WikiVet English - User contributions [en]

Parturition Behaviour - Ewe

2019-09-06T18:47:55Z

DrNdaba:

Similar to the [[Parturition Behaviour - Cow|cow]], except incidence of twinning and triplets is high.

=== Stage 2 ===

* Completed within 1 hour usually.
* Lambs normally in anterior presentation.
* In twin births where one foetus occupies each horn, one horn develops contractions before the other.
** Hence distocia due to simultaneous presentation is more common when both foetuses occupy the same horn.

=== Stage 3 ===

* Placenta usually expelled within 2-3 hours after birth of the lamb.

[[Category:Parturition]][[Category:Reproductive Behaviour]]
[[Category:Bullet Points]]

Foot and Mouth Disease

2019-05-01T22:15:06Z

DrNdaba: /* Introduction */

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Also known as: '''''FMDV — FMD'''''

== Introduction ==

This [[:Category:Apthoviruses|Apthovirus]] is a small (25nm) +ss RNA virus, unenveloped and has 7 serotypes, namely '''Oise (O), ''''''Allemagne (A), ''''''C (also German), '''South African Territories (SAT) 1, 2, and 3 and Asia-1.

This disease affects all '''cloven-hoofed animals, '''namely cattle, sheep, goats, pigs, deer, elephants and other wild ruminants such as buffalo and kudu etc. It does NOT affect the horse. The main presentation of the disease is the formation of '''vesicles'''.

The disease is NOTIFIABLE in the UK and any animals with the disease, or in contact with the disease have to be destroyed.

The virus replicates primarily in the upper respiratory tract, tonsils, or upper alimentary tract and there is '''aerosol''' excretion during this incubation period. This is then followed by a viremia. Virus targets stratum spinosum of stratified squamous epithelia and mucus membranes and secondary '''vesicles''' appear after incubation of 2-14 days. Lesions also affect the feet with cutaneous erosions in interdigital cleft, at coronet and bulbs of heals . These feet lesions often take a long time to heal as secondary bacterial infections may ensue and produce true deep ulcerative dermatitis. In the young, without maternal antibody, virus will localize in the heart, particularly the wall of the left ventricle, resulting in multi-focal necrosis of the myocardium and subsequent death. Persistent infection of cattle can occur in unkeratinized lesions, but subclinical carriers do not usually transfer infection except for subclinical buffalo that can transmit the disease.

FMDV causes loss of condition and productivity but is NOT typically fatal. Approximately 5% mortality (usually young animals); older animals recover. The virus is highly contagious and spread is by aerosol, direct contact, saliva, infected swill and fomites. Pigs produce 3000 times more aerosol virus than cows, but cows are much more susceptible to infection than pigs.

In 1967 and 2001 there were major outbreaks in the UK. The disease is still widespread in many parts of world especially S. America and far East.

== Clinical Signs ==

Main clinical signs include pyrexia, depression, separation away from the herd, drooling, excess salivation, anorexia pain while eating as well as smacking of the lips. Lameness is also a key clinical sign and in pigs may often be the first noticeable sign as mouth lesions in this specie are less severe.

Lesions in the mouth and on the tongue have the following characteristics depending on age of lesions.
: At 0- 2 days there will be unruptured vesicles.
: At 1-3 days newly ruptured vesicles with adherent epithelia at margins will appear.
: By 3-7 days there will be ruptured vesicles, loss of epithelia, no marked fibrous margin.
: At days 7-10+ open lesions with marked fibrous margin will be present.

'''Teats''' on animals that are suckling may also develop vesicles.

In pigs and sheep, lesions are less obvious, but vesicles around nose, mouth, and coronary band are present. Pigs have vesicles on snout, which are quickly traumatised to leave an eroded lesion. Presence of a lesion at '''coronary band''' means infection is usually less than a week old. The lesions grow down the claw at a rate of 1mm per week.

In cattle, lesions are seen inside mouth, around muzzle, in the interdigital cleft, around coronary band, and on teats. There will be excessive salivation, anorexia, secondary mastitis and on PM there will be lesions in oesophagus and forestomachs.

== Diagnosis ==

Clinical signs are enough to make a provisional diagnosis. This must be confirmed by [[ELISA testing|'''ELISA''']] for virus '''antigen. '''ELISAs are serotype-specific. This method is soon to be replaced by immunochromatography-bedside ELISA to allow on-farm diagnosis. '''Virus isolation''' can also be performed in kidney culture cells, and then serotyped by ELISA. Serology for virus '''antibody''' can determine past infection and ELISAs are used to detect subclinical carrier sheep. This cannot be done on vaccinated animals.

RT-PCR has been suggested for on-farm diagnosis, but has flaws such as, RNA is readily degraded by tissue enzymes, RNA must be purified before converting to DNA for PCR, false positives can occur easily by contamination with previously amplified DNA.

Samples should be taken from the vesicle itself and include the vesicle fluid as well as the tissue. These should be placed in transport medium and sent for testing.

== Control ==

Recovered animals show immunity ONLY to the serotype of first exposure, and even this is relatively short-lived, therefore re-exposure to the original serotype after immunity has waned will still result in virus excretion, even without clinical symptoms. Infection by a second serotype will result in clinical disease. It is for these reasons, that '''vaccination is not practiced''' in the UK. Further, vaccination would mean a loss of meat export markets.

===== Prevention in the UK =====

Imported stock must come from virus-free countries that DO NOT vaccinate. Any meat imported from endemic countries must be de-boned.

ANY sign of lesions in a susceptible animal is '''NOTIFIABLE''' to the Divisional Veterinary Officer and local police. Once diagnosis is confirmed, all animals on the premises must be '''slaughtered and incinerated''' and the premises fully disinfected. Movement is controlled within a 10-mile radius and follow-up serology must be performed to ensure no spread has taken place on any nearby farms. '''Ring vaccination''' with relevant subtype to create a barrier of immune animals (although this was not done in the 2001 outbreak) can be used. There is to be no movement on or off the farm as soon as a case is suspected.

'''In Endemic Areas''' disease cannot be prevented by slaughter due to large numbers of carrier stock. Annual '''inactivated whole virus vaccination''' using local subtypes is used. This vaccine is inactivated by azuridines, using alhydrogel adjuvant for cows, and oil for pigs. Subunit vaccines are ineffective. The course involves 2 initial injections at 4 months (if dams are vaccinated), followed by boosters every 6-12 months, which induces virus-neutralizing antibodies. Vaccination DOES NOT render meat harmful to consumers, but does affect when it can be exported.

== References ==

Andrews, A.H, Blowey, R.W, Boyd, H and Eddy, R.G. (2004)'''Bovine Medicine '''(Second edition), ''Blackwell Publishing''

Brownlie, J (2007) '''Virology Study Guide, '''''Royal Veterinary College.''

Radostits, O.M, Arundel, J.H, and Gay, C.C. (2000) '''Veterinary Medicine: a textbook of the diseases of cattle, sheep, pigs, goats and horses '''''Elsevier Health Sciences''

Taylor, D.J. (2006) '''Pig Diseases''' (Eighth edition)'' St Edmunsdbury Press ltd''

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[[Category:Apthoviruses]] [[Category:Oral_Diseases_-_Cattle]] [[Category:Oral_Diseases_-_Sheep]] [[Category:Oral_Diseases_-_Goat]] [[Category:Oral_Diseases_-_Pig]] [[Category:Dermatological_Diseases_-_Cattle]] [[Category:Dermatological_Diseases_-_Sheep]] [[Category:Dermatological_Diseases_-_Goat]] [[Category:Dermatological_Diseases_-_Pig]] [[Category:Oral_Cavity_-_Vesicular_Pathology]] [[Category:Integumentary_System_-_Viral_Infections]] [[Category:Viral_Myositis]]
[[Category:Expert Review - Farm Animal]]

Vitamin B1 (Thiamin) - Nutrition

2018-09-30T13:05:44Z

DrNdaba: /* Roles in the Body */

==What is Vitamin B1 (Thiamin)?==
Vitamin B1, also called '''thiamin''', is an '''[[Nutrition Glossary#Essential Nutrients|essential]] water-soluble vitamin''' used in [[Sugars - Nutrition|glucose]] and [[Amino Acids Overview - Nutrition|amino acid]] metabolism and energy production. Thiamin is readily absorbed across the intestinal mucosa via [[Active Transport - Physiology|active carrier-mediated transport]] as well as via [[Diffusion - Physiology|passive diffusion]]. Once in the enterocyte, thiamin can either be converted to thiamin pyrophosphate (TPP) for immediate use in the cell, or transported as thiamin into the portal circulation to the [[Liver - Anatomy & Physiology|liver]]. Once in the liver it is rapidly distributed throughout the body. Thiamin can be found as a free vitamin within the [[plasma]], but is largely found as part of TPP within [[Erythrocyte|erythrocytes]] and [[leukocytes]]. '''Thiamin is not stored in the body and is freely filtered by the [[Nephron Microscopic Anatomy#Proximal Tubule|renal tubules]]'''.

==Why is it Important?==
Thiamin is required for formation of (TPP), a [[Nutrition Glossary#Coenzyme|coenzyme]] used during energy production, and is required by transketolase enzymes used during glucose metabolism<ref>McCormick DB. Niacin, Riboflavin, and Thiamin. In Biochemical and physiological aspects of human nutrition. 2000 Philadelphia, PA: WB Saunders Company p.475-481.</ref>. Cats require approximately 3x the amount of thiamin on a metabolic body weight basis relative to dogs<ref name="NRC">National Research Council (NRC). Vitamins. In Nutrient Requirements for Dogs and Cats. 2006 Washington, DC: National Academies Press p.212-216.</ref>.

==Roles in the Body==
Thiamin (as TPP) is responsible for the decarboxylation of α-ketoacids and aceyl-CoA derivatives during amino acid and glucose metabolism. The TPP-dependant enzyme transketolase is also involved in metabolism of glucose and ribose synthesis via the pentose phosphate pathway.
Thiamin is one of the [[Nutrition Glossary#Essential Nutrients|essential nutrients]] involved with the clinical sequelae of refeeding syndrome<ref>Mehanna HM, et al. Refeeding syndrome: what it is, and how to prevent and treat it. BMJ 2008;336:1495-1498.</ref>. Refeeding syndrome can occurs when chronically starved animals are given a large bolus of readily absorbed carbohydrates without adequate amount of rate-limiting essential nutrients, specifically thiamin, [[Potassium - Nutrition|potassium]], and [[Magnesium - Nutrition|magnesium]]. The intracellular shift of these nutrients can cause rapid and profound clinical signs, leading to death if untreated.

==Consequences of Thiamin Deficiency==
====Dogs:====
Puppies fed thiamin deficient diets experience '''slow growth, inappetance, weight loss, coprophagia, neurological abnormalities (circling, torticollis, ataxia, and central nervous system depression) and sudden death'''. Dogs with acute thiamin deficiency develop bilaterally symmetric grey matter necrosis; chronic deficiencies can progress to myocardial and peripheral nerve degeneration<ref name="NRC"/>.
====Cats:====
Cats fed thiamin deficient diet develop '''anorexia initially, followed by progressive clinical signs of neurological involvement in 1-2 weeks'''. The neurological signs include flexion of the head, impaired proprioception and righting reflexes, seizures, progressive weakness, and death<ref name="NRC"/>. Kittens fed thiamin deficient diets can also develop ataxia and [[Eye - Anatomy & Physiology#Reflexes with Optic Nerve as the Sensory Arm|mydriasis]]. Bilaterally symmetric grey matter necrosis is also a feature of thiamin deficiency in cats and kittens<ref>Moon S, et al. Clinical signs, MRI features, and outcomes of two cats with thiamine deficiency secondary to diet change. J Vet Sci 2013;14:499-502.</ref>. 
Conditions associated with diuresis (e.g. chronic disease, such as [[:Category:Kidney - Pathology|renal disease]] or [[Diabetes Insipidus|diabetes]], or therapeutic intervention, such as [[Fluid therapy|intravenous fluids]] or increased water intake to manage [[Cystitis|lower urinary disease]]) can result in increased loss of thiamin and may increase daily requirements. Patients on chronic haemodialysis are also at an increased risk for developing a deficiency. 
Thiamin deficiencies can also occur due to low dietary intake, presence of compounds in food that directly antagonise thiamin, and vitamin degradation during cooking. Thiaminases are present in certain freshwater and marine fishes, but this enzyme is readily denatured with heating<ref name="NRC"/>. Additionally sulphite preservatives in meats can degrade thiamin resulting in clinical signs of deficiency<ref>Studdert VP and Labuc RH. Thiamin deficiency in cats and dogs associated with feeding meat preserved with sulphur dioxide. Aust Vet J 1991;68:54-57.</ref>. Thiamin is particularly sensitive to degradation with increased temperature especially under alkaline conditions, such as can occur during canned foods production. This higher rate of thiamin degradation requires commercial pet food manufacturers to monitor and supplement thiamin according to expected losses.

