https://en.wikivet.net/api.php?action=feedcontributions&feedformat=atom&user=Signarski 2026-05-01T23:36:49Z User contributions MediaWiki 1.35.0 https://en.wikivet.net/index.php?title=Hepatic_Abscessation&diff=93547 2010-09-29T20:58:29Z

<p>Signarski: </p> <hr /> <div>{unfinished}}<br /> <br /> ==Description==<br /> Hepatic abscessation occurs most commonly in cattle and is associated with a roughage-deficient or high concentrate diet. The disease is an important cause of economic losses due to reduced production efficiency and carcass condemnation or trimming. <br /> <br /> ==Pathogenesis==<br /> The main causative agent of hepatic abscessation is ''Fusobacterium necrophorum'', a gram-negative obligate anaerobe and a component of normal rumenal microflora. ''Arcanobacter pyogenes'', Staphylococci and Streptococci have also been associated with the disease. Damage of the wall of the rumen secondary to rumenal acidosis leads to embolisation of bacteria emboli from the inflamed rumen wall. The bacteria enter the hepatic portal system and are transmitted to the liver, leading to bacterial proliferation and abscess formation. Eventually the abscesses may heal via formation of a fibrous scar.<br /> <br /> ==Clinical Signs==<br /> Clinical signs are a rare feature of the disease and abscesses are frequently only observed as incidental findings at slaughter or post mortem. Detailed clinical examination may reveal signs including pyrexia, depression and weight loss. Evidence of abdominal pain may be present including signs such as bruxism, grunting and abduction of the elbows. There may be a history of change in diet from pasture to a high-concentrate ration, as well as anorexia and reduced milk production. Clinical signs of caudal vena cava thrombosis may be apparent if abscesses have involved the posterior vena cava, including chronic diarrhoea, emaciation, ascites and distension of subcutaneous abdominal veins. <br /> <br /> Rupture of hepatic abscesses is associated with anaphylactic shock and death. In these cases, the lungs appear markedly oedematous and collapsed at post mortem.<br /> <br /> ==Diagnosis==<br /> Ultrasonographic examination of the liver is a valuable diagnostic tool for determing the location and size of the abscesses and for determining a prognosis. Serum biochemistry may reveal a neutrophilic leucocytosis and increased serum globulin and fibrinogen. Other laboratory changes frequently observed include increased GGT, SDH and bilirubin. Occasionally, radiographs may reveal displacement of the diaphragm if the liver abscess is large. <br /> <br /> ==Treatment==<br /> If hepatic abscesses have been diagnosed and located it is possible to consider antibiotic or surgical therapy. Systemically administered penicillin treatment may be successful in cows with smaller, hypoechoic abscesses but recurrence of disease is common unless treatment is given for 4 weeks or longer. Successful surgical treatment has been described but the prognosis is poor for animals with large, hyperechoic abscesses that have caused clinical signs.<br /> <br /> ==Prevention==<br /> The main aim of prevention of hepatic abscessation is to control rumen acidosis by feeding a diet that is adequate in roughage. Multiple daily feedings may aid in increasing mastication and saliva production, increasing buffer to the rumen and reducing intrarumenal acidity.<br /> <br /> ==References==<br /> *Divers, T. J., Peek, S. F. (2008) '''Rebhun's Diseases of Dairy Cattle''' ''Elsevier Health Sciences''<br /> <br /> [[Category:To_Do_-_SophieIgnarski]]<br /> [[Category:To_Do_-_Review]]</div>

Signarski https://en.wikivet.net/index.php?title=Hepatic_Abscessation&diff=93546 2010-09-29T20:55:59Z

<p>Signarski: </p> <hr /> <div>{unfinished}}<br /> <br /> ==Description==<br /> Hepatic abscessation occurs most commonly in cattle and is associated with a roughage-deficient or high concentrate diet. The disease is an important cause of economic losses due to reduced production efficiency and carcass condemnation or trimming. <br /> <br /> ==Pathogenesis==<br /> The main causative agent of hepatic abscessation is ''Fusobacterium necrophorum'', a gram-negative obligate anaerobe and a component of normal rumenal microflora. ''Arcanobacter pyogenes'', Staphylococci and Streptococci have also been associated with the disease. Damage of the wall of the rumen secondary to rumenal acidosis leads to embolisation of bacteria emboli from the inflamed rumen wall. The bacteria enter the hepatic portal system and are transmitted to the liver, leading to bacterial proliferation and abscess formation. Eventually the abscesses may heal via formation of a fibrous scar.<br /> <br /> ==Clinical Signs==<br /> Clinical signs are a rare feature of the disease and abscesses are frequently only observed as incidental findings at slaughter or post mortem. Detailed clinical examination may reveal signs of pyrexia, depression and weight loss. Evidence of abdominal pain may be present such as bruxism, grunting and abduction of the elbows. There may be a history of change in diet from pasture to a high-concentrate ration, as well as anorexia and reduced milk production. Clinical signs of caudal vena cava thrombosis may be apparent if abscesses have involved the posterior vena cava, including chronic diarrhoea, emaciation, ascites and distension of subcutaneous abdominal veins. <br /> <br /> Rupture of hepatic abscesses is associated with anaphylactic shock and death. In these cases, the lungs appear markedly oedematous and collapsed at post mortem.<br /> <br /> ==Diagnosis==<br /> Ultrasonographic examination of the liver is a valuable diagnostic tool for determing the location and size of the abscesses and for determining a prognosis. Serum biochemistry may reveal a neutrophilic leucocytosis and increased serum globulin and fibrinogen. Other laboratory changes frequently observed include increased GGT, SDH and bilirubin. Occasionally, radiographs may reveal displacement of the diaphragm if the liver abscess is large. <br /> <br /> ==Treatment==<br /> If hepatic abscesses have been diagnosed and located it is possible to consider antibiotic or surgical therapy. Systemically administered penicillin treatment may be successful in cows with smaller, hypoechoic abscesses but recurrence of disease is common unless treatment is given for 4 weeks or longer. Successful surgical treatment has been described but the prognosis is poor for animals with large, hyperechoic abscesses that have caused clinical signs.<br /> <br /> ==Prevention==<br /> The main aim of prevention of hepatic abscessation is to control rumen acidosis by feeding a diet that is adequate in roughage. Multiple daily feedings may aid in increasing mastication and saliva production, increasing buffer to the rumen and reducing intrarumenal acidity.<br /> <br /> ==References==<br /> *Divers, T. J., Peek, S. F. (2008) '''Rebhun's Diseases of Dairy Cattle''' ''Elsevier Health Sciences''<br /> <br /> [[Category:To_Do_-_SophieIgnarski]]<br /> [[Category:To_Do_-_Review]]</div>

Signarski https://en.wikivet.net/index.php?title=Hepatic_Abscessation&diff=93545 2010-09-29T20:51:42Z

<p>Signarski: </p> <hr /> <div>{unfinished}}<br /> <br /> ==Description==<br /> Hepatic abscessation occurs most commonly in cattle and is associated with a roughage-deficient or high concentrate diet. The disease is an important cause of economic losses due to reduced production efficiency and carcass condemnation or trimming. <br /> <br /> ==Pathogenesis==<br /> The main causative agent of hepatic abscessation is ''Fusobacterium necrophorum'', a gram-negative obligate anaerobe and a component of normal rumenal microflora. ''Arcanobacter pyogenes'', Staphylococci and Streptococci have also been associated with the disease. Damage of the wall of the rumen secondary to rumenal acidosis leads to embolisation of bacteria emboli from the inflamed rumen wall. The bacteria enter the hepatic portal system and are transmitted to the liver, leading to bacterial proliferation and abscess formation. Eventually the abscesses may heal via formation of a fibrous scar.<br /> <br /> ==Clinical Signs==<br /> Clinical signs are a rare feature of the disease and abscesses are frequently only observed as incidental findings at slaughter or post mortem. Detailed clinical examination may reveal signs of pyrexia, depression and weight loss. Evidence of abdominal pain may be present such as bruxism, grunting and abduction of the elbows. There may be a history of change in diet from pasture to a high-concentrate ration, as well as anorexia and reduced milk production. Clinical signs of caudal vena cava thrombosis may be apparent if abscesses have involved the posterior vena cava, including chronic diarrhoea, emaciation, ascites and distension of subcutaneous abdominal veins. <br /> <br /> Rupture of hepatic abscesses is associated with anaphylactic shock and death. In these cases, the lungs appear markedly oedematous and collapsed at post mortem.<br /> <br /> ==Diagnosis==<br /> Ultrasonographic examination of the liver is a valuable diagnostic tool for determing the location and size of the abscesses and for determining a prognosis. Serum biochemistry may reveal a neutrophilic leucocytosis and increased serum globulin and fibrinogen. Other laboratory changes frequently observed include increased GGT, SDH and bilirubin. Occasionally, radiographs may reveal displacement of the diaphragm if the liver abscess is large. <br /> <br /> ==Treatment==<br /> If hepatic abscesses have been diagnosed and located it is possible to consider antibiotic or surgical therapy. Penicillin treatment may be successful in cows with smaller, hypoechoic abscesses but recurrence of disease is common unless treatment is given for 4 weeks or longer. Successful surgical treatment has been described but the prognosis is poor for animals with large, hyperechoic abscesses that have caused clinical signs.<br /> <br /> ==References==<br /> *Divers, T. J., Peek, S. F. (2008) '''Rebhun's Diseases of Dairy Cattle''' ''Elsevier Health Sciences''<br /> <br /> [[Category:To_Do_-_Clinical]]</div>

Signarski https://en.wikivet.net/index.php?title=Hepatic_Abscessation&diff=93544 2010-09-29T20:43:12Z

<p>Signarski: </p> <hr /> <div>{unfinished}}<br /> <br /> ==Description==<br /> Hepatic abscessation occurs most commonly in cattle and is associated with a roughage-deficient or high concentrate diet. The disease is a common cause of economic losses due to reduced production efficiency and carcass condemnation or trimming. <br /> <br /> ==Pathogenesis==<br /> The main causative agent of hepatic abscessation is ''Fusobacterium necrophorum'', a gram-negative obligate anaerobe and a component of normal rumenal microflora. ''Arcanobacter pyogenes'', Staphylococci and Streptococci have also been associated with the disease. Damage of the wall of the rumen secondary to rumenal acidosis leads to embolisation of bacteria emboli from the inflamed rumen wall. The bacteria enter the hepatic portal system and are transmitted to the liver, leading to bacterial proliferation and abscess formation. Eventually the abscesses may heal via formation of a fibrous scar.<br /> <br /> ==Clinical Signs==<br /> Clinical signs are a rare feature of the disease and abscesses are frequently only observed as incidental findings at slaughter or post mortem. Detailed clinical examination may reveal signs of pyrexia, depression and weight loss. Evidence of abdominal pain may be present such as bruxism, grunting and abduction of the elbows. There may be a history of change in diet from pasture to a high-concentrate ration, as well as anorexia and reduced milk production. Clinical signs of caudal vena cava thrombosis may be apparent if abscesses have involved the posterior vena cava, including chronic diarrhoea, emaciation, ascites and distension of subcutaneous abdominal veins. <br /> <br /> Rupture of hepatic abscesses is associated with anaphylactic shock and death. In these cases, the lungs appear markedly oedematous and collapsed at post mortem.<br /> <br /> ==Diagnosis==<br /> Ultrasonographic examination of the liver is a valuable diagnostic tool for determing the location and size of the abscesses and for determining a prognosis. Serum biochemistry may reveal a neutrophilic leucocytosis and increased serum globulin and fibrinogen. Other laboratory changes frequently observed include increased GGT, SDH and bilirubin. Occasionally, radiographs may reveal displacement of the diaphragm if the liver abscess is large. <br /> <br /> ==Treatment==<br /> If hepatic abscesses have been diagnosed and located it is possible to consider antibiotic or surgical therapy.<br /> <br /> ==References==<br /> *Divers, T. J., Peek, S. F. (2008) '''Rebhun's Diseases of Dairy Cattle''' ''Elsevier Health Sciences''<br /> <br /> [[Category:To_Do_-_Clinical]]</div>

Signarski https://en.wikivet.net/index.php?title=Hepatic_Abscessation&diff=93543 2010-09-29T20:35:12Z

<p>Signarski: </p> <hr /> <div>{unfinished}}<br /> <br /> ==Description==<br /> Hepatic abscessation occurs most commonly in cattle and is associated with a roughage-deficient or high concentrate diet. The disease is a common cause of economic losses due to reduced production efficiency and carcass condemnation or trimming. <br /> <br /> ==Pathogenesis==<br /> The main causative agent of hepatic abscessation is ''Fusobacterium necrophorum'', a gram-negative obligate anaerobe and a component of normal rumenal microflora. ''Arcanobacter pyogenes'', Staphylococci and Streptococci have also been associated with the disease. Damage of the wall of the rumen secondary to rumenal acidosis leads to embolisation of bacteria emboli from the inflamed rumen wall. The bacteria enter the hepatic portal system and are transmitted to the liver, leading to bacterial proliferation and abscess formation. Eventually the abscesses may heal via formation of a fibrous scar.<br /> <br /> ==Clinical Signs==<br /> Clinical signs are a rare feature of the disease and abscesses are frequently only observed as incidental findings at slaughter or post mortem. Detailed clinical examination may reveal signs of pyrexia, depression and weight loss. Evidence of abdominal pain may be present such as bruxism, grunting and abduction of the elbows. There may be a history of change in diet from pasture to a high-concentrate ration, as well as anorexia and reduced milk production. Clinical signs of caudal vena cava thrombosis may be apparent if abscesses have involved the posterior vena cava, including chronic diarrhoea, emaciation, ascites and distension of subcutaneous abdominal veins. <br /> <br /> Rupture of hepatic abscesses is associated with anaphylactic shock and death. In these cases, the lungs appear markedly oedematous and collapsed at post mortem.<br /> <br /> ==Diagnosis==<br /> <br /> <br /> <br /> ==References==<br /> *Divers, T. J., Peek, S. F. (2008) '''Rebhun's Diseases of Dairy Cattle''' ''Elsevier Health Sciences''<br /> <br /> [[Category:To_Do_-_Clinical]]</div>

Signarski https://en.wikivet.net/index.php?title=Hepatic_Abscessation&diff=93526 2010-09-29T20:05:53Z

<p>Signarski: </p> <hr /> <div>{unfinished}}<br /> <br /> ==Description==<br /> Hepatic abscessation occurs most commonly in cattle and is a common cause of economic losses due to carcass condemnation and reduced production efficiency. The disease is associated with a change from pasture to a high concentrate ration that predisposes to the development of rumenitis. <br /> <br /> ==Pathogenesis==<br /> The main causative agent of the disease is ''Fusobacterium necrophorum'', a gram-negative obligate anaerobe and a component of normal rumenal microflora. ''Arcanobacter pyogenes'' has also been implicated in the disease. Damage of the wall of the rumen secondary to rumenal acidosis leads to bacteraemia. Bacterial emboli from the inflamed rumen wall enter the hepatic portal system and are transmitted to the liver, leading to abscess formation. <br /> <br /> ==Clinical Signs==<br /> Clinical signs are a rare feature of the disease and abscesses are frequently only observed as incidental findings at slaughter or post mortem. Detailed clinical examination may reveal signs of pyrexia, depression and weight loss. Evidence of abdominal pain may be present such as bruxism, grunting when pressure is applied to the xiphisternum and abduction of the elbows. There may be a history of feeding of a high-concentrate ration, anorexia and reduced milk production. <br /> Rupture of the abscesses is associated with anaphylactic shock and death.<br /> <br /> <br /> ==References==<br /> *Divers, T. J., Peek, S. F. (2008) '''Rebhun's Diseases of Dairy Cattle''' ''Elsevier Health Sciences''<br /> <br /> [[Category:To_Do_-_Clinical]]</div>

Signarski https://en.wikivet.net/index.php?title=Newcastle_Disease_Virus&diff=93515 2010-09-29T19:36:51Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Newcastle disease virus (NDV) (Avian Paramyxovirus type 1) is the causative agent of Newcastle Disease, an acute viral disease of domestic poultry and many other bird species that is usually fatal. It is characterised primarily by respiratory signs but neurological and gastrointestinal forms of the disease may also be seen. The disease is notifiable in the UK but virulent strains of the virus are endemic in most of Asia and Africa and South America. Sporadic cases of the disease have been reported in North America following importation of infected birds.<br /> <br /> ==Transmission==<br /> Hosts of the virus include gallinaceous birds, pigeons, parrots and finches and the disease may be carried subclinically by ducks and ostriches. Infected birds are the primary source of infection and shed the virus through droppings and secretions from the nose, mouth and eyes. The virus may also be present in eggs laid during clinical disease. NDV is commonly transferred by the movement of people and contaminated equipment and birds are easily infected by inhalation of the virus or ingestion of contaminated feed or water.<br /> <br /> ==Clinical signs==<br /> NDV affects the gastrointestinal, respiratory and nervous systems and clinical signs reflect the system(s) affected. Clinical signs are usually acute and may appear throughout the flock within 2-12 days with young birds particularly susceptible to the disease. Signs in affected birds may be variable and a subclinical form of the disease can occur, which may only be suspected following a drop in egg production. Respiratory signs may include dyspnoea, sneezing, nasal discharge and coughing and are common with low virulence infections. Neurological signs such as tremors, paralysis, circling and depression may accompany respiratory signs and are often seen in cormorants and exotic bird species. Pigeons frequently display neurological signs accompanied by diarrhoea.<br /> <br /> Post mortem lesions include sacculitis, tracheitis and petechiae on the serous membranes. The proventricular mucosa is frequently haemorrhagic with necrotic plaques. In birds infected with the less virulent strains of NDV the lesions may be restricted to congestion of the respiratory tract and thickening and opacification of the air sacs.<br /> <br /> [[Image:Newcastle Disease.jpg|150px|thumb|right|''Newcastle Disease'' &lt;br&gt; L. Mahin, Wikimedia Commons]]<br /> <br /> ==Diagnosis and management==<br /> Diagnosis is commonly performed using ELISA or PCR. In the UK, Newcastle Disease is notifiable and if suspected, must be reported to DEFRA. If the disease is suspected, movement of birds, people, animals, eggs and vehicles may be prevented pending investigation by an Animal Health Veterinary Inspector. If the disease is confirmed, all poultry on the premises must be slaughtered and eggs must be destroyed. Thorough cleaning and disinfection of the premises must be carried out and an infected premises may not be re-stocked until at least 21 days after this has been completed.<br /> <br /> ==Control==<br /> In the event of an outbreak of Newcastle Disease, a compulsory vaccination zone is imposed. Two types of vaccine are available; inactivated and live vaccines. Live vaccines are more commonly used as they can be delivered by spray, drinking water or aerosolisation, whereas inactivated vaccines can only be delivered via direct innoculation.<br /> <br /> Prevention of the disease may be achieved by adopting stringent biosecurity measures, vaccinating birds, ensuring good sanitation, using all-in-all-out management systems and ensuring new stock are quarantined before entering the flock.<br /> <br /> ==References==<br /> *DEFRA website: http://www.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/newcastle/disease-factsheet.htm#7<br /> *Kahn, C. M., Merck, Line, S. (2010) '''The Merck Veterinary Manual''' ''John Wiley and Sons''<br /> <br /> [[Category:Paramyxovirinae]][[Category:Poultry]][[Category:Birds]]<br /> [[Category:To_Do_-_SophieIgnarski]]<br /> [[Category:To_Do_-_Review]]</div>

