Difference between revisions of "Lamb Dysentery"

 
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Also known as: '''''Clostridium perfringens'' type B Enterotoxaemia
  
Also known as: Clostridium perfringens type B Enterotoxaemia
+
==Introduction==
==Description==
+
Lamb dysentery is a peracute and fatal enterotoxaemia of young lambs caused by the beta and epsilon toxins of ''Clostridium perfringens'' type B. ''C. perfringens'' is a large, gram positive, anaerobic bacillus that is ubiquitous in the environment and commensalises the gastrointestinal tract of most mammals<sup>1</sup>. Five genotypes of ''Clostridium perfringens'' exist, named A-E, and all genotypes produce potent exotoxins. There are 12 exotoxins in total, some of which are lethal and others which are of minor significance<sup>2</sup>. These are produced as pro-toxins, and are converted to their toxic forms by digestive enzymes. The enterotoxaemias are a group of diseases caused by proliferation of ''C. perfringens'' in the lumen of the gastrointestinal tract and excessive production of exotoxin.
 +
[[Image:clostridium perfringens.jpg|thumb|right|200px|Clostridium Perfingens. Source: Wikimedia Commons; Author:Don Stalons (1974)]]
 +
In healthy animals, there is a balance between multiplication of ''Clostridium perfringens'' and its passage in the faeces. This ensures that infection is maintained at a low level. However, ''C. perfringens'' is saccharolytic and is therefore able to multiply rapidly when large quantities of fermentable carbohydrate are introduced to the anaerobic conditions of the abomasum and small intestine, leading to build-up of exotoxin. Gut stasis, for example due to insufficient dietray fibre or a high gastrointestinal parasite burden, can also contribute to the accumulation of toxins.
  
Lamb dysentery is a peracute and fatal enterotoxaemia of young lambs caused by the beta and epsilon toxins of ''Clostridium perfringens'' type B. ''C. perfringens'' is a large, gram positive, anaerobic bacillus that is ubiquitous in the environment and commensalises the gastrointestinal tract of most mammals<sup>ivis</sup>. Five genotypes of ''Clostridium perfringens'' exist, named A-E, and all genotypes produce potent exotoxins. There are 12 exotoxins in total, some of which are lethal and others which are of minor significance<sup>lewis</sup>. These are produced as pro-toxins, and are converted to their toxic froms by digestive enzymes. The enterotoxaemias are a group of diseases caused by proliferation of ''C. perfringens'' in the lumen of the gastrointestinal tract and excessive production of exotoxin.
+
Enterotoxaemia due to ''Clostridium  perfringens''  type B causes severe enteritis and dysentery with a high mortality in young lambs (lamb dysentery), but also affects calves, pigs, and foals. The &beta; toxin it produces is highly necrotising and is responsible for severe intestinal damage. &epsilon; toxin also plays a part in pathogenesis. The incidence of lamb dysentery declined over the past 20 years or so, due to the widespread use of clostridial vaccines<sup>3</sup>, but the condition is now becoming a problem again as complacency reduces the use of vaccination. Outbreaks of lamb dysentery typically occur during cold, wet lambing periods when lambing ewes are confined to small areas of shelter which rapidly become unhygienic. Most cases are seen in stronger, single lambs<sup>3</sup> because these animals consume the largest quantities of milk, which functions as a growth medium for ''C. perfringens''.
 
 
In healthy animals, there is a balance between multiplication of ''Clostridium perfringens'' and its passage in the faeces. This ensures that infection is maintained at a low level.  However, ''C. perfringens'' is saccharolytic and is therefore able to multiply rapidly when large quantities of fermentable carbohydrate are introduced to the anaerobic conditions of the abomasum and small intestine, leading to build-up of exotoxin. Gut statis, for example due to insufficient dietray fibre or a high gastrointestinal parasite burden, can also contribute to the accumulation of toxins.
 
 
 
Enterotoxaemia due to ''Clostridium  perfringens''  type B causes severe enteritis and dysentery with a high mortality in young lambs and also calves, pigs, and foals. The &beta; toxin its produces is highly necrotising andis responsible for severe intestinal damage. &Epsilon; toxin also plays a part in pathogenesis.
 
