Porcine Adenomatosis Complex - Revision history

Bara: Redirected page to Lawsonia intracellularis

2011-03-14T15:12:40Z

Redirected page to Lawsonia intracellularis

Bara at 14:53, 14 March 2011

2011-03-14T14:53:31Z

Kthompson at 21:26, 7 March 2011

2011-03-07T21:26:20Z

Kthompson at 21:25, 7 March 2011

2011-03-07T21:25:35Z

Kthompson at 21:19, 7 March 2011

2011-03-07T21:19:52Z

Kthompson at 21:16, 7 March 2011

2011-03-07T21:16:36Z

Kthompson at 21:08, 7 March 2011

2011-03-07T21:08:02Z

Kthompson at 21:05, 7 March 2011

2011-03-07T21:05:50Z

Kthompson at 21:01, 7 March 2011

2011-03-07T21:01:02Z

Kthompson at 20:57, 7 March 2011

2011-03-07T20:57:05Z

← Older revision		Revision as of 15:12, 14 March 2011
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−	~~{{review}}~~	+	#redirect[[Lawsonia intracellularis]]
−
−	~~Also known as: '''''Porcine intestinal adenomatosis - Porcine Proliferative Enteropathy '''''~~
−
−	~~== Introduction ==~~
−
−	~~This is a disease caused by the obligatory intracellular organism ''~~[[Lawsonia intracellularis]]'', a spirochete that does not grow well in the laboratory except in tissue culture. It is only seen in pigs, worldwide, including the United Kingdom. It is characterised by proliferative changes in the epithelium of the small and large intestinal mucosa.
−
−	~~==Signalment==~~
−
−	~~It is a disease that can affect pigs of all ages, but most severe clinical signs tend to appear in weanlings and growers. The infection is transmitted orally.~~
−
−	~~==Pathogenesis==~~
−
−	~~The disease appears in four different presentations:~~
−
−	~~'''Intestinal adenomatosis - '''The basic hyperplastic and metaplastic changes are seen in the epithelium, which causes chronic weight loss and diarrhoea.~~
−
−	'''Necrotic enteritis''' - Predominately affects the colon and terminal ileum and parts of the hyperplastic mucosa develop erosions and ulcerations which then become colonised by ''Fusiformis'' baceria.
−
−	'''Terminal ileitis - '''Characterised by marked hypertrophic thickening of the muscular portion of the wall of the terminal ileum and there is associated thickening of the mucosa due to hypertrophy and secondary granulomatous inflammation, which is caused by a degree of obstruction to the passage of ingesta along the bowel caused by the mucosal hypertrophy. Its appearance is very similar to [[Johne's Disease\|Johnes disease]] with lots of mononuclear cells and a chronic granulomatous type of inflammation.
−
−	'''Proliferative haemorrhagic syndrome - '''The bowel shows proliferation but with ulceration and copious haemorrhage into the bowel lumen. Animals are often found dead. The pathogenesis is unclear but may involve a type of hypersensitivity reaction or secondary infection of some type.
−
−	~~== Clinical Signs ==~~
−
−	~~Clinical signs are variable and can range from anything from poor weight gain to diarrhoea, weight loss, cachexia and death and appears usually in weaned pigs from age 3-4 weeks to adulthood.~~
−
−	~~It is seen often as a problem in closed, low infection herds and can lead to a decrease in production of up to 8%. It is not seen in pigs with lots of other pathogens in guts.~~
−
−	~~== Diagnosis ==~~
−
−	Clinical signs of a failure to thrive and history of a closed herd plus signalment of pigs is indicative. On post mortem examination, the terminal [[Small Intestine Overview - Anatomy & Physiology\|small intestine]] and [[Colon - Anatomy & Physiology\|colon]] are affected by proliferation of the mucosal epithelium. Signs will include thickened mucosal epithelium, polypoid-like nodules several millimetres in diameter. There may also be undifferentiated epithelium replacing goblet cells. Its appearance is almost neoplastic.
−
−	Histologically it will appear similar to a virus induced proliferation. Organisms seen in the apical part of epithelial cells lining glands of terminal [[Ileum - Anatomy & Physiology\|ileum]], [[Colon - Anatomy & Physiology\|colon]] and [[Caecum - Anatomy & Physiology\|caecum]]. The organism can be stained by silver staining by the use of antibody in immunofluorescence or PCR.
−
−	~~== Treatment and Control ==~~
−
−	~~Individually affected animals may be treated with tetracyclines parenterally. These animals must be isolated. In affected groups the same treatment can be given via the drinking water.~~
−
−	~~Any new genetic material into the herd should be by A.I. or embryo transfer only so as to reduce risk of introduction of the disease into the herd.~~
−
−	Vaccination as a control measure is now readily available and will reduce clinical signs of the disease and improve performance. Vaccine is given orally from 3 weeks of age and provides protection for up to 17 weeks. This is excellent for finishing stock, but boosters will need to be given for stock kept on as breeding herd if this is farm protocol.
−
−	~~== References ==~~
−
−	~~Cowart, R.P. and Casteel, S.W. (2001) An Outline of Swine diseases: a handbook Wiley-Blackwell~~
−
−	~~Jackson, G.G. and Cockcroft, P.D. (2007) Handbook of Pig Medicine Saunders Elsevier~~
−
−	~~Straw, B.E. and Taylor, D.J. (2006) Disease of Swine Wiley-Blackwell~~
−
−	~~Taylor, D.J. (2006) Pig Diseases (Eighth edition) St Edmunsdbury Press~~
−
−
−
−
−	~~[[Category:Enteritis,_Proliferative]] [[Category:Intestinal_Diseases_-_Pig]] [[Category:Enteritis,_Bacterial]] [[Category:Expert_Review - Farm Animal~~]]