Signarski https://en.wikivet.net/index.php?title=Newcastle_Disease_Virus&diff=93514 2010-09-29T19:34:06Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Newcastle disease virus (NDV) (Avian Paramyxovirus type 1) is the causative agent of Newcastle Disease, an acute viral disease of domestic poultry and many other bird species that is usually fatal. It is characterised primarily by respiratory signs but neurological and gastrointestinal forms of the disease may also be seen. The disease is notifiable in the UK but virulent strains of the virus are endemic in most of Asia and Africa and South America. Sporadic cases of the disease have been reported in North America following importation of infected birds.<br /> <br /> ==Transmission==<br /> Hosts of the virus include gallinaceous birds, pigeons, parrots and finches and the disease may be carried subclinically by ducks and ostriches. Infected birds are the primary source of infection and shed the virus through droppings and secretions from the nose, mouth and eyes. The virus may also be present in eggs laid during clinical disease. NDV is commonly transferred by the movement of people and contaminated equipment and birds are easily infected by inhalation of the virus or ingestion of contaminated feed or water.<br /> <br /> ==Clinical signs==<br /> NDV affects the gastrointestinal, respiratory and nervous systems and clinical signs reflect the system(s) affected. Clinical signs are usually acute and may appear throughout the flock within 2-12 days with young birds particularly susceptible to the disease. Signs in affected birds may be variable and a subclinical form of the disease can occur, which may only be suspected following a drop in egg production. Respiratory signs may include dyspnoea, sneezing, nasal discharge and coughing and are common with low virulence infections. Neurological signs such as tremors, paralysis, circling and depression may accompany respiratory signs and are often seen in cormorants and exotic bird species. Pigeons frequently display neurological signs accompanied by diarrhoea.<br /> <br /> Post mortem lesions include sacculitis, tracheitis and petechiae on the serous membranes. The proventricular mucosa is frequently haemorrhagic with necrotic plaques. In birds infected with the less virulent strains of NDV the lesions may be restricted to congestion of the respiratory tract and thickening and opacification of the air sacs.<br /> <br /> [[Image:Newcastle Disease.jpg|150px|thumb|right|''Newcastle Disease'' &lt;br&gt; L. Mahin, Wikimedia Commons]]<br /> <br /> ==Diagnosis and management==<br /> Diagnosis is commonly performed using ELISA or PCR. In the UK, Newcastle Disease is notifiable and if suspected, must be reported to DEFRA. If the disease is suspected, movement of birds, people, animals, eggs and vehicles may be prevented pending investigation by an Animal Health Veterinary Inspector. If the disease is confirmed, all poultry on the premises must be slaughtered and eggs must be destroyed. Thorough cleaning and disinfection of the premises must be carried out and an infected premises may not be re-stocked until at least 21 days after this has been completed.<br /> <br /> ==Control==<br /> In the event of an outbreak of Newcastle Disease, a compulsory vaccination zone is imposed. Two types of vaccine are available; inactivated and live vaccines. Live vaccines are more commonly used as they can be delivered by spray, drinking water or aerosolisation, whereas inactivated vaccines can only be delivered via direct innoculation.<br /> <br /> ==References==<br /> *DEFRA website: http://www.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/newcastle/disease-factsheet.htm#7<br /> *Kahn, C. M., Merck, Line, S. (2010) '''The Merck Veterinary Manual''' ''John Wiley and Sons''<br /> <br /> [[Category:Paramyxovirinae]][[Category:Poultry]][[Category:Birds]]<br /> [[Category:To_Do_-_SophieIgnarski]]<br /> [[Category:To_Do_-_Review]]</div>

Signarski https://en.wikivet.net/index.php?title=Newcastle_Disease_Virus&diff=93513 2010-09-29T19:33:13Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Newcastle disease virus (NDV) (Avian Paramyxovirus type 1) is the causative agent of Newcastle Disease, an acute viral disease of domestic poultry and many other bird species that is usually fatal. It is characterised primarily by respiratory signs but neurological and gastrointestinal forms of the disease may also be seen. The disease is notifiable in the UK but virulent strains of the virus are endemic in most of Asia and Africa and South America. Sporadic cases of the disease have been reported in North America following importation of infected birds.<br /> <br /> ==Transmission==<br /> Hosts of the virus include gallinaceous birds, pigeons, parrots and finches and the disease may be carried subclinically by ducks and ostriches. Infected birds are the primary source of infection and shed the virus through droppings and secretions from the nose, mouth and eyes. The virus may also be present in eggs laid during clinical disease. NDV is commonly transferred by the movement of people and contaminated equipment and birds are easily infected by inhalation of the virus or ingestion of contaminated feed or water.<br /> <br /> ==Clinical signs==<br /> NDV affects the gastrointestinal, respiratory and nervous systems and clinical signs reflect the system(s) affected. Clinical signs are usually acute and may appear throughout the flock within 2-12 days with young birds particularly susceptible to the disease. Signs in affected birds may be variable and a subclinical form of the disease can occur, which may only be suspected following a drop in egg production. Respiratory signs may include dyspnoea, sneezing, nasal discharge and coughing and are common with low virulence infections. Neurological signs such as tremors, paralysis, circling and depression may accompany respiratory signs and are often seen in cormorants and exotic bird species. Pigeons frequently display neurological signs accompanied by diarrhoea.<br /> <br /> Post mortem lesions include sacculitis, tracheitis and petechiae on the serous membranes. The proventricular mucosa is frequently haemorrhagic with necrotic plaques. In birds infected with the less virulent strains of NDV the lesions may be restricted to congestion of the respiratory tract and thickening and opacification of the air sacs.<br /> <br /> [[Image:Newcastle Disease.jpg|150px|thumb|right|''Newcastle Disease'' &lt;br&gt; L. Mahin, Wikimedia Commons]]<br /> <br /> ==Diagnosis==<br /> Diagnosis is commonly performed using ELISA or PCR. In the UK, Newcastle Disease is notifiable and if suspected, must be reported to DEFRA. If the disease is suspected, movement of birds, people, animals, eggs and vehicles may be prevented pending investigation by an Animal Health Veterinary Inspector. If the disease is confirmed, all poultry on the premises must be slaughtered and eggs must be destroyed. Thorough cleaning and disinfection of the premises must be carried out and an infected premises may not be re-stocked until at least 21 days after this has been completed.<br /> <br /> ==Control==<br /> In the event of an outbreak of Newcastle Disease, a compulsory vaccination zone is imposed. Two types of vaccine are available; inactivated and live vaccines. Live vaccines are more commonly used as they can be delivered by spray, drinking water or aerosolisation, whereas inactivated vaccines can only be delivered via direct innoculation.<br /> <br /> ==References==<br /> *DEFRA website: http://www.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/newcastle/disease-factsheet.htm#7<br /> *Kahn, C. M., Merck, Line, S. (2010) '''The Merck Veterinary Manual''' ''John Wiley and Sons''<br /> <br /> [[Category:Paramyxovirinae]][[Category:Poultry]][[Category:Birds]]<br /> [[Category:To_Do_-_Clinical]]</div>

Signarski https://en.wikivet.net/index.php?title=Newcastle_Disease_Virus&diff=93512 2010-09-29T19:32:42Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Newcastle disease virus (NDV) (Avian Paramyxovirus type 1) is the causative agent of Newcastle Disease, an acute viral disease of domestic poultry and many other bird species that is usually fatal. It is characterised primarily by respiratory signs but neurological and gastrointestinal forms of the disease may also be seen. The disease is notifiable in the UK but virulent strains of the virus are endemic in most of Asia and Africa and South America. Sporadic cases of the disease have been reported in North America following importation of infected birds.<br /> <br /> ==Transmission==<br /> Hosts of the virus include gallinaceous birds, pigeons, parrots and finches and the disease may be carried subclinically by ducks and ostriches. Infected birds are the primary source of infection and shed the virus through droppings and secretions from the nose, mouth and eyes. The virus may also be present in eggs laid during clinical disease. NDV is commonly transferred by the movement of people and contaminated equipment and birds are easily infected by inhalation of the virus or ingestion of contaminated feed or water.<br /> <br /> ==Clinical signs==<br /> NDV affects the gastrointestinal, respiratory and nervous systems and clinical signs reflect the system(s) affected. Clinical signs are usually acute and may appear throughout the flock within 2-12 days with young birds particularly susceptible to the disease. Signs in affected birds may be variable and a subclinical form of the disease can occur, which may only be suspected following a drop in egg production. Respiratory signs may include dyspnoea, sneezing, nasal discharge and coughing and are common with low virulence infections. Neurological signs such as tremors, paralysis, circling and depression may accompany respiratory signs and are often seen in cormorants and exotic bird species. Pigeons frequently display neurological signs accompanied by diarrhoea.<br /> <br /> Post mortem lesions include sacculitis, tracheitis and petechiae on the serous membranes. The proventricular mucosa is frequently haemorrhagic with necrotic plaques. In birds infected with the less virulent strains of NDV the lesions may be restricted to congestion of the respiratory tract. <br /> <br /> [[Image:Newcastle Disease.jpg|150px|thumb|right|''Newcastle Disease'' &lt;br&gt; L. Mahin, Wikimedia Commons]]<br /> <br /> ==Diagnosis==<br /> Diagnosis is commonly performed using ELISA or PCR. In the UK, Newcastle Disease is notifiable and if suspected, must be reported to DEFRA. If the disease is suspected, movement of birds, people, animals, eggs and vehicles may be prevented pending investigation by an Animal Health Veterinary Inspector. If the disease is confirmed, all poultry on the premises must be slaughtered and eggs must be destroyed. Thorough cleaning and disinfection of the premises must be carried out and an infected premises may not be re-stocked until at least 21 days after this has been completed.<br /> <br /> ==Control==<br /> In the event of an outbreak of Newcastle Disease, a compulsory vaccination zone is imposed. Two types of vaccine are available; inactivated and live vaccines. Live vaccines are more commonly used as they can be delivered by spray, drinking water or aerosolisation, whereas inactivated vaccines can only be delivered via direct innoculation.<br /> <br /> ==References==<br /> *DEFRA website: http://www.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/newcastle/disease-factsheet.htm#7<br /> *Kahn, C. M., Merck, Line, S. (2010) '''The Merck Veterinary Manual''' ''John Wiley and Sons''<br /> <br /> [[Category:Paramyxovirinae]][[Category:Poultry]][[Category:Birds]]<br /> [[Category:To_Do_-_Clinical]]</div>

Signarski https://en.wikivet.net/index.php?title=Newcastle_Disease_Virus&diff=93511 2010-09-29T19:32:17Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Newcastle disease virus (NDV) (Avian Paramyxovirus type 1) is the causative agent of Newcastle Disease, an acute viral disease of domestic poultry and many other bird species that is usually fatal. It is characterised primarily by respiratory signs but neurological and gastrointestinal forms of the disease may also be seen. The disease is notifiable in the UK but virulent strains of the virus are endemic in most of Asia and Africa and South America. Sporadic cases of the disease have been reported in North America following importation of infected birds.<br /> <br /> ==Transmission==<br /> Hosts of the virus include gallinaceous birds, pigeons, parrots and finches and the disease may be carried subclinically by ducks and ostriches. Infected birds are the primary source of infection and shed the virus through droppings and secretions from the nose, mouth and eyes. The virus may also be present in eggs laid during clinical disease. NDV is commonly transferred by the movement of people and contaminated equipment and birds are easily infected by inhalation of the virus or ingestion of contaminated feed or water.<br /> <br /> ==Clinical signs==<br /> NDV affects the gastrointestinal, respiratory and nervous systems and clinical signs reflect the system(s) affected. Clinical signs are usually acute and may appear throughout the flock within 2-12 days with young birds particularly susceptible to the disease. Signs in affected birds may be variable and a subclinical form of the disease can occur, which may only be suspected following a drop in egg production. Respiratory signs may include dyspnoea, sneezing, nasal discharge and coughing and are common with low virulence infections. Neurological signs such as tremors, paralysis, circling and depression may accompany respiratory signs and are often seen in cormorants and exotic bird species. Pigeons frequently display neurological signs accompanied by diarrhoea.<br /> <br /> Post mortem lesions include sacculitis, tracheitis and petechia on the serous membranes. The proventricular mucosa is frequently haemorrhagic with necrotic plaques. In birds infected with the less virulent strains of NDV the lesions may be restricted to congestion of the respiratory tract. <br /> <br /> [[Image:Newcastle Disease.jpg|150px|thumb|right|''Newcastle Disease'' &lt;br&gt; L. Mahin, Wikimedia Commons]]<br /> <br /> ==Diagnosis==<br /> Diagnosis is commonly performed using ELISA or PCR. In the UK, Newcastle Disease is notifiable and if suspected, must be reported to DEFRA. If the disease is suspected, movement of birds, people, animals, eggs and vehicles may be prevented pending investigation by an Animal Health Veterinary Inspector. If the disease is confirmed, all poultry on the premises must be slaughtered and eggs must be destroyed. Thorough cleaning and disinfection of the premises must be carried out and an infected premises may not be re-stocked until at least 21 days after this has been completed.<br /> <br /> ==Control==<br /> In the event of an outbreak of Newcastle Disease, a compulsory vaccination zone is imposed. Two types of vaccine are available; inactivated and live vaccines. Live vaccines are more commonly used as they can be delivered by spray, drinking water or aerosolisation, whereas inactivated vaccines can only be delivered via direct innoculation.<br /> <br /> ==References==<br /> *DEFRA website: http://www.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/newcastle/disease-factsheet.htm#7<br /> *Kahn, C. M., Merck, Line, S. (2010) '''The Merck Veterinary Manual''' ''John Wiley and Sons''<br /> <br /> [[Category:Paramyxovirinae]][[Category:Poultry]][[Category:Birds]]<br /> [[Category:To_Do_-_Clinical]]</div>

Signarski https://en.wikivet.net/index.php?title=Newcastle_Disease_Virus&diff=93510 2010-09-29T19:31:27Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Newcastle disease virus (NDV) (Avian Paramyxovirus type 1) is the causative agent of Newcastle Disease, an acute viral disease of domestic poultry and many other bird species that is usually fatal. It is characterised primarily by respiratory signs but neurological and gastrointestinal forms of the disease may also be seen. The disease is notifiable in the UK but virulent strains of the virus are endemic in most of Asia and Africa and South America. Sporadic cases of the disease have been reported in North America following importation of infected birds.<br /> <br /> ==Transmission==<br /> Hosts of the virus include gallinaceous birds, pigeons, parrots and finches and the disease may be carried subclinically by ducks and ostriches. Infected birds are the primary source of infection and shed the virus through droppings and secretions from the nose, mouth and eyes. The virus may also be present in eggs laid during clinical disease. NDV is commonly transferred by the movement of people and contaminated equipment and birds are easily infected by inhalation of the virus or ingestion of contaminated feed or water.<br /> <br /> ==Clinical signs==<br /> NDV affects the gastrointestinal, respiratory and nervous systems and clinical signs reflect the system(s) affected. Clinical signs are usually acute and may appear throughout the flock within 2-12 days with young birds particularly susceptible. Signs in affected birds may be variable and a subclinical form of the disease can occur, which may only be suspected following a drop in egg production. Respiratory signs may include dyspnoea, sneezing, nasal discharge and coughing and are common with low virulence infections. Neurological signs such as tremors, paralysis, circling and depression may accompany respiratory signs and are often seen in cormorants and exotic bird species. Pigeons frequently display neurological signs accompanied by diarrhoea.<br /> <br /> Post mortem lesions include sacculitis, tracheitis and petechia on the serous membranes. The proventricular mucosa is frequently haemorrhagic with necrotic plaques. In birds infected with the less virulent strains of NDV the lesions may be restricted to congestion of the respiratory tract. <br /> <br /> [[Image:Newcastle Disease.jpg|150px|thumb|right|''Newcastle Disease'' &lt;br&gt; L. Mahin, Wikimedia Commons]]<br /> <br /> ==Diagnosis==<br /> Diagnosis is commonly performed using ELISA or PCR. In the UK, Newcastle Disease is notifiable and if suspected, must be reported to DEFRA. If the disease is suspected, movement of birds, people, animals, eggs and vehicles may be prevented pending investigation by an Animal Health Veterinary Inspector. If the disease is confirmed, all poultry on the premises must be slaughtered and eggs must be destroyed. Thorough cleaning and disinfection of the premises must be carried out and an infected premises may not be re-stocked until at least 21 days after this has been completed.<br /> <br /> ==Control==<br /> In the event of an outbreak of Newcastle Disease, a compulsory vaccination zone is imposed. Two types of vaccine are available; inactivated and live vaccines. Live vaccines are more commonly used as they can be delivered by spray, drinking water or aerosolisation, whereas inactivated vaccines can only be delivered via direct innoculation.<br /> <br /> ==References==<br /> *DEFRA website: http://www.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/newcastle/disease-factsheet.htm#7<br /> *Kahn, C. M., Merck, Line, S. (2010) '''The Merck Veterinary Manual''' ''John Wiley and Sons''<br /> <br /> [[Category:Paramyxovirinae]][[Category:Poultry]][[Category:Birds]]<br /> [[Category:To_Do_-_Clinical]]</div>

