II. Bordetellosis
III. Colibacillosis
IV. Tyzzer's Disease
V. Staphylococcus Infections
VI. Venereal Spirochetosis (Rabbit Syphilis, Vent Disease, Cuniculosis)
VII. Proliferative Ileotyphlitis
VIII. Salmonellosis
IX. Tularemia
A. Etiology: Pasteurella multocida is a small, Gram-negative, nonspore-forming bipolar rod.
B. Transmission: Transmission occurs by direct contact, aerosol, venereal, and hematogenous routes. Incidence of infection and disease is high (probably > 90%). Many rabbits are asymptomatic carriers. The incidence of bacterial carriage is no different in antibiotic-treated rabbits.
C. Disease Forms: Upper respiratory disease ("snuffles"), pneumonia, otitis media, pyometra, orchitis, subcutaneous abscesses, conjunctivitis and septicemia are manifestations of P. multocida infection.
1. Snuffles - This is the most common manifestation of pasteurellosis.
Clinical signs characteristically include serous to mucopurulent nasal
exudate with sneezing and coughing. Exudate may be seen on the medial
aspect of the forepaws. Signs may subside temporarily only to recur
throughout life. Lesions include reddened mucosa in acute infections,
thickened mucosa in chronic infections, and exudate in nasal cavity and
paranasal sinuses. Antibiotic therapy (see Table 1) usually causes
abatement of clinical signs. The prognosis for disease improvement
or remission is good, however there is a good chance of recurrence. 
2. Enzootic Pneumonia - Affected rabbits frequently die
acutely with no signs (especially young rabbits); anorexia and depression
may be observed. Acute pneumonia lesions include red-grey foci of
consolidation of the cranioventral lung lobes with or without hemorrhage.
Chronic pneumonia is characterized by generalized consolidation, encapsulated
abscesses, fibrinopurulent or mucopurulent pleuritis and pyothorax.
If the pneumonia is recognized early, aggressive antibiotic therapy may
be of some value. The prognosis for all cases of pneumonia is poor. 
3. Otitis Media - Usually there are no clinical signs.
Torticollis will occur if the function of the internal ear is compromised,
either by direct bacterial invasion or by the damaging effects of the bacterial
toxins. Nervous signs and incoordination are observed if the bacteria
extends to the meninges. Creamy, white exudate in middle ear is found either
uni- or bilaterally. When treated with antibiotics at the first indication
of a head tilt, rabbits with otitis media may improve or stabilize.
In rabbits with severe torticollis, NSAID or corticosteroid therapy may
be indicated. Bulla osteotomies and lavage of the tympanic bullae
has proven to be a fruitless approach to treatment. The torticollis
may progress in spite of antibiotic therapy, so the prognosis is guarded. 
4. Genital Infections - Venereal or hematogenous transmission
may occur. Affected rabbits may have a vaginal discharge which may
be serous to mucopurulent and/or a history of infertility. The uterus
can be palpably enlarged with pyometra. Acute infection of the uterus
is characterized by slightly dilated horns filled with grey exudate.
In chronic infections the uterine horns are greatly dilated with purulent
exudate, and are fragile. In affected bucks, one or both testicles
may be enlarged, tender, firm and may contain abscesses. The health
of affected rabbits can be salvaged by surgical removal of diseased tissues
coupled with antibiotic therapy. The prognosis for recovery after
surgery is good. 
5. Abscesses - Contaminated wounds and septicemia are common routes for abscess development in a variety of locations, but especially in the subcutis. The presence of subcutaneous swellings which are filled with creamy exudate and may have draining fistulous tracts is typical of Pasteurella abscesses. Treatments include sedation of the rabbit prior to lancing and flushing superficial abscesses t.i.d. with Betadine or chlorhexidine. Systemic antibiotic therapy should be provided for 1 week. If the infections persist, surgical resection may be required.
