Difference between revisions of "Pulpy Kidney"

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Also known as: '''''Clostridium perfringens type D enterotoxaemia
+
 
 +
==Description==
  
−
==Introduction==
 
 
[[Image:clostridium perfringens.jpg|thumb|right|200px|Clostridium Perfingens. Source: Wikimedia Commons; Author:Don Stalons (1974)]]
 
[[Image:clostridium perfringens.jpg|thumb|right|200px|Clostridium Perfingens. Source: Wikimedia Commons; Author:Don Stalons (1974)]]
−
Pulpy kidney is a common, peracute and usually fatal enterotoxaemia of sheep of all ages, caused by the &epsilon; toxin of ''Clostridium perfringens'' type D. ''Clostridium perfringens'' type D causes the highest number of sheep fatalities due to clostridial disease<sup>1</sup>. It is a large, gram positive, anaerobic bacillus that is ubiquitous in the environment and commensalises the gastrointestinal tract of most mammals, although type D is found less abundantly in healthy animals than the other genotypes<sup>2</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>3</sup>. These are produced as pro-toxins, and are converted to their toxic forms by digestive enzymes such as trypsin. 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.
+
Pulpy kidney is a common, peracute and usually fatal enterotoxaemia of sheep of all ages, caused by the &epsilon; toxin of ''Clostridium perfringens'' type D. ''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 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 dietary fibre or a high gastrointestinal parasite burden, can also contribute to the accumulation of toxins.  
+
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 D causes sudden death in sheep of any age, particularly well-grown lambs of between 4 and 10 weeks of age and fattening lambs of 6 months to 1 year old<sup>3</sup>. Rams are also susceptible when they are subjected to an increased plane of nutrition prior to mating. The condition is associated with a change in diet, for example the introdcution of lush grass or high proportions of concentrate. This leads to rapid multiplication of the bacterium and excessive production of its &epsilon; toxin. &epsilon; toxin causes loss of epithelial integrity, increasing the permeability of the intestinal mucosa to facilitate its rapid absorption<sup>1</sup>. It then gives degeneration of vascular endothelium elsewhere, particularly in the brain, leading to increased capiliary permeability and oedema formation<sup>2, 4</sup>. Hepatic glycogen is mobilised by &epsilon; toxin and so hyperglycaemia and glycosuria are frequently seen<sup>1</sup>.Endothelial damage results in protein-rich effusions. The incidence of pulpy kidney declined over the past 25 years due to the widespread use of clostridial vaccines<sup>5</sup>, but the condition is becoming a problem again as complacency reduces the use of vaccination. At its most extreme, pulpy kidney can cause losses of 10-15% of the lamb crop. The disease can also occur in cattle, but this is rare<sup>2</sup>.
+
Enterotoxaemia due to ''Clostridium  perfringens''  type D causes sudden death in sheep of any age, particularly well-grown lambs of between 4 and 10 weeks of age and fattening lambs of 6 months to 1 year old,sup>ref</sup>. The condition is associated with a change in diet, for example to include lush grass or high proportions of concentrate. This causes rapid multiplication of the bacterium and excessive production of its &epsilon; toxin. The incidence of pulpy kidney declined over the past 25 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. At its most extreme, pulpy kidney can cause losses of 10-15% of the lamb crop. The disease can also occur in cattle, but this is rare<sup>ref 2?</sup>.
 +
 
 +
lewis: Pulpy kidney disease, which is caused by C perfringens
 +
type D, is by far the commonest of the enterotoxaemias.
 +
It is usually encountered in growing lambs of four to 10
 +
weeks of age, and in finishing lambs of six months of
 +
age and above. However, it is not unusual for adults to
 +
be sporadically affected. Rams, in particular, appear to
 +
be susceptible when they are on a rising plane of nutrition
 +
in preparation for mating.
 +
C perfringens elaborates a non-toxic protoxin, which
 +
is converted to the lethal epsilon toxin by the action of
 +
Very congested small intestine and ecchymosal
 +
haemorrhages on the abomasum of a three-month-old lamb
 +
with acute pulpy kidney disease (Picture, Shrewsbury VIC)
 +
Congested small intestine in
 +
a lamb under 14 days of age
 +
with lamb dysentery
 +
(Picture, Carmarthen VIC)
 +
trypsin. The disease is peracute and the majority of cases
 +
are found dead. In the rare instances that animals survive
 +
for a short time, diarrhoea is a feature, as are CNS signs
 +
due to the development of focal symmetrical encephalomalacia;
 +
typcially, there is ataxia, progressing to
 +
recumbency, opisthotonos, convulsions with or without
 +
nystagmus, and death.
 +
 