==Toxicity==
No reports of toxicity in dogs and cats with excess oral intake. High doses given intravenously to dogs can result in dramatic and potentially fatal hypotension<ref name="NRC"/>, while high doses given intravenously to cats can result in neuromuscular blockade and associated signs of weakness<ref>Freye E and Agoutin H. The action of vitamin B1 (thiamine) on the cardiovascular system of the cat. Biomedicine 1978;28:315-319.</ref>.

==Dietary Sources==
Thiamin is naturally occurring in nuts and seeds, muscle and organ meats (especially liver and kidney), yeast, and pulses (e.g. legumes). It is also supplemented into all commercially-prepared complete and balanced dog and cat foods.

==Diagnosing Thiamin Deficiency==
Diagnosis of thiamine deficiency is based on measurement of low [[Erythrocytes|erythrocyte]] transketolase activity or low plasma thiamine phosphorylated esters serum [[Nutrition Glossary#Retinol|retinol]], though not routinely tested through veterinary reference laboratories. Submission of samples to a human reference laboratory may be possible, though often concurrent submission of normal reference samples is required. Magnetic resonance imaging (MRI) images show changes consistent with thiamine deficient grey matter degeneration.

Diagnosis is also made on clinical signs consistent with deficiency, evaluation of diet, and response to parenteral thiamine supplementation.

==References==
<references/>
 
{{Reviewed Nutrition 1
|date = 22 May 2015}}
{{Waltham}}
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[[Category:Vitamins]]

Intussusception

2018-09-30T09:28:44Z

DrNdaba: /* Pathogenesis */

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==Introduction==
[[Image:intussusception.jpg|thumb|right|300px|Diagram of intussuscception (Courtesy of Elspeth Milne)]]
'''Intussusception''' is the invagination of one portion of the gastrointestinal tract into the lumen of the adjacent portion. The '''intussusceptum''' is the invaginated segment and the '''intussuscipien''' is the enveloping segment. A normograde intussusception is most common, but retrograde intussusception has also been reported.

Intussusceptions can be classified according to their location in the gastrointestinal tract. They usually occur in regions where there is a significant change in lumen diameter, such as ileocolic and gastroesphageal junctions. Ileocolic intussusceptions are most common, they frequently protrude from the rectum and must be distinguished from a rectal prolapse. In the case of an intussusception, it is possible to pass a probe next to the anus, but not in a [[Rectal Prolapse - Cat and Dog|rectal prolapse]].

Depending on the site and severity, an intussusception results in a partial or complete obstruction to the gastrointestinal tract causing hypovolaemia, dehydration and shock. The condition is potentially serious and should be treated as an emergency.

Also see: [[Intussusception - Horse|Intussusception in horses]].

===Pathogenesis===
Intussusception results from abnormal peristalsis. Vigorous contractions force the more proximal intestine to invaginate into the adjacent distal portion, taking its mesenteric attachment with it. Obstruction of the gastrointestinal tract causes distention which may lead to rupture and peritonitis. Compression of the mesenteric vessels cause vascular compromise to the intestine, resulting in venous congestion, oedema and if the aterial supply is damaged, full thickness necrosis. An inflammatory exudate is released from the serosal surface and fibrinous adhesions may form, making the structure irreducible.

Intussusception normally occurs due to gastrointestinal disease, although it is often hard to identify the cause. It is associated with any condition that increases peristalsis such as
* Enteritis
* Foreign body
* Heavy parasitism
* Previous intestinal surgery
* Intramural abscess/tumour
* Motility disorders.
* Change in diet
* Bacterial infection

==Signalment==
Intussusception occurs in dogs and cats, but gastroesophageal intussusception has only been reported in dogs.

German shepherd dogs and Siamese cats are over represented. German Shepherd dogs are particularly predisposed to gastroesophageal intussusception.

Young animals are most commonly affected, 80% of cases are less than a year old.

==Diagnosis==
===Clinical Signs===
Clinical signs vary depending on location, duration and the degree of obstruction and vascular compromise.
====Acute Intussusception====
*[[Vomiting|Vomiting]]
*Regurgitation
*Haematemesis
*Abdominal discomfort
*Collapse
*Palpable abdominal tubular mass
*Diarrhoea- bloody and mucoid
*Tenesmus and Haematochezia in cases of ileocaecocolic intussusception
*Ileocolic intussusception protruding through the anus

====Chronic Intussusception====
*Intermittent diarrhoea- bloody and mucoid
*Tenesmus
*Depression
*Anorexia
*Weight loss

===Radiography===
Plain abdominal radiographs do not always provide a definitive diagnosis. In cases of complete obstruction distented loops of intestine and a tubular soft tissue mass are usually obvious, but a partial obstruction will produce much more subtle signs which may be missed.

A barium enema or upper gastrointestinal contrast study can be useful in identifying the site of obstruction but may result in delay of treatment and should be used cautiously as leakage of contrast into the abdominal cavity will result in peritonitis.
The classic appearance of an intussusception is described as a 'coiled spring'.

===Ultrasound===
Abdominal ultrasound will reveal a cylindrical mass with layering of the intestinal wall. The intestines may also be hypomotile, with distension proximal to the obstruction.

===Endoscopy===
Colonoscopy can identify ileocolic or caecocolic intussusception. Oesopgagoscopy can reveal a gastroesophageal intussusception, a soft tissue mass is visible in the lumen of the oesophagus.

===Pathology===
The degree of damage to the intestine depends on the severity of the intussusception. In severe or chronic cases fibrinous adhesions form between surfaces making the structure irreducible. Necrosis of the tissue usually follows.

Intussusception may occur due to post mortem change, in this case there are no other associated changes and the invaginated intestine is easily reducible.

==Treatment==
[[Principles of Fluid Therapy|Fluid therapy]] and correction of electrolyte and acid-base abnormalities should be carried out prior to surgical correction.

'''Surgery''' is required to manually reduce the intussusception, it may be necessary to '''resect and anastomose''' the intestine in cases where the adhesions have formed. This decision depends on the viability of the intestines, as determined by the colour, vascular supply and presence or absence of peristalsis.It is important to preserve as much of the intestine as possible to avoid [[Short Bowel Syndrome|short bowel syndrome]].

Complications include dehiscence at the site of anastomosis, [[Peritonitis - Cats and Dogs|peritonitis]], recurrence (11-20%, most common within 1-5 days post surgery), ileus, intestinal obstruction and short bowel syndrome.

Recurrence can be prevented by '''enteroplication''' of the small intestine, or by a left-sided gastroplexy of the fundus in cases of gastroesophageal intussusception.

==Prognosis==
This depends on the location, completeness and duration of the intusussception. The prognosis is good in animals treated with early surgical intervention and aggressive supportive care. The prognosis is poor for animals with perforated intestine and peritonitis.

{{Learning
|Vetstream = [https://www.vetstream.com/canis/Content/Disease/dis00651.asp, Canine intussusception] [https://www.vetstream.com/canis/Content/Illustration/ill00400.asp, Intussusception barium radiograph]
|flashcards = [[Small Animal Abdominal and Metabolic Disorders Q&A 14]]
|literature search = [http://www.cabdirect.org/search.html?q=title%3A%28Intussusception%29 Intussusception publications]

[http://www.cabdirect.org/search.html?q=%28%28od%3A%28dogs%29%29%29+AND+%28%28title%3A%28Intussusception%29%29%29 Intussusception in dogs publications]

[http://www.cabdirect.org/search.html?q=%28%28od%3A%28cats%29%29%29+AND+%28%28title%3A%28Intussusception%29%29%29 Intussusception in cats publications]

[http://www.cabdirect.org/search.html?q=%28%28od%3A%28horses%29%29%29+AND+%28%28title%3A%28Intussusception%29%29%29 Intussusception in horses publications]

[http://www.cabdirect.org/search.html?q=%28%28od%3A%28cattle%29+OR+od%3A%28sheep%29+OR+od%3A%28goats%29+OR+od%3A%28pigs%29%29%29+AND+%28%28title%3A%28Intussusception%29%29%29 Intussusception in farm animals publications]
}}

==References==
*Barreau, P. (2008) '''Intussusception: Diagnosis and Treatment''' ''33rd WSAVA Congress''
*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''.
*Fossum, T. W. et. al. (2007) '''Small Animal Surgery (Third Edition)''' ''Mosby Elsevier''
*Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''
*Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine (Fourth Edition)''' ''Mosby Elsevier''.
*Tilley, L.P. and Smith, F.W.K.(2004)'''The 5-minute Veterinary Consult(Third edition)''' ''Lippincott, Williams & Wilkins''.

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[[Category:Intestine_-_Physical_Disturbances]]
[[Category:Intestinal Diseases - Dog]][[Category:Intestinal Diseases - Cat]]
[[Category:Expert_Review]]

Paramyxoviridae - Overview

2018-05-31T08:41:58Z

DrNdaba: /* Types and Subtypes */

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==Introduction==
The Paramyxoviridae have a helical nucleocapsid surrounded by an envelope comprised of host cell membrane spiked with viral glycoproteins responsible for haemagglutinin, neuraminidase and haemolytic activities. The genome of the Paramyxoviridae is single-stranded, negative-sense RNA which is used as a template for the production of messenger (positive-sense) RNA and further genomic material. Paramyxoviridae are sensitive to heat, dessication and most disinfectants, and so are not resistant in the environment. The Paramyxovididae family is divided to two sub-families, the [[Paramyxovirinae]] and the [[Pneumovirinae]]. It is within the Paramyxovirinae sub-family that [[morbilliviruses]] fall, along with respiroviruses, henipaviruses, rubulaviruses and avulaviruses. As well as [[Canine Distemper Virus|canine distemper virus (CDV)]], the morbilliviruses include [[rinderpest]], [[Peste des Petits Ruminants|peste des petits ruminants]], measles, phocine (seal) distemper and dolphin distemper.

==Morphology==
The virus is constructed of single-stranded negative-sense unsegmented RNA. Reassortment and antigenic shift cannot occur with this virus.

Spike proteins include '''HN''' (Haemagglutinin and Neuraminidase) and '''F''' (Fusion glycoprotein), which allows the virus to fuse directly to the plasma membrane and release its RNA. F also causes syncitium to form, which aids diagnosis. The host antibody response to the F protein is the basis for vaccination.

==Virulence==
Paramyxoviruses replicate in the epithelium of the upper respiratory tract as well as occasionally in the gut as these are sites of spike protein cleavage. Virulence varies by virus, see below.

==Types and Subtypes==
Paramyxoviridae was reclassified in 2000 to include 2 subfamilies and 5 genera, of interest including the subfamily ''[[Paramyxovirinae]]'' and subfamily ''[[Pneumovirinae]]''.

==Antigenic Variation==
Antigenic conservation allows some cross protection by vaccination as conservation of major virus-specific F/HN antigens means vaccines protect against '''all isolates''' of the same virus.
Minor morbillivirus-specific epitopes on F allows some cross protection between '''canine distemper, measles, and rinderpest'''.

Antigenic "fingerprinting" is possible for some viruses based on minor variable epitopes of HN, F and NP on specific isolates as detected by monoclonal antibodies. These are detected by immunostaining infected cells.

==Other resources==
*[http://www.pitt.edu/~super1/lecture/lec3401/index.htm On line Paramyxoviridae lecture by P. Russell]

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[[Category:Expert_Review]]
[[Category:Paramyxoviridae|A]]

Erythropoiesis

2018-05-13T12:59:12Z

DrNdaba: /* Regulation */

[[Image:LH Developing Erythrocyte Histology.jpg|right|thumb|200px|'''Developing erythrocytes''' ©RVC 2008]]
==Introduction==
[[Erythrocytes|Erythrocytes]] contain no nucleus and are thus only produced from stem cells. During the fetal stage production is in both the [[Liver - Anatomy & Physiology|liver]] and [[Spleen - Anatomy & Physiology|spleen]] however production is transferred to the [[Bone Marrow - Anatomy & Physiology|bone marrow]] ([[Bone Marrow - Anatomy & Physiology#Red marrow|red marrow]]) in the final stages of gestation. Initially erythropoiesis occurs in all bones, however after puberty production is limited to membranous bones (ribs, vertebrae, pelvic bones etc.) as the long bones contain adipose tissue in place of red marrow.