@@ Line 1: / Line 1: @@
-== Synonyms  ==
+{{review}}
-Porcine intestinal adenomatosis or Porcine Proliferative Enteropathy
+Also known as: '''''Porcine intestinal adenomatosis - Porcine Proliferative Enteropathy '''''
-<br>
+== Introduction  ==
-== Introduction  ==
+==Pathogenesis==
-This is a disease caused by the obligatory intracellular organism Lawsonia intracellularis, a spirochete that does not grow well in the laboratory excpet in tissue culture. It is only seen in pigs, worldwide, including&nbsp;the United Kingdom. It is characterised by proliferative&nbsp;changes in&nbsp;the epithelium of the&nbsp;small and large intestinal mucosa.&nbsp;<br>It is a disease that can affect pigs of all ages, but most severe clinical signs tend to appear in weanlings and growers. The infection is transmitted orally.
+'''Necrotic enteritis''' - Predominately affects the colon and terminal ileum and parts of the hyperplastic mucosa develop erosions and ulcerations which then become colonised by ''Fusiformis'' baceria.
-The disease appears in four different presentations:<br>'''Intestinal adenomatosis - '''The basic hyperplastic and metaplastic changes are seen in the epithelium, which causes&nbsp;chronic weight loss and diarrhoea. <br>'''Necrotic enteritis''' - Predominately affects the colon and terminal ileum and parts of the hyperplastic mucosa develop erosions and ulcerations which then&nbsp;become colonised by Fusiformis baceria. <br>'''Terminal ileitis -&nbsp;'''Characterised by marked hypertrophic thickening of the muscular portion of the wall of the terminal ileum and there is associated thickening of the mucosa due to hypertrophy and secondary granulomatous inflammation, which is caused by a degree of obstruction to the passage of ingesta along the bowel caused by the mucosal hypertrophy. Its appearance is&nbsp;very similar to Johnes disease with lots of mononuclear cells and a chronic granulomatous type of inflammation. <br>'''Proliferative haemorrhagic syndrome - '''The bowel shows proliferation but with ulceration and copious haemorrhage into the bowel lumen.&nbsp;Animals are often be found dead. The pathogenesis is unclear but may involve a type of hypersensitivity reaction or secondary infection of some type. <br>
+'''Terminal ileitis - '''Characterised by marked hypertrophic thickening of the muscular portion of the wall of the terminal ileum and there is associated thickening of the mucosa due to hypertrophy and secondary granulomatous inflammation, which is caused by a degree of obstruction to the passage of ingesta along the bowel caused by the mucosal hypertrophy. Its appearance is very similar to [[Johne's Disease|Johnes disease]] with lots of mononuclear cells and a chronic granulomatous type of inflammation.
-<br>
+'''Proliferative haemorrhagic syndrome - '''The bowel shows proliferation but with ulceration and copious haemorrhage into the bowel lumen. Animals are often found dead. The pathogenesis is unclear but may involve a type of hypersensitivity reaction or secondary infection of some type.
 == Clinical Signs  ==
-Clinical signs are variable and can range from anything from poor weight gain to diarrhoea, weight loss, cachexia and death and appears usually in weaned pigs from age 3-4 weeks to adulthood.<br>It is seen often as a problem in closed, low infection herds and can lead to a decrease in production of up to 8%. It is not seen in pigs with lots of other pathogens in guts.
+Clinical signs are variable and can range from anything from poor weight gain to diarrhoea, weight loss, cachexia and death and appears usually in weaned pigs from age 3-4 weeks to adulthood.
-<br>
+It is seen often as a problem in closed, low infection herds and can lead to a decrease in production of up to 8%. It is not seen in pigs with lots of other pathogens in guts.
 == Diagnosis  ==