Signarski https://en.wikivet.net/index.php?title=Newcastle_Disease_Virus&diff=93509 2010-09-29T19:31:06Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Newcastle disease virus (NDV) (Avian Paramyxovirus type 1) is the causative agent of Newcastle Disease, an acute viral disease of domestic poultry and many other bird species that is usually fatal. It is characterised primarily by respiratory signs but neurological and gastrointestinal forms of the disease may also be seen. The disease is notifiable in the UK but virulent strains of the virus are endemic in most of Asia and Africa and South America. Sporadic cases of the disease have been reported in North America following importaion of infected birds.<br /> <br /> ==Transmission==<br /> Hosts of the virus include gallinaceous birds, pigeons, parrots and finches and the disease may be carried subclinically by ducks and ostriches. Infected birds are the primary source of infection and shed the virus through droppings and secretions from the nose, mouth and eyes. The virus may also be present in eggs laid during clinical disease. NDV is commonly transferred by the movement of people and contaminated equipment and birds are easily infected by inhalation of the virus or ingestion of contaminated feed or water.<br /> <br /> ==Clinical signs==<br /> NDV affects the gastrointestinal, respiratory and nervous systems and clinical signs reflect the system(s) affected. Clinical signs are usually acute and may appear throughout the flock within 2-12 days with young birds particularly susceptible. Signs in affected birds may be variable and a subclinical form of the disease can occur, which may only be suspected following a drop in egg production. Respiratory signs may include dyspnoea, sneezing, nasal discharge and coughing and are common with low virulence infections. Neurological signs such as tremors, paralysis, circling and depression may accompany respiratory signs and are often seen in cormorants and exotic bird species. Pigeons frequently display neurological signs accompanied by diarrhoea.<br /> <br /> Post mortem lesions include sacculitis, tracheitis and petechia on the serous membranes. The proventricular mucosa is frequently haemorrhagic with necrotic plaques. In birds infected with the less virulent strains of NDV the lesions may be restricted to congestion of the respiratory tract. <br /> <br /> [[Image:Newcastle Disease.jpg|150px|thumb|right|''Newcastle Disease'' &lt;br&gt; L. Mahin, Wikimedia Commons]]<br /> <br /> ==Diagnosis==<br /> Diagnosis is commonly performed using ELISA or PCR. In the UK, Newcastle Disease is notifiable and if suspected, must be reported to DEFRA. If the disease is suspected, movement of birds, people, animals, eggs and vehicles may be prevented pending investigation by an Animal Health Veterinary Inspector. If the disease is confirmed, all poultry on the premises must be slaughtered and eggs must be destroyed. Thorough cleaning and disinfection of the premises must be carried out and an infected premises may not be re-stocked until at least 21 days after this has been completed.<br /> <br /> ==Control==<br /> In the event of an outbreak of Newcastle Disease, a compulsory vaccination zone is imposed. Two types of vaccine are available; inactivated and live vaccines. Live vaccines are more commonly used as they can be delivered by spray, drinking water or aerosolisation, whereas inactivated vaccines can only be delivered via direct innoculation.<br /> <br /> ==References==<br /> *DEFRA website: http://www.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/newcastle/disease-factsheet.htm#7<br /> *Kahn, C. M., Merck, Line, S. (2010) '''The Merck Veterinary Manual''' ''John Wiley and Sons''<br /> <br /> [[Category:Paramyxovirinae]][[Category:Poultry]][[Category:Birds]]<br /> [[Category:To_Do_-_Clinical]]</div>

Signarski https://en.wikivet.net/index.php?title=Newcastle_Disease_Virus&diff=93508 2010-09-29T19:22:29Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Newcastle disease virus (NDV) (Avian Paramyxovirus type 1) is the causative agent of Newcastle Disease, an acute viral disease of domestic poultry and many other bird species that is usually fatal. It is characterised primarily by respiratory signs but neurological and gastrointestinal forms of the diseas may also be seen. <br /> <br /> ==Transmission==<br /> Virulent strains of the virus are endemic in most of Asia and Africa and South America. Sporadic cases of the disease have been reported in North America following importaion of infected birds. Hosts of the virus include gallinaceous birds, pigeons, parrots and finches and the disease may be carried subclinically by ducks and ostriches.<br /> Infected birds are the primary source of infection and shed the virus through droppings and secretions from the nose, mouth and eyes. The virus may also be present in eggs laid during the clinical disease. NDV is commonly transferred by the movement of people and contaminated equipment and birds are easily infected by inhalation of the virus or ingestion of contaminated feed or water.<br /> <br /> ==Clinical signs==<br /> NDV affects the gastrointestinal, respiratory and nervous systems and clinical signs reflect the system(s) affected. Clinical signs are usually acute and may appear throughout the flock within 2-12 days with young birds particularly susceptible.<br /> <br /> Clinical signs in affected birds are variable and a subclinical form of the disease can occur which may only be suspected following a drop in egg production. Respiratory signs may include dyspnoea, sneezing, nasal discharge and coughing and are common with low virulence infections. Neurological signs such as tremors, paralysis, circling and depression may accompany respiratory signs and are often seen in cormorants and exotic bird species. Pigeons frequently display neurological signs accompanied by diarrhoea.<br /> <br /> Post mortem lesions include sacculitis, tracheitis and petechia on the serous membranes. The proventricular mucosa is frequently haemorrhagic with necrotic plaques. In birds infected with the less virulent strains of NDV the lesions may be restricted to congestion of the respiratory tract. <br /> <br /> [[Image:Newcastle Disease.jpg|150px|thumb|right|''Newcastle Disease'' &lt;br&gt; L. Mahin, Wikimedia Commons]]<br /> <br /> ==Diagnosis==<br /> Diagnosis is commonly performed using ELISA or PCR. In the UK, Newcastle Disease is notifiable and if suspected, must be reported to DEFRA. If the disesae is suspected, movement of birds, people, animals, eggs and vehicles may be restricted pending investigation by an Animal Health Veterinary Inspector. If the disease is confirmed, all poultry on the premises must be slaughtered and eggs must be destroyed. Thorough cleaning and disinfection of the premises must be carried out and an infected premises may not be re-stocked until at least 21 days after this as been completed.<br /> <br /> ==Control==<br /> *Newcastle Disease is '''NOTIFIABLE'''<br /> *Vaccination of chickens and racing pigeons<br /> *Surveillance of imported exotic birds<br /> *Isolation of infected stock<br /> *Infected premises to be culled and firebreak cull if spread<br /> [[Category:Paramyxovirinae]][[Category:Poultry]][[Category:Birds]]<br /> [[Category:To_Do_-_Clinical]]</div>

Signarski https://en.wikivet.net/index.php?title=Newcastle_Disease_Virus&diff=93507 2010-09-29T18:49:43Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Newcastle disease virus (NDV) is the causative agent of Newcastle Disease, an acute viral disease of domestic poultry and many other bird species that is usually fatal. It is characterised primarily by respiratory disease but neurological and gastrointestinal signs may also be a feature of Newcastle Disease. Virulent strains of the virus are endemic in most of Asia, Africa and South, Central and North America. Hosts of the virus include gallinaceous birds, pigeons, parrots and finches and the disease may be carried subclinically by ducks and ostriches.<br /> <br /> ==Transmission==<br /> Infected birds shed the virus through droppings and secretions from the nose, mouth and eyes. The virus may also be present in eggs laid during the clinical disease. The virus is commonly transferred by the movement of people and contaminated equipment.<br /> <br /> ==Clinical signs==<br /> NDV affects the gastrointestinal, respiratory and nervous systems and clinical signs reflect the system(s) affected. Clinical signs are usually acute and may appear throughout the flock within 2-12 days. Respiratory signs may include dyspnoea, sneezing, nasal discharge and coughing and are common with low virulence infections. Neurological signs such as tremors, paralysis, circling and depression may accompany respiratory signs and are often seen in cormorants and exotic bird species. Pigeons frequently display neurological signs accompanied by diarrhoea.<br /> <br /> [[Image:Newcastle Disease.jpg|150px|thumb|right|''Newcastle Disease'' &lt;br&gt; L. Mahin, Wikimedia Commons]]<br /> <br /> <br /> <br /> ==Pathogenesis==<br /> Transmission via aerosol and direct contact<br /> Disease ranges from subclinical respiratory tract infections -&gt; torticollis -&gt; haemorrhages and death<br /> <br /> ==Diagnosis==<br /> Two diagnostic tests currently exist:<br /> Animal test:<br /> 1. Samples of trachea and gut of 20 birds are tested in eggs<br /> '''HI''' using anti-NDV serum (to differentiate '''HA''' caused by [[Avian Influenza]]<br /> Virulence of isolate tested by the speed it kills chicks<br /> <br /> 2. DNA test (which will soon replace the animal test):<br /> Sequencing the cleavage site of H gene<br /> The more basic amino acids the more virulent the virus<br /> <br /> ==Control==<br /> *Newcastle Disease is '''NOTIFIABLE'''<br /> *Vaccination of chickens and racing pigeons<br /> *Surveillance of imported exotic birds<br /> *Isolation of infected stock<br /> *Infected premises to be culled and firebreak cull if spread<br /> [[Category:Paramyxovirinae]][[Category:Poultry]][[Category:Birds]]<br /> [[Category:To_Do_-_Clinical]]</div>

Signarski https://en.wikivet.net/index.php?title=Newcastle_Disease_Virus&diff=93506 2010-09-29T18:43:44Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Newcastle disease virus is the causative agent of Newcastle Disease, an acute viral disease of domestic poultry and many other bird species that is usually fatal.<br /> <br /> ==Transmission==<br /> Infected birds shed the virus through droppings and secretions from the nose, mouth and eyes. The virus may also be present in eggs laid during the clinical disease. The virus is commonly transferred by the movement of people and contaminated equipment.<br /> <br /> ==Clinical signs==<br /> NDV affects the gastrointestinal, respiratory and nervous systems and clinical signs reflect the system(s) affected. Clinical signs are usually acute and may appear throughout the flock within 2-12 days. Respiratory signs may include dyspnoea, sneezing, nasal discharge and coughing and are common with low virulence infections.<br /> <br /> [[Image:Newcastle Disease.jpg|150px|thumb|right|''Newcastle Disease'' &lt;br&gt; L. Mahin, Wikimedia Commons]]<br /> <br /> ==Hosts==<br /> Gallinaceous birds, pigeons, parrots, finches<br /> <br /> Subclinical carriers: ducks, ostriches<br /> <br /> ==Pathogenesis==<br /> Transmission via aerosol and direct contact<br /> Disease ranges from subclinical respiratory tract infections -&gt; torticollis -&gt; haemorrhages and death<br /> <br /> ==Diagnosis==<br /> Two diagnostic tests currently exist:<br /> Animal test:<br /> 1. Samples of trachea and gut of 20 birds are tested in eggs<br /> '''HI''' using anti-NDV serum (to differentiate '''HA''' caused by [[Avian Influenza]]<br /> Virulence of isolate tested by the speed it kills chicks<br /> <br /> 2. DNA test (which will soon replace the animal test):<br /> Sequencing the cleavage site of H gene<br /> The more basic amino acids the more virulent the virus<br /> <br /> ==Control==<br /> *Newcastle Disease is '''NOTIFIABLE'''<br /> *Vaccination of chickens and racing pigeons<br /> *Surveillance of imported exotic birds<br /> *Isolation of infected stock<br /> *Infected premises to be culled and firebreak cull if spread<br /> [[Category:Paramyxovirinae]][[Category:Poultry]][[Category:Birds]]<br /> [[Category:To_Do_-_Clinical]]</div>

Signarski https://en.wikivet.net/index.php?title=Telangiectasis&diff=93505 2010-09-29T18:30:11Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Telangiectasis ('plum-pudding liver') is a condition of the liver affecting cattle, sheep, poultry and horses. The lesions are characterised by focal dilatation and congestion of the hepatic sinusoids. All animals may be affected by the lesions but they are more commonly seen in older animals. There is little clinical significance to the disease but affected animals are a significant cause of direct economic loss due to carcass condemnation at slaughter. <br /> <br /> ==Pathogenesis==<br /> Various aetiologies for the condition have been suggested. It has been widely proposed that telangiectasis occurs due to ischaemic necrosis of the liver relating to a number underlying causes. These include thromboembolism, pregnancy, abdominal tympany and bacterial infection with ''Fusobacterium necrophorum''. Other theories include high levels of vitamin A, metabolic disturbances and neoplastic or immune-mediated processes. <br /> <br /> Following slaughter, animals with mildly affected livers may be passed for food following trimming but severely affected carcasses must be condemned. <br /> <br /> ==Pathology==<br /> Lesions commonly develop at the parietal portion of the liver or at the periphery. They uually appear as irregularly-shaped red depressions on the surface of the liver that extend into the parenchyma and consist of dilated sinusoids filled with blood and lined with epithelium. Livers containing a few lesions are commonly seen in young animals. <br /> <br /> On histopathology, hepatocytes appear swollen and degenerate with intracytoplasmic vacuoles and dilated sinusoids. The dilated sinusoids are filled with erythrocytes and fibrin strands and leucocytes are occasionally seen. The hepatic parenchyma surrounding the lesions is frequently normal.<br /> <br /> ==References==<br /> *Gracey, J. F., Collins, D. S., Huey, R. J. (1999) '''Meat Hygiene''' ''Elsevier Health Sciences''<br /> *Hubbert, W. T. (1996) '''Food Safety and Quality Assurance: foods of animal origin''' ''Wiley-Blackwell''<br /> <br /> [[Category:Liver - Circulatory Disturbances]]<br /> [[Category:To_Do_-_SophieIgnarski]]<br /> [[Category:To_Do_-_Review]]</div>

Signarski https://en.wikivet.net/index.php?title=Telangiectasis&diff=93504 2010-09-29T18:28:12Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Telangiectasis ('plum-pudding liver') is a condition of the liver affecting cattle, sheep, poultry and horses. The lesions are characterised by focal dilatation and congestion of the hepatic sinusoids. All animals may be affected by the lesions but they are more commonly seen in older animals. There is little clinical significance to the disease but affected animals are a significant cause of direct economic loss due to carcass condemnation at slaughter. <br /> <br /> ==Pathogenesis==<br /> Various aetiologies for the condition have been suggested. It has been widely proposed that telangiectasis occurs due to ischaemic necrosis of the liver relating to a number underlying causes. These include thromboembolism, pregnancy, abdominal tympany and bacterial infection with ''Fusobacterium necrophorum''. Other theories include high levels of vitamin A, metabolic disturbances and neoplastic or immune-mediated processes. <br /> <br /> Following slaughter, animals with mildly affected livers may be passed for food following trimming but severely affected carcasses must be condemned. <br /> <br /> ==Pathology==<br /> Lesions commonly develop at the parietal portion of the liver or at the periphery. They uually appear as irregularly-shaped red depressions on the surface of the liver that extend into the parenchyma. They consist of dilated sinusoids filled with blood and lined with epithelium. Livers containing a few lesions are commonly seen in young animals. <br /> <br /> On histopathology, hepatocytes appear swollen and degenerate with intracytoplasmic vacuoles and dilated sinusoids. The dilated sinusoids are filled with erythrocytes and occasionally fibrin strands and leucocytes. The hepatic parenchyma surrounding the lesions is frequently normal.<br /> <br /> ==References==<br /> *Gracey, J. F., Collins, D. S., Huey, R. J. (1999) '''Meat Hygiene''' ''Elsevier Health Sciences''<br /> *Hubbert, W. T. (1996) '''Food Safety and Quality Assurance: foods of animal origin''' ''Wiley-Blackwell''<br /> <br /> [[Category:Liver - Circulatory Disturbances]]<br /> [[Category:To_Do_-_SophieIgnarski]]<br /> [[Category:To_Do_-_Review]]</div>

Signarski https://en.wikivet.net/index.php?title=Telangiectasis&diff=93499 2010-09-29T18:21:28Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Telangiectasis ('plum-pudding liver') is a condition of the liver affecting cattle, sheep, poultry and horses. The lesions are characterised by focal dilatation and congestion of the hepatic sinusoids. All animals may be affected by the lesions but they are more commonly seen in older animals. There is little clinical significance to the disease but affected animals are a significant cause of direct economic loss due to carcass condemnation at slaughter. <br /> <br /> ==Pathogenesis==<br /> Various aetiologies for the condition have been suggested. It has been widely proposed that telangiectasis occurs due to ischaemic necrosis of the liver relating to a number underlying causes. These include pregnancy, abdominal tympany and bacterial infection with ''Fusobacterium necrophorum''. Other theories include a neoplastic or immune-mediated process. <br /> <br /> Following slaughter, animals with mildly affected livers may be passed for food following trimming but severely affected carcasses must be condemned. <br /> <br /> ==Pathology==<br /> Lesions usually appear as irregularly-shaped red depressions on the surface of the liver that extend into the parenchyma. They consist of dilated sinusoids filled with blood and lined with epithelium. On histopathology, hepatocytes appear swollen and degenerate with intracytoplasmic vacuoles and dilated sinusoids.<br /> <br /> ==References==<br /> *Gracey, J. F., Collins, D. S., Huey, R. J. (1999) '''Meat Hygiene''' ''Elsevier Health Sciences''<br /> *Hubbert, W. T. (1996) '''Food Safety and Quality Assurance: foods of animal origin''' ''Wiley-Blackwell''<br /> <br /> [[Category:Liver - Circulatory Disturbances]]<br /> [[Category:To_Do_-_SophieIgnarski]]<br /> [[Category:To_Do_-_Review]]</div>

Signarski https://en.wikivet.net/index.php?title=Telangiectasis&diff=93498 2010-09-29T18:20:41Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Telangiectasis ('plum-pudding liver') is a condition of the liver affecting cattle, sheep, poultry and horses. The lesions are characterised by focal dilatation and congestion of the hepatic sinusoids. All animals may be affected by the lesions but they are more commonly seen in older animals. There is little clinical significance to the disease but affected animals are a significant cause of direct economic loss due to carcass condemnation at slaughter. <br /> <br /> ==Pathogenesis==<br /> Various aetiologies for the condition have been suggested. It has been widely proposed that telangiectasis occurs due to ischaemic necrosis of the liver relating to a number underlying causes. These include pregnancy, abdominal tympany and bacterial infection with ''Fusobacterium necrophorum''. Other theories include a neoplastic or immune-mediated process. <br /> <br /> Following slaughter, animals with mildly affected livers may be passed for food following trimming but severely affected carcasses must be condemned. <br /> <br /> ==Pathology==<br /> Lesions usually appear as irregularly-shaped red depressions on the surface of the liver that extend into the parenchyma. They consist of dilated sinusoids filled with blood and lined with epithelium. On histopathology, hepatocytes appear swollen and degenerate with intracytoplasmic vacuoles and dilated sinusoids.<br /> <br /> ==References==<br /> *Gracey, J. F., Collins, D. S., Huey, R. J. (1999) '''Meat Hygiene''' ''Elsevier Health Sciences''<br /> *Hubbert, W. T. (1996) '''Food Safety and Quality Assurance: foods of animal origin''' ''Wiley-Blackwell''<br /> <br /> [[Category:Liver - Circulatory Disturbances]]<br /> [[Category:To_Do_-_SophieIgnarski]]</div>