Erythrocyte stem cells contain no haemoglobin and it is only after several cell divisions that pro-erythrocyte haemoglobin starts to be generated within the cells. When the haemoglobin levels are at the correct concentration the nucleus reduces in size and is removed from cell. Cells at this stage still have ribosomes and other organelles and stain differently to mature erythrocytes; they are known as '''reticulocytes'''. Reticulocytes contain some RNA and continue to produce haemoglobin. After a few days these mature having reached a final haemoglobin concentration of 34%.

Reticulocytes and mature [[Erythrocytes|erythrocytes]] leave the [[Bone Marrow - Anatomy & Physiology|bone marrow]] by ‘squeezing’ through the capillary endothelial cells. Precursors to these stages cannot change shape and therefore remain confined to the bone marrow.

==Development==
[[Erythrocytes|Erythrocyte]] development is divided into several stages and at each stage the cell will divide several times. As bone marrow does not act as storage, all erythrocytes produced are immediately released into the circulation.

===Stem cell ===
Stem cells give rise to precursors which eventually mature to form the fully developed erythrocyte.
Initially, the multipotential myeloid stem cell ([[Haematopoiesis - Overview#Colony Forming Units|CFU-GEMM]]) differentiates into the erythroid CFU ([[Haematopoiesis - Overview#Colony Forming Units|CFU-E]]). This develops into the first erythrocyte precursor, the proerythroblast.
The development process is controlled and influenced by a number of different factors including erythropoietin, IL-3, IL-4 and granulocyte-macrophage colony stimulating factor (GM-CSF).

===Nomenclature===
The naming of the stages of the erythrocyte precursors varies.

The main headings for this section refer to each stage in terms of a histological description, namely the proerythroblast, basophilic erythroblast, polychromatic erythroblast, orthochromatic erythroblast and polychromatophilic erythrocyte.

Another classification of the stages is based upon the [[Haematopoiesis - Overview#Colony Forming Units|CFU-E]] being referred to as ‘rubri’. This system gives all developing blood cell lineages similar names. For example the first stage for erythrocytes is referred to as a [rubri]blast and the first stage for lymphocytes is called a [lympho]blast. The stages for the erythrocyte are rubriblast, prorubriblast, rubricyte and metarubricye.

Finally the stages can also be named according to the development of the normoblast stage. This gives the stages pronormoblast, early normoblast, intermediate normoblast, late normoblast, polychromatic cell.

===Stages of Development===
[[Image:Erythropoiesis pathway.jpg|right|thumb|175px|'''Erythropoiesis pathway''']]
====Proerythroblast====
The first [[Erythrocytes|erythrocyte]] precursor produced directly from the [[Haematopoiesis - Overview#Colony Forming Units|CFU-GEMM]] under the influence of erythropoietin. It has a large nucleus with free ribosomes in the cytoplasm giving the cytoplasm a basophilic appearance.

Alternative nomenclature: Pronormoblast or Rubriblast

====Basophilic erythroblast====
Smaller than the proerythroblast with a smaller nucleus but a more basophilic cytoplasm due to increased numbers of ribosomes in the cytoplasm. These ribosomes are involved in the production of haemoglobin.

Alternative nomenclature: Early normoblast or Rubriblast

====Polychromatic erythroblast====
This is the last precursor cell capable of mitosis and is smaller than the basophilic erythroblast. Its cytoplasm appears greyer due to the increased acidophilic staining caused by the presence of haemoglobin.

Alternative nomenclature: Intermediate normoblast or Prorubricyte

==== Orthochromatic erythroblast ====
Also called a normoblast. It is incapable of cell division and is only slightly larger than a mature erythrocyte but it does contain a small dense nucleus.

Alternative nomenclature: Late normoblast or Rubricyte

==== Polychromatophilic erythrocyte ====
Also called a reticulocyte and is formed when the nucleus is extruded from the normoblast. It still contains some ribosomes and therefore retains a slight basophilic stain. The clustering of the ribosomes forms a reticular network giving the name, reticulocyte. These cells can carry oxygen and enter the blood stream and are found in low concentrations in normal blood.

Alternative nomenclature: Polychromatic cell or Metarubricyte

====Erythrocyte====
Commonly called the red blood cell. It is the final product of erythropoiesis and is released from the [[Bone Marrow - Anatomy & Physiology|bone marrow]] into circulation.

Alternative nomenclature: None

==Nutritional factors==
Normal erythrocyte production requires protein, copper, iron, folic acid and vitamins B6 and B12. Deficiencies lead to inadequate production of haemoglobin.
===Iron===
Iron is found within each haem component of haemoglobin and binds oxygen.
===Folic acid and vitamin B12===
These elements are required for DNA synthesis and are important for the formation of new erythrocytes. Deficiencies leads to the formation of '''macrocytes''', which are enlarged erythrocytes with a higher than normal mean corpuscular volume (MCV).

==Regulation==
Production of [[Erythrocytes|erythrocytes]] is regulated by '''erythropoietin''' (EPO) which is produced in the yolk sac, [[Liver - Anatomy & Physiology|liver]] and kidney from embryonic life until early neonatal life. In the adult it is produced only in the kidneys. Erythropoietin is a glycoprotein hormone and is controled by a negative feedback mechanism. Normal levels are low with sufficient amounts to maintain a basal level of new erythrocyte production. If blood oxygen concentration falls, the release of erythropoietin rises.

EPO is transported from kidneys to [[Bone Marrow - Anatomy & Physiology|bone marrow]] where it acts upon receptors on the CFU-E’s and causes differentiation into erythrocyte precursors. It also increases the rate of division and maturation of developing erythrocyte precursors by increasing the rate of gene transcription. Thus it is not the number of [[Erythrocytes|erythrocytes]] but the oxygen concentration that controls erythrocyte numbers. EPO release can be affected by any form of renal pathology. Inflammatory induced release of interleukins reduces the secretion of erythropoietin.

The mechanism of oxygen concentration detection is via HIF-1 (hypoxia inducible factor 1) which is a transcription activator that is oxygen sensitive.

[[Category:Haematopoiesis]]

Cowdriosis

2018-05-09T10:59:45Z

DrNdaba: /* Clinical Signs */

{{OpenPagesTop}}
{{Taxobox
|name = ''Cowdria ruminantium''
|kingdom = Bacteria
|sub-kingdom =
|phylum = Proteobacteria
|super-class =
|class = Alphaproteobacteria
|sub-class =
|super-order =
|order = [[Rickettsiales]]
|sub-order =
|super-family =
|family = Ehrlichiaceae
|sub-family =
|genus = Cowdria
|species = ''C. ruminantium''
}}
Also Known As: '''''Heartwater — Ehrlichiosis — Nintas (South Africa)'''''

Caused by: '''''Cowdria ruminantium''''' Also known as: '''''Rickettsia ruminantium'''''

==Introduction==
''C. ruminantium'' is a '''[[Bacteria | bacterial]] gram negative coccal''' pathogen causing the '''[[Tick Disease Transmission |tickborne]] disease “Heartwater”''' in ruminants in '''Subsaharan Africa'''. Animals often acquire the disease when moved on to heartwater infected grazing.

It is an '''intracellular bacteria''', residing in endothelial cells and affecting the cardiovascular, respiratory and neurological systems.

Cowdriosis has a huge economic impact in Africa, both in direct losses and as an obstruction to the improvement of breeding stock due to the susceptibility of introduced high producing breeds.<ref> Uilenberg, G. (1982) '''Disease problems associated with the introduction of European cattle in the tropics. '''''Proc 12th World Cong Diseases Cattle, The Netherlands, ''1025-1032</ref>

Cowdriosis is '''notifiable''' to the World Organisation for Animal Health [http://www.oie.int/ (OIE)].

==Distribution==
Cowdriosis occurs across the African continent, particularly in '''South Africa'''.

Cowdriosis is transmitted by '''bont [[Ticks |ticks]]''', mainly of the [[Amblyomma spp.|''Amblyomma'' genus]] (''A. variegatum'' and ''A. hebraeum'') but also [[Rhipicephalus spp.|''Rhipicephalus'']], [[Hyalomma spp.|''Hyalomma'']], and ''Glossina'' species and the ''[[Sarcoptes|Sarcoptes scabei]]'' mite. Both adults and nymphs of tick species can transmit disease.

Heartwater is therefore also a risk for countries where the ''Amblyomma'' tick is present, such as mainland America, Asia and the Caribbean, although disease may cutrently not be.

''C. ruminantium'' develops and replicates within both its mammalian and invertebrate hosts.

Although speculated to be potentially zoonotic, there is no evidence of cowdriosis affecting humans.

==Signalment==
Cowdriosis affects a wide range of domestic and wild ruminants, although not all develop clinical disease. Clinical disease is most common in '''young animals.'''

''Bos indicus'' (zebu) cattle appear more '''resistant''' than European breeds<ref> Uilenberg, G. (1983) '''Heartwater (''Cowdria ruminantium ''infection): current status.''' ''Adv Vet Sci Comp Med'', 27:427-480</ref>

==Clinical Signs==
Clinical signs are attributable to '''increased vascular permeability''' due to '''vascular endothelial cell invasion''' and consequent oedema and hypovolaemia:

'''Tachycardia, petechiae''' on mucous membranes\conjunctiva, weak pulses, muffled heart sounds.

Dull areas on percussion of the thorax, '''cough''', purulent nasal discharge, abnormal respiratory noises, '''tachypnoea'''.

'''Head tilt, tremors''', coma, circling, abnormal reflexes, '''hyperaesthesia, aggression''', head pressing, depression, nystagmus, mydriasis and blindness.

Animals display a '''high fever''' which may progress to hypothermia. They gradually stop feeding and their behaviour changes.

Cowdriosis can also cause reproductive and gastrointestinal disease.

Various factors such as species, breed, age, natural resistance, vector efficiency and immune status dictate whether clinical disease develops and its severity.

==Diagnosis==
On '''post-mortem examination''', a '''light yellow [[Transudate | transudate]]''' that '''coagulates on exposure to air''' is often found within the '''thorax, [[Pericardial - Pathology |pericardium]] and abdomen.''' Volume may vary but may be several litres in cattle.
Most fatal cases will display the '''hydropericardium''' that gives the disease its common name, although this is seen more commonly in sheep and goats than cattle. <ref> Henning, M. W. (1956) '''Heartwater'''. In: Anim Dis S Africa, ed 3. South Africa: ''Central News Agency Ltd'', 1155-1178</ref>

'''Pulmonary oedema''' and mucosal congestion are regularly seen along with '''frothy fluid''' in the airways and cut surfaces of the [[Lungs - Anatomy & Physiology |lungs]].

The [[Spleen |spleen]] may be enlarged and pulpy in consistency.

Although neurological signs are often attributed to '''cerebral oedema''', this is not always obvious macroscopically although in some cases the brain and '''gyri''' may be strikingly swollen and/or petechiated.

The organism may be visible in '''smears''' of peripheral '''blood''' or the '''buffy coat'''.

In all suspect cases, presence of ''C. ruminantium'' must be demonstrated in preparations of the '''hippocampus''' under Giemsa staining or '''histopathology''' of brain or kidney.

==Treatment==
During the '''early febrile''' stages, '''sulphonamides and tetracyclines''' appear effective.

In advanced disease, prognosis is poor due to the intensive support therapy required and degree of cell death.

==Control==
'''Tetracyclines''' can be used '''prophylactically''' when animals are introduced into an area endemic with cowdriosis.

There is also a '''blood vaccine''' available for protection from heartwater in calves, lambs and kids in South Africa. As it contains '''live''' ''C. ruminantium'' organisms, treatment may be required in some animals post vaccination.

'''Control''' of exposure to '''bont ticks''', whether total or strategic allowing a level of immunity to develop, is also vital but often difficult. It can be achieved through dipping with [[Ectoparasiticides | ectoparasiticides]].

