https://en.wikivet.net/api.php?action=feedcontributions&feedformat=atom&user=Stuartd 2026-05-02T16:16:10Z User contributions MediaWiki 1.35.0 https://en.wikivet.net/index.php?title=Coccidia_-_Poultry&diff=72325 2010-07-14T17:12:35Z

<p>Stuartd: </p> <hr /> <div>[[Image:Buff orpington.jpg|thumb|right|150px|Buff orpington - nabrown RVC]]<br /> [[Image:Eimeria Sporulated.jpg|thumb|right|150px|Sporulated ''Eimeria'' - Joaquim Castellà Veterinary Parasitology Universitat Autònoma de Barcelona]]<br /> <br /> Domestic poultry and birds are affected by coccidia called Eimeria. Different species of Eimeria that effect poultry are host-specific – meaning that a species that infects chickens does not infect turkeys and vice versa.<br /> <br /> Nine species of Eimeria infect chickens. The species important in broiler production include Eimeria tenella (90%), E. maxima, E. acervulina, and E. mivati; the species important in breeder and egg- layers are E. burnetti and E. necatrix. Seven species infect turkeys – the big three of concern are Eimeria meleagrimitis, E. adenoeides, and E. gallapovonis.<br /> <br /> *Direct life cycle<br /> <br /> *1 week prepatent period<br /> <br /> *After oocysts are ingested, sporozoites are released which penetrate the intestinal epithelium<br /> <br /> *2 asexual phases of multiplication called schizogony occur followed by a phase of sexual multiplication called gametogony<br /> <br /> *Zygote develops into an oocyst which is then shed in the faeces<br /> **Oocyst measures 20-30μm<br /> <br /> *For each oocyst ingested, thousands are shed<br /> <br /> *Life cycle is '''self-limiting'''<br /> **Organisms from a single infection go through the sequence of developmental stages synchronously<br /> **Organisms leave the body simultaneously as oocysts<br /> <br /> *Oocysts are only infective once they have sporulated<br /> **Sporulation requires warmth, moisture and oxygen<br /> **Takes 2-3 days in broiler houses<br /> <br /> *Oocysts contain 4 sporocysts each with 2 sporozoites<br /> <br /> [[Category:Coccidia]][[Category:Poultry]]<br /> [[Category:To_Do_-_Stuartd]]</div>

Stuartd https://en.wikivet.net/index.php?title=Coccidiosis&diff=72307 2010-07-14T16:48:38Z

<p>Stuartd: </p> <hr /> <div>== Coccidiosis ==<br /> Coccidiosis is the disease caused by coccidian infection. Coccidiosis is a parasitic disease of the intestinal tract of animals, caused by coccidian [[protozoa]]. The disease spreads from one animal to another by contact with infected faeces or ingestion of infected tissue. The primary sympton is usally watery [[Diarrhoea|diarrhoea]], dysentery and weight loss. It usually presents in young animals which are living in overcrowded and unhygienic conditions. Most adult animals infected with coccidia are asymptomatic; however, immuno-compromised animals may suffer severe symptoms, including death. <br /> <br /> Pathogenicity of coccidiosis is related to the size of the endogenous stages, the location of the infection in the mucosa and the site of infection. For example, infection in the small intestine can lead to compensation whereas infection in the large intestine will affect water absorption. If mucosal stem cells are affected, it will cause villous atrophy and a prolonged recovery.<br /> <br /> While coccidian organisms can infect a wide variety of animals, including humans, birds, and livestock, they are usually species-specific. One well-known exception is [[toxoplasmosis]], caused by ''Toxoplasma gondii''.<br /> <br /> Species specific descriptions of the disease are found on individual wikivet pages.<br /> <br /> [[Category:Coccidia]]<br /> [[Category:To_Do_-_Review]]</div>

Stuartd https://en.wikivet.net/index.php?title=Enteritis,_Parasitic&diff=72295 2010-07-14T16:35:29Z

<p>Stuartd: </p> <hr /> <div>[[Image:trichuris ovis.jpg|thumb|right|150px|Trichuris ovis in the sheep caecum (Courtesy of Bristol BioMed Image Archive)]]<br /> [[Image:trichuris vulpis caecum.jpg|thumb|right|150px|Trichuris vulpis in the caecum (Courtesy of Bristol BioMed Image Archive)]]<br /> [[Image:trichuris vulpis caecum comparative.jpg|thumb|right|150px|Comparison- caecum unaffected and affected by Trichuris vulpis (Courtesy of Bristol BioMed Image Archive)]]<br /> * This is the most important condition causing cattarhal enteritis worldwide. <br /> * Seen mainly in grazing animals.<br /> ** Especially in sheep - causes large production losses. <br /> * Particularly problematic since some parasites are resistant to anthelmintics.<br /> ** Especially in Australia.<br /> ** e.g. [[Nematodirus|''Nematodirus'']] and [[Trichuris|''Trichuris'']].<br /> * A pre-patent period of 7-10 days is followed by the development of greenish [[Diarrhoea|diarrhoea]].<br /> ** The gut becomes filled with greenish soupy material.<br /> ** Oedema and hyperaemia of mucosa occurs.<br /> * In young animals, parasites can cause serious disease and even death.<br /> <br /> [[Category:Enteritis, Catarrhal]]<br /> [[Category:Enteritis,_Parasitic]]<br /> [[Category:To_Do_-_Stuartd]]</div>

Stuartd https://en.wikivet.net/index.php?title=Enteritis,_Lymphocytic_-_Plasmacytic&diff=72294 2010-07-14T16:34:58Z

<p>Stuartd: </p> <hr /> <div>{{unfinished}}<br /> <br /> {{dog}}<br /> {{cat}}<br /> <br /> <br /> ==Signalment==<br /> *Often affects older animals but kittens of 16 weeks old and puppies of 20 weeks old have been reported. <br /> *Basenjis have been reported to suffer from a severe form known as immunoproliferative disease.<br /> <br /> <br /> ==Description==<br /> '''Lymphocytic - plasmacytic enteritis (LPE)''' is the most common form of [[Inflammatory Bowel Disease|Inflammatory Bowel Disease]] (IBD). As its name suggests, the predominant cell type in the intestinal mucosa is [[Lymphocytes|'''lymphocytes''']] and '''plasma cells'''. Enteric parasites, bacteria in dogs and [[Toxoplasma|''Toxoplasma'']] in cats have been reported to associated with LPE. This disorder in cats have also been shown to associate with concurrent disease of the pancreas and liver such as [[Pancreatitis - Dog and Cat|pancreatitis]], [[Cholangitis|cholangitis]] and [[Hepatic Lipidosis|hepatic lipidosis]]. LPE is believed to be caused by an abnormal [[Regional Lymphoid Tissue - Anatomy &amp; Physiology|mucosal associated lymphoid tissue (MALT)]] response to luminal bacterial, dietary or self-antigens. <br /> <br /> The [[Small Intestine - Anatomy &amp; Physiology|small intestines]] are affected to a variable degree of severity. It has also been known to affect other parts of the gastrointestinal tract such as the [[:Category:Stomach and Abomasum - Pathology|stomach]] and the [[Colon - Anatomy &amp; Physiology|colon]]. In severely affected animals, this will result in a protein-losing enteropathy (PLE).<br /> <br /> ==Diagnosis==<br /> ===Clinical Signs===<br /> Most common:<br /> *small intestinal diarrhoea<br /> *weight loss<br /> *protein - losing enteropathy in severe cases<br /> *chronic vomiting (more common presentation in cats compared to the other signs)<br /> *thickened small intestinal loops and mesenteric lymphadenopathy may be detected on physical examination in cats<br /> <br /> Others:<br /> *appetite changes<br /> *excessive borborygmi<br /> *abdominal discomfort<br /> *ascites or subcutaneous oedema if severe PLE resulting in hypoproteinaemia<br /> *concurrent systemic immune-mediated response and [[Thromboembolism|thromboembolism]] (rare)<br /> <br /> ===Laboratory Tests===<br /> ====Haematology====<br /> *Panhypoproteinaemia (non-specific)<br /> <br /> ====Biochemistry====<br /> *Leucocytosis (non-specific)<br /> <br /> ====Other Tests====<br /> *Serum trypsin-like immunoassay (TLI) to rule out [[Exocrine Pancreatic Insufficiency|exocrine pancreatic insufficiency (EPI)]].<br /> *Faecal analysis to rule out endoparasite and pathogenic bacteria.<br /> <br /> ===Diagnostic Imaging===<br /> *Abdominal radiography is unremarkable, but it can be used to eliminate other differential diagnosis.<br /> *Abdominal ultrasonography may reveal thickened intestinal walls, mesenteric lymphadenopathy or abdominal effusion.<br /> <br /> ===Histopathology===<br /> Intestinal biopsy is needed for a definitive diagnosis once all the other differential diagnoses have been eliminated.<br /> <br /> Refer to [[Inflammatory Bowel Disease#Lymphocytic - Plasmacytic Enteritis|Lymphocytic - Plasmacytic Enteritis]] for pathology.<br /> <br /> <br /> ==Treatment==<br /> Refer to [[Inflammatory Bowel Disease#Treatment|IBD]]<br /> <br /> ==Prognosis==<br /> Refer to [[Inflammatory Bowel Disease#Prognosis|IBD]]<br /> <br /> <br /> ==References==<br /> *Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2''' (Fifth Edition) ''W.B. Saunders Company''.<br /> *Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''<br /> *Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine (Fourth Edition)''' ''Mosby Elsevier''.<br /> <br /> ==Lymphocytic - Plasmacytic Enteritis== <br /> <br /> ====Pathology====<br /> <br /> * Hypersensitivity reaction results in increased GIT permeablility and recruitment of inflammatory cells. <br /> * Histologically:<br /> ** Mucosal epithelial-glandular alterations.<br /> ** Variably increased mucosal infiltrate of lymphocytes and plasma cells.<br /> *** In these dogs there is an increase in the number of [[IgA]] and [[IgG]] containing cells and CD3+ T-cells.<br /> **** Can develop into lymphoma.<br /> *** Changes in the relative and absolute numbers of plasma cells and lymphocytes have been associated with IBD in humans.<br /> <br /> [[Category:Intestine_-_Inflammatory_Pathology_by_Type]][[Category:To_Do_-_Stuartd]]</div>

Stuartd https://en.wikivet.net/index.php?title=Enteritis,_Eosinophilic_Idiopathic&diff=72292 2010-07-14T16:34:11Z

<p>Stuartd: </p> <hr /> <div>==Idiopathic Eosinophilic Enteritis==<br /> <br /> *Dairy cows<br /> *Thickened [[Small Intestine - Anatomy &amp; Physiology|small intestine]], mesenteric lymphadenopathy.<br /> *[[Small Intestine - Anatomy &amp; Physiology|small intestine]]<br /> **Marked oedema, lymphangiectasia without vasculitis<br /> **Eosinophilic infiltration of the intestinal mucosa (esp. at the villus tip).<br /> *Eosinophilic enteritis associated with hypoalbuminaemia, hypoglobulinaemia and eosinophilia in other species. The extent of the biochemical changes reflect the extent of the histological changes in the gut. <br /> **Not so in these cases.<br /> *In man, eosinophilic enteritis called if ≥20 eosinophils per HPF in the gut.<br /> *No cause in these cattle found … although loweed ingestion can cause eosinophilic gastroenteritis.<br /> <br /> [Idiopathic eosinophilic enteritis in 4 cattle. JAVMA (1998) 212 258-61]<br /> [[Category:Cattle]][[Category:Intestine_-_Inflammatory_Pathology_by_Type]]<br /> [[Category:To_Do_-_Stuartd]]</div>

Stuartd https://en.wikivet.net/index.php?title=Enteritis,_Eosinophilic&diff=72291 2010-07-14T16:33:50Z

<p>Stuartd: </p> <hr /> <div>{{unfinished}}<br /> <br /> {{dog}}<br /> {{cat}}<br /> <br /> <br /> ==Signalment==<br /> *Seen in any breed or age<br /> *However, more common in younger animal<br /> *More common in<br /> **Boxers<br /> **Dobermans<br /> **German Shepherd Dogs<br /> <br /> <br /> ==Description==<br /> '''Eosinophilic enteritis (EE)''' is the second most common form of IBD, characterised by a mixed, but predominantly eosiphilic, mucosal inflammatory infiltration. EGE may be limited to the small intestine or it may affect other areas of the gastrointestinal tract such as stomach or colon.<br /> <br /> An eosinophilic infiltrate may indicate a diet-induced, type 1 hypersensitivity. However, most dogs do not respond to a purely exclusion diet. Endoparasitism should also be excluded prior to immunosuppressive therapy for EE.<br /> <br /> ==Diagnosis==<br /> ===Clinical Signs===<br /> *Vomiting<br /> *Diarrhoea; small intestinal is more common<br /> **Haematoemesis or malena, and/or haematochezia; EGE is associated with mucosal erosion or ulceration<br /> *Protein-losing enteropathy in severe cases<br /> *Hypoproteinaemia in severe casese<br /> <br /> <br /> <br /> ===Laboratory Tests===<br /> ====Haematology====<br /> *Anaemia if gastrointestinal haemorrhage is severe.<br /> <br /> ====Biochemistry====<br /> *Eosinophilia<br /> **This is not always present. Even when present, alone, it cannot prove the presence of EE.<br /> **It is also a marker for parasitism, hypoadrenocorticism, allergic dermatological disease, allergic respiratory disease and mast cell tumour.<br /> *Panhypoproteinaemia<br /> **Secoondary to concurrent protein-losing enteropathy<br /> <br /> <br /> ===Diagnostic Imaging===<br /> *Endoscopically, linear ulcers within the duodenal mucosa may be seen grossly.<br /> <br /> <br /> ===Histopathology===<br /> Biopsy is required for a definitive diagnosis.<br /> <br /> ==Treatment==<br /> *Anti-parasiticide<br /> **Fenbendazole may be given due to the possible endoparasitism or dietary sensitivity<br /> *Dietary modification<br /> **A hypoallergenic diet should be used<br /> *Immunosuppressive therapy<br /> <br /> Refer to [[Inflammatory Bowel Disease#Treatment|IBD]] for further information<br /> <br /> <br /> ==Prognosis==<br /> Guarded if the initial response to treatment is poor. Good if the underlying cause is detected and successfully treated.<br /> <br /> <br /> ==References==<br /> *Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2''' (Fifth Edition) ''W.B. Saunders Company''.<br /> *Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''<br /> *Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine (Fourth Edition)''' ''Mosby Elsevier''.<br /> <br /> <br /> ==Eosinophilic Enteritis==<br /> <br /> * Can be either focal or diffuse.<br /> <br /> ===Focal===<br /> <br /> * A disease of young dogs.<br /> * Associated with [[Toxocara canis|''Toxocara canis'']] infection.<br /> ** Pin-head sized white nodules can be seen under the serosa in the bowel.<br /> *** Consist of of eosinophils and occasionally macrophages and plasma cells.<br /> *** Can sometimes see [[Toxocara canis|''Toxocara'']] larvae in the nodules.<br /> <br /> ===Diffuse===<br /> <br /> * Seen in the dog, cat and horse.<br /> * Idiopathic<br /> * Has a predilection for German Shepherd Dogs, but also occcurs in other breeds of dogs and in cats.<br /> ** Recurrent episodes of diarrhoea with tissue and circulatory eosinophilia.<br /> *** Eosinophils heavily infiltrate all layers of stomach and intestines.<br /> **It has been suggested that it is a type of hypersensitivity reaction.<br /> <br /> <br /> [[Image:eosinophilic_enteritis.jpg|thumb|right|150px|Eosinophilic enteritis - horse(Courtesy of Susan Rhind, University of Edinburgh)]]<br /> [[Category:Dog]][[Category:Intestine_-_Inflammatory_Pathology_by_Type]][[Category:To_Do_-_Stuartd]]</div>

Stuartd https://en.wikivet.net/index.php?title=Coccidiosis_-_Turkey&diff=72290 2010-07-14T16:33:07Z

<p>Stuartd: </p> <hr /> <div>*5 ''[[Eimeria spp.|Eimeria]]'' species<br /> **2 important pathogenically<br /> <br /> *''[[Eimeria spp.|Eimeria]]'' in [[Caecum - Anatomy &amp; Physiology|caeca]] causes petechial haemorrhages and caseous [[Caecum - Anatomy &amp; Physiology|caecal]] cores<br /> <br /> *''[[Eimeria spp.|Eimeria]]'' in the anterior and mid-intestine causes necrotic enteritis and petechial haemorrhages<br /> <br /> *Causes watery [[Diarrhoea|diarrhoea]] in young poults and some mortality<br /> <br /> [[Coccidiosis]]<br /> <br /> [[Category:Coccidia]][[Category:Avian]]<br /> [[Category:To_Do_-_Stuartd]]</div>

Stuartd https://en.wikivet.net/index.php?title=Coccidiosis_-_Sheep&diff=72289 2010-07-14T16:32:46Z

<p>Stuartd: </p> <hr /> <div>*11 different Coccidia species although only two are of clinical significance<br /> **Giant schizonts visible as white spots<br /> <br /> *''[[Eimeria spp.|Eimeria]] ovinoidalis''<br /> **Highly pathogenic<br /> **[[Diarrhoea|Diarrhoea]]<br /> **Parasitises the [[Caecum - Anatomy &amp; Physiology|caecum]] and [[Colon - Anatomy &amp; Physiology|colon]]<br /> <br /> *''[[Eimeria spp.|Eimeria]] crandalis''<br /> **Varying pathogenicity<br /> **Scours, grey, foul-smelling faeces<br /> **Parasitises the [[Small Intestine - Anatomy &amp; Physiology|small intestine]], [[Caecum - Anatomy &amp; Physiology|caecum]] and [[Colon - Anatomy &amp; Physiology|colon]]<br /> <br /> *2 week prepatent period<br /> <br /> *Disease frequently seen in lambs under 6 months old<br /> **More often in twins and triplets when single lambs<br /> <br /> *Oocyts from ewes (immune carriers) accumulate in poorly managed litter or around feed and water troughs<br /> <br /> *Lambs born early in the year amplify the parasite problem increasing the parasite risk to lambs born later in the year<br /> <br /> *Affected lambs may die before oocysts are found in the faeces<br /> **Post-mortem diagnosis difficult<br /> <br /> *Different species of ''[[Eimeria spp.|Eimeria]]'' occurs in sheep and goats<br /> <br /> *Infection may be coincident with ''Neospora'' or ''Cryptosporidium'' infections<br /> **Mixed infections complicate the diagnosis as oocyst differentiation is difficult<br /> <br /> *Other non-pathogenic species can cause papillomatous mucosal growths<br /> <br /> '''Control'''<br /> *Improve husbandry<br /> **Avoid overcrowding<br /> **Decrease stress<br /> <br /> *Improve hygiene by dagging ewes<br /> <br /> *Avoid mixing lambs of different ages<br /> <br /> *Preventative measures include creep feeding lambs with decoquinate or oral dosing with diclazuril when lambs are 4-6 weeks<br /> **A second dose can be given after 3 weeks[[Category:Coccidia]][[Category:Sheep]]<br /> [[Category:To_Do_-_Stuartd]]</div>

Stuartd https://en.wikivet.net/index.php?title=Coccidiosis_-_Rabbit&diff=72287 2010-07-14T16:32:24Z

<p>Stuartd: </p> <hr /> <div>*3 pathogenic ''[[Eimeria spp.|Eimeria]]'' species<br /> **2 in the [[Caecum - Anatomy &amp; Physiology|caecum]]<br /> **1 in the bile duct<br /> <br /> *''[[Eimeria spp.|Eimeria]] steidae''<br /> **Parasitises the bile duct epithelium<br /> **Travels via the bile duct to the [[Liver - Anatomy &amp; Physiology|liver]] where it forms large white nodules<br /> **Oocysts travel in the bile and are passed out in the faeces<br /> **Causes ascites, [[Diarrhoea|diarrhoea]], weight loss and polyuria<br /> <br /> *Serious disease of both pet and farmed rabbits<br /> <br /> *Treatment is by administration of drugs in drinking water<br /> **E.g. Toltrazuril<br /> <br /> *Hygiene is the best method of prevention to prevent sporocysts from sporulating<br /> <br /> *Medicated feed can be used in commercial units<br /> **E.g. Rabenidine<br /> [[Category:Coccidia]][[Category:Rabbit]]<br /> [[Category:To_Do_-_Stuartd]]</div>

Stuartd https://en.wikivet.net/index.php?title=Coccidiosis_-_Poultry&diff=72286 2010-07-14T16:32:03Z

<p>Stuartd: </p> <hr /> <div>[[Coccidia - Poultry]]<br /> <br /> '''Pathogenesis'''<br /> *7 important ''[[Eimeria spp.|Eimeria]]'' species<br /> <br /> *4 malabsorptive species<br /> **''[[Eimeria spp.|Eimeria]] acervulina'' which is moderately pathogenic<br /> **''[[Eimeria spp.|Eimeria]] maxima'' which is moderately pathogenic<br /> **''[[Eimeria spp.|Eimeria]] mitis'' which has low pathogenicity<br /> **''[[Eimeria spp.|Eimeria]] praecox'' which has low pathogenicity<br /> <br /> *3 haemorrhagic species<br /> **''[[Eimeria spp.|Eimeria]] tenella''<br /> **''[[Eimeria spp.|Eimeria]] necatrix''<br /> **''[[Eimeria spp.|Eimeria]] brunetti''<br /> **All highly pathogenic<br /> **Form large sub-epithelial second generation schizonts at the base of intestinal crypts<br /> **Deep eruptions form when cells rupture to release merozoites<br /> **Destruction of crypt stem cells and marked haemorrhage<br /> **Blood stained faeces<br /> **High morbidity and high mortality<br /> <br /> '''Diagnosis'''<br /> *Post-mortem diagnosis of lesion severity<br /> **Region of intestine affected<br /> **Appearance of lesion<br /> **Presence or absence of haemorrhage<br /> **Size of schizonts and oocysts found in mucosal scrapings<br /> <br /> *''[[Eimeria spp.|Eimeria]] acervulina'' <br /> **Proximal gut <br /> **Thickening of walls<br /> **'White ladder lesions' produced by dense foci of gamonts and oocysts<br /> **Watery exudate<br /> <br /> *''[[Eimeria spp.|Eimeria]] maxima''<br /> **Mid-gut<br /> **Thickening of walls<br /> **Pink exudate <br /> <br /> *''[[Eimeria spp.|Eimeria]] tenella''<br /> **Swollen [[Caecum - Anatomy &amp; Physiology|caeca]]<br /> **Thickening of wall<br /> **Dark colouring containing a core of necrotic tissue and blood<br /> <br /> *Lesion scoring is the best method of diagnosing the severity of the lesions and therefore the causative ''[[Eimeria spp.|Eimeria]]'' species<br /> <br /> *''[[Eimeria spp.|Eimeria]] necatrix''<br /> **Mid-gut<br /> **Ballooning of wall<br /> **White spots and petechiae forming 'salt and pepper' lesions<br /> **Haemorrhage into lumen<br /> <br /> '''Immunity'''<br /> *Different ''[[Eimeria spp.|Eimeria]]'' species produce different levels of protective immunity<br /> **''E.maxima'' -&gt; ''E.brunetti'' and ''E.acervulina'' -&gt; ''E.tenella'' and ''E.necatrix''<br /> <br /> *There is no cross immunity between species<br /> <br /> *There is very little passive immunity<br /> <br /> *Evokes a cell-mediated response<br /> <br /> *All ages of poultry are susceptible<br /> <br /> '''Epidemiology'''<br /> *Oocysts are ubiquitous and robust<br /> **Able to survive several months to years<br /> <br /> *It is impossible to keep buildings free from infection<br /> **Chicks become infected by pecking the ground shortly after being placed in the poultry house<br /> <br /> *Biotic potential is enormous<br /> **Generation time is short<br /> **Massive infections can build up rapidly<br /> <br /> *Immunity develops relatively slowly<br /> **With high stocking densities the situation is explosive<br /> <br /> '''Control'''<br /> *Chemical<br /> **Intensive poultry production is largely dependent on the use of anticoccidial drugs<br /> **For more information see [[Anti-Protozoal Drugs|here]]<br /> <br /> *[[Vaccines - WikiBlood|Vaccines]]<br /> **Paracox<br /> ***Multivalent attenuated [[Vaccines - WikiBlood#What antigen(s) do we use in the vaccine?|live vaccine]] for replacement layers and broilers<br /> ***Contains 7 live strains of ''[[Eimeria spp.|Eimeria]]''<br /> ***Lack the most pathogenic life cycle stage making the prepatent period shorter<br /> ***Known as '''precocious''' strains<br /> ***Chicks [[Vaccines - WikiBlood|vaccinated]] on a single occasion when 1-9 days old through oocyst suspension in the feed or water<br /> ***[[Vaccines - WikiBlood|Vaccinated]] birds have sub-optimal growth rates so is not used for broilers<br /> **Paracox 5<br /> ***Contains 5 strains of the most pathogenic ''[[Eimeria spp.|Eimeria]]''<br /> ***Used for broilers<br /> ***Sprayed onto the first feed offered to new batches of chicks<br /> <br /> *Integrated control<br /> **Careful management is needed so in-feed prophylaxis and [[Vaccines - WikiBlood|vaccination]] do not fail<br /> **Remove litter and thoroughly clean houses in between crops<br /> ***Optimum turn-around time is 10 days<br /> **Use the lowest stocking density which is compatible with economic production<br /> **Water bowls, roofs and walls should be well maintained to prevent litter becoming damp<br /> **Stress factors should be avoided and adequate nutrition provided[[Category:Coccidia]][[Category:Poultry]]<br /> [[Category:To_Do_-_Stuartd]]</div>

Stuartd https://en.wikivet.net/index.php?title=Coccidiosis_-_Pig&diff=72285 2010-07-14T16:31:36Z

<p>Stuartd: </p> <hr /> <div>[[Image:Isospora suis oocyst.jpg|thumb|right|150px|''Isospora suis'' oocyst from pig faeces - Joaquim Castellà Veterinary Parasitology Universitat Autònoma de Barcelona]]<br /> *Many species of ''[[Eimeria spp.|Eimeria]]'' and ''[[Isospora spp.|Isospora]]''<br /> <br /> *Only ''[[Isospora spp.|Isospora]] suis'' is of clinical pathogenic importance<br /> <br /> *Causes sporadic, serious and sometimes fatal disease in unweaned piglets<br /> **Causes profuse [[Diarrhoea|diarrhoea]]<br /> <br /> *Very short 1 week prepatent period <br /> <br /> *[[Diarrhoea|Diarrhoea]] starts before oocysts are shed in faeces<br /> **Ante-mortem diagnosis is difficult<br /> <br /> *Death usually occurs after parasites have left the host<br /> **Post-mortem diagnosis difficult<br /> **''[[Isospora spp.|Isospora]]'' infections are '''self-limiting'''<br /> [[Category:Coccidia]][[Category:Pig]]<br /> [[Category:To_Do_-_Stuartd]]</div>

Stuartd https://en.wikivet.net/index.php?title=Coccidiosis_-_Horse&diff=72284 2010-07-14T16:31:15Z

<p>Stuartd: </p> <hr /> <div>[[Image:Eimeria leukarti horse.jpg|thumb|right|150px|''Eimeria leukarti'' - Joaquim Castellà Veterinary Parasitology Universitat Autònoma de Barcelona]]<br /> *Only one atypical ''[[Eimeria spp.|Eimeria]]''<br /> <br /> *Forms large subepithelial gametocytes in villi<br /> <br /> *Large, dark coloured oocysts<br /> **Approximately 12μm<br /> <br /> *Occasionally causes [[Diarrhoea|diarrhoea]]<br /> <br /> *'''''Besnoitia bennetti''''' in [[Respiratory Parasitic Infections - Pathology#Besnoitia bennetti|larynx]] of horses<br /> **Papilloma like lesions in [[Larynx Inflammatory - Pathology#Infectious causes of laryngitis|larynx]], skin and sclera<br /> **Thick walled parasitic cysts, covered by hyperplastic epithelium, may be ulcerated<br /> <br /> <br /> <br /> <br /> <br /> <br /> [[Category:Coccidia]][[Category:Horse]]<br /> [[Category:To_Do_-_Stuartd]]</div>

Stuartd https://en.wikivet.net/index.php?title=Coccidiosis_-_Goat&diff=72283 2010-07-14T16:30:56Z

<p>Stuartd: </p> <hr /> <div>[[Image:Goats.jpg|thumb|right|150px|Goats - nabrown RVC]]<br /> *Many ''[[Eimeria spp.|Eimeria]]'' species<br /> <br /> *2 ''[[Eimeria spp.|Eimeria]]'' are pathogenic<br /> **Cause [[Diarrhoea|diarrhoea]] and a decreased growth rate<br /> <br /> *Different species of ''[[Eimeria spp.|Eimeria]]'' occurs in sheep and goats[[Category:Coccidia]][[Category:Goat]]<br /> [[Category:To_Do_-_Stuartd]]</div>

Stuartd https://en.wikivet.net/index.php?title=Coccidiosis_-_Geese&diff=72282 2010-07-14T16:30:39Z

<p>Stuartd: </p> <hr /> <div>*3 ''[[Eimeria spp.|Eimeria]]'' species<br /> <br /> *2 intestinal species causing macroscopic lesions in [[Urinary System - Anatomy &amp; Physiology#The Kidney|kidney tubules]]<br /> **Oocysts carried in urine and pass out with faeces<br /> <br /> *Renal species cause severe disease in goslings<br /> **Depression, emaciation, [[Diarrhoea|diarrhoea]] and sometimes death[[Category:Avian]][[Category:Coccidia]]<br /> [[Category:To_Do_-_Stuartd]]</div>

Stuartd https://en.wikivet.net/index.php?title=Coccidiosis_-_Game_Birds&diff=72281 2010-07-14T16:30:17Z

<p>Stuartd: </p> <hr /> <div>*3 main species<br /> <br /> *[[Caecum - Anatomy &amp; Physiology|Caecal]] species most pathogenic causing white [[Caecum - Anatomy &amp; Physiology|caecal]] cores[[Category:Coccidia]][[Category:Avian]]<br /> [[Category:To_Do_-_Stuartd]]</div>

Stuartd https://en.wikivet.net/index.php?title=Coccidiosis_-_Duck&diff=72280 2010-07-14T16:29:56Z

<p>Stuartd: </p> <hr /> <div>[[Image:Crested duck.jpg|thumb|right|150px|Crested duck - nabrown RVC]]<br /> *Several ''[[Eimeria spp.|Eimeria]]'' species<br /> <br /> *Another coccidia species which produces 8 sporozoites but these are not enclosed in a sporocyst<br /> <br /> *Causes severe enteritis and mortality in ducklings<br /> **Haemorrhages and pale focal lesions in [[Small Intestine - Anatomy &amp; Physiology|small intestine]] [[Category:Coccidia]][[Category:Avian]]<br /> [[Category:To_Do_-_Stuartd]]</div>

Stuartd https://en.wikivet.net/index.php?title=Coccidiosis_-_Cattle&diff=72279 2010-07-14T16:29:24Z

<p>Stuartd: </p> <hr /> <div>[[Image:Coccidia ruminant.jpg|thumb|right|150px|''Eimeria'' sp. of ruminants - Joaquim Castellà Veterinary Parasitology Universitat Autònoma de Barcelona]]<br /> [[Image:Coccidia oocyst ruminant.jpg|thumb|right|150px|Coccidia oocyst from ruminant faeces - Joaquim Castellà Veterinary Parasitology Universitat Autònoma de Barcelona]]<br /> *Many species affect cattle<br /> <br /> *Cattle under a year old are usually infected sporadically<br /> <br /> *2-3 week prepatent period<br /> <br /> *''Eimeria bovis''<br /> **Endogenous stages in central lacteal of villi and epithelial cells of [[Caecum - Anatomy &amp; Physiology|caecum]] and [[Colon - Anatomy &amp; Physiology|colon]]<br /> **Causes [[Diarrhoea|diarrhoea]] and enteritis<br /> **Oocysts are 28x20μm<br /> **Moderately pathogenic<br /> <br /> *''Eimeria zuernii''<br /> **Endogenous stages in connective tissue of lamina propria of the lower [[Small Intestine - Anatomy &amp; Physiology|small intestine]] and in the epithelial cells of the [[Caecum - Anatomy &amp; Physiology|caecum]] and [[Colon - Anatomy &amp; Physiology|colon]]<br /> **More pathogenic than ''Eimeria bovis''<br /> **Causes blood stained dysentery, tenesmus and sloughed mucosa<br /> **Oocysts are spherical and measure 16μm<br /> <br /> *Mainly occurs in calves in poor conditions and bought-in calves<br /> **Also occurs in suckler calves turned out in spring<br /> <br /> *''Eimeria alabamensis'' associated with [[Diarrhoea|diarrhoea]] in calves after spring turnout<br /> <br /> *[[Materno-fetal immunity - WikiBlood#Passive transfer via colostrum|Passive immunity]] is sufficient during the neonatal period<br /> <br /> *Can be concurrent with cryptosporidium, viral and bacterial agents<br /> <br /> '''Diagnosis'''<br /> *History, clinical signs, [[Diarrhoea|diarrhoea]] (often with blood) and a decrease in weight gain<br /> <br /> *Post-mortem<br /> **Diffuse inflammation and thickening of [[Caecum - Anatomy &amp; Physiology|caecal]] mucosa (and sometimes [[Ileum - Anatomy &amp; Physiology|ileal]] and [[Colon - Anatomy &amp; Physiology|colonic]] mucosa)<br /> **Masses of gamonts and oocysts in scrapings<br /> <br /> *High faecal oocyst count<br /> **However, healthy animals can pass millions of oocysts from mixed species infections which have no pathogenic significance<br /> **Animals may die before oocysts are shed<br /> <br /> '''Control'''<br /> *Improve husbandry<br /> **Improve sanitation<br /> **Increase bedding<br /> **Raise food and water troughs to avoid faecal contamination<br /> <br /> *Preventative in-feed medication<br /> **E.g. Decoquinate<br /> <br /> *Injectable antiprotozoals may limit oocyst production but animals should still be moved to a clean environment<br /> **E.g. Sulphamethoxypyridazine[[Category:Coccidia]][[Category:Cattle]]<br /> [[Category:To_Do_-_Stuartd]]</div>