 
 
sargison: Laimb dysentery is aI peracute and fatal disease of youLng
 
lamiibs caused by the beta and epsilon toxins of Clost-
 
i'ridiiio peJri-ingens type B. Over the past 20 years, the
 
disease had become rai-e due to the svidespread LIse of
 
clostr-idial xvaccines. Howverer, lamb dysenltery is becom-ing a conimon problem again due to reductions in ewe
 
vaccinations in many flocks. Affected lambs are usually
 
less than twvo vxeeks old and most commonly one to three
 
days old. The majority of cases are characterised by the
 
sporadic sudden death of stronger single lambs which
 
had been consuming the largest quantities of milk.
 
Outbreaks of lamb dysentery can occur during cold and
 
wvet springs wvhen lambing ewes are confined to small
 
sheltered areas and conditions become unhygienic. In
 
extreme cases, losses of between 20 and 30 per cent of
 
animals in a flock have been reported.
 
  
 
==Signalment==
 
==Signalment==
 +
Affected animals are unvaccinated lambs of less than two to three weeks old. The condition is most common in neonates between one and three days of age, and typically affects well-fed singletons<sup>3</sup>.
  
 
==Diagnosis==
 
==Diagnosis==
 +
A provisional diagnosis of lamb dysentery can be made on the basis of a history of sudden deaths in well-grown, unvaccinated lambs. This is supported by post-mortem findings and laboratory testing may also be useful.
  
The initial diagnosis of enterotoxaemia is made on the basis of history of sudden deaths in well-grown, unvaccinated lambs fed on a carbohydrate rich diet, supported by post-mortem finsings. Positive ELISA rtest results for identification of toxins in intestinal contents or peritoneal fluid support, but do not confirm the diagnosis because iimmune animals may have high concentrations of toxin but not suffer from its effects. The diagnosis can be confirmed by brain histopathology.
+
===Clinical Signs===
===Clincal Signs===
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Lamb dysentery often presents as sudden death of lambs less than 2-3 weeks old<sup>2, 3, 4, 5</sup>. When clinical signs are seen, these include cessation of suckling, depression and recumbency<sup>4</sup>. Animals suffer acute abdominal pain, and semi-fluid blood-stained faeces may be passed<sup>2, 3, 4, 5</sup>. However, the rapid course of disease means that faeces are often observed to be normal. In 2-3 week old lambs, lamb dysentery may present with non-specific neurological signs<sup>3</sup>.
 
 
 
 
Affected lambs are usually less than two weeks old, but sporadic suffen death of stronger single lambs does occur. Lambs may be seen with acute abdominal pain but die within four hours. Faeces are usually normal, but can be semi-fluid and blood stained.
 
 
 
merck: Lamb dysentery is an acute disease of lambs <3 wk old. Many may die before signs are seen, but some newborn lambs stop nursing, become listless, and remain recumbent. A fetid, blood-tinged diarrhea is common, and death usually occurs within a few days
 
 
 
songer: In lambs, inappetence, abdominal
 
pain and bloody diarrhea are followed
 
by recumbency and coma. Lesions consist
 
primarily of hemorrhagic enteritis,
 
with evidence of enterotoxemia (Frank,
 
1956). Chronic disease in older lambs
 
(’pine’) is characterized by chronic
 
abdominal pain without diarrhea
 
 
 
sargison: Outbreaks of lamb dysentery are initially characterised
 
by the sudden death of young lambs, but slower
 
onset disease, manifesting as acute abdominal pain and
 
non-specific nervous signs, is sometimes seen in older,
 
two- to three-\veek-old lambs. Faeces may be semi-fluid
 
and blood stained although, in most cases, they are normal
 
due to the rapid course of the disease.
 
  
 
===Laboratory Tests===
 
===Laboratory Tests===
 +
Intestinal contents or peritoneal fluid may be collected post-mortem and submitted for an [[ELISA testing|ELISA test]] to identify clostridial exotoxins. A positive result supports a diagnosis of enterotoxaemia but does not confirm it: animals with immunity to ''Clostridium perfringens'' may have high concentrations of toxin without suffering from its effects.
  