-Clinical signs of a failure to thirve and history of a closed herd plus signalment of pigs is indicative. On post mortem examination the terminal [[Small Intestine Overview - Anatomy & Physiology|small intestine]] and [[Colon - Anatomy & Physiology|colon]] are affected by proliferation of the mucosal epithelium. Signs will include thickened mucosal epithelium, polypoid-like nodules several millimetres in diameter. there may also be undifferentiated epithelium replaces goblet cells. Its appearance is almost neoplastic. <br>Histologically it will appear similar to a virus induced proliferation. Organisms seen in the apical part of epithelial cells lining glands of terminal [[Ileum - Anatomy & Physiology|ileum]], [[Colon - Anatomy & Physiology|colon]] and [[Caecum - Anatomy & Physiology|caecum]]. The organism can be stained by silver staining by the use of aintibody in immunofluresence or PCR.
+Clinical signs of a failure to thrive and history of a closed herd plus signalment of pigs is indicative. On post mortem examination, the terminal [[Small Intestine Overview - Anatomy & Physiology|small intestine]] and [[Colon - Anatomy & Physiology|colon]] are affected by proliferation of the mucosal epithelium. Signs will include thickened mucosal epithelium, polypoid-like nodules several millimetres in diameter. There may also be undifferentiated epithelium replacing goblet cells. Its appearance is almost neoplastic.
-<br>
+Histologically it will appear similar to a virus induced proliferation. Organisms seen in the apical part of epithelial cells lining glands of terminal [[Ileum - Anatomy & Physiology|ileum]], [[Colon - Anatomy & Physiology|colon]] and [[Caecum - Anatomy & Physiology|caecum]]. The organism can be stained by silver staining by the use of antibody in immunofluorescence or PCR.
 == Treatment and Control  ==
-Individually affected animals may be treated with tetracyclines parenterally. These animals must be isolated. In affected groups the same treatment can be given via the drinking water.<br>Any new genetic material into the herd should be by A.I. or embryo transfer only so as to reduce risk of introduction of the disease into the herd.
+Individually affected animals may be treated with tetracyclines parenterally. These animals must be isolated. In affected groups the same treatment can be given via the drinking water.
-Vaccination as a control measure is now readily avaliable and will reduce clinical signs of the disease and imporove performance. Vaccine is given orally from 3 weeks of age and provides protection for up to 17 weeks. This is excellent for finishing stock, but boosters will need to be given for stock kept on as breeding herd if this is farm protocol.
+Any new genetic material into the herd should be by A.I. or embryo transfer only so as to reduce risk of introduction of the disease into the herd.
-<br>
+Vaccination as a control measure is now readily available and will reduce clinical signs of the disease and improve performance. Vaccine is given orally from 3 weeks of age and provides protection for up to 17 weeks. This is excellent for finishing stock, but boosters will need to be given for stock kept on as breeding herd if this is farm protocol.
 == References  ==
-Cowart, R.P. and Casteel, S.W. (2001) An Outline of Swine diseases: a handbook Wiley-Blackwell <br>Jackson, G.G. and Cockcroft, P.D. (2007) Handbook of Pig Medicine Saunders Elsevier <br>Straw, B.E. and Taylor, D.J. (2006) Disease of Swine Wiley-Blackwell <br>Taylor, D.J. (2006) Pig Diseases (Eighth edition) St Edmunsdbury Press
+Cowart, R.P. and Casteel, S.W. (2001) An Outline of Swine diseases: a handbook Wiley-Blackwell
-[[Category:Enteritis,_Proliferative]] [[Category:Intestinal_Diseases_-_Pig]] [[Category:Enteritis,_Bacterial]] [[Category:To_Do_-_Review]]
+[[Category:Enteritis,_Proliferative]] [[Category:Intestinal_Diseases_-_Pig]] [[Category:Enteritis,_Bacterial]] [[Category:Expert_Review - Farm Animal]]