Stuartd https://en.wikivet.net/index.php?title=Coccidiosis_-_Dog&diff=72278 2010-07-14T16:28:53Z

<p>Stuartd: </p> <hr /> <div>[[Image:Isospora canis.jpg|thumb|right|150px|''Isospora canis'' - Joaquim Castellà Veterinary Parasitology Universitat Autònoma de Barcelona]]<br /> *2 common and 2 less common ''[[Isospora spp.|Isospora]]'' species<br /> <br /> *Occasionally can cause disease<br /> <br /> *Little pathogenicity<br /> <br /> *Even if faecal oocyst count is high, other causes of [[Diarrhoea|diarrhoea]] should be looked for<br /> <br /> *''Hepatozoon americanum'' and subclinical ''H. canis'' in [[Bones Hyperplastic and Neoplastic - Pathology#Hepatozoon|periosteal bone formation]]<br /> **Both are Tick borne diseases<br /> ***''H. canis'' – ''Rhipicephalus sanguineus''<br /> ***Ticks become infected by ingesting a blood meal containing macrophages and [[Neutrophils|neutrophils]] infected with the parasite gamonts -&gt; sexual replication in the gut of the tick -&gt; oocysts containing infective sporozoites -&gt; dogs ingest the tick  schizogony occurs in numerous tissues[[Category:Coccidia]]<br /> [[Category:Dog]<br /> [[Category:To_Do_-_Stuartd]]</div>

Stuartd https://en.wikivet.net/index.php?title=Coccidiosis_-_Cat_%26_Dog&diff=72277 2010-07-14T16:28:20Z

<p>Stuartd: </p> <hr /> <div>[[Image:Isospora felis sporulated.jpg|thumb|left|150px|''Isospora felis'' sporulated - Courtesy of the Laboratory of Parasitology, University of Pennsylvania School of Veterinary Medicine]][[Image:Isospora felis.jpg|thumb|right|150px|''Isospora felis'' - Joaquim Castellà Veterinary Parasitology Universitat Autònoma de Barcelona]]<br /> [[Image:Isospora felis unsporulated.jpg|thumb|left|150px|''Isospora felis'' unsporulated - Courtesy of the Laboratory of Parasitology, University of Pennsylvania School of Veterinary Medicine]][[Image:Coccidia.jpg|thumb|right|150px|Coccidia in Cat Faeces - Joel Mills]]<br /> <br /> *2 common ''Isospora'' species with little clinical significance<br /> <br /> *Oocysts in faeces have to be distinguised from those of ''Toxoplasma'' (smaller) and ''Sarcocytis'' (sporulated or naked sporocyts in faeces)[[Category:Coccidia]][[Category:Cat]]<br /> [[Category:To_Do_-_Stuartd]]</div>

Stuartd https://en.wikivet.net/index.php?title=Coccidiosis&diff=72275 2010-07-14T16:27:22Z

<p>Stuartd: </p> <hr /> <div>Poultry coccidiosis is caused by ''[[Eimeria spp.|Eimeria]]'' species. The poultry industry has grown to its massive size through the development and administration of anticoccidial drugs. Most growing birds are fed compounded rations containing anticoccidial drugs which has radically reduced the deaths from coccidiosis bringing the mortality rate down to negligible levels. Careful management is needed to prevent decreased productivity from infection through decreased egg production, weight gain and feed conversion ratios.<br /> <br /> Mammalian coccidiosis is usually associated with watery [[Diarrhoea|diarrhoea]], dysentery and weight loss. It usually presents in young animals which are living in overcrowded and unhygienic conditions.<br /> <br /> Pathogenicity of coccidiosis is related to the size of the endogenous stages, the location of the infection in the mucosa and the site of infection. For example, infection in the small intestine can lead to compensation whereas infection in the large intestine will affect water absorption. If mucosal stem cells are affected, it will cause villous atrophy and a prolonged recovery.<br /> [[Category:Coccidia]]<br /> [[Category:To_Do_-_Stuartd]]</div>

Stuartd https://en.wikivet.net/index.php?title=Gastric_Dilatation_and_Volvulus&diff=70115 2010-07-05T16:28:15Z

<p>Stuartd: </p> <hr /> <div>{{unfinished}}<br /> <br /> {|cell padding=''10'' cellspacing=''0'' border=''1''<br /> |Also known as:<br /> |'''GDV&lt;br&gt;<br /> |-|}<br /> <br /> ==Signalment==<br /> *Large deep chested breeds including:<br /> <br /> Akitas, Bloodhounds, Collies, Great Danes, Irish Setters, Wolfhounds, Newfoundlands, Rottweilers, Saint Bernards, Standard Poodles, Weirmaraners<br /> <br /> <br /> ==Description==<br /> Gastric dilatation (GD) and Gastric dilatation and volvulus (GDV) are caused by the stomach distending with air. In GDV the stomach twists around its axis mainly in a clockwise direction with both conditions leading to compression of the caudal vena cava. GDV can lead to [[Shock - Pathology#Hypovolaemic shock|hypovolaemic shock]], splenic torsion, gastric wall ischaemia, abdominal viscera congestion, [[Shock - Pathology#Endotoxic shock|endotoxic shock]] and [[Disseminated Intravascular Coagulation|disseminated intravascular coagulation (DIC)]]. The exact pathogenesis is unclear but risk factors for GDV include age, fast eating, once- daily feeding, aerophagia, raised feeding bowl and a close relative with GDV.<br /> <br /> ==Diagnosis==<br /> ===History and Clinical signs===<br /> *Abdominal distension<br /> *Non-productive retching<br /> *Weakness<br /> *Collapse<br /> *Salivation<br /> *Abdominal tympany<br /> *Tachycardia<br /> *Pallor<br /> *Hypothermia<br /> *[[:Category:Arrhythmia|Cardiac arrythmias]] (present in 40-50% of patients) ([[Ventricular Premature Complexes|ventricular premature beats]], [[Ventricular Tachycardia|ventricular tachycardia]])<br /> <br /> ===Haematology===<br /> *Increased haematocrit<br /> *DIC (thrombocytopaenia, increased firbin degradation products, prolonged patial thromboplastin time and reduced antithrombin III.)<br /> <br /> ===Biochemistry===<br /> Most commonly find hypokalaemia and metabolic acidosis. The acidosis is caused hypoperfusion and anaerobic metabolism leading to lactic acid accumulation. Respiratory acidosis and alkalosis may also be present due to hypo- and hyperventilation.<br /> <br /> ===Diagnostic imaging===<br /> Best performed after [[Principles of Fluid Therapy|fluid therapy]] and gastric decompression. It allows distinction between GD and GDV:<br /> *Gastric dilatation: gas distension, on right lateral shows air in the fundus.<br /> *Gastric dilatation and volvulus: pylorus moves dorsally and left with a compartmentalized stomach. (GDV x-ray from WikiCommons[[http://commons.wikimedia.org/wiki/File:GDV_x-ray.JPG]])<br /> A right lateral view will show a large fundus ventrally, with a smaller gas filled pylorus located dorsally to that. These are seperated by a soft tissue strip. The contrast of the abdomen may be lost indicating peritonitis or [[Haemoabdomen|haemoabdomen]]. Gastric rupture would show as pneumoperitoneum and increased contrast.<br /> <br /> ==Treatment==<br /> The most important first line treatments are [[Principles of Fluid Therapy|fluid therapy]] and gastric decompression.<br /> <br /> ===Fluid therapy===<br /> Should be individualised to the patient due to the varying nature of the [[Essential Ion and Compound Balance and Homeostasis - Anatomy &amp; Physiology#Acid / Base|acid-base]] disturbances. Large bore (16 or 18 gauge) catheters should be placed into cephalic or jugular veins (ideally two into both cephalic veins). Shock doses of Compound Sodium Lactate (Lactated Ringer's Solution) (60-90ml/kg/h). Hypertonic saline can also be used. Monitoring of the situation should be done by regular blood pressure measurements, heart rates, PCV and total solids and urine output. Potassium can be supplemented to bags in the form of KCl after the initial shock doses.<br /> <br /> ===Gastric decompression===<br /> Performed by introduction of a lubricated premeasured (from nostril to last rib) stomach tube or by trocharizing the most tympanic area caudal to the ribs with a 14 to 16 gauge catheter. Sedation may be required to allow the passage of the stomach tube. Suitable drugs for this include [[Opioids#Butorphanol|butorphanol]], [[Opioids#Fentanyl|fentanyl]] or oxymorphone and [[Benzodiazepines#Diazepam|diazepam]].<br /> <br /> ===Other treatment===<br /> *For shock: [[Steroids|Prednisolone sodium succinate]] or [[Steroids|dexamethasone sodium phosphate]].<br /> *For bacterial translocation and endotoxaemia: Broad spectrum antibiotics (e.g. [[Cephalosporins|cephalosporin]] and a [[Fluoroquinolones|fluoroquinolone]]) should also be given at surgical induction through to the postoperative period.<br /> *For cardiac arrythmias: indicated if weakness, syncope, tachycardia runs with R on T complexes, ventricular tachycardia at rates &gt;150bpm. Treated by correcting [[Essential Ion and Compound Balance and Homeostasis - Anatomy &amp; Physiology#Acid / Base|acid-base]], [[Essential Ion and Compound Balance and Homeostasis - Anatomy &amp; Physiology|electrolyte]] and [[Haemostasis - Pathology|haemostatic]] disturbances. The treatment is [[Local Anaesthetics#Lidocaine|lidocaine]] by bolus or continuous rate infusion or procainamide if they persist.<br /> *For analgesia: Pure [[Opioids|opioid]] of [[Opioids#Morphine|morphine]], [[Opioids#Methadone|methadone]] or [[Opioids#Fentanyl|fentanyl]].<br /> *General: Oxygen supplementation if possible<br /> <br /> ===Anaesthesia===<br /> Anaesthesia must be carried out with care even after the patient has been stabilised. There are limited protocols but included [[Opioids#Fentanyl|fentanyl]] and [[Benzodiazepines#Diazepam|diazepam]] bolus or titrated [[Propofol|propofol]]. Maintenance can be achieved with the use of [[Isoflurane|isoflurane]] and [[Sevoflurane|sevoflurane]] in oxygen however [[Nitrous Oxide|nitrous oxide]] should be avoided due to third spacing. Regular routine monitoring of urine production, blood pressure, [[Blood Pressure#Central Venous Pressure|central venous pressure]], PCV, total solids, blood gas and serum electrolytes. High rates of fluids should be used to maintain tissue perfusion and arterial [[Blood Pressure|blood pressure]].<br /> <br /> ===Surgery===<br /> Surgical aims include:<br /> *Gastric decompression and repositioning<br /> *Assessing the organ viability<br /> *Removing necrotic tissue<br /> *Gastropexy (can perform incisional, tube, belt-loop and circumcostal techniques) to prevent recurrence<br /> <br /> If gastric necrosis (happens in 10-37% of patients) is present (discoloured dark purple or grey/green, don't bleed when incised or feel paper thin) then a parital gastrectomy is required. Damage to the spleen via avulsion or torsion may need partial or complete splenectomy.<br /> <br /> ===Post-operative complications===<br /> These are wide and varied and include:<br /> *Hypoperfusion<br /> *Hypotension<br /> *Cardiac arrythmias<br /> *[[Lungs Inflammatory - Pathology#Aspiration pneumonia|Aspiration pneumonia]]<br /> *[[Gastric Motility Disorders|Abnormal gastric motility]]<br /> *Gastric necrosis<br /> *[[Disseminated Intravascular Coagulation|DIC]]<br /> *[[Systemic Inflammatory Response Syndrome|Systemic Inflammatory Response Syndrome (SIRS)]]<br /> <br /> ==Prognosis==<br /> Simple GDV mortality rates are around 15%. Patients suffering from gastric necrosis, gastric resection or splenectomy have a higher mortality rate at over 30%. Gastric necorsis can be predicted by measuring plasma lactate. Values &gt;6mmol/l indicates necrosis (Specificity 88%, Sensitivity 66%)<br /> <br /> ==References==<br /> <br /> Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''<br /> <br /> King, L. and Hammond, R. (1999) '''BSAVA Manual of Canine and Feline Emergency and Critical Care''' ''BSAVA''<br /> <br /> Tivers, M. and Brockman, D. (2009) '''[[http://inpractice.bvapublications.com/cgi/reprint/31/2/66?maxtoshow=&amp;HITS=10&amp;hits=10&amp;RESULTFORMAT=&amp;author1=brockman&amp;searchid=1&amp;FIRSTINDEX=0&amp;sortspec=relevance&amp;resourcetype=HWCIT|Gastric dilation–volvulus syndrome in dogs 1. Pathophysiology, diagnosis and stabilisation]]''' 31(2):66 ''In Practice''<br /> <br /> Tivers, M. and Brockman, D. (2009) '''[[http://inpractice.bvapublications.com/cgi/reprint/31/3/114?maxtoshow=&amp;HITS=10&amp;hits=10&amp;RESULTFORMAT=&amp;author1=brockman&amp;andorexactfulltext=and&amp;searchid=1&amp;FIRSTINDEX=0&amp;sortspec=relevance&amp;resourcetype=HWCIT|Gastric dilation–volvulus syndromein dogs 2. Surgical and postoperative management]]''' 31(3):114 ''In Practice''<br /> <br /> ==From pathology section==<br /> <br /> * Is a consequence of '''gastric dilation'''.<br /> ** Gastric dilation occurs in dogs, cats, horses, rabbits and primates.<br /> ** Cause unclear but may be associated with overeating. <br /> ** Gastric dilation is most studied in dog, since it can lead to displacement of the [[Forestomach - Anatomy &amp; Physiology|stomach]] within the abdomen.<br /> <br /> ===Clinical===<br /> <br /> * Mainly affects large, deep-chested dogs - Great Dane, St. Bernard's and occasionally German Shepherd dogs.<br /> ** A similar condition also occurs in the pig.<br /> * Animal collapses suddenly and must be operated on rapidly.<br /> <br /> ===Pathogenesis===<br /> <br /> * Usually occurs around 30 minutes after a meal, or following aerophagia.<br /> ** [[Forestomach - Anatomy &amp; Physiology|Stomach]] is distended (gastric dilation).<br /> ** Animal excercises, and the [[Forestomach - Anatomy &amp; Physiology|stomach]] twists 180 degrees clockwise on its mesentery.<br /> * Torsion impairs the blood supply- the arterial supply is maintained BUT venous drainage is blocked.<br /> ** [[Forestomach - Anatomy &amp; Physiology|Stomach]] wall becomes severely congested and infarction of gastric mucosa may occur.<br /> * [[Forestomach - Anatomy &amp; Physiology|Stomach]] blows up with gas and fluid.<br /> ** Block venous return to heart.<br /> ** Compresses diaphragm and interferes with respiration.<br /> <br /> * '''The actual cause of the problem and the reason for accumulation of gas is unclear.'''<br /> ** It is better to feed big dogs small amounts more frequently.<br /> <br /> ===Pathology===<br /> <br /> ====Gross====<br /> <br /> * Following the pathogenesis above the [[Forestomach - Anatomy &amp; Physiology|stomach]] contents appear dark red/black and bloody, and the organ may rupture.<br /> * The [[Spleen - Anatomy &amp; Physiology|spleen]] is also affected by venous occlusion.<br /> ** Becomes very congested and moves from left to right side of abdomen.<br /> <br /> ====Histological====<br /> <br /> * Venous obstruction gives rise to congestion, oedema and necrosis of gastric mucosa.[[Category:Stomach_and_Abomasum_-_Pathology]][[Category:Dog]]<br /> [[Category:To_Do_-_Stuart]]</div>

Stuartd https://en.wikivet.net/index.php?title=Gastric_Dilatation_and_Volvulus&diff=70108 2010-07-05T16:22:16Z

<p>Stuartd: </p> <hr /> <div>{{unfinished}}<br /> <br /> {|cell padding=''10'' cellspacing=''0'' border=''1''<br /> |Also known as:<br /> |'''GDV&lt;br&gt;<br /> |-|}<br /> <br /> ==Signalment==<br /> *Large deep chested breeds including:<br /> &lt;gallery&gt;<br /> Image:Akita.jpg|Akitas<br /> Image:Bloodhound.jpg|Bloodhounds<br /> Image:Smooth Collie.jpg|Collies<br /> Image:Greatdane.jpg|Great Danes<br /> Image:Irish Setter.jpg|Irish Setters<br /> Image:Irish Wolfhound.jpg|Wolfhounds<br /> Image:Newfoundland.jpg|Newfoundlands<br /> Image:Rottweiler.jpg|Rottweilers<br /> Image:Stbernard.jpg|Saint Bernards<br /> Image:Standard poodle.jpg|Standard Poodles<br /> Image:Weimaraner.jpg|Weirmaraners<br /> &lt;/gallery&gt;<br /> <br /> ==Description==<br /> Gastric dilatation (GD) and Gastric dilatation and volvulus (GDV) are caused by the stomach distending with air. In GDV the stomach twists around its axis mainly in a clockwise direction with both conditions leading to compression of the caudal vena cava. GDV can lead to [[Shock - Pathology#Hypovolaemic shock|hypovolaemic shock]], splenic torsion, gastric wall ischaemia, abdominal viscera congestion, [[Shock - Pathology#Endotoxic shock|endotoxic shock]] and [[Disseminated Intravascular Coagulation|disseminated intravascular coagulation (DIC)]]. The exact pathogenesis is unclear but risk factors for GDV include age, fast eating, once- daily feeding, aerophagia, raised feeding bowl and a close relative with GDV.<br /> <br /> ==Diagnosis==<br /> ===History and Clinical signs===<br /> *Abdominal distension<br /> *Non-productive retching<br /> *Weakness<br /> *Collapse<br /> *Salivation<br /> *Abdominal tympany<br /> *Tachycardia<br /> *Pallor<br /> *Hypothermia<br /> *[[:Category:Arrhythmia|Cardiac arrythmias]] (present in 40-50% of patients) ([[Ventricular Premature Complexes|ventricular premature beats]], [[Ventricular Tachycardia|ventricular tachycardia]])<br /> <br /> ===Haematology===<br /> *Increased haematocrit<br /> *DIC (thrombocytopaenia, increased firbin degradation products, prolonged patial thromboplastin time and reduced antithrombin III.)<br /> <br /> ===Biochemistry===<br /> Most commonly find hypokalaemia and metabolic acidosis. The acidosis is caused hypoperfusion and anaerobic metabolism leading to lactic acid accumulation. Respiratory acidosis and alkalosis may also be present due to hypo- and hyperventilation.<br /> <br /> ===Diagnostic imaging===<br /> Best performed after [[Principles of Fluid Therapy|fluid therapy]] and gastric decompression. It allows distinction between GD and GDV:<br /> *Gastric dilatation: gas distension, on right lateral shows air in the fundus.<br /> *Gastric dilatation and volvulus: pylorus moves dorsally and left with a compartmentalized stomach. (GDV x-ray from WikiCommons[[http://commons.wikimedia.org/wiki/File:GDV_x-ray.JPG]])<br /> A right lateral view will show a large fundus ventrally, with a smaller gas filled pylorus located dorsally to that. These are seperated by a soft tissue strip. The contrast of the abdomen may be lost indicating peritonitis or [[Haemoabdomen|haemoabdomen]]. Gastric rupture would show as pneumoperitoneum and increased contrast.<br /> <br /> ==Treatment==<br /> The most important first line treatments are [[Principles of Fluid Therapy|fluid therapy]] and gastric decompression.<br /> <br /> ===Fluid therapy===<br /> Should be individualised to the patient due to the varying nature of the [[Essential Ion and Compound Balance and Homeostasis - Anatomy &amp; Physiology#Acid / Base|acid-base]] disturbances. Large bore (16 or 18 gauge) catheters should be placed into cephalic or jugular veins (ideally two into both cephalic veins). Shock doses of Compound Sodium Lactate (Lactated Ringer's Solution) (60-90ml/kg/h). Hypertonic saline can also be used. Monitoring of the situation should be done by regular blood pressure measurements, heart rates, PCV and total solids and urine output. Potassium can be supplemented to bags in the form of KCl after the initial shock doses.<br /> <br /> ===Gastric decompression===<br /> Performed by introduction of a lubricated premeasured (from nostril to last rib) stomach tube or by trocharizing the most tympanic area caudal to the ribs with a 14 to 16 gauge catheter. Sedation may be required to allow the passage of the stomach tube. Suitable drugs for this include [[Opioids#Butorphanol|butorphanol]], [[Opioids#Fentanyl|fentanyl]] or oxymorphone and [[Benzodiazepines#Diazepam|diazepam]].<br /> <br /> ===Other treatment===<br /> *For shock: [[Steroids|Prednisolone sodium succinate]] or [[Steroids|dexamethasone sodium phosphate]].<br /> *For bacterial translocation and endotoxaemia: Broad spectrum antibiotics (e.g. [[Cephalosporins|cephalosporin]] and a [[Fluoroquinolones|fluoroquinolone]]) should also be given at surgical induction through to the postoperative period.<br /> *For cardiac arrythmias: indicated if weakness, syncope, tachycardia runs with R on T complexes, ventricular tachycardia at rates &gt;150bpm. Treated by correcting [[Essential Ion and Compound Balance and Homeostasis - Anatomy &amp; Physiology#Acid / Base|acid-base]], [[Essential Ion and Compound Balance and Homeostasis - Anatomy &amp; Physiology|electrolyte]] and [[Haemostasis - Pathology|haemostatic]] disturbances. The treatment is [[Local Anaesthetics#Lidocaine|lidocaine]] by bolus or continuous rate infusion or procainamide if they persist.<br /> *For analgesia: Pure [[Opioids|opioid]] of [[Opioids#Morphine|morphine]], [[Opioids#Methadone|methadone]] or [[Opioids#Fentanyl|fentanyl]].<br /> *General: Oxygen supplementation if possible<br /> <br /> ===Anaesthesia===<br /> Anaesthesia must be carried out with care even after the patient has been stabilised. There are limited protocols but included [[Opioids#Fentanyl|fentanyl]] and [[Benzodiazepines#Diazepam|diazepam]] bolus or titrated [[Propofol|propofol]]. Maintenance can be achieved with the use of [[Isoflurane|isoflurane]] and [[Sevoflurane|sevoflurane]] in oxygen however [[Nitrous Oxide|nitrous oxide]] should be avoided due to third spacing. Regular routine monitoring of urine production, blood pressure, [[Blood Pressure#Central Venous Pressure|central venous pressure]], PCV, total solids, blood gas and serum electrolytes. High rates of fluids should be used to maintain tissue perfusion and arterial [[Blood Pressure|blood pressure]].<br /> <br /> ===Surgery===<br /> Surgical aims include:<br /> *Gastric decompression and repositioning<br /> *Assessing the organ viability<br /> *Removing necrotic tissue<br /> *Gastropexy (can perform incisional, tube, belt-loop and circumcostal techniques) to prevent recurrence<br /> <br /> If gastric necrosis (happens in 10-37% of patients) is present (discoloured dark purple or grey/green, don't bleed when incised or feel paper thin) then a parital gastrectomy is required. Damage to the spleen via avulsion or torsion may need partial or complete splenectomy.<br /> <br /> ===Post-operative complications===<br /> These are wide and varied and include:<br /> *Hypoperfusion<br /> *Hypotension<br /> *Cardiac arrythmias<br /> *[[Lungs Inflammatory - Pathology#Aspiration pneumonia|Aspiration pneumonia]]<br /> *[[Gastric Motility Disorders|Abnormal gastric motility]]<br /> *Gastric necrosis<br /> *[[Disseminated Intravascular Coagulation|DIC]]<br /> *[[Systemic Inflammatory Response Syndrome|Systemic Inflammatory Response Syndrome (SIRS)]]<br /> <br /> ==Prognosis==<br /> Simple GDV mortality rates are around 15%. Patients suffering from gastric necrosis, gastric resection or splenectomy have a higher mortality rate at over 30%. Gastric necorsis can be predicted by measuring plasma lactate. Values &gt;6mmol/l indicates necrosis (Specificity 88%, Sensitivity 66%)<br /> <br /> ==References==<br /> <br /> Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''<br /> <br /> King, L. and Hammond, R. (1999) '''BSAVA Manual of Canine and Feline Emergency and Critical Care''' ''BSAVA''<br /> <br /> Tivers, M. and Brockman, D. (2009) '''[[http://inpractice.bvapublications.com/cgi/reprint/31/2/66?maxtoshow=&amp;HITS=10&amp;hits=10&amp;RESULTFORMAT=&amp;author1=brockman&amp;searchid=1&amp;FIRSTINDEX=0&amp;sortspec=relevance&amp;resourcetype=HWCIT|Gastric dilation–volvulus syndrome in dogs 1. Pathophysiology, diagnosis and stabilisation]]''' 31(2):66 ''In Practice''<br /> <br /> Tivers, M. and Brockman, D. (2009) '''[[http://inpractice.bvapublications.com/cgi/reprint/31/3/114?maxtoshow=&amp;HITS=10&amp;hits=10&amp;RESULTFORMAT=&amp;author1=brockman&amp;andorexactfulltext=and&amp;searchid=1&amp;FIRSTINDEX=0&amp;sortspec=relevance&amp;resourcetype=HWCIT|Gastric dilation–volvulus syndromein dogs 2. Surgical and postoperative management]]''' 31(3):114 ''In Practice''<br /> <br /> ==From pathology section==<br /> <br /> * Is a consequence of '''gastric dilation'''.<br /> ** Gastric dilation occurs in dogs, cats, horses, rabbits and primates.<br /> ** Cause unclear but may be associated with overeating. <br /> ** Gastric dilation is most studied in dog, since it can lead to displacement of the [[Forestomach - Anatomy &amp; Physiology|stomach]] within the abdomen.<br /> <br /> ===Clinical===<br /> <br /> * Mainly affects large, deep-chested dogs - Great Dane, St. Bernard's and occasionally German Shepherd dogs.<br /> ** A similar condition also occurs in the pig.<br /> * Animal collapses suddenly and must be operated on rapidly.<br /> <br /> ===Pathogenesis===<br /> <br /> * Usually occurs around 30 minutes after a meal, or following aerophagia.<br /> ** [[Forestomach - Anatomy &amp; Physiology|Stomach]] is distended (gastric dilation).<br /> ** Animal excercises, and the [[Forestomach - Anatomy &amp; Physiology|stomach]] twists 180 degrees clockwise on its mesentery.<br /> * Torsion impairs the blood supply- the arterial supply is maintained BUT venous drainage is blocked.<br /> ** [[Forestomach - Anatomy &amp; Physiology|Stomach]] wall becomes severely congested and infarction of gastric mucosa may occur.<br /> * [[Forestomach - Anatomy &amp; Physiology|Stomach]] blows up with gas and fluid.<br /> ** Block venous return to heart.<br /> ** Compresses diaphragm and interferes with respiration.<br /> <br /> * '''The actual cause of the problem and the reason for accumulation of gas is unclear.'''<br /> ** It is better to feed big dogs small amounts more frequently.<br /> <br /> ===Pathology===<br /> <br /> ====Gross====<br /> <br /> * Following the pathogenesis above the [[Forestomach - Anatomy &amp; Physiology|stomach]] contents appear dark red/black and bloody, and the organ may rupture.<br /> * The [[Spleen - Anatomy &amp; Physiology|spleen]] is also affected by venous occlusion.<br /> ** Becomes very congested and moves from left to right side of abdomen.<br /> <br /> ====Histological====<br /> <br /> * Venous obstruction gives rise to congestion, oedema and necrosis of gastric mucosa.[[Category:Stomach_and_Abomasum_-_Pathology]][[Category:Dog]]<br /> [[Category:To_Do_-_Stuart]]</div>

Stuartd https://en.wikivet.net/index.php?title=Gastric_Dilatation_and_Volvulus&diff=70105 2010-07-05T16:19:17Z

