Rabbit diseases diagnosis, prevention and control

1-Salmonellosis

Etiology
Various serotypes of Salmonella enteritidis, usually typhimurium or enteritidis.
Gram negative, non-spore forming bacilli. Grow on enriched media for 24 hours then transmitted to MacConkey agar (White dew drops colonies) or S-S agar.
Epizootiology:
Morbidity and mortality can be high. Transmission is via fecal contamination
from carriers or affected animals. Potentially zoonotic.
Transmission:
-Direct by the fecal-oral route.

- Bedding and nest cages, Rodent excretion that contaminate both food and water. Rabbits housed in unhygienic conditions.
Clinical:
Usually nonspecific (General clinical signs), include depression, fever many are found dead. Some have diarrhea, some abort.
Disease may spread rapidly, with many cases appearing in a short time.
P.M:
-Rabbits dying of peracute septicemic disease may have no lesions or only congestion of the organs, a few petechial hemorrhages.

-Those living a little longer may have multiple pinpoint focal necrosis on liver, and heart splenomegaly, lymphadenopathy (mesenteric L.N), and ulceration of Peyer’s patches.
- In some cases there is fibrinous enteritis.

-Metritis is found in pregnant Does
-Acute form: Polyserositis, focal hepatic necrosis, splenomegaly, enteritis with fibrinous exudate and suppurative metritis.
Diagnosis:
Morphology, culture, serotyping.

D.D:

Systemic diseases Viral (VHD),

Bacterial (pseudotuberculosis, acute pasteurellosis, listeriosis, spirochetosis ,Staphylococcosis.

 Protozoal: diseases (Toxaplasmosis)
Control:
Good husbandry. Feed and bedding contaminated by fecal matter of rodents are a potential source of infection. Human carriers also are a possible.

Treatment and Prevention:

Broad spectrum antibiotics are recommended. However, when administrated orally, most antibiotics do not attain sufficient concentration in the blood stream to be effective against septicemia. Best results obtained with fluoroquinolone antibiotic.

Recommendation:

Treated adults become carriers. Therefore, elimination of carrier is best method for control.

2-Colibacillosis

Etiology: Attaching and effacing (enteropathogenic) strains of Escherichia coli.
General: E. coli is a major cause of enteritis in commercial rabbitries and is occasionally a problem in research facilities. The organism is not normally present or is present in small numbers within the gastrointestinal tract of suckling and weanling rabbits.

-When a change in intestinal pH occurs, there is a rapid proliferation of the bacteria.

- Factors that promote this growth are intestinal coccidiosis and diets that require a high hydrochloric acid content for digestion.

 -The isolated strains are enteropathogenic (cause intestinal disease, but do not
produce enterotoxins).

- Some strains affect only suckling rabbits and attach to the full length of the small and large intestine, while other strains affect weanlings only and attach only to the ileum and large intestine.
Pathogenesis:

- The organism colonizes and attaches to the Peyer’s patches then later colonizes and attaches to enterocytes. Intestinal lesions are most severe at 7-14 days post-inoculation (in experimental infection).

Clinical signs and PM findings
-Morbidity may be sporadic or epizootic and mortality is high.
- Dehydrated carcasses, perineal staining with watery, yellow to brown fecal material.
-The small intestine is usually grossly normal.
-The cecum and colon may be distended with watery yellow to gray-brown contents.
-Serosal ecchymoses may be found,

-Edema in the cecal and colonic walls.

- Enlarged mesenteric lymph nodes.

- In the very young (1-14 day old), Watery diarrhea colors the belly and the posterior part of the body with yellow to brown.

- The stomach is full of undigested clotted milk. The whole nest usually affected at the same time.
-Changes are most severe and extensive in weanlings. lesions are limited to caecum and large intestine with watery content, foul smelling light brown diarrhea tinged with blood.

- longitudinal hemorrhages from outer surface of caecum( paint brush) .

Diagnosis:
1- History and gross and microscopic lesions are suggestive.

2- Morphology, culture on MacConky give red colonies,
EMB give green metallic chain, serotyping, eliminate other diseases.
And biochemical characterization of the organism.
Differential diagnosis :
Acute coccidiosis, clostridiosis, viral enteridities, Tyzzer’s disease and mucoid
enteropathy.
Control: 1-Vet. Biosecurity. 2-Antibiotic sensitivity test ( danofloxacin, Enrofloxacin)

3-Tyzzer’s Disease

Etiology:
“Bacillus” piliformis, a gram-variable, large pleomorphic filamentous sporeformer of uncertain classification.
It has not been grown on artificial medium grow only on tissue culture also it can be cultivated in eggs as the bacteria is obligatory intracellular.

Epizootiology:
Weanling rabbit 6-12 weeks are susceptible and stress plays a role in infection
Not often recognized, but possibly widespread; many cases probably is diagnosed.
-Predisposing factors are important and include poor sanitation, stress and sulfonamide therapy.