@@ Line 31: / Line 31: @@
 Vaccination as a control measure is now readily avaliable and will reduce clinical signs of the disease and imporove performance. Vaccine is given orally from 3 weeks of age and provides protection for up to 17 weeks. This is excellent for finishing stock, but boosters will need to be given for stock kept on as breeding herd if this is farm protocol.
+== References  ==
 Cowart, R.P. and Casteel, S.W. (2001) An Outline of Swine diseases: a handbook Wiley-Blackwell <br>Jackson, G.G. and Cockcroft, P.D. (2007) Handbook of Pig Medicine Saunders Elsevier <br>Straw, B.E. and Taylor, D.J. (2006) Disease of Swine Wiley-Blackwell <br>Taylor, D.J. (2006) Pig Diseases (Eighth edition) St Edmunsdbury Press
@@ Line 41: / Line 41: @@
 <br>
-[[Category:Enteritis,_Proliferative]] [[Category:Intestinal_Diseases_-_Pig]] [[Category:Enteritis,_Bacterial]] [[Category:To_Do_-_Kate]]
+[[Category:Enteritis,_Proliferative]] [[Category:Intestinal_Diseases_-_Pig]] [[Category:Enteritis,_Bacterial]] [[Category:To_Do_-_Review]]

@@ Line 29: / Line 29: @@
 Individually affected animals may be treated with tetracyclines parenterally. These animals must be isolated. In affected groups the same treatment can be given via the drinking water.<br>Any new genetic material into the herd should be by A.I. or embryo transfer only so as to reduce risk of introduction of the disease into the herd.
 Vaccination as a control measure is now readily avaliable and will reduce clinical signs of the disease and imporove performance. Vaccine is given orally from 3 weeks of age and provides protection for up to 17 weeks. This is excellent for finishing stock, but boosters will need to be given for stock kept on as breeding herd if this is farm protocol.
 &nbsp;