Positive ELISA rtest results for identification of toxins in intestinal contents or peritoneal fluid support, but do not confirm the diagnosis because iimmune animals may have high concentrations of toxin but not suffer from its effects.
+
Intestinal smears and scrapings readily reveal gram-positive rods<sup>3, 6</sup>. Culture of intestinal contents can yield almost pure growths of ''C. perfringens''<sup>6</sup>, but again this is supportive rather than diagnostic of lamb dysentery<sup>3</sup>.
  
 +
===Pathology===
 +
On post-mortem examination, segments of the intestines appear dark red-purple and distended, and show mucosal ulceration<sup>3, 6</sup>. The peritoneal fluid is blood-stained and liver may be pale and friable. The kidneys are often enlarged<sup>3</sup>.
  
watt: similar lesions has been described involving
+
Histologically, numerous gram-positive rods are present in intestinal smears and scrapings<sup>3, 6</sup>.
Cl wet1ihil type C.) The causal organism is readily demonstrated
 
on1 s.mear anld its cxact identity can be conifirmed in the
 
laboratory.
 
  
===Pathology===
+
==Treatment and Control==
 +
Presentation of lamb dysentery is usually peracute, with sudden deaths occurring before treatment can be implemented. Even if animals are found prior to death, treatment is usually unrewarding as organs are irreversibly damaged by toxins by the time signs present<sup>2</sup>. Instead, a definitive diagnosis should be pursued before greater losses occur, and the farmer should be encouraged to submit the carcase for further investigations.
  
Hemorrhagic enteritis with ulceration of the mucosa is the major lesion in all species. Grossly, the affected portion of the intestine is deep blue-purple and appears at first glance to be an infarction associated with mesenteric torsion. Smears of intestinal contents can be examined for large numbers of gram-positive, rod-shaped bacteria, and filtrates made for detection of toxin and subsequent identification by neutralization with specific antiserum
+
As treatment is so ineffective, much emphasis is put on to the control of lamb dysentery. '''Vaccination''' in the face of an outbreak has been shown to be effective<sup>7</sup>, and specific hyperimmune serum can also be administered<sup>4, 6t</sup>. Oral antibiotics may be given<sup>4</sup> but are regarded as a less appropriate therepautic. Management measures such as removing the flock from a particular pasture or reducing concentrate feeding may be implemented in other clostridial diseases but are of no benefit in lamb dysentery: over-ingestion of the dam's milk combined with poor hygiene are responsible for this disease. Therefore, sufficient supervision should be given at lambing time to ensure adequate intakes of colostrum and the maintenance of good hygiene.
  
watt: Diagnosis on post mortem examination is
+
Lamb dysentery can be controlled through vaccination against clostridial diseases. Before the development of modern clostridial vaccines in the 1970s, catastrophic losses of up to 30% of the lamb crop could occur due to lamb dysentery<sup>2</sup>. The vaccines used today are effective against a variety of clostridial diseases and some vaccines are combined for effects against ''Pasteurella''. The vaccines consist of toxoids which are inactivated forms of the toxins produced by clostridial organisms. The principles of vaccination are the same whether a clostridium-only or ''Pasteurella''-combined product is used: a sensitising dose must be given 4-6 weeks before a second, confirming dose<sup>2</sup>. As immunity wanes over a period of a year booster doses are required annually. Therefore, ewes should receive the primary vaccination course before entering the breeding flock and an annual booster approximately six weeks before lambing. Timing the booster vaccination in this way affords passive protection to lambs until they are around sixteen weeks of age. Lambs born to unvaccinated ewes should be vaccinated between 3 and 12 weeks old, with a second injection given at least four weeks later.
usually obx ious with areas of the small intestine markedly
 
hy peraemic and with characteristic ulceration of the mucosa.
 
(Disease presentinig similar lesions has been described involving
 
Cl wet1ihil type C.)
 