6. Conjunctivitis - Signs include epiphora with blephorospasm,
eyelids closed by excessive mucopurulent exudate and facial staining.
Reddened conjuctiva with serous to mucopurulent adherent exudate are found.
Often there is inflammation and eventual stenosis of the nasolacrimal duct,
resulting in chronic epiphora and hair loss. The use of antibiotic
ophthalmic ointments will improve most cases. Occasionally, the nasolacrimal
duct may need to be flushed to remove inspissated purulent material. 
7. Septicemia - Septicemic rabbits usually die acutely; however, one may see pneumonia or infertility prior to death. Diffuse congestion and petechiation of thoracic and abdominal viscera as well as abscesses in viscera (kidneys, liver, lungs) may be seen on necropsy.
D. Predisposing Factors: Onset of clinical disease is often associated with some underlying stressor, such as a marked change in environmental temperature or humidity, poor ventilation, poor sanitation, and overcrowding. Physiologic conditions that also predispose to disease is age (very young or very old), pregnancy, nutritional state, and genetics. Some rabbit stocks are genetically hardier, and can carry Pasteurella throughout life without developing clinical disease.
E. Diagnosis: Tentative diagnosis of pasteurellosis is based on clinical signs and gross necropsy findings of a mucopurulent exudate associated with inflamed body parts such as the respiratory tract, subcutis, middle ears, and reproductive tract. A presumptive diagnosis may be reached by making a smear or scraping from the affected area and staining with a gram stain. With torticollis, radiographs of the tympanic bulla may disclose the presence of exudate or bony reaction (increased density in the bulla). Definitive diagnosis requires isolation of the bacteria by culturing the affected site(s).
F. Treatment: Most Pasteurella isolates are sensitive to penicillin. Only sulfaquinoxaline and tetracycline have known withdrawal times and can be used for rabbits raised for slaughter. Short term use of certain oral antibiotics, such as ampicillin or amoxicillin, or prolonged systemic antibiotic therapy with any drug may upset the cecal bacterial flora. If anorexia or diarrhea occurs during therapy, stop treatment immediately. Dietary supplementation with high fiber foods, such as alfalfa cubes or high fiber pelleted diets, or with yogurt containing live Lactobacillus cultures may reduce intestinal upsets.
TABLE 1: Antibiotics Commonly Dispensed for Rabbits
Enrofloxicin 2.5 to 5 mg/kg b.i.d. for 5 to 7 days (oral and injectable)
Procaine penicillin 40 to 60,000 IU/kg body weight IM s.i.d. for 3 to 10 days
Sulfaquinoxaline 0.256 gm/50 gm feed for 30 days or 226 gm/ton of feed
Tetracycline 300 mg/liter of water for 7 days, or 5 mg/kg q.i.d. for 7 days
G. Control: The best control for pasteurellosis is good husbandry techniques and culling of rabbits with clinical disease. Since most all rabbits carry Pasteurella multocida in the nasal cavity, management measures are aimed at controlling the clinical disease expression. The rabbitry must have good ventilation, low ammonia levels, and low humidity to decrease incidence of this disease. In a breeding colony situation, all infected rabbits with clinical disease should be culled for many reasons. (In spite of antibiotic therapy, the chance of disease recurrence is high. Rabbits with clinical signs shed large numbers of organisms into the environment. The best way to improve the genetic hardiness is to remove breeders with clinical disease.) Clean automatic waterers and cages in which diseased rabbits were housed and then spray with 1% bleach solution to kill residual bacteria. (Bleach will eventually damage galvanized caging, so alternative disinfectants can be used.) All new arrivals should be quarantined prior to introduction into the rabbitry. If possible, weanling rabbits should be raised separately from the breeding colony.
A. Etiology: Bordetella bronchiseptica is a small gram-negative, alpha-hemolytic, nonfermenting rod. Incidence of infection is high with a low incidence of disease.
B. Transmission: Routes of transmission include aerosol and direct contact. Many rabbits are asymptomatic carriers, and may harbor both Bordetella and Pasteurella.