<p>Stuartd: </p> <hr /> <div>{{unfinished}}<br /> <br /> {|cell padding=''10'' cellspacing=''0'' border=''1''<br /> |Also known as:<br /> |'''GDV&lt;br&gt;<br /> |-|}<br /> <br /> ==Signalment==<br /> *Large deep chested breeds including:<br /> &lt;gallery&gt;<br /> Image:Akita.jpg|Akitas<br /> Image:Bloodhound.jpg|Bloodhounds<br /> Image:Smooth Collie.jpg|Collies<br /> Image:Greatdane.jpg|Great Danes<br /> Image:Irish Setter.jpg|Irish Setters<br /> Image:Irish Wolfhound.jpg|Wolfhounds<br /> Image:Newfoundland.jpg|Newfoundlands<br /> Image:Rottweiler.jpg|Rottweilers<br /> Image:Stbernard.jpg|Saint Bernards<br /> Image:Standard poodle.jpg|Standard Poodles<br /> Image:Weimaraner.jpg|Weirmaraners<br /> &lt;/gallery&gt;<br /> <br /> ==Description==<br /> Gastric dilatation (GD) and Gastric dilatation and volvulus (GDV) are caused by the stomach distending with air. In GDV the stomach twists around its axis mainly in a clockwise direction with both conditions leading to compression of the caudal vena cava. GDV can lead to [[Shock - Pathology#Hypovolaemic shock|hypovolaemic shock]], splenic torsion, gastric wall ischaemia, abdominal viscera congestion, [[Shock - Pathology#Endotoxic shock|endotoxic shock]] and [[Disseminated Intravascular Coagulation|disseminated intravascular coagulation (DIC)]]. The exact pathogenesis is unclear but risk factors for GDV include age, fast eating, once- daily feeding, aerophagia, raised feeding bowl and a close relative with GDV.<br /> <br /> ==Diagnosis==<br /> ===History and Clinical signs===<br /> *Abdominal distension<br /> *Non-productive retching<br /> *Weakness<br /> *Collapse<br /> *Salivation<br /> *Abdominal tympany<br /> *Tachycardia<br /> *Pallor<br /> *Hypothermia<br /> *[[:Category:Arrhythmia|Cardiac arrythmias]] (present in 40-50% of patients) ([[Ventricular Premature Complexes|ventricular premature beats]], [[Ventricular Tachycardia|ventricular tachycardia]])<br /> <br /> ===Haematology===<br /> *Increased haematocrit<br /> *DIC (thrombocytopaenia, increased firbin degradation products, prolonged patial thromboplastin time and reduced antithrombin III.)<br /> <br /> ===Biochemistry===<br /> Most commonly find hypokalaemia and metabolic acidosis. The acidosis is caused hypoperfusion and anaerobic metabolism leading to lactic acid accumulation. Respiratory acidosis and alkalosis may also be present due to hypo- and hyperventilation.<br /> <br /> ===Diagnostic imaging===<br /> Best performed after [[Principles of Fluid Therapy|fluid therapy]] and gastric decompression. It allows distinction between GD and GDV:<br /> *Gastric dilatation: gas distension, on right lateral shows air in the fundus.<br /> *Gastric dilatation and volvulus: pylorus moves dorsally and left with a compartmentalized stomach. (GDV x-ray from WikiCommons[[http://commons.wikimedia.org/wiki/File:GDV_x-ray.JPG]])<br /> A right lateral view will show a large fundus ventrally, with a smaller gas filled pylorus located dorsally to that. These are seperated by a soft tissue strip. The contrast of the abdomen may be lost indicating peritonitis or [[Haemoabdomen|haemoabdomen]]. Gastric rupture would show as pneumoperitoneum and increased contrast.<br /> <br /> ==Treatment==<br /> The most important first line treatments are [[Principles of Fluid Therapy|fluid therapy]] and gastric decompression.<br /> <br /> ===Fluid therapy===<br /> Should be individualised to the patient due to the varying nature of the [[Essential Ion and Compound Balance and Homeostasis - Anatomy &amp; Physiology#Acid / Base|acid-base]] disturbances. Large bore (16 or 18 gauge) catheters should be placed into cephalic or jugular veins (ideally two into both cephalic veins). Shock doses of Compound Sodium Lactate (Lactated Ringer's Solution) (60-90ml/kg/h). Hypertonic saline can also be used. Monitoring of the situation should be done by regular blood pressure measurements, heart rates, PCV and total solids and urine output. Potassium can be supplemented to bags in the form of KCl after the initial shock doses.<br /> <br /> ===Gastric decompression===<br /> Performed by introduction of a lubricated premeasured (from nostril to last rib) stomach tube or by trocharizing the most tympanic area caudal to the ribs with a 14 to 16 gauge catheter. Sedation may be required to allow the passage of the stomach tube. Suitable drugs for this include [[Opioids#Butorphanol|butorphanol]], [[Opioids#Fentanyl|fentanyl]] or oxymorphone and [[Benzodiazepines#Diazepam|diazepam]].<br /> <br /> ===Other treatment===<br /> *For shock: [[Steroids|Prednisolone sodium succinate]] or [[Steroids|dexamethasone sodium phosphate]].<br /> *For bacterial translocation and endotoxaemia: Broad spectrum antibiotics (e.g. [[Cephalosporins|cephalosporin]] and a [[Fluoroquinolones|fluoroquinolone]]) should also be given at surgical induction through to the postoperative period.<br /> *For cardiac arrythmias: indicated if weakness, syncope, tachycardia runs with R on T complexes, ventricular tachycardia at rates &gt;150bpm. Treated by correcting [[Essential Ion and Compound Balance and Homeostasis - Anatomy &amp; Physiology#Acid / Base|acid-base]], [[Essential Ion and Compound Balance and Homeostasis - Anatomy &amp; Physiology|electrolyte]] and [[Haemostasis - Pathology|haemostatic]] disturbances. The treatment is [[Local Anaesthetics#Lidocaine|lidocaine]] by bolus or continuous rate infusion or procainamide if they persist.<br /> *For analgesia: Pure [[Opioids|opioid]] of [[Opioids#Morphine|morphine]], [[Opioids#Methadone|methadone]] or [[Opioids#Fentanyl|fentanyl]].<br /> *General: Oxygen supplementation if possible<br /> <br /> ===Anaesthesia===<br /> Anaesthesia must be carried out with care even after the patient has been stabilised. There are limited protocols but included [[Opioids#Fentanyl|fentanyl]] and [[Benzodiazepines#Diazepam|diazepam]] bolus or titrated [[Propofol|propofol]]. Maintenance can be achieved with the use of [[Isoflurane|isoflurane]] and [[Sevoflurane|sevoflurane]] in oxygen however [[Nitrous Oxide|nitrous oxide]] should be avoided due to third spacing. Regular routine monitoring of urine production, blood pressure, [[Blood Pressure#Central Venous Pressure|central venous pressure]], PCV, total solids, blood gas and serum electrolytes. High rates of fluids should be used to maintain tissue perfusion and arterial [[Blood Pressure|blood pressure]].<br /> <br /> ===Surgery===<br /> Surgical aims include:<br /> *Gastric decompression and repositioning<br /> *Assessing the organ viability<br /> *Removing necrotic tissue<br /> *Gastropexy (can perform incisional, tube, belt-loop and circumcostal techniques) to prevent recurrence<br /> <br /> If gastric necrosis (happens in 10-37% of patients) is present (discoloured dark purple or grey/green, don't bleed when incised or feel paper thin) then a parital gastrectomy is required. Damage to the spleen via avulsion or torsion may need partial or complete splenectomy.<br /> <br /> ===Post-operative complications===<br /> These are wide and varied and include:<br /> *Hypoperfusion<br /> *Hypotension<br /> *Cardiac arrythmias<br /> *[[Lungs Inflammatory - Pathology#Aspiration pneumonia|Aspiration pneumonia]]<br /> *[[Gastric Motility Disorders|Abnormal gastric motility]]<br /> *Gastric necrosis<br /> *[[Disseminated Intravascular Coagulation|DIC]]<br /> *Systemic Inflammatory Response Syndrome (SIRS)<br /> <br /> ==Prognosis==<br /> Simple GDV mortality rates are around 15%. Patients suffering from gastric necrosis, gastric resection or splenectomy have a higher mortality rate at over 30%. Gastric necorsis can be predicted by measuring plasma lactate. Values &gt;6mmol/l indicates necrosis (Specificity 88%, Sensitivity 66%)<br /> <br /> ==References==<br /> <br /> Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''<br /> <br /> King, L. and Hammond, R. (1999) '''BSAVA Manual of Canine and Feline Emergency and Critical Care''' ''BSAVA''<br /> <br /> Tivers, M. and Brockman, D. (2009) '''[[http://inpractice.bvapublications.com/cgi/reprint/31/2/66?maxtoshow=&amp;HITS=10&amp;hits=10&amp;RESULTFORMAT=&amp;author1=brockman&amp;searchid=1&amp;FIRSTINDEX=0&amp;sortspec=relevance&amp;resourcetype=HWCIT|Gastric dilation–volvulus syndrome in dogs 1. Pathophysiology, diagnosis and stabilisation]]''' 31(2):66 ''In Practice''<br /> <br /> Tivers, M. and Brockman, D. (2009) '''[[http://inpractice.bvapublications.com/cgi/reprint/31/3/114?maxtoshow=&amp;HITS=10&amp;hits=10&amp;RESULTFORMAT=&amp;author1=brockman&amp;andorexactfulltext=and&amp;searchid=1&amp;FIRSTINDEX=0&amp;sortspec=relevance&amp;resourcetype=HWCIT|Gastric dilation–volvulus syndromein dogs 2. Surgical and postoperative management]]''' 31(3):114 ''In Practice''<br /> <br /> ==From pathology section==<br /> <br /> * Is a consequence of '''gastric dilation'''.<br /> ** Gastric dilation occurs in dogs, cats, horses, rabbits and primates.<br /> ** Cause unclear but may be associated with overeating. <br /> ** Gastric dilation is most studied in dog, since it can lead to displacement of the [[Forestomach - Anatomy &amp; Physiology|stomach]] within the abdomen.<br /> <br /> ===Clinical===<br /> <br /> * Mainly affects large, deep-chested dogs - Great Dane, St. Bernard's and occasionally German Shepherd dogs.<br /> ** A similar condition also occurs in the pig.<br /> * Animal collapses suddenly and must be operated on rapidly.<br /> <br /> ===Pathogenesis===<br /> <br /> * Usually occurs around 30 minutes after a meal, or following aerophagia.<br /> ** [[Forestomach - Anatomy &amp; Physiology|Stomach]] is distended (gastric dilation).<br /> ** Animal excercises, and the [[Forestomach - Anatomy &amp; Physiology|stomach]] twists 180 degrees clockwise on its mesentery.<br /> * Torsion impairs the blood supply- the arterial supply is maintained BUT venous drainage is blocked.<br /> ** [[Forestomach - Anatomy &amp; Physiology|Stomach]] wall becomes severely congested and infarction of gastric mucosa may occur.<br /> * [[Forestomach - Anatomy &amp; Physiology|Stomach]] blows up with gas and fluid.<br /> ** Block venous return to heart.<br /> ** Compresses diaphragm and interferes with respiration.<br /> <br /> * '''The actual cause of the problem and the reason for accumulation of gas is unclear.'''<br /> ** It is better to feed big dogs small amounts more frequently.<br /> <br /> ===Pathology===<br /> <br /> ====Gross====<br /> <br /> * Following the pathogenesis above the [[Forestomach - Anatomy &amp; Physiology|stomach]] contents appear dark red/black and bloody, and the organ may rupture.<br /> * The [[Spleen - Anatomy &amp; Physiology|spleen]] is also affected by venous occlusion.<br /> ** Becomes very congested and moves from left to right side of abdomen.<br /> <br /> ====Histological====<br /> <br /> * Venous obstruction gives rise to congestion, oedema and necrosis of gastric mucosa.[[Category:Stomach_and_Abomasum_-_Pathology]][[Category:Dog]]<br /> [[Category:To_Do_-_Stuart]]</div>

Stuartd https://en.wikivet.net/index.php?title=Gastric_Dilatation_and_Volvulus&diff=70096 2010-07-05T16:13:53Z

<p>Stuartd: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Signalment==<br /> *Large deep chested breeds including:<br /> &lt;gallery&gt;<br /> Image:Akita.jpg|Akitas<br /> Image:Bloodhound.jpg|Bloodhounds<br /> Image:Smooth Collie.jpg|Collies<br /> Image:Greatdane.jpg|Great Danes<br /> Image:Irish Setter.jpg|Irish Setters<br /> Image:Irish Wolfhound.jpg|Wolfhounds<br /> Image:Newfoundland.jpg|Newfoundlands<br /> Image:Rottweiler.jpg|Rottweilers<br /> Image:Stbernard.jpg|Saint Bernards<br /> Image:Standard poodle.jpg|Standard Poodles<br /> Image:Weimaraner.jpg|Weirmaraners<br /> &lt;/gallery&gt;<br /> <br /> ==Description==<br /> Gastric dilatation (GD) and Gastric dilatation and volvulus (GDV) are caused by the stomach distending with air. In GDV the stomach twists around its axis mainly in a clockwise direction with both conditions leading to compression of the caudal vena cava. GDV can lead to [[Shock - Pathology#Hypovolaemic shock|hypovolaemic shock]], splenic torsion, gastric wall ischaemia, abdominal viscera congestion, [[Shock - Pathology#Endotoxic shock|endotoxic shock]] and [[Disseminated Intravascular Coagulation|disseminated intravascular coagulation (DIC)]]. The exact pathogenesis is unclear but risk factors for GDV include age, fast eating, once- daily feeding, aerophagia, raised feeding bowl and a close relative with GDV.<br /> <br /> ==Diagnosis==<br /> ===History and Clinical signs===<br /> *Abdominal distension<br /> *Non-productive retching<br /> *Weakness<br /> *Collapse<br /> *Salivation<br /> *Abdominal tympany<br /> *Tachycardia<br /> *Pallor<br /> *Hypothermia<br /> *[[:Category:Arrhythmia|Cardiac arrythmias]] (present in 40-50% of patients) ([[Ventricular Premature Complexes|ventricular premature beats]], [[Ventricular Tachycardia|ventricular tachycardia]])<br /> <br /> ===Haematology===<br /> *Increased haematocrit<br /> *DIC (thrombocytopaenia, increased firbin degradation products, prolonged patial thromboplastin time and reduced antithrombin III.)<br /> <br /> ===Biochemistry===<br /> Most commonly find hypokalaemia and metabolic acidosis. The acidosis is caused hypoperfusion and anaerobic metabolism leading to lactic acid accumulation. Respiratory acidosis and alkalosis may also be present due to hypo- and hyperventilation.<br /> <br /> ===Diagnostic imaging===<br /> Best performed after [[Principles of Fluid Therapy|fluid therapy]] and gastric decompression. It allows distinction between GD and GDV:<br /> *Gastric dilatation: gas distension, on right lateral shows air in the fundus.<br /> *Gastric dilatation and volvulus: pylorus moves dorsally and left with a compartmentalized stomach. (GDV x-ray from WikiCommons[[http://commons.wikimedia.org/wiki/File:GDV_x-ray.JPG]])<br /> A right lateral view will show a large fundus ventrally, with a smaller gas filled pylorus located dorsally to that. These are seperated by a soft tissue strip. The contrast of the abdomen may be lost indicating peritonitis or [[Haemoabdomen|haemoabdomen]]. Gastric rupture would show as pneumoperitoneum and increased contrast.<br /> <br /> ==Treatment==<br /> The most important first line treatments are [[Principles of Fluid Therapy|fluid therapy]] and gastric decompression.<br /> <br /> ===Fluid therapy===<br /> Should be individualised to the patient due to the varying nature of the [[Essential Ion and Compound Balance and Homeostasis - Anatomy &amp; Physiology#Acid / Base|acid-base]] disturbances. Large bore (16 or 18 gauge) catheters should be placed into cephalic or jugular veins (ideally two into both cephalic veins). Shock doses of Compound Sodium Lactate (Lactated Ringer's Solution) (60-90ml/kg/h). Hypertonic saline can also be used. Monitoring of the situation should be done by regular blood pressure measurements, heart rates, PCV and total solids and urine output. Potassium can be supplemented to bags in the form of KCl after the initial shock doses.<br /> <br /> ===Gastric decompression===<br /> Performed by introduction of a lubricated premeasured (from nostril to last rib) stomach tube or by trocharizing the most tympanic area caudal to the ribs with a 14 to 16 gauge catheter. Sedation may be required to allow the passage of the stomach tube. Suitable drugs for this include [[Opioids#Butorphanol|butorphanol]], [[Opioids#Fentanyl|fentanyl]] or oxymorphone and [[Benzodiazepines#Diazepam|diazepam]].<br /> <br /> ===Other treatment===<br /> *For shock: [[Steroids|Prednisolone sodium succinate]] or [[Steroids|dexamethasone sodium phosphate]].<br /> *For bacterial translocation and endotoxaemia: Broad spectrum antibiotics (e.g. [[Cephalosporins|cephalosporin]] and a [[Fluoroquinolones|fluoroquinolone]]) should also be given at surgical induction through to the postoperative period.<br /> *For cardiac arrythmias: indicated if weakness, syncope, tachycardia runs with R on T complexes, ventricular tachycardia at rates &gt;150bpm. Treated by correcting [[Essential Ion and Compound Balance and Homeostasis - Anatomy &amp; Physiology#Acid / Base|acid-base]], [[Essential Ion and Compound Balance and Homeostasis - Anatomy &amp; Physiology|electrolyte]] and [[Haemostasis - Pathology|haemostatic]] disturbances. The treatment is [[Local Anaesthetics#Lidocaine|lidocaine]] by bolus or continuous rate infusion or procainamide if they persist.<br /> *For analgesia: Pure [[Opioids|opioid]] of [[Opioids#Morphine|morphine]], [[Opioids#Methadone|methadone]] or [[Opioids#Fentanyl|fentanyl]].<br /> *General: Oxygen supplementation if possible<br /> <br /> ===Anaesthesia===<br /> Anaesthesia must be carried out with care even after the patient has been stabilised. There are limited protocols but included [[Opioids#Fentanyl|fentanyl]] and [[Benzodiazepines#Diazepam|diazepam]] bolus or titrated [[Propofol|propofol]]. Maintenance can be achieved with the use of [[Isoflurane|isoflurane]] and [[Sevoflurane|sevoflurane]] in oxygen however [[Nitrous Oxide|nitrous oxide]] should be avoided due to third spacing. Regular routine monitoring of urine production, blood pressure, [[Blood Pressure#Central Venous Pressure|central venous pressure]], PCV, total solids, blood gas and serum electrolytes. High rates of fluids should be used to maintain tissue perfusion and arterial [[Blood Pressure|blood pressure]].<br /> <br /> ===Surgery===<br /> Surgical aims include:<br /> *Gastric decompression and repositioning<br /> *Assessing the organ viability<br /> *Removing necrotic tissue<br /> *Gastropexy (can perform incisional, tube, belt-loop and circumcostal techniques) to prevent recurrence<br /> <br /> If gastric necrosis (happens in 10-37% of patients) is present (discoloured dark purple or grey/green, don't bleed when incised or feel paper thin) then a parital gastrectomy is required. Damage to the spleen via avulsion or torsion may need partial or complete splenectomy.<br /> <br /> ===Post-operative complications===<br /> These are wide and varied and include:<br /> *Hypoperfusion<br /> *Hypotension<br /> *Cardiac arrythmias<br /> *[[Lungs Inflammatory - Pathology#Aspiration pneumonia|Aspiration pneumonia]]<br /> *[[Gastric Motility Disorders|Abnormal gastric motility]]<br /> *Gastric necrosis<br /> *[[Disseminated Intravascular Coagulation|DIC]]<br /> *Systemic Inflammatory Response Syndrome (SIRS)<br /> <br /> ==Prognosis==<br /> Simple GDV mortality rates are around 15%. Patients suffering from gastric necrosis, gastric resection or splenectomy have a higher mortality rate at over 30%. Gastric necorsis can be predicted by measuring plasma lactate. Values &gt;6mmol/l indicates necrosis (Specificity 88%, Sensitivity 66%)<br /> <br /> ==References==<br /> <br /> Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''<br /> <br /> King, L. and Hammond, R. (1999) '''BSAVA Manual of Canine and Feline Emergency and Critical Care''' ''BSAVA''<br /> <br /> Tivers, M. and Brockman, D. (2009) '''[[http://inpractice.bvapublications.com/cgi/reprint/31/2/66?maxtoshow=&amp;HITS=10&amp;hits=10&amp;RESULTFORMAT=&amp;author1=brockman&amp;searchid=1&amp;FIRSTINDEX=0&amp;sortspec=relevance&amp;resourcetype=HWCIT|Gastric dilation–volvulus syndrome in dogs 1. Pathophysiology, diagnosis and stabilisation]]''' 31(2):66 ''In Practice''<br /> <br /> Tivers, M. and Brockman, D. (2009) '''[[http://inpractice.bvapublications.com/cgi/reprint/31/3/114?maxtoshow=&amp;HITS=10&amp;hits=10&amp;RESULTFORMAT=&amp;author1=brockman&amp;andorexactfulltext=and&amp;searchid=1&amp;FIRSTINDEX=0&amp;sortspec=relevance&amp;resourcetype=HWCIT|Gastric dilation–volvulus syndromein dogs 2. Surgical and postoperative management]]''' 31(3):114 ''In Practice''<br /> <br /> ==From pathology section==<br /> <br /> * Is a consequence of '''gastric dilation'''.<br /> ** Gastric dilation occurs in dogs, cats, horses, rabbits and primates.<br /> ** Cause unclear but may be associated with overeating. <br /> ** Gastric dilation is most studied in dog, since it can lead to displacement of the [[Forestomach - Anatomy &amp; Physiology|stomach]] within the abdomen.<br /> <br /> ===Clinical===<br /> <br /> * Mainly affects large, deep-chested dogs - Great Dane, St. Bernard's and occasionally German Shepherd dogs.<br /> ** A similar condition also occurs in the pig.<br /> * Animal collapses suddenly and must be operated on rapidly.<br /> <br /> ===Pathogenesis===<br /> <br /> * Usually occurs around 30 minutes after a meal, or following aerophagia.<br /> ** [[Forestomach - Anatomy &amp; Physiology|Stomach]] is distended (gastric dilation).<br /> ** Animal excercises, and the [[Forestomach - Anatomy &amp; Physiology|stomach]] twists 180 degrees clockwise on its mesentery.<br /> * Torsion impairs the blood supply- the arterial supply is maintained BUT venous drainage is blocked.<br /> ** [[Forestomach - Anatomy &amp; Physiology|Stomach]] wall becomes severely congested and infarction of gastric mucosa may occur.<br /> * [[Forestomach - Anatomy &amp; Physiology|Stomach]] blows up with gas and fluid.<br /> ** Block venous return to heart.<br /> ** Compresses diaphragm and interferes with respiration.<br /> <br /> * '''The actual cause of the problem and the reason for accumulation of gas is unclear.'''<br /> ** It is better to feed big dogs small amounts more frequently.<br /> <br /> ===Pathology===<br /> <br /> ====Gross====<br /> <br /> * Following the pathogenesis above the [[Forestomach - Anatomy &amp; Physiology|stomach]] contents appear dark red/black and bloody, and the organ may rupture.<br /> * The [[Spleen - Anatomy &amp; Physiology|spleen]] is also affected by venous occlusion.<br /> ** Becomes very congested and moves from left to right side of abdomen.<br /> <br /> ====Histological====<br /> <br /> * Venous obstruction gives rise to congestion, oedema and necrosis of gastric mucosa.[[Category:Stomach_and_Abomasum_-_Pathology]][[Category:Dog]]<br /> [[Category:To_Do_-_Stuart]]</div>

Stuartd https://en.wikivet.net/index.php?title=Gastric_Dilatation_and_Volvulus&diff=70093 2010-07-05T16:12:02Z

<p>Stuartd: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Signalment==<br /> *Large deep chested breeds including:<br /> &lt;gallery&gt;<br /> Image:Akita.jpg|Akitas<br /> Image:Bloodhound.jpg|Bloodhounds<br /> Image:Smooth Collie.jpg|Collies<br /> Image:Greatdane.jpg|Great Danes<br /> Image:Irish Setter.jpg|Irish Setters<br /> Image:Irish Wolfhound.jpg|Wolfhounds<br /> Image:Newfoundland.jpg|Newfoundlands<br /> Image:Rottweiler.jpg|Rottweilers<br /> Image:Stbernard.jpg|Saint Bernards<br /> Image:Standard poodle.jpg|Standard Poodles<br /> Image:Weimaraner.jpg|Weirmaraners<br /> &lt;/gallery&gt;<br /> <br /> ==Description==<br /> Gastric dilatation (GD) and Gastric dilatation and volvulus (GDV) are caused by the stomach distending with air. In GDV the stomach twists around its axis mainly in a clockwise direction with both conditions leading to compression of the caudal vena cava. GDV can lead to [[Shock - Pathology#Hypovolaemic shock|hypovolaemic shock]], splenic torsion, gastric wall ischaemia, abdominal viscera congestion, [[Shock - Pathology#Endotoxic shock|endotoxic shock]] and [[Disseminated Intravascular Coagulation|disseminated intravascular coagulation (DIC)]]. The exact pathogenesis is unclear but risk factors for GDV include age, fast eating, once- daily feeding, aerophagia, raised feeding bowl and a close relative with GDV.<br /> <br /> ==Diagnosis==<br /> ===History and Clinical signs===<br /> *Abdominal distension<br /> *Non-productive retching<br /> *Weakness<br /> *Collapse<br /> *Salivation<br /> *Abdominal tympany<br /> *Tachycardia<br /> *Pallor<br /> *Hypothermia<br /> *[[:Category:Arrhythmia|Cardiac arrythmias]] (present in 40-50% of patients) ([[Ventricular Premature Complexes|ventricular premature beats]], [[Ventricular Tachycardia|ventricular tachycardia]])<br /> <br /> ===Haematology===<br /> *Increased haematocrit<br /> *DIC (thrombocytopaenia, increased firbin degradation products, prolonged patial thromboplastin time and reduced antithrombin III.)<br /> <br /> ===Biochemistry===<br /> Most commonly find hypokalaemia and metabolic acidosis. The acidosis is caused hypoperfusion and anaerobic metabolism leading to lactic acid accumulation. Respiratory acidosis and alkalosis may also be present due to hypo- and hyperventilation.<br /> <br /> ===Diagnostic imaging===<br /> Best performed after [[Principles of Fluid Therapy|fluid therapy]] and gastric decompression. It allows distinction between GD and GDV:<br /> *Gastric dilatation: gas distension, on right lateral shows air in the fundus.<br /> *Gastric dilatation and volvulus: pylorus moves dorsally and left with a compartmentalized stomach. (GDV x-ray from WikiCommons[[http://commons.wikimedia.org/wiki/File:GDV_x-ray.JPG]])<br /> A right lateral view will show a large fundus ventrally, with a smaller gas filled pylorus located dorsally to that. These are seperated by a soft tissue strip. The contrast of the abdomen may be lost indicating peritonitis or [[Haemoabdomen|haemoabdomen]]. Gastric rupture would show as pneumoperitoneum and increased contrast.<br /> <br /> ==Treatment==<br /> The most important first line treatments are [[Principles of Fluid Therapy|fluid therapy]] and gastric decompression.<br /> <br /> ===Fluid therapy===<br /> Should be individualised to the patient due to the varying nature of the [[Essential Ion and Compound Balance and Homeostasis - Anatomy &amp; Physiology#Acid / Base|acid-base]] disturbances. Large bore (16 or 18 gauge) catheters should be placed into cephalic or jugular veins (ideally two into both cephalic veins). Shock doses of Compound Sodium Lactate (Lactated Ringer's Solution) (60-90ml/kg/h). Hypertonic saline can also be used. Monitoring of the situation should be done by regular blood pressure measurements, heart rates, PCV and total solids and urine output. Potassium can be supplemented to bags in the form of KCl after the initial shock doses.<br /> <br /> ===Gastric decompression===<br /> Performed by introduction of a lubricated premeasured (from nostril to last rib) stomach tube or by trocharizing the most tympanic area caudal to the ribs with a 14 to 16 gauge catheter. Sedation may be required to allow the passage of the stomach tube. Suitable drugs for this include [[Opioids#Butorphanol|butorphanol]], [[Opioids#Fentanyl|fentanyl]] or oxymorphone and [[Benzodiazepines#Diazepam|diazepam]].<br /> <br /> ===Other treatment===<br /> *For shock: [[Steroids|Prednisolone sodium succinate]] or [[Steroids|dexamethasone sodium phosphate]].<br /> *For bacterial translocation and endotoxaemia: Broad spectrum antibiotics (e.g. [[Cephalosporins|cephalosporin]] and a [[Fluoroquinolones|fluoroquinolone]]) should also be given at surgical induction through to the postoperative period.<br /> *For cardiac arrythmias: indicated if weakness, syncope, tachycardia runs with R on T complexes, ventricular tachycardia at rates &gt;150bpm. Treated by correcting [[Essential Ion and Compound Balance and Homeostasis - Anatomy &amp; Physiology#Acid / Base|acid-base]], [[Essential Ion and Compound Balance and Homeostasis - Anatomy &amp; Physiology|electrolyte]] and [[Haemostasis - Pathology|haemostatic]] disturbances. The treatment is [[Local Anaesthetics#Lidocaine|lidocaine]] by bolus or continuous rate infusion or procainamide if they persist.<br /> *For analgesia: Pure [[Opioids|opioid]] of [[Opioids#Morphine|morphine]], [[Opioids#Methadone|methadone]] or [[Opioids#Fentanyl|fentanyl]].<br /> *General: Oxygen supplementation if possible<br /> <br /> ===Anaesthesia===<br /> Anaesthesia must be carried out with care even after the patient has been stabilised. There are limited protocols but included [[Opioids#Fentanyl|fentanyl]] and [[Benzodiazepines#Diazepam|diazepam]] bolus or titrated [[Propofol|propofol]]. Maintenance can be achieved with the use of [[Isoflurane|isoflurane]] and [[Sevoflurane|sevoflurane]] in oxygen however [[Nitrous Oxide|nitrous oxide]] should be avoided due to third spacing. Regular routine monitoring of urine production, blood pressure, [[Blood Pressure#Central Venous Pressure|central venous pressure]], PCV, total solids, blood gas and serum electrolytes. High rates of fluids should be used to maintain tissue perfusion and arterial [[Blood Pressure|blood pressure]].<br /> <br /> ===Surgery===<br /> Surgical aims include:<br /> *Gastric decompression and repositioning<br /> *Assessing the organ viability<br /> *Removing necrotic tissue<br /> *Gastropexy (can perform incisional, tube, belt-loop and circumcostal techniques) to prevent recurrence<br /> <br /> If gastric necrosis (happens in 10-37% of patients) is present (discoloured dark purple or grey/green, don't bleed when incised or feel paper thin) then a parital gastrectomy is required. Damage to the spleen via avulsion or torsion may need partial or complete splenectomy.<br /> <br /> ===Post-operative complications===<br /> These are wide and varied and include:<br /> *Hypoperfusion<br /> *Hypotension<br /> *Cardiac arrythmias<br /> *[[Lungs Inflammatory - Pathology#Aspiration pneumonia|Aspiration pneumonia]]<br /> *[[Gastric Motility Disorders|Abnormal gastric motility]]<br /> *Gastric necrosis<br /> *[[Disseminated Intravascular Coagulation|DIC]]<br /> *Systemic Inflammatory Response Syndrome (SIRS)<br /> <br /> ==Prognosis==<br /> Simple GDV mortality rates are around 15%. Patients suffering from gastric necrosis, gastric resection or splenectomy have a higher mortality rate at over 30%. Gastric necorsis can be predicted by measuring plasma lactate. Values &gt;6mmol/l indicates necrosis (Specificity 88%, Sensitivity 66%)<br /> <br /> ==References==<br /> <br /> Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''<br /> <br /> King, L. and Hammond, R. (1999) '''BSAVA Manual of Canine and Feline Emergency and Critical Care''' ''BSAVA''<br /> <br /> Tivers, M. and Brockman, D. (2009) '''[[http://inpractice.bvapublications.com/cgi/reprint/31/2/66?maxtoshow=&amp;HITS=10&amp;hits=10&amp;RESULTFORMAT=&amp;author1=brockman&amp;searchid=1&amp;FIRSTINDEX=0&amp;sortspec=relevance&amp;resourcetype=HWCIT|Gastric dilation–volvulus syndrome in dogs 1. Pathophysiology, diagnosis and stabilisation]]''' 31(2):66 ''In Practice''<br /> <br /> Tivers, M. and Brockman, D. (2009) '''[[http://inpractice.bvapublications.com/cgi/reprint/31/3/114?maxtoshow=&amp;HITS=10&amp;hits=10&amp;RESULTFORMAT=&amp;author1=brockman&amp;andorexactfulltext=and&amp;searchid=1&amp;FIRSTINDEX=0&amp;sortspec=relevance&amp;resourcetype=HWCIT|Gastric dilation–volvulus syndromein dogs 2. Surgical and postoperative management]]''' 31(3):114 ''In Practice''<br /> <br /> ==From pathology section==<br /> <br /> * Is a consequence of '''gastric dilation'''.<br /> ** Gastric dilation occurs in dogs, cats, horses, rabbits and primates.<br /> ** Cause unclear but may be associated with overeating. <br /> ** Gastric dilation is most studied in dog, since it can lead to displacement of the [[Forestomach - Anatomy &amp; Physiology|stomach]] within the abdomen.<br /> <br /> ===Clinical===<br /> <br /> * Mainly affects large, deep-chested dogs - Great Dane, St. Bernard's and occasionally German Shepherd dogs.<br /> ** A similar condition also occurs in the pig.<br /> * Animal collapses suddenly and must be operated on rapidly.<br /> <br /> ===Pathogenesis===<br /> <br /> * Usually occurs around 30 minutes after a meal, or following aerophagia.<br /> ** [[Forestomach - Anatomy &amp; Physiology|Stomach]] is distended (gastric dilation).<br /> ** Animal excercises, and the [[Forestomach - Anatomy &amp; Physiology|stomach]] twists 180 degrees clockwise on its mesentery.<br /> * Torsion impairs the blood supply- the arterial supply is maintained BUT venous drainage is blocked.<br /> ** [[Forestomach - Anatomy &amp; Physiology|Stomach]] wall becomes severely congested and infarction of gastric mucosa may occur.<br /> * [[Forestomach - Anatomy &amp; Physiology|Stomach]] blows up with gas and fluid.<br /> ** Block venous return to heart.<br /> ** Compresses diaphragm and interferes with respiration.<br /> <br /> * '''The actual cause of the problem and the reason for accumulation of gas is unclear.'''<br /> ** It is better to feed big dogs small amounts more frequently.<br /> <br /> ===Pathology===<br /> <br /> ====Gross====<br /> <br /> * Following the pathogenesis above the [[Forestomach - Anatomy &amp; Physiology|stomach]] contents appear dark red/black and bloody, and the organ may rupture.<br /> * The [[Spleen - Anatomy &amp; Physiology|spleen]] is also affected by venous occlusion.<br /> ** Becomes very congested and moves from left to right side of abdomen.<br /> <br /> ====Histological====<br /> <br /> * Venous obstruction gives rise to congestion, oedema and necrosis of gastric mucosa.[[Category:Stomach_and_Abomasum_-_Pathology]][[Category:Dog]]<br /> [[Category:To_Do_-_Clinical]]</div>

Stuartd https://en.wikivet.net/index.php?title=Ceratopogonidae&diff=70064 2010-07-05T15:58:31Z

<p>Stuartd: </p> <hr /> <div>==Introduction==<br /> <br /> {| cellpadding=&quot;10&quot; cellspacing=&quot;0&quot; border=&quot;1&quot; <br /> | Also known as:<br /> | '''Midges<br /> |-<br /> | The most important veterinary species<br /> |'''''Culicoides''''' <br /> |-<br /> |}<br /> <br /> <br /> This parasite is found worldwide and attacks humans and a wide variety of animals.<br /> <br /> <br /> '''Recognition'''<br /> Culicoides are small flies 2-5mm long with a dark colouring. They have a characteristic arched thorax giving a 'hump-backed' appearance. The wings are mottled. <br /> <br /> <br /> '''Life cycle'''<br /> Eggs are laid onto plants near water and the larvae fall into water and pupate. The life cycle takes '''6-12 months''' to complete in temperate climates but is only '''1 month''' in tropical climates.<br /> <br /> <br /> '''Pathogenesis'''<br /> Culicoides is most active in late afternoon and early evening. Bites are painful and irritating. Only females suck blood.<br /> <br /> A bite causes [[Skin Immunologic - Pathology#Culicoides hypersensitivity|'Sweet itch']], a culicoides hypersensitivity reaction<br /> *Seasonally occurring allergic dermatitis of horses<br /> *Affects the base of the tail and the withers<br /> *Intermediate-type hypersensitivity reaction to the midge saliva<br /> <br /> The midge is a vector for several viruses:<br /> *[[Bluetongue Virus|Bluetongue]] <br /> *[[African Horse Sickness|African horse sickness]]<br /> <br /> It is also a vector for several other parasites:<br /> *''Onchocerca spp.'' in cattle and horses <br /> *[[Parasitic skin infections - Pathology#Onchocerciasis|Onchocerciasis]] <br /> *[[Parasitic skin infections - Pathology#Cutaneous habronemiasis|cutaneous habronemiasis]] <br /> *[[Parasitic skin infections - Pathology#Stephanofilariasis|stephanofilariasis]]<br /> <br /> <br /> '''Control'''<br /> This is difficult due to the extensive breeding sites but can include drainage of breeding sites, stabling horses at peak midge activity times e.g. from late afternoon to early morning, the use of insecticide fly strips in stables and topical fly repellent.<br /> <br /> <br /> [[Category:Biting_Flies]]<br /> [[Category:To_Do_-_Parasites]]<br /> [[Category:To_Do_-_Workshop]]</div>

Stuartd https://en.wikivet.net/index.php?title=Ceratopogonidae&diff=70063 2010-07-05T15:57:21Z

<p>Stuartd: </p> <hr /> <div>==Introduction==<br /> <br /> {| cellpadding=&quot;10&quot; cellspacing=&quot;0&quot; border=&quot;1&quot; <br /> | Also known as:<br /> | '''Midges<br /> |-<br /> | The most important veterinary species<br /> |'''''Culicoides''''' <br /> |-<br /> |}<br /> <br /> <br /> This parasite is found worldwide and attacks a wide variety of animals and also attacks humans.<br /> <br /> <br /> '''Recognition'''<br /> Small flies 2-5mm long with a dark colouring. They have a characteristic arched thorax giving a 'hump-backed' appearance. The wings are mottled. <br /> <br /> <br /> '''Life cycle'''<br /> Eggsare laid on to plants near water and the larvae fall into water and pupate. The life cycle takes '''6-12 months''' to complete in temperate climates but is only '''1 month''' in tropical climates.<br /> <br /> <br /> '''Pathogenesis'''<br /> Culicoides is most active in late afternoon and early evening. Bites are painful and irritating. Only females suck blood.<br /> <br /> A bite causes [[Skin Immunologic - Pathology#Culicoides hypersensitivity|'Sweet itch']], a culicoides hypersensitivity reaction<br /> *Seasonally occurring allergic dermatitis of horses<br /> *Affects the base of the tail and the withers<br /> *Intermediate-type hypersensitivity reaction to the midge saliva<br /> <br /> The midge is a vector for several viruses:<br /> *[[Bluetongue Virus|Bluetongue]] <br /> *[[African Horse Sickness|African horse sickness]]<br /> <br /> It is also a vector for several other parasites:<br /> *''Onchocerca spp.'' in cattle and horses <br /> *[[Parasitic skin infections - Pathology#Onchocerciasis|Onchocerciasis]] <br /> *[[Parasitic skin infections - Pathology#Cutaneous habronemiasis|cutaneous habronemiasis]] <br /> *[[Parasitic skin infections - Pathology#Stephanofilariasis|stephanofilariasis]]<br /> <br /> <br /> '''Control'''<br /> This is difficult due to the extensive breeding sites but can include drainage of breeding sites, stabling horses at peak midge activity times e.g. from late afternoon to early morning, the use of insecticide fly strips in stables and topical fly repellent.<br /> <br /> <br /> [[Category:Biting_Flies]]<br /> [[Category:To_Do_-_Parasites]]<br /> [[Category:To_Do_-_Workshop]]</div>