  
==Treatment==
+
==Literature Search==
 +
[[File:CABI logo.jpg|left|90px]]
  
Presentation of lamb dysentery is usually peracute, with sudden deaths occuring before treatment can be implemented. Even if animals are seen in the stages of disease preceeding death, treatment is usually ineffective. Suggested drugs include oral antibiotics and specific hyperimmune serum<sup>Merck</sup>.
 
  
Lamb dysentery can be controlled through vaccination against clostridial diseases. Before ewes enter the breeding flock, they should be given two vaccinations separated by an interval of 4-6 weeks. An annual booster should be given about six weeks before lambing to afford passive protection to lambs until around sixteen weeks of age. Lambs born to unvaccinated ewes should themselves be vaccinated at between 3 and 12 weeks old, with a second injection given at least four weeks later. Good husbandry is also critical to the control of lamb dysentery. Lambing is a particularly important period where supervision and hygiene should be maintainted and adequate colostrum intake should be ensured. Care should be taken when introducing animals to an improved plane of nutrition.
+
Use these links to find recent scientific publications via CAB Abstracts (log in required unless accessing from a subscribing organisation).
 +
<br><br><br>
 +
[http://www.cabdirect.org/search.html?q=title%3A%28%27%27Clostridium+perfringens%27%27+type+B+Enterotoxaemia%29+OR+title%3A%28%22lamb+dysentery%22%29 Lamb dysentery publications]
  
watt: In the face of ain outbreak each lamb born must be
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==Links==
treated with atntiserumii and a programme of ewe % accination
 
instituted be tote subsequent lambings.
 
  
==Links==
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*[http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/50713.htm The Merck Veterinary Manual: Enterotoxemia Caused by ''Clostridium perfringens'' Types B and C]
 +
*[http://www.ivis.org/advances/Disease_Factsheets/epsilon_toxin_clostridium.pdf The Center for Food Security and Public Health Animal Disease Factsheet: Epsilon toxin of ''Clostridium perfringens''.]
 +
*[http://www.noah.co.uk/issues/briefingdoc/22-vaccfarmanimals.htm NOAH: Vaccination of farm animals]
 +
*[http://www.clostridia.net/Cperfringens.htm Clostridia.net - ''Clostridium perfringens'']
  
 
==References==
 
==References==
  
 +
#Van Metre (2006) Clostridial Infections of the Ruminant GI Tract. ''Proceedings of the North American Veterinary Conference 2006''.
 +
#Lewis, C (1998) Aspects of clostridial disease in sheep. ''In Practice'', '''20(9)''', 494-499.
 +
#Sargison, N (2004) Differential diagnosis of diarrhoea in lambs. ''In Practice'', '''26(1)''', 20-27.
 
#Merck & Co (2008) '''The Merck Veterinary Manual (Eighth Edition)''', ''Merial''.
 
#Merck & Co (2008) '''The Merck Veterinary Manual (Eighth Edition)''', ''Merial''.
#The Center for Food Security and Public Health, Iowa State University (2004) [http://www.ivis.org/advances/Disease_Factsheets/epsilon_toxin_clostridium.pdf Animal Disease Factsheet: Epsilon toxin of Clostridium Perfringens.]
 
 
#Songer, J G (1998) Clostridial diseases of small ruminants. ''Veterinary Research'', '''29''', 219-232.
 
#Songer, J G (1998) Clostridial diseases of small ruminants. ''Veterinary Research'', '''29''', 219-232.
#Van Metre (2006) Clostridial Infections of the Ruminant GI Tract. ''Proceedings of the North American Veterinary Conference 2006''
 
#Lewis, C (1998) Aspects of clostridial disease in sheep. ''In Practice'', '''20(9)''', 494-499.
 
#Sargison, N (2004) Differential diagnosis of diarrhoea in lambs. ''In Practice'', '''26(1)''', 20-27.
 
 
#Watt, A (1980) Neonatal losses in lambs. ''In Practice'', '''2(2)''', 5-9.
 