 +
 
 +
ivis: perfringens type D causes enterotoxemia in small ruminants of all ages; [1,10] disease in cattle appears to be very rare [27]. Clostridium perfringens  type D is not considered to be a common inhabitant of the gastrointestinal tract of normal ruminants, although it can be carried sporadically by healthy animals [10]. As for type C enterotoxemia, passage of soluble carbohydrates or protein into the small intestine is thought to induce rapid replication and elaboration of epsilon toxin from this organism [24]. Unlike beta toxin, however, epsilon toxin is activated by intestinal and pancreatic proteases [1]. Once absorbed into the bloodstream, epsilon toxin causes loss of endothelial integrity, increased capillary permeability, and edema formation in multiple tissues [28].
 +
 
 +
Type D enterotoxemia in sheep is typically a peracute illness, with many cases simply being found dead. If a live ovine case is detected, neurologic signs predominate. Lethargy and ataxia are evident early on, with collapse, hyperesthesia, lateral recumbency, convulsive paddling, and opisthotonus following within hours. Diarrhea is inconsistently seen. Glucosuria is frequently present [29].
  
 
==Signalment==
 
==Signalment==
Line 16: Line 46:
 
==Diagnosis==
 
==Diagnosis==
  
−
A presumptive diagnosis of pulpy kidney can be made on the basis a history of sudden deaths in lambs recently introduced to carbohydrate-rich feed. If animals are seen before they die, certain clinical signs may be suggestive of pulpy kidney, and post-mortem examination may also aid diagnosis. However, histopathology of the brain is the most useful diagnostic test.  
+
* Location of the organism in the gut contents is not helpful, since it is always present (as a commensal).
 +
** Therefore, diagnosis is by location of the toxin in the gut contents.
 +
* Toxin is tested for by administering filtered intestinal fluid intravenously to a mouse (mouse protection test).
 +
** If the toxin is present, the mouse should die within minutes or hours.
 +
** Another mouse can be protected from the effect of the toxin with a specific antibody.
 +
* An ELISA test is also possible.
 +
** However, an ELISA is often too sensitive as the toxin can be present in the normal sheep gut and the ELISA can pick this up.
 +
===Clinical Signs===
  
−
===Clinical Signs===
+
Animals are occasionally seen alive with hyperaesthesis and ataxia, which rapidly progresses to recumbency, opisthotonus, convulsions and death. In lambs which live longer, diarrhoea and signs associated with focal symmetrical encephalomalacia can be seen.
  
−
The first indication of pulpy kidney disease is the occurence of sudden death in the best-grown lambs<sup>1-4</sup>. Occasionally, animals may be seen alive displaying clinical signs suggestive of the condition. Signs are typically neurological and include hyperaesthesia, ataxia, circling or head-pressing, with rapid progression to recumbency, opisthotonus, convulsions and death<sup>1-4</sup>. Diarrhoea may also be seen, and hyperglycemia or glycosuria is frequently reported<sup>1-4</sup>.
 
  
−
Adult sheep are sometimes affected and show weakness, incoordination, and convulsions. Death occurs within 24 hours<sup>4</sup>.
+
The time course from onset to death is only a few hours, so sheep are normally found dead and only occasionally seen alive.
 +
* Nervous signs, such as head pressing, may be seen.
 +
* Paralysis of the [[Oesophagus - Anatomy & Physiology|oesophagus]] may result in severe [[Bloat|bloat]].
 +
* Profuse greenish [[Diarrhoea|diarrhoea]] is seen occasionally just before death.
 +
* Only mild catarrhal enteritis is seen in the gut.
  
 
===Laboratory Tests===
 
===Laboratory Tests===
−
[[Image:pulpy kidney disease.jpg|thumb|right|150px|Pulpy kidney disease- histological (Courtesy of Bristol BioMed Image Archive)]]
 
−
 
−
Short, thick gram-positive rods are easily visualised on smears of intestinal contents. Culture under anaerobic conditions usually gives pure cultures of ''C. perfringens'', which can be demonstrated as being type D by PCR techniques. An ELISA may be used to demonstrate the presence of  ɛ toxin in the small intestinal or peritoneal fluid. In contrast to lamb dysentery, in pulpy kidney &epsilon; toxin will be demonstrated in the absence of &beta; toxin<sup>1</sup>. A positive toxin ELISA supports but does not confirm a diagnosis, since immune animals may experience elevated toxin levels without suffering ill effects.
 