C. Clinical Signs: Signs are similar to snuffles and include upper respiratory infection with serous to mucopurulent nasal exudate and sneezing. Pneumonia uncommonly develops.
D. Gross Pathology: The characteristic lesion is erythematous nasal mucosa with adherent exudate.
E. Diagnosis: Definitive diagnosis is made by culture of the organism. Smear and gram stain of nasal exudate may be helpful.
F. Treatment: Enrofloxian (2.5 to 5.0 mg/kg bid for 5 to 7 days), oxytetracycline (0.1 mg/ml drinking water) or Tylosin (2 to 4 mg/kg IM b.i.d., then s.i.d. for 3 to 5 days) are effective in reducing clinical signs. As with pasteurellosis, antibiotic therapy may have to be repeated when rhinitis recurs, which may happen. Antibiotic therapy does not eliminate the carrier state.
G. Control: Isolation and treatment of sick animals, decreasing stressful conditions, and preparation of and vaccination with an autogenous bacterin are all adequate control measures. The bacterin may not eliminate the carrier state, but may help prevent expression of clinical disease.
BACTERIAL DIARRHEAL DISEASES
The initial approach to treating diarrhea in a rabbit is similar to that used for companion animals, and is similar for all infectious etiologies. Obtaining a thorough history is imperative. Questions to ask include recent changes in the rabbits' environment, husbandry, diet, including supplemental foods, antibiotics or home remedies. Even the addition of a new pet, especially a carnivore, can serve as a sufficient stressor. A diagnostic workup should include a complete physical exam including abdominal palpation, fecal flotation for coccidia, and fecal cultures. Ancillary tests may include blood work, and abdominal radiographs (plain and contrast studies) if warranted. Supportive therapy should be directed at correcting and maintaining hydration (via parenteral and oral fluid therapy) and stimulating the appetite in an attempt to restore normal gut flora using live yogurt cultures and fiber-containing treats. Antibiotics should be judiciously used as they may further upset the gut flora.
A. Etiology: Escherichia coli is a gram-negative, lactose-fermenting, indole positive rod. Rabbits are known to be affected by non-toxin producing, enteropathogenic E. coli (EPEC). EPEC adhere to the intestinal mucosa through a 2-step process. First, a bacterial pilus first allows attachment of the bacterial cell to the enterocyte. Second, a more intimate attachment through the eae pathogenicity island disrupts the cytoskeleton and destroys microvilli. A secretory diarrhea is induced by an unknown mechanism. Receptors for EPEC attachment to the epithelial cells are not present in newborn rabbits. They first appear at 21 days and reach normal adult levels by 35 days. The stress of weaning and loss of passively acquired maternal antibody contribute to susceptibility at this time.
B. Clinical Signs: Rabbits have diarrhea, fever, anorexia, and may consume more water than usual.
C. Pathology: Fecal-stained perineal fur and fluid-filled
intestinal contents with serosal vascular injection are seen.
Edema and pyogranulomatous cellularity of the lamina propria without
mucosal ulceration are prominent histopathologic findings. Edema or hemorrhage
can be seen in the submucosa. Small bacterial rods (arrow) adhered
to and effacing enterocyte margins are common in the ileum and cecum.
D. Treatment: Fluid therapy and supportive care are indicated.
The salicylates in Pepto bismol may be protective. Chlorpromazine
(1 to 10 mg/kg IM) may help decrease fluid loss from the the secretory
diarrhea.
A. Etiology: Clostridium piliforme, an obligate intracellular bacterium, is a Gram-negative, pleomorphic, filamentous organism that can produce spores.
B. Transmission: The disease is spread by spore ingestion (fecal-oral). Spores can remain viable at moderate to freezing temperatures for extended periods of time (> 1 year). The disease is perpetuated in breeding colonies by the infection of bunnies born into the colony. The incidence of disease is moderate.