Signarski https://en.wikivet.net/index.php?title=Telangiectasis&diff=93497 2010-09-29T18:11:46Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Telangiectasis ('plum-pudding liver') is a condition of the liver affecting cattle, sheep, poultry and horses. The lesions are characterised by focal dilatation and congestion of the hepatic sinusoids. All animals may be affected by the lesions but they are more commonly seen in older animals. There is little clinical significance to the disease but affected animals are a significant cause of direct economic loss due to carcass condemnation at slaughter. <br /> <br /> ==Pathogenesis==<br /> Various aetiologies for the condition have been suggested. It has been widely proposed that telangiectasis occurs due to ischaemic necrosis of the liver relating to a number underlying causes. These include pregnancy, abdominal tympany and bacterial infection with ''Fusobacterium necrophorum''. Other theories include a neoplastic or immune-mediated process. <br /> <br /> Following slaughter, animals with mildly affected livers may be passed for food following trimming but severely affected carcasses must be condemned. <br /> <br /> ==Pathology==<br /> Lesions usually appear as red spots on the surface of the liver that extend into the parenchyma. They consist of dilated sinusoids filled with blood and lined with epithelium.<br /> <br /> ===Gross pathology===<br /> Affected livers are irregular in shape <br /> Affected livers <br /> <br /> ==References==<br /> *Gracey, J. F., Collins, D. S., Huey, R. J. (1999) '''Meat Hygiene''' ''Elsevier Health Sciences''<br /> *Hubbert, W. T. (1996) '''Food Safety and Quality Assurance: foods of animal origin''' ''Wiley-Blackwell''<br /> <br /> [[Category:Liver - Circulatory Disturbances]]<br /> [[Category:To_Do_-_SophieIgnarski]]</div>

Signarski https://en.wikivet.net/index.php?title=Telangiectasis&diff=93496 2010-09-29T17:57:44Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Telangiectasis is a condition of the liver affecting cattle, sheep, poultry and horses. The lesions are characterised by focal dilatation and congestion of the hepatic sinusoids. All animals may be affected by the lesions but they are more commonly seen in older animals. There is little clinical significance to the disease but affected animals are a significant cause of direct economic loss due to carcass condemnation at slaughter. <br /> <br /> ==Pathogenesis==<br /> Various aetiologies for the condition have been suggested. It has been widely proposed that telangiectasis occurs due to ischaemic necrosis of the liver relating to a number underlying causes. These include pregnancy, abdominal tympany and bacterial infection with ''Fusobacterium necrophorum''. Other theories include a neoplastic or immune-mediated process. <br /> <br /> Following slaughter, animals with mildly affected livers may be passed for food following trimming but severely affected carcasses must be condemned. <br /> <br /> ==References==<br /> <br /> [[Category:Liver - Circulatory Disturbances]]<br /> [[Category:To_Do_-_SophieIgnarski]]</div>

Signarski https://en.wikivet.net/index.php?title=Telangiectasis&diff=93495 2010-09-29T17:10:34Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Telangiectasis is a condition of the liver affecting cattle, sheep, poultry and horses. The lesions are characterised by focal dilatation and congestion of the hepatic sinusoids. All animals may be affected by the lesions but they are more commonly seen in older animals. There is little clinical significance to the disease but affected animals are a significant cause of direct economic loss due to carcass condemnation at slaughter. <br /> <br /> ==Pathogenesis==<br /> Various aetiologies for the condition have been suggested. It has been widely proposed that telangiectasis occurs due to ischaemic necrosis of the liver relating to a number underlying causes. These include pregnancy, abdominal tympany and bacterial infection with ''Fusobacterium necrophorum''. Other theories include a neoplastic or immune-mediated process. <br /> <br /> Following slaughter, animals with mildly affected livers may be passed for food following trimming but severely affected carcasses must be condemned. <br /> <br /> ==References==<br /> <br /> [[Category:Liver - Circulatory Disturbances]]<br /> [[Category:To_Do_-_Clinical]]</div>

Signarski https://en.wikivet.net/index.php?title=Telangiectasis&diff=93494 2010-09-29T17:07:11Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> <br /> Telangiectasis is a condition of the liver affecting cattle, sheep poultry and horses. The lesions are characterised by focal dilatation and congestion of the hepatic sinusoids.<br /> <br /> All animals may be affected by the lesions but they are more commonly seen in older animals. There is little clinical significance to the disease but affected animals are a significant cause of direct economic loss due to carcass condemnation at slaughter. <br /> Various aetiologies for the condition have been suggested. It has been proposed that telangiectasis is caused by ischaemic necrosis relating to a number underlying causes including pregnancy, abdominal tympany and bacterial infection with ''Fusobacterium necrophorum''. Other theories include a neoplastic or immune-mediated process. <br /> <br /> Following slaughter, animals with mildly affected livers may be passed for food following trimming but severely affected carcasses must be condemned. <br /> <br /> <br /> <br /> [[Category:Liver - Circulatory Disturbances]]<br /> [[Category:To_Do_-_Clinical]]</div>

Signarski https://en.wikivet.net/index.php?title=Myxomatosis&diff=93476 2010-09-29T13:45:57Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> [[Image:Myxomatosis_rabbit_logo.jpg|200px|right|thumb|A European Rabbit afflicted by Myxomatosis &lt;br&gt; Chris Bayley, WikiMedia Commons]]<br /> <br /> ==Description==<br /> Myxomatosis is a highly contagious viral condition of rabbits caused by the myxoma virus, a member of the poxvirus group. It was first recognised in the UK in 1953 after it crossed the channel from France where it was illegally introduced in 1952. It is carried mainly by arthropods, particularly the rabbit flea, ''Spilopsyllus cuniculi''. The disease is also transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors. The disease is characterised by subcutaneous mucinous lesions and nodular tumours and is associated with a high mortality rate.<br /> <br /> Myxomatosis is enzootic in cottontail rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia. All other animals are resistant to the disease. <br /> <br /> ==Pathogenesis==<br /> The myxoma virus infects several cell types including mucosal cells, lymphocytes and fibroblasts. In addition to primary and secondary tumour development, there is severe immunosuppression leading to overwhelming infections by opportunistic gram-negative bacteria particularly affecting the conjunctiva and nasal passages. <br /> <br /> Virus multiplication and tumour-like lesions occur initially at the site of intradermal inoculation. This is followed by spread to regional lymph nodes and cell-associated viraemia, with generalization to the skin and internal organs. Gelatinous proliferative nodules develop all over the body, especially at orifices such as the eyes, anus, nose. The rabbit usually dies within 12 days.<br /> <br /> ==Clinical signs==<br /> The clinical disease varies with the virus strain and host species. Lepus species (hares are highly resistant; occasional individuals develop mild to severe generalized myxomatosis. Sylvilagus species are relatively resistant and are probably the natural host of the virus. In this species, infection usually results in the development of skin tumours at the site of innoculation. The tumours appear 4-8 days after exposure and persist for up to 40 days. <br /> <br /> In the European rabbit (Oryctolagus cuniculus), infection with a virulent virus (i.e. the South American or California strains) results in severe disease with up to a 99% case fatality rate. Initial signs include oedema of the eyelids accompanied by inflammation and oedema of the anal, genital, oral and nasal orifices. Oedema of the head and ears, drooping ears and bacterial infections resulting in mucopurulent conjunctivitis and pneumonia are seen. Severe pyrexia is frequently reported. Death (8-15 days post infection) is usually preceded by dyspnoea and seizures. The mortality rate is affected by environmental temperature, with the disease being more lethal at low temperatures.<br /> <br /> ==Pathology==<br /> The most prominent gross lesions in European rabbits with myxomatosis are the skin tumours and the pronounced cutaneous and subcutaneous oedema, particularly in the area of the face and around body orifices. Skin hemorrhages and subserosal petechiae and ecchymoses may be observed in the stomach and intestines. Subepicardial and subendocardial hemorrhages may also occur.<br /> <br /> Adult rabbits of the genus Sylvilagus usually develop localized skin tumours resembling fibromas. Hares or young Sylvilagus rabbits may develop fibromatous to myxomatous nodules, however, lesions are usually mild and localized.<br /> <br /> ==Prevention==<br /> Vaccination and control of insect parasites are the most important means of disease prevention in domestic rabbits. In order to control fleas, wild rabbits should be kept away from pet rabbits and spot-on products may be used. Mosquito control can be achieved using insect repellent strips and fine mesh netting.<br /> <br /> The myxomatosis vaccine currently used in the UK is a live vaccine containing ''Shope fibroma'' virus (Nobivac Myxo, Intervet). Antibodies made against ''Shope fibroma'' provide cross immunity against myxomatosis. Intradermal vaccination is performed in order to achieve adequate immunity and annual booster vaccination is recommended. Live attenuated vaccines have been used elsewhere in Europe but have been associated with other side effects such as immunosuppression.<br /> <br /> ==Treatment==<br /> Although the mortality rate in affected rabbits is high, recovery is possible. High ambient temperatures have been reported to increase recovery rates and a warm environment should be provided. Antibiotics and non-steroidal anti-inflammatories are commonly used to treat the disease, however corticosteroids are contraindicated due to their immunosuppressive effects.<br /> <br /> ==References==<br /> *Fraser, S. G. (2009) '''Rabbit Medicine and Surgery for Veterinary Nurses''' ''Wiley-Blackwell''<br /> *Harcourt-Brown, F. (2002) '''Textbook of Rabbit Medicine''' ''Elsevier Health Sciences''<br /> *Kayne, S. B., Jepson, M. H. (2004) '''Veterinary Pharmacy''' ''Pharmaceutical Press''<br /> <br /> [[Category:Leporipoxviruses]][[Category:Rabbit Viruses]]<br /> <br /> [[Category:To_Do_-_SophieIgnarski]]<br /> [[Category:To_Do_-_Review]]</div>

Signarski https://en.wikivet.net/index.php?title=Myxomatosis&diff=93360 2010-09-28T20:12:44Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> [[Image:Myxomatosis_rabbit_logo.jpg|200px|right|thumb|A European Rabbit afflicted by Myxomatosis &lt;br&gt; Chris Bayley, WikiMedia Commons]]<br /> <br /> ==Description==<br /> Myxomatosis is a highly contagious viral condition of rabbits caused by the myxoma virus, a member of the poxvirus group. It was first recognised in the UK in 1953 after it crossed the channel from France where it was illegally introduced in 1952. It is carried mainly by arthropods, particularly the rabbit flea, ''Spilopsyllus cuniculi''. The disease is also transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors. The disease is characterised by subcutaneous mucinous lesions and nodular tumours and is associated with a high mortality rate.<br /> <br /> Myxomatosis is enzootic in cottontail rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia. All other animals are resistant to the disease. <br /> <br /> ==Pathogenesis==<br /> The myxoma virus infects several cell types including mucosal cells, lymphocytes, and fibroblasts. In addition to primary and secondary tumour development, there is severe immunosuppression leading to overwhelming infections by opportunistic gram-negative bacteria particularly affecting the conjunctiva and nasal passages. <br /> <br /> Virus multiplication and tumour-like lesions occur initially at the site of intradermal inoculation. This is followed by spread to regional lymph nodes and cell-associated viraemia, with generalization to the skin and internal organs. Gelatinous proliferative nodules develop all over the body, especially at orifices such as the eyes, anus, nose. The rabbit usually dies within 12 days, if not killed by predators.<br /> <br /> ==Clinical signs==<br /> The clinical disease varies with the virus strain and host species. Sylvilagus species are relatively resistant, and are probably the natural host of the virus. In this species, infection usually results in the development of skin tumours at the site of innoculation. The tumours appear 4-8 days after exposure and persist for up to 40 days. <br /> <br /> In the European rabbit (Oryctolagus cuniculus), infection with a virulent virus (i.e. the South American or California strains) results in severe disease with up to a 99% case fatality rate. Initial signs include oedema of the eyelids accompanied by inflammation and oedema around the anal, genital, oral, and nasal orifices. Oedema of the head and ears, drooping ears, and bacterial infections resulting in mucopurulent conjunctivitis and pneumonia are seen. Severe pyrexia is frequently reported. Death (8-15 days post infection) is usually preceded by dyspnoea and seizures. Lepus species (hares) however are highly resistant; occasional individuals develop mild to severe generalized myxomatosis. The mortality rate is affected by environmental temperature, with the disease being more lethal at low temperatures.<br /> <br /> ==Pathology==<br /> The most prominent gross lesions in European rabbits with myxomatosis are the skin tumours and the pronounced cutaneous and subcutaneous oedema, particularly in the area of the face and around body orifices. Skin hemorrhages and subserosal petechiae and ecchymoses may be observed in the stomach and intestines. Subepicardial and subendocardial hemorrhages may also occur.<br /> <br /> Adult rabbits of the genus Sylvilagus usually develop localized skin tumours resembling fibromas. Hares or young Sylvilagus rabbits may develop fibromatous to myxomatous nodules, however, lesions are usually mild and localized.<br /> <br /> ==Prevention==<br /> Vaccination and control of insect parasites are the most important means of disease prevention in domestic rabbits. In order to control fleas, wild rabbits should be kept away from pet rabbits and spot-on products may be used. Mosquito control can be achieved using insect repellent strips and fine mesh netting.<br /> The myxomatosis vaccine currently used in the UK is a live vaccine containing ''Shope fibroma'' virus (Nobivac Myxo, Intervet). Antibodies made against ''Shope fibroma'' provide cross immunity against myxomatosis. Intradermal vaccination is performed in order to achieve adequate immunity and annual booster vaccination is recommended. Live attenuated vaccines have been used elsewhere in Europe but have been associated with other side effects such as immunosuppression.<br /> <br /> ==Treatment==<br /> Although the mortality rate in affected rabbits is high, recovery is possible. High ambient temperatures have been reported to increase recovery rates and a warm environment should be provided. Antibiotics and non-steroidal anti-inflammatories are commonly used to treat the disease, however corticosteroids are contraindicated due to their immunosuppressive effects.<br /> <br /> ==References==<br /> <br /> *Fraser, S. G. (2009) '''Rabbit Medicine and Surgery for Veterinary Nurses''' ''Wiley-Blackwell''<br /> *Harcourt-Brown, F. (2002) '''Textbook of Rabbit Medicine''' ''Elsevier Health Sciences''<br /> *Kayne, S. B., Jepson, M. H. (2004) '''Veterinary Pharmacy''' ''Pharmaceutical Press''<br /> <br /> [[Category:Leporipoxviruses]][[Category:Rabbit Viruses]]<br /> <br /> [[Category:To_Do_-_SophieIgnarski]]</div>

Signarski https://en.wikivet.net/index.php?title=Myxomatosis&diff=93359 2010-09-28T20:08:03Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> [[Image:Myxomatosis_rabbit_logo.jpg|200px|right|thumb|A European Rabbit afflicted by Myxomatosis &lt;br&gt; Chris Bayley, WikiMedia Commons]]<br /> <br /> ==Description==<br /> Myxomatosis is a highly contagious viral condition of rabbits caused by the myxoma virus, a member of the poxvirus group. It was first recognised in the UK in 1953 after it crossed the channel from France where it was illegally introduced in 1952. It is carried mainly by arthropods, particularly the rabbit flea,''Spilopsyllus cuniculi''. The disease is also transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors. The disease is characterised by subcutaneous mucinous lesions and nodular tumours and is associated with a high mortality rate.<br /> <br /> Myxomatosis is enzootic in cottontail rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia. All other animals are resistant to the disease. <br /> <br /> ==Pathogenesis==<br /> The myxoma virus infects several cell types including mucosal cells, lymphocytes, and fibroblasts. In addition to primary and secondary tumour development, there is severe immunosuppression leading to overwhelming infections by opportunistic gram-negative bacteria particularly affecting the conjunctiva and nasal passages. <br /> <br /> Virus multiplication and tumour-like lesions occur initially at the site of intradermal inoculation. This is followed by spread to regional lymph nodes and cell-associated viraemia, with generalization to the skin and internal organs. Gelatinous proliferative nodules develop all over the body, especially at orifices such as the eyes, anus, nose. The rabbit usually dies within 12 days, if not killed by predators.<br /> <br /> ==Clinical signs==<br /> The clinical disease varies with the virus strain and host species. Sylvilagus species are relatively resistant, and are probably the natural host of the virus. In this species, infection usually results in the development of skin tumours at the site of innoculation. The tumours appear 4-8 days after exposure and persist for up to 40 days. <br /> <br /> In the European rabbit (Oryctolagus cuniculus), infection with a virulent virus (i.e. the South American or California strains) results in severe disease with up to a 99% case fatality rate. Initial signs include oedema of the eyelids accompanied by inflammation and oedema around the anal, genital, oral, and nasal orifices. Oedema of the head and ears, drooping ears, and bacterial infections resulting in mucopurulent conjunctivitis and pneumonia are seen. Severe pyrexia is frequently reported. Death (8-15 days post infection) is usually preceded by dyspnoea and seizures. Lepus species (hares) however are highly resistant; occasional individuals develop mild to severe generalized myxomatosis. The mortality rate is affected by environmental temperature, with the disease being more lethal at low temperatures.<br /> <br /> ==Pathology==<br /> The most prominent gross lesions in European rabbits with myxomatosis are the skin tumours and the pronounced cutaneous and subcutaneous oedema, particularly in the area of the face and around body orifices. Skin hemorrhages and subserosal petechiae and ecchymoses may be observed in the stomach and intestines. Subepicardial and subendocardial hemorrhages may also occur.<br /> <br /> Adult rabbits of the genus Sylvilagus usually develop localized skin tumors resembling fibromas. Hares or young Sylvilagus rabbits may develop fibromatous to myxomatous nodules, however, lesions are usually mild and localized.<br /> <br /> ==Prevention==<br /> Vaccination and control of insect parasites are the most important means of disease prevention in domestic rabbits. In order to control flease, wild rabbits should be kept away from pet rabbits and spot-on products may be used. Mosquito control can be achieved using insect repellent strips and fine mesh netting.<br /> The myxomatosis vaccine currently used in the UK is a live vaccine containing ''Shope fibroma'' virus (Nobivac Myxo, Intervet). Antibodies made against ''Shope fibroma'' provide cross immunity against myxomatosis. Intradermal vaccination is performed in order to achieve adequate immunity and annual booster vaccination is recommended. Live attenuated vaccines have been used elsewhere in Europe but have been associated with other side effects such as immunosuppression.<br /> <br /> ==Treatment==<br /> Although the mortality rate in affected rabbits is high, recovery is possible. High ambient temperatures have been reported to increase recovery rates and a warm environment should be provided. Antibiotics and non-steroidal anti-inflammatories are commonly used to treat the disease, however corticosteroids are contraindicated due to their immunosuppressive effects.<br /> <br /> ==References==<br /> <br /> *Fraser, S. G. (2009) '''Rabbit Medicine and Surgery for Veterinary Nurses''' ''Wiley-Blackwell''<br /> *Harcourt-Brown, F. (2002) '''Textbook of Rabbit Medicine''' ''Elsevier Health Sciences''<br /> *Kayne, S. B., Jepson, M. H. (2004) '''Veterinary Pharmacy''' ''Pharmaceutical Press''<br /> <br /> [[Category:Leporipoxviruses]][[Category:Rabbit Viruses]]<br /> <br /> [[Category:To_Do_-_SophieIgnarski]]</div>