Stuartd https://en.wikivet.net/index.php?title=Ceratopogonidae&diff=70061 2010-07-05T15:56:53Z

<p>Stuartd: </p> <hr /> <div>==Introduction==<br /> <br /> {| cellpadding=&quot;10&quot; cellspacing=&quot;0&quot; border=&quot;1&quot; <br /> | Also known as:<br /> | '''Midges<br /> |-<br /> | The most important veterinary species<br /> |'''''Culicoides''''' <br /> |-<br /> |}<br /> <br /> <br /> This parasite is found worldwide and attacks a wide variety of animals and also attacks humans.<br /> <br /> <br /> '''Recognition'''<br /> Small flies 2-5mm long with a dark colouring. They have a characteristic arched thorax giving a 'hump-backed' appearance. The wings are mottled. <br /> <br /> <br /> '''Life cycle'''<br /> Eggsare laid on to plants near water and the larvae fall into water and pupate. The life cycle takes '''6-12 months''' to complete in temperate climates but is only '''1 month''' in tropical climates.<br /> <br /> <br /> '''Pathogenesis'''<br /> Culicoides is most active in late afternoon and early evening. Bites are painful and irritating. Only females suck blood.<br /> <br /> A bite causes [[Skin Immunologic - Pathology#Culicoides hypersensitivity|'Sweet itch']], a culicoides hypersensitivity reaction<br /> *Seasonally occurring allergic dermatitis of horses<br /> *Affects the base of the tail and the withers<br /> *Intermediate-type hypersensitivity reaction to the midge saliva<br /> <br /> The midge is a vector for several viruses:<br /> *[[Bluetongue Virus|Bluetongue]] <br /> *[[African Horse Sickness|African horse sickness]]<br /> <br /> It is also a vector for several other parasites:<br /> *''Onchocerca spp.'' in cattle and horses <br /> *[[Parasitic skin infections - Pathology#Onchocerciasis|Onchocerciasis]] <br /> *Involved in [[Parasitic skin infections - Pathology#Cutaneous habronemiasis|cutaneous habronemiasis]] <br /> *Involved in [[Parasitic skin infections - Pathology#Stephanofilariasis|stephanofilariasis]]<br /> <br /> <br /> '''Control'''<br /> This is difficult due to the extensive breeding sites but can include drainage of breeding sites, stabling horses at peak midge activity times e.g. from late afternoon to early morning, the use of insecticide fly strips in stables and topical fly repellent.<br /> <br /> <br /> [[Category:Biting_Flies]]<br /> [[Category:To_Do_-_Parasites]]<br /> [[Category:To_Do_-_Workshop]]</div>

Stuartd https://en.wikivet.net/index.php?title=Ceratopogonidae&diff=70060 2010-07-05T15:55:20Z

<p>Stuartd: </p> <hr /> <div>==Introduction==<br /> <br /> {| cellpadding=&quot;10&quot; cellspacing=&quot;0&quot; border=&quot;1&quot; <br /> | Also known as:<br /> | '''Midges<br /> |-<br /> | The most important veterinary species<br /> |'''''Culicoides''''' <br /> |-<br /> |}<br /> <br /> <br /> This parasite is found worldwide and attacks a wide variety of animals and also attacks humans.<br /> <br /> <br /> '''Recognition'''<br /> Small flies 2-5mm long with a dark colouring. They have a characteristic arched thorax giving a 'hump-backed' appearance. The wings are mottled. <br /> <br /> <br /> '''Life cycle'''<br /> Eggsare laid on to plants near water and the larvae fall into water and pupate. The life cycle takes '''6-12 months''' to complete in temperate climates but is only '''1 month''' in tropical climates.<br /> <br /> <br /> '''Pathogenesis'''<br /> Culicoides is most active in late afternoon and early evening. Bites are painful and irritating. Only females suck blood.<br /> <br /> A bite causes [[Skin Immunologic - Pathology#Culicoides hypersensitivity|'Sweet itch']], a culicoides hypersensitivity reaction<br /> *Seasonally occurring allergic dermatitis of horses<br /> *Affects the base of the tail and the withers<br /> *Intermediate-type hypersensitivity reaction to the midge saliva<br /> <br /> The midge is a vector for several viruses:<br /> *[[Bluetongue Virus|Bluetongue]] <br /> *[[African Horse Sickness|African horse sickness]]<br /> <br /> It is also a vector for several parasites:<br /> *''Onchocerca spp.'' in cattle and horses<br /> *[[Parasitic skin infections - Pathology#Protozoa|Protozoal skin infections]]<br /> <br /> *Causes [[Parasitic skin infections - Pathology#Flies|skin infections]] <br /> **[[Parasitic skin infections - Pathology#Onchocerciasis|Onchocerciasis]] <br /> **Involved in [[Parasitic skin infections - Pathology#Cutaneous habronemiasis|cutaneous habronemiasis]] <br /> **Involved in [[Parasitic skin infections - Pathology#Stephanofilariasis|stephanofilariasis]]<br /> <br /> <br /> '''Control'''<br /> This is difficult due to the extensive breeding sites but can include drainage of breeding sites, stabling horses at peak midge activity times e.g. from late afternoon to early morning, the use of insecticide fly strips in stables and topical fly repellent.<br /> <br /> Cause [[Culicoides Hypersensitivity]]<br /> <br /> [[Category:Biting_Flies]]<br /> [[Category:To_Do_-_Parasites]]<br /> [[Category:To_Do_-_Workshop]]</div>

Stuartd https://en.wikivet.net/index.php?title=Myxomatosis&diff=70045 2010-07-05T15:45:16Z

<p>Stuartd: </p> <hr /> <div>{{unfinished}}<br /> <br /> [[Image:MyxoRabbit.JPG|200px|right|thumb|A European Rabbit afflicted by Myxomatosis in Shropshire, England. Courtesy of WikiMedia]]<br /> <br /> This page explains the viral cause of Myxomatosis and the associated clinical signs, pathology and pathogenesis, treatment, control and prognosis.<br /> <br /> <br /> ===Myxoma virus===<br /> ====Hosts====<br /> *Causes Myxomatosis in rabbits<br /> ====Transmission====<br /> *Infectious myxomatosis is highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors. <br /> *Arthropod vectors such as mosquitoes and fleas provide the principal means of transmission. <br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia. <br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain. <br /> *The naturally attenuated viruses cause a milder disease of longer duration which favors vector transmission and persistence of the virus in nature. <br /> *High ambient environmental temperatures are associated with increased survival of infected animals. Some authors consider the California strains of the virus (California rabbit fibroma virus) as distinct from the myxoma virus, while others feel that the antigenic differences do not justify the separate distinction.<br /> *Several proteins encoded by the virus are immunosubversive in that they mimic host ligands or regulators (virokines) or are homologues of cellular cytokine receptors (viroceptors)<br /> ====Antigenicity====<br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia<br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain<br /> <br /> ===Clinical signs===<br /> *Clinical disease varies with virus strain and host species. <br /> **Sylvilagus species are relatively resistant, and are probably the natural host of the virus. In Sylvilagus species, infection usually results only in the development of skin tumors at the site of inoculation. The tumors appear 4-8 days after exposure and persist for up to 40 days. Very young rabbits may succumb to generalized disease.<br /> **Lepus species (hares) are highly resistant. Occasional individuals develop mild to severe generalized myxomatosis.<br /> **In the European rabbit (Oryctolagus cuniculus), infection with virulent virus (South American or California strains) results in severe disease with up to a 99% case fatality rate. <br /> ***Initial signs include edema of the eyelids accompanied by inflammation and edema around the anal, genital, oral, and nasal orifices. <br /> ***Edema of the head and ears, drooping ears, and bacterial infections resulting in mucopurulent conjunctivitis and pneumonia are seen. <br /> ***The primary tumor may be evident by 3-4 days after infection. Generalized tumors develop by 6-7 days after infection. <br /> ***Subcutaneous swellings become mucoid, gelatinous masses (hence the name myxomatosis). <br /> ***More chronic wart-like nodules appear, especially at mucocutaneous borders, after 10-14 days. <br /> ***Death (8-15 days post infection) is usually preceded by labored breathing and convulsions.<br /> <br /> ===Pathology===<br /> <br /> ====Gross Pathology====<br /> <br /> *The most prominent gross lesions in European rabbits with myxomatosis are the skin tumors and the pronounced cutaneous and subcutaneous edema, particularly in the area of the face and around body orifices. <br /> *Skin hemorrhages and subserosal petechiae and ecchymoses may be observed in the stomach and intestines. Subepicardial and subendocardial hemorrhages may also occur.<br /> *Adult rabbits of the genus Sylvilagus usually develop localized skin tumors resembling the fibromas produced in European rabbits by Shope fibroma virus.<br /> *Hares or young Sylvilagus rabbits may develop fibromatous to myxomatous nodules, however, lesions are usually mild and localized.<br /> <br /> ====Histopathology====<br /> <br /> *The lesions are proliferative to degenerative, depending on the virus strain. <br /> *The skin tumors result from proliferation of undifferentiated mesenchymal cells which become large stellate cells (myxoma cells). These cells may contain intracytoplasmic eosinophilic inclusions. These cells lie in a homogeneous matrix of mucinous material interspersed with capillaries and inflammatory cells. Endothelial proliferation with narrowing of the lumen and extrusion of stellate &quot;myxoma&quot; cells has been described. <br /> *Epithelial cells overlying the tumor may show hyperplasia or degeneration, or may appear normal. Epithelial proliferation is characterized by ballooning of cells in the stratum granulosum and hyperkeratosis. Epithelial vesiculation progresses to crust formation. Large, eosinophilic, intracytoplasmic inclusions are especially prominent in the stratum spinosum. Lesions in other organs include cellular proliferation of alveolar epithelium and the reticulum cells of lymph nodes and spleen. Focal hemorrhage may be present in skin, kidneys, lymph nodes, testes, heart, stomach, and intestinal walls. Myxoma cells may be present in lymph nodes, bone marrow, uterus, ovaries, testes, and lungs.<br /> <br /> <br /> ===Pathogenesis===<br /> *Infects several cell types including mucosal cells, lymphocytes, and fibroblasts<br /> *In addition to primary and secondary tumor development, there is severe immunosuppression leading to overwhelming infections by opportunistic gram-negative bacteria (esp. conjunctiva and nasal passages)<br /> *Virus multiplication and tumor-like lesions occur initially at the site of intradermal inoculation <br /> *This is followed by spread to regional lymph nodes and cell-associated viremia, with generalization to the skin and internal organs<br /> *Gelatinous proliferative nodules all over body, especially at orifices (eyes, anus, nose)<br /> *Rabbit dies within 12 days, if not killed by predators<br /> <br /> =====In more detail=====<br /> *Virulent strains of MYX and MRV secrete a T2 gene product with significant homology to the T2 protein secreted by Shope fibroma virus. This protein acts as a receptor for TNFα and TNFβ. TNF is active in killing virus infected and tumor cells. Cytotoxicity is correlated with the induction of toxic superoxide radicals. The T2 gene product enhances viral virulence by interfering with TNF-dependent immune response pathways of the host.<br /> *Myxoma virus and MRV have also been shown to compromise cell-mediated immunity by inducing a loss of class I MHC antigens from the surface of infected cells. MHC class I-restricted cytotoxic T lymphocytes play a major role in clearing poxvirus infections from susceptible animal hosts, and are an important factor in limiting virus spread within the host. Class I molecules are present on all nucleated cells and platelets. Cytotoxic T cells (CD8+) recognize intracellular viral antigen in association with class I MHC glycoproteins on the cell surface. MYX and MRV infection results in a specific, rapid decrease in detectable surface class I epitopes. It has been suggested that a late viral gene product may interact with the class I complex to either physically sequester the complex away from the cell surface and inhibit its recycling to the surface, or induce a conformational change in the complex rendering it unrecognizable by cytotoxic T lymphocytes.<br /> *Myxoma growth factor (MGF) and a gene product designated M11L are also associated with MYX virulence. MGF and M11L deleted mutants are markedly attenuated, capable of inducing only benign localized nodules that regress spontaneously, similar to lesions induced by Shope fibroma virus. MGF has significant sequence homology with epidermal growth factor and transforming growth factor β. It has been postulated that the presence of EGF/TGFβ-like growth factors in tumorigenic poxviruses affects the growth and progression of poxvirus-infected cells.<br /> *Another myxoma virus virulence factor designated MYXOMA SERPIN 1 (SERP 1) has significant sequence homology with members of the family of serine proteases inhibitors (serpins). The exact role of SERP 1 is unknown but it may theoretically affect antigen presentation by interfering with viral protein degradation, or might reduce cytoxic T cell killing mediated by serine proteases in the effector cell.<br /> *Rabbit poxvirus gene sequences coding for products related to the C4 and C5 components of the complement cascade have been identified. It is postulated that complement-like viral protein products may block the activation or action of complement. The virulence factor T7 is an IFNγ receptor homologue.<br /> <br /> <br /> ===Epidemiology===<br /> *Highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors<br /> *Mosquitoes act as mechanical vectors<br /> *High ambient environmental temperatures are associated with increased survival of infected animals<br /> <br /> ===Differentials===<br /> *[[Shope fibroma virus|Shope Fibroma Virus]]<br /> **Localised benign tumours that spontaneously regress in adult immunocompetent rabbits<br /> *[[Malignant rabbit fibroma virus|Malignant Rabbit Fibroma Virus]]<br /> **MRV is a recombinant between Myxoma virus and Shope fibroma virus.<br /> **Causes a lethal disease with numerous primary and secondary tumours and immunosuppression.<br /> <br /> ===Control===<br /> *Attenuated vaccines are used for farmed and pet rabbits<br /> *Wild suspect animals should be culled<br /> <br /> [[Category:Leporipoxviruses]][[Category:Rabbit]]<br /> [[Category:To_Do_-_Review]]<br /> [[Category:To_Do_-_Stuart]]</div>

Stuartd https://en.wikivet.net/index.php?title=Myxomatosis&diff=70037 2010-07-05T14:55:34Z

<p>Stuartd: </p> <hr /> <div>{{unfinished}}<br /> <br /> [[Image:MyxoRabbit.JPG|200px|right|thumb|A European Rabbit afflicted by Myxomatosis in Shropshire, England. Courtesy of WikiMedia]]<br /> <br /> This page explains the viral cause of Myxomatosis and the associated clinical signs, pathology and pathogenesis, treatment, control and prognosis.<br /> <br /> <br /> ===Myxoma virus===<br /> ====Hosts====<br /> *Causes Myxomatosis in rabbits<br /> ====Transmission====<br /> *Infectious myxomatosis is highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors. <br /> *Arthropod vectors such as mosquitoes and fleas provide the principal means of transmission. <br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia. <br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain. <br /> *The naturally attenuated viruses cause a milder disease of longer duration which favors vector transmission and persistence of the virus in nature. <br /> *High ambient environmental temperatures are associated with increased survival of infected animals. Some authors consider the California strains of the virus (California rabbit fibroma virus) as distinct from the myxoma virus, while others feel that the antigenic differences do not justify the separate distinction.<br /> *Several proteins encoded by the virus are immunosubversive in that they mimic host ligands or regulators (virokines) or are homologues of cellular cytokine receptors (viroceptors)<br /> ====Antigenicity====<br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia<br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain<br /> <br /> ===Clinical signs===<br /> *Clinical disease varies with virus strain and host species. <br /> **Sylvilagus species are relatively resistant, and are probably the natural host of the virus. In Sylvilagus species, infection usually results only in the development of skin tumors at the site of inoculation. The tumors appear 4-8 days after exposure and persist for up to 40 days. Very young rabbits may succumb to generalized disease.<br /> **Lepus species (hares) are highly resistant. Occasional individuals develop mild to severe generalized myxomatosis.<br /> **In the European rabbit (Oryctolagus cuniculus), infection with virulent virus (South American or California strains) results in severe disease with up to a 99% case fatality rate. <br /> ***Initial signs include edema of the eyelids accompanied by inflammation and edema around the anal, genital, oral, and nasal orifices. <br /> ***Edema of the head and ears, drooping ears, and bacterial infections resulting in mucopurulent conjunctivitis and pneumonia are seen. <br /> ***The primary tumor may be evident by 3-4 days after infection. Generalized tumors develop by 6-7 days after infection. <br /> ***Subcutaneous swellings become mucoid, gelatinous masses (hence the name myxomatosis). <br /> ***More chronic wart-like nodules appear, especially at mucocutaneous borders, after 10-14 days. <br /> ***Death (8-15 days post infection) is usually preceded by labored breathing and convulsions.<br /> <br /> ===Pathology===<br /> <br /> ====Gross Pathology====<br /> <br /> *The most prominent gross lesions in European rabbits with myxomatosis are the skin tumors and the pronounced cutaneous and subcutaneous edema, particularly in the area of the face and around body orifices. <br /> *Skin hemorrhages and subserosal petechiae and ecchymoses may be observed in the stomach and intestines. Subepicardial and subendocardial hemorrhages may also occur.<br /> *Adult rabbits of the genus Sylvilagus usually develop localized skin tumors resembling the fibromas produced in European rabbits by Shope fibroma virus.<br /> *Hares or young Sylvilagus rabbits may develop fibromatous to myxomatous nodules, however, lesions are usually mild and localized.<br /> <br /> ====Histopathology====<br /> <br /> *The lesions are proliferative to degenerative, depending on the virus strain. <br /> *The skin tumors result from proliferation of undifferentiated mesenchymal cells which become large stellate cells (myxoma cells). These cells may contain intracytoplasmic eosinophilic inclusions. These cells lie in a homogeneous matrix of mucinous material interspersed with capillaries and inflammatory cells. Endothelial proliferation with narrowing of the lumen and extrusion of stellate &quot;myxoma&quot; cells has been described. <br /> *Epithelial cells overlying the tumor may show hyperplasia or degeneration, or may appear normal. Epithelial proliferation is characterized by ballooning of cells in the stratum granulosum and hyperkeratosis. Epithelial vesiculation progresses to crust formation. Large, eosinophilic, intracytoplasmic inclusions are especially prominent in the stratum spinosum. Lesions in other organs include cellular proliferation of alveolar epithelium and the reticulum cells of lymph nodes and spleen. Focal hemorrhage may be present in skin, kidneys, lymph nodes, testes, heart, stomach, and intestinal walls. Myxoma cells may be present in lymph nodes, bone marrow, uterus, ovaries, testes, and lungs.<br /> <br /> <br /> ===Pathogenesis===<br /> *Infects several cell types including mucosal cells, lymphocytes, and fibroblasts<br /> *In addition to primary and secondary tumor development, there is severe immunosuppression leading to overwhelming infections by opportunistic gram-negative bacteria (esp. conjunctiva and nasal passages)<br /> *Virus multiplication and tumor-like lesions occur initially at the site of intradermal inoculation <br /> *This is followed by spread to regional lymph nodes and cell-associated viremia, with generalization to the skin and internal organs<br /> *Gelatinous proliferative nodules all over body, especially at orifices (eyes, anus, nose)<br /> *Rabbit dies within 12 days, if not killed by predators<br /> <br /> =====In more detail=====<br /> *Virulent strains of MYX and MRV secrete a T2 gene product with significant homology to the T2 protein secreted by Shope fibroma virus. This protein acts as a receptor for TNFα and TNFβ. TNF is active in killing virus infected and tumor cells. Cytotoxicity is correlated with the induction of toxic superoxide radicals. The T2 gene product enhances viral virulence by interfering with TNF-dependent immune response pathways of the host.<br /> *Myxoma virus and MRV have also been shown to compromise cell-mediated immunity by inducing a loss of class I MHC antigens from the surface of infected cells. MHC class I-restricted cytotoxic T lymphocytes play a major role in clearing poxvirus infections from susceptible animal hosts, and are an important factor in limiting virus spread within the host. Class I molecules are present on all nucleated cells and platelets. Cytotoxic T cells (CD8+) recognize intracellular viral antigen in association with class I MHC glycoproteins on the cell surface. MYX and MRV infection results in a specific, rapid decrease in detectable surface class I epitopes. It has been suggested that a late viral gene product may interact with the class I complex to either physically sequester the complex away from the cell surface and inhibit its recycling to the surface, or induce a conformational change in the complex rendering it unrecognizable by cytotoxic T lymphocytes.<br /> *Myxoma growth factor (MGF) and a gene product designated M11L are also associated with MYX virulence. MGF and M11L deleted mutants are markedly attenuated, capable of inducing only benign localized nodules that regress spontaneously, similar to lesions induced by Shope fibroma virus. MGF has significant sequence homology with epidermal growth factor and transforming growth factor β. It has been postulated that the presence of EGF/TGFβ-like growth factors in tumorigenic poxviruses affects the growth and progression of poxvirus-infected cells.<br /> *Another myxoma virus virulence factor designated MYXOMA SERPIN 1 (SERP 1) has significant sequence homology with members of the family of serine proteases inhibitors (serpins). The exact role of SERP 1 is unknown but it may theoretically affect antigen presentation by interfering with viral protein degradation, or might reduce cytoxic T cell killing mediated by serine proteases in the effector cell.<br /> *Rabbit poxvirus gene sequences coding for products related to the C4 and C5 components of the complement cascade have been identified. It is postulated that complement-like viral protein products may block the activation or action of complement. The virulence factor T7 is an IFNγ receptor homologue.<br /> <br /> <br /> ===Epidemiology===<br /> *Highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors<br /> *Mosquitoes act as mechanical vectors<br /> *High ambient environmental temperatures are associated with increased survival of infected animals<br /> <br /> ===Differentials===<br /> *[[Shope fibroma virus|Shope Fibroma Virus]]<br /> **Localised benign tumours that spontaneously regress in adult immunocompetent rabbits<br /> *[[Malignant rabbit fibroma virus|Malignant Rabbit Fibroma Virus]]<br /> **MRV is a recombinant between Myxoma virus and Shope fibroma virus.<br /> **Causes a lethal disease with numerous primary and secondary tumours and immunosuppression.<br /> <br /> ===Control===<br /> *Attenuated vaccines are used for farmed and pet rabbits<br /> *Wild suspect animals should be culled<br /> <br /> [[Category:Leporipoxviruses]][[Category:Rabbit]]<br /> [[Category:To_Do_-_Viruses]]<br /> [[Category:To_Do_-_Stuart]]</div>

Stuartd https://en.wikivet.net/index.php?title=Myxomatosis&diff=70034 2010-07-05T14:54:24Z

<p>Stuartd: </p> <hr /> <div>{{unfinished}}<br /> <br /> [[Image:MyxoRabbit.JPG|200px|right|thumb|A European Rabbit afflicted by Myxomatosis in Shropshire, England. Courtesy of WikiMedia]]<br /> <br /> This page explains the viral cause of Myxomatosis and the associated clinical signs, pathology and pathogenesis, treatment, control and prognosis.<br /> <br /> <br /> ===Myxoma virus===<br /> ====Hosts====<br /> *Causes Myxomatosis in rabbits<br /> ====Transmission====<br /> *Infectious myxomatosis is highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors. <br /> *Arthropod vectors such as mosquitoes and fleas provide the principal means of transmission. <br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia. <br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain. <br /> *The naturally attenuated viruses cause a milder disease of longer duration which favors vector transmission and persistence of the virus in nature. <br /> *High ambient environmental temperatures are associated with increased survival of infected animals. Some authors consider the California strains of the virus (California rabbit fibroma virus) as distinct from the myxoma virus, while others feel that the antigenic differences do not justify the separate distinction.<br /> *Several proteins encoded by the virus are immunosubversive in that they mimic host ligands or regulators (virokines) or are homologues of cellular cytokine receptors (viroceptors)<br /> ====Antigenicity====<br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia<br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain<br /> <br /> ===Clinical signs===<br /> *Clinical disease varies with virus strain and host species. <br /> **Sylvilagus species are relatively resistant, and are probably the natural host of the virus. In Sylvilagus species, infection usually results only in the development of skin tumors at the site of inoculation. The tumors appear 4-8 days after exposure and persist for up to 40 days. Very young rabbits may succumb to generalized disease.<br /> **Lepus species (hares) are highly resistant. Occasional individuals develop mild to severe generalized myxomatosis.<br /> **In the European rabbit (Oryctolagus cuniculus), infection with virulent virus (South American or California strains) results in severe disease with up to a 99% case fatality rate. <br /> ***Initial signs include edema of the eyelids accompanied by inflammation and edema around the anal, genital, oral, and nasal orifices. <br /> ***Edema of the head and ears, drooping ears, and bacterial infections resulting in mucopurulent conjunctivitis and pneumonia are seen. <br /> ***The primary tumor may be evident by 3-4 days after infection. Generalized tumors develop by 6-7 days after infection. <br /> ***Subcutaneous swellings become mucoid, gelatinous masses (hence the name myxomatosis). <br /> ***More chronic wart-like nodules appear, especially at mucocutaneous borders, after 10-14 days. <br /> ***Death (8-15 days post infection) is usually preceded by labored breathing and convulsions.<br /> <br /> ===Pathology===<br /> <br /> ====Gross Pathology====<br /> <br /> *The most prominent gross lesions in European rabbits with myxomatosis are the skin tumors and the pronounced cutaneous and subcutaneous edema, particularly in the area of the face and around body orifices. <br /> *Skin hemorrhages and subserosal petechiae and ecchymoses may be observed in the stomach and intestines. Subepicardial and subendocardial hemorrhages may also occur.<br /> *Adult rabbits of the genus Sylvilagus usually develop localized skin tumors resembling the fibromas produced in European rabbits by Shope fibroma virus.<br /> *Hares or young Sylvilagus rabbits may develop fibromatous to myxomatous nodules, however, lesions are usually mild and localized.<br /> <br /> ====Histopathology====<br /> <br /> *The lesions are proliferative to degenerative, depending on the virus strain. <br /> *The skin tumors result from proliferation of undifferentiated mesenchymal cells which become large stellate cells (myxoma cells). These cells may contain intracytoplasmic eosinophilic inclusions. These cells lie in a homogeneous matrix of mucinous material interspersed with capillaries and inflammatory cells. Endothelial proliferation with narrowing of the lumen and extrusion of stellate &quot;myxoma&quot; cells has been described. <br /> *Epithelial cells overlying the tumor may show hyperplasia or degeneration, or may appear normal. Epithelial proliferation is characterized by ballooning of cells in the stratum granulosum and hyperkeratosis. Epithelial vesiculation progresses to crust formation. Large, eosinophilic, intracytoplasmic inclusions are especially prominent in the stratum spinosum. Lesions in other organs include cellular proliferation of alveolar epithelium and the reticulum cells of lymph nodes and spleen. Focal hemorrhage may be present in skin, kidneys, lymph nodes, testes, heart, stomach, and intestinal walls. Myxoma cells may be present in lymph nodes, bone marrow, uterus, ovaries, testes, and lungs.<br /> <br /> <br /> ===Pathogenesis===<br /> *Infects several cell types including mucosal cells, lymphocytes, and fibroblasts<br /> *In addition to primary and secondary tumor development, there is severe immunosuppression leading to overwhelming infections by opportunistic gram-negative bacteria (esp. conjunctiva and nasal passages)<br /> *Virus multiplication and tumor-like lesions occur initially at the site of intradermal inoculation <br /> *This is followed by spread to regional lymph nodes and cell-associated viremia, with generalization to the skin and internal organs<br /> *Gelatinous proliferative nodules all over body, especially at orifices (eyes, anus, nose)<br /> *Rabbit dies within 12 days, if not killed by predators<br /> <br /> =====In more detail=====<br /> *Virulent strains of MYX and MRV secrete a T2 gene product with significant homology to the T2 protein secreted by Shope fibroma virus. This protein acts as a receptor for TNFα and TNFβ. TNF is active in killing virus infected and tumor cells. Cytotoxicity is correlated with the induction of toxic superoxide radicals. The T2 gene product enhances viral virulence by interfering with TNF-dependent immune response pathways of the host.<br /> *Myxoma virus and MRV have also been shown to compromise cell-mediated immunity by inducing a loss of class I MHC antigens from the surface of infected cells. MHC class I-restricted cytotoxic T lymphocytes play a major role in clearing poxvirus infections from susceptible animal hosts, and are an important factor in limiting virus spread within the host. Class I molecules are present on all nucleated cells and platelets. Cytotoxic T cells (CD8+) recognize intracellular viral antigen in association with class I MHC glycoproteins on the cell surface. MYX and MRV infection results in a specific, rapid decrease in detectable surface class I epitopes. It has been suggested that a late viral gene product may interact with the class I complex to either physically sequester the complex away from the cell surface and inhibit its recycling to the surface, or induce a conformational change in the complex rendering it unrecognizable by cytotoxic T lymphocytes.<br /> *Myxoma growth factor (MGF) and a gene product designated M11L are also associated with MYX virulence. MGF and M11L deleted mutants are markedly attenuated, capable of inducing only benign localized nodules that regress spontaneously, similar to lesions induced by Shope fibroma virus. MGF has significant sequence homology with epidermal growth factor and transforming growth factor β. It has been postulated that the presence of EGF/TGFβ-like growth factors in tumorigenic poxviruses affects the growth and progression of poxvirus-infected cells.<br /> *Another myxoma virus virulence factor designated MYXOMA SERPIN 1 (SERP 1) has significant sequence homology with members of the family of serine proteases inhibitors (serpins). The exact role of SERP 1 is unknown but it may theoretically affect antigen presentation by interfering with viral protein degradation, or might reduce cytoxic T cell killing mediated by serine proteases in the effector cell.<br /> *Rabbit poxvirus gene sequences coding for products related to the C4 and C5 components of the complement cascade have been identified. It is postulated that complement-like viral protein products may block the activation or action of complement. The virulence factor T7 is an IFNγ receptor homologue.<br /> <br /> <br /> ===Epidemiology===<br /> *Highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors<br /> *Mosquitoes act as mechanical vectors<br /> *High ambient environmental temperatures are associated with increased survival of infected animals<br /> <br /> ===Differentials===<br /> *[[Shope fibroma virus|Shope Fibroma Virus]]<br /> **Localised benign tumours that spontaneously regress in adult immunocompetent rabbits<br /> *[[Malignant rabbit fibroma virus|Malignant Rabbit Fibroma Virus]]<br /> **MRV is a recombinant between Myxoma virus and Shope fibroma virus.<br /> **Causes a lethal disease with numerous primary and secondary tumours and immunosuppression.<br /> <br /> ===Control===<br /> *Attenuated vaccines are used for farmed and pet rabbits<br /> *Wild suspect animals should be culled<br /> <br /> [[Category:Leporipoxviruses]][[Category:Rabbit]]<br /> [[Category:To_Do_-_Review]]<br /> [[Category:To_Do_-_Stuart]]</div>

Stuartd https://en.wikivet.net/index.php?title=Myxomatosis&diff=70022 2010-07-05T14:50:24Z