C. Clinical Signs: Usually rabbits are affected shortly after weaning when passive immunity, if present, has waned. Acute, profuse watery to mucoid diarrhea, dehydration and death within 12 to 48 hours after onset of diarrhea are typical. The mortality rate is high. Exposure of naive adult rabbits may cause little to no clinical disease.
D. Pathology: Lesions in weanling rabbits include edema and hemorrhage
of mucosa, submucosa, and musculature of intestinal tract (A.). It is unusual
to see an enlarged liver with multifocal tan to yellow foci of necrosis
or hemorrhage of the myocardium as is described in the literature.
Extensive mucosal necrosis with a granulomatous cellular mucosal infiltrate
may occur in the ileum, cecum, and proximal colon. Visualization of the
bacterium is enhanced with use of silver stains. Argyrophilic intracellular
bacteria in clusters or "pick-up-sticks" or haystack clumps are present
in viable enterocytes in areas of granulomatous enteritis (B.), and if
heaptic necrosis is observed, in hepatocytes adjacent to an area of necrosis.
E. Diagnosis: Histopathological examination of liver or cecum stained with silver will be diagnostic if intracellular bacterial rods are observed. PCR of feces, intestinal tissue or liver can be used to document the presence of the bacterium. An ELISA is useful to detect antibody in recovered or asymptomatically infected rabbits.
F. Treatment: No therapy has been uniformly successful. Supportive therapy may help when the enteric disease is mild and the rabbit is still eating.
G. Control: Prevent overcrowding and use good sanitation techniques. Stresses such as weaning and high environmental temperature may precipitate an outbreak. To minimize the stress of weaning, let the bunnies stay in the original cage and remove the doe. Work to prevent temperature fluctuations and keep the rabbits well-ventilated in high temperatures with fans. The spores are resistant to many disinfectants. A 1% bleach solution will inactivate spores that remain after the fecal material has been washed off soiled cages. Temperatures of water used to clean cages may also inactivate spores if the cages and supplies are allowed to contact 180oF water for no less than 15 minutes.
A. Etiology: Staphylococcus aureus is a Gram-positive, hemolytic, coagulase-positive coccus.
B. Transmission: Aerosol and direct contact (organism present in oral cavity of non-clinical carriers) are primary routes of infection. Incidence of infection is moderate, but the incidence of disease is low.
C. Clinical Signs: There is a wide range of clinical disease forms. S. aureus may cause suppurative infection in any organ or any site. Subcutaneous abscesses, mastitis with abscess formation, dermatitis, upper respiratory infection with mucopurulent nasal discharge, and septicemia with depression, anorexia, fever, and death have been reported. Of these disease syndromes, abscess formation and mastitis are most commonly reported.
1. Abscesses - Abscesses may occur subcutaneously or in the viscera. At necropsy thick-walled abscesses filled with purulent exudate are found. Diffuse congestion and petechiation of viscera may be seen in septicemic animals. Clinicopathologic lesions are similar to those of pasteurellosis. Presumptive diagnosis may be made by making a smear and gram stain of the exudate. Culture and antibiotic sensitivities are needed for a definitive diagnosis and choice of treatment. If the organism is sensitive to penicillin, 40,000 IU/kg procaine penicillin, IM s.i.d., for 3 to 5 days may be effective. Subcutaneous abscesses should be lanced and flushed with germicidal solution along with administration of systemic antibiotics. Surgical extirpation may be necessary to resolve chronic abscesses. To decrease the incidence of abscesses, the cages must be kept clean, fighting animals separated, and clinically ill rabbits isolated.VI. Venereal Spirochetosis (Rabbit Syphilis, Vent Disease, Cuniculosis)2. Mastitis - Mastitis or blue breast disease is commonly found in herds with intensified production. Infection of gland occurs through trauma to the teat, ascending infection through the teat canal, or secondary to septicemia. Mastitis occurs just after kindling. The mammary glands are swollen, usually not discolored, and may develop abscesses. Frequently there is loss of function of the affected gland and rarely the doe may die. Bunnies may die because of infected milk or not grow as well because of decreased function of the gland. Therapy includes hot packing the affected gland, systemic antibiotic therapy, and transfer of bunnies to a healthy lactating doe. To prevent mastitis, keep nest boxes clean and dry. Limit feed to the doe just prior to kindling to prevent excessive milk production and stagnation. Cull all affected does.