{{Learning
|literature search = [http://www.cabdirect.org/search.html?q=title%3A+Cowdriosis Cowdriosis Publications]
|flashcards = [[Cowdriosis Flashcards]]
}}

==References==
<references/>
{{CABI source
|datasheet = [http://www.cabi.org/ahpc/?compid=3&dsid=87241&loadmodule=datasheet&page=2144&site=160 cowdriosis] and [http://www.cabi.org/ahpc/Default.aspx?site=160&page=2144&LoadModule=datasheet&CompID=3&dsID=87240 ''Cowdria ruminantium'']
|date =06 June 2011
}}
 

{{review}}

{{OpenPages}}

[[Category:Cardiovascular Diseases - Cattle]][[Category:Neurological Diseases - Cattle]][[Category:Respiratory Diseases - Cattle]]
[[Category:CABI Expert Review]][[Category:CABI AHPC Pages]]
[[Category:Nick L]]
[[Category:Cardiology Section]]

Reticulum - Anatomy & Physiology

2018-02-18T06:49:10Z

DrNdaba: /* Ruminoreticular contraction */

{{OpenPagesTop}}
==Introduction==

The reticulum is the second chamber of the ruminant stomach. It has regular contractions which precede the biphasic ruminal contraction for digestion of food particles. Mechanical digestion and microbial fermentation occur to breakdown food particles for absorption. [[Volatile Fatty Acids|Volatile fatty acids]] are the major product of ruminant digestion.

==Structure==

[[Image:Reticulum Anatomy Sheep.jpg|thumb|right|250px|Reticulum Anatomy (Sheep) - Copyright RVC 2008]]

The reticulum is covered by greater omentum. The rumino-reticular fold often gets objects lodged. When the [[Rumen - Anatomy & Physiology|rumen]] contracts, the object can be pushed through the reticulum wall into the [[Heart Structure - Anatomy & Physiology#Pericardium|pericardium]] and [[Heart - Anatomy & Physiology|heart]].

Opening at the cardia into both the reticulum and the [[Rumen - Anatomy & Physiology|rumen]] is called the reticular groove (see [[Oesophageal Groove|oseophageal groove]]). The reticular groove also opens into the [[Omasum - Anatomy & Physiology|omasum]].

The reticulum is cranial to the [[Rumen - Anatomy & Physiology|rumen]] at ribs 6-8. It is located from cardia to the diaphragm. It lies above the xiphoid process of the sternum. Serosa covers the surface.

==Function==

The functions of the reticulum include waste removal and movement. Simpler products of digestion are assimilated directly, others continue down the digestive tract for further digestion.

See [[Rumination|rumination]] and [[Eructation|eructation]].

==Ruminoreticular contraction==

[[Image:Contractions of the ruminoreticulum diagram.jpg|thumb|right|250px|Diagram of the contractions of the ruminoreticulum - Copyright RVC 2008]]

The contractions have two main functions:
:Primary contraction mixes food by a ruminoreticuluar mixing cycle. There are 2 contractions of the reticulum (2nd most powerful) which continue over the [[Rumen - Anatomy & Physiology|rumen]]. Ingesta flows from the reticulum to cranial rumenal sac and then to reticulum (or ventral sac). It occurs every 60 seconds.

:The secondary contraction lets gas out (see [[Eructation|eructation]]). Ingesta flows from the ventral blind sac to the dorsal blind sac then to dorsal sac (eructation) and to the ventral sac.

==Vasculature==

The reticulum receives blood supply from the '''cranial mesenteric artery''', '''celiac artery''' and '''right and left ruminal arteries'''.

==Innervation==

The reticulum is innervated by the '''dorsal vagus''' ([[Cranial Nerves - Anatomy & Physiology|CN X]]) (most important) and the '''ventral vagus''' nerve ([[Cranial Nerves - Anatomy & Physiology|CN X]]).

==Lymphatics==

Numerous small lymph nodes are scattered in the grooves. The lymph drains to larger atrial nodes between the cardia and [[Omasum - Anatomy & Physiology|omasum]], then to the cistera chyli.

==Histology==

[[Image:Reticulum Histology Sheep.jpg|thumb|right|250px|Reticulum Histology (Sheep) - Copyright RVC 2008]]
The reticulum is lined by a '''keratinised stratified squamous epithelium''' and there are no glands present. The characteristic honeycomb appearance is formed by the mucosal layer trown into short and tall folds. The folds gradually merge into '''papillae''', where the reticulum meets the rumen. [[Tongue - Anatomy & Physiology#Types of Papillae|Conical papillae]], also called secondary papillae, are present on folds, providing a rough surface to increase food breakdown.

The '''lamina muscularis''' is present as discrete bands of smooth muscle (not continuous). There are two thick layers of '''tunica muscularis''', the inner circular and the outer longitudinal. The upper keratinised layer of the reticulum protects against abrasion and the deeper layers metabolise [[Volatile Fatty Acids|volatile fatty acids]].

==Species Differences==

===Small Ruminants===

Small ruminants have a larger reticulum compared to cattle. In sheep and goats, the ridges of the reticular cells are lower and have more prominent serrated edges than in cattle. The papillated ruminal mucosa expands over a greater proportion of the reticulum.
 
 

==Links==

'''Click here for information on [[Rumen - Anatomy & Physiology|Rumen]]'''

'''Click here for information on [[Omasum - Anatomy & Physiology|Omasum]]'''

'''Click here for information on [[Abomasum - Anatomy & Physiology|Abomasum]]'''

{{Template:Learning
|flashcards = [[Reticulum Flashcards]]
}}

{{OpenPages}}
[[Category:Stomach - Anatomy & Physiology]]
[[Category:A&P Done]]
[[Category:Alimentary Anatomy - Cattle]]

Oestrous Cycle Pharmacological Manipulation - Anatomy & Physiology

2017-10-24T10:11:45Z

DrNdaba: /* Pharmacological: Melatonin */

= Introduction =

The manipulation of normal cyclic activity ensures optimum production or is convenient for the herdsmen or owner. In the case of seasonal breeders, it allows them to breed out of season, or to advance the onset of cyclic activity. There are also advantages in ensuring all animals in a group come into oestrus at the same time for ease of management.
There are two methods of oestrus synchronisation. One is physiological manipulation of the oestrous cycle, and the other pharmacological manipulation of the cycle. Various factors must be considered before deciding which method to use. These factors will be specific to the type of production unit and species, also the stage of the natural oestrous cycle in the animal/herd involved.

= Factors Influencing Reproduction =

== Physiological ==

=== Light ===

* Cyclic activity in the mare, ewe, goat and cat depend on changes in the number of daylight hours.
* Tungsten and fluorescent lamps can be used to artificially manipulate the photoperiod.
* Mare and queen are stimulated by increasing day length (long day breeders)
** If mares are stabled in December and exposed to artificial light for increasing duration, the onset of oestrous cyclicity and ovulation will be advanced.
* Ewe and goat are stimulated by decreasing day length (short day breeders)
** Providing ewes with controlled light housing enables change in the breeding season from autumn and winter to spring and summer.
** If there is no change in duration of light stimulus, it is possible to make ewes cycle all year round.

=== Nutrition ===

* Improved nutrition prior to mating (flushing) will increase the number of follicles which mature and ovulate.
* Used in the ewe and sow successfully.

=== Other Methods ===

* The presence of a male can stimulate the onset of cyclic activity in some species (see 'Ram Effect' for more detail).
* In sows and gilts, removing piglets will cause a more rapid return to cyclic activity post-partum.
* If litters are weaned from a group of sows at the same time, there will also be some synchronisation of oestrus.
* Also in gilts and sows, the stress of changing environment or transport stress can stimulate the onset of oestrus post-partum.

== Pharmacalogical ==

=== Preparations which Stimulate Release of Anterior Pituitary Hormones ===

* Ovarian steroids, particularly oestrogens, exert a positive-feedback on the anterior pituitary gland and hypothalamus.
* Oestrogens and synthetic oestrogens are used to stimulate oestrus.
* They have a direct effect on stimulating oestrus behaviour and changes in the genital tract.
* They may also stimulate release of pituitary gonadotrophins.
* Synthetic GnRH can be used to stimulate the release of endogenous gonadotrophins.

=== Preparations which Supplement or Replace Pituitary Gonadotrophins ===

* Purified LH and FSH can be extracted from the pituitary gland in the abbatoir, but this is too time consuming to be practiced commercially. There is also the risk of transmitting diseases such as BSE.
* Instead, two substitutes are used commercially:
** Equine Chorionic Gonadotrophin (eCG): obtained from the serum of pregnant mares. This has an 'FSH-like' effect, but with some 'LH-like' activity.
** Human Chorionic Gonadotrophin (hCG): obtained from the urine of pregnant women. It has mainly an 'LH-like' effect, but with some 'FSH-like' activity.

=== Oestrogens ===

* Used to induce oestrus in anoestrous animals.
* Have a direct effect on oestrus behaviour and the genital tract.
* May inhibit the pituitary release of gonadotrophins in high doses.
* Do not initiate ovarian activity or ovulation.

=== Progestogens ===

* Progesterone and its synthetic analogues are used extensively in most domestic species to synchronize oestrus.
* Exogenous progestogens act in the same way as the corpus luteum, resulting in a negative feedback effect on the anterior pituitary gland.
* This in turn results in supression of gonadotrophin release, so cyclic activity ceases.
* When the progestogen is withdrawn, the negative feedback block on the anterior pituitary gland is removed. This initiates a retun to cyclic activity.

=== Prostaglandins ===

* The length of the interoestrus interval in most domestic species is controlled by the duration of the lifespan of the corpus luteum.
* Administration of PGF2α or its analogues will cause premature luteolysis of the corpus luteum.
* This can be used to manipulate the normal pattern of cyclic activity.
* Prostaglandins will induce luteal regression. As a result, progesterone levels fall and negative feedback on the anterior pituitary gland is removed. Subsequently, levels of gonadotrophins begin to rise, leading to increased follicular growth under the influence of FSH. Oestradiol production begins to rise as follicles become dominant. When oestradiol rises above the threshold, it feeds back positively at the level of the hypothalamus. The hypothalamus then releases a surge of GnRH. This then stimulates the anterior pituitary gland to release a surge of LH which is responsible for ovulation.
* The corpora lutea of the cow, mare, sow, ewe and goat respond to administration of exogenous prostaglandins.
* In the cow, mare, ewe and goat the new developing corpus luteum is refractory to prostaglandins for 3-5 days after ovulation.
* At the end of the cycle, the corpus luteum is unaffected by exogenous prostaglandin because it is already regressing under the influence of its own endogenous luteolytic hormones.
* The corpus luteum is resonsive for:
** Cow: 13 days
** Goat: 13 days
** Mare: 10 days
** Ewe: 9 days
* In the sow, the corpus luteum is refractory for up to 11 days after ovulation. It is only resposive for a period of 7-8 days.
* In the bitch and queen, corpora lutea are unresponsive to exogenous prostaglandins unless they are given repeated doses.
* Prostaglandins will cause abortion, do not use in animals that might be pregnant!

=== Melatonin ===

* The pineal gland controls reproductive cyclicity in seasonal breeders (sheep, goats, horses and cats) by the secretion of melatonin as the daylight hours are reduced. For more information on this mechanism, click [[Seasonality_of_Reproduction_- Anatomy & Physiology#Mechanism_of_seasonality|here]]
* Melatonin can be used successfully to modify seasonal activity in the species mentioned, most practically the ewe.

= Manipulation of the Oestrous Cycle in Various Species =

== Ewe ==

True synchronization in the ewe is not achieved even with the combined use of prostaglandins and progestogens with much time and effort under controlled conditions of a lab setting. Thus, in practice these methods are never completely effective for the ewe.

=== Factors to Consider Before Deciding which Method to Use ===

* Degree of synchronization required
* The season
* Economic and market factors
* Physiological manipulation is usually cheaper, but it does not result in tight synchronization and can only be used under certain conditions.
* Pharmacological methods tend to give tight synchronization throughout the year, but are more expensive in terms of both drugs and labour.

=== Physiological: The Ram Effect ===

* Ram stimulate gonadotrophin secretion form the anterior pituitary gland and subsequent ovulation in anoestrus ewes through chemosensory cues.
* Isolate ewes for 3-4 weeks before introducing the ram.
* Only effective at certain times of the year - just before commencement of the natural breeding season. This method is not effective for ewes in deep anoestrus.
* The majority of ewes ovulate within 6 days of introducing the ram.
* Priming with progesterone (intravaginal sponge or intramuscular injection) prior to the introduction of the ram will increase the percentage of ewes showing oestrus behaviour.
* Cheap and easy, but not very effective as a sole method.

=== Pharmacological: Gonadotrophins ===

* Use of eCG alone to induce oestrus in anoestrus ewes is not very successful.
* Administration of progesterone before the injection of eCG causes synchronised oestrus and ovulation in seasonally anoestrus ewes.