  
 
===Pathology===
 
===Pathology===
  
−
 
+
[[Image:pulpy kidney disease.jpg|thumb|right|150px|Pulpy kidney disease- histological (Courtesy of Bristol BioMed Image Archive)]]
 +
At necropsy examination, the peritoneal, pleural, and / or pericardial spaces are filled with variable volumes of straw- or red-colored fluid that may contain fibrin clots. Petechial hemorrhages are often visible on the visceral surfaces. Pulmonary and mesenteric edema may be evident. Gross lesions of the intestinal tract are frequently absent in affected sheep. Dipstick analysis of urine collected from the bladder frequently reveals the presence of glucose. The renal cortex may be softened (hence the term "pulpy kidney"), although this is a nonspecific autolytic change seen on occasion in small ruminant cadavers. The thalamus and cerebellum may be appreciably soft, with scattered hemorrhages therein. Occasionally, no gross lesions are seen in ovine cases of type D enterotoxemia [24].
 +
* Animals are very bloated.
 +
* Often lack lesions.
 +
* Guts appear slightly flaccid, and a bit hyperaemic.
 +
* The toxaemic carcase has petechial and echymotic haemorrhages, and hydropericardium.
 +
* The '''kidneys''' are characteristically affected.
 +
** Become oedematous, mushy and red within about 1 hour of death.
 +
** A stream of water on cut surface of the kidney washes away the epithelium (since it is necrotic) and leaves fronds of tissue (This is the case with any kidney if the post mortem is more than a few hours after death).
 +
*** This accelerated post mortem change is a characteristic of the disease.
 +
* '''Glycosuria''' is a feature
 +
** The toxin affects the  epithelium of the proximal part of nephron, stopping resorption of glucose. 
 +
** Note: the swelling of cells in the kidney means that anuria occurs, meaning there is no urine avaialable to rest for glucose.
 +
*** It is sometimes possible to get a positive reaction to a stick test by wiping it on the inside of the bladder.
 +
* Periportal hepatic fatty change occurs.
 +
** This is only really seen histologically.
 +
** Grossly, the liver looks "half cooked", but this is true of many bacterial diseases.
 +
* Histopathology is often not helpful.
 +
** Necrosis of cells in proximal convoluted tubules.
 +
** There is also a characteristic degeneration in parts of the brain - focal symmetrical encephalomalacia
 
[[Image:pulpy kidney gross.jpg|thumb|right|150px|Pulpy kidney disease- gross (Courtesy of Bristol BioMed Image Archive)]]
 
[[Image:pulpy kidney gross.jpg|thumb|right|150px|Pulpy kidney disease- gross (Courtesy of Bristol BioMed Image Archive)]]
−
 
+
* Lesions due to effect of epsilon toxin on blood vessels.
−
In young lambs, the only change observable on post-mortem examination may be the presence of a few hyperaemic areas on the intestine and a fluid-filled pericardial sac<sup>4</sup>. Intestinal lesions may even be absent<sup>2</sup>. Animals, particularly older ones, may have myocardial haemorrhages as well as petechiation of visceral surfaces and abdominal muscles<sup>2, 4, 6</sup>. Pulmonary oedema and congestion is often present and there may be pleural, peritoneal or pericardial effusions<sup>2, 4</sup>. The fluid is variable in volume and can be straw or red coloured, sometimes containing fibrin clots<sup>ivis</sup>. The kidneys often rapidly autolyse, as suggested by the name "pulpy kidney", but this is not a pathognomic finding.
 
−
 
 
−
Lesions of the central nervous system account for the neurologic signs. There is a bilaterally symmetrical focal malacia of the basal ganglia and thalamus, with demyelination occuring in the internal capsule, subcortical white matter and cerebellar peduncles<sup>6</sup>. Histological examination of the brain is often used to confirm a diagnosis of pulpy kidney<sup>1</sup>. Capillaries are occluded by aggregated platelets, and grossly this gives petechiation of the damaged areas. The cerebellar white matter shows periaxonal and intramyelinic oedema, and there is swelling of axon terminals and dendrites near the lateral ventricles<sup>6</sup>. The nuceli of damaged endothelial cells appear pyknotic, and astrocyte end feet are markedly swollen. Swelling of mitochondria may also be seen <sup>6</sup>.
 