A. Etiology: Treponema paraluis cuniculi is a spiral-shaped bacterium related to the human syphilis organism, Treponema pallidum.
B. Transmission: Genital transmission is most common.
C. Clinical Signs: Cutaneous Infections - Erythema
of mucous membrane of external genitalia which progresses to focal, raised,
crusty ulcerations is the most common sign. Lesions can occur on
the perineal area and face due to auto-inoculation. As ulcerations
heal, a dry scaly condition follows. Spontaneous regression usually
occurs in several weeks. The bacteria causes only superficial, cutaneous
pathology. There may be popliteal and inguinal lymph node enlargement.
Mild or subclinical disease is common. Reluctance to breed and decreased
reproductive efficiency may occur. 
D. Diagnosis: Serological tests to identify antibody in actively or recently infected rabbits include the hemagglutination test, Rapid Plasma Reagin (RPR), or fluorescent treponema antigen preparation. (FTA). T. paraluis cuniculi may be found in histosections with silver stain or with darkfield microscopy of fresh specimens.
E. Treatment: A regimen of procaine penicillin, 40,000 IU IM s.i.d. for 3 to 5 days is curative. Once the spirochete is eliminated, serum antibody drops gradually to undetectable levels.
F. Control: If spirochetosis is a herd problem, treat the entire herd. Do not breed infected animals. If animals are for meat production, do not treat weanlings or fryers; treat only breeding stock. Maintain a closed breeding colony or quarantine and medicate new arrivals. Recovered animals can be used as breeding stock without danger of transmitting infection.
VII. Proliferative Ileotyphlitis
Chronic diarrhea with wasting and a proliferative enteritis in rabbits have been associated with infection with a Lawsonia-like organism. The bacterium can be demonstrated within ileal or cecal enterocytes by use of silver chemical stains or amplified by a Lawsonia-specific PCR assay.. There is little known about the disease pathogenesis, but the etiologic agent (and the resultant disease) is similar to that of proliferative enteritis of swine. Concurrent diseases or stressors seem to be associated with development of the proliferative enteric lesion with intracellular bacteria. Oral administration of kaolin may be helpful when this infection is suspected.
A. Etiology: Salmonella enterica serovars are Gram-negative aerobic, nonlactose fermenting, H2S producing rods.
B. Transmission: Salmonellae are transmitted by ingestion through direct contact with contaminated feces, food or fomites. Incidence of infection is rare.
C. Clinical Signs: Acute disease is characterized by anorexia, fever, dehydration, diarrhea (hemorrhagic), death, and abortions. Rabbits that recover from acute disease are asymptomatic shedders.
D. Pathology: Lesions are consistent with those of septicemia and include congestion and hemorrhage of the viscera associated with septicemia, ulcerative colitis, and focal necrosis of liver.
E. Diagnosis: Definitive diagnosis is made by isolation of the bacteria through culture of blood, spleen, mesenteric lymph nodes and feces on selective media (brilliant green, selenite, citrate, or tetrathionate).
F. Treatment: Since antibiotic therapy does not eliminate bacterial carriage, it is advisable to eliminate the colony and restock.
G. Control: Good management practices will prevent infection. Disinfection, replacement with clean stock and prevention of wild bird or rodent contamination of bedding, water, or food should prevent future or continued problems.
Public Health Significance: Man can contract Salmonella from infected rabbits.
A. Etiology: Francisella tularensis is a Gram-negative, pleomorphic rod.