Difference between revisions of "Lamb Dysentery"

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Also known as: '''''Clostridium perfringens'' type B Enterotoxaemia
+
{{unfinished}}
  
==Introduction==
+
Also known as: Clostridium perfringens type B Enterotoxaemia
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.
+
==Description==
[[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.
 
  
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''.
+
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.
 +
 
 +
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 (lamb dysentery), but also in 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 vaccins<sup>sargison</sup>, but the condition is now becoming a problem again as complacency reduces flocks vaccinating for the disease. 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>sargison</sup>, because these animals consume the largest quantities of milk which functions as a growth medium for ''C. perfringens''. In extreme cases, 20-30% of lambs can be lost to lamb dysentery.
  
 
==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>.
+
 
 +
Affected animals are unvaccinated lambs of less than two weeks old. The condition is most common in neonates between one and three days of age, and typically affects well-fed singletons<sup>sargison</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.
 
  
===Clinical Signs===
+
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.
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>.
+
 
 +
===Clincal Signs===
 +
 
 +
Lamb dysentery often presents as sudden death of lambs less than 2-3 weeks old<sup>sargison, lewis, merk, songer</sup>. When clinical signs are seen, these include cessation of suckling, depression and recumbency<sup>merck</sup>. Animals suffer acute abdominal pain, and semi-fluid blood-stained faeces may be passed<sup>sargison, leis merck, sanger</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>sargison</sup>.
  
 
===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.
 
  
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>.
+
Intestinal contents or pertioneal 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 with suffering from its effects.
 +
 
 +
Intestinal smears and scrapings readily reveal gram-positive rods<sup>sargison, watt</sup>. Culture of intestinal contents can yield almost pure growths of ''C. perfringens''<sup>watt</sup>, but this is again supportive rather than diagnostic<sup>sargison</sup>.
  
 
===Pathology===
 
===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>.
 
  
Histologically, numerous gram-positive rods are present in intestinal smears and scrapings<sup>3, 6</sup>.
+
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
 +
 
 +
watt: Diagnosis on post mortem examination is
 +
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 and Control==
+
sargison At postmortem examination. localised
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.  
+
areaLs ot the intestinies appear dark red and distended,
 +
with ulceration otl the mucosa and serous, blood-stained
 +
peritoneal fluid. The liver may be pale and friable and
 +
the kidnieys enlarged. Numerous Gram-positixe rods are
 +
present in smears from intestinal scrapings.
  
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.
+
==Treatment==
  
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.
+
Presentation of lamb dysentery is usually peracute, with sudden deaths occuring 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>lewis</lewis>. Instead, a definitive diagnosis should be pursued before great losses occur,and the farmer should be encouraged to submit the carcase for further investigations.  
  
==Literature Search==
+
Suggested drugs include oral antibiotics<sup>merck</sup> and specific hyperimmune serum<sup>Merck, watt</sup>.  
[[File:CABI logo.jpg|left|90px]]
 
  
 +
Control of an outbreak of clostridial
 +
disease involves a dual approach of
 +
management techniques and therapy.
 +
In the case of the enterotoxaemias,
 +
vaccination in the face of an outbreak
 +
has proved effective (West 1993).
 +
Alternatively, particularly for lamb
 +
dysentery and tetanus, antisera can be
 +
administered. Management measures
 +
for some of the clostridial conditions
 +
include the removal of the remainder
 +
of the flock from a particular pasture
 +
or a reduction in concentrate feeding.
 +
The reduction of stress factors, as well
 +
as the gradual introduction of any
 +
new feeds or feeding regimens, also
 +
reduces the likelihood of disease. The
 +
cost of controls can be high in terms of
 +
time, labour and possibly further losses
 +
due to the stress of gathering the
 +
animals for treatment. Of all the diseases
 +
that afflict sheep, the clostridials
 +
are the ideal candidates for control by
 +
vaccination
  
