Difference between revisions of "Pulpy Kidney"

Revision as of 19:22, 6 June 2010

Caused by Clostridium welchii / Clostridium perfringens type D.
- The organisms are found everywhere cannot be got rid of.
- Found in the soil and as a gut commensal, but can explosively multiply and produce toxin under certain conditions.
  - Often occurs when the animal had just changed from one feed to another (i.e. just put out onto lush grass).
Seen mostly in sheep and goats.
- Disease was commonly vaccintated against, but this may not be done in times of financial difficulty.
  - Diagnosis of the disease is important in deciding if should sheep be vaccinated.
    - If the animal has been vaccinated it is important to need to diagnose pulpy kidney accurately in case of possible legal proceedings.
      
      Pulpy kidney disease- histological (Courtesy of Bristol BioMed Image Archive)

Clinical

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.

Pathogenesis

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

Lesions due to effect of epsilon toxin on blood vessels.

Pathology

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

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.

Pulpy kidney disease in well-fed 3-10 week-old lambs
Caused by Clostridium perfringens type D
Follows overeating high grain diet or luchious pasture
Starch from partially digested food enterering the intestine from the rumen allows rapid clostridial proliferation
Epsilon toxin activated by proteolytic enzymes causes toxaemia
Epsilon toxin increases intestinal and capillary permeability; also alpha toxin
Lambs found dead or with opisthotonos, convulsions, coma in acute phases
Blindness and head pressing in subacute disease; bloat in later stages
Hyperglycaemia, glycosuria
Post mortem: hyperaemia in intestine; fluid in pericardial sac; kidney autolysis with pulpy cortical softening (acute death)
Subacute death causes symmetrical encephalomalacia and haemorrhage in basal ganglia and midbrain
Enterotoxaemia in kids and adult goats

@@ Line 1: / Line 1: @@
-{{OpenPagesTop}}
+* Caused by [[:Category:Clostridium species|''Clostridium welchii'' / ''Clostridium perfringens'']] type D.
-Also known as: '''''Clostridium perfringens type D enterotoxaemia
+** The organisms are found everywhere cannot be got rid of.
+** Found in the soil and as a gut commensal, but can explosively multiply and produce toxin under certain conditions.
+*** Often occurs when the animal had just changed from one feed to another (i.e. just put out onto lush grass).
+* Seen mostly in sheep and goats.
+** Disease was commonly vaccintated against, but this may not be done in times of financial difficulty.
+*** Diagnosis of the disease is important in deciding if should sheep be vaccinated.
+**** If the animal has been vaccinated it is important to need to diagnose pulpy kidney accurately in case of possible legal proceedings. [[Image:pulpy kidney disease.jpg|thumb|right|150px|Pulpy kidney disease- histological (Courtesy of Bristol BioMed Image Archive)]]
-==Introduction==
+=====Clinical=====
-[[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.
-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.
-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>.
-==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==
-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.
-===Clinical Signs===
-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>.
-===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===
+* 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.
+=====Pathogenesis=====
 [[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.
+=====Pathology=====
-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==
-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.
-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.
+* 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
-{{Learning
+=====Diagnosis=====
-|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==
+* 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.
-*[http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/50714.htm The Merck Veterinary Manual: Pulpy Kidney]
-*[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==
-#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''.]
-{{review}}
-==Webinars==
+*Pulpy kidney disease in well-fed 3-10 week-old lambs
-<rss max="10" highlight="none">https://www.thewebinarvet.com/urogenital-and-reproduction/webinars/feed</rss>
+*Caused by Clostridium perfringens type D
+*Follows overeating high grain diet or luchious pasture
+*Starch from partially digested food enterering the intestine from the rumen allows rapid clostridial proliferation
+*Epsilon toxin activated by proteolytic enzymes causes toxaemia
+*Epsilon toxin increases intestinal and capillary permeability; also alpha toxin
+*Lambs found dead or with opisthotonos, convulsions, coma in acute phases
+*Blindness and head pressing in subacute disease; bloat in later stages
+*Hyperglycaemia, glycosuria
+*Post mortem: hyperaemia in intestine; fluid in pericardial sac; kidney autolysis with pulpy cortical softening (acute death)
+*Subacute death causes symmetrical encephalomalacia and haemorrhage in basal ganglia and midbrain
+*Enterotoxaemia in kids and adult goats
-[[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]]
+[[Category:Enteropathogenic_and_Enterotoxaemic_Clostridia]][[Category:Sheep]][[Category:Goat]]
 [[Category:Enteritis,_Bacterial]][[Category:Enteritis,_Catarrhal]]
-[[Category:Expert_Review - Farm Animal]]

Difference between revisions of "Pulpy Kidney"

Revision as of 19:22, 6 June 2010

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