Difference between revisions of "Bacterial Enteropathies – Rabbit"

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==Clostridial diseases==
 
==Clostridial diseases==
  
These are addressed in many papers by Carman(1994) who refers to several factors that lead to the establishment of C spiroforme in the rabbit gut, including parturition, weaning, change of diet, heat and dehydration,  taking blood, removal from germ-free isolation, shipping, old age and over-crowding. The diseases produced by ''Clostridia''  are usually so acute that they are seldom possible to treat successfully
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These are addressed in many papers by Carman (1994) who refers to several factors that lead to the establishment of C spiroforme in the rabbit gut, including parturition, weaning, change of diet, heat and dehydration,  taking blood, removal from germ-free isolation, shipping, old age and over-crowding. The diseases produced by ''Clostridia''  are usually so acute that they are seldom possible to treat successfully
''C. spiroforme'' colonises gut more frequently after weaning (young rabbits do not digest and absorb starch as efficiently as adults and carry a greater risk of unabsorbed carbohydrate reaching the caecum to act as a bacterial substrate from which toxins may be produced by the organism) and less frequently after antibiotics (Carman 1994) and may be seen in Gram-stained faecal smears and is obvious morphologically  as it forms helices, U-, S- and C-shapes. ''C. spiroforme'' produces two types of toxins, iotaa  and iotaa which have antigenic properties, a property which might be exploited for the protection of baby rabbits after suitable research (Carman 1994).  
+
''C. spiroforme'' colonises gut more frequently after weaning (young rabbits do not digest and absorb starch as efficiently as adults and carry a greater risk of unabsorbed carbohydrate reaching the caecum to act as a bacterial substrate from which toxins may be produced by the organism) and less frequently after antibiotics (Carman, 1994) and may be seen in Gram-stained faecal smears and is obvious morphologically  as it forms helices, U-, S- and C-shapes. ''C. spiroforme'' produces two types of toxins, iotaa  and iotaa which have antigenic properties, a property which might be exploited for the protection of baby rabbits after suitable research (Carman, 1994).  
The role of ''C. perfringens'' types A and E in the production of diarrhoea in rabbits has yet to be clarified (Carman 1994).
+
The role of ''C. perfringens'' types A and E in the production of diarrhoea in rabbits has yet to be clarified (Carman, 1994).
  
'''''C. difficile''''' diarrhoea is a frequently fatal disease of rabbits encountered after the use of oral antibiotics (Carman 1994). It is interesting to note that this is not listed as a zoonosis by Bell et al (1988).
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'''''C. difficile''''' diarrhoea is a frequently fatal disease of rabbits encountered after the use of oral antibiotics (Carman, 1994). It is interesting to note that this is not listed as a zoonosis by Bell et al (1988).
  
 
'''''C. sordelli''''' - experimental.
 
'''''C. sordelli''''' - experimental.
  
'''''C tympani cuniculi''''' - one case only  (Carman 1994).
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'''''C tympani cuniculi''''' - one case only  (Carman, 1994).
  
 
===Treatment of clostridial enteritis===
 
===Treatment of clostridial enteritis===

Revision as of 21:48, 20 July 2010



Bacterial enteropathies should really be regarded as "overgrowths".

Clostridial diseases

These are addressed in many papers by Carman (1994) who refers to several factors that lead to the establishment of C spiroforme in the rabbit gut, including parturition, weaning, change of diet, heat and dehydration, taking blood, removal from germ-free isolation, shipping, old age and over-crowding. The diseases produced by Clostridia are usually so acute that they are seldom possible to treat successfully C. spiroforme colonises gut more frequently after weaning (young rabbits do not digest and absorb starch as efficiently as adults and carry a greater risk of unabsorbed carbohydrate reaching the caecum to act as a bacterial substrate from which toxins may be produced by the organism) and less frequently after antibiotics (Carman, 1994) and may be seen in Gram-stained faecal smears and is obvious morphologically as it forms helices, U-, S- and C-shapes. C. spiroforme produces two types of toxins, iotaa and iotaa which have antigenic properties, a property which might be exploited for the protection of baby rabbits after suitable research (Carman, 1994). The role of C. perfringens types A and E in the production of diarrhoea in rabbits has yet to be clarified (Carman, 1994).

C. difficile diarrhoea is a frequently fatal disease of rabbits encountered after the use of oral antibiotics (Carman, 1994). It is interesting to note that this is not listed as a zoonosis by Bell et al (1988).

C. sordelli - experimental.

C tympani cuniculi - one case only (Carman, 1994).