Signarski https://en.wikivet.net/index.php?title=Myxomatosis&diff=93358 2010-09-28T20:07:02Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> [[Image:Myxomatosis_rabbit_logo.jpg|200px|right|thumb|A European Rabbit afflicted by Myxomatosis &lt;br&gt; Chris Bayley, WikiMedia Commons]]<br /> <br /> ==Description==<br /> Myxomatosis is a highly contagious viral condition of rabbits caused by the myxoma virus, a member of the poxvirus group. It was first recognised in the UK in 1953 after it crossed the channel from France where it was illegally introduced in 1952. It is carried mainly by arthropods, particularly the rabbit flea,''Spilopsyllus cuniculi''. The disease is also transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors. The disease is characterised by subcutaneous mucinous lesions and nodular tumours and is associated with a high mortality rate.<br /> <br /> Myxomatosis is enzootic in cottontail rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia. All other animals are resistant to the disease. <br /> <br /> ==Pathogenesis==<br /> The myxoma virus infects several cell types including mucosal cells, lymphocytes, and fibroblasts. In addition to primary and secondary tumour development, there is severe immunosuppression leading to overwhelming infections by opportunistic gram-negative bacteria particularly affecting the conjunctiva and nasal passages. <br /> <br /> Virus multiplication and tumour-like lesions occur initially at the site of intradermal inoculation. This is followed by spread to regional lymph nodes and cell-associated viraemia, with generalization to the skin and internal organs. Gelatinous proliferative nodules develop all over the body, especially at orifices such as the eyes, anus, nose. The rabbit usually dies within 12 days, if not killed by predators.<br /> <br /> ==Clinical signs==<br /> The clinical disease varies with the virus strain and host species. Sylvilagus species are relatively resistant, and are probably the natural host of the virus. In this species, infection usually results in the development of skin tumours at the site of innoculation. The tumours appear 4-8 days after exposure and persist for up to 40 days. <br /> <br /> In the European rabbit (Oryctolagus cuniculus), infection with a virulent virus (i.e. the South American or California strains) results in severe disease with up to a 99% case fatality rate. Initial signs include oedema of the eyelids accompanied by inflammation and oedema around the anal, genital, oral, and nasal orifices. Oedema of the head and ears, drooping ears, and bacterial infections resulting in mucopurulent conjunctivitis and pneumonia are seen. Severe pyrexia is frequently reported. Death (8-15 days post infection) is usually preceded by dyspnoea and seizures. Lepus species (hares) however are highly resistant; occasional individuals develop mild to severe generalized myxomatosis. The mortality rate is affected by environmental temperature, with the disease being more lethal at low temperatures.<br /> <br /> ==Pathology==<br /> The most prominent gross lesions in European rabbits with myxomatosis are the skin tumours and the pronounced cutaneous and subcutaneous oedema, particularly in the area of the face and around body orifices. Skin hemorrhages and subserosal petechiae and ecchymoses may be observed in the stomach and intestines. Subepicardial and subendocardial hemorrhages may also occur.<br /> <br /> Adult rabbits of the genus Sylvilagus usually develop localized skin tumors resembling fibromas. Hares or young Sylvilagus rabbits may develop fibromatous to myxomatous nodules, however, lesions are usually mild and localized.<br /> <br /> ==Prevention==<br /> Vaccination and control of insect parasites are the most important means of disease prevention in domestic rabbits. In order to control flease, wild rabbits should be kept away from pet rabbits and spot-on products may be used. Mosquito control can be achieved using insect repellent strips and fine mesh netting.<br /> The myxomatosis vaccine currently used in the UK is a live vaccine containing ''Shope fibroma'' virus (Nobivac Myxo, Intervet). Antibodies made against ''Shope fibroma'' provide cross immunity against myxomatosis. Annual booster vaccination is recommended. Live attenuated vaccines have been used elsewhere in Europe but have been associated with other side effects such as immunosuppression.<br /> <br /> ==Treatment==<br /> Although the mortality rate in affected rabbits is high, recovery is possible. High ambient temperatures have been reported to increase recovery rates and a warm environment should be provided. Antibiotics and non-steroidal anti-inflammatories are commonly used to treat the disease, however corticosteroids are contraindicated due to their immunosuppressive effects.<br /> <br /> ==References==<br /> <br /> *Fraser, S. G. (2009) '''Rabbit Medicine and Surgery for Veterinary Nurses''' ''Wiley-Blackwell''<br /> *Harcourt-Brown, F. (2002) '''Textbook of Rabbit Medicine''' ''Elsevier Health Sciences''<br /> *Kayne, S. B., Jepson, M. H. (2004) '''Veterinary Pharmacy''' ''Pharmaceutical Press''<br /> <br /> [[Category:Leporipoxviruses]][[Category:Rabbit Viruses]]<br /> <br /> [[Category:To_Do_-_SophieIgnarski]]</div>

Signarski https://en.wikivet.net/index.php?title=Myxomatosis&diff=93357 2010-09-28T19:53:10Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> [[Image:Myxomatosis_rabbit_logo.jpg|200px|right|thumb|A European Rabbit afflicted by Myxomatosis &lt;br&gt; Chris Bayley, WikiMedia Commons]]<br /> <br /> ==Description==<br /> Myxomatosis is a highly contagious viral condition of rabbits caused by the myxoma virus, a member of the poxvirus group. It was first recognised in the UK in 1953 after it crossed the channel from France where it was illegally introduced in 1952. It is carried prinicpally by mosquitoes and the rabbit flea,''Spilopsyllus cuniculi'', but is also transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors. The disease is characterised by mucinous skin lesions and nodular tumours and is associated with a high mortality rate.<br /> <br /> Myxomatosis is enzootic in cottontail rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia. All other animals are resistant to the disease. <br /> <br /> ==Pathogenesis==<br /> The myxoma virus infects several cell types including mucosal cells, lymphocytes, and fibroblasts. In addition to primary and secondary tumour development, there is severe immunosuppression leading to overwhelming infections by opportunistic gram-negative bacteria particularly affecting the conjunctiva and nasal passages. <br /> <br /> Virus multiplication and tumour-like lesions occur initially at the site of intradermal inoculation. This is followed by spread to regional lymph nodes and cell-associated viraemia, with generalization to the skin and internal organs. Gelatinous proliferative nodules develop all over the body, especially at orifices such as the eyes, anus, nose. The rabbit usually dies within 12 days, if not killed by predators.<br /> <br /> ==Clinical signs==<br /> The clinical disease varies with the virus strain and host species. Sylvilagus species are relatively resistant, and are probably the natural host of the virus. In this species, infection usually results in the development of skin tumours at the site of innoculation. The tumours appear 4-8 days after exposure and persist for up to 40 days. <br /> <br /> In the European rabbit (Oryctolagus cuniculus), infection with a virulent virus (i.e. the South American or California strains) results in severe disease with up to a 99% case fatality rate. Initial signs include oedema of the eyelids accompanied by inflammation and oedema around the anal, genital, oral, and nasal orifices. Oedema of the head and ears, drooping ears, and bacterial infections resulting in mucopurulent conjunctivitis and pneumonia are seen. Severe pyrexia is frequently reported. Death (8-15 days post infection) is usually preceded by dyspnoea and seizures. Lepus species (hares) however are highly resistant; occasional individuals develop mild to severe generalized myxomatosis.<br /> <br /> ==Pathology==<br /> The most prominent gross lesions in European rabbits with myxomatosis are the skin tumours and the pronounced cutaneous and subcutaneous oedema, particularly in the area of the face and around body orifices. Skin hemorrhages and subserosal petechiae and ecchymoses may be observed in the stomach and intestines. Subepicardial and subendocardial hemorrhages may also occur.<br /> <br /> Adult rabbits of the genus Sylvilagus usually develop localized skin tumors resembling fibromas. Hares or young Sylvilagus rabbits may develop fibromatous to myxomatous nodules, however, lesions are usually mild and localized.<br /> <br /> ==Prevention==<br /> Vaccination and control of insect parasites are the most important means of disease prevention in domestic rabbits. In order to control flease, wild rabbits should be kept away from pet rabbits and spot-on products may be used. Mosquito control can be achieved using insect repellent strips and fine mesh netting.<br /> The myxomatosis vaccine currently used in the UK is a live vaccine containing ''Shope fibroma'' virus. Antibodies made against ''Shope fibroma'' provide cross immunity against myxomatosis. Annual booster vaccination is recommended. Live attenuated vaccines have been used elsewhere in Europe but have been associated with other side effects such as immunosuppression.<br /> <br /> ==References==<br /> *Fraser, S. G. (2009) '''Rabbit Medicine and Surgery for Veterinary Nurses''' ''Wiley-Blackwell''<br /> *Kayne, S. B., Jepson, M. H. (2004) '''Veterinary Pharmacy''' ''Pharmaceutical Press''<br /> <br /> [[Category:Leporipoxviruses]][[Category:Rabbit Viruses]]<br /> <br /> [[Category:To_Do_-_SophieIgnarski]]</div>

Signarski https://en.wikivet.net/index.php?title=Myxomatosis&diff=93338 2010-09-28T19:22:58Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> [[Image:Myxomatosis_rabbit_logo.jpg|200px|right|thumb|A European Rabbit afflicted by Myxomatosis &lt;br&gt; Chris Bayley, WikiMedia Commons]]<br /> <br /> ==Description==<br /> Myxomatosis is a highly contagious viral condition of rabbits caused by the myxoma virus and carried prinicpally by the rabbit flea,''Spilopsyllus cuniculi''. It is also transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors. Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia. <br /> <br /> ==Pathogenesis==<br /> The myxoma virus infects several cell types including mucosal cells, lymphocytes, and fibroblasts. In addition to primary and secondary tumour development, there is severe immunosuppression leading to overwhelming infections by opportunistic gram-negative bacteria particularly affecting the conjunctiva and nasal passages. <br /> <br /> Virus multiplication and tumour-like lesions occur initially at the site of intradermal inoculation. This is followed by spread to regional lymph nodes and cell-associated viraemia, with generalization to the skin and internal organs. Gelatinous proliferative nodules develop all over the body, especially at orifices such as the eyes, anus, nose. The rabbit usually dies within 12 days, if not killed by predators.<br /> <br /> ==Clinical signs==<br /> The clinical disease varies with the virus strain and host species. Sylvilagus species are relatively resistant, and are probably the natural host of the virus. In this species, infection usually results in the development of skin tumours at the site of innoculation. The tumours appear 4-8 days after exposure and persist for up to 40 days. <br /> <br /> In the European rabbit (Oryctolagus cuniculus), infection with a virulent virus (i.e. the South American or California strains) results in severe disease with up to a 99% case fatality rate. Initial signs include oedema of the eyelids accompanied by inflammation and oedema around the anal, genital, oral, and nasal orifices. Oedema of the head and ears, drooping ears, and bacterial infections resulting in mucopurulent conjunctivitis and pneumonia are seen. Death (8-15 days post infection) is usually preceded by labored breathing and convulsions.Very young rabbits may succumb to generalized disease. Lepus species (hares) however are highly resistant; occasional individuals develop mild to severe generalized myxomatosis.<br /> <br /> ==Pathology==<br /> The most prominent gross lesions in European rabbits with myxomatosis are the skin tumours and the pronounced cutaneous and subcutaneous oedema, particularly in the area of the face and around body orifices. Skin hemorrhages and subserosal petechiae and ecchymoses may be observed in the stomach and intestines. Subepicardial and subendocardial hemorrhages may also occur.<br /> <br /> Adult rabbits of the genus Sylvilagus usually develop localized skin tumors resembling fibromas. Hares or young Sylvilagus rabbits may develop fibromatous to myxomatous nodules, however, lesions are usually mild and localized.<br /> <br /> <br /> [[Category:Leporipoxviruses]][[Category:Rabbit Viruses]]<br /> <br /> [[Category:To_Do_-_SophieIgnarski]]</div>

Signarski https://en.wikivet.net/index.php?title=Myxomatosis&diff=93337 2010-09-28T19:22:07Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> [[Image:Myxomatosis_rabbit_logo.jpg|200px|right|thumb|A European Rabbit afflicted by Myxomatosis &lt;br&gt; Chris Bayley, WikiMedia Commons]]<br /> <br /> ==Description==<br /> Myxomatosis is a highly contagious viral condition of rabbits caused by the myxoma virus and carried prinicpally by the rabbit flea,''Spilopsyllus cuniculi''. It is also transmitted by direct or indirect contact with ocular or skin discharges or by mechanical vectors. Myxomatosis is enzootic in rabbits of the genus Sylvilagus in both South and North America and in wild rabbits of the genus Oryctolagus in South America, Europe, and Australia. <br /> <br /> ===Pathogenesis===<br /> The myxoma virus infects several cell types including mucosal cells, lymphocytes, and fibroblasts. In addition to primary and secondary tumour development, there is severe immunosuppression leading to overwhelming infections by opportunistic gram-negative bacteria particularly affecting the conjunctiva and nasal passages. <br /> <br /> Virus multiplication and tumour-like lesions occur initially at the site of intradermal inoculation. This is followed by spread to regional lymph nodes and cell-associated viraemia, with generalization to the skin and internal organs. Gelatinous proliferative nodules develop all over the body, especially at orifices such as the eyes, anus, nose. The rabbit usually dies within 12 days, if not killed by predators.<br /> <br /> ==Clinical signs==<br /> The clinical disease varies with the virus strain and host species. Sylvilagus species are relatively resistant, and are probably the natural host of the virus. In this species, infection usually results in the development of skin tumours at the site of innoculation. The tumours appear 4-8 days after exposure and persist for up to 40 days. <br /> <br /> In the European rabbit (Oryctolagus cuniculus), infection with a virulent virus (i.e. the South American or California strains) results in severe disease with up to a 99% case fatality rate. Initial signs include oedema of the eyelids accompanied by inflammation and oedema around the anal, genital, oral, and nasal orifices. Oedema of the head and ears, drooping ears, and bacterial infections resulting in mucopurulent conjunctivitis and pneumonia are seen. Death (8-15 days post infection) is usually preceded by labored breathing and convulsions.Very young rabbits may succumb to generalized disease. Lepus species (hares) however are highly resistant; occasional individuals develop mild to severe generalized myxomatosis.<br /> <br /> ===Pathology===<br /> <br /> ====Gross Pathology====<br /> <br /> The most prominent gross lesions in European rabbits with myxomatosis are the skin tumours and the pronounced cutaneous and subcutaneous oedema, particularly in the area of the face and around body orifices. Skin hemorrhages and subserosal petechiae and ecchymoses may be observed in the stomach and intestines. Subepicardial and subendocardial hemorrhages may also occur.<br /> <br /> Adult rabbits of the genus Sylvilagus usually develop localized skin tumors resembling fibromas. Hares or young Sylvilagus rabbits may develop fibromatous to myxomatous nodules, however, lesions are usually mild and localized.<br /> <br /> <br /> [[Category:Leporipoxviruses]][[Category:Rabbit Viruses]]<br /> <br /> [[Category:To_Do_-_SophieIgnarski]]</div>

Signarski https://en.wikivet.net/index.php?title=Feline_Miliary_Dermatitis&diff=92805 2010-09-24T20:49:28Z

<p>Signarski: </p> <hr /> <div>[[Category:Allergic Skin Diseases]]<br /> [[Category:To Do - Blood]][[Category:To Do - Clinical]]<br /> <br /> {{unfinished]]<br /> <br /> ==Description==<br /> Feline Miliary Dermatitis (FMD) is a multifactorial disease of cats characterised by multiple papulocrustous lesions of the skin. The term &quot;miliary&quot; is commonly used to describe the millet-seed like appearance of the typical lesions of miliary dermatitis.<br /> <br /> ==Signalment==<br /> There is no age, breed or sex predilection for the condition.<br /> ==Pathogenesis==<br /> Most cases of FMD occur due to an allergic response, most commonly to fleas. Other conditions such as nutritional deficiencies, ectoparasitism, immune-mediated disease and other allergies may lead to the development of FMD. <br /> <br /> ==Clinical signs==<br /> The characteristic papulocrustous lesions develop<br /> <br /> <br /> [[Category:Allergic Skin Diseases]]<br /> [[Category:To Do - Blood]][[Category:To Do - Clinical]]</div>

Signarski https://en.wikivet.net/index.php?title=Myxomatosis&diff=92800 2010-09-24T19:35:11Z

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

Signarski https://en.wikivet.net/index.php?title=Myxomatosis&diff=92750 2010-09-23T21:10:10Z