<p>Stuartd: </p> <hr /> <div>{{unfinished}}<br /> <br /> [[Image:MyxoRabbit.JPG|200px|right|thumb|A European Rabbit afflicted by Myxomatosis in Shropshire, England. Courtesy of WikiMedia]]<br /> <br /> This page explains the viral cause of Myxomatosis and the associated clinical signs, pathology and pathogenesis, treatment, control and prognosis.<br /> <br /> <br /> ===Myxoma virus===<br /> ====Hosts====<br /> *Causes Myxomatosis in rabbits<br /> ====Transmission====<br /> *Infectious myxomatosis is highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors. <br /> *Arthropod vectors such as mosquitoes and fleas provide the principal means of transmission. <br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia. <br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain. <br /> *The naturally attenuated viruses cause a milder disease of longer duration which favors vector transmission and persistence of the virus in nature. <br /> *High ambient environmental temperatures are associated with increased survival of infected animals. Some authors consider the California strains of the virus (California rabbit fibroma virus) as distinct from the myxoma virus, while others feel that the antigenic differences do not justify the separate distinction.<br /> *Several proteins encoded by the virus are immunosubversive in that they mimic host ligands or regulators (virokines) or are homologues of cellular cytokine receptors (viroceptors)<br /> ====Antigenicity====<br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia<br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain<br /> <br /> ===Clinical signs===<br /> *Clinical disease varies with virus strain and host species. <br /> **Sylvilagus species are relatively resistant, and are probably the natural host of the virus. In Sylvilagus species, infection usually results only in the development of skin tumors at the site of inoculation. The tumors appear 4-8 days after exposure and persist for up to 40 days. Very young rabbits may succumb to generalized disease.<br /> **Lepus species (hares) are highly resistant. Occasional individuals develop mild to severe generalized myxomatosis.<br /> **In the European rabbit (Oryctolagus cuniculus), infection with virulent virus (South American or California strains) results in severe disease with up to a 99% case fatality rate. <br /> ***Initial signs include edema of the eyelids accompanied by inflammation and edema around the anal, genital, oral, and nasal orifices. <br /> ***Edema of the head and ears, drooping ears, and bacterial infections resulting in mucopurulent conjunctivitis and pneumonia are seen. <br /> ***The primary tumor may be evident by 3-4 days after infection. Generalized tumors develop by 6-7 days after infection. <br /> ***Subcutaneous swellings become mucoid, gelatinous masses (hence the name myxomatosis). <br /> ***More chronic wart-like nodules appear, especially at mucocutaneous borders, after 10-14 days. <br /> ***Death (8-15 days post infection) is usually preceded by labored breathing and convulsions.<br /> <br /> ===Pathology===<br /> <br /> ====Gross Pathology====<br /> <br /> *The most prominent gross lesions in European rabbits with myxomatosis are the skin tumors and the pronounced cutaneous and subcutaneous edema, particularly in the area of the face and around body orifices. <br /> *Skin hemorrhages and subserosal petechiae and ecchymoses may be observed in the stomach and intestines. Subepicardial and subendocardial hemorrhages may also occur.<br /> *Adult rabbits of the genus Sylvilagus usually develop localized skin tumors resembling the fibromas produced in European rabbits by Shope fibroma virus.<br /> *Hares or young Sylvilagus rabbits may develop fibromatous to myxomatous nodules, however, lesions are usually mild and localized.<br /> <br /> ====Histopathology====<br /> <br /> *The lesions are proliferative to degenerative, depending on the virus strain. <br /> *The skin tumors result from proliferation of undifferentiated mesenchymal cells which become large stellate cells (myxoma cells). These cells may contain intracytoplasmic eosinophilic inclusions. These cells lie in a homogeneous matrix of mucinous material interspersed with capillaries and inflammatory cells. Endothelial proliferation with narrowing of the lumen and extrusion of stellate &quot;myxoma&quot; cells has been described. <br /> *Epithelial cells overlying the tumor may show hyperplasia or degeneration, or may appear normal. Epithelial proliferation is characterized by ballooning of cells in the stratum granulosum and hyperkeratosis. Epithelial vesiculation progresses to crust formation. Large, eosinophilic, intracytoplasmic inclusions are especially prominent in the stratum spinosum. Lesions in other organs include cellular proliferation of alveolar epithelium and the reticulum cells of lymph nodes and spleen. Focal hemorrhage may be present in skin, kidneys, lymph nodes, testes, heart, stomach, and intestinal walls. Myxoma cells may be present in lymph nodes, bone marrow, uterus, ovaries, testes, and lungs.<br /> <br /> <br /> ===Pathogenesis===<br /> *Infects several cell types including mucosal cells, lymphocytes, and fibroblasts<br /> *In addition to primary and secondary tumor development, there is severe immunosuppression leading to overwhelming infections by opportunistic gram-negative bacteria (esp. conjunctiva and nasal passages)<br /> *Virus multiplication and tumor-like lesions occur initially at the site of intradermal inoculation <br /> *This is followed by spread to regional lymph nodes and cell-associated viremia, with generalization to the skin and internal organs<br /> *Gelatinous proliferative nodules all over body, especially at orifices (eyes, anus, nose)<br /> *Rabbit dies within 12 days, if not killed by predators<br /> <br /> =====In more detail=====<br /> *Virulent strains of MYX and MRV secrete a T2 gene product with significant homology to the T2 protein secreted by Shope fibroma virus. This protein acts as a receptor for TNFα and TNFβ. TNF is active in killing virus infected and tumor cells. Cytotoxicity is correlated with the induction of toxic superoxide radicals. The T2 gene product enhances viral virulence by interfering with TNF-dependent immune response pathways of the host.<br /> *Myxoma virus and MRV have also been shown to compromise cell-mediated immunity by inducing a loss of class I MHC antigens from the surface of infected cells. MHC class I-restricted cytotoxic T lymphocytes play a major role in clearing poxvirus infections from susceptible animal hosts, and are an important factor in limiting virus spread within the host. Class I molecules are present on all nucleated cells and platelets. Cytotoxic T cells (CD8+) recognize intracellular viral antigen in association with class I MHC glycoproteins on the cell surface. MYX and MRV infection results in a specific, rapid decrease in detectable surface class I epitopes. It has been suggested that a late viral gene product may interact with the class I complex to either physically sequester the complex away from the cell surface and inhibit its recycling to the surface, or induce a conformational change in the complex rendering it unrecognizable by cytotoxic T lymphocytes.<br /> *Myxoma growth factor (MGF) and a gene product designated M11L are also associated with MYX virulence. MGF and M11L deleted mutants are markedly attenuated, capable of inducing only benign localized nodules that regress spontaneously, similar to lesions induced by Shope fibroma virus. MGF has significant sequence homology with epidermal growth factor and transforming growth factor β. It has been postulated that the presence of EGF/TGFβ-like growth factors in tumorigenic poxviruses affects the growth and progression of poxvirus-infected cells.<br /> *Another myxoma virus virulence factor designated MYXOMA SERPIN 1 (SERP 1) has significant sequence homology with members of the family of serine proteases inhibitors (serpins). The exact role of SERP 1 is unknown but it may theoretically affect antigen presentation by interfering with viral protein degradation, or might reduce cytoxic T cell killing mediated by serine proteases in the effector cell.<br /> *Rabbit poxvirus gene sequences coding for products related to the C4 and C5 components of the complement cascade have been identified. It is postulated that complement-like viral protein products may block the activation or action of complement. The virulence factor T7 is an IFNγ receptor homologue.<br /> <br /> <br /> ===Epidemiology===<br /> *Highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors<br /> *Mosquitoes act as mechanical vectors<br /> *High ambient environmental temperatures are associated with increased survival of infected animals<br /> <br /> ===Differentials===<br /> *[[Shope fibroma virus|Shope Fibroma Virus]]<br /> **Localised benign tumours that spontaneously regress in adult immunocompetent rabbits<br /> *[[Malignant rabbit fibroma virus|Malignant Rabbit Fibroma Virus]]<br /> **MRV is a recombinant between Myxoma virus and Shope fibroma virus.<br /> **Causes a lethal disease with numerous primary and secondary tumours and immunosuppression.<br /> <br /> ===Control===<br /> *Attenuated vaccines are used for farmed and pet rabbits<br /> *Wild suspect animals should be culled<br /> <br /> [[Category:Leporipoxviruses]][[Category:Rabbit]]<br /> [[Category:To_Do_-_Viruses]]<br /> [[Category:To_Do_-_Stuart]]</div>

Stuartd https://en.wikivet.net/index.php?title=Myxomatosis&diff=70018 2010-07-05T14:48:30Z

<p>Stuartd: </p> <hr /> <div>{{unfinished}}<br /> <br /> [[Image:MyxoRabbit.JPG|200px|right|thumb|A European Rabbit afflicted by Myxomatosis in Shropshire, England. Courtesy of WikiMedia]]<br /> <br /> This page explains the viral cause of Myxomatosis and the associated clinical signs, pathology and pathogenesis, treatment, control and prognosis.<br /> <br /> <br /> ===Myxoma virus===<br /> ====Hosts====<br /> *Causes Myxomatosis in rabbits<br /> ====Transmission====<br /> *Infectious myxomatosis is highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors. <br /> *Arthropod vectors such as mosquitoes and fleas provide the principal means of transmission. <br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia. <br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain. <br /> *The naturally attenuated viruses cause a milder disease of longer duration which favors vector transmission and persistence of the virus in nature. <br /> *High ambient environmental temperatures are associated with increased survival of infected animals. Some authors consider the California strains of the virus (California rabbit fibroma virus) as distinct from the myxoma virus, while others feel that the antigenic differences do not justify the separate distinction.<br /> *Several proteins encoded by the virus are immunosubversive in that they mimic host ligands or regulators (virokines) or are homologues of cellular cytokine receptors (viroceptors)<br /> ====Antigenicity====<br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia<br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain<br /> <br /> ===Clinical signs===<br /> *Clinical disease varies with virus strain and host species. <br /> **Sylvilagus species are relatively resistant, and are probably the natural host of the virus. In Sylvilagus species, infection usually results only in the development of skin tumors at the site of inoculation. The tumors appear 4-8 days after exposure and persist for up to 40 days. Very young rabbits may succumb to generalized disease.<br /> **Lepus species (hares) are highly resistant. Occasional individuals develop mild to severe generalized myxomatosis.<br /> **In the European rabbit (Oryctolagus cuniculus), infection with virulent virus (South American or California strains) results in severe disease with up to a 99% case fatality rate. <br /> ***Initial signs include edema of the eyelids accompanied by inflammation and edema around the anal, genital, oral, and nasal orifices. <br /> ***Edema of the head and ears, drooping ears, and bacterial infections resulting in mucopurulent conjunctivitis and pneumonia are seen. <br /> ***The primary tumor may be evident by 3-4 days after infection. Generalized tumors develop by 6-7 days after infection. <br /> ***Subcutaneous swellings become mucoid, gelatinous masses (hence the name myxomatosis). <br /> ***More chronic wart-like nodules appear, especially at mucocutaneous borders, after 10-14 days. <br /> ***Death (8-15 days post infection) is usually preceded by labored breathing and convulsions.<br /> <br /> ===Pathology===<br /> <br /> ====Gross Pathology====<br /> <br /> *The most prominent gross lesions in European rabbits with myxomatosis are the skin tumors and the pronounced cutaneous and subcutaneous edema, particularly in the area of the face and around body orifices. <br /> *Skin hemorrhages and subserosal petechiae and ecchymoses may be observed in the stomach and intestines. Subepicardial and subendocardial hemorrhages may also occur.<br /> *Adult rabbits of the genus Sylvilagus usually develop localized skin tumors resembling the fibromas produced in European rabbits by Shope fibroma virus.<br /> *Hares or young Sylvilagus rabbits may develop fibromatous to myxomatous nodules, however, lesions are usually mild and localized.<br /> <br /> ====Histopathology====<br /> <br /> *The lesions are proliferative to degenerative, depending on the virus strain. <br /> *The skin tumors result from proliferation of undifferentiated mesenchymal cells which become large stellate cells (myxoma cells). These cells may contain intracytoplasmic eosinophilic inclusions. These cells lie in a homogeneous matrix of mucinous material interspersed with capillaries and inflammatory cells. Endothelial proliferation with narrowing of the lumen and extrusion of stellate &quot;myxoma&quot; cells has been described. <br /> *Epithelial cells overlying the tumor may show hyperplasia or degeneration, or may appear normal. Epithelial proliferation is characterized by ballooning of cells in the stratum granulosum and hyperkeratosis. Epithelial vesiculation progresses to crust formation. Large, eosinophilic, intracytoplasmic inclusions are especially prominent in the stratum spinosum. Lesions in other organs include cellular proliferation of alveolar epithelium and the reticulum cells of [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]] and [[Spleen - Anatomy &amp; Physiology|spleen]]. Focal hemorrhage may be present in skin, kidneys, lymph nodes, testes, heart, stomach, and intestinal walls. Myxoma cells may be present in lymph nodes, bone marrow, uterus, ovaries, testes, and lungs.<br /> <br /> <br /> ===Pathogenesis===<br /> *Infects several cell types including mucosal cells, lymphocytes, and fibroblasts<br /> *In addition to primary and secondary tumor development, there is severe immunosuppression leading to overwhelming infections by opportunistic gram-negative bacteria (esp. conjunctiva and nasal passages)<br /> *Virus multiplication and tumor-like lesions occur initially at the site of intradermal inoculation <br /> *This is followed by spread to regional lymph nodes and cell-associated viremia, with generalization to the skin and internal organs<br /> *Gelatinous proliferative nodules all over body, especially at orifices (eyes, anus, nose)<br /> *Rabbit dies within 12 days, if not killed by predators<br /> <br /> =====In more detail=====<br /> *Virulent strains of MYX and MRV secrete a T2 gene product with significant homology to the T2 protein secreted by Shope fibroma virus. This protein acts as a receptor for TNFα and TNFβ. TNF is active in killing virus infected and tumor cells. Cytotoxicity is correlated with the induction of toxic superoxide radicals. The T2 gene product enhances viral virulence by interfering with TNF-dependent immune response pathways of the host.<br /> *Myxoma virus and MRV have also been shown to compromise cell-mediated immunity by inducing a loss of class I MHC antigens from the surface of infected cells. MHC class I-restricted cytotoxic T lymphocytes play a major role in clearing poxvirus infections from susceptible animal hosts, and are an important factor in limiting virus spread within the host. Class I molecules are present on all nucleated cells and platelets. Cytotoxic T cells (CD8+) recognize intracellular viral antigen in association with class I MHC glycoproteins on the cell surface. MYX and MRV infection results in a specific, rapid decrease in detectable surface class I epitopes. It has been suggested that a late viral gene product may interact with the class I complex to either physically sequester the complex away from the cell surface and inhibit its recycling to the surface, or induce a conformational change in the complex rendering it unrecognizable by cytotoxic T lymphocytes.<br /> *Myxoma growth factor (MGF) and a gene product designated M11L are also associated with MYX virulence. MGF and M11L deleted mutants are markedly attenuated, capable of inducing only benign localized nodules that regress spontaneously, similar to lesions induced by Shope fibroma virus. MGF has significant sequence homology with epidermal growth factor and transforming growth factor β. It has been postulated that the presence of EGF/TGFβ-like growth factors in tumorigenic poxviruses affects the growth and progression of poxvirus-infected cells.<br /> *Another myxoma virus virulence factor designated MYXOMA SERPIN 1 (SERP 1) has significant sequence homology with members of the family of serine proteases inhibitors (serpins). The exact role of SERP 1 is unknown but it may theoretically affect antigen presentation by interfering with viral protein degradation, or might reduce cytoxic T cell killing mediated by serine proteases in the effector cell.<br /> *Rabbit poxvirus gene sequences coding for products related to the C4 and C5 components of the complement cascade have been identified. It is postulated that complement-like viral protein products may block the activation or action of complement. The virulence factor T7 is an IFNγ receptor homologue.<br /> <br /> <br /> ===Epidemiology===<br /> *Highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors<br /> *Mosquitoes act as mechanical vectors<br /> *High ambient environmental temperatures are associated with increased survival of infected animals<br /> <br /> ===Differentials===<br /> *[[Shope fibroma virus|Shope Fibroma Virus]]<br /> **Localised benign tumours that spontaneously regress in adult immunocompetent rabbits<br /> *[[Malignant rabbit fibroma virus|Malignant Rabbit Fibroma Virus]]<br /> **MRV is a recombinant between Myxoma virus and Shope fibroma virus.<br /> **Causes a lethal disease with numerous primary and secondary tumours and immunosuppression.<br /> <br /> ===Control===<br /> *Attenuated vaccines are used for farmed and pet rabbits<br /> *Wild suspect animals should be culled<br /> <br /> [[Category:Leporipoxviruses]][[Category:Rabbit]]<br /> [[Category:To_Do_-_Viruses]]<br /> [[Category:To_Do_-_Stuart]]</div>

Stuartd https://en.wikivet.net/index.php?title=Myxomatosis&diff=70016 2010-07-05T14:47:02Z

<p>Stuartd: </p> <hr /> <div>{{unfinished}}<br /> <br /> [[Image:MyxoRabbit.JPG|200px|right|thumb|A European Rabbit afflicted by Myxomatosis in Shropshire, England. Courtesy of WikiMedia]]<br /> <br /> This page explains the viral cause of Myxomatosis and the associated clinical signs, pathology and pathogenesis, treatment, control and prognosis.<br /> <br /> <br /> ===Myxoma virus===<br /> ====Hosts====<br /> *Causes Myxomatosis in rabbits<br /> ====Transmission====<br /> *Infectious myxomatosis is highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors. <br /> *Arthropod vectors such as mosquitoes and fleas provide the principal means of transmission. <br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia. <br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain. <br /> *The naturally attenuated viruses cause a milder disease of longer duration which favors vector transmission and persistence of the virus in nature. <br /> *High ambient environmental temperatures are associated with increased survival of infected animals. Some authors consider the California strains of the virus (California rabbit fibroma virus) as distinct from the myxoma virus, while others feel that the antigenic differences do not justify the separate distinction.<br /> *Several proteins encoded by the virus are immunosubversive in that they mimic host ligands or regulators (virokines) or are homologues of cellular cytokine receptors (viroceptors)<br /> ====Antigenicity====<br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia<br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain<br /> <br /> ===Clinical signs===<br /> *Clinical disease varies with virus strain and host species. <br /> **Sylvilagus species are relatively resistant, and are probably the natural host of the virus. In Sylvilagus species, infection usually results only in the development of skin tumors at the site of inoculation. The tumors appear 4-8 days after exposure and persist for up to 40 days. Very young rabbits may succumb to generalized disease.<br /> **Lepus species (hares) are highly resistant. Occasional individuals develop mild to severe generalized myxomatosis.<br /> **In the European rabbit (Oryctolagus cuniculus), infection with virulent virus (South American or California strains) results in severe disease with up to a 99% case fatality rate. <br /> ***Initial signs include edema of the eyelids accompanied by inflammation and edema around the anal, genital, oral, and nasal orifices. <br /> ***Edema of the head and ears, drooping ears, and bacterial infections resulting in mucopurulent conjunctivitis and pneumonia are seen. <br /> ***The primary tumor may be evident by 3-4 days after infection. Generalized tumors develop by 6-7 days after infection. <br /> ***Subcutaneous swellings become mucoid, gelatinous masses (hence the name myxomatosis). <br /> ***More chronic wart-like nodules appear, especially at mucocutaneous borders, after 10-14 days. <br /> ***Death (8-15 days post infection) is usually preceded by labored breathing and convulsions.<br /> <br /> ===Pathology===<br /> <br /> ====Gross Pathology====<br /> <br /> *The most prominent gross lesions in European rabbits with myxomatosis are the skin tumors and the pronounced cutaneous and subcutaneous edema, particularly in the area of the face and around body orifices. <br /> *Skin hemorrhages and subserosal petechiae and ecchymoses may be observed in the stomach and intestines. Subepicardial and subendocardial hemorrhages may also occur.<br /> *Adult rabbits of the genus Sylvilagus usually develop localized skin tumors resembling the fibromas produced in European rabbits by Shope fibroma virus.<br /> *Hares or young Sylvilagus rabbits may develop fibromatous to myxomatous nodules, however, lesions are usually mild and localized.<br /> <br /> ====Histopathology====<br /> <br /> *The lesions are proliferative to degenerative, depending on the virus strain. <br /> *The skin tumors result from proliferation of undifferentiated mesenchymal cells which become large stellate cells (myxoma cells). These cells may contain intracytoplasmic eosinophilic inclusions. These cells lie in a homogeneous matrix of mucinous material interspersed with capillaries and inflammatory cells. Endothelial proliferation with narrowing of the lumen and extrusion of stellate &quot;myxoma&quot; cells has been described. <br /> *Epithelial cells overlying the tumor may show hyperplasia or degeneration, or may appear normal. Epithelial proliferation is characterized by ballooning of cells in the stratum granulosum and hyperkeratosis. Epithelial vesiculation progresses to crust formation. Large, eosinophilic, intracytoplasmic inclusions are especially prominent in the stratum spinosum. Lesions in other organs include cellular proliferation of alveolar epithelium and the reticulum cells of [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]] and [[Spleen - Anatomy &amp; Physiology|spleen]]. Focal hemorrhage may be present in skin, kidneys, lymph nodes, testes, heart, stomach, and intestinal walls. Myxoma cells may be present in [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]], [[Bone Marrow - Anatomy &amp; Physiology|bone marrow]], uterus, ovaries, testes, and lungs.<br /> <br /> <br /> ===Pathogenesis===<br /> *Infects several cell types including mucosal cells, lymphocytes, and fibroblasts<br /> *In addition to primary and secondary tumor development, there is severe immunosuppression leading to overwhelming infections by opportunistic gram-negative bacteria (esp. conjunctiva and nasal passages)<br /> *Virus multiplication and tumor-like lesions occur initially at the site of intradermal inoculation <br /> *This is followed by spread to regional lymph nodes and cell-associated viremia, with generalization to the skin and internal organs<br /> *Gelatinous proliferative nodules all over body, especially at '''orifices''' (eyes, anus, nose)<br /> *Rabbit dies within 12 days, if not killed by predators<br /> <br /> =====In more detail=====<br /> *Virulent strains of MYX and MRV secrete a T2 gene product with significant homology to the T2 protein secreted by Shope fibroma virus. This protein acts as a receptor for TNFα and TNFβ. TNF is active in killing virus infected and tumor cells. Cytotoxicity is correlated with the induction of toxic superoxide radicals. The T2 gene product enhances viral virulence by interfering with TNF-dependent immune response pathways of the host.<br /> *Myxoma virus and MRV have also been shown to compromise cell-mediated immunity by inducing a loss of class I MHC antigens from the surface of infected cells. MHC class I-restricted cytotoxic T lymphocytes play a major role in clearing poxvirus infections from susceptible animal hosts, and are an important factor in limiting virus spread within the host. Class I molecules are present on all nucleated cells and platelets. Cytotoxic T cells (CD8+) recognize intracellular viral antigen in association with class I MHC glycoproteins on the cell surface. MYX and MRV infection results in a specific, rapid decrease in detectable surface class I epitopes. It has been suggested that a late viral gene product may interact with the class I complex to either physically sequester the complex away from the cell surface and inhibit its recycling to the surface, or induce a conformational change in the complex rendering it unrecognizable by cytotoxic T lymphocytes.<br /> *Myxoma growth factor (MGF) and a gene product designated M11L are also associated with MYX virulence. MGF and M11L deleted mutants are markedly attenuated, capable of inducing only benign localized nodules that regress spontaneously, similar to lesions induced by Shope fibroma virus. MGF has significant sequence homology with epidermal growth factor and transforming growth factor β. It has been postulated that the presence of EGF/TGFβ-like growth factors in tumorigenic poxviruses affects the growth and progression of poxvirus-infected cells.<br /> *Another myxoma virus virulence factor designated MYXOMA SERPIN 1 (SERP 1) has significant sequence homology with members of the family of serine proteases inhibitors (serpins). The exact role of SERP 1 is unknown but it may theoretically affect antigen presentation by interfering with viral protein degradation, or might reduce cytoxic T cell killing mediated by serine proteases in the effector cell.<br /> *Rabbit poxvirus gene sequences coding for products related to the C4 and C5 components of the complement cascade have been identified. It is postulated that complement-like viral protein products may block the activation or action of complement. The virulence factor T7 is an IFNγ receptor homologue.<br /> <br /> <br /> ===Epidemiology===<br /> *Highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors<br /> *Mosquitoes act as mechanical vectors<br /> *High ambient environmental temperatures are associated with increased survival of infected animals<br /> <br /> ===Differentials===<br /> *[[Shope fibroma virus|Shope Fibroma Virus]]<br /> **Localised benign tumours that spontaneously regress in adult immunocompetent rabbits<br /> *[[Malignant rabbit fibroma virus|Malignant Rabbit Fibroma Virus]]<br /> **MRV is a recombinant between Myxoma virus and Shope fibroma virus.<br /> **Causes a lethal disease with numerous primary and secondary tumours and immunosuppression.<br /> <br /> ===Control===<br /> *Attenuated vaccines are used for farmed and pet rabbits<br /> *Wild suspect animals should be culled<br /> <br /> [[Category:Leporipoxviruses]][[Category:Rabbit]]<br /> [[Category:To_Do_-_Viruses]]<br /> [[Category:To_Do_-_Stuart]]</div>

Stuartd https://en.wikivet.net/index.php?title=Myxomatosis&diff=70012 2010-07-05T14:45:12Z

<p>Stuartd: </p> <hr /> <div>{{unfinished}}<br /> <br /> [[Image:MyxoRabbit.JPG|200px|right|thumb|A European Rabbit afflicted by Myxomatosis in Shropshire, England. Courtesy of WikiMedia]]<br /> <br /> This page explains the viral cause of Myxomatosis and the associated clinical signs, pathology and pathogenesis, treatment, control and prognosis.<br /> <br /> <br /> ===Myxoma virus===<br /> ====Hosts====<br /> *Causes Myxomatosis in rabbits<br /> ====Transmission====<br /> *Infectious myxomatosis is highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors. <br /> *Arthropod vectors such as mosquitoes and fleas provide the principal means of transmission. <br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia. <br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain. <br /> *The naturally attenuated viruses cause a milder disease of longer duration which favors vector transmission and persistence of the virus in nature. <br /> *High ambient environmental temperatures are associated with increased survival of infected animals. Some authors consider the California strains of the virus (California rabbit fibroma virus) as distinct from the myxoma virus, while others feel that the antigenic differences do not justify the separate distinction.<br /> *Several proteins encoded by the virus are immunosubversive in that they mimic host ligands or regulators (virokines) or are homologues of cellular cytokine receptors (viroceptors)<br /> ====Antigenicity====<br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia<br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain<br /> <br /> ===Clinical signs===<br /> *Clinical disease varies with virus strain and host species. <br /> **Sylvilagus species are relatively resistant, and are probably the natural host of the virus. In Sylvilagus species, infection usually results only in the development of skin tumors at the site of inoculation. The tumors appear 4-8 days after exposure and persist for up to 40 days. Very young rabbits may succumb to generalized disease.<br /> **Lepus species (hares) are highly resistant. Occasional individuals develop mild to severe generalized myxomatosis.<br /> **In the European rabbit (Oryctolagus cuniculus), infection with virulent virus (South American or California strains) results in severe disease with up to a 99% case fatality rate. <br /> ***Initial signs include edema of the eyelids accompanied by inflammation and edema around the anal, genital, oral, and nasal orifices. <br /> ***Edema of the head and ears, drooping ears, and bacterial infections resulting in mucopurulent conjunctivitis and pneumonia are seen. <br /> ***The primary tumor may be evident by 3-4 days after infection. Generalized tumors develop by 6-7 days after infection. <br /> ***Subcutaneous swellings become mucoid, gelatinous masses (hence the name myxomatosis). <br /> ***More chronic wart-like nodules appear, especially at mucocutaneous borders, after 10-14 days. <br /> ***Death (8-15 days post infection) is usually preceded by labored breathing and convulsions.<br /> <br /> ===Pathology===<br /> <br /> ====Gross Pathology====<br /> <br /> *The most prominent gross lesions in European rabbits with myxomatosis are the skin tumors and the pronounced cutaneous and subcutaneous edema, particularly in the area of the face and around body orifices. <br /> *Skin hemorrhages and subserosal petechiae and ecchymoses may be observed in the stomach and intestines. Subepicardial and subendocardial hemorrhages may also occur.<br /> *Adult rabbits of the genus Sylvilagus usually develop localized skin tumors resembling the fibromas produced in European rabbits by Shope fibroma virus.<br /> *Hares or young Sylvilagus rabbits may develop fibromatous to myxomatous nodules, however, lesions are usually mild and localized.<br /> <br /> ====Histopathology====<br /> <br /> *The lesions are proliferative to degenerative, depending on the virus strain. <br /> *The skin tumors result from proliferation of undifferentiated mesenchymal cells which become large stellate cells (myxoma cells). These cells may contain intracytoplasmic eosinophilic inclusions. These cells lie in a homogeneous matrix of mucinous material interspersed with capillaries and inflammatory cells. Endothelial proliferation with narrowing of the lumen and extrusion of stellate &quot;myxoma&quot; cells has been described. <br /> *Epithelial cells overlying the tumor may show hyperplasia or degeneration, or may appear normal. Epithelial proliferation is characterized by ballooning of cells in the stratum granulosum and hyperkeratosis. Epithelial vesiculation progresses to crust formation. Large, eosinophilic, intracytoplasmic inclusions are especially prominent in the stratum spinosum. Lesions in other organs include cellular proliferation of alveolar epithelium and the reticulum cells of [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]] and [[Spleen - Anatomy &amp; Physiology|spleen]]. Focal hemorrhage may be present in skin, kidneys, lymph nodes, testes, heart, stomach, and intestinal walls. Myxoma cells may be present in [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]], [[Bone Marrow - Anatomy &amp; Physiology|bone marrow]], uterus, ovaries, testes, and lungs.<br /> <br /> <br /> ===Pathogenesis===<br /> *Infects several cell types including mucosal cells, lymphocytes, and fibroblasts<br /> *In addition to primary and secondary tumor development, there is severe immunosuppression leading to overwhelming infections by opportunistic gram-negative bacteria (esp. conjunctiva and nasal passages)<br /> *Virus multiplication and tumor-like lesions occur initially at the site of intradermal inoculation <br /> *This is followed by spread to regional lymph nodes and cell-associated viremia, with generalization to the skin and internal organs<br /> *Gelatinous proliferative nodules all over body, especially at '''orifices''' (eyes, anus, nose)<br /> *Rabbit dies within 12 days, if not killed by predators<br /> <br /> =====In more detail=====<br /> *Virulent strains of MYX and MRV secrete a T2 gene product with significant homology to the T2 protein secreted by Shope fibroma virus. This protein acts as a receptor for TNFα and TNFβ. TNF is active in killing virus infected and tumor cells. Cytotoxicity is correlated with the induction of toxic superoxide radicals. The T2 gene product enhances viral virulence by interfering with TNF-dependent immune response pathways of the host.<br /> *Myxoma virus and MRV have also been shown to compromise cell-mediated immunity by inducing a loss of class I MHC antigens from the surface of infected cells. MHC class I-restricted cytotoxic T lymphocytes play a major role in clearing poxvirus infections from susceptible animal hosts, and are an important factor in limiting virus spread within the host. Class I molecules are present on all nucleated cells and platelets. Cytotoxic T cells (CD8+) recognize intracellular viral antigen in association with class I MHC glycoproteins on the cell surface. MYX and MRV infection results in a specific, rapid decrease in detectable surface class I epitopes. It has been suggested that a late viral gene product may interact with the class I complex to either physically sequester the complex away from the cell surface and inhibit its recycling to the surface, or induce a conformational change in the complex rendering it unrecognizable by cytotoxic T lymphocytes.<br /> *Myxoma growth factor (MGF) and a gene product designated M11L are also associated with MYX virulence. MGF and M11L deleted mutants are markedly attenuated, capable of inducing only benign localized nodules that regress spontaneously, similar to lesions induced by Shope fibroma virus. MGF has significant sequence homology with epidermal growth factor and transforming growth factor β. It has been postulated that the presence of EGF/TGFβ-like growth factors in tumorigenic poxviruses affects the growth and progression of poxvirus-infected cells.<br /> *Another myxoma virus virulence factor designated MYXOMA SERPIN 1 (SERP 1) has significant sequence homology with members of the family of serine proteases inhibitors (serpins). The exact role of SERP 1 is unknown but it may theoretically affect antigen presentation by interfering with viral protein degradation, or might reduce cytoxic T cell killing mediated by serine proteases in the effector cell.<br /> *Rabbit poxvirus gene sequences coding for products related to the C4 and C5 components of the complement cascade have been identified. It is postulated that complement-like viral protein products may block the activation or action of complement. The virulence factor T7 is an IFNγ receptor homologue.<br /> <br /> <br /> ===Epidemiology===<br /> *Highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors<br /> *'''Mosquitoes''' act as mechanical vectors<br /> *High ambient environmental temperatures are associated with increased survival of infected animals<br /> <br /> ===Differentials===<br /> *[[Shope fibroma virus|Shope Fibroma Virus]]<br /> **Localised benign tumours that spontaneously regress in adult immunocompetent rabbits<br /> *[[Malignant rabbit fibroma virus|Malignant Rabbit Fibroma Virus]]<br /> **MRV is a recombinant between Myxoma virus and Shope fibroma virus.<br /> **Causes a lethal disease with numerous primary and secondary tumours and immunosuppression.<br /> <br /> ===Control===<br /> *Attenuated vaccines are used for farmed and pet rabbits<br /> *Wild suspect animals should be culled<br /> <br /> [[Category:Leporipoxviruses]][[Category:Rabbit]]<br /> [[Category:To_Do_-_Viruses]]<br /> [[Category:To_Do_-_Stuart]]</div>

Stuartd https://en.wikivet.net/index.php?title=Myxomatosis&diff=70008 2010-07-05T14:42:55Z