@@ Line 23: / Line 23: @@
 Clinical signs of a failure to thirve and history of a closed herd plus signalment of pigs is indicative. On post mortem examination the terminal [[Small Intestine Overview - Anatomy & Physiology|small intestine]] and [[Colon - Anatomy & Physiology|colon]] are affected by proliferation of the mucosal epithelium. Signs will include thickened mucosal epithelium, polypoid-like nodules several millimetres in diameter. there may also be undifferentiated epithelium replaces goblet cells. Its appearance is almost neoplastic. <br>Histologically it will appear similar to a virus induced proliferation. Organisms seen in the apical part of epithelial cells lining glands of terminal [[Ileum - Anatomy & Physiology|ileum]], [[Colon - Anatomy & Physiology|colon]] and [[Caecum - Anatomy & Physiology|caecum]]. The organism can be stained by silver staining by the use of aintibody in immunofluresence or PCR.
-== Treatment and Control ==
+Individually affected animals may be treated with tetracyclines parenterally. These animals must be isolated. In affected groups the same treatment can be given via the drinking water.<br>Any new genetic material into the herd should be by A.I. or embryo transfer only so as to reduce risk of introduction of the disease into the herd.
-Individually affected animals may be treated with tetracyclines parenterally. These animals must be isolated. In affected groups the same treatment can be given via the drinking water.<br>Any new genetic material into the herd should be by A.I. or embryo transfer only so as to reduce risk of introduction of the disease into the herd.
+Vaccination as a control measure is now readily avaliable and will reduce clinical signs of the disease and imporove performance. Vaccine is given orally from 3 weeks of age and provides protection for up to 17 weeks. This is excellent for finishing stock, but boosters will need to be given for stock kept on as breeding herd if this is farm protocol.
 &nbsp;

@@ Line 21: / Line 21: @@
 == Diagnosis  ==
-==== Pathology  ====
+Clinical signs and history of a closed herd plus signalment of pigs is indicative. On post mortem examination the terminal [[Small Intestine Overview - Anatomy & Physiology|small intestine]] and [[Colon - Anatomy & Physiology|colon]] are affected by proliferation of the mucosal epithelium. Signs will include thickened mucosal epithelium, polypoid-like nodules several millimetres in diameter. there may also be undifferentiated epithelium replaces goblet cells. Its appearance is almost neoplastic. <br>Histologically it will appear similar to a virus induced proliferation. Organisms seen in the apical part of epithelial cells lining glands of terminal [[Ileum - Anatomy & Physiology|ileum]], [[Colon - Anatomy & Physiology|colon]] and [[Caecum - Anatomy & Physiology|caecum]].
-*The terminal [[Small Intestine Overview - Anatomy & Physiology|small intestine]] and [[Colon - Anatomy & Physiology|colon]] are affected by proliferation of the mucosal epithelium.
+&nbsp;
 <br>
 [[Category:Enteritis,_Proliferative]] [[Category:Intestinal_Diseases_-_Pig]] [[Category:Enteritis,_Bacterial]] [[Category:To_Do_-_Kate]]

@@ Line 11: / Line 11: @@
 The disease appears in four different presentations:<br>'''Intestinal adenomatosis - '''The basic hyperplastic and metaplastic changes are seen in the epithelium, which causes&nbsp;chronic weight loss and diarrhoea. <br>'''Necrotic enteritis''' - Predominately affects the colon and terminal ileum and parts of the hyperplastic mucosa develop erosions and ulcerations which then&nbsp;become colonised by Fusiformis baceria. <br>'''Terminal ileitis -&nbsp;'''Characterised by marked hypertrophic thickening of the muscular portion of the wall of the terminal ileum and there is associated thickening of the mucosa due to hypertrophy and secondary granulomatous inflammation, which is caused by a degree of obstruction to the passage of ingesta along the bowel caused by the mucosal hypertrophy. Its appearance is&nbsp;very similar to Johnes disease with lots of mononuclear cells and a chronic granulomatous type of inflammation. <br>'''Proliferative haemorrhagic syndrome - '''The bowel shows proliferation but with ulceration and copious haemorrhage into the bowel lumen.&nbsp;Animals are often be found dead. The pathogenesis is unclear but may involve a type of hypersensitivity reaction or secondary infection of some type. <br>
-== Clinical Signs ==
+Clinical signs are variable and can range from anything from poor weight gain to diarrhoea, weight loss, cachexia and death.
-<br><br>
+It is seen often as a problem in closed, low infection herds and is not seen in pigs with lots of other pathogens in guts.
-*Anything from poor weight gain to diarrhoea, weight loss, cachexia and death.
-*Seen often as problem in closed, low infection herds.
+== Diagnosis ==
 ==== Pathology  ====