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

Signarski https://en.wikivet.net/index.php?title=Coccidiosis_-_Horse&diff=92748 2010-09-23T20:58:38Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Equine coccidiosis is an infection of the intestinal tract of equids by protozoa of the genera ''Eimeria''. Horses may be infected by 3 species of ''Eimeria''; ''Eimeria leukarti'', ''E. solipedum'' and ''E. uniungulsti''. The most common coccidial oocyst identified in equine faeces is that of ''E. leukarti''. The prepatent period of infection by the protozoa is 16-35 days. Infection follows the ingestion of sporulated oocysts in contaminated food or water. After exposure to bile in the small intestine, the oocysts excyst and individual sporozoites emerge. Oocysts, released as the final product of the sexual reproductive cycle are shed in the faeces and are infective to new hosts. Coccidia are a common incidental finding in normal foals aged 30-125 days and suggest that this organism does not cause clinical signs in foals. <br /> <br /> ==Clinical signs==<br /> Clinical signs associated with the condition occur due to the damaged intestinal epithelium and connective tissue underlying the mucosa. These may include profuse diarrhoea, weight loss, ventral oedema, intestinal haemorrhage and catarrhal inflammation of the intestinal tract.<br /> <br /> ==Diagnosis==<br /> A diagnosis of coccidiosis is made by detection of oocysts in the faeces using faecal flotation. A solution of saturated sugar or sodium nitrate solution is used. Oocysts are approximately 12μm in diameter and are identified by their dark brown colour and thick-walled, ovoid shape. They also contain a prominent micropyle on the narrower end. <br /> <br /> [[Image:Eimeria leukarti horse.jpg|thumb|right|150px|''Eimeria leukarti'' - Joaquim Castellà Veterinary Parasitology Universitat Autònoma de Barcelona]]<br /> <br /> ==Treatment==<br /> The treatment of choice for the disease is the sulphonamide antimicrobial agents. Sulphamethazine or Sulphathiazole are commonly used. Prevention of coccidiosis is obtained by providing adequate nutrition and hygiene and minimising stress. <br /> <br /> ==References==<br /> *Bertone, J., Horspool, L. J. I. (2004) '''Equine Clinical Pharmacology''' ''Elsevier Health Sciences''<br /> *Lavoie, J. P., Hinchcliff, K. W. (2009) '''Blackwell's Five-Minute Veterinary Consult: Equine''' ''John Wiley and Sons''<br /> *Sellon, D. C., Long, M. T. (2007) '''Equine Infectious Diseases''' ''Elsevier Health Sciences''<br /> <br /> <br /> <br /> [[Category:Coccidia]]<br /> [[Category:To_Do_-_SophieIgnarski]]<br /> [[Category:To Do - Review]]<br /> [[Category:Respiratory Parasitic Infections]]<br /> [[Category:Respiratory_Disorders_-_Horse]][[Category:Alimentary_Disorders_-_Horse]]</div>

Signarski https://en.wikivet.net/index.php?title=Coccidiosis_-_Horse&diff=92747 2010-09-23T20:57:57Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Equine coccidiosis is an infection of the intestinal tract of equids by protozoa of the genera ''Eimeria''. Horses may be infected by 3 species of ''Eimeria''; ''Eimeria leukarti'', ''E. solipedum'' and ''E. uniungulsti''. The most common coccidial oocyst identified in equine faeces is that of ''E. leukarti''. The prepatent period of infection by the protozoa is 16-35 days. Infection follows the ingestion of sporulated oocysts in contaminated food or water. After exposure to bile in the small intestine, the oocysts excyst and individual sporozoites emerge. Oocysts, released as the final product of the sexual reproductive cycle are shed in the faeces and are infective to new hosts. Coccidia are a common incidental findings in normal foals aged 30-125 days and suggest that this organism does not cause clinical signs in foals. <br /> <br /> ==Clinical signs==<br /> Clinical signs associated with the condition occur due to the damaged intestinal epithelium and connective tissue underlying the mucosa. These may include profuse diarrhoea, weight loss, ventral oedema, intestinal haemorrhage and catarrhal inflammation of the intestinal tract.<br /> <br /> ==Diagnosis==<br /> A diagnosis of coccidiosis is made by detection of oocysts in the faeces using faecal flotation. A solution of saturated sugar or sodium nitrate solution is used. Oocysts are approximately 12μm in diameter and are identified by their dark brown colour and thick-walled, ovoid shape. They also contain a prominent micropyle on the narrower end. <br /> <br /> [[Image:Eimeria leukarti horse.jpg|thumb|right|150px|''Eimeria leukarti'' - Joaquim Castellà Veterinary Parasitology Universitat Autònoma de Barcelona]]<br /> <br /> ==Treatment==<br /> The treatment of choice for the disease is the sulphonamide antimicrobial agents. Sulphamethazine or Sulphathiazole are commonly used. Prevention of coccidiosis is obtained by providing adequate nutrition and hygiene and minimising stress. <br /> <br /> ==References==<br /> *Bertone, J., Horspool, L. J. I. (2004) '''Equine Clinical Pharmacology''' ''Elsevier Health Sciences''<br /> *Lavoie, J. P., Hinchcliff, K. W. (2009) '''Blackwell's Five-Minute Veterinary Consult: Equine''' ''John Wiley and Sons''<br /> *Sellon, D. C., Long, M. T. (2007) '''Equine Infectious Diseases''' ''Elsevier Health Sciences''<br /> <br /> <br /> <br /> [[Category:Coccidia]]<br /> [[Category:To_Do_-_SophieIgnarski]]<br /> [[Category:To Do - Review]]<br /> [[Category:Respiratory Parasitic Infections]]<br /> [[Category:Respiratory_Disorders_-_Horse]][[Category:Alimentary_Disorders_-_Horse]]</div>

Signarski https://en.wikivet.net/index.php?title=Coccidiosis_-_Horse&diff=92746 2010-09-23T20:56:24Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Equine coccidiosis is an infection of the intestinal tract of equids by protozoa of the genera ''Eimeria''. Horses may be infected by 3 species of ''Eimeria''; ''Eimeria leukarti'', ''E. solipedum'' and ''E. uniungulsti''. The most common coccidial oocyst identified in equine faeces is that of ''E. leukarti''. The prepatent period of infection by the protozoa is 16-35 days. Infection follows the ingestion of sporulated oocysts in contaminated food or water. After exposure to bile in the small intestine, the oocysts excyst and individual sporozoites emerge. Oocysts, released as the final product of the sexual reproductive cycle are shed in the faeces and are infective to new hosts. Coccidia are a common incidental findings in normal foals aged 30-125 days and suggest that this organism does not cause clinical signs in foals. <br /> <br /> ==Clinical signs==<br /> Clinical signs associated with the condition occur due to the damaged intestinal epithelium and connective tissue underlying the mucosa. These may include profuse diarrhoea, weight loss, ventral oedema, intestinal haemorrhage and catarrhal inflammation of the intestinal tract.<br /> <br /> ==Diagnosis==<br /> A diagnosis of coccidiosis is made by detection of oocysts in the faeces using faecal flotation. A solution of saturated sugar or sodium nitrate solution is used. Oocysts are approximately 12μm in diameter and are identified by their dark brown colour and thick-walled, ovoid shape. They also contain a prominent micropyle on the narrower end. <br /> <br /> [[Image:Eimeria leukarti horse.jpg|thumb|right|150px|''Eimeria leukarti'' - Joaquim Castellà Veterinary Parasitology Universitat Autònoma de Barcelona]]<br /> <br /> ==Treatment==<br /> The treatment of choice for the disease is the sulphonamide antimicrobial agents. Sulphamethazine or Sulphathiazole are commonly used. Prevention of coccidiosis is obtained by ensuring adequate nutrition, hygiene and minimising stress. <br /> <br /> ==References==<br /> *Bertone, J., Horspool, L. J. I. (2004) '''Equine Clinical Pharmacology''' ''Elsevier Health Sciences''<br /> *Lavoie, J. P., Hinchcliff, K. W. (2009) '''Blackwell's Five-Minute Veterinary Consult: Equine''' ''John Wiley and Sons''<br /> *Sellon, D. C., Long, M. T. (2007) '''Equine Infectious Diseases''' ''Elsevier Health Sciences''<br /> <br /> <br /> <br /> [[Category:Coccidia]]<br /> [[Category:To_Do_-_Clinical]]<br /> [[Category:Respiratory Parasitic Infections]]<br /> [[Category:Respiratory_Disorders_-_Horse]][[Category:Alimentary_Disorders_-_Horse]]</div>

Signarski https://en.wikivet.net/index.php?title=Coccidiosis_-_Horse&diff=92745 2010-09-23T20:53:06Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Equine coccidiosis is an infection of the intestinal tract of equids by protozoa of the genera ''Eimeria''. Horses may be infected by 3 species of ''Eimeria''; ''Eimeria leukarti'', ''E. solipedum'' and ''E. uniungulsti''. The most common coccidial oocyst identified in equine faeces is that of ''E. leukarti''. The prepatent period of infection by the protozoa is 16-35 days. Infection follows the ingestion of sporulated oocysts in contaminated food or water. After exposure to bile in the small intestine, the oocysts excyst and individual sporozoites emerge. Oocysts, released as the final product of the sexual reproductive cycle are shed in the faeces and are infective to new hosts. Coccidia are a common incidental findings in normal foals aged 30-125 days and suggest that this organism does not cause clinical signs in foals. <br /> <br /> ==Clinical signs==<br /> Clinical signs associated with the condition occur due to the damaged intestinal epithelium and connective tissue underlying the mucosa. These may include profuse diarrhoea, weight loss, ventral oedema, intestinal haemorrhage and catarrhal inflammation of the intestinal tract.<br /> <br /> ==Diagnosis==<br /> A diagnosis of coccidiosis is made by detection of oocysts in the faeces using faecal flotation. A solution of saturated sugar or sodium nitrate solution is used. Oocysts are identified by their dark brown colour and thick-walled, ovoid shape. They also contain a prominent micropyle on the narrower end. <br /> <br /> ==Treatment==<br /> The treatment of choice for the disease is the sulphonamide antimicrobial agents. Sulphamethazine or Sulphathiazole are commonly used. Prevention of coccidiosis is obtained by ensuring adequate nutrition, hygiene and minimising stress. <br /> <br /> <br /> <br /> <br /> [[Image:Eimeria leukarti horse.jpg|thumb|right|150px|''Eimeria leukarti'' - Joaquim Castellà Veterinary Parasitology Universitat Autònoma de Barcelona]]<br /> *Only one atypical ''[[Eimeria spp.|Eimeria]]''<br /> <br /> *Forms large subepithelial gametocytes in villi<br /> <br /> *Large, dark coloured oocysts<br /> **Approximately 12μm<br /> <br /> *Occasionally causes [[Diarrhoea|diarrhoea]]<br /> <br /> *'''''Besnoitia bennetti''''' in [[Respiratory Parasitic Infections - Pathology#Besnoitia bennetti|larynx]] of horses<br /> **Papilloma like lesions in [[Larynx Inflammatory - Pathology#Infectious causes of laryngitis|larynx]], skin and sclera<br /> **Thick walled parasitic cysts, covered by hyperplastic epithelium, may be ulcerated<br /> <br /> <br /> <br /> ==References==<br /> *Bertone, J., Horspool, L. J. I. (2004) '''Equine Clinical Pharmacology''' ''Elsevier Health Sciences''<br /> *Lavoie, J. P., Hinchcliff, K. W. (2009) '''Blackwell's Five-Minute Veterinary Consult: Equine''' ''John Wiley and Sons''<br /> <br /> <br /> <br /> [[Category:Coccidia]]<br /> [[Category:To_Do_-_Clinical]]<br /> [[Category:Respiratory Parasitic Infections]]<br /> [[Category:Respiratory_Disorders_-_Horse]][[Category:Alimentary_Disorders_-_Horse]]</div>

Signarski https://en.wikivet.net/index.php?title=Coccidiosis_-_Horse&diff=92740 2010-09-23T20:38:32Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Equine coccidiosis is an infection of the intestinal tract of equids by the protozoal organism ''Eimeria leukarti''. Infection follows the ingestion of sporulated oocysts in contaminated food or water. After exposure to bile in the small intestine, the oocysts excyst and individual sporozoites emerge. Oocysts, released as the final product of the sexual reproductive cycle are shed in the faeces and are infective to new hosts. The prepatent period is 16-35 days. Coccidia are a common incidental findings in normal foals aged 30-125 days and suggest that this organism does not cause clinical signs in foals. <br /> <br /> ==Clinical signs==<br /> Clinical signs associated with the condition occur due to the damaged intestinal epithelium and connective tissue underlying the mucosa. These may include profuse diarrhoea, weight loss, ventral oedema <br /> <br /> <br /> <br /> <br /> [[Image:Eimeria leukarti horse.jpg|thumb|right|150px|''Eimeria leukarti'' - Joaquim Castellà Veterinary Parasitology Universitat Autònoma de Barcelona]]<br /> *Only one atypical ''[[Eimeria spp.|Eimeria]]''<br /> <br /> *Forms large subepithelial gametocytes in villi<br /> <br /> *Large, dark coloured oocysts<br /> **Approximately 12μm<br /> <br /> *Occasionally causes [[Diarrhoea|diarrhoea]]<br /> <br /> *'''''Besnoitia bennetti''''' in [[Respiratory Parasitic Infections - Pathology#Besnoitia bennetti|larynx]] of horses<br /> **Papilloma like lesions in [[Larynx Inflammatory - Pathology#Infectious causes of laryngitis|larynx]], skin and sclera<br /> **Thick walled parasitic cysts, covered by hyperplastic epithelium, may be ulcerated<br /> <br /> <br /> <br /> ==References==<br /> *Bertone, J., Horspool, L. J. I. (2004) '''Equine Clinical Pharmacology''' ''Elsevier Health Sciences''<br /> *Lavoie, J. P., Hinchcliff, K. W. (2009) '''Blackwell's Five-Minute Veterinary Consult: Equine''' ''John Wiley and Sons''<br /> <br /> <br /> <br /> [[Category:Coccidia]]<br /> [[Category:To_Do_-_Clinical]]<br /> [[Category:Respiratory Parasitic Infections]]<br /> [[Category:Respiratory_Disorders_-_Horse]][[Category:Alimentary_Disorders_-_Horse]]</div>

Signarski https://en.wikivet.net/index.php?title=User:Signarski&diff=92736 2010-09-23T20:15:12Z

<p>Signarski: </p> <hr /> <div>|[[File:sophieignarski.jpg|300px|thumb|right|]]<br /> <br /> ==About me==<br /> <br /> I qualifed in veterinary medicine at the Royal Veterinary College in 2010. I also hold a BSc (Hons) in Zoology from Bristol University. <br /> <br /> ==What I hope to get out of the project==<br /> <br /> I'd like to become more familiar with WikiVet in general so that I will be able to make more use of it as a resource in the future. I'd also like to consolidate my own knowledge through authoring articles. <br /> <br /> ==Improvements that I'd like to see on WikiVet==<br /> <br /> More complete articles. <br /> <br /> ==Pages I'm working on==<br /> <br /> [[Tetanus - Overview]]<br /> <br /> <br /> <br /> <br /> {| cellpadding=&quot;10&quot; cellspacing=&quot;0&quot; border=&quot;1&quot;<br /> | My recent pages:<br /> | '''[[Tetanus - Horse]]&lt;br&gt;<br /> '''[[Cyathostomosis]]&lt;br&gt;<br /> '''[[Colitis X]]&lt;br&gt;<br /> '''[[Tetanus - Dog]]&lt;br&gt;<br /> '''[[Hepatitis, Equine Serum]]&lt;br&gt;<br /> '''[[Impaction of the Oesophagus]]&lt;br&gt;<br /> '''[[Anthrax]]&lt;br&gt;<br /> '''[[Lipoma, Pedunculated - Horse]]&lt;br&gt;<br /> '''[[Tyzzer's Disease]]&lt;br&gt;<br /> '''[[Sand Impaction - Horse]]&lt;br&gt;<br /> '''[[Small Intestine Volvulus - Horse]]&lt;br&gt;<br /> |-}<br /> <br /> ==Hours worked==<br /> <br /> <br /> {| class=&quot;wikitable collapsible&quot;<br /> |Day<br /> |'''Week 1''' (5-11th July)<br /> |'''Week 2''' (12-18th July)<br /> |'''Week 3''' (19-25th July)<br /> |'''Week 4''' (26th Jul-1st Aug)<br /> |'''Week 5''' (2-8th Aug)<br /> |'''Week 6''' (9-13th Aug)<br /> |'''Week 7''' (16-20th Aug)<br /> |'''Week 8''' (23-27th Aug)<br /> |-<br /> |Monday<br /> | 1 <br /> | 0<br /> | 0<br /> | 2<br /> | 5<br /> | 3.5<br /> | 0 <br /> | 3<br /> |-<br /> |Tuesday<br /> | 7.5<br /> | 0<br /> | 0<br /> | 3.5<br /> | 4 <br /> | 4<br /> | 3.5<br /> | 2<br /> |-<br /> |Wednesday<br /> | 4.5 <br /> | 0<br /> | 0<br /> | 0 <br /> | 2.5<br /> | 0<br /> | 0<br /> | 4<br /> |-<br /> |Thursday<br /> | 0<br /> | 0<br /> | 2.5<br /> | 4.5<br /> | 1<br /> | 1 <br /> | 4 <br /> | 4<br /> |-<br /> |Friday<br /> | 0<br /> | 0<br /> | 3<br /> | 4.5<br /> | 4.5<br /> | 0<br /> | 0 <br /> | 4<br /> |-<br /> |Saturday<br /> | 0<br /> | 0<br /> | 5<br /> | 0 <br /> | 4 <br /> | 3 <br /> | 4<br /> | 2<br /> |-<br /> |Sunday<br /> | 0<br /> | 0<br /> | 5 <br /> | 0 <br /> | 3<br /> | 0 <br /> | 2<br /> | 4<br /> |-<br /> |'''Total hours'''<br /> | 13<br /> | 0<br /> | 15.5<br /> | 14.5<br /> | 24<br /> | 11.5<br /> | 13.5<br /> | 23<br /> |-<br /> |}<br /> <br /> {| class=&quot;wikitable collapsible&quot;<br /> |Day<br /> |'''Week 9''' (30th Aug - 3rd Sep)<br /> |'''Week 10''' (6th Sept - 10th Sept)<br /> |'''Week 11''' (13th Sept - 17th Sept)<br /> |-<br /> |Monday<br /> | 0 <br /> | 3<br /> | 0 <br /> |-<br /> |Tuesday<br /> | 3<br /> | 0<br /> | 0 <br /> |-<br /> |Wednesday<br /> | 3<br /> | 0<br /> | 3<br /> |-<br /> |Thursday<br /> | 0<br /> | 1<br /> | 0 <br /> |-<br /> |Friday<br /> | 2<br /> | 0<br /> | 0 <br /> |-<br /> |Saturday<br /> | 4<br /> | 0<br /> | 4<br /> |-<br /> |Sunday<br /> | 2<br /> | 0<br /> | 0 <br /> |-<br /> |'''Total hours'''<br /> | 14<br /> | 4<br /> | 7<br /> |-<br /> |}<br /> <br /> <br /> [[:Category:To Do - SophieIgnarski]]</div>