<p>Stuartd: </p> <hr /> <div>{{unfinished}}<br /> <br /> [[Image:MyxoRabbit.JPG|200px|right|thumb|A European Rabbit afflicted by Myxomatosis in Shropshire, England. Courtesy of WikiMedia]]<br /> <br /> This page explains the viral cause of Myxomatosis and the associated clinical signs, pathology and pathogenesis, treatment, control and prognosis.<br /> <br /> ===Hosts===<br /> *Rabbits<br /> <br /> ===Myxoma virus===<br /> *Causes Myxomatosis in rabbits<br /> *Infectious myxomatosis is highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors. <br /> *Arthropod vectors such as mosquitoes and fleas provide the principal means of transmission. <br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia. <br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain. <br /> *The naturally attenuated viruses cause a milder disease of longer duration which favors vector transmission and persistence of the virus in nature. <br /> *High ambient environmental temperatures are associated with increased survival of infected animals. Some authors consider the California strains of the virus (California rabbit fibroma virus) as distinct from the myxoma virus, while others feel that the antigenic differences do not justify the separate distinction.<br /> *Several proteins encoded by the virus are immunosubversive in that they mimic host ligands or regulators (virokines) or are homologues of cellular cytokine receptors (viroceptors)<br /> <br /> ===Clinical signs===<br /> *Clinical disease varies with virus strain and host species. <br /> **Sylvilagus species are relatively resistant, and are probably the natural host of the virus. In Sylvilagus species, infection usually results only in the development of skin tumors at the site of inoculation. The tumors appear 4-8 days after exposure and persist for up to 40 days. Very young rabbits may succumb to generalized disease.<br /> **Lepus species (hares) are highly resistant. Occasional individuals develop mild to severe generalized myxomatosis.<br /> **In the European rabbit (Oryctolagus cuniculus), infection with virulent virus (South American or California strains) results in severe disease with up to a 99% case fatality rate. <br /> ***Initial signs include edema of the eyelids accompanied by inflammation and edema around the anal, genital, oral, and nasal orifices. <br /> ***Edema of the head and ears, drooping ears, and bacterial infections resulting in mucopurulent conjunctivitis and pneumonia are seen. <br /> ***The primary tumor may be evident by 3-4 days after infection. Generalized tumors develop by 6-7 days after infection. <br /> ***Subcutaneous swellings become mucoid, gelatinous masses (hence the name myxomatosis). <br /> ***More chronic wart-like nodules appear, especially at mucocutaneous borders, after 10-14 days. <br /> ***Death (8-15 days post infection) is usually preceded by labored breathing and convulsions.<br /> <br /> ===Pathology===<br /> <br /> ====Gross Pathology====<br /> <br /> *The most prominent gross lesions in European rabbits with myxomatosis are the skin tumors and the pronounced cutaneous and subcutaneous edema, particularly in the area of the face and around body orifices. <br /> *Skin hemorrhages and subserosal petechiae and ecchymoses may be observed in the stomach and intestines. Subepicardial and subendocardial hemorrhages may also occur.<br /> *Adult rabbits of the genus Sylvilagus usually develop localized skin tumors resembling the fibromas produced in European rabbits by Shope fibroma virus.<br /> *Hares or young Sylvilagus rabbits may develop fibromatous to myxomatous nodules, however, lesions are usually mild and localized.<br /> <br /> ====Histopathology====<br /> <br /> *The lesions are proliferative to degenerative, depending on the virus strain. <br /> *The skin tumors result from proliferation of undifferentiated mesenchymal cells which become large stellate cells (myxoma cells). These cells may contain intracytoplasmic eosinophilic inclusions. These cells lie in a homogeneous matrix of mucinous material interspersed with capillaries and inflammatory cells. Endothelial proliferation with narrowing of the lumen and extrusion of stellate &quot;myxoma&quot; cells has been described. <br /> *Epithelial cells overlying the tumor may show hyperplasia or degeneration, or may appear normal. Epithelial proliferation is characterized by ballooning of cells in the stratum granulosum and hyperkeratosis. Epithelial vesiculation progresses to crust formation. Large, eosinophilic, intracytoplasmic inclusions are especially prominent in the stratum spinosum. Lesions in other organs include cellular proliferation of alveolar epithelium and the reticulum cells of [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]] and [[Spleen - Anatomy &amp; Physiology|spleen]]. Focal hemorrhage may be present in skin, kidneys, lymph nodes, testes, heart, stomach, and intestinal walls. Myxoma cells may be present in [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]], [[Bone Marrow - Anatomy &amp; Physiology|bone marrow]], uterus, ovaries, testes, and lungs.<br /> ====Antigenicity====<br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia<br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain<br /> <br /> <br /> ===Pathogenesis===<br /> *Infects several cell types including mucosal cells, lymphocytes, and fibroblasts<br /> *In addition to primary and secondary tumor development, there is severe immunosuppression leading to overwhelming infections by opportunistic gram-negative bacteria (esp. conjunctiva and nasal passages)<br /> *Virus multiplication and tumor-like lesions occur initially at the site of intradermal inoculation <br /> *This is followed by spread to regional lymph nodes and cell-associated viremia, with generalization to the skin and internal organs<br /> *Gelatinous proliferative nodules all over body, especially at '''orifices''' (eyes, anus, nose)<br /> *Rabbit dies within 12 days, if not killed by predators<br /> <br /> =====In more detail=====<br /> *Virulent strains of MYX and MRV secrete a T2 gene product with significant homology to the T2 protein secreted by Shope fibroma virus. This protein acts as a receptor for TNFα and TNFβ. TNF is active in killing virus infected and tumor cells. Cytotoxicity is correlated with the induction of toxic superoxide radicals. The T2 gene product enhances viral virulence by interfering with TNF-dependent immune response pathways of the host.<br /> *Myxoma virus and MRV have also been shown to compromise cell-mediated immunity by inducing a loss of class I MHC antigens from the surface of infected cells. MHC class I-restricted cytotoxic T lymphocytes play a major role in clearing poxvirus infections from susceptible animal hosts, and are an important factor in limiting virus spread within the host. Class I molecules are present on all nucleated cells and platelets. Cytotoxic T cells (CD8+) recognize intracellular viral antigen in association with class I MHC glycoproteins on the cell surface. MYX and MRV infection results in a specific, rapid decrease in detectable surface class I epitopes. It has been suggested that a late viral gene product may interact with the class I complex to either physically sequester the complex away from the cell surface and inhibit its recycling to the surface, or induce a conformational change in the complex rendering it unrecognizable by cytotoxic T lymphocytes.<br /> *Myxoma growth factor (MGF) and a gene product designated M11L are also associated with MYX virulence. MGF and M11L deleted mutants are markedly attenuated, capable of inducing only benign localized nodules that regress spontaneously, similar to lesions induced by Shope fibroma virus. MGF has significant sequence homology with epidermal growth factor and transforming growth factor β. It has been postulated that the presence of EGF/TGFβ-like growth factors in tumorigenic poxviruses affects the growth and progression of poxvirus-infected cells.<br /> *Another myxoma virus virulence factor designated MYXOMA SERPIN 1 (SERP 1) has significant sequence homology with members of the family of serine proteases inhibitors (serpins). The exact role of SERP 1 is unknown but it may theoretically affect antigen presentation by interfering with viral protein degradation, or might reduce cytoxic T cell killing mediated by serine proteases in the effector cell.<br /> *Rabbit poxvirus gene sequences coding for products related to the C4 and C5 components of the complement cascade have been identified. It is postulated that complement-like viral protein products may block the activation or action of complement. The virulence factor T7 is an IFNγ receptor homologue.<br /> <br /> <br /> ===Epidemiology===<br /> *Highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors<br /> *'''Mosquitoes''' act as mechanical vectors<br /> *High ambient environmental temperatures are associated with increased survival of infected animals<br /> <br /> ===Differentials===<br /> *[[Shope fibroma virus|Shope Fibroma Virus]]<br /> **Localised benign tumours that spontaneously regress in adult immunocompetent rabbits<br /> *[[Malignant rabbit fibroma virus|Malignant Rabbit Fibroma Virus]]<br /> **MRV is a recombinant between Myxoma virus and Shope fibroma virus.<br /> **Causes a lethal disease with numerous primary and secondary tumours and immunosuppression.<br /> <br /> ===Control===<br /> *Attenuated vaccines are used for farmed and pet rabbits<br /> *Wild suspect animals should be culled<br /> <br /> [[Category:Leporipoxviruses]][[Category:Rabbit]]<br /> [[Category:To_Do_-_Viruses]]<br /> [[Category:To_Do_-_Stuart]]</div>

Stuartd https://en.wikivet.net/index.php?title=Myxomatosis&diff=70002 2010-07-05T14:42:14Z

<p>Stuartd: </p> <hr /> <div>{{unfinished}}<br /> <br /> [[Image:MyxoRabbit.JPG|200px|right|thumb|A European Rabbit afflicted by Myxomatosis in Shropshire, England. Courtesy of WikiMedia]]<br /> <br /> This page explains the viral cause of Myxomatosis and the associated clinical signs, pathology, treatment, control and prognosis.<br /> <br /> ===Hosts===<br /> *Rabbits<br /> <br /> ===Myxoma virus===<br /> *Causes Myxomatosis in rabbits<br /> *Infectious myxomatosis is highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors. <br /> *Arthropod vectors such as mosquitoes and fleas provide the principal means of transmission. <br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia. <br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain. <br /> *The naturally attenuated viruses cause a milder disease of longer duration which favors vector transmission and persistence of the virus in nature. <br /> *High ambient environmental temperatures are associated with increased survival of infected animals. Some authors consider the California strains of the virus (California rabbit fibroma virus) as distinct from the myxoma virus, while others feel that the antigenic differences do not justify the separate distinction.<br /> *Several proteins encoded by the virus are immunosubversive in that they mimic host ligands or regulators (virokines) or are homologues of cellular cytokine receptors (viroceptors)<br /> <br /> ===Clinical signs===<br /> *Clinical disease varies with virus strain and host species. <br /> **Sylvilagus species are relatively resistant, and are probably the natural host of the virus. In Sylvilagus species, infection usually results only in the development of skin tumors at the site of inoculation. The tumors appear 4-8 days after exposure and persist for up to 40 days. Very young rabbits may succumb to generalized disease.<br /> **Lepus species (hares) are highly resistant. Occasional individuals develop mild to severe generalized myxomatosis.<br /> **In the European rabbit (Oryctolagus cuniculus), infection with virulent virus (South American or California strains) results in severe disease with up to a 99% case fatality rate. <br /> ***Initial signs include edema of the eyelids accompanied by inflammation and edema around the anal, genital, oral, and nasal orifices. <br /> ***Edema of the head and ears, drooping ears, and bacterial infections resulting in mucopurulent conjunctivitis and pneumonia are seen. <br /> ***The primary tumor may be evident by 3-4 days after infection. Generalized tumors develop by 6-7 days after infection. <br /> ***Subcutaneous swellings become mucoid, gelatinous masses (hence the name myxomatosis). <br /> ***More chronic wart-like nodules appear, especially at mucocutaneous borders, after 10-14 days. <br /> ***Death (8-15 days post infection) is usually preceded by labored breathing and convulsions.<br /> <br /> ===Pathology===<br /> <br /> ====Gross Pathology====<br /> <br /> *The most prominent gross lesions in European rabbits with myxomatosis are the skin tumors and the pronounced cutaneous and subcutaneous edema, particularly in the area of the face and around body orifices. <br /> *Skin hemorrhages and subserosal petechiae and ecchymoses may be observed in the stomach and intestines. Subepicardial and subendocardial hemorrhages may also occur.<br /> *Adult rabbits of the genus Sylvilagus usually develop localized skin tumors resembling the fibromas produced in European rabbits by Shope fibroma virus.<br /> *Hares or young Sylvilagus rabbits may develop fibromatous to myxomatous nodules, however, lesions are usually mild and localized.<br /> <br /> ====Histopathology====<br /> <br /> *The lesions are proliferative to degenerative, depending on the virus strain. <br /> *The skin tumors result from proliferation of undifferentiated mesenchymal cells which become large stellate cells (myxoma cells). These cells may contain intracytoplasmic eosinophilic inclusions. These cells lie in a homogeneous matrix of mucinous material interspersed with capillaries and inflammatory cells. Endothelial proliferation with narrowing of the lumen and extrusion of stellate &quot;myxoma&quot; cells has been described. <br /> *Epithelial cells overlying the tumor may show hyperplasia or degeneration, or may appear normal. Epithelial proliferation is characterized by ballooning of cells in the stratum granulosum and hyperkeratosis. Epithelial vesiculation progresses to crust formation. Large, eosinophilic, intracytoplasmic inclusions are especially prominent in the stratum spinosum. Lesions in other organs include cellular proliferation of alveolar epithelium and the reticulum cells of [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]] and [[Spleen - Anatomy &amp; Physiology|spleen]]. Focal hemorrhage may be present in skin, kidneys, lymph nodes, testes, heart, stomach, and intestinal walls. Myxoma cells may be present in [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]], [[Bone Marrow - Anatomy &amp; Physiology|bone marrow]], uterus, ovaries, testes, and lungs.<br /> ====Antigenicity====<br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia<br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain<br /> <br /> <br /> ===Pathogenesis===<br /> *Infects several cell types including mucosal cells, lymphocytes, and fibroblasts<br /> *In addition to primary and secondary tumor development, there is severe immunosuppression leading to overwhelming infections by opportunistic gram-negative bacteria (esp. conjunctiva and nasal passages)<br /> *Virus multiplication and tumor-like lesions occur initially at the site of intradermal inoculation <br /> *This is followed by spread to regional lymph nodes and cell-associated viremia, with generalization to the skin and internal organs<br /> *Gelatinous proliferative nodules all over body, especially at '''orifices''' (eyes, anus, nose)<br /> *Rabbit dies within 12 days, if not killed by predators<br /> <br /> =====In more detail=====<br /> *Virulent strains of MYX and MRV secrete a T2 gene product with significant homology to the T2 protein secreted by Shope fibroma virus. This protein acts as a receptor for TNFα and TNFβ. TNF is active in killing virus infected and tumor cells. Cytotoxicity is correlated with the induction of toxic superoxide radicals. The T2 gene product enhances viral virulence by interfering with TNF-dependent immune response pathways of the host.<br /> *Myxoma virus and MRV have also been shown to compromise cell-mediated immunity by inducing a loss of class I MHC antigens from the surface of infected cells. MHC class I-restricted cytotoxic T lymphocytes play a major role in clearing poxvirus infections from susceptible animal hosts, and are an important factor in limiting virus spread within the host. Class I molecules are present on all nucleated cells and platelets. Cytotoxic T cells (CD8+) recognize intracellular viral antigen in association with class I MHC glycoproteins on the cell surface. MYX and MRV infection results in a specific, rapid decrease in detectable surface class I epitopes. It has been suggested that a late viral gene product may interact with the class I complex to either physically sequester the complex away from the cell surface and inhibit its recycling to the surface, or induce a conformational change in the complex rendering it unrecognizable by cytotoxic T lymphocytes.<br /> *Myxoma growth factor (MGF) and a gene product designated M11L are also associated with MYX virulence. MGF and M11L deleted mutants are markedly attenuated, capable of inducing only benign localized nodules that regress spontaneously, similar to lesions induced by Shope fibroma virus. MGF has significant sequence homology with epidermal growth factor and transforming growth factor β. It has been postulated that the presence of EGF/TGFβ-like growth factors in tumorigenic poxviruses affects the growth and progression of poxvirus-infected cells.<br /> *Another myxoma virus virulence factor designated MYXOMA SERPIN 1 (SERP 1) has significant sequence homology with members of the family of serine proteases inhibitors (serpins). The exact role of SERP 1 is unknown but it may theoretically affect antigen presentation by interfering with viral protein degradation, or might reduce cytoxic T cell killing mediated by serine proteases in the effector cell.<br /> *Rabbit poxvirus gene sequences coding for products related to the C4 and C5 components of the complement cascade have been identified. It is postulated that complement-like viral protein products may block the activation or action of complement. The virulence factor T7 is an IFNγ receptor homologue.<br /> <br /> <br /> ===Epidemiology===<br /> *Highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors<br /> *'''Mosquitoes''' act as mechanical vectors<br /> *High ambient environmental temperatures are associated with increased survival of infected animals<br /> <br /> ===Differentials===<br /> *[[Shope fibroma virus|Shope Fibroma Virus]]<br /> **Localised benign tumours that spontaneously regress in adult immunocompetent rabbits<br /> *[[Malignant rabbit fibroma virus|Malignant Rabbit Fibroma Virus]]<br /> **MRV is a recombinant between Myxoma virus and Shope fibroma virus.<br /> **Causes a lethal disease with numerous primary and secondary tumours and immunosuppression.<br /> <br /> ===Control===<br /> *Attenuated vaccines are used for farmed and pet rabbits<br /> *Wild suspect animals should be culled<br /> <br /> [[Category:Leporipoxviruses]][[Category:Rabbit]]<br /> [[Category:To_Do_-_Viruses]]<br /> [[Category:To_Do_-_Stuart]]</div>

Stuartd https://en.wikivet.net/index.php?title=Myxomatosis&diff=69993 2010-07-05T14:40:42Z

<p>Stuartd: </p> <hr /> <div>{{unfinished}}<br /> <br /> [[Image:MyxoRabbit.JPG|200px|right|thumb|A European Rabbit afflicted by Myxomatosis in Shropshire, England. Courtesy of WikiMedia]]<br /> <br /> This page explains the viral cause of Myxomatosis and the associated clinical signs, pathology, treatment, control and prognosis.<br /> <br /> ===Hosts===<br /> *Rabbits<br /> <br /> ===Myxoma virus===<br /> *Causes Myxomatosis in rabbits<br /> *Infectious myxomatosis is highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors. <br /> *Arthropod vectors such as mosquitoes and fleas provide the principal means of transmission. <br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia. <br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain. <br /> *The naturally attenuated viruses cause a milder disease of longer duration which favors vector transmission and persistence of the virus in nature. <br /> *High ambient environmental temperatures are associated with increased survival of infected animals. Some authors consider the California strains of the virus (California rabbit fibroma virus) as distinct from the myxoma virus, while others feel that the antigenic differences do not justify the separate distinction.<br /> *Several proteins encoded by the virus are immunosubversive in that they mimic host ligands or regulators (virokines) or are homologues of cellular cytokine receptors (viroceptors)<br /> <br /> ===Clinical signs===<br /> *Clinical disease varies with virus strain and host species. <br /> **Sylvilagus species are relatively resistant, and are probably the natural host of the virus. In Sylvilagus species, infection usually results only in the development of skin tumors at the site of inoculation. The tumors appear 4-8 days after exposure and persist for up to 40 days. Very young rabbits may succumb to generalized disease.<br /> **Lepus species (hares) are highly resistant. Occasional individuals develop mild to severe generalized myxomatosis.<br /> **In the European rabbit (Oryctolagus cuniculus), infection with virulent virus (South American or California strains) results in severe disease with up to a 99% case fatality rate. <br /> ***Initial signs include edema of the eyelids accompanied by inflammation and edema around the anal, genital, oral, and nasal orifices. <br /> ***Edema of the head and ears, drooping ears, and bacterial infections resulting in mucopurulent conjunctivitis and pneumonia are seen. <br /> ***The primary tumor may be evident by 3-4 days after infection. Generalized tumors develop by 6-7 days after infection. <br /> ***Subcutaneous swellings become mucoid, gelatinous masses (hence the name myxomatosis). <br /> ***More chronic wart-like nodules appear, especially at mucocutaneous borders, after 10-14 days. <br /> ***Death (8-15 days post infection) is usually preceded by labored breathing and convulsions.<br /> <br /> ===Pathology===<br /> <br /> ====Gross Pathology====<br /> <br /> *The most prominent gross lesions in European rabbits with myxomatosis are the skin tumors and the pronounced cutaneous and subcutaneous edema, particularly in the area of the face and around body orifices. <br /> *Skin hemorrhages and subserosal petechiae and ecchymoses may be observed in the stomach and intestines. Subepicardial and subendocardial hemorrhages may also occur.<br /> *Adult rabbits of the genus Sylvilagus usually develop localized skin tumors resembling the fibromas produced in European rabbits by Shope fibroma virus.<br /> *Hares or young Sylvilagus rabbits may develop fibromatous to myxomatous nodules, however, lesions are usually mild and localized.<br /> <br /> ====Histopathology====<br /> <br /> *The lesions are proliferative to degenerative, depending on the virus strain. <br /> *The skin tumors result from proliferation of undifferentiated mesenchymal cells which become large stellate cells (myxoma cells). These cells may contain intracytoplasmic eosinophilic inclusions. These cells lie in a homogeneous matrix of mucinous material interspersed with capillaries and inflammatory cells. Endothelial proliferation with narrowing of the lumen and extrusion of stellate &quot;myxoma&quot; cells has been described. <br /> *Epithelial cells overlying the tumor may show hyperplasia or degeneration, or may appear normal. Epithelial proliferation is characterized by ballooning of cells in the stratum granulosum and hyperkeratosis. Epithelial vesiculation progresses to crust formation. Large, eosinophilic, intracytoplasmic inclusions are especially prominent in the stratum spinosum. Lesions in other organs include cellular proliferation of alveolar epithelium and the reticulum cells of [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]] and [[Spleen - Anatomy &amp; Physiology|spleen]]. Focal hemorrhage may be present in skin, kidneys, lymph nodes, testes, heart, stomach, and intestinal walls. Myxoma cells may be present in [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]], [[Bone Marrow - Anatomy &amp; Physiology|bone marrow]], uterus, ovaries, testes, and lungs.<br /> ====Antigenicity====<br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia<br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain<br /> <br /> <br /> ===Pathogenesis===<br /> *Infects several cell types including mucosal cells, lymphocytes, and fibroblasts<br /> *In addition to primary and secondary tumor development, there is severe immunosuppression leading to overwhelming infections by opportunistic gram-negative bacteria (esp. conjunctiva and nasal passages)<br /> *Virus multiplication and tumor-like lesions occur initially at the site of intradermal inoculation <br /> *This is followed by spread to regional lymph nodes and cell-associated viremia, with generalization to the skin and internal organs<br /> *Gelatinous proliferative nodules all over body, especially at '''orifices''' (eyes, anus, nose)<br /> *Rabbit dies within 12 days, if not killed by predators<br /> <br /> =====In more detail=====<br /> *Virulent strains of MYX and MRV secrete a T2 gene product with significant homology to the T2 protein secreted by Shope fibroma virus. This protein acts as a receptor for TNFα and TNFβ. TNF is active in killing virus infected and tumor cells. Cytotoxicity is correlated with the induction of toxic superoxide radicals. The T2 gene product enhances viral virulence by interfering with TNF-dependent immune response pathways of the host.<br /> *Myxoma virus and MRV have also been shown to compromise cell-mediated immunity by inducing a loss of class I MHC antigens from the surface of infected cells. MHC class I-restricted cytotoxic T lymphocytes play a major role in clearing poxvirus infections from susceptible animal hosts, and are an important factor in limiting virus spread within the host. Class I molecules are present on all nucleated cells and platelets. Cytotoxic T cells (CD8+) recognize intracellular viral antigen in association with class I MHC glycoproteins on the cell surface. MYX and MRV infection results in a specific, rapid decrease in detectable surface class I epitopes. It has been suggested that a late viral gene product may interact with the class I complex to either physically sequester the complex away from the cell surface and inhibit its recycling to the surface, or induce a conformational change in the complex rendering it unrecognizable by cytotoxic T lymphocytes.<br /> *Myxoma growth factor (MGF) and a gene product designated M11L are also associated with MYX virulence. MGF and M11L deleted mutants are markedly attenuated, capable of inducing only benign localized nodules that regress spontaneously, similar to lesions induced by Shope fibroma virus. MGF has significant sequence homology with epidermal growth factor and transforming growth factor β. It has been postulated that the presence of EGF/TGFβ-like growth factors in tumorigenic poxviruses affects the growth and progression of poxvirus-infected cells.<br /> *Another myxoma virus virulence factor designated MYXOMA SERPIN 1 (SERP 1) has significant sequence homology with members of the family of serine proteases inhibitors (serpins). The exact role of SERP 1 is unknown but it may theoretically affect antigen presentation by interfering with viral protein degradation, or might reduce cytoxic T cell killing mediated by serine proteases in the effector cell.<br /> *Rabbit poxvirus gene sequences coding for products related to the C4 and C5 components of the complement cascade have been identified. It is postulated that complement-like viral protein products may block the activation or action of complement. The virulence factor T7 is an IFNγ receptor homologue.<br /> <br /> <br /> ===Epidemiology===<br /> *Highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors<br /> *'''Mosquitoes''' act as mechanical vectors<br /> *High ambient environmental temperatures are associated with increased survival of infected animals<br /> <br /> ===Differentials===<br /> *[[Shope fibroma virus|Shope Fibroma Virus]]<br /> **Localised benign tumours that spontaneously regress in adult immunocompetent rabbits<br /> *Malignant rabbit fibroma virus<br /> **MRV is a recombinant between Myxoma virus and Shope fibroma virus.<br /> **Causes a lethal disease with numerous primary and secondary tumours and immunosuppression.<br /> <br /> ===Control===<br /> *Attenuated vaccines are used for farmed and pet rabbits<br /> *Wild suspect animals should be culled<br /> <br /> [[Category:Leporipoxviruses]][[Category:Rabbit]]<br /> [[Category:To_Do_-_Viruses]]<br /> [[Category:To_Do_-_Stuart]]</div>

Stuartd https://en.wikivet.net/index.php?title=Myxomatosis&diff=69990 2010-07-05T14:40:05Z

<p>Stuartd: </p> <hr /> <div>{{unfinished}}<br /> <br /> [[Image:MyxoRabbit.JPG|200px|right|thumb|A European Rabbit afflicted by Myxomatosis in Shropshire, England. Courtesy of WikiMedia]]<br /> <br /> This page explains the viral cause of Myxomatosis and the associated clinical signs, pathology, treatment, control and prognosis.<br /> <br /> ===Hosts===<br /> *Rabbits<br /> <br /> ===Myxoma virus===<br /> *Causes Myxomatosis in rabbits<br /> *Infectious myxomatosis is highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors. <br /> *Arthropod vectors such as mosquitoes and fleas provide the principal means of transmission. <br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia. <br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain. <br /> *The naturally attenuated viruses cause a milder disease of longer duration which favors vector transmission and persistence of the virus in nature. <br /> *High ambient environmental temperatures are associated with increased survival of infected animals. Some authors consider the California strains of the virus (California rabbit fibroma virus) as distinct from the myxoma virus, while others feel that the antigenic differences do not justify the separate distinction.<br /> *Several proteins encoded by the virus are immunosubversive in that they mimic host ligands or regulators (virokines) or are homologues of cellular cytokine receptors (viroceptors)<br /> <br /> ===Clinical signs===<br /> *Clinical disease varies with virus strain and host species. <br /> **Sylvilagus species are relatively resistant, and are probably the natural host of the virus. In Sylvilagus species, infection usually results only in the development of skin tumors at the site of inoculation. The tumors appear 4-8 days after exposure and persist for up to 40 days. Very young rabbits may succumb to generalized disease.<br /> **Lepus species (hares) are highly resistant. Occasional individuals develop mild to severe generalized myxomatosis.<br /> **In the European rabbit (Oryctolagus cuniculus), infection with virulent virus (South American or California strains) results in severe disease with up to a 99% case fatality rate. <br /> ***Initial signs include edema of the eyelids accompanied by inflammation and edema around the anal, genital, oral, and nasal orifices. <br /> ***Edema of the head and ears, drooping ears, and bacterial infections resulting in mucopurulent conjunctivitis and pneumonia are seen. <br /> ***The primary tumor may be evident by 3-4 days after infection. Generalized tumors develop by 6-7 days after infection. <br /> ***Subcutaneous swellings become mucoid, gelatinous masses (hence the name myxomatosis). <br /> ***More chronic wart-like nodules appear, especially at mucocutaneous borders, after 10-14 days. <br /> ***Death (8-15 days post infection) is usually preceded by labored breathing and convulsions.<br /> <br /> ===Pathology===<br /> <br /> ====Gross Pathology====<br /> <br /> *The most prominent gross lesions in European rabbits with myxomatosis are the skin tumors and the pronounced cutaneous and subcutaneous edema, particularly in the area of the face and around body orifices. <br /> *Skin hemorrhages and subserosal petechiae and ecchymoses may be observed in the stomach and intestines. Subepicardial and subendocardial hemorrhages may also occur.<br /> *Adult rabbits of the genus Sylvilagus usually develop localized skin tumors resembling the fibromas produced in European rabbits by Shope fibroma virus.<br /> *Hares or young Sylvilagus rabbits may develop fibromatous to myxomatous nodules, however, lesions are usually mild and localized.<br /> <br /> ====Histopathology====<br /> <br /> *The lesions are proliferative to degenerative, depending on the virus strain. <br /> *The skin tumors result from proliferation of undifferentiated mesenchymal cells which become large stellate cells (myxoma cells). These cells may contain intracytoplasmic eosinophilic inclusions. These cells lie in a homogeneous matrix of mucinous material interspersed with capillaries and inflammatory cells. Endothelial proliferation with narrowing of the lumen and extrusion of stellate &quot;myxoma&quot; cells has been described. <br /> *Epithelial cells overlying the tumor may show hyperplasia or degeneration, or may appear normal. Epithelial proliferation is characterized by ballooning of cells in the stratum granulosum and hyperkeratosis. Epithelial vesiculation progresses to crust formation. Large, eosinophilic, intracytoplasmic inclusions are especially prominent in the stratum spinosum. Lesions in other organs include cellular proliferation of alveolar epithelium and the reticulum cells of [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]] and [[Spleen - Anatomy &amp; Physiology|spleen]]. Focal hemorrhage may be present in skin, kidneys, lymph nodes, testes, heart, stomach, and intestinal walls. Myxoma cells may be present in [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]], [[Bone Marrow - Anatomy &amp; Physiology|bone marrow]], uterus, ovaries, testes, and lungs.<br /> ====Antigenicity====<br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia<br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain<br /> <br /> <br /> ===Pathogenesis===<br /> *Infects several cell types including mucosal cells, lymphocytes, and fibroblasts<br /> *In addition to primary and secondary tumor development, there is severe immunosuppression leading to overwhelming infections by opportunistic gram-negative bacteria (esp. conjunctiva and nasal passages)<br /> *Virus multiplication and tumor-like lesions occur initially at the site of intradermal inoculation <br /> *This is followed by spread to regional lymph nodes and cell-associated viremia, with generalization to the skin and internal organs<br /> *Gelatinous proliferative nodules all over body, especially at '''orifices''' (eyes, anus, nose)<br /> *Rabbit dies within 12 days, if not killed by predators<br /> <br /> =====In more detail=====<br /> *Virulent strains of MYX and MRV secrete a T2 gene product with significant homology to the T2 protein secreted by Shope fibroma virus. This protein acts as a receptor for TNFα and TNFβ. TNF is active in killing virus infected and tumor cells. Cytotoxicity is correlated with the induction of toxic superoxide radicals. The T2 gene product enhances viral virulence by interfering with TNF-dependent immune response pathways of the host.<br /> *Myxoma virus and MRV have also been shown to compromise cell-mediated immunity by inducing a loss of class I MHC antigens from the surface of infected cells. MHC class I-restricted cytotoxic T lymphocytes play a major role in clearing poxvirus infections from susceptible animal hosts, and are an important factor in limiting virus spread within the host. Class I molecules are present on all nucleated cells and platelets. Cytotoxic T cells (CD8+) recognize intracellular viral antigen in association with class I MHC glycoproteins on the cell surface. MYX and MRV infection results in a specific, rapid decrease in detectable surface class I epitopes. It has been suggested that a late viral gene product may interact with the class I complex to either physically sequester the complex away from the cell surface and inhibit its recycling to the surface, or induce a conformational change in the complex rendering it unrecognizable by cytotoxic T lymphocytes.<br /> *Myxoma growth factor (MGF) and a gene product designated M11L are also associated with MYX virulence. MGF and M11L deleted mutants are markedly attenuated, capable of inducing only benign localized nodules that regress spontaneously, similar to lesions induced by Shope fibroma virus. MGF has significant sequence homology with epidermal growth factor and transforming growth factor β. It has been postulated that the presence of EGF/TGFβ-like growth factors in tumorigenic poxviruses affects the growth and progression of poxvirus-infected cells.<br /> *Another myxoma virus virulence factor designated MYXOMA SERPIN 1 (SERP 1) has significant sequence homology with members of the family of serine proteases inhibitors (serpins). The exact role of SERP 1 is unknown but it may theoretically affect antigen presentation by interfering with viral protein degradation, or might reduce cytoxic T cell killing mediated by serine proteases in the effector cell.<br /> *Rabbit poxvirus gene sequences coding for products related to the C4 and C5 components of the complement cascade have been identified. It is postulated that complement-like viral protein products may block the activation or action of complement. The virulence factor T7 is an IFNγ receptor homologue.<br /> <br /> <br /> ===Epidemiology===<br /> *Highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors<br /> *'''Mosquitoes''' act as mechanical vectors<br /> *High ambient environmental temperatures are associated with increased survival of infected animals<br /> <br /> ===Differentials===<br /> *[[Shope Fibroma Virus|Shope fibroma virus]]<br /> **Localised benign tumours that spontaneously regress in adult immunocompetent rabbits<br /> *Malignant rabbit fibroma virus<br /> **MRV is a recombinant between Myxoma virus and Shope fibroma virus.<br /> **Causes a lethal disease with numerous primary and secondary tumours and immunosuppression.<br /> <br /> ===Control===<br /> *Attenuated vaccines are used for farmed and pet rabbits<br /> *Wild suspect animals should be culled<br /> <br /> [[Category:Leporipoxviruses]][[Category:Rabbit]]<br /> [[Category:To_Do_-_Viruses]]<br /> [[Category:To_Do_-_Stuart]]</div>

Stuartd https://en.wikivet.net/index.php?title=Myxomatosis&diff=69975 2010-07-05T14:33:15Z