=== Pharmacological: Progestogens ===

* Used alone or in conjunction with other hormones.
* Used to induce oestrus in the anoestrus ewe during the non-breeding season and for oestrus synchronization in cyclic ewes.
* To be effective, treatment must last for the length of the normal luteal phase (12-14 days).
* In the anoestrus ewe, progesterone withdrawal is complemented by follicle stimulating treatments such as eCG. This will stimulate oestradiol secretion due to its 'FSH-like' effect.
* Progestogens are now used more commonly than progesterone itself, because progesterone has a short-half life. These include:
** Fluorogestone acetate (FGA)
** Medroxyprogesterone acetate (MAP)

==== Intravaginal Sponges ====

* The sponge is impregnated with progestogens and inserted into the vagina.
* Progestogen is absorbed in sufficient quantities to cause a negative feedback effect on pituitary function.
* When used outside of the normal breeding season, eCG is administered at the end of the progestogen priming period.
* Fertility may be reduced at first mating after synchronized oestrus. This may be due to poor absorbtion of progestogen from the sponge. It may also be the effect of abnormal hormone levels on sperm survival.

=== Pharmacological: Prostaglandins ===

* Used to induce luteal regression and subsequent cyclicity in cyclic ewes.
* Administration of PGF2α or its analogues during the period when there is a sensitive corpus luteum present induces oestrus 36-46 hours after injection.
* Ovulation will then occur shortly afterwards.
* In order to synchronize a group of ewes in randomly different stages of the oestrous cycle, two injections are required 8-9 days apart in order to ensure administration at a time when there is a sensitive corpus luteum present in all animals of the group.
* Uses are limited for a number of reasons:
** Having to give two injections is impractical under field conditions
** The induced oestrus leads to poor fertility, probably due to the limited exposure of the tract to progesterone.
** Prostaglandins can only be used in cyclic animals, not in seasonal anoestrus.
* It is usually only used in combination with progestogens.

=== Pharmacological: Melatonin ===

* Used commercially to advance the onset of the breeding season.
* The breeding season can be advanced by 2-3 months with good fertility.
* Administered as an implant containing 18mg of melatonin, which is inserted subcutaneously at the base of the ear.
* Ewes should be completely isolated from rams at least 7 days before insertion of the implant.
* They should remain separated for at least 30 days, and no more than 40 days.
* Rams should then be reintroduced.
* Peak mating activity occurs 25-35 days later.
* However, this is much work for little benefit because it cannot be used for ewes in deep anoestrus.

=== Immunization ===

* Use of an immunogen, produced by conjugating a derivative of adrostenedione with human serum albumin, increases lambing rates.
* When injected, it stimulates the production of antibodies to androstenedione.
* The antibodies bind free androstendione in the blood.
* This results in an increase in the number of lambs born, although the precise reason for this is unknown.
* Inject twice:
** 8 weeks before tupping
** 4 weeks before tupping
* If ewes have been treated in the previous season, only one injection is required at 4 weeks before tupping.
* Only inject ewes which are to be fed adequately during pregnancy, due to the dangers of pregnancy toxaemia.
* Immunization against inhibin will soon be available for commercial use.
** This will reduce the inhibitory effect of inhibin on FSH secretion from the anterior pituitary gland.
** The subsequent increase in FSH will lead to an increase in the nuber of developing follicles, thus better lambing rates.

== Cow ==

=== Controlling Oestrous ===

* The main reasons for controlling oestrus are:
** Induction of oestrus in dairy cows that are not observed in oestrus by 45 days post-partum.
** Synchronization of groups of heifers for insemination with semen of 'easy calving' bulls.
** Reducuction in the time necessary for oestrus detection.
** To facillitate the use of artificial insemination.
** Synchronization of donor and recipient cows for embryo transfer.
** Induction of ovarian activity in beef cows with lactational anoestrus.

=== Pharmacological: Gonadotrophins ===

* eCG can be used to stimulate follicular growth and ovulation in the anoestrus cow.
* Dose response is variable and can result in multiple ovulations.
* Withold insemination at the induced oestrus.
* The cow often returns to anoestrus, so overall the use of eCH is not recommended.

=== Pharmacological: Prostaglandins ===

* Used to synchronize oestrus in groups of cows and heifers. Oestrus detection is difficult in this species, so this is advantageous for optimum timing of artificial insemination.
* Give two injections of PGF2α or an analogue such as cloprostenol at an interval of 11 days to a group of cows/heifers all at different stages of the oestrous cycle.
* 3-5 days after the second injection, all animals treated will come into oestrus and ovulate at about the same time.
* If only a single injection is given, conception rates are lower after subsequent artificial insemination.
* Two injections are required in order to ensure the prostaglandins are administered to all animals in a period where the corpus luteum is sensitive.
* To reduce cost and improve pregnancy rates, the following regime is used:
** All animals are injected with PGF2α on the same day and observed for oestrus during the following 5 days.
* The length of time between the injection and onset of oestrus does vary slightly, depending on the ovarian status at the time of the injection. If there is a large, dominant follicle, the time until oestrus onset will be short, whereas if only small follicles are present, the period will be longer.
* Lactating dairy cows have a more variable interval between the injection and onset of oestrus.
** Any identified in oestrus are inseminated
** Any not identified as being in oestrus receive a second injection of prostaglandin followed by artificial insemination.
** Any animals that exhibit oestrus following the first insemination are reinseminated.

=== Pharmacological: Progestogens ===

* Used to synchronize groups of cows and heifers for artificial insemination and to overcome problems with oestrus detection.
* Treatment of random cycling animals for 18-21 days results in synchronization of oestrus.
* When the treatment ceases, oestrus occurs in 4-6 days.
* Fertility at first oestrus is lower, due to impaired sperm transort as a result of the atypical hormone balance after treatment is withdrawn.
* To ensure the natural corpus luteum of the cycle has regressed by the time of progestogen withdrawal, progestogen treatment is often combined with a luteolytic factor:
** Oestradiol at the start of treatment or prostaglandin analogues at the end of treatment.
** Oestradiol is best because as well as inducing luteal regression, it affects follicular dynamics so improves fertility at first oestrus.
* In non-cyclic cows, progestogens sensitize the hypothalamic-anterior pituitary-gonadal axis. This approach can be used in cattle with innactive ovaries.
* Injecting with eCG at progestogen removal stimulates follicular maturation and ovulation.
* Oestrus and ovulation after treatment with progestogens occurs earlier and with more precise timing than following injection of prostaglandin alone.

==== Progesterone Releasing Intravaginal Device (PRID) ====

* Stainless steel coil covered with an inert elastomer incorporating 1.55g of progesterone.
* Placed in the vagina using a speculum.
* Whilst in place, progesterone is absorbed to produce plasma concentrations that mimic maximum levels at dioestrus.
* When removed after 12 days, the cow will come into oestrus in 2-3 days.
* Some may also contain Oestradiol Benzoate.
* Oestradiol Benzoate is anti-luteotrophic and mildly luteolytic.
* Almost 100% synchronization can be achieved if an injection of PGF2α is administered 24 hours before removing the device. This has a far greater luteolytic effect than Oestradiol Benzoate alone.
* Can be used in cyclic cows to synchronize oestrus, best inserted on day 13-14.
* Can be used in anoestrus dairy and beef cows to induce oestrus.

==== Controlled Internal Drug Release Device (CIDR) ====

* A hinged T-shaped device impregnated with progesterone.
* Placed in the vagina using a speculum.
* Whilst in place, progesterone is absorbed to produce plasma concentrations that mimic maximum levels at dioestrus.
* When removed after 12 days, the cow will come into oestrus in 2-3 days.
* Can be used in cyclic cows to synchronize oestrus, best inserted on day 13-14.
* Can be used in anoestrus dairy and beef cows to induce oestrus.

== Mare ==

=== Reasons to Control the Oestrous Cycle ===

* Better planning in studs
* Synchronizing the donor and recipient for embryo transfer.
* In racehorses, performance of 2-year olds is important. The age of a horse is measured from 1st January, so it is important that foals are born as soon as possible after 1st January in order to produce the oldest '2 year old' possible.

=== Control in the Transition Period ===

* Day length is an important stimulus for cyclicity.
* Aim is to simulate the natural photoperiod that would occur later on in the year.
* Exposure to ~116 hours of daylight in mid-November can advance the first ovulation from early April to early February.
* Combining photoperiod manipulation with GnRH achieved optimal results.

=== Control in the Breeding Period ===

* During the natural breeding period, manipulation is mainly carried out to treat fertility disorders.
** Prolonged oestrus can be treated with a Progesterone Rleasing Intravaginal Device (PRID)
** A persistent corpus luteum can be treated with prostaglandins.
* Other reasons for manipulation include:
** Shortening anoestrus after foaling
** Synchronizing oestrus in a group of mares

===== Pharmacological: Progestogens =====

* In competition horses, it is desirable to prevent the mare from coming into oestrus at inopportune times.
* In some cases it is desirable to synchronize a group of animals.
* A daily injection of progesterone (0.3mg/Kg) will prevent oestrus.
* The mare will return to oestrus 3-7 days after treatment ceases.
* Oral progestoges recommended include:
** Allytrenbolone
** Altrenogest
* These can be used in a number of ways:
1. '''To stimulate the onset of cyclic activity'''
* Administer 0.044mg/Kg mixed in with the feed for 10 days and then stop.
* Give in the late transition period from anoestrus to cyclic activity when follicles are present.
* Better results when combined with increased lighting.
2. '''To suppress oestrus for an event'''
* Feed for 15 days at 0.044mg/Kg
3. '''To suppress oestrus in mares with prolonged oestrus'''
4. '''To control the time of oestrus for effective use of the stallion'''
* Feed for 15 days, then stop.
* Mare should come into oestrus 2-3 days later.

===== Pharmacological: Prostaglandins =====

* Eliminates the need for frequent testing for oestrus. It is also useful if a heat is missed, particularly the 'foal heat'.
* PGF2α and the synthetic analogue clonprostenol are used.
* Onset of oestrus is well synchronized 3 days after treatment.
* Subsequent ovulation occurs 7-12 days after treatment.
* Injecting hCG or GnRH on day 2-3 of the induced oestrus achieves the best results.

=== Inducing Ovulation ===

* The main method is the use of hCG
* In the presence of a follicle >2.5 cm, hCG will induce ovulation 24-48 (on average 35) hours after administration.

== Sow ==

=== Pharmacological: Progestagens ===

* Used to synchronize cyclic gilts and sows
* Difficult to treat group-fed animals, since it is contraindicated for pregnant animals and boars.
* Progestogens used are:
** Altrenogest
** Allytrenbolone
* Supress follicular maturation when fed daily at 15-20mg with no effect on the life span of corpora lutea.
* Feed for 18 days to achieve synchronization of oestrus 5-7 days after withdrawal.

=== Pharmacological: Prostaglandins ===

* Theoretically gives reliable synchronization of oestrus in groups of gilts and sows.
* Enables ease of artificial insemination and batch farrowing.
* But, prostaglandins and their analogues are not luteolytic until day 11-12 of the oestrous cycle.
* Thus, an injection regime for groups of animals at random periods of the oestrous cycle is not possible.
* However, it is possible after injection of oestrogen (see below)
* Another indication for use of prostaglandins is to induce luteolysis of accessory corpora lutea after use of eCG or hCG at any stage of the oestrous cycle.

=== Pharmacological: Oestrogens ===

* Prolong the lifespan of corpora lutea
* Inject oestrogen on day 10-14 of the oestrus cycle.
* Then, prostaglandins can be injected after 5-20 days.
* Oestrus will occur 4-6 days later.

=== Pharmacological: Gonadotrophins ===

* In anoestrus gilts and sows eCG, or a combination of eCG and hCG will promote follicular growth and oestrus.
* If this is followed by another injection of hCG 72 hours later, this will ensure ovulation occurs.
* This can also be used to synchronize cyclic activity, especially if used in combination with progestogen.

== Bitch ==

=== Pharmacological: Gonadotrophins ===

* Combinations of eCG and hCG can induce oestrus in the anoestrus bitch.
* Sometimes this is combined with oestrogens.
* However, conception rates after the induced ovulation tend to be poor.

=== Pharmacological: Synthetic Progestogens ===

* Used to suppress oestrus.
* Commonly used progestogens include:
** Megoestrol acetate
** Proligestone
** Medroxyprogesterone
* These are available orally or for injection.
* They can be used to postpone the onset of oestrus when administered during anoestrus.
** Can be postponed for up to a year by injecting progestogens at intervals of 3-5 months or giving a 40 day course of oral tablets twice a week.
* Another use is to prevent oestrus from occuring if administered at the fist signs of pro-oestrus.
** This is achieved by a single injection or oral progestogen at a higher dose rate than for postmonement, but for a shorter duration.
* Following administration of progestogens, the interval before onset of the next oestrus is unpredictable if treatment is not continued.
* Frequent use can predispose the bitch to reproductive disorders, particularly cystic glandular hyperplasia of the endometrium.
* First generation progestogens such as Medroxyprogesterone acetate (MPA) carry the risk of stimulating growth hormone (GH) secretion. This leads to an increased risk of acromegaly, mammary tumours and diabetes mellitus.