Signarski https://en.wikivet.net/index.php?title=Ameloblastoma,_Central&diff=92495 2010-09-19T19:31:05Z

<p>Signarski: </p> <hr /> <div><br /> {{unfinished}}<br /> <br /> ==Description==<br /> The central or intraosseous ameloblastoma is one of the most common odontogenic tumours. The tumour is locally invasive and destructive to bone but metastasis has not been reported. Ameloblastomas are usually slow growing. The tumours have been reported to occur in dogs and cattle and occasionally in cats and horses.<br /> <br /> ==Diagnosis==<br /> The histological appearance of an ameloblastoma is a follicular arrangement of ameloblasts and stellate reticulum cells. There may be occasional keratinisation. <br /> &lt;/small&gt;[[Category:Teeth_-_Proliferative_Pathology]]<br /> [[Category:Neoplasia]][[Category:To_Do_-_Clinical]]</div>

Signarski https://en.wikivet.net/index.php?title=User:Signarski&diff=92494 2010-09-19T19:11:37Z

<p>Signarski: </p> <hr /> <div>|[[File:sophieignarski.jpg|300px|thumb|right|]]<br /> <br /> ==About me==<br /> <br /> I qualifed in veterinary medicine at the Royal Veterinary College in 2010. I also hold a BSc (Hons) in Zoology from Bristol University. <br /> <br /> ==What I hope to get out of the project==<br /> <br /> I'd like to become more familiar with WikiVet in general so that I will be able to make more use of it as a resource in the future. I'd also like to consolidate my own knowledge through authoring articles. <br /> <br /> ==Improvements that I'd like to see on WikiVet==<br /> <br /> More complete articles. <br /> <br /> ==Pages I'm working on==<br /> <br /> [[Tetanus - Overview]]<br /> <br /> <br /> <br /> <br /> {| cellpadding=&quot;10&quot; cellspacing=&quot;0&quot; border=&quot;1&quot;<br /> | My recent pages:<br /> | '''[[Tetanus - Horse]]&lt;br&gt;<br /> '''[[Cyathostomosis]]&lt;br&gt;<br /> '''[[Colitis X]]&lt;br&gt;<br /> '''[[Tetanus - Dog]]&lt;br&gt;<br /> '''[[Hepatitis, Equine Serum]]&lt;br&gt;<br /> '''[[Impaction of the Oesophagus]]&lt;br&gt;<br /> '''[[Anthrax]]&lt;br&gt;<br /> '''[[Lipoma, Pedunculated - Horse]]&lt;br&gt;<br /> '''[[Tyzzer's Disease]]&lt;br&gt;<br /> '''[[Sand Impaction - Horse]]&lt;br&gt;<br /> '''[[Small Intestine Volvulus - Horse]]&lt;br&gt;<br /> |-}<br /> <br /> ==Hours worked==<br /> <br /> <br /> {| class=&quot;wikitable collapsible&quot;<br /> |Day<br /> |'''Week 1''' (5-11th July)<br /> |'''Week 2''' (12-18th July)<br /> |'''Week 3''' (19-25th July)<br /> |'''Week 4''' (26th Jul-1st Aug)<br /> |'''Week 5''' (2-8th Aug)<br /> |'''Week 6''' (9-13th Aug)<br /> |'''Week 7''' (16-20th Aug)<br /> |'''Week 8''' (23-27th Aug)<br /> |-<br /> |Monday<br /> | 1 <br /> | 0<br /> | 0<br /> | 2<br /> | 5<br /> | 3.5<br /> | 0 <br /> | 3<br /> |-<br /> |Tuesday<br /> | 7.5<br /> | 0<br /> | 0<br /> | 3.5<br /> | 4 <br /> | 4<br /> | 3.5<br /> | 2<br /> |-<br /> |Wednesday<br /> | 4.5 <br /> | 0<br /> | 0<br /> | 0 <br /> | 2.5<br /> | 0<br /> | 0<br /> | 4<br /> |-<br /> |Thursday<br /> | 0<br /> | 0<br /> | 2.5<br /> | 4.5<br /> | 1<br /> | 1 <br /> | 4 <br /> | 4<br /> |-<br /> |Friday<br /> | 0<br /> | 0<br /> | 3<br /> | 4.5<br /> | 4.5<br /> | 0<br /> | 0 <br /> | 4<br /> |-<br /> |Saturday<br /> | 0<br /> | 0<br /> | 5<br /> | 0 <br /> | 4 <br /> | 3 <br /> | 4<br /> | 2<br /> |-<br /> |Sunday<br /> | 0<br /> | 0<br /> | 5 <br /> | 0 <br /> | 3<br /> | 0 <br /> | 2<br /> | 4<br /> |-<br /> |'''Total hours'''<br /> | 13<br /> | 0<br /> | 15.5<br /> | 14.5<br /> | 24<br /> | 11.5<br /> | 13.5<br /> | 23<br /> |-<br /> |}<br /> <br /> {| class=&quot;wikitable collapsible&quot;<br /> |Day<br /> |'''Week 9''' (30th Aug - 3rd Sep)<br /> |'''Week 10''' (6th Sept - 10th Sept)<br /> |'''Week 11''' (13th Sept - 17th Sept)<br /> |-<br /> |Monday<br /> | 0 <br /> | 3<br /> | 0 <br /> |-<br /> |Tuesday<br /> | 3<br /> | 0<br /> | 0 <br /> |-<br /> |Wednesday<br /> | 3<br /> | 0<br /> | 3<br /> |-<br /> |Thursday<br /> | 0<br /> | 1<br /> | 0 <br /> |-<br /> |Friday<br /> | 2<br /> | 0<br /> | 0 <br /> |-<br /> |Saturday<br /> | 4<br /> | 0<br /> | 4<br /> |-<br /> |Sunday<br /> | 2<br /> | 0<br /> |-<br /> |'''Total hours'''<br /> | 14<br /> | 4<br /> |-<br /> |}<br /> <br /> <br /> [[:Category:To Do - SophieIgnarski]]</div>

Signarski https://en.wikivet.net/index.php?title=Haemangioma&diff=92493 2010-09-19T19:07:11Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Haemangiomas are benign tumours of the vascular epithelium and soft tissues. They occur most commonly in dogs, occasionally in cats and horses and rarely in cattle and pigs. In dogs the tumours frequently occur on the distal extremities and the trunk. A widespread, disseminated form of the disease has been reported in dairy cattle affecting the skin and internal organs.<br /> <br /> The tumours are classified as cavernous or capillary haemangiomas depending on the size of the vascular spaces.<br /> <br /> ==Signalment==<br /> In horses, young animals less than a year of age are most frequently affected. Cats and dogs most frequently develop haemangiomas as adults; the average age of affected dogs is nine years. <br /> <br /> ==Clinical signs==<br /> Haemangiomas usually appear as single to multiple circumscribed nodules that are red to black in colour. Those on the skin may be ulcerated and may bleed due to self-trauma, particularly if located on the face. Feline hemangiomas appear as solitary tumors in the dermis and subcutis without any site predilection.<br /> <br /> ==Histological features==<br /> Haemangiomas are often well circumscribed and are composed of vascular spaces filled with red blood cells and lined by a layer of well-differentiated endothelial cells. Evidence for acute or chronic haemorrhage is often noted resulting in erythrophagocytosis or haemosiderin-laden macrophages, and organised thrombi are a frequent finding.<br /> <br /> ==Treatment==<br /> Haemangiomas are generally slow growing and the treatment of choice is surgical excision. Local haemangiomas of the skin and mouth may also respond to thermocautery or radiation therapy. Cryosurgery may be required to successfully treat some of the verrucous variants reported in large animals. <br /> <br /> ==Prognosis==<br /> Surgical treatment of cutaneous haemangioma generally has a good prognosis following surgical excision and metastasis is rare.<br /> <br /> ==References==<br /> *Meuten, D. J. (2002) '''Tumours in Domestic Animals''' ''Wiley-Blackwell'' <br /> *Radostits, O. M., Arundel, J. H., Gay, C. C. (2000) '''Veterinary Medicine: a textbook of the diseases of cattle, sheep, pigs, goats and horses''' ''Elsevier Health Sciences''<br /> *Raskin, R., Meyer, D. J. (Atlas of Canine and Feline Cytology''' ''Elsevier Health Sciences'' <br /> <br /> [[Category:Neoplasia]]<br /> [[Category:To Do - SophieIgnarski]][[Category: To Do - Review]]<br /> [[Category:Splenic Neoplasia]]</div>

Signarski https://en.wikivet.net/index.php?title=Urticaria&diff=92492 2010-09-19T19:06:24Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Urticaria is a condition of the skin characterised by the development of multiple flat-topped, oedematous swellings (wheals) in the dermis that dent or 'pit' with digital pressure. Episodes may be acute, chronic or recurrent. The condition occurs in all domestic animals but most commonly in the horse.<br /> <br /> ==Pathogenesis==<br /> The aetiopathogenesis of urticaria is complex and many causes have been suggested. The basic pathogenesis is thought to be due to degranulation of mast cells and basophils leading to the release of inflammatory mediators and an increase in vascular permeability. This may be due to either an exogenous or endogenous type I hypersensitivity reaction. Exogenous urticaria may occur as a result of exposure to chemicals, medication and insect bites or stings, shampoos or insecticides. Endogenous urticaria occurs following inhalation of allergens such as pollens. For a large number of cases no underlying cause is identified and these cases are termed idiopathic urticaria.<br /> <br /> ==Signalment==<br /> Horses between 1 and 10 years of age are most prone to developing the condition. There is no sex predilection but Thoroughbreds and Arabs appear to be more commonly affected than other breeds. <br /> <br /> ==History and clinical signs==<br /> Multiple wheals are often observed and occur within a few minutes or hours of exposure to the causative agent. A history of recurrence or repeated episodes is often reported. Affected areas can vary from small, localised lesions up to 3 cm in diameter, to extensive generalised areas involving large areas of skin. Lesions can occur on any part of the body but usually develop on the back, legs, flanks, neck and eyelids. Dermatographism is a specific pressure-induced type of urticaria in which wheals form in reponse to exogenous pressure, commonly these are observed in the saddle area of the horse. In severe cases the mucous membranes of the nose, mouth, anus and vulva may be involved. Pruritus may or may not be present and the lesions usually disappear rapidly.<br /> <br /> ==Diagnosis and treatment==<br /> Because of the numerous underlying causes of urticaria, definitive diagnosis may be difficult. Historical and clinical findings may lead to suspicion of the condition. The localisation of lesions (e.g. site of contact with saddle or insect repellent) or history of medication or exposure to chemicals may help to determine an underlying cause. <br /> <br /> Acute urticaria often resolves spontaneouly without requiring treatment. If urticaria is susupected all current medications should be stopped. Dexamethasone given once at a dose of 0.1 mg/kg IM usually results in resolution of clinical signs within 24 hours. In rare cases, epinephrine may be required if the urticaria is associated with signs of anaphylaxis.<br /> <br /> Recurrent cases may require further investigation in order to determine the underlying cause. This may include further questioning about the animal's history and response to withdrawal of drugs or topical products. If no underlying cause is found, an investigation for allergies is indicated and may include intradermal allergy testing, insect control trials and an elimination (novel protein) diet. Biopsy of lesions is generally unrewarding but helps to rule out vasculitis as an underlying cause of the clinical signs. Antihistamines such as Hydroxyzine may be useful in the management of chronic urticaria but are ineffective in treating the acute form of the condition. Acupuncture has been reported to be effective in one horse.<br /> <br /> ==Prognosis==<br /> The prognosis with urticaria is dependent on the underlying cause. If this can be identified and removed the prognosis is excellent. Horses with recurrent (idiopathic) urticaria generally have a poor prognosis.<br /> ==References==<br /> *Mair, T. S., Love, S., Schumacher, J., Watson, A. E. (1998) '''Equine Medicine, Surgery and Reproduction''' ''Elsevier Health Sciences''<br /> *Pascoe, R. R., Knottenbelt, D. C. (1999) '''Manual of Equine Dermatology''' ''Elsevier Health Sciences''<br /> *Rose, R. J., Hodgson, D. R. (2000) '''Manual of Equine Practice''' ''Elsevier Health Sciences''<br /> *Scott, D. W., Miller, W. H. (2003) '''Equine Dermatology''' ''Elsevier Health Sciences''<br /> <br /> [[Category:Allergic Skin Diseases]]<br /> [[Category:To Do - SophieIgnarski]]<br /> [[Category:To Do - Review]]</div>

Signarski https://en.wikivet.net/index.php?title=Urticaria&diff=92491 2010-09-19T19:05:28Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Urticaria is a condition of the skin characterised by the development of multiple flat-topped, oedematous swellings (wheals) in the dermis that dent or 'pit' with digital pressure. Episodes may be acute, chronic or recurrent. The condition occurs in all domestic animals but most commonly in the horse.<br /> <br /> ==Pathogenesis==<br /> The aetiopathogenesis of urticaria is complex and many causes have been suggested. The basic pathogenesis is thought to be due to degranulation of mast cells and basophils leading to the release of inflammatory mediators and an increase in vascular permeability. This may be due to either an exogenous or endogenous type I hypersensitivity reaction. Exogenous urticaria may occur as a result of exposure to chemicals, medication and insect bites or stings, shampoos or insecticides. Endogenous urticaria occurs following inhalation of allergens such as pollens. For a large number of cases no underlying cause is identified and these cases are termed idiopathic urticaria.<br /> <br /> ==Signalment==<br /> Horses between 1 and 10 years of age are most prone to developing the condition. There is no sex predilection but Thoroughbreds and Arabs appear to be more commonly affected than other breeds. <br /> <br /> ==History and clinical signs==<br /> Multiple wheals are often observed and occur within a few minutes or hours of exposure to the causative agent. A history of recurrence or repeated episodes is often reported. Affected areas can vary from small, localised lesions up to 3 cm in diameter, to extensive generalised areas involving large areas of skin. Lesions can occur on any part of the body but usually develop on the back, legs, flanks, neck and eyelids. Dermatographism is a specific pressure-induced type of urticaria in which wheals form in reponse to exogenous pressure, commonly these are observed in the saddle area of the horse. In severe cases the mucous membranes of the nose, mouth, anus and vulva may be involved. Pruritus may or may not be present and the lesions usually disappear rapidly.<br /> <br /> ==Diagnosis and treatment==<br /> Because of the numerous underlying causes of urticaria, definitive diagnosis may be difficult. Historical and clinical findings may lead to suspicion of the condition. The localisation of lesions (e.g. site of contact with saddle or insect repellent) or history of medication or exposure to chemicals may help to determine an underlying cause. <br /> <br /> Acute urticaria often resolves spontaneouly without requiring treatment. If urticaria is susupected all current medications should be stopped. Dexamethasone given once at a dose of 0.1 mg/kg IM usually results in resolution of clinical signs within 24 hours. In rare cases, epinephrine may be required if the urticaria is associated with signs of anaphylaxis.<br /> <br /> Recurrent cases may require further investigation in order to determine the underlying cause. This may include further questioning about the animal's history and response to withdrawal of drugs or topical products. If no underlying cause is found, an investigation for allergies is indicated and may include intradermal allergy testing, insect control trials and an elimination (novel protein) diet. Biopsy of lesions is generally unrewarding but helps to rule out vasculitis as an underlying cause of the clinical signs. Antihistamines such as Hydroxyzine may be useful in the management of chronic urticaria but are ineffective in treating the acute form of the condition. Acupuncture has been reported to be effective in one horse.<br /> <br /> ==Prognosis==<br /> The prognosis with urticaria is dependent on the underlying cause. If this can be identified and removed the prognosis is excellent. Horses with recurrent (idiopathic) urticaria generally have a poor prognosis.<br /> ==References==<br /> *Mair, T. S., Love, S., Schumacher, J., Watson, A. E. (1998) '''Equine Medicine, Surgery and Reproduction''' ''Elsevier Health Sciences''<br /> *Pascoe, R. R., Knottenbelt, D. C. (1999) '''Manual of Equine Dermatology''' ''Elsevier Health Sciences''<br /> *Rose, R. J., Hodgson, D. R. (2000) '''Manual of Equine Practice''' ''Elsevier Health Sciences''<br /> *Scott, D. W., Miller, W. H. (2003) '''Equine Dermatology''' ''Elsevier Health Sciences''<br /> <br /> [[Category:Allergic Skin Diseases]]<br /> [[Category:To Do - Blood]][[Category:To Do - SophieIgnarski]]<br /> [[Category:To Do - Review]]</div>