<p>Stuartd: </p> <hr /> <div>{{unfinished}}<br /> <br /> [[Image:MyxoRabbit.JPG|200px|right|thumb|A European Rabbit afflicted by Myxomatosis in Shropshire, England. Courtesy of WikiMedia]]<br /> <br /> This page explains the viral cause of Myxomatosis and the associated clinical signs, pathology, treatment, control and prognosis.<br /> <br /> ===Myxoma virus===<br /> *Causes Myxomatosis in rabbits<br /> *Infectious myxomatosis is highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors. <br /> *Arthropod vectors such as mosquitoes and fleas provide the principal means of transmission. <br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia. <br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain. <br /> *The naturally attenuated viruses cause a milder disease of longer duration which favors vector transmission and persistence of the virus in nature. <br /> *High ambient environmental temperatures are associated with increased survival of infected animals. Some authors consider the California strains of the virus (California rabbit fibroma virus) as distinct from the myxoma virus, while others feel that the antigenic differences do not justify the separate distinction.<br /> <br /> ====Morphology====<br /> *Several proteins encoded by the virus are immunosubversive in that they mimic host ligands or regulators (virokines) or are homologues of cellular cytokine receptors (viroceptors)<br /> <br /> ====Pathogenesis====<br /> *MYX infects several cell types including mucosal cells, lymphocytes, and fibroblasts. <br /> *In addition to primary and secondary tumor development, there is severe immunosuppression leading to overwhelming infections by opportunistic gram-negative bacteria. <br /> *Viral antigen is present within primary as well as secondary tumors. <br /> *Virus multiplication and tumor-like lesions occur initially at the site of intradermal inoculation. This is followed by spread to regional lymph nodes and cell-associated viremia, with generalization to the skin and internal organs. <br /> *With immunosuppression, severe secondary gram-negative bacterial infections of the conjunctiva and nasal passages occur. <br /> *Death follows within 14 days of inoculation. <br /> *Several proteins encoded by the virus are immunosubversive in that they mimic host ligands or regulators (virokines) or are homologues of cellular cytokine receptors (viroceptors) <br /> **Virulent strains of MYX and MRV secrete a T2 gene product with significant homology to the T2 protein secreted by Shope fibroma virus. This protein acts as a receptor for TNFα and TNFβ. TNF is active in killing virus infected and tumor cells. Cytotoxicity is correlated with the induction of toxic superoxide radicals. The T2 gene product enhances viral virulence by interfering with TNF-dependent immune response pathways of the host.<br /> *Myxoma virus and MRV have also been shown to compromise cell-mediated immunity by inducing a loss of class I MHC antigens from the surface of infected cells. MHC class I-restricted cytotoxic T lymphocytes play a major role in clearing poxvirus infections from susceptible animal hosts, and are an important factor in limiting virus spread within the host. Class I molecules are present on all nucleated cells and platelets. Cytotoxic T cells (CD8+) recognize intracellular viral antigen in association with class I MHC glycoproteins on the cell surface. MYX and MRV infection results in a specific, rapid decrease in detectable surface class I epitopes. It has been suggested that a late viral gene product may interact with the class I complex to either physically sequester the complex away from the cell surface and inhibit its recycling to the surface, or induce a conformational change in the complex rendering it unrecognizable by cytotoxic T lymphocytes.<br /> *Myxoma growth factor (MGF) and a gene product designated M11L are also associated with MYX virulence. MGF and M11L deleted mutants are markedly attenuated, capable of inducing only benign localized nodules that regress spontaneously, similar to lesions induced by Shope fibroma virus. MGF has significant sequence homology with epidermal growth factor and transforming growth factor β. It has been postulated that the presence of EGF/TGFβ-like growth factors in tumorigenic poxviruses affects the growth and progression of poxvirus-infected cells.<br /> *Another myxoma virus virulence factor designated MYXOMA SERPIN 1 (SERP 1) has significant sequence homology with members of the family of serine proteases inhibitors (serpins). The exact role of SERP 1 is unknown but it may theoretically affect antigen presentation by interfering with viral protein degradation, or might reduce cytoxic T cell killing mediated by serine proteases in the effector cell.<br /> *Rabbit poxvirus gene sequences coding for products related to the C4 and C5 components of the complement cascade have been identified. It is postulated that complement-like viral protein products may block the activation or action of complement. The virulence factor T7 is an IFNγ receptor homologue.<br /> <br /> ====Clinical signs====<br /> *Clinical disease varies with virus strain and host species. <br /> **Sylvilagus species are relatively resistant, and are probably the natural host of the virus. In Sylvilagus species, infection usually results only in the development of skin tumors at the site of inoculation. The tumors appear 4-8 days after exposure and persist for up to 40 days. Very young rabbits may succumb to generalized disease.<br /> **Lepus species (hares) are highly resistant. Occasional individuals develop mild to severe generalized myxomatosis.<br /> **In the European rabbit (Oryctolagus cuniculus), infection with virulent virus (South American or California strains) results in severe disease with up to a 99% case fatality rate. <br /> ***Initial signs include edema of the eyelids accompanied by inflammation and edema around the anal, genital, oral, and nasal orifices. <br /> ***Edema of the head and ears, drooping ears, and bacterial infections resulting in mucopurulent conjunctivitis and pneumonia are seen. <br /> ***The primary tumor may be evident by 3-4 days after infection. Generalized tumors develop by 6-7 days after infection. <br /> ***Subcutaneous swellings become mucoid, gelatinous masses (hence the name myxomatosis). <br /> ***More chronic wart-like nodules appear, especially at mucocutaneous borders, after 10-14 days. <br /> ***Death (8-15 days post infection) is usually preceded by labored breathing and convulsions.<br /> <br /> ====Pathology====<br /> *The most prominent gross lesions in European rabbits with myxomatosis are the skin tumors and the pronounced cutaneous and subcutaneous edema, particularly in the area of the face and around body orifices. <br /> *Skin hemorrhages and subserosal petechiae and ecchymoses may be observed in the stomach and intestines. Subepicardial and subendocardial hemorrhages may also occur.<br /> *Adult rabbits of the genus Sylvilagus usually develop localized skin tumors resembling the fibromas produced in European rabbits by Shope fibroma virus.<br /> *Hares or young Sylvilagus rabbits may develop fibromatous to myxomatous nodules, however, lesions are usually mild and localized.<br /> <br /> ====Histopathology====<br /> <br /> *The lesions are proliferative to degenerative, depending on the virus strain. <br /> *The skin tumors result from proliferation of undifferentiated mesenchymal cells which become large stellate cells (myxoma cells). These cells may contain intracytoplasmic eosinophilic inclusions. These cells lie in a homogeneous matrix of mucinous material interspersed with capillaries and inflammatory cells. Endothelial proliferation with narrowing of the lumen and extrusion of stellate &quot;myxoma&quot; cells has been described. <br /> *Epithelial cells overlying the tumor may show hyperplasia or degeneration, or may appear normal. Epithelial proliferation is characterized by ballooning of cells in the stratum granulosum and hyperkeratosis. Epithelial vesiculation progresses to crust formation. Large, eosinophilic, intracytoplasmic inclusions are especially prominent in the stratum spinosum. Lesions in other organs include cellular proliferation of alveolar epithelium and the reticulum cells of [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]] and [[Spleen - Anatomy &amp; Physiology|spleen]]. Focal hemorrhage may be present in skin, kidneys, lymph nodes, testes, heart, stomach, and intestinal walls. Myxoma cells may be present in [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]], [[Bone Marrow - Anatomy &amp; Physiology|bone marrow]], uterus, ovaries, testes, and lungs.<br /> ====Antigenicity====<br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia<br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain<br /> <br /> <br /> ====Hosts====<br /> *Rabbits<br /> <br /> <br /> ====Pathogenesis====<br /> *Infects several cell types including mucosal cells, lymphocytes, and fibroblasts<br /> *In addition to primary and secondary tumor development, there is severe immunosuppression leading to overwhelming infections by opportunistic gram-negative bacteria (esp. conjunctiva and nasal passages)<br /> *Virus multiplication and tumor-like lesions occur initially at the site of intradermal inoculation <br /> *This is followed by spread to regional lymph nodes and cell-associated viremia, with generalization to the skin and internal organs<br /> *Gelatinous proliferative nodules all over body, especially at '''orifices''' (eyes, anus, nose)<br /> *Rabbit dies within 12 days, if not killed by predators<br /> <br /> =====In more detail=====<br /> *Virulent strains of MYX and MRV secrete a T2 gene product with significant homology to the T2 protein secreted by Shope fibroma virus. This protein acts as a receptor for TNFα and TNFβ. TNF is active in killing virus infected and tumor cells. Cytotoxicity is correlated with the induction of toxic superoxide radicals. The T2 gene product enhances viral virulence by interfering with TNF-dependent immune response pathways of the host.<br /> *Myxoma virus and MRV have also been shown to compromise cell-mediated immunity by inducing a loss of class I MHC antigens from the surface of infected cells. MHC class I-restricted cytotoxic T lymphocytes play a major role in clearing poxvirus infections from susceptible animal hosts, and are an important factor in limiting virus spread within the host. Class I molecules are present on all nucleated cells and platelets. Cytotoxic T cells (CD8+) recognize intracellular viral antigen in association with class I MHC glycoproteins on the cell surface. MYX and MRV infection results in a specific, rapid decrease in detectable surface class I epitopes. It has been suggested that a late viral gene product may interact with the class I complex to either physically sequester the complex away from the cell surface and inhibit its recycling to the surface, or induce a conformational change in the complex rendering it unrecognizable by cytotoxic T lymphocytes.<br /> *Myxoma growth factor (MGF) and a gene product designated M11L are also associated with MYX virulence. MGF and M11L deleted mutants are markedly attenuated, capable of inducing only benign localized nodules that regress spontaneously, similar to lesions induced by Shope fibroma virus. MGF has significant sequence homology with epidermal growth factor and transforming growth factor β. It has been postulated that the presence of EGF/TGFβ-like growth factors in tumorigenic poxviruses affects the growth and progression of poxvirus-infected cells.<br /> *Another myxoma virus virulence factor designated MYXOMA SERPIN 1 (SERP 1) has significant sequence homology with members of the family of serine proteases inhibitors (serpins). The exact role of SERP 1 is unknown but it may theoretically affect antigen presentation by interfering with viral protein degradation, or might reduce cytoxic T cell killing mediated by serine proteases in the effector cell.<br /> *Rabbit poxvirus gene sequences coding for products related to the C4 and C5 components of the complement cascade have been identified. It is postulated that complement-like viral protein products may block the activation or action of complement. The virulence factor T7 is an IFNγ receptor homologue.<br /> <br /> =====Clinical Signs=====<br /> *Clinical disease varies with virus strain and host species. <br /> **Sylvilagus species are relatively resistant, and are probably the natural host of the virus. In Sylvilagus species, infection usually results only in the development of skin tumors at the site of inoculation. The tumors appear 4-8 days after exposure and persist for up to 40 days. Very young rabbits may succumb to generalized disease.<br /> **Lepus species (hares) are highly resistant. Occasional individuals develop mild to severe generalized myxomatosis.<br /> **In the European rabbit (Oryctolagus cuniculus), infection with virulent virus (South American or California strains) results in severe disease with up to a 99% case fatality rate. <br /> ***Initial signs include edema of the eyelids accompanied by inflammation and edema around the anal, genital, oral, and nasal orifices. <br /> ***Edema of the head and ears, drooping ears, and bacterial infections resulting in mucopurulent conjunctivitis and pneumonia are seen. <br /> ***The primary tumor may be evident by 3-4 days after infection. Generalized tumors develop by 6-7 days after infection. <br /> ***Subcutaneous swellings become mucoid, gelatinous masses (hence the name myxomatosis). <br /> ***More chronic wart-like nodules appear, especially at mucocutaneous borders, after 10-14 days. <br /> ***Death (8-15 days post infection) is usually preceded by labored breathing and convulsions.<br /> <br /> =====Pathology=====<br /> *The most prominent gross lesions in European rabbits with myxomatosis are the '''skin tumors''' and the pronounced '''cutaneous and subcutaneous edema''', particularly in the area of the face and around body orifices. <br /> *'''Skin hemorrhages''', '''subserosal petechiae''' and '''ecchymoses''' may be observed in the stomach and intestines. Subepicardial and subendocardial hemorrhages may also occur.<br /> *Adult rabbits of the genus Sylvilagus usually develop localized skin tumors resembling the fibromas produced in European rabbits by Shope fibroma virus.<br /> *Hares or young Sylvilagus rabbits may develop fibromatous to myxomatous nodules, however, lesions are usually mild and localized.<br /> <br /> =====Histopathology=====<br /> *The lesions are proliferative to degenerative, depending on the virus strain. <br /> *The skin tumors result from proliferation of undifferentiated mesenchymal cells which become large stellate cells (myxoma cells). These cells may contain '''intracytoplasmic eosinophilic inclusions'''. These cells lie in a homogeneous matrix of mucinous material interspersed with capillaries and inflammatory cells. Endothelial proliferation with narrowing of the lumen and extrusion of stellate &quot;myxoma&quot; cells has been described. <br /> *Epithelial cells overlying the tumor may show hyperplasia or degeneration, or may appear normal. Epithelial proliferation is characterized by ballooning of cells in the stratum granulosum and hyperkeratosis. Epithelial vesiculation progresses to crust formation. Large, eosinophilic, intracytoplasmic inclusions are especially prominent in the stratum spinosum. Lesions in other organs include cellular proliferation of alveolar epithelium and the reticulum cells of lymph nodes and [[Spleen - Anatomy &amp; Physiology|spleen]]. Focal hemorrhage may be present in skin, kidneys, [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]], testes, heart, stomach, and intestinal walls. Myxoma cells may be present in [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]], [[Bone Marrow - Anatomy &amp; Physiology|bone marrow]], uterus, ovaries, testes, and lungs.<br /> <br /> ====Epidemiology====<br /> *Highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors<br /> *'''Mosquitoes''' act as mechanical vectors<br /> *High ambient environmental temperatures are associated with increased survival of infected animals<br /> <br /> ====Differentials====<br /> *Shope fibroma virus<br /> **Localised benign tumours that spontaneously regress in adult immunocompetent rabbits<br /> *Malignant rabbit fibroma virus<br /> **MRV is a recombinant between Myxoma virus and Shope fibroma virus.<br /> **Causes a lethal disease with numerous primary and secondary tumours and immunosuppression.<br /> <br /> ====Control====<br /> *Attenuated vaccines are used for farmed and pet rabbits<br /> *Wild suspect animals should be culled<br /> <br /> [[Category:Leporipoxviruses]][[Category:Rabbit]]<br /> [[Category:To_Do_-_Viruses]]<br /> [[Category:To_Do_-_Stuart]]</div>

Stuartd https://en.wikivet.net/index.php?title=Myxomatosis&diff=69974 2010-07-05T14:32:42Z

<p>Stuartd: </p> <hr /> <div>{{unfinished}}<br /> <br /> [[Image:MyxoRabbit.JPG|200px|right|thumb|A European Rabbit afflicted by Myxomatosis in Shropshire, England. Courtesy of WikiMedia]]<br /> <br /> This page explains the viral cause of Myxomatosis and the associated clinical signs, treatment, control and prognosis.<br /> <br /> ===Myxoma virus===<br /> *Causes Myxomatosis in rabbits<br /> *Infectious myxomatosis is highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors. <br /> *Arthropod vectors such as mosquitoes and fleas provide the principal means of transmission. <br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia. <br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain. <br /> *The naturally attenuated viruses cause a milder disease of longer duration which favors vector transmission and persistence of the virus in nature. <br /> *High ambient environmental temperatures are associated with increased survival of infected animals. Some authors consider the California strains of the virus (California rabbit fibroma virus) as distinct from the myxoma virus, while others feel that the antigenic differences do not justify the separate distinction.<br /> <br /> ====Morphology====<br /> *Several proteins encoded by the virus are immunosubversive in that they mimic host ligands or regulators (virokines) or are homologues of cellular cytokine receptors (viroceptors)<br /> <br /> ====Pathogenesis====<br /> *MYX infects several cell types including mucosal cells, lymphocytes, and fibroblasts. <br /> *In addition to primary and secondary tumor development, there is severe immunosuppression leading to overwhelming infections by opportunistic gram-negative bacteria. <br /> *Viral antigen is present within primary as well as secondary tumors. <br /> *Virus multiplication and tumor-like lesions occur initially at the site of intradermal inoculation. This is followed by spread to regional lymph nodes and cell-associated viremia, with generalization to the skin and internal organs. <br /> *With immunosuppression, severe secondary gram-negative bacterial infections of the conjunctiva and nasal passages occur. <br /> *Death follows within 14 days of inoculation. <br /> *Several proteins encoded by the virus are immunosubversive in that they mimic host ligands or regulators (virokines) or are homologues of cellular cytokine receptors (viroceptors) <br /> **Virulent strains of MYX and MRV secrete a T2 gene product with significant homology to the T2 protein secreted by Shope fibroma virus. This protein acts as a receptor for TNFα and TNFβ. TNF is active in killing virus infected and tumor cells. Cytotoxicity is correlated with the induction of toxic superoxide radicals. The T2 gene product enhances viral virulence by interfering with TNF-dependent immune response pathways of the host.<br /> *Myxoma virus and MRV have also been shown to compromise cell-mediated immunity by inducing a loss of class I MHC antigens from the surface of infected cells. MHC class I-restricted cytotoxic T lymphocytes play a major role in clearing poxvirus infections from susceptible animal hosts, and are an important factor in limiting virus spread within the host. Class I molecules are present on all nucleated cells and platelets. Cytotoxic T cells (CD8+) recognize intracellular viral antigen in association with class I MHC glycoproteins on the cell surface. MYX and MRV infection results in a specific, rapid decrease in detectable surface class I epitopes. It has been suggested that a late viral gene product may interact with the class I complex to either physically sequester the complex away from the cell surface and inhibit its recycling to the surface, or induce a conformational change in the complex rendering it unrecognizable by cytotoxic T lymphocytes.<br /> *Myxoma growth factor (MGF) and a gene product designated M11L are also associated with MYX virulence. MGF and M11L deleted mutants are markedly attenuated, capable of inducing only benign localized nodules that regress spontaneously, similar to lesions induced by Shope fibroma virus. MGF has significant sequence homology with epidermal growth factor and transforming growth factor β. It has been postulated that the presence of EGF/TGFβ-like growth factors in tumorigenic poxviruses affects the growth and progression of poxvirus-infected cells.<br /> *Another myxoma virus virulence factor designated MYXOMA SERPIN 1 (SERP 1) has significant sequence homology with members of the family of serine proteases inhibitors (serpins). The exact role of SERP 1 is unknown but it may theoretically affect antigen presentation by interfering with viral protein degradation, or might reduce cytoxic T cell killing mediated by serine proteases in the effector cell.<br /> *Rabbit poxvirus gene sequences coding for products related to the C4 and C5 components of the complement cascade have been identified. It is postulated that complement-like viral protein products may block the activation or action of complement. The virulence factor T7 is an IFNγ receptor homologue.<br /> <br /> ====Clinical signs====<br /> *Clinical disease varies with virus strain and host species. <br /> **Sylvilagus species are relatively resistant, and are probably the natural host of the virus. In Sylvilagus species, infection usually results only in the development of skin tumors at the site of inoculation. The tumors appear 4-8 days after exposure and persist for up to 40 days. Very young rabbits may succumb to generalized disease.<br /> **Lepus species (hares) are highly resistant. Occasional individuals develop mild to severe generalized myxomatosis.<br /> **In the European rabbit (Oryctolagus cuniculus), infection with virulent virus (South American or California strains) results in severe disease with up to a 99% case fatality rate. <br /> ***Initial signs include edema of the eyelids accompanied by inflammation and edema around the anal, genital, oral, and nasal orifices. <br /> ***Edema of the head and ears, drooping ears, and bacterial infections resulting in mucopurulent conjunctivitis and pneumonia are seen. <br /> ***The primary tumor may be evident by 3-4 days after infection. Generalized tumors develop by 6-7 days after infection. <br /> ***Subcutaneous swellings become mucoid, gelatinous masses (hence the name myxomatosis). <br /> ***More chronic wart-like nodules appear, especially at mucocutaneous borders, after 10-14 days. <br /> ***Death (8-15 days post infection) is usually preceded by labored breathing and convulsions.<br /> <br /> ====Pathology====<br /> *The most prominent gross lesions in European rabbits with myxomatosis are the skin tumors and the pronounced cutaneous and subcutaneous edema, particularly in the area of the face and around body orifices. <br /> *Skin hemorrhages and subserosal petechiae and ecchymoses may be observed in the stomach and intestines. Subepicardial and subendocardial hemorrhages may also occur.<br /> *Adult rabbits of the genus Sylvilagus usually develop localized skin tumors resembling the fibromas produced in European rabbits by Shope fibroma virus.<br /> *Hares or young Sylvilagus rabbits may develop fibromatous to myxomatous nodules, however, lesions are usually mild and localized.<br /> <br /> ====Histopathology====<br /> <br /> *The lesions are proliferative to degenerative, depending on the virus strain. <br /> *The skin tumors result from proliferation of undifferentiated mesenchymal cells which become large stellate cells (myxoma cells). These cells may contain intracytoplasmic eosinophilic inclusions. These cells lie in a homogeneous matrix of mucinous material interspersed with capillaries and inflammatory cells. Endothelial proliferation with narrowing of the lumen and extrusion of stellate &quot;myxoma&quot; cells has been described. <br /> *Epithelial cells overlying the tumor may show hyperplasia or degeneration, or may appear normal. Epithelial proliferation is characterized by ballooning of cells in the stratum granulosum and hyperkeratosis. Epithelial vesiculation progresses to crust formation. Large, eosinophilic, intracytoplasmic inclusions are especially prominent in the stratum spinosum. Lesions in other organs include cellular proliferation of alveolar epithelium and the reticulum cells of [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]] and [[Spleen - Anatomy &amp; Physiology|spleen]]. Focal hemorrhage may be present in skin, kidneys, lymph nodes, testes, heart, stomach, and intestinal walls. Myxoma cells may be present in [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]], [[Bone Marrow - Anatomy &amp; Physiology|bone marrow]], uterus, ovaries, testes, and lungs.<br /> ====Antigenicity====<br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia<br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain<br /> <br /> <br /> ====Hosts====<br /> *Rabbits<br /> <br /> <br /> ====Pathogenesis====<br /> *Infects several cell types including mucosal cells, lymphocytes, and fibroblasts<br /> *In addition to primary and secondary tumor development, there is severe immunosuppression leading to overwhelming infections by opportunistic gram-negative bacteria (esp. conjunctiva and nasal passages)<br /> *Virus multiplication and tumor-like lesions occur initially at the site of intradermal inoculation <br /> *This is followed by spread to regional lymph nodes and cell-associated viremia, with generalization to the skin and internal organs<br /> *Gelatinous proliferative nodules all over body, especially at '''orifices''' (eyes, anus, nose)<br /> *Rabbit dies within 12 days, if not killed by predators<br /> <br /> =====In more detail=====<br /> *Virulent strains of MYX and MRV secrete a T2 gene product with significant homology to the T2 protein secreted by Shope fibroma virus. This protein acts as a receptor for TNFα and TNFβ. TNF is active in killing virus infected and tumor cells. Cytotoxicity is correlated with the induction of toxic superoxide radicals. The T2 gene product enhances viral virulence by interfering with TNF-dependent immune response pathways of the host.<br /> *Myxoma virus and MRV have also been shown to compromise cell-mediated immunity by inducing a loss of class I MHC antigens from the surface of infected cells. MHC class I-restricted cytotoxic T lymphocytes play a major role in clearing poxvirus infections from susceptible animal hosts, and are an important factor in limiting virus spread within the host. Class I molecules are present on all nucleated cells and platelets. Cytotoxic T cells (CD8+) recognize intracellular viral antigen in association with class I MHC glycoproteins on the cell surface. MYX and MRV infection results in a specific, rapid decrease in detectable surface class I epitopes. It has been suggested that a late viral gene product may interact with the class I complex to either physically sequester the complex away from the cell surface and inhibit its recycling to the surface, or induce a conformational change in the complex rendering it unrecognizable by cytotoxic T lymphocytes.<br /> *Myxoma growth factor (MGF) and a gene product designated M11L are also associated with MYX virulence. MGF and M11L deleted mutants are markedly attenuated, capable of inducing only benign localized nodules that regress spontaneously, similar to lesions induced by Shope fibroma virus. MGF has significant sequence homology with epidermal growth factor and transforming growth factor β. It has been postulated that the presence of EGF/TGFβ-like growth factors in tumorigenic poxviruses affects the growth and progression of poxvirus-infected cells.<br /> *Another myxoma virus virulence factor designated MYXOMA SERPIN 1 (SERP 1) has significant sequence homology with members of the family of serine proteases inhibitors (serpins). The exact role of SERP 1 is unknown but it may theoretically affect antigen presentation by interfering with viral protein degradation, or might reduce cytoxic T cell killing mediated by serine proteases in the effector cell.<br /> *Rabbit poxvirus gene sequences coding for products related to the C4 and C5 components of the complement cascade have been identified. It is postulated that complement-like viral protein products may block the activation or action of complement. The virulence factor T7 is an IFNγ receptor homologue.<br /> <br /> =====Clinical Signs=====<br /> *Clinical disease varies with virus strain and host species. <br /> **Sylvilagus species are relatively resistant, and are probably the natural host of the virus. In Sylvilagus species, infection usually results only in the development of skin tumors at the site of inoculation. The tumors appear 4-8 days after exposure and persist for up to 40 days. Very young rabbits may succumb to generalized disease.<br /> **Lepus species (hares) are highly resistant. Occasional individuals develop mild to severe generalized myxomatosis.<br /> **In the European rabbit (Oryctolagus cuniculus), infection with virulent virus (South American or California strains) results in severe disease with up to a 99% case fatality rate. <br /> ***Initial signs include edema of the eyelids accompanied by inflammation and edema around the anal, genital, oral, and nasal orifices. <br /> ***Edema of the head and ears, drooping ears, and bacterial infections resulting in mucopurulent conjunctivitis and pneumonia are seen. <br /> ***The primary tumor may be evident by 3-4 days after infection. Generalized tumors develop by 6-7 days after infection. <br /> ***Subcutaneous swellings become mucoid, gelatinous masses (hence the name myxomatosis). <br /> ***More chronic wart-like nodules appear, especially at mucocutaneous borders, after 10-14 days. <br /> ***Death (8-15 days post infection) is usually preceded by labored breathing and convulsions.<br /> <br /> =====Pathology=====<br /> *The most prominent gross lesions in European rabbits with myxomatosis are the '''skin tumors''' and the pronounced '''cutaneous and subcutaneous edema''', particularly in the area of the face and around body orifices. <br /> *'''Skin hemorrhages''', '''subserosal petechiae''' and '''ecchymoses''' may be observed in the stomach and intestines. Subepicardial and subendocardial hemorrhages may also occur.<br /> *Adult rabbits of the genus Sylvilagus usually develop localized skin tumors resembling the fibromas produced in European rabbits by Shope fibroma virus.<br /> *Hares or young Sylvilagus rabbits may develop fibromatous to myxomatous nodules, however, lesions are usually mild and localized.<br /> <br /> =====Histopathology=====<br /> *The lesions are proliferative to degenerative, depending on the virus strain. <br /> *The skin tumors result from proliferation of undifferentiated mesenchymal cells which become large stellate cells (myxoma cells). These cells may contain '''intracytoplasmic eosinophilic inclusions'''. These cells lie in a homogeneous matrix of mucinous material interspersed with capillaries and inflammatory cells. Endothelial proliferation with narrowing of the lumen and extrusion of stellate &quot;myxoma&quot; cells has been described. <br /> *Epithelial cells overlying the tumor may show hyperplasia or degeneration, or may appear normal. Epithelial proliferation is characterized by ballooning of cells in the stratum granulosum and hyperkeratosis. Epithelial vesiculation progresses to crust formation. Large, eosinophilic, intracytoplasmic inclusions are especially prominent in the stratum spinosum. Lesions in other organs include cellular proliferation of alveolar epithelium and the reticulum cells of lymph nodes and [[Spleen - Anatomy &amp; Physiology|spleen]]. Focal hemorrhage may be present in skin, kidneys, [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]], testes, heart, stomach, and intestinal walls. Myxoma cells may be present in [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]], [[Bone Marrow - Anatomy &amp; Physiology|bone marrow]], uterus, ovaries, testes, and lungs.<br /> <br /> ====Epidemiology====<br /> *Highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors<br /> *'''Mosquitoes''' act as mechanical vectors<br /> *High ambient environmental temperatures are associated with increased survival of infected animals<br /> <br /> ====Differentials====<br /> *Shope fibroma virus<br /> **Localised benign tumours that spontaneously regress in adult immunocompetent rabbits<br /> *Malignant rabbit fibroma virus<br /> **MRV is a recombinant between Myxoma virus and Shope fibroma virus.<br /> **Causes a lethal disease with numerous primary and secondary tumours and immunosuppression.<br /> <br /> ====Control====<br /> *Attenuated vaccines are used for farmed and pet rabbits<br /> *Wild suspect animals should be culled<br /> <br /> [[Category:Leporipoxviruses]][[Category:Rabbit]]<br /> [[Category:To_Do_-_Viruses]]<br /> [[Category:To_Do_-_Stuart]]</div>

Stuartd https://en.wikivet.net/index.php?title=Myxomatosis&diff=69970 2010-07-05T14:30:47Z