Transmission:
- thought to occur via fecal contamination

Infections are thought to be subclinical parasitism of small numbers of enterocytes unless animals are stressed or predisposed to disease by other unknown factors.
Morbidity can be sporadic with only a few rabbits affected, Survivors can become
chronically infected and serve as carriers.
Outbreaks can be severe with 50% or more affected. Mortality is near 100%.
Clinical:
Acute onset of profuse watery diarrhea, depression, dehydration, death in a day or two.
Chronic: chronic weight loss.
P.M:
Primarily the cecum is affected and sometimes the distal ileum and proximal colon.
Serosal surfaces are reddened and sometimes petechiated. The wall is edematous.
Contents are brown, flocculent, and watery and the mucosa is rough and granular with adherent exudate or necrotic debris.
Lesion is necrotizing and multifocal to diffuse.
Multifocal necrotizing hepatitis is common; usually the foci are small (up to 2-3 mm).
A few rabbits may have myocarditis.
Diagnosis:
-Culture the suspected sample in tissue culture Morphology; silver impregnation (Warthin-Starry) to demonstrate intracellular bacilli
-Serological tests.
-Histopathological detect the intracellular bacilli.

Control:
Closed colony establish bacilli.
Tetracycline at half dose for one month 250 ppm in ration or 125mg /liter in drinking water.

4-Clostridiosis (Enterotoxemia)

Etiology :
Clostridium difficile and C. spiroforme (C.spiroforme appears to be more common).
All are Gram positive, anaerobic bacilli. C. spiroforme produces a type E iota toxin.
Epizootiology:
-C. difficile is a ubiquitous anaerobe and may be carried in low numbers by normal rabbits.
C. difficile causes colitis in rabbits following prolonged therapy with penicillin and
ampicillin ( as antibiotic destruct normal flora).
-C. spiroforme is reported not to be part of normal flora, but may colonize if flora upset (e.g., by antibiotic treatment) At necropsy of diarrheic rabbits, it was isolated from over 50% of the cases, and of those, 90% of the strains isolated were toxigenic in one study.
-C. perfringens causes an enterotoxemia-like condition in young rabbits that results in cecal hemorrhage and edema.
-High carbohydrate diet is one of the predisposing factors for enterotoxiaemia and
treatment with following antibiotic: Lincomycin, penicillin, clindomycin ,erythromycin, amoxycillin.
Clinical:
Acute sudden death
Peracute form brown watery diarrhea and death in young or lactating rabbits. Loss of appetite, anorexia collaose, death may occur within 2days to3 weeks due to loss of electrolyte.
Abdomens may be enlarged by gas-filled intestines.
Chronic: anorexia, wasting and intermittent diarrhea over several days.

P.M:
Necrotizing enterocolitis, often with extensive edema and hemorrhage. thin and dehydrated carcass; staining of the ventral abdomen, perineum and near legs with watery green to tarry brown feces; straw colored peritoneal effusion; ecchymoses in the cecal serosa with very liquid content and gases. Ulcer may be found on mucosal surface of cecum
Diagnosis:
1- Lesions, gram-stained fecal smear, anaerobic culture, toxin demonstration.

2- Stain caecal wall scrap u shaped bacteria or spiral G+ve bacteria
3-Toxins can be demonstrated by cytotoxicity assay, ELISA, CIE (counter immunoelectrophoresis), and latex immunoassays.

Latex immunoassays are to be fastest and cheapest, and results agree well with those of ELISA tests (at least in the case of C.difficile toxin). Both tests offer positive and negative predictive values approaching or exceeding 90%. This is better than the cytotoxicity assay, which is not very good at detecting low concentrations of toxin.
N.B: We have done cytotoxicity assays in several rabbit diarrhea outbreaks, but have not yet found an unequivocal case of clostridiosis.

Differential diagnosis: Coccidiosis, Tyzzer’s disease, and colibacillosis.
Treatment:
Tetracycline, Nitrofuran, Metronidazole these drugs could be effective.

5-Enteritis Complex

Synonyms: Mucoid Enteropathy (Mucoid Enteritis)

Etiology:
Multifactorial; one or combinations of bacteria, toxins, dietary irregularity and/or
obstruction are suggested.
General: A major cause of disease and mortality in young rabbits. This disease can be reproduced experimentally by ligating sections of the large intestine. It is a subacute, frequently fatal disease, characterized by the passage of copious quantities of gelatinous mucus with feces. Rabbits 7-10 weeks of age are most often affected; however, rabbits aged between 5-20 weeks may also be affected.
Pathogenesis:
It is suggested that an alteration in the cecal environment results in the production of a goblet cell secrete by an undetermined bacterium. The secreta  is absorbed
through the cecal mucosa and is transported to the colon where it exerts its effect.
Clinical signs:
-Anorexia, polydipsia and subnormal temperature in addition to the abnormal feces.
- Gastric distention by fluid and gas; distention of the jejunum by translucent, watery fluid; cecal impaction by dry contents and gas; distention of the sacculated colon by clear, gelatinous mucoid exudate.
PM: Striking goblet cell hyperplasia in the jejunal, ileal and colonic mucosa with minimal or no inflammation. In the colon, the crypts and lumen are distended with mucus and mucus plugs. There are minimal to absent lesions in the cecum. Goblet cell hyperplasia of the gallbladder and mild nephrosis has been described.
Diagnosis:

-Characteristic histologic appearance. Demonstrate goblet cells with periodic
acid schiff or Alcian blue stains.
Differential diagnosis: Any infectious or management problem that results in disruption of normal microbial environment (coccidiosis, clostridiosis, trichobezars or constipation).
Carbohydrate Overload: low fiber, high starch diets fed to young animals results in high concentrations of starch in the cecum and colon which may result in the proliferation of E. coli, Clostridium perfringens, or Clostridium spiroforme. Bacterial toxins produced during the fermentation process may damage the mucosal surface and cause movement of water and electrolytes into the lumen, resulting in diarrhea and dehydration followed by death.