Use these links to find recent scientific publications via CAB Abstracts (log in required unless accessing from a subscribing organisation).
+
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.
<br><br><br>
+
Before the advent of modern vaccines,
[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]
+
losses from clostridial diseases could
 +
be cata-strophic, on occasion running
 +
at over 30 per cent. By the mid-1970s,
 +
efficient multicomponent vaccines
 +
were widely available and in the mid-
 +
1980s the clostridial components were
 +
combined with multicomponent pasteurella
 +
antigens. Clostridial vaccines
 +
are, except for the C chauvoei component,
 +
directed at the toxins produced
 +
by the various pathogenic members of
 +
the clostridial family. Referred to as
 +
toxoids, they are inactivated and
 +
require an adjuvant for better stimulation
 +
of the immune system.
 +
Whether a straight clostridial vaccine
 +
or a combined vaccine is used, the principles
 +
underlying efficacious vaccination
 +
programmes are identical. For
 +
effective protection of sheep, of whatever
 +
age, a primary course of two
 +
doses, administered four to six weeks
 +
apart, is required. The first dose can be
 +
considered a sensitising dose and, the
 +
second, the confirming dose. Immunity
 +
wanes over a period of a year and,
 +
consequently, booster doses are
 +
required annually.
 +
* EWES. Vaccination should be performed
 +
four to six weeks before lambing
 +
is due. Where lambing is prolonged,
 +
the late lambers should be
 +
identified and boosted later, closer to
 +
their lambing date.
 +
* LAMBS. By virtue of the ewe's
 +
enhanced ability to concentrate circulating
 +
antibodies into the colostrum
 +
(Cooper 1967), lambs ingesting sufficient
 +
colostrum from adequately fed
 +
ewes receive sufficient maternal antitoxins
 +
to protect them for about 12
 +
weeks. Such maternal protection is
 +
essential to prevent lamb dysentery,
 +
tetanus and early enterotoxaemia
 +
caused by C perfringens type D.
 +
Lambs from fully vaccinated ewes
 +
can start their primary course from
 +
eight weeks of age, as maternally
 +
derived antitoxin does not appear to
 +
interfere with the response to the vaccine.
 +
The choice and combination of
 +
antigens to be used depends on the
 +
ultimate fate of the lamb. Those to be
 +
retained for breeding require the full
 +
complement of antigens. Those for
 +
early slaughter may only require protection
 +
against pulpy kidney disease
 +
and tetanus, while lambs aimed at the
 +
store market or autumn finishing
 +
require a wider range of antigens to
 +
give additional protection against
 +
braxy, blackleg and malignant oedema.
  
 
==Links==
 
==Links==
  
*[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.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.noah.co.uk/issues/briefingdoc/22-vaccfarmanimals.htm NOAH: Vaccination of farm animals]
 
*[http://www.clostridia.net/Cperfringens.htm Clostridia.net - ''Clostridium perfringens'']
 
*[http://www.clostridia.net/Cperfringens.htm Clostridia.net - ''Clostridium perfringens'']
Line 51: Line 149:
 
==References==
 
==References==
  
#Van Metre (2006) Clostridial Infections of the Ruminant GI Tract. ''Proceedings of the North American Veterinary Conference 2006''.
+
#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.
 +
#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.
 
#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.
 
#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''.
 
#Songer, J G (1998) Clostridial diseases of small ruminants. ''Veterinary Research'', '''29''', 219-232.
 
 
#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.
#West, D M (1993) Vaccines as therapeutics. ''Proceedings of the Third International Sheep Veterinary Society Conference'', '''17''', 111-115.
+
#Lewis, C (2000) Vaccination of sheep: an update. ''In Practice'', ''22(1)'', 34-39.
#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.
 
 
 
  
{{review}}
+
[[Category:Enteritis,_Bacterial]][[Category:Enteritis,_Fibrinous/Haemorrhagic]] [[Category: WikiClinical Ovine]]
[[Category:Enteritis,_Bacterial]][[Category:Enteritis,_Fibrinous/Haemorrhagic]] [[Category:Intestinal Diseases - Sheep]]
+
[[Category:To_Do_-_Lizzie]]
[[Category:Brian Aldridge reviewing]]
 

Revision as of 18:38, 24 August 2010



Also known as: Clostridium perfringens type B Enterotoxaemia

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 mammalsivis. 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 significancelewis. 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.

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 (lamb dysentery), but also in 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 vaccinssargison, but the condition is now becoming a problem again as complacency reduces flocks vaccinating for the disease. 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 lambssargison, because these animals consume the largest quantities of milk which functions as a growth medium for C. perfringens. In extreme cases, 20-30% of lambs can be lost to lamb dysentery.

Signalment

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

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.