<p>Stuartd: </p> <hr /> <div>{{unfinished}}<br /> <br /> [[Image:MyxoRabbit.JPG|200px|right|thumb|A European Rabbit afflicted by Myxomatosis in Shropshire, England. Courtesy of WikiMedia]]<br /> <br /> ===Myxoma virus===<br /> *Causes Myxomatosis in rabbits<br /> *Infectious myxomatosis is highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors. <br /> *Arthropod vectors such as mosquitoes and fleas provide the principal means of transmission. <br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia. <br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain. <br /> *The naturally attenuated viruses cause a milder disease of longer duration which favors vector transmission and persistence of the virus in nature. <br /> *High ambient environmental temperatures are associated with increased survival of infected animals. Some authors consider the California strains of the virus (California rabbit fibroma virus) as distinct from the myxoma virus, while others feel that the antigenic differences do not justify the separate distinction.<br /> <br /> ====Morphology====<br /> *Several proteins encoded by the virus are immunosubversive in that they mimic host ligands or regulators (virokines) or are homologues of cellular cytokine receptors (viroceptors)<br /> <br /> ====Pathogenesis====<br /> *MYX infects several cell types including mucosal cells, lymphocytes, and fibroblasts. <br /> *In addition to primary and secondary tumor development, there is severe immunosuppression leading to overwhelming infections by opportunistic gram-negative bacteria. <br /> *Viral antigen is present within primary as well as secondary tumors. <br /> *Virus multiplication and tumor-like lesions occur initially at the site of intradermal inoculation. This is followed by spread to regional lymph nodes and cell-associated viremia, with generalization to the skin and internal organs. <br /> *With immunosuppression, severe secondary gram-negative bacterial infections of the conjunctiva and nasal passages occur. <br /> *Death follows within 14 days of inoculation. <br /> *Several proteins encoded by the virus are immunosubversive in that they mimic host ligands or regulators (virokines) or are homologues of cellular cytokine receptors (viroceptors) <br /> **Virulent strains of MYX and MRV secrete a T2 gene product with significant homology to the T2 protein secreted by Shope fibroma virus. This protein acts as a receptor for TNFα and TNFβ. TNF is active in killing virus infected and tumor cells. Cytotoxicity is correlated with the induction of toxic superoxide radicals. The T2 gene product enhances viral virulence by interfering with TNF-dependent immune response pathways of the host.<br /> *Myxoma virus and MRV have also been shown to compromise cell-mediated immunity by inducing a loss of class I MHC antigens from the surface of infected cells. MHC class I-restricted cytotoxic T lymphocytes play a major role in clearing poxvirus infections from susceptible animal hosts, and are an important factor in limiting virus spread within the host. Class I molecules are present on all nucleated cells and platelets. Cytotoxic T cells (CD8+) recognize intracellular viral antigen in association with class I MHC glycoproteins on the cell surface. MYX and MRV infection results in a specific, rapid decrease in detectable surface class I epitopes. It has been suggested that a late viral gene product may interact with the class I complex to either physically sequester the complex away from the cell surface and inhibit its recycling to the surface, or induce a conformational change in the complex rendering it unrecognizable by cytotoxic T lymphocytes.<br /> *Myxoma growth factor (MGF) and a gene product designated M11L are also associated with MYX virulence. MGF and M11L deleted mutants are markedly attenuated, capable of inducing only benign localized nodules that regress spontaneously, similar to lesions induced by Shope fibroma virus. MGF has significant sequence homology with epidermal growth factor and transforming growth factor β. It has been postulated that the presence of EGF/TGFβ-like growth factors in tumorigenic poxviruses affects the growth and progression of poxvirus-infected cells.<br /> *Another myxoma virus virulence factor designated MYXOMA SERPIN 1 (SERP 1) has significant sequence homology with members of the family of serine proteases inhibitors (serpins). The exact role of SERP 1 is unknown but it may theoretically affect antigen presentation by interfering with viral protein degradation, or might reduce cytoxic T cell killing mediated by serine proteases in the effector cell.<br /> *Rabbit poxvirus gene sequences coding for products related to the C4 and C5 components of the complement cascade have been identified. It is postulated that complement-like viral protein products may block the activation or action of complement. The virulence factor T7 is an IFNγ receptor homologue.<br /> <br /> ====Clinical signs====<br /> *Clinical disease varies with virus strain and host species. <br /> **Sylvilagus species are relatively resistant, and are probably the natural host of the virus. In Sylvilagus species, infection usually results only in the development of skin tumors at the site of inoculation. The tumors appear 4-8 days after exposure and persist for up to 40 days. Very young rabbits may succumb to generalized disease.<br /> **Lepus species (hares) are highly resistant. Occasional individuals develop mild to severe generalized myxomatosis.<br /> **In the European rabbit (Oryctolagus cuniculus), infection with virulent virus (South American or California strains) results in severe disease with up to a 99% case fatality rate. <br /> ***Initial signs include edema of the eyelids accompanied by inflammation and edema around the anal, genital, oral, and nasal orifices. <br /> ***Edema of the head and ears, drooping ears, and bacterial infections resulting in mucopurulent conjunctivitis and pneumonia are seen. <br /> ***The primary tumor may be evident by 3-4 days after infection. Generalized tumors develop by 6-7 days after infection. <br /> ***Subcutaneous swellings become mucoid, gelatinous masses (hence the name myxomatosis). <br /> ***More chronic wart-like nodules appear, especially at mucocutaneous borders, after 10-14 days. <br /> ***Death (8-15 days post infection) is usually preceded by labored breathing and convulsions.<br /> <br /> ====Pathology====<br /> *The most prominent gross lesions in European rabbits with myxomatosis are the skin tumors and the pronounced cutaneous and subcutaneous edema, particularly in the area of the face and around body orifices. <br /> *Skin hemorrhages and subserosal petechiae and ecchymoses may be observed in the stomach and intestines. Subepicardial and subendocardial hemorrhages may also occur.<br /> *Adult rabbits of the genus Sylvilagus usually develop localized skin tumors resembling the fibromas produced in European rabbits by Shope fibroma virus.<br /> *Hares or young Sylvilagus rabbits may develop fibromatous to myxomatous nodules, however, lesions are usually mild and localized.<br /> <br /> ====Histopathology====<br /> <br /> *The lesions are proliferative to degenerative, depending on the virus strain. <br /> *The skin tumors result from proliferation of undifferentiated mesenchymal cells which become large stellate cells (myxoma cells). These cells may contain intracytoplasmic eosinophilic inclusions. These cells lie in a homogeneous matrix of mucinous material interspersed with capillaries and inflammatory cells. Endothelial proliferation with narrowing of the lumen and extrusion of stellate &quot;myxoma&quot; cells has been described. <br /> *Epithelial cells overlying the tumor may show hyperplasia or degeneration, or may appear normal. Epithelial proliferation is characterized by ballooning of cells in the stratum granulosum and hyperkeratosis. Epithelial vesiculation progresses to crust formation. Large, eosinophilic, intracytoplasmic inclusions are especially prominent in the stratum spinosum. Lesions in other organs include cellular proliferation of alveolar epithelium and the reticulum cells of [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]] and [[Spleen - Anatomy &amp; Physiology|spleen]]. Focal hemorrhage may be present in skin, kidneys, lymph nodes, testes, heart, stomach, and intestinal walls. Myxoma cells may be present in [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]], [[Bone Marrow - Anatomy &amp; Physiology|bone marrow]], uterus, ovaries, testes, and lungs.<br /> ====Antigenicity====<br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia<br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain<br /> <br /> <br /> ====Hosts====<br /> *Rabbits<br /> <br /> <br /> ====Pathogenesis====<br /> *Infects several cell types including mucosal cells, lymphocytes, and fibroblasts<br /> *In addition to primary and secondary tumor development, there is severe immunosuppression leading to overwhelming infections by opportunistic gram-negative bacteria (esp. conjunctiva and nasal passages)<br /> *Virus multiplication and tumor-like lesions occur initially at the site of intradermal inoculation <br /> *This is followed by spread to regional lymph nodes and cell-associated viremia, with generalization to the skin and internal organs<br /> *Gelatinous proliferative nodules all over body, especially at '''orifices''' (eyes, anus, nose)<br /> *Rabbit dies within 12 days, if not killed by predators<br /> <br /> =====In more detail=====<br /> *Virulent strains of MYX and MRV secrete a T2 gene product with significant homology to the T2 protein secreted by Shope fibroma virus. This protein acts as a receptor for TNFα and TNFβ. TNF is active in killing virus infected and tumor cells. Cytotoxicity is correlated with the induction of toxic superoxide radicals. The T2 gene product enhances viral virulence by interfering with TNF-dependent immune response pathways of the host.<br /> *Myxoma virus and MRV have also been shown to compromise cell-mediated immunity by inducing a loss of class I MHC antigens from the surface of infected cells. MHC class I-restricted cytotoxic T lymphocytes play a major role in clearing poxvirus infections from susceptible animal hosts, and are an important factor in limiting virus spread within the host. Class I molecules are present on all nucleated cells and platelets. Cytotoxic T cells (CD8+) recognize intracellular viral antigen in association with class I MHC glycoproteins on the cell surface. MYX and MRV infection results in a specific, rapid decrease in detectable surface class I epitopes. It has been suggested that a late viral gene product may interact with the class I complex to either physically sequester the complex away from the cell surface and inhibit its recycling to the surface, or induce a conformational change in the complex rendering it unrecognizable by cytotoxic T lymphocytes.<br /> *Myxoma growth factor (MGF) and a gene product designated M11L are also associated with MYX virulence. MGF and M11L deleted mutants are markedly attenuated, capable of inducing only benign localized nodules that regress spontaneously, similar to lesions induced by Shope fibroma virus. MGF has significant sequence homology with epidermal growth factor and transforming growth factor β. It has been postulated that the presence of EGF/TGFβ-like growth factors in tumorigenic poxviruses affects the growth and progression of poxvirus-infected cells.<br /> *Another myxoma virus virulence factor designated MYXOMA SERPIN 1 (SERP 1) has significant sequence homology with members of the family of serine proteases inhibitors (serpins). The exact role of SERP 1 is unknown but it may theoretically affect antigen presentation by interfering with viral protein degradation, or might reduce cytoxic T cell killing mediated by serine proteases in the effector cell.<br /> *Rabbit poxvirus gene sequences coding for products related to the C4 and C5 components of the complement cascade have been identified. It is postulated that complement-like viral protein products may block the activation or action of complement. The virulence factor T7 is an IFNγ receptor homologue.<br /> <br /> =====Clinical Signs=====<br /> *Clinical disease varies with virus strain and host species. <br /> **Sylvilagus species are relatively resistant, and are probably the natural host of the virus. In Sylvilagus species, infection usually results only in the development of skin tumors at the site of inoculation. The tumors appear 4-8 days after exposure and persist for up to 40 days. Very young rabbits may succumb to generalized disease.<br /> **Lepus species (hares) are highly resistant. Occasional individuals develop mild to severe generalized myxomatosis.<br /> **In the European rabbit (Oryctolagus cuniculus), infection with virulent virus (South American or California strains) results in severe disease with up to a 99% case fatality rate. <br /> ***Initial signs include edema of the eyelids accompanied by inflammation and edema around the anal, genital, oral, and nasal orifices. <br /> ***Edema of the head and ears, drooping ears, and bacterial infections resulting in mucopurulent conjunctivitis and pneumonia are seen. <br /> ***The primary tumor may be evident by 3-4 days after infection. Generalized tumors develop by 6-7 days after infection. <br /> ***Subcutaneous swellings become mucoid, gelatinous masses (hence the name myxomatosis). <br /> ***More chronic wart-like nodules appear, especially at mucocutaneous borders, after 10-14 days. <br /> ***Death (8-15 days post infection) is usually preceded by labored breathing and convulsions.<br /> <br /> =====Pathology=====<br /> *The most prominent gross lesions in European rabbits with myxomatosis are the '''skin tumors''' and the pronounced '''cutaneous and subcutaneous edema''', particularly in the area of the face and around body orifices. <br /> *'''Skin hemorrhages''', '''subserosal petechiae''' and '''ecchymoses''' may be observed in the stomach and intestines. Subepicardial and subendocardial hemorrhages may also occur.<br /> *Adult rabbits of the genus Sylvilagus usually develop localized skin tumors resembling the fibromas produced in European rabbits by Shope fibroma virus.<br /> *Hares or young Sylvilagus rabbits may develop fibromatous to myxomatous nodules, however, lesions are usually mild and localized.<br /> <br /> =====Histopathology=====<br /> *The lesions are proliferative to degenerative, depending on the virus strain. <br /> *The skin tumors result from proliferation of undifferentiated mesenchymal cells which become large stellate cells (myxoma cells). These cells may contain '''intracytoplasmic eosinophilic inclusions'''. These cells lie in a homogeneous matrix of mucinous material interspersed with capillaries and inflammatory cells. Endothelial proliferation with narrowing of the lumen and extrusion of stellate &quot;myxoma&quot; cells has been described. <br /> *Epithelial cells overlying the tumor may show hyperplasia or degeneration, or may appear normal. Epithelial proliferation is characterized by ballooning of cells in the stratum granulosum and hyperkeratosis. Epithelial vesiculation progresses to crust formation. Large, eosinophilic, intracytoplasmic inclusions are especially prominent in the stratum spinosum. Lesions in other organs include cellular proliferation of alveolar epithelium and the reticulum cells of lymph nodes and [[Spleen - Anatomy &amp; Physiology|spleen]]. Focal hemorrhage may be present in skin, kidneys, [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]], testes, heart, stomach, and intestinal walls. Myxoma cells may be present in [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]], [[Bone Marrow - Anatomy &amp; Physiology|bone marrow]], uterus, ovaries, testes, and lungs.<br /> <br /> ====Epidemiology====<br /> *Highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors<br /> *'''Mosquitoes''' act as mechanical vectors<br /> *High ambient environmental temperatures are associated with increased survival of infected animals<br /> <br /> ====Differentials====<br /> *Shope fibroma virus<br /> **Localised benign tumours that spontaneously regress in adult immunocompetent rabbits<br /> *Malignant rabbit fibroma virus<br /> **MRV is a recombinant between Myxoma virus and Shope fibroma virus.<br /> **Causes a lethal disease with numerous primary and secondary tumours and immunosuppression.<br /> <br /> ====Control====<br /> *Attenuated vaccines are used for farmed and pet rabbits<br /> *Wild suspect animals should be culled<br /> <br /> [[Category:Leporipoxviruses]][[Category:Rabbit]]<br /> [[Category:To_Do_-_Viruses]]<br /> [[Category:To_Do_-_Stuart]]</div>

Stuartd https://en.wikivet.net/index.php?title=Bovine_Viral_Diarrhoea_Virus&diff=69946 2010-07-05T14:25:03Z

<p>Stuartd: </p> <hr /> <div>{{unfinished}}<br /> <br /> ====Antigenicity====<br /> *RNA virus closely related to [[Classical Swine Fever]] and [[Border Disease Virus]]<br /> *2 Serological Types<br /> **BVDV-1 is traditional, existing as two biotypes<br /> ***BVDV-1nc: noncytopathogenic<br /> ***BVDV-1c: cytopathogenic<br /> **BVDV-2 is an emerging hemorrhagic virus<br /> <br /> ====Hosts====<br /> *Cattle<br /> <br /> ====Pathogenesis====<br /> [[Image:BVD-MD.gif|right|thumb|125px|&lt;small&gt;&lt;center&gt;Small erosions of MDV/BVDV - vesicles are microscopic (Courtesy of Alun Williams (RVC))&lt;/center&gt;&lt;/small&gt;]]<br /> [[Image:Bvd2.gif|right|thumb|125px|&lt;small&gt;&lt;center&gt;Coalescing lesions of BVDV (Courtesy of Alun Williams (RVC))&lt;/center&gt;&lt;/small&gt;]]<br /> '''BVDV-1c'''<br /> *Infects cattle regardless of age<br /> *Usually mild: diarrhoea with recovery in 10 dyas<br /> *Immunosuppression can lead to secondary infection<br /> '''BVDV-2nc'''<br /> *Transient '''thrombocytopenia''' and '''leukopenia''' over 2 weeks<br /> *Hemorrhages <br /> *Secondary infection<br /> *Death<br /> '''BVDV-1nc'''<br /> *'''Transplacental''' infection of naive heifers<br /> *Outcome depends on age of fetus at contraction<br /> **0-110 days: '''abortion''' or '''persistently infected (PI)''' calves born<br /> **110-220 days: congenital damage with noticeable '''CNS''' and '''musculoskeletal''' lesions<br /> **220 days to term: '''active immunity''' developed<br /> '''Mucosal Disease'''<br /> *Mucosal disease is caused by a '''superinfection''' of PI animals with a second homologous cytopathic biotype (eg BVDV-1nc followed by BVDV-1c)<br /> *Infection typically occurs between '''6-18 months of age''' but is variable<br /> *Superinfection will quickly '''spread horizontally''' among PI animals<br /> *Invariable '''fatal'''<br /> *Characterized by '''oral and enteric erosions''', particularly overlying Peyer's patches, and ulceration of the feet<br /> *Animals can show anorexia, depression and/or diarrhoea for 2-5 days before death<br /> *Vaccination can lead to '''iatrogenic''' infection in undiagnosed PI calves<br /> <br /> ====Pathology====<br /> <br /> *'''Mucosal Disease''': erosive condition produces small multiple, cleanly punched out lesion in mouth<br /> *[[Neutrophils|Neutrophils]] invade the ulcer and if bacterial colonisation occurs, further excavation follows. Either:<br /> ::#This lesion develops a granular base and becomes diphtheritic. <br /> ::#If bacterial colonisation does not take place, healing occurs within fourteen days. <br /> *Seen in most parts of mouth (or maybe on muzzle) e.g. dental pad, [[Cheeks - Anatomy &amp; Physiology|cheeks]], sides of [[Oral Cavity - Tongue - Anatomy &amp; Physiology|tongue]]<br /> *Lesions extend throughout gut with particularly big ulcers in small intestine over [[Peyer's Patches - Anatomy &amp; Physiology|Peyers patches]]. Necrosis occurs in lymph nodes and [[Spleen - Anatomy &amp; Physiology|spleen]]<br /> <br /> ====&lt;span id=&quot;BVDHistology&quot;&gt;Histology&lt;/span&gt;====<br /> *No vesicular stage, prickle cells die off from surface resulting in layer of necrotic debris over epithelial layer<br /> *Infection penetrates inward through stratum germinativum.<br /> *Epithelium does not recover as animal does not recover<br /> ====Epidemiology====<br /> *A major concern is that it can be confused with [[Foot and Mouth Disease (FMDV)|FMD]] (especially as it often occurs with clinical signs of salivation and depression)<br /> *Virus is widespread: 60-70% exposure by 4 years of age<br /> **Often may sweep through a whole colony of young stock causing profuse diarrhoea (perhaps febrile) for a few days and then recover<br /> **Due to primary exposure to cytopathic strain of virus<br /> *PI cows: <br /> **100% vertical transmission to offspring<br /> **Are infected with BVDV-1nc and NEVER BVDV-1c<br /> **Are often antibody-negative (though they can show low levels of Ab to ''heterologous'' virus)<br /> **Show a wide range of clinical signs:<br /> ***Severe congenital damage (ataxia)<br /> ***Poor body condition<br /> ***Increased susceptibility to enteric and respiratory disease<br /> **Act as the herd '''reservoir''' of BVDV<br /> **Can ONLY be identified by blood testing<br /> *Transfer via '''semen''', '''direct contact''' with acutely infected animals, or vertical from dam to offspring<br /> *Transfer can be iatrogenic: repeated use of needles and gloves, etc.<br /> <br /> ====Diagnosis====<br /> *Traditional test: virus isolation followed by serology on infected cells<br /> *'''ELISA''' for virus '''antigen''' in animals with persistent viremia (will show up 3-8 days post-infection)<br /> *PI calves often appear virus negative as a result of receiving neutralizing Ab in colostrum: can be countered by RT-PCR<br /> *'''Paired serum samples''' from cows with acute BVDV<br /> *'''Herd sampling''' by ELISA for antibody on bulk milk<br /> <br /> ====Control====<br /> *No known treatment to reverse persistent infection or to cure mucosal disease<br /> *BUT, without exposure to BVDV, the whole herd is at risk as there is no developed immunity<br /> *'''Vaccination of dams''' before pregnancy will prevent PI calves being born<br /> **'''Beta-propiolactone inactivated''' vaccine<br /> **Combine with screening for antigen and removal of PI animals<br /> <br /> <br /> <br /> <br /> <br /> <br /> &lt;br&gt;A pestivirus which may result in abortion of fresh, autolysed or mummified foetuses. <br /> Calves may also be born alive and may be weak, uncoordinated due to cerebellar hypoplasia (cerebellar hypoplasia also seen with feline panleukopenia infection).<br /> [[Category:Pestiviruses]][[Category:Cattle]]<br /> [[Category:Oral_Cavity_-_Erosive_&amp;_Ulcerative_Pathology]]<br /> [[Category:Enteritis,_Ulcerative]][[Category:Enteritis,_Viral]][[Category:To_Do_-_Stuart]]</div>

Stuartd https://en.wikivet.net/index.php?title=User:Stuartd&diff=69926 2010-07-05T14:20:26Z

<p>Stuartd: </p> <hr /> <div>[[Image:Stuartd.jpg|thumb|right|400px|Copyright Stuart Davenport 2010]]<br /> ==About Me==<br /> Originally from Warwickshire I graduated with a BVM&amp;S degree from the University of Edinburgh. I also hold an intercalated BSc in Veterinary Pathology from the [[Royal Veterinary College, London, UK|Royal Veterinary College, London]]. From October 2010 I will be undertaking a Wellcome Trust funded PhD in Infection and Immunity at the University of Cambridge.<br /> <br /> ==What I Hope to Get Out of this Project==<br /> This summer I hope to contribute to the Veterinary information revolution. <br /> ==Pages I Edit==<br /> [[:Category:To_Do_-_Stuart]]</div>

Stuartd https://en.wikivet.net/index.php?title=Myxomatosis&diff=69904 2010-07-05T14:17:55Z

<p>Stuartd: </p> <hr /> <div>{{unfinished}}<br /> <br /> [[Image:MyxoRabbit.JPG|200px|right|thumb|A European Rabbit afflicted by Myxomatosis in Shropshire, England. Courtesy of WikiMedia]]<br /> ====Antigenicity====<br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia<br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain<br /> <br /> ====Morphology====<br /> *Several proteins encoded by the virus are immunosubversive in that they mimic host ligands or regulators (virokines) or are homologues of cellular cytokine receptors (viroceptors)<br /> <br /> <br /> ====Hosts====<br /> *Rabbits<br /> <br /> <br /> ====Pathogenesis====<br /> *Infects several cell types including mucosal cells, lymphocytes, and fibroblasts<br /> *In addition to primary and secondary tumor development, there is severe immunosuppression leading to overwhelming infections by opportunistic gram-negative bacteria (esp. conjunctiva and nasal passages)<br /> *Virus multiplication and tumor-like lesions occur initially at the site of intradermal inoculation <br /> *This is followed by spread to regional lymph nodes and cell-associated viremia, with generalization to the skin and internal organs<br /> *Gelatinous proliferative nodules all over body, especially at '''orifices''' (eyes, anus, nose)<br /> *Rabbit dies within 12 days, if not killed by predators<br /> <br /> =====In more detail=====<br /> *Virulent strains of MYX and MRV secrete a T2 gene product with significant homology to the T2 protein secreted by Shope fibroma virus. This protein acts as a receptor for TNFα and TNFβ. TNF is active in killing virus infected and tumor cells. Cytotoxicity is correlated with the induction of toxic superoxide radicals. The T2 gene product enhances viral virulence by interfering with TNF-dependent immune response pathways of the host.<br /> *Myxoma virus and MRV have also been shown to compromise cell-mediated immunity by inducing a loss of class I MHC antigens from the surface of infected cells. MHC class I-restricted cytotoxic T lymphocytes play a major role in clearing poxvirus infections from susceptible animal hosts, and are an important factor in limiting virus spread within the host. Class I molecules are present on all nucleated cells and platelets. Cytotoxic T cells (CD8+) recognize intracellular viral antigen in association with class I MHC glycoproteins on the cell surface. MYX and MRV infection results in a specific, rapid decrease in detectable surface class I epitopes. It has been suggested that a late viral gene product may interact with the class I complex to either physically sequester the complex away from the cell surface and inhibit its recycling to the surface, or induce a conformational change in the complex rendering it unrecognizable by cytotoxic T lymphocytes.<br /> *Myxoma growth factor (MGF) and a gene product designated M11L are also associated with MYX virulence. MGF and M11L deleted mutants are markedly attenuated, capable of inducing only benign localized nodules that regress spontaneously, similar to lesions induced by Shope fibroma virus. MGF has significant sequence homology with epidermal growth factor and transforming growth factor β. It has been postulated that the presence of EGF/TGFβ-like growth factors in tumorigenic poxviruses affects the growth and progression of poxvirus-infected cells.<br /> *Another myxoma virus virulence factor designated MYXOMA SERPIN 1 (SERP 1) has significant sequence homology with members of the family of serine proteases inhibitors (serpins). The exact role of SERP 1 is unknown but it may theoretically affect antigen presentation by interfering with viral protein degradation, or might reduce cytoxic T cell killing mediated by serine proteases in the effector cell.<br /> *Rabbit poxvirus gene sequences coding for products related to the C4 and C5 components of the complement cascade have been identified. It is postulated that complement-like viral protein products may block the activation or action of complement. The virulence factor T7 is an IFNγ receptor homologue.<br /> <br /> =====Clinical Signs=====<br /> *Clinical disease varies with virus strain and host species. <br /> **Sylvilagus species are relatively resistant, and are probably the natural host of the virus. In Sylvilagus species, infection usually results only in the development of skin tumors at the site of inoculation. The tumors appear 4-8 days after exposure and persist for up to 40 days. Very young rabbits may succumb to generalized disease.<br /> **Lepus species (hares) are highly resistant. Occasional individuals develop mild to severe generalized myxomatosis.<br /> **In the European rabbit (Oryctolagus cuniculus), infection with virulent virus (South American or California strains) results in severe disease with up to a 99% case fatality rate. <br /> ***Initial signs include edema of the eyelids accompanied by inflammation and edema around the anal, genital, oral, and nasal orifices. <br /> ***Edema of the head and ears, drooping ears, and bacterial infections resulting in mucopurulent conjunctivitis and pneumonia are seen. <br /> ***The primary tumor may be evident by 3-4 days after infection. Generalized tumors develop by 6-7 days after infection. <br /> ***Subcutaneous swellings become mucoid, gelatinous masses (hence the name myxomatosis). <br /> ***More chronic wart-like nodules appear, especially at mucocutaneous borders, after 10-14 days. <br /> ***Death (8-15 days post infection) is usually preceded by labored breathing and convulsions.<br /> <br /> =====Pathology=====<br /> *The most prominent gross lesions in European rabbits with myxomatosis are the '''skin tumors''' and the pronounced '''cutaneous and subcutaneous edema''', particularly in the area of the face and around body orifices. <br /> *'''Skin hemorrhages''', '''subserosal petechiae''' and '''ecchymoses''' may be observed in the stomach and intestines. Subepicardial and subendocardial hemorrhages may also occur.<br /> *Adult rabbits of the genus Sylvilagus usually develop localized skin tumors resembling the fibromas produced in European rabbits by Shope fibroma virus.<br /> *Hares or young Sylvilagus rabbits may develop fibromatous to myxomatous nodules, however, lesions are usually mild and localized.<br /> <br /> =====Histopathology=====<br /> *The lesions are proliferative to degenerative, depending on the virus strain. <br /> *The skin tumors result from proliferation of undifferentiated mesenchymal cells which become large stellate cells (myxoma cells). These cells may contain '''intracytoplasmic eosinophilic inclusions'''. These cells lie in a homogeneous matrix of mucinous material interspersed with capillaries and inflammatory cells. Endothelial proliferation with narrowing of the lumen and extrusion of stellate &quot;myxoma&quot; cells has been described. <br /> *Epithelial cells overlying the tumor may show hyperplasia or degeneration, or may appear normal. Epithelial proliferation is characterized by ballooning of cells in the stratum granulosum and hyperkeratosis. Epithelial vesiculation progresses to crust formation. Large, eosinophilic, intracytoplasmic inclusions are especially prominent in the stratum spinosum. Lesions in other organs include cellular proliferation of alveolar epithelium and the reticulum cells of lymph nodes and [[Spleen - Anatomy &amp; Physiology|spleen]]. Focal hemorrhage may be present in skin, kidneys, [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]], testes, heart, stomach, and intestinal walls. Myxoma cells may be present in [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]], [[Bone Marrow - Anatomy &amp; Physiology|bone marrow]], uterus, ovaries, testes, and lungs.<br /> <br /> ====Epidemiology====<br /> *Highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors<br /> *'''Mosquitoes''' act as mechanical vectors<br /> *High ambient environmental temperatures are associated with increased survival of infected animals<br /> <br /> ====Differentials====<br /> *Shope fibroma virus<br /> **Localised benign tumours that spontaneously regress in adult immunocompetent rabbits<br /> *Malignant rabbit fibroma virus<br /> **MRV is a recombinant between Myxoma virus and Shope fibroma virus.<br /> **Causes a lethal disease with numerous primary and secondary tumours and immunosuppression.<br /> <br /> ====Control====<br /> *Attenuated vaccines are used for farmed and pet rabbits<br /> *Wild suspect animals should be culled<br /> <br /> <br /> <br /> ===Myxoma virus===<br /> *Causes Myxomatosis in rabbits<br /> *Infectious myxomatosis is highly contagious and transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors. <br /> *Arthropod vectors such as mosquitoes and fleas provide the principal means of transmission. <br /> *Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia. <br /> *Following introduction into Europe and Australia, genetic modification of the myxoma virus produced markedly attenuated strains that replaced the virulent virus as the dominant virus strain. <br /> *The naturally attenuated viruses cause a milder disease of longer duration which favors vector transmission and persistence of the virus in nature. <br /> *High ambient environmental temperatures are associated with increased survival of infected animals. Some authors consider the California strains of the virus (California rabbit fibroma virus) as distinct from the myxoma virus, while others feel that the antigenic differences do not justify the separate distinction.<br /> <br /> ====Pathogenesis====<br /> *MYX infects several cell types including mucosal cells, lymphocytes, and fibroblasts. <br /> *In addition to primary and secondary tumor development, there is severe immunosuppression leading to overwhelming infections by opportunistic gram-negative bacteria. <br /> *Viral antigen is present within primary as well as secondary tumors. <br /> *Virus multiplication and tumor-like lesions occur initially at the site of intradermal inoculation. This is followed by spread to regional lymph nodes and cell-associated viremia, with generalization to the skin and internal organs. <br /> *With immunosuppression, severe secondary gram-negative bacterial infections of the conjunctiva and nasal passages occur. <br /> *Death follows within 14 days of inoculation. <br /> *Several proteins encoded by the virus are immunosubversive in that they mimic host ligands or regulators (virokines) or are homologues of cellular cytokine receptors (viroceptors) <br /> **Virulent strains of MYX and MRV secrete a T2 gene product with significant homology to the T2 protein secreted by Shope fibroma virus. This protein acts as a receptor for TNFα and TNFβ. TNF is active in killing virus infected and tumor cells. Cytotoxicity is correlated with the induction of toxic superoxide radicals. The T2 gene product enhances viral virulence by interfering with TNF-dependent immune response pathways of the host.<br /> *Myxoma virus and MRV have also been shown to compromise cell-mediated immunity by inducing a loss of class I MHC antigens from the surface of infected cells. MHC class I-restricted cytotoxic T lymphocytes play a major role in clearing poxvirus infections from susceptible animal hosts, and are an important factor in limiting virus spread within the host. Class I molecules are present on all nucleated cells and platelets. Cytotoxic T cells (CD8+) recognize intracellular viral antigen in association with class I MHC glycoproteins on the cell surface. MYX and MRV infection results in a specific, rapid decrease in detectable surface class I epitopes. It has been suggested that a late viral gene product may interact with the class I complex to either physically sequester the complex away from the cell surface and inhibit its recycling to the surface, or induce a conformational change in the complex rendering it unrecognizable by cytotoxic T lymphocytes.<br /> *Myxoma growth factor (MGF) and a gene product designated M11L are also associated with MYX virulence. MGF and M11L deleted mutants are markedly attenuated, capable of inducing only benign localized nodules that regress spontaneously, similar to lesions induced by Shope fibroma virus. MGF has significant sequence homology with epidermal growth factor and transforming growth factor β. It has been postulated that the presence of EGF/TGFβ-like growth factors in tumorigenic poxviruses affects the growth and progression of poxvirus-infected cells.<br /> *Another myxoma virus virulence factor designated MYXOMA SERPIN 1 (SERP 1) has significant sequence homology with members of the family of serine proteases inhibitors (serpins). The exact role of SERP 1 is unknown but it may theoretically affect antigen presentation by interfering with viral protein degradation, or might reduce cytoxic T cell killing mediated by serine proteases in the effector cell.<br /> *Rabbit poxvirus gene sequences coding for products related to the C4 and C5 components of the complement cascade have been identified. It is postulated that complement-like viral protein products may block the activation or action of complement. The virulence factor T7 is an IFNγ receptor homologue.<br /> <br /> ====Clinical signs====<br /> *Clinical disease varies with virus strain and host species. <br /> **Sylvilagus species are relatively resistant, and are probably the natural host of the virus. In Sylvilagus species, infection usually results only in the development of skin tumors at the site of inoculation. The tumors appear 4-8 days after exposure and persist for up to 40 days. Very young rabbits may succumb to generalized disease.<br /> **Lepus species (hares) are highly resistant. Occasional individuals develop mild to severe generalized myxomatosis.<br /> **In the European rabbit (Oryctolagus cuniculus), infection with virulent virus (South American or California strains) results in severe disease with up to a 99% case fatality rate. <br /> ***Initial signs include edema of the eyelids accompanied by inflammation and edema around the anal, genital, oral, and nasal orifices. <br /> ***Edema of the head and ears, drooping ears, and bacterial infections resulting in mucopurulent conjunctivitis and pneumonia are seen. <br /> ***The primary tumor may be evident by 3-4 days after infection. Generalized tumors develop by 6-7 days after infection. <br /> ***Subcutaneous swellings become mucoid, gelatinous masses (hence the name myxomatosis). <br /> ***More chronic wart-like nodules appear, especially at mucocutaneous borders, after 10-14 days. <br /> ***Death (8-15 days post infection) is usually preceded by labored breathing and convulsions.<br /> <br /> ====Pathology====<br /> *The most prominent gross lesions in European rabbits with myxomatosis are the skin tumors and the pronounced cutaneous and subcutaneous edema, particularly in the area of the face and around body orifices. <br /> *Skin hemorrhages and subserosal petechiae and ecchymoses may be observed in the stomach and intestines. Subepicardial and subendocardial hemorrhages may also occur.<br /> *Adult rabbits of the genus Sylvilagus usually develop localized skin tumors resembling the fibromas produced in European rabbits by Shope fibroma virus.<br /> *Hares or young Sylvilagus rabbits may develop fibromatous to myxomatous nodules, however, lesions are usually mild and localized.<br /> <br /> ====Histopathology====<br /> <br /> *The lesions are proliferative to degenerative, depending on the virus strain. <br /> *The skin tumors result from proliferation of undifferentiated mesenchymal cells which become large stellate cells (myxoma cells). These cells may contain intracytoplasmic eosinophilic inclusions. These cells lie in a homogeneous matrix of mucinous material interspersed with capillaries and inflammatory cells. Endothelial proliferation with narrowing of the lumen and extrusion of stellate &quot;myxoma&quot; cells has been described. <br /> *Epithelial cells overlying the tumor may show hyperplasia or degeneration, or may appear normal. Epithelial proliferation is characterized by ballooning of cells in the stratum granulosum and hyperkeratosis. Epithelial vesiculation progresses to crust formation. Large, eosinophilic, intracytoplasmic inclusions are especially prominent in the stratum spinosum. Lesions in other organs include cellular proliferation of alveolar epithelium and the reticulum cells of [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]] and [[Spleen - Anatomy &amp; Physiology|spleen]]. Focal hemorrhage may be present in skin, kidneys, lymph nodes, testes, heart, stomach, and intestinal walls. Myxoma cells may be present in [[Lymph Nodes - Anatomy &amp; Physiology|lymph nodes]], [[Bone Marrow - Anatomy &amp; Physiology|bone marrow]], uterus, ovaries, testes, and lungs.<br /> <br /> <br /> <br /> <br /> [[Category:Leporipoxviruses]][[Category:Rabbit]]<br /> [[Category:To_Do_-_Viruses]]<br /> [[Category:To_Do_-_Stuart]]</div>

Stuartd https://en.wikivet.net/index.php?title=User:Stuartd&diff=69839 2010-07-05T12:02:06Z

<p>Stuartd: </p> <hr /> <div>[[Image:Stuartd.jpg|thumb|right|400px|Copyright Stuart Davenport 2010]]<br /> ==About Me==<br /> Originally from Warwickshire I graduated with a BVM&amp;S degree from the University of Edinburgh. I also hold an intercalated BSc in Veterinary Pathology from the [[Royal Veterinary College, London, UK|Royal Veterinary College, London]]. From October 2010 I will be undertaking a Wellcome Trust funded PhD in Infection and Immunity at the University of Cambridge.<br /> <br /> ==What I Hope to Get Out of this Project==<br /> This summer I hope to contribute to the Veterinary information revolution. <br /> ==Pages I Edit==</div>

Stuartd https://en.wikivet.net/index.php?title=User:Stuartd&diff=69829 2010-07-05T11:59:40Z

<p>Stuartd: </p> <hr /> <div>[[Image:Stuartd.jpg|thumb|right|400px|Copyright Stuart Davenport 2010]]<br /> ==About Me==<br /> Originally from Warwickshire I graduated with a BVM&amp;S degree from the University of Edinburgh. I also hold an intercalated BSc in Veterinary Pathology from the [[Royal Veterinary College, London, UK|Royal Veterinary College, London]]. From October 2010 I will be undertaking a Wellcome Trust funded PhD in Infection and Immunity at the University of Cambridge.<br /> <br /> ==What I Hope to Get Out of this Project==<br /> To contribute to the Veterinary information revolution. <br /> ==Pages I Edit==</div>

Stuartd https://en.wikivet.net/index.php?title=User:Stuartd&diff=69821 2010-07-05T11:56:40Z

<p>Stuartd: /* About Me */</p> <hr /> <div>[[Image:Stuartd.jpg|thumb|right|400px|Copyright Stuart Davenport 2010]]<br /> ==About Me==<br /> Originally from Warwickshire I graduated with a BVM&amp;S degree from the University of Edinburgh. I also hold an intercalated BSc in Veterinary Pathology from the Royal Veterinary College, London. From October 2010 I will be undertaking a Wellcome Trust funded PhD in Infection and Immunity at the University of Cambridge.<br /> <br /> ==What I Hope to Get Out of this Project==<br /> To contribute to the Veterinary information revolution. <br /> ==Pages I Edit==</div>

Stuartd https://en.wikivet.net/index.php?title=User:Stuartd&diff=69816 2010-07-05T11:55:55Z

<p>Stuartd: /* About Me */</p> <hr /> <div>[[Image:Stuartd.jpg|thumb|right|400px|Copyright Stuart Davenport 2010]]<br /> ==About Me==<br /> Originally from Warwickshire I graduated with a BVM&amp;S degree from the University of Edinburgh. I also hold an intercalated BSc in Veterinary Pathology from the Royal Veterinary College, London. In the future I will be pursuing a Wellcome Trust funded PhD in Infection and Immunity at the University of Cambridge.<br /> <br /> ==What I Hope to Get Out of this Project==<br /> To contribute to the Veterinary information revolution. <br /> ==Pages I Edit==</div>

Stuartd