#Watt, A (1980) Neonatal losses in lambs. ''In Practice'', '''2(2)''', 5-9.
#Lewis, C (2000) Vaccination of sheep: an update. ''In Practice'', ''22(1)'', 34-39.
+
#West, D M (1993) Vaccines as therapeutics. ''Proceedings of the Third International Sheep Veterinary Society Conference'', '''17''', 111-115.
 +
#The Center for Food Security and Public Health, Iowa State University (2004) [http://www.ivis.org/advances/Disease_Factsheets/epsilon_toxin_clostridium.pdf Animal Disease Factsheet: Epsilon toxin of ''Clostridium perfringens''.]
 +
#Lewis, C (2000) Vaccination of sheep: an update. ''In Practice'', '''22(1)''', 34-39.
 +
 
  
[[Category:Enteritis,_Bacterial]][[Category:Enteritis,_Fibrinous/Haemorrhagic]] [[Category: WikiClinical Ovine]]
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{{review}}
[[Category:To_Do_-_Lizzie]]
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[[Category:Enteritis,_Bacterial]][[Category:Enteritis,_Fibrinous/Haemorrhagic]] [[Category:Intestinal Diseases - Sheep]]
 +
[[Category:Brian Aldridge reviewing]]

Latest revision as of 17:57, 10 May 2011

Also known as: Clostridium perfringens type B Enterotoxaemia

Introduction

Lamb dysentery is a peracute and fatal enterotoxaemia of young lambs caused by the beta and epsilon toxins of Clostridium perfringens type B. C. perfringens is a large, gram positive, anaerobic bacillus that is ubiquitous in the environment and commensalises the gastrointestinal tract of most mammals1. Five genotypes of Clostridium perfringens exist, named A-E, and all genotypes produce potent exotoxins. There are 12 exotoxins in total, some of which are lethal and others which are of minor significance2. These are produced as pro-toxins, and are converted to their toxic forms by digestive enzymes. The enterotoxaemias are a group of diseases caused by proliferation of C. perfringens in the lumen of the gastrointestinal tract and excessive production of exotoxin.

Clostridium Perfingens. Source: Wikimedia Commons; Author:Don Stalons (1974)

In healthy animals, there is a balance between multiplication of Clostridium perfringens and its passage in the faeces. This ensures that infection is maintained at a low level. However, C. perfringens is saccharolytic and is therefore able to multiply rapidly when large quantities of fermentable carbohydrate are introduced to the anaerobic conditions of the abomasum and small intestine, leading to build-up of exotoxin. Gut stasis, for example due to insufficient dietray fibre or a high gastrointestinal parasite burden, can also contribute to the accumulation of toxins.

Enterotoxaemia due to Clostridium perfringens type B causes severe enteritis and dysentery with a high mortality in young lambs (lamb dysentery), but also affects calves, pigs, and foals. The β toxin it produces is highly necrotising and is responsible for severe intestinal damage. ε toxin also plays a part in pathogenesis. The incidence of lamb dysentery declined over the past 20 years or so, due to the widespread use of clostridial vaccines3, but the condition is now becoming a problem again as complacency reduces the use of vaccination. Outbreaks of lamb dysentery typically occur during cold, wet lambing periods when lambing ewes are confined to small areas of shelter which rapidly become unhygienic. Most cases are seen in stronger, single lambs3 because these animals consume the largest quantities of milk, which functions as a growth medium for C. perfringens.

Signalment

Affected animals are unvaccinated lambs of less than two to three weeks old. The condition is most common in neonates between one and three days of age, and typically affects well-fed singletons3.

Diagnosis

A provisional diagnosis of lamb dysentery can be made on the basis of a history of sudden deaths in well-grown, unvaccinated lambs. This is supported by post-mortem findings and laboratory testing may also be useful.

Clinical Signs

Lamb dysentery often presents as sudden death of lambs less than 2-3 weeks old2, 3, 4, 5. When clinical signs are seen, these include cessation of suckling, depression and recumbency4. Animals suffer acute abdominal pain, and semi-fluid blood-stained faeces may be passed2, 3, 4, 5. However, the rapid course of disease means that faeces are often observed to be normal. In 2-3 week old lambs, lamb dysentery may present with non-specific neurological signs3.