  
 
==Treatment and Control==
 
==Treatment and Control==
−
The first sign of pulpy kidney is sudden death, and so there is often no opportunity for treatment. Even if affected animals are found prior to death, treatment is usually unrewarding as organs are irreversibly damaged by toxins by the time signs present<sup>3</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.
+
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>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.  
−
 
 
−
Control of pulpy kidney involves avoiding the factors that can precipitate disease. Diets should not be changed suddenly and concentrate feeding should always be introduced slowly<sup>1</sup>. Feeding of whole grain slows the transit of feed to the small intestine, so cereals should be fed in this form. ''C.. perfringens'' type D is ubiquitously distributed and so management measure will never completely prevent disease. The best method of disease prevention is vaccination.
 
  
−
Before the development of modern clostridial vaccines in the 1970s, losses of up to 15% of the lamb crop could occur due to pulpy kidney<sup>3</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>3</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 16 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.
+
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 colostrium and the maintenance of good hygiene.
  
−
{{Learning
+
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.
−
|literature search = [http://www.cabdirect.org/search.html?q=title%3A%28pulpy+kidney%29+OR+title%3A%28Clostridium+perfringens+type+D+enterotoxaemia%29 Pulpy Kidney publications]
 
−
}}
 
  
 
==Links==
 
==Links==
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==References==
 
==References==
  
−
#Aitken, I D (2007) '''Diseases of sheep''', ''Wiley-Blackwell''.
 
−
#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.
 
−
#Merck & Co (2008) '''The Merck Veterinary Manual (Eighth Edition)''', ''Merial''.
 
−
#Sargison, N (2004) Differential diagnosis of diarrhoea in lambs. ''In Practice'', '''26(1)''', 20-27.
 
−
#Jones, T C et al (1997) '''Veterinary Pathology''', ''Wiley-Blackwell''.
 
−
#Songer, J G (1998) Clostridial diseases of small ruminants. ''Veterinary Research'', '''29''', 219-232.
 
−
#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''.]
 
  
  
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{{review}}
 
  
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==Webinars==
 
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<rss max="10" highlight="none">https://www.thewebinarvet.com/urogenital-and-reproduction/webinars/feed</rss>
 
  
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[[Category:Enteropathogenic_and_Enterotoxaemic_Clostridia]][[Category:Neurological Diseases - Sheep]][[Category:Urological Diseases - Sheep]][[Category:Neurological Diseases - Goat]][[Category:Urological Diseases - Sheep]][[Category:Urological Diseases - Goat]]
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[[Category:Enteropathogenic_and_Enterotoxaemic_Clostridia]][[Category:Sheep]][[Category:Goat]]
 
[[Category:Enteritis,_Bacterial]][[Category:Enteritis,_Catarrhal]]
 
[[Category:Enteritis,_Bacterial]][[Category:Enteritis,_Catarrhal]]
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[[Category:Expert_Review - Farm Animal]]
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[[Category:To_Do_-_Lizzie]]

Revision as of 20:30, 24 August 2010


 This article is still under construction.


Description

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

Pulpy kidney is a common, peracute and usually fatal enterotoxaemia of sheep of all ages, caused by the ε toxin of Clostridium perfringens type D. 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 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 D causes sudden death in sheep of any age, particularly well-grown lambs of between 4 and 10 weeks of age and fattening lambs of 6 months to 1 year old,sup>ref. The condition is associated with a change in diet, for example to include lush grass or high proportions of concentrate. This causes rapid multiplication of the bacterium and excessive production of its ε toxin. The incidence of pulpy kidney declined over the past 25 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. At its most extreme, pulpy kidney can cause losses of 10-15% of the lamb crop. The disease can also occur in cattle, but this is rareref 2?.

lewis: Pulpy kidney disease, which is caused by C perfringens type D, is by far the commonest of the enterotoxaemias. It is usually encountered in growing lambs of four to 10 weeks of age, and in finishing lambs of six months of age and above. However, it is not unusual for adults to be sporadically affected. Rams, in particular, appear to be susceptible when they are on a rising plane of nutrition in preparation for mating. C perfringens elaborates a non-toxic protoxin, which is converted to the lethal epsilon toxin by the action of Very congested small intestine and ecchymosal haemorrhages on the abomasum of a three-month-old lamb with acute pulpy kidney disease (Picture, Shrewsbury VIC) Congested small intestine in a lamb under 14 days of age with lamb dysentery (Picture, Carmarthen VIC) trypsin. The disease is peracute and the majority of cases are found dead. In the rare instances that animals survive for a short time, diarrhoea is a feature, as are CNS signs due to the development of focal symmetrical encephalomalacia; typcially, there is ataxia, progressing to recumbency, opisthotonos, convulsions with or without nystagmus, and death.


ivis: perfringens type D causes enterotoxemia in small ruminants of all ages; [1,10] disease in cattle appears to be very rare [27]. Clostridium perfringens type D is not considered to be a common inhabitant of the gastrointestinal tract of normal ruminants, although it can be carried sporadically by healthy animals [10]. As for type C enterotoxemia, passage of soluble carbohydrates or protein into the small intestine is thought to induce rapid replication and elaboration of epsilon toxin from this organism [24]. Unlike beta toxin, however, epsilon toxin is activated by intestinal and pancreatic proteases [1]. Once absorbed into the bloodstream, epsilon toxin causes loss of endothelial integrity, increased capillary permeability, and edema formation in multiple tissues [28].