Clincal Signs

Lamb dysentery often presents as sudden death of lambs less than 2-3 weeks oldsargison, lewis, merk, songer. When clinical signs are seen, these include cessation of suckling, depression and recumbencymerck. Animals suffer acute abdominal pain, and semi-fluid blood-stained faeces may be passedsargison, leis merck, sanger. 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 signssargison.

Laboratory Tests

Intestinal contents or pertioneal 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 with suffering from its effects.

Intestinal smears and scrapings readily reveal gram-positive rodssargison, watt. Culture of intestinal contents can yield almost pure growths of C. perfringenswatt, but this is again supportive rather than diagnosticsargison.

Pathology

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

watt: Diagnosis on post mortem examination is 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.)

sargison At postmortem examination. localised areaLs ot the intestinies appear dark red and distended, with ulceration otl the mucosa and serous, blood-stained peritoneal fluid. The liver may be pale and friable and the kidnieys enlarged. Numerous Gram-positixe rods are present in smears from intestinal scrapings.

Treatment

Presentation of lamb dysentery is usually peracute, with sudden deaths occuring 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 presentlewis</lewis>. Instead, a definitive diagnosis should be pursued before great losses occur,and the farmer should be encouraged to submit the carcase for further investigations.

Suggested drugs include oral antibioticsmerck and specific hyperimmune serumMerck, watt.

Control of an outbreak of clostridial disease involves a dual approach of management techniques and therapy. In the case of the enterotoxaemias, vaccination in the face of an outbreak has proved effective (West 1993). Alternatively, particularly for lamb dysentery and tetanus, antisera can be administered. Management measures for some of the clostridial conditions include the removal of the remainder of the flock from a particular pasture or a reduction in concentrate feeding. The reduction of stress factors, as well as the gradual introduction of any new feeds or feeding regimens, also reduces the likelihood of disease. The cost of controls can be high in terms of time, labour and possibly further losses due to the stress of gathering the animals for treatment. Of all the diseases that afflict sheep, the clostridials are the ideal candidates for control by vaccination

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. Before the advent of modern vaccines, losses from clostridial diseases could be cata-strophic, on occasion running at over 30 per cent. By the mid-1970s, efficient multicomponent vaccines were widely available and in the mid- 1980s the clostridial components were combined with multicomponent pasteurella antigens. Clostridial vaccines are, except for the C chauvoei component, directed at the toxins produced by the various pathogenic members of the clostridial family. Referred to as toxoids, they are inactivated and require an adjuvant for better stimulation of the immune system. Whether a straight clostridial vaccine or a combined vaccine is used, the principles underlying efficacious vaccination programmes are identical. For effective protection of sheep, of whatever age, a primary course of two doses, administered four to six weeks apart, is required. The first dose can be considered a sensitising dose and, the second, the confirming dose. Immunity wanes over a period of a year and, consequently, booster doses are required annually.

  • EWES. Vaccination should be performed

four to six weeks before lambing is due. Where lambing is prolonged, the late lambers should be identified and boosted later, closer to their lambing date.

  • LAMBS. By virtue of the ewe's

enhanced ability to concentrate circulating antibodies into the colostrum (Cooper 1967), lambs ingesting sufficient colostrum from adequately fed ewes receive sufficient maternal antitoxins to protect them for about 12 weeks. Such maternal protection is essential to prevent lamb dysentery, tetanus and early enterotoxaemia caused by C perfringens type D. Lambs from fully vaccinated ewes can start their primary course from eight weeks of age, as maternally derived antitoxin does not appear to interfere with the response to the vaccine. The choice and combination of antigens to be used depends on the ultimate fate of the lamb. Those to be retained for breeding require the full complement of antigens. Those for early slaughter may only require protection against pulpy kidney disease and tetanus, while lambs aimed at the store market or autumn finishing require a wider range of antigens to give additional protection against braxy, blackleg and malignant oedema.

Links

References

  1. Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial.
  2. The Center for Food Security and Public Health, Iowa State University (2004) Animal Disease Factsheet: Epsilon toxin of Clostridium Perfringens.
  3. Songer, J G (1998) Clostridial diseases of small ruminants. Veterinary Research, 29, 219-232.
  4. Van Metre (2006) Clostridial Infections of the Ruminant GI Tract. Proceedings of the North American Veterinary Conference 2006
  5. Lewis, C (1998) Aspects of clostridial disease in sheep. In Practice, 20(9), 494-499.
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