==== Proligestone (PRG) ====

* A new drug specifically designed to prevent oestrus in bitches and queens.
* It is particularly suitable because:
** Strongly anti-gonadotrophic
** Weakly progestagenic
** Antioestrogenic, so effectively controls vulval swelling and bleeding.

== Queen ==

Suppression of oestrus may be desireable for a number of reasons, but mostly to plan litters throughout the year and allow the queen a rest from sexual activity after a litter. This allows the queen to regain condition before being bred again. If the queen is allowed to call without mating, it may lead to loss in condition due to innapetance during oestrus.

=== Physiological ===

* Pseudopregnancy can be achieved by mating queens with a castrated Tom, or through stimulating coitus by swabbing the vagina.
* Pseudopregnant queens will not return to oestrus for 4-8 weeks.

=== Pharmacological: hCG ===

* Administration of hCG can be used to induce ovulation.
* This will cause pseudopregnancy.
* Pseudopregnant queens will not return to oestrus for 4-8 weeks.

=== Pharmacological: Androgens ===

* Androgen anabolic steroids used daily postpone calling.
* Give daily oral doses ~30 days before anticipated oestrus.
* Induces masculinization

=== Pharmacological: Progestogens ===

* Used to suppress oestrus
* Injectable forms include:
** Medroxyprogesterone acetate
*** Will suppress oestrus for 7 months or more following a single injection
*** Can be repeated every 5 months to achieve permanent oestrus suppression.
** Proligestone
* Oral progestogens are more flexible.
* The most commonly used oral progestogen is Megoestrol acetate.
** Used to prevent oestrus period by administering 5mg as soon as signs of oestrus are observed.
** Postponment is achieved by administering 2.5mg daily or weekly depending on whether the treatment is in the breeding season or the period of anoestrus.
* Side effects include lethargy and weight gain, there is also a predisposal to diabetes mellitus.

[[Category:Female Reproduction]][[Category:Pharmacology]]
[[Category:Bullet Points]]

Foot and Mouth Disease

2017-05-31T08:46:13Z

DrNdaba: /* Introduction */

{{OpenPagesTop}}
Also known as: '''''FMDV — FMD'''''

== Introduction ==

This [[:Category:Apthoviruses|Apthovirus]] is a small (25nm) +ss RNA virus, unenveloped and has 7 serotypes, namely '''Oise (O), ''''''Allemagne (A), ''''''C (also German), '''South African Territories (SAT) 1, 2, and 3 and Asia-1.

This disease affects all '''cloven-hoofed animals, '''namely cattle, sheep, goats, pigs, deer, elephants and other wild ruminants such as buffalo and kudu etc. It does NOT afferct the horse. The main presentation of the disease is the formation of '''vesicles'''.

The disease is NOTIFIABLE in the UK and any animals with the disease, or in contact with the disease have to be destroyed.

The virus replicates primarily in the upper respiratory tract, tonsils, or upper alimentary tract and there is '''aerosol''' excretion during this incubation period. This is then followed by a viremia. Virus targets stratum spinosum of stratified squamous epithelia and mucus membranes and secondary '''vesicles''' appear after incubation of 2-14 days. Lesions also affect the feet with cutaneous erosions in interdigital cleft, at coronet and bulbs of heals . These feet lesions often take a long time to heal as secondary bacterial infections may ensue and produce true deep ulcerative dermatitis. In the young, without maternal antibody, virus will localize in the heart, particularly the wall of the left ventricle, resulting in multi-focal necrosis of the myocardium and subsequent death. Persistent infection of cattle can occur in unkeratinized lesions, but subclinical carriers do not usually transfer infection except for subclinical buffalo that can transmit the disease.

FMDV causes loss of condition and productivity but is NOT typically fatal. Approximately 5% mortality (usually young animals); older animals recover. The virus is highly contagious and spread is by aerosol, direct contact, saliva, infected swill and fomites. Pigs produce 3000 times more aerosol virus than cows, but cows are much more susceptible to infection than pigs.

In 1967 and 2001 there were major outbreaks in the UK. The disease is still widespread in many parts of world especially S. America and far East.

== Clinical Signs ==

Main clinical signs include pyrexia, depression, separation away from the herd, drooling, excess salivation, anorexia pain while eating as well as smacking of the lips. Lameness is also a key clinical sign and in pigs may often be the first noticeable sign as mouth lesions in this specie are less severe.

Lesions in the mouth and on the tongue have the following characteristics depending on age of lesions.
: At 0- 2 days there will be unruptured vesicles.
: At 1-3 days newly ruptured vesicles with adherent epithelia at margins will appear.
: By 3-7 days there will be ruptured vesicles, loss of epithelia, no marked fibrous margin.
: At days 7-10+ open lesions with marked fibrous margin will be present.

'''Teats''' on animals that are suckling may also develop vesicles.

In pigs and sheep, lesions are less obvious, but vesicles around nose, mouth, and coronary band are present. Pigs have vesicles on snout, which are quickly traumatised to leave an eroded lesion. Presence of a lesion at '''coronary band''' means infection is usually less than a week old. The lesions grow down the claw at a rate of 1mm per week.

In cattle, lesions are seen inside mouth, around muzzle, in the interdigital cleft, around coronary band, and on teats. There will be excessive salivation, anorexia, secondary mastitis and on PM there will be lesions in oesophagus and forestomachs.

== Diagnosis ==

Clinical signs are enough to make a provisional diagnosis. This must be confirmed by [[ELISA testing|'''ELISA''']] for virus '''antigen. '''ELISAs are serotype-specific. This method is soon to be replaced by immunochromatography-bedside ELISA to allow on-farm diagnosis. '''Virus isolation''' can also be performed in kidney culture cells, and then serotyped by ELISA. Serology for virus '''antibody''' can determine past infection and ELISAs are used to detect subclinical carrier sheep. This cannot be done on vaccinated animals.

RT-PCR has been suggested for on-farm diagnosis, but has flaws such as, RNA is readily degraded by tissue enzymes, RNA must be purified before converting to DNA for PCR, false positives can occur easily by contamination with previously amplified DNA.

Samples should be taken from the vesicle itself and include the vesicle fluid as well as the tissue. These should be placed in transport medium and sent for testing.

== Control ==

Recovered animals show immunity ONLY to the serotype of first exposure, and even this is relatively short-lived, therefore re-exposure to the original serotype after immunity has waned will still result in virus excretion, even without clinical symptoms. Infection by a second serotype will result in clinical disease. It is for these reasons, that '''vaccination is not practiced''' in the UK. Further, vaccination would mean a loss of meat export markets.

===== Prevention in the UK =====

Imported stock must come from virus-free countries that DO NOT vaccinate. Any meat imported from endemic countries must be de-boned.

ANY sign of lesions in a susceptible animal is '''NOTIFIABLE''' to the Divisional Veterinary Officer and local police. Once diagnosis is confirmed, all animals on the premises must be '''slaughtered and incinerated''' and the premises fully disinfected. Movement is controlled within a 10-mile radius and follow-up serology must be performed to ensure no spread has taken place on any nearby farms. '''Ring vaccination''' with relevant subtype to create a barrier of immune animals (although this was not done in the 2001 outbreak) can be used. There is to be no movement on or off the farm as soon as a case is suspected.

'''In Endemic Areas''' disease cannot be prevented by slaughter due to large numbers of carrier stock. Annual '''inactivated whole virus vaccination''' using local subtypes is used. This vaccine is inactivated by azuridines, using alhydrogel adjuvant for cows, and oil for pigs. Subunit vaccines are ineffective. The course involves 2 initial injections at 4 months (if dams are vaccinated), followed by boosters every 6-12 months, which induces virus-neutralizing antibodies. Vaccination DOES NOT render meat harmful to consumers, but does affect when it can be exported.

== References ==

Andrews, A.H, Blowey, R.W, Boyd, H and Eddy, R.G. (2004)'''Bovine Medicine '''(Second edition), ''Blackwell Publishing''

Brownlie, J (2007) '''Virology Study Guide, '''''Royal Veterinary College.''

Radostits, O.M, Arundel, J.H, and Gay, C.C. (2000) '''Veterinary Medicine: a textbook of the diseases of cattle, sheep, pigs, goats and horses '''''Elsevier Health Sciences''

Taylor, D.J. (2006) '''Pig Diseases''' (Eighth edition)'' St Edmunsdbury Press ltd''

{{review}}

{{OpenPages}}

[[Category:Apthoviruses]] [[Category:Oral_Diseases_-_Cattle]] [[Category:Oral_Diseases_-_Sheep]] [[Category:Oral_Diseases_-_Goat]] [[Category:Oral_Diseases_-_Pig]] [[Category:Dermatological_Diseases_-_Cattle]] [[Category:Dermatological_Diseases_-_Sheep]] [[Category:Dermatological_Diseases_-_Goat]] [[Category:Dermatological_Diseases_-_Pig]] [[Category:Oral_Cavity_-_Vesicular_Pathology]] [[Category:Integumentary_System_-_Viral_Infections]] [[Category:Viral_Myositis]]
[[Category:Expert Review - Farm Animal]]

Angiotensin Converting Enzyme

2016-10-20T08:15:35Z

DrNdaba: /* Overview */

{{OpenPagesTop}}
==Overview==

Angiotensin converting enzyme is known as '''ACE'''. It is a membrane bound '''metalloproteinase''' and converts Angiotensin 1 to Angiotensin 2.
[[Image:angiotensin.png|right|thumb|250px|Fvasconcellos 2006, Spacefilling models of angiotensin I (left) and angiotensin II (right).]]

It is very important in the [[Renin Angiotensin Aldosterone System|Renin Angiotensin Aldosterone System (RAAS)]]. ACE is predominantly expressed on epithelial cell membranes in the pulmonary circulation and this is therefore, the site of action of the ACE inhibitor drugs.

{{OpenPages}}
[[Category:Kidney Hormonal Regulators]]
[[Category:To Do - AimeeHicks]]

Alimentary System Overview - Anatomy & Physiology

2016-10-04T13:27:17Z

DrNdaba: /* Introduction */

{{OpenPagesTop}}
[[Image:Alimentary Canine.jpg|thumb|right|300px|The Alimentary Tract (Canine) - Copyright Prof. Pat Mccarthy]]
==Introduction==
The anatomy of the alimentary system begins rostrally with the [[Oral Cavity Overview - Anatomy & Physiology|oral cavity]], which is the first section of the alimentary tract that receives food. It provides the digestive functions of prehension, [[Mastication|mastication]] and insalivation and also plays a role in the respiratory system through oral breathing when the nasopharynx is impaired. The oral cavity or mouth, includes accessory structures - [[Salivary Glands - Anatomy & Physiology|the salivary glands]], projecting structures - [[:Category:Teeth - Anatomy & Physiology|the teeth]] and [[Tongue - Anatomy & Physiology|tongue]], and the boundaries enclosing the oral cavity; the [[Lips|lips]], [[Cheeks|cheeks]], [[Soft Palate|soft]] and [[Hard Palate|hard palates]], and the [[Oropharynx - Anatomy & Physiology|oropharynx]]. In anatomical terms, the oropharynx is common to both the alimentary and the respiratory system, and the hard and soft palate forms the boundary between the oral and nasal cavities in many species.

Food passes from the oral cavity into the [[oesophagus - Anatomy & Physiology|oesophagus]] and from here to the stomach. In evolutionary terms, various adaptations to the anatomy of the stomach reflect the digestive needs of the species based on their natural diet. The [[Ruminant Stomach - Anatomy & Physiology|ruminant stomach]] for example, is composed of 4 separate compartments; the rumen, the reticulum, the omasum and the abomasum. The first three compartments are adapted to digest complex carbohydrates with the aid of microorganisms which produce [[Volatile Fatty Acids|volatile fatty acids]] - the major energy source of ruminants. The last compartment, the abomasum resembles the simple [[Monogastric Stomach - Anatomy & Physiology|monogastric stomach]] of a carnivore in structure and function. As a further adaptation, the [[Oesophageal Groove|oesophageal groove]] is present in newborn ruminants; it is a channel which directs milk from the oesophagus into the rumen, omasum and then abomasum, bypassing the reticulum.