Type D enterotoxemia in sheep is typically a peracute illness, with many cases simply being found dead. If a live ovine case is detected, neurologic signs predominate. Lethargy and ataxia are evident early on, with collapse, hyperesthesia, lateral recumbency, convulsive paddling, and opisthotonus following within hours. Diarrhea is inconsistently seen. Glucosuria is frequently present [29].

Signalment

Pulpy kidney can affect unvaccinated sheep of all ages. However, it is most common in 4-10 week old lambs, and fattening lambs between 6 months and 1 year of age.

Diagnosis

  • Location of the organism in the gut contents is not helpful, since it is always present (as a commensal).
    • Therefore, diagnosis is by location of the toxin in the gut contents.
  • Toxin is tested for by administering filtered intestinal fluid intravenously to a mouse (mouse protection test).
    • If the toxin is present, the mouse should die within minutes or hours.
    • Another mouse can be protected from the effect of the toxin with a specific antibody.
  • An ELISA test is also possible.
    • However, an ELISA is often too sensitive as the toxin can be present in the normal sheep gut and the ELISA can pick this up.

Clinical Signs

Animals are occasionally seen alive with hyperaesthesis and ataxia, which rapidly progresses to recumbency, opisthotonus, convulsions and death. In lambs which live longer, diarrhoea and signs associated with focal symmetrical encephalomalacia can be seen.


The time course from onset to death is only a few hours, so sheep are normally found dead and only occasionally seen alive.

  • Nervous signs, such as head pressing, may be seen.
  • Paralysis of the oesophagus may result in severe bloat.
  • Profuse greenish diarrhoea is seen occasionally just before death.
  • Only mild catarrhal enteritis is seen in the gut.

Laboratory Tests

Pathology

Pulpy kidney disease- histological (Courtesy of Bristol BioMed Image Archive)

At necropsy examination, the peritoneal, pleural, and / or pericardial spaces are filled with variable volumes of straw- or red-colored fluid that may contain fibrin clots. Petechial hemorrhages are often visible on the visceral surfaces. Pulmonary and mesenteric edema may be evident. Gross lesions of the intestinal tract are frequently absent in affected sheep. Dipstick analysis of urine collected from the bladder frequently reveals the presence of glucose. The renal cortex may be softened (hence the term "pulpy kidney"), although this is a nonspecific autolytic change seen on occasion in small ruminant cadavers. The thalamus and cerebellum may be appreciably soft, with scattered hemorrhages therein. Occasionally, no gross lesions are seen in ovine cases of type D enterotoxemia [24].

  • Animals are very bloated.
  • Often lack lesions.
  • Guts appear slightly flaccid, and a bit hyperaemic.
  • The toxaemic carcase has petechial and echymotic haemorrhages, and hydropericardium.
  • The kidneys are characteristically affected.
    • Become oedematous, mushy and red within about 1 hour of death.
    • A stream of water on cut surface of the kidney washes away the epithelium (since it is necrotic) and leaves fronds of tissue (This is the case with any kidney if the post mortem is more than a few hours after death).
      • This accelerated post mortem change is a characteristic of the disease.
  • Glycosuria is a feature
    • The toxin affects the epithelium of the proximal part of nephron, stopping resorption of glucose.
    • Note: the swelling of cells in the kidney means that anuria occurs, meaning there is no urine avaialable to rest for glucose.
      • It is sometimes possible to get a positive reaction to a stick test by wiping it on the inside of the bladder.
  • Periportal hepatic fatty change occurs.
    • This is only really seen histologically.
    • Grossly, the liver looks "half cooked", but this is true of many bacterial diseases.
  • Histopathology is often not helpful.
    • Necrosis of cells in proximal convoluted tubules.
    • There is also a characteristic degeneration in parts of the brain - focal symmetrical encephalomalacia
Pulpy kidney disease- gross (Courtesy of Bristol BioMed Image Archive)
  • Lesions due to effect of epsilon toxin on blood vessels.

Treatment and Control

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 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 colostrium 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.

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