Laboratory Tests

Intestinal contents or peritoneal fluid may be collected post-mortem and submitted for an ELISA test to identify clostridial exotoxins. A positive result supports a diagnosis of enterotoxaemia but does not confirm it: animals with immunity to Clostridium perfringens may have high concentrations of toxin without suffering from its effects.

Intestinal smears and scrapings readily reveal gram-positive rods3, 6. Culture of intestinal contents can yield almost pure growths of C. perfringens6, but again this is supportive rather than diagnostic of lamb dysentery3.

Pathology

On post-mortem examination, segments of the intestines appear dark red-purple and distended, and show mucosal ulceration3, 6. The peritoneal fluid is blood-stained and liver may be pale and friable. The kidneys are often enlarged3.

Histologically, numerous gram-positive rods are present in intestinal smears and scrapings3, 6.

Treatment and Control

Presentation of lamb dysentery is usually peracute, with sudden deaths occurring before treatment can be implemented. Even if animals are found prior to death, treatment is usually unrewarding as organs are irreversibly damaged by toxins by the time signs present2. Instead, a definitive diagnosis should be pursued before greater losses occur, and the farmer should be encouraged to submit the carcase for further investigations.

As treatment is so ineffective, much emphasis is put on to the control of lamb dysentery. Vaccination in the face of an outbreak has been shown to be effective7, and specific hyperimmune serum can also be administered4, 6t. Oral antibiotics may be given4 but are regarded as a less appropriate therepautic. Management measures such as removing the flock from a particular pasture or reducing concentrate feeding may be implemented in other clostridial diseases but are of no benefit in lamb dysentery: over-ingestion of the dam's milk combined with poor hygiene are responsible for this disease. Therefore, sufficient supervision should be given at lambing time to ensure adequate intakes of colostrum and the maintenance of good hygiene.

Lamb dysentery can be controlled through vaccination against clostridial diseases. Before the development of modern clostridial vaccines in the 1970s, catastrophic losses of up to 30% of the lamb crop could occur due to lamb dysentery2. The vaccines used today are effective against a variety of clostridial diseases and some vaccines are combined for effects against Pasteurella. The vaccines consist of toxoids which are inactivated forms of the toxins produced by clostridial organisms. The principles of vaccination are the same whether a clostridium-only or Pasteurella-combined product is used: a sensitising dose must be given 4-6 weeks before a second, confirming dose2. As immunity wanes over a period of a year booster doses are required annually. Therefore, ewes should receive the primary vaccination course before entering the breeding flock and an annual booster approximately six weeks before lambing. Timing the booster vaccination in this way affords passive protection to lambs until they are around sixteen weeks of age. Lambs born to unvaccinated ewes should be vaccinated between 3 and 12 weeks old, with a second injection given at least four weeks later.

Literature Search

CABI logo.jpg


Use these links to find recent scientific publications via CAB Abstracts (log in required unless accessing from a subscribing organisation).


Lamb dysentery publications

Links

References

  1. Van Metre (2006) Clostridial Infections of the Ruminant GI Tract. Proceedings of the North American Veterinary Conference 2006.
  2. Lewis, C (1998) Aspects of clostridial disease in sheep. In Practice, 20(9), 494-499.
  3. Sargison, N (2004) Differential diagnosis of diarrhoea in lambs. In Practice, 26(1), 20-27.
  4. Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial.
  5. Songer, J G (1998) Clostridial diseases of small ruminants. Veterinary Research, 29, 219-232.
  6. Watt, A (1980) Neonatal losses in lambs. In Practice, 2(2), 5-9.
  7. West, D M (1993) Vaccines as therapeutics. Proceedings of the Third International Sheep Veterinary Society Conference, 17, 111-115.
  8. The Center for Food Security and Public Health, Iowa State University (2004) Animal Disease Factsheet: Epsilon toxin of Clostridium perfringens.
  9. Lewis, C (2000) Vaccination of sheep: an update. In Practice, 22(1), 34-39.