Signarski https://en.wikivet.net/index.php?title=Urticaria&diff=92490 2010-09-19T19:02:25Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Urticaria is a condition of the skin characterised by the development of multiple flat-topped, oedematous swellings (wheals) in the dermis that dent or 'pit' with digital pressure. Episodes may be acute, chronic or recurrent. The condition occurs in all domestic animals but most commonly in the horse.<br /> <br /> ==Pathogenesis==<br /> The aetiopathogenesis of urticaria is complex and many causes have been suggested. The basic pathogenesis is thought to be due to degranulation of mast cells and basophils leading to the release of inflammatory mediators and an increase in vascular permeability. This may be due to either an exogenous or endogenous type I hypersensitivity reaction. Exogenous urticaria may occur as a result of exposure to chemicals, medication and insect bites or stings, shampoos or insecticides. Endogenous urticaria occurs following inhalation of allergens such as pollens. For a large number of cases no underlying cause is identified and these cases are termed idiopathic urticaria.<br /> <br /> ==Signalment==<br /> Horses between 1 and 10 years of age are most prone to developing the condition. There is no sex predilection but Thoroughbreds and Arabs appear to be more commonly affected than other breeds. <br /> <br /> ==History and clinical signs==<br /> Multiple wheals are often observed and occur within a few minutes or hours of exposure to the causative agent. A history of recurrence or repeated episodes is often reported. Affected areas can vary from small, localised lesions up to 3 cm in diameter, to extensive generalised areas involving large areas of skin. Lesions can occur on any part of the body but usually develop on the back, legs, flanks, neck and eyelids. Dermatographism is a specific pressure-induced type of urticaria in which wheals form in reponse to exogenous pressure, commonly these are observed in the saddle area of the horse. In severe cases the mucous membranes of the nose, mouth, anus and vulva may be involved. Pruritus may or may not be present and the lesions usually disappear rapidly.<br /> <br /> ==Diagnosis and treatment==<br /> Because of the numerous underlying causes of urticaria, definitive diagnosis may be difficult. Historical and clinical findings may lead to suspicion of the condition. The localisation of lesions (e.g. site of contact with saddle or insect repellent) or history of medication or exposure to chemicals may help to determine an underlying cause. <br /> <br /> Acute urticaria often resolves spontaneouly without requiring treatment. If urticaria is susupected all current medications should be stopped. Dexamethasone given once at a dose of 0.1 mg/kg IM usually results in resolution of clinical signs within 24 hours. In rare cases, epinephrine may be required if the urticaria is associated with signs of anaphylaxis.<br /> <br /> Recurrent cases may require further investigation in order to determine the underlying cause. This may include further questioning about the animal's history and response to withdrawal of drugs or topical products. If no underlying cause is found, an investigation for allergies is indicated and may include intradermal allergy testing, insect control trials and an elimination (novel protein) diet. Biopsy of lesions is generally unrewarding but helps to rule out vasculitis as an underlying cause of the clinical signs. Antihistamines such as Hydroxyzine may be useful in the management of chronic urticaria but are ineffective in treating acute urticaria. Acupuncture has been reported to be effective in one horse.<br /> <br /> ==Prognosis==<br /> The prognosis with urticaria is dependent on the underlying cause. If this can be identified and removed the prognosis is excellent. Horses with recurrent (idiopathic) urticaria generally have a poor prognosis.<br /> ==References==<br /> *Mair, T. S., Love, S., Schumacher, J., Watson, A. E. (1998) '''Equine Medicine, Surgery and Reproduction''' ''Elsevier Health Sciences''<br /> *Pascoe, R. R., Knottenbelt, D. C. (1999) '''Manual of Equine Dermatology''' ''Elsevier Health Sciences''<br /> *Rose, R. J., Hodgson, D. R. (2000) '''Manual of Equine Practice''' ''Elsevier Health Sciences''<br /> *Scott, D. W., Miller, W. H. (2003) '''Equine Dermatology''' ''Elsevier Health Sciences''<br /> <br /> [[Category:Allergic Skin Diseases]]<br /> [[Category:To Do - Blood]][[Category:To Do - SophieIgnarski]]</div>

Signarski https://en.wikivet.net/index.php?title=Urticaria&diff=92489 2010-09-19T19:01:42Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Urticaria is a condition of the skin characterised by the development of multiple flat-topped, oedematous swellings (wheals) in the dermis that dent or 'pit' with digital pressure. Episodes may be acute, chronic or recurrent. The condition occurs in all domestic animals but most commonly in the horse.<br /> <br /> ==Pathogenesis==<br /> The aetiopathogenesis of urticaria is complex and many causes have been suggested. The basic pathogenesis is thought to be due to degranulation of mast cells and basophils leading to the release of inflammatory mediators and an increase in vascular permeability. This may be due to either an exogenous or endogenous type I hypersensitivity reaction. Exogenous urticaria may occur as a result of exposure to chemicals, medication and insect bites or stings, shampoos or insecticides. Endogenous urticaria occurs following inhalation of allergens such as pollens. For a large number of cases no underlying cause is identified and these cases are termed idiopathic urticaria.<br /> <br /> ==Signalment==<br /> Horses between 1 and 10 years of age are most prone to developing the condition. There is no sex predilection but Thoroughbreds and Arabs appear to be more commonly affected than other breeds. <br /> <br /> ==History and clinical signs==<br /> Multiple wheals are often observed and occur within a few minutes or hours of exposure to the causative agent. A history of recurrence or repeated episodes is often reported. Affected areas can vary from small, localised lesions up to 3cm in diameter, to extensive generalised areas involving large areas of skin. Lesions can occur on any part of the body but usually develop on the back, legs, flanks, neck and eyelids. Dermatographism is a specific pressure-induced type of urticaria in which wheals form in reponse to exogenous pressure, commonly these are observed in the saddle area of the horse. In severe cases the mucous membranes of the nose, mouth, anus and vulva may be involved. Pruritus may or may not be present and the lesions usually disappear rapidly.<br /> <br /> ==Diagnosis and treatment==<br /> Because of the numerous underlying causes of urticaria, definitive diagnosis may be difficult. Historical and clinical findings may lead to suspicion of the condition. The localisation of lesions (e.g. site of contact with saddle or insect repellent) or history of medication or exposure to chemicals may help to determine an underlying cause. <br /> <br /> Acute urticaria often resolves spontaneouly without requiring treatment. If urticaria is susupected all current medications should be stopped. Dexamethasone given once at a dose of 0.1 mg/kg IM usually results in resolution of clinical signs within 24 hours. In rare cases, epinephrine may be required if the urticaria is associated with signs of anaphylaxis.<br /> <br /> Recurrent cases may require further investigation in order to determine the underlying cause. This may include further questioning about the animal's history and response to withdrawal of drugs or topical products. If no underlying cause is found, an investigation for allergies is indicated and may include intradermal allergy testing, insect control trials and an elimination (novel protein) diet. Biopsy of lesions is generally unrewarding but helps to rule out vasculitis as an underlying cause of the clinical signs. Antihistamines such as Hydroxyzine may be useful in the management of chronic urticaria but are ineffective in treating acute urticaria. Acupuncture has been reported to be effective in one horse.<br /> <br /> ==Prognosis==<br /> The prognosis with urticaria is dependent on the underlying cause. If this can be identified and removed the prognosis is excellent. Horses with recurrent (idiopathic) urticaria generally have a poor prognosis.<br /> ==References==<br /> *Mair, T. S., Love, S., Schumacher, J., Watson, A. E. (1998) '''Equine Medicine, Surgery and Reproduction''' ''Elsevier Health Sciences''<br /> *Pascoe, R. R., Knottenbelt, D. C. (1999) '''Manual of Equine Dermatology''' ''Elsevier Health Sciences''<br /> *Rose, R. J., Hodgson, D. R. (2000) '''Manual of Equine Practice''' ''Elsevier Health Sciences''<br /> *Scott, D. W., Miller, W. H. (2003) '''Equine Dermatology''' ''Elsevier Health Sciences''<br /> <br /> [[Category:Allergic Skin Diseases]]<br /> [[Category:To Do - Blood]][[Category:To Do - SophieIgnarski]]</div>

Signarski https://en.wikivet.net/index.php?title=Urticaria&diff=92488 2010-09-19T18:52:12Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Urticaria is a condition of the skin characterised by the development of multiple flat-topped, oedematous swellings (wheals) that dent or 'pit' with digital pressure. Episodes may be acute, chronic or recurrent. The condition occurs in all domestic animals but most commonly in the horse.<br /> <br /> ==Pathogenesis==<br /> The aetiopathogenesis of urticaria is complex and many causes have been suggested. The basic pathogenesis is thought to be due to degranulation of mast cells and basophils leading to the release of inflammatory mediators and an increase in vascular permeability. This may be due to either an exogenous or endogenous hypersensitivity reaction. Exogenous urticaria may occur as a result of exposure to chemicals, medication and insect bites or stings, shampoos or insecticides. Endogenous urticaria occurs following inhalation of allergens such as pollens. <br /> <br /> ==Signalment==<br /> Horses between 1 and 10 years of age are most prone to developing the condition. There is no sex predilection but Thoroughbreds and Arabs appear to be more commonly affected than other breeds. <br /> <br /> ==History and clinical signs==<br /> Multiple wheals are often observed and occur within a few minutes or hours of exposure to the causative agent. A history of recurrence or repeated episodes is often reported. Affected areas can vary from small, localised lesions up to 3cm in diameter, to extensive generalised areas involving large areas of skin. Lesions can occur on any part of the body but usually develop on the back, legs, flanks, neck and eyelids. Dermatographism is a specific pressure-induced type of urticaria in which wheals form in reponse to exogenous pressure, commonly these are observed in the saddle area of the horse. In severe cases the mucous membranes of the nose, mouth, anus and vulva may be involved. Pruritus may or may not be present and the lesions usually disappear rapidly.<br /> <br /> ==Diagnosis and treatment==<br /> Because of the numerous underlying causes of urticaria, definitive diagnosis may be difficult. Historical and clinical findings may lead to suspicion of the condition. The localisation of lesions (e.g. site of contact with saddle or insect repellent) or history of medication or exposure to chemicals may help to determine an underlying cause. <br /> <br /> Acute urticaria often resolves spontaneouly without requiring treatment. If urticaria is susupected all current medications should be stopped. Dexamethasone given once at a dose of 0.1 mg/kg IM usually results in resolution of clinical signs within 24 hours. Recurrent cases may require further investigation in order to determine the underlying cause. This may include further questioning about the animal's history and response to withdrawal of drugs or topical products. If no underlying cause is found, an investigation for allergies is indicated and may include intradermal allergy testing, insect control trials and an elimination (novel protein) diet. Biopsy of lesions is generally unrewarding but may reveal a mild to moderate perivascular to interstitial dermatitis. Antihistamines such as Hydroxyzine may be useful in the management of chronic urticaria but are ineffective in treating acute urticaria. Acupuncture has been reported to be effective in one horse.<br /> <br /> ==Prognosis==<br /> The prognosis with urticaria is generally favourable because general health is not usually affected. Recurrent con<br /> <br /> ==References==<br /> *Mair, T. S., Love, S., Schumacher, J., Watson, A. E. (1998) '''Equine Medicine, Surgery and Reproduction''' ''Elsevier Health Sciences''<br /> *Pascoe, R. R., Knottenbelt, D. C. (1999) '''Manual of Equine Dermatology''' ''Elsevier Health Sciences''<br /> *Rose, R. J., Hodgson, D. R. (2000) '''Manual of Equine Practice''' ''Elsevier Health Sciences''<br /> *Scott, D. W., Miller, W. H. (2003) '''Equine Dermatology''' ''Elsevier Health Sciences''<br /> <br /> [[Category:Allergic Skin Diseases]]<br /> [[Category:To Do - Blood]][[Category:To Do - SophieIgnarski]]</div>

Signarski https://en.wikivet.net/index.php?title=Urticaria&diff=92487 2010-09-19T18:50:56Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Urticaria is a condition of the skin characterised by the development of multiple flat-topped, oedematous swellings (wheals) that dent or 'pit' with digital pressure. Episodes may be acute, chronic or recurrent. The condition occurs in all domestic animals but most commonly in the horse.<br /> <br /> ==Pathogenesis==<br /> The aetiopathogenesis of urticaria is complex and many causes have been suggested. The basic pathogenesis is thought to be due to degranulation of mast cells and basophils leading to the release of inflammatory mediators and an increase in vascular permeability. This may be due to exogenous or endogenous hypersensitivity reactions. Exogenous urticaria may occur as a result of exposure to chemicals, medication and insect bites or stings, shampoos or insecticides. Endogenous urticaria occurs following inhalation of allergens such as pollens. <br /> <br /> ==Signalment==<br /> Horses between 1 and 10 years of age are most prone to developing the condition. There is no sex predilection but Thoroughbreds and Arabs appear to be more commonly affected than other breeds. <br /> <br /> ==History and clinical signs==<br /> Multiple wheals are often observed and occur within a few minutes or hours of exposure to the causative agent. A history of recurrence or repeated episodes is often reported. Affected areas can vary from small, localised lesions up to 3cm in diameter, to extensive generalised areas involving large areas of skin. Lesions can occur on any part of the body but usually develop on the back, legs, flanks, neck and eyelids. Dermatographism is a specific pressure-induced type of urticaria in which wheals form in reponse to exogenous pressure, commonly these are observed in the saddle area of the horse. In severe cases the mucous membranes of the nose, mouth, anus and vulva may be involved. Pruritus may or may not be present and the lesions usually disappear rapidly.<br /> <br /> ==Diagnosis and treatment==<br /> Because of the numerous underlying causes of urticaria, definitive diagnosis may be difficult. Historical and clinical findings may lead to suspicion of the condition. The localisation of lesions (e.g. site of contact with saddle or insect repellent) or history of medication or exposure to chemicals may help to determine an underlying cause. <br /> <br /> Acute urticaria often resolves spontaneouly without requiring treatment. If urticaria is susupected all current medications should be stopped. Dexamethasone given once at a dose of 0.1 mg/kg IM usually results in resolution of clinical signs within 24 hours. Recurrent cases may require further investigation in order to determine the underlying cause. This may include further questioning about the animal's history and response to withdrawal of drugs or topical products. If no underlying cause is found, an investigation for allergies is indicated and may include intradermal allergy testing, insect control trials and an elimination (novel protein) diet. Biopsy of lesions is generally unrewarding but may reveal a mild to moderate perivascular to interstitial dermatitis. Antihistamines such as Hydroxyzine may be useful in the management of chronic urticaria but are ineffective in treating acute urticaria. Acupuncture has been reported to be effective in one horse.<br /> <br /> ==Prognosis==<br /> The prognosis with urticaria is generally favourable because general health is not usually affected. Recurrent con<br /> <br /> ==References==<br /> *Mair, T. S., Love, S., Schumacher, J., Watson, A. E. (1998) '''Equine Medicine, Surgery and Reproduction''' ''Elsevier Health Sciences''<br /> *Pascoe, R. R., Knottenbelt, D. C. (1999) '''Manual of Equine Dermatology''' ''Elsevier Health Sciences''<br /> *Rose, R. J., Hodgson, D. R. (2000) '''Manual of Equine Practice''' ''Elsevier Health Sciences''<br /> *Scott, D. W., Miller, W. H. (2003) '''Equine Dermatology''' ''Elsevier Health Sciences''<br /> <br /> [[Category:Allergic Skin Diseases]]<br /> [[Category:To Do - Blood]][[Category:To Do - SophieIgnarski]]</div>

Signarski https://en.wikivet.net/index.php?title=Urticaria&diff=92486 2010-09-19T18:50:19Z

<p>Signarski: </p> <hr /> <div>{{unfinished}}<br /> <br /> ==Description==<br /> Urticaria is a condition of the skin characterised by the development of multiple flat-topped, oedematous swellings (wheals) that dent or 'pit' with digital pressure. Episodes may be acute, chronic or recurrent. The condition occurs in all domestic animals but most commonly in the horse.<br /> <br /> ==Pathogenesis==<br /> The aetiopathogenesis of urticaria is complex and many causes have been suggested. The basic pathogenesis is thought to be due to degranulation of mast cells and basophils leading to the release of inflammatory mediators and an increase in vascular permeability. The condition may occur due to exogenous or endogenous hypersensitivity reactions. Exogenous urticaria may occur as a result of exposure to chemicals, medication and insect bites or stings, shampoos or insecticides. Endogenous urticaria occurs following inhalation of allergens such as pollens. <br /> <br /> ==Signalment==<br /> Horses between 1 and 10 years of age are most prone to developing the condition. There is no sex predilection but Thoroughbreds and Arabs appear to be more commonly affected than other breeds. <br /> <br /> ==History and clinical signs==<br /> Multiple wheals are often observed and occur within a few minutes or hours of exposure to the causative agent. A history of recurrence or repeated episodes is often reported. Affected areas can vary from small, localised lesions up to 3cm in diameter, to extensive generalised areas involving large areas of skin. Lesions can occur on any part of the body but usually develop on the back, legs, flanks, neck and eyelids. Dermatographism is a specific pressure-induced type of urticaria in which wheals form in reponse to exogenous pressure, commonly these are observed in the saddle area of the horse. In severe cases the mucous membranes of the nose, mouth, anus and vulva may be involved. Pruritus may or may not be present and the lesions usually disappear rapidly.<br /> <br /> ==Diagnosis and treatment==<br /> Because of the numerous underlying causes of urticaria, definitive diagnosis may be difficult. Historical and clinical findings may lead to suspicion of the condition. The localisation of lesions (e.g. site of contact with saddle or insect repellent) or history of medication or exposure to chemicals may help to determine an underlying cause. <br /> <br /> Acute urticaria often resolves spontaneouly without requiring treatment. If urticaria is susupected all current medications should be stopped. Dexamethasone given once at a dose of 0.1 mg/kg IM usually results in resolution of clinical signs within 24 hours. Recurrent cases may require further investigation in order to determine the underlying cause. This may include further questioning about the animal's history and response to withdrawal of drugs or topical products. If no underlying cause is found, an investigation for allergies is indicated and may include intradermal allergy testing, insect control trials and an elimination (novel protein) diet. Biopsy of lesions is generally unrewarding but may reveal a mild to moderate perivascular to interstitial dermatitis. Antihistamines such as Hydroxyzine may be useful in the management of chronic urticaria but are ineffective in treating acute urticaria. Acupuncture has been reported to be effective in one horse.<br /> <br /> ==Prognosis==<br /> The prognosis with urticaria is generally favourable because general health is not usually affected. Recurrent con<br /> <br /> ==References==<br /> *Mair, T. S., Love, S., Schumacher, J., Watson, A. E. (1998) '''Equine Medicine, Surgery and Reproduction''' ''Elsevier Health Sciences''<br /> *Pascoe, R. R., Knottenbelt, D. C. (1999) '''Manual of Equine Dermatology''' ''Elsevier Health Sciences''<br /> *Rose, R. J., Hodgson, D. R. (2000) '''Manual of Equine Practice''' ''Elsevier Health Sciences''<br /> *Scott, D. W., Miller, W. H. (2003) '''Equine Dermatology''' ''Elsevier Health Sciences''<br /> <br /> [[Category:Allergic Skin Diseases]]<br /> [[Category:To Do - Blood]][[Category:To Do - SophieIgnarski]]</div>

Signarski