Treatment of clostridial enteritis

It is usually unrewarding and follows the same regime as for other causes but, in addition:

  • Ascorbic acid may limit the absorption of toxins and improve mucosal integrity
  • Metronidazole, used parenterally (intraperitoneal use of the 0.5% solution), is the antibiotic of choice.

Colibacillosis

It can be encountered in pet rabbits of all ages, especially if they have been receiving doses of antibiotics that include gram-positive organisms in their spectrum of activity (Morisse 1978). This can be a particular problem if animals from different sources are mixed together on acquisition, especially in conditions of indifferent hygiene. The quality of the diet (especially the protein/cellulose ratio) and of the drinking water is also of aetiological importance. The levels of E. coli in the intestinal lumen of a rabbit rises directly in proportion to infestation with Eimeria species (coccidians).

Clinical Signs

  • profuse diarrhoea
  • fur-chewing
  • anorexia

Treatment

Treatment is usually unrewarding.

  • Oral administration of broad-spectrum antibiotics with known activity against gram-negative organisms, including E. coli.
  • Antispasmolytic agents such as hysocine (Buscopan Compositum; Boehringer Ingelheim 1 mg per kilogram I/M or S/C once only or daily until the desired results are obtained)
  • Fluids. Okerman (1994 p 37) warns that finding E. coli in large numbers merely reflects the ability of the organism to reproduce post-mortem and does not necessarily prove the diagnosis.


Tyzzer's disease (or bacillary typhilitis)

Tyzzer's disease is caused by the obligatory intracellular Clostridium (formerly Bacillus) piliformis, a gram-variable organism diagnosed on post-mortem examination by histopathology utilising Giemsa or Warthin-Starry staining techniques (Walden 1990). The organism may be seen on impression smears of the ileum lining (see Okerman 1994). The organism does not grow on broth or agar. Predisposing causes in rabbits are not known (Carman 1994) but weanlings are most frequently affected.

Symptoms include acute depression, watery diarrhoea and a high mortality rate) or chronic weight loss. Post-mortem findings include dehydration, oedema of the intestinal wall, necrosis of the colonic and caecal mucosa, and occasionally many necrotic foci in the liver.

Treatment is not generally recommended but may be attempted (tetracyclines). The disease has also been reported under circumstances which suggested that it may be spread by wild mice (MAFF monthly report 080892).

Salmonellosis

Salmonellosis is due to Salmonella typhimurium which has been recorded as manifesting a severe enteritis in baby rabbits. Clinical signs include depression, fever, +/- diarrhoea, abortion (Okerman 1994). Salmonellosis is a zoonosis.

Pseudotuberculosis

(syn: rodentiosis) Pseudotuberculosis is not just a condition of the gastrointestinal tract. Infection with Yersinia pseudotuberculosis as a result of direct or indirect contact with infected rodents or wild birds is encountered occasionally. The provision of freshly gathered wild plants or unwashed vegetables must be considered as a source of infection. Clinical signs include cachexia with an enlarged spleen being detected on abdominal palpation. Diagnosis is usually made on post-mortem examination, the organism being isolated from the typical lesions - necrotic foci in the lymphoid tissue of the spleen, caecum and ileo-caecal. Treatment and prevention of spread of the infection to contact animals is by the use of oral fluoroquinolones. Further prevention is via rodent control.

Synopsis of treatment for enterotoxaemia and bacterial enteritis

  • Warmth up to 27°C
  • Fluid therapy
    • Hartmann’s is probably better than dextrose-containing fluids (Clostridial toxins “feed” on monosaccharides)
    • intravenous or intraosseous.
    • maintenance = 100ml/kg/day
  • Analgesia
    • buprenorphine
    • butorphanol
    • carprofen
  • Cholestyramine resin (Questran, Bristol-Myers Pharmaceuticals) - rabbit must be well-hydrated because the same chain of events occur when ispaghula husk (psyllium) is given to rabbits (see anatomy and physiology of the digestive tract).
  • Antibiotics are indicated if it is a true bacterial enteritis but should be avoided if Salmonbella sp. is isolated.
  • Probiotics. Lactobacillus spp are claimed to attach to mucosa and compete with pathogenic bacteria.
  • Transfaunation
    • Caecotrophs collected from a healthy rabbit
    • Elizabethan collars
    • Fed whole to maintain the protective mucus coating
  • Rabbits with diarrhoea should never be starved
    • Ad lib hay and leafy greens. Dandelions, parsley, freshly pulled (not cut) grass and groundsel
    • Assisted feeding – commercial high fibre products for herbivores are available (eg). Most rabbits will accept food orally may be necessary.
    • Vitamin C may be of use in limiting the absorption of iota toxins and improving mucosal integrity
    • Oxbow Critical care for herbivores,
    • Supreme Recovery Diet via a syringe or nasogastric intubation