The stomach passes into the [[Small Intestine Overview - Anatomy & Physiology|small intestine]], which is subdivided into three sections; the [[Duodenum - Anatomy & Physiology|duodenum]], the [[Jejunum - Anatomy & Physiology|jejunum]] and the [[Ileum - Anatomy & Physiology|ileum]]. The small intestine receives the ingested food from the stomach and is the main site of the chemical degradation and absorption of ingesta. Fats are exclusively broken down in this part of the alimentary tract. Carbohydrates and proteins that are not degraded in the small intestine are available for microbial fermentation in the large intestine. The wall of the small intestine produces enzymes for the digestion of protein, carbohydrate and fat. The [[Pancreas - Anatomy & Physiology|pancreas]] also produces digestive enzymes to aid this process. The [[Gall Bladder - Anatomy & Physiology|gall bladder]] stores bile which is produced in the [[Liver - Anatomy & Physiology|liver]] and emulsifies fats for digestion. Absorption in the small intestine is facilitated by ridges in the small intestine and by the presence of villi and microvilli.

The [[Large Intestine - Anatomy & Physiology|large intestine]] begins at the [[Caecum - Anatomy & Physiology|caecum]], and includes the [[Colon - Anatomy & Physiology|colon]], the [[Rectum - Anatomy & Physiology|rectum]] and the [[Anus - Anatomy & Physiology|anus]]. Water, electrolytes and nutrients are absorbed which concentrates the ingesta into faeces. There is no secretion of enzymes and any digestion that takes place is carried out by microbes. All species have a large microbial population living in the large intestine, which is of particular importance to the [[Hindgut Fermenters - Anatomy & Physiology|hindgut fermenters]] such as the horse. For this reason, hindgut fermenters have a more complex large intestine with highly specialised regions for fermentation. The volatile fatty acid products of microbial fermentation are absorbed in the colon.

The stomach, small intestines and large intestines are situatied within the abdominal or [[Peritoneal Cavity - Anatomy & Physiology|peritoneal cavity]]. The peritoneum is the serous membrane that lines the abdominal cavity; it produces fluid to lubricate abdominal viscera and enhances the immune response and walls off infection in the abdomen to prevent peritonitis.

*[[Camelid Stomach - Anatomy & Physiology|The Camelid Stomach]]

==The Physiology of feeding==
Different hormones, neurotransmitters and reflexes are involved in the complicated [[Control of Feeding - Anatomy & Physiology|process of feeding]] in animals. [[Control of Feeding - Anatomy & Physiology#Control of GIT Secretions|Secretions]] and [[Control of Feeding - Anatomy & Physiology#Control of Motility|motility]] of the gastrointestinal tract are stimulated and carefully regulated by numerous factors, including environmental stimuli and the presence of food in different parts of the gastrointestinal tract, which is detected by chemoreceptors and mechanical receptors. Motility is modified by both intrinsic and extrinsic nervous sytems, and neurological reflex mechanisms prevent food from accidentally passing into the trachea during [[Deglutition|deglutition]], or swallowing.

When a harmful substance is ingested the body acts to eliminate it in different ways to prevent the animal becoming ill, for example, through [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|vomiting]] or diarrhoea. If one or more of the [[Control of Feeding - Anatomy & Physiology#Neuroendocrine Regulation of Feeding|neuroendocrine pathways]] involved with the control of feeding is damaged or inhibited, then problems such as obesity can occur.

There are many species differences in the phsiology of feeding, from different [[Control of Feeding - Anatomy & Physiology#Feeding Methods|feeding methods]] to adaptations during the digestive process such as additional cycles of [[Mastication|mastication]] which is seen during [[Rumination|rumination]] and [[Eructation|eructation]].

==The Avian Digestive Tract==
[[Image:Cockatiel.jpg|thumb|right|200px|Cockatiel - Copyright nabrown 2008]]

The [[Avian Digestive Tract - Anatomy & Physiology|avian alimentary system]] differs immensely from the basic mammalian design. Food can move in a retrograde fashion from the [[Proventriculus - Anatomy & Physiology|proventriculus]] to the [[Crop - Anatomy and Physiology|crop]]. Food can also pass from the [[Gizzard - Anatomy & Physiology|gizzard]], which is the equivalent of a muscular stomach back into the [[Proventriculus - Anatomy & Physiology|proventriculus]], or glandular stomach depending on particle size. The egestion of bones occurs once the nutritious material has been ingested. During reflux, gastric motility is inhibited and the pellet is expelled through the [[Avian Oral Cavity - Anatomy & Physiology|oral cavity]] by oesophageal antiperistaltis. This cleans the [[Crop - Anatomy and Physiology|crop]] out and checking the pellet of captive birds should be undertaken daily to assess health.

The [[Avian Intestines - Anatomy & Physiology|avian intestines]] shows some species specific anatomical variety, and the hindgut of the avian digestive system differs from mammalian anatomy as it terminates in the [[Avian Vent and Cloaca - Anatomy & Physiology|cloaca]]. The external opening through which faecal matter and uric acid is excreted is called the [[Avian Vent and Cloaca - Anatomy & Physiology|vent]]. The shape of the vent varies depending on species. Avian species vary in the presence or absence of a [[Avian_Liver_- Anatomy & Physiology#Gallbladder:_Species_Differences|gall bladder]], and the avian [[Avian Liver - Anatomy & Physiology|liver]] differs from the mammalian liver, being bilobular.

==Test yourself with the Alimentary Flashcards==
[[:Category:Alimentary System Anatomy & Physiology Flashcards|Alimentary Flashcards]]

[[The Avian Alimentary Tract - Anatomy & Physiology - Flashcards|Avian Alimentary Tract Flashcards]]

==References==
BOOKS
*Dyce, Sack and Wensing: Textbook of Veterinary Anatomy, 3rd Edition
*Sjaastad, Hove and Sand: Physiology of Domestic Animals, Scandinavian Veterinary Press, Oslo. (735pp)
*Konig and Liebich: Veterinary Anatomy of Domestic Mammals, 3rd Edition
*John E. Harkness and Joseph E. Wagner.: The Biology and Medicine of Rabbits and Rodents, 4th Edition
*Bloom and Fawcett: A Textbook of Histology
*Ian Kay: Introduction to Animal Physiology
*McGeady, Quinn, FitzPatrick, Ryan: Veterinary Embryology, pp. 205-220
*McGavin DM & Zachary, JF: Pathologic Basis of Veterinary Disease, 4th ed, pp. 301-393. Elsevier, St. Louis, Missouri, 2007.
*Reece, WO: Functional Anatomy and Physiology of Domestic Animals, 3rd ed., pp. 312-368. Lippincott Williams & Wilkins, London, England, 2005.
*Young B, Heath, JW: Wheater's Functional Histology: A Text and Colour Atlas, 4th ed, pp. 249-274. Churchill Livingstone, London, England, 2000.
*Andrew A.Mckenzie et al The Capture and Care Manual
*O.Charnock Bradley The Structure of the Fowl, 3rd ed, J.B.Lippincott Company, 1950

IMAGES
*Royal Veterinary College Histology Department
*Dr. Thomas Caceci and Dr. Ihab El-Zhogby Department of Histology, Faculty of Veterinary Medicine, Zagazig University, Egypt
*Nottingham Veterinary School

{{OpenPages}}
[[Category:Alimentary System - Anatomy & Physiology]]

Alimentary System Overview - Anatomy & Physiology

2016-10-04T13:27:02Z

DrNdaba: /* Introduction */

{{OpenPagesTop}}
[[Image:Alimentary Canine.jpg|thumb|right|300px|The Alimentary Tract (Canine) - Copyright Prof. Pat Mccarthy]]
==Introduction==
The anatomy of the alimentary system begins rostrally with the [[Oral Cavity Overview - Anatomy & Physiology|oral cavity]], which is the first section of the alimentary tract that receives food. It provides the digestive functions of prehension, [[Mastication|mastication]] and insalivation and also plays a role in the respiratory system through oral breathing when the nasopharynx is impaired. The oral cavity or mouth, includes accessory structures - [[Salivary Glands - Anatomy & Physiology|the salivary glands]], projecting structures - [[:Category:Teeth - Anatomy & Physiology|the teeth]] and [[Tongue - Anatomy & Physiology|tongue]], and the boundaries enclosing the oral cavity; the [[Lips|lips]], [[Cheeks|cheeks]], [[Soft Palate|soft]] and [[Hard Palate|hard palates]], and the [[Oropharynx - Anatomy & Physiology|oropharynx]]. In anatomical terms, the oropharynx is common to both the alimentary and the respiratory system, and the hard and soft palate forms the boundary between the oral and nasal cavities in many species.

Food passes from the oral cavity into the [[oesophagus - Anatomy & Physiology|oesophagus]] and from here to the stomach. In evolutionary terms, various adaptations to the anatomy of the stomach reflect the digestive needs of the species based on their natural diet. The [[Ruminant Stomach - Anatomy & Physiology|ruminant stomach]] for example, is composed of 4 separate compartments; the rumen, the reticulum, the omasum and the abomasum. The first three compartments are adapted to digest complex carbohydrates with the aid of microorganisms which produce [[Volatile Fatty Acids|volatile fatty acids]] - the major energy source of ruminants. The last compartment, the abomasum resembles the simple [[Monogastric Stomach - Anatomy & Physiology|monogastric stomach]] of a carnivore in structure and function. As a further adaptation, the [[Oesophageal Groove|oesophageal groove]] is present in newborn ruminants; it is a channel which directs milk from the oesophagus into the rumen, omasum and then abomasum, bypassing the reticulum.

The stomach passes into the [[Small Intestine Overview - Anatomy & Physiology|small intestine]], which is subdivided into three sections; the [[Duodenum - Anatomy & Physiology|duodenum]], the [[Jejunum - Anatomy & Physiology|jejunum]] and the [[Ileum - Anatomy & Physiology|ileum]]. The small intestine recieves the ingested food from the stomach and is the main site of the chemical degradation and absorption of ingesta. Fats are exclusively broken down in this part of the alimentary tract. Carbohydrates and proteins that are not degraded in the small intestine are available for microbial fermentation in the large intestine. The wall of the small intestine produces enzymes for the digestion of protein, carbohydrate and fat. The [[Pancreas - Anatomy & Physiology|pancreas]] also produces digestive enzymes to aid this process. The [[Gall Bladder - Anatomy & Physiology|gall bladder]] stores bile which is produced in the [[Liver - Anatomy & Physiology|liver]] and emulsifies fats for digestion. Absorption in the small intestine is facilitated by ridges in the small intestine and by the presence of villi and microvilli.

The [[Large Intestine - Anatomy & Physiology|large intestine]] begins at the [[Caecum - Anatomy & Physiology|caecum]], and includes the [[Colon - Anatomy & Physiology|colon]], the [[Rectum - Anatomy & Physiology|rectum]] and the [[Anus - Anatomy & Physiology|anus]]. Water, electrolytes and nutrients are absorbed which concentrates the ingesta into faeces. There is no secretion of enzymes and any digestion that takes place is carried out by microbes. All species have a large microbial population living in the large intestine, which is of particular importance to the [[Hindgut Fermenters - Anatomy & Physiology|hindgut fermenters]] such as the horse. For this reason, hindgut fermenters have a more complex large intestine with highly specialised regions for fermentation. The volatile fatty acid products of microbial fermentation are absorbed in the colon.

The stomach, small intestines and large intestines are situatied within the abdominal or [[Peritoneal Cavity - Anatomy & Physiology|peritoneal cavity]]. The peritoneum is the serous membrane that lines the abdominal cavity; it produces fluid to lubricate abdominal viscera and enhances the immune response and walls off infection in the abdomen to prevent peritonitis.

*[[Camelid Stomach - Anatomy & Physiology|The Camelid Stomach]]

==The Physiology of feeding==
Different hormones, neurotransmitters and reflexes are involved in the complicated [[Control of Feeding - Anatomy & Physiology|process of feeding]] in animals. [[Control of Feeding - Anatomy & Physiology#Control of GIT Secretions|Secretions]] and [[Control of Feeding - Anatomy & Physiology#Control of Motility|motility]] of the gastrointestinal tract are stimulated and carefully regulated by numerous factors, including environmental stimuli and the presence of food in different parts of the gastrointestinal tract, which is detected by chemoreceptors and mechanical receptors. Motility is modified by both intrinsic and extrinsic nervous sytems, and neurological reflex mechanisms prevent food from accidentally passing into the trachea during [[Deglutition|deglutition]], or swallowing.

When a harmful substance is ingested the body acts to eliminate it in different ways to prevent the animal becoming ill, for example, through [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|vomiting]] or diarrhoea. If one or more of the [[Control of Feeding - Anatomy & Physiology#Neuroendocrine Regulation of Feeding|neuroendocrine pathways]] involved with the control of feeding is damaged or inhibited, then problems such as obesity can occur.

There are many species differences in the phsiology of feeding, from different [[Control of Feeding - Anatomy & Physiology#Feeding Methods|feeding methods]] to adaptations during the digestive process such as additional cycles of [[Mastication|mastication]] which is seen during [[Rumination|rumination]] and [[Eructation|eructation]].

==The Avian Digestive Tract==
[[Image:Cockatiel.jpg|thumb|right|200px|Cockatiel - Copyright nabrown 2008]]

The [[Avian Digestive Tract - Anatomy & Physiology|avian alimentary system]] differs immensely from the basic mammalian design. Food can move in a retrograde fashion from the [[Proventriculus - Anatomy & Physiology|proventriculus]] to the [[Crop - Anatomy and Physiology|crop]]. Food can also pass from the [[Gizzard - Anatomy & Physiology|gizzard]], which is the equivalent of a muscular stomach back into the [[Proventriculus - Anatomy & Physiology|proventriculus]], or glandular stomach depending on particle size. The egestion of bones occurs once the nutritious material has been ingested. During reflux, gastric motility is inhibited and the pellet is expelled through the [[Avian Oral Cavity - Anatomy & Physiology|oral cavity]] by oesophageal antiperistaltis. This cleans the [[Crop - Anatomy and Physiology|crop]] out and checking the pellet of captive birds should be undertaken daily to assess health.

The [[Avian Intestines - Anatomy & Physiology|avian intestines]] shows some species specific anatomical variety, and the hindgut of the avian digestive system differs from mammalian anatomy as it terminates in the [[Avian Vent and Cloaca - Anatomy & Physiology|cloaca]]. The external opening through which faecal matter and uric acid is excreted is called the [[Avian Vent and Cloaca - Anatomy & Physiology|vent]]. The shape of the vent varies depending on species. Avian species vary in the presence or absence of a [[Avian_Liver_- Anatomy & Physiology#Gallbladder:_Species_Differences|gall bladder]], and the avian [[Avian Liver - Anatomy & Physiology|liver]] differs from the mammalian liver, being bilobular.

==Test yourself with the Alimentary Flashcards==
[[:Category:Alimentary System Anatomy & Physiology Flashcards|Alimentary Flashcards]]

[[The Avian Alimentary Tract - Anatomy & Physiology - Flashcards|Avian Alimentary Tract Flashcards]]

==References==
BOOKS
*Dyce, Sack and Wensing: Textbook of Veterinary Anatomy, 3rd Edition
*Sjaastad, Hove and Sand: Physiology of Domestic Animals, Scandinavian Veterinary Press, Oslo. (735pp)
*Konig and Liebich: Veterinary Anatomy of Domestic Mammals, 3rd Edition
*John E. Harkness and Joseph E. Wagner.: The Biology and Medicine of Rabbits and Rodents, 4th Edition
*Bloom and Fawcett: A Textbook of Histology
*Ian Kay: Introduction to Animal Physiology
*McGeady, Quinn, FitzPatrick, Ryan: Veterinary Embryology, pp. 205-220
*McGavin DM & Zachary, JF: Pathologic Basis of Veterinary Disease, 4th ed, pp. 301-393. Elsevier, St. Louis, Missouri, 2007.
*Reece, WO: Functional Anatomy and Physiology of Domestic Animals, 3rd ed., pp. 312-368. Lippincott Williams & Wilkins, London, England, 2005.
*Young B, Heath, JW: Wheater's Functional Histology: A Text and Colour Atlas, 4th ed, pp. 249-274. Churchill Livingstone, London, England, 2000.
*Andrew A.Mckenzie et al The Capture and Care Manual
*O.Charnock Bradley The Structure of the Fowl, 3rd ed, J.B.Lippincott Company, 1950

IMAGES
*Royal Veterinary College Histology Department
*Dr. Thomas Caceci and Dr. Ihab El-Zhogby Department of Histology, Faculty of Veterinary Medicine, Zagazig University, Egypt
*Nottingham Veterinary School

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[[Category:Alimentary System - Anatomy & Physiology]]

Introduction to General Pathology

2016-09-06T04:53:22Z

DrNdaba: /* Pathological changes to cells */

==Introduction==
The term '''pathology''' is derived from '''Pathos''', or suffering and '''Logos''', or reasoning/logic. Pathology is defined as the study of disease including:
* '''Aetiology''' - causal factor(s)
* '''Pathogenesis''' - the development of the disease within the body.
* '''Lesions''' - the observable structural changes in the tissues and fluids of the body.
* '''Pathophysiology''' - the functional changes in diseased tissues.
* '''Sequel''' - the consequences of the disease in the body.
* '''Remote effects''' - the effect of disease in one tissue on other tissues in the body.

==Lesions==
Lesions are the abnormalities or changes seen in living tissues due to disease, and can be observed in:
* The live animal
* Tissues surgically removed from the live animal during biopsy or excision
* Necropsy or post-mortem examination.

===Description of Lesions===
[[Recognition and Description of Lesions|Descriptions of lesions]] are very important. Whole organs, tissues or individual lesions are described under headings such as:
# Size
# Shape
# Colour
# Weight (generally in relation to body weight)
# Texture and Consistency
# Appearance of the cut surface
# Contents of hollow organs
# Position, relationships and effects on adjacent tissues

==Pathological changes to cells==
Generally, disruptions at a cellular level usually involve changes or damage to the cells themselves, or they involve the presence of unexpected material within the cell, such as [[Pigmentation - Pathology|pigments]] or [[Mineralisation_-_Pathology#Calcification|calcified material]]. When cells begin to [[:Category:Degenerations and Infiltrations|degenerate]] or become [[:Category:Degenerations and Infiltrations|infiltrated]] by foreign material then cellular metabolism has been disrupted. The alteration in the structure of the cell can be suggestive of the metabolic abnormality that has occurred, and result in the cellular parameters extending beyond the normal physiological range for the cell.

There are several [[Cell Growth Disorders|changes in the size of cells]] and their respective organs that are commonly seen in pathological states:
*'''Atrophy''' is a decrease in the size of the cells and respective organ(s), occurring after the organ has reached it's normal size.
*'''Hypertrophy''' is an increase in the number of an organ due to an increase in size of the individual cells.
*'''Hypoplasia''' is a reduction in the number of cells and tissues due to a failure to grow to the normal size which ranges from mild hypoplasia to almost complete absence. Almost complete absence is also called vestigial or rudimentary.
*'''Aplasia''' and '''agensis''' refer to complete absence of tissue.
*'''Hyperplasia''' is an increase in the size of an organ due to an increase in the numbers of cells present within it. Hypertrophy and hyperplasia may occur concurrently.
*'''Metaplasia''' is a transformation of one type of tissue into another and occurs solely in connective tissue and epithelium.
*'''Dysplasia''' is abnormal growth within a tissue
*'''Anaplasia''' is a marked and irreversible loss of cellular differentiation with return to a more primitive state, which can be a feature of highly malignant tumours.
*'''Neoplasia''' is a serious disturbance of growth of tissues

The final pathological process that occurs at a cellular level is [[Necrosis - Pathology|necrosis]], which is the death of cells within the living body.
Two things happen when [[Necrosis - Pathology|necrosis]] occurs:
#Further changes can take place in the tissue itself.
#The surrounding unaffected living tissue can react to the necrotic tissue.

==Disease==
===Definition and Type===
'''Disease''' is a morbid (illness producing) process, having a characteristic train of symptoms or signs. It may affect the whole body or any of its parts, and the disease's aetiology, pathology and prognosis may be known or unknown.

There are two main categories of disease:
# '''Acute''' - characterised by sudden onset and short duration.
#* The outcome of acute disease may be:
#** Death
#** Resolution due to [[:Category:Immunology|host defence response]] or clinical therapy
#** Progression to chronic disease
# '''Chronic''' - characterised by insidious onset and protracted course.
#* The outcome of chronic disease may be:
#** Progressive destruction of tissue, which compromises function and endangers life,
#** The halting of the course of disease, with tissue repair by scarring.

===Factors Involved in the Development of Disease===
There are three factors which conspire with each other to produce disease.
#'''The individual animal''' - in particular, the animal's nutritional and immune status, which may be modified by recent or concurrent disease, and/or previous exposure to the agent(s) responsible.
#'''The disease-causing agent(s)'''. Most do not cause a uniform pattern of disease. The host defences are important in determining the presentation of the disease. An agent's capacity to produce disease depends upon the dose and the virulence of the agent. Bear in mind that several agents may be involved - often one agent debilitates, allowing others to exert a greater effect that normal within the body. The presence of an agent does not necessarily mean it is the cause of the disease! On occasions, a pathogenic agent may be absent from the tissues, due to either clinical therapy or the action of the host defence systems
#'''Environment''', for example: in the overcrowding of animals, mixing animals from differing origins and interaction with carriers are allowed to infect susceptible animals. Carriers are animals which harbour the pathogenic agent but do not show signs of disease. Changes in management routine may also affect susceptibility to disease.

===Types of Agents Causing Disease===
# '''Infectious organisms'''
#* [[Viruses|Viruses]]
#* [[Bacteria|Bacteria]]
#* [[Fungi|Fungi]]
#* [[Parasites|Parasites]]
# '''Physical'''
#* Trauma
#* Pressure
#* Heat
#* Cold
#* Radiation
# '''Chemical'''
#* Toxic organic and inorganic substances
#* Toxins produced by infectious organisms
# '''Nutritional'''
#* Deficiencies of vitamins and trace elements
#* Excess vitamins and trace elements
# '''[[Congenital and Neonatal Disease - Pathology|Genetic defects]]'''
#* There is a very wide range of potential defects; some are incompatible with life whilst others affect specific systems within the body

===Aspects of Disease===
There are many aspects of a disease that must be considered in order to understand it in full.
# '''Incidence''' refers to how much of the disease is present, where the disease is found and in what species is the disease seen?
# '''Aetiology''' refers to the causal agent(s) and includes predisposing factors
# '''Transmission''' describes how a disease is spread between individuals, and includes the important question 'is the disease zoonotic'?
# '''Pathogenesis''' describes how the causal agent(s) exert their effect within the body.
# '''Diagnosis''' - this is reached on considering the clinical history and findings with reference to the clinical examination and the presence of any pathology. Confirmation is reached by monitoring the response to treatment or by biopsy or post-mortem examination
# '''Prognosis and Treatment'''
# '''Control and Prevention'''

==Post-Mortem Examination==
Post-mortem examination (PME) investigates the observable structural changes in the animal. Information relating to the disease within the body or specific tissue is gained from PME, including information on the disease's aetiology and pathogenesis.

Several types of changes are encountered at post-mortem examination.
* Those due to the '''disease''', including [[Recognition and Description of Lesions|visible lesions]]
*Those occurring '''immediately prior to death''', known as [[Post-Mortem Change - Pathology#Agonal Changes|agonal changes]]
* Those occurring '''after death''', or [[Post-Mortem Change - Pathology|post-mortem]]

==Techniques Involved in Pathological Examination==

* '''Fluid examination''' e.g. blood, urine, discharges.
* '''Cytology''' - collect and examine cells in smears, aspirates and fluids.
* '''Necropsy''', which is a visual examination of the gross changes in the dead body.
* '''Histopathology'''; microscopic examination of:
** Tissues selected from the dead body after necropsy.
** Biopsy/excision materials from lesions in the living animal.
* '''Histochemistry'''; microscopic visualisation of enzymatic activity in tissues.
* '''Immunological methods''' such as testing for specific antibody activity in tissues and fluids.
** Examination of serum can show prior exposure to a particular infectious agent (i.e. specific antibodies).
** Specific antigens can be detected in tissues.
** When linked to a marking agent (e.g. a fluorescent dye), an antibody can localise its antigen in the tissue.
* '''Electronmicroscopy''' which reveals the fine detail of the surfaces or internal structures of cells.
* '''Bacteriology/ Virology/ Parasitology'''; these techniques allow the isolation and identification of pathogenic bacteria, viruses and parasites.
* '''Toxicology'''; analysis of tissues for particular poisons and toxins.

[[Category:General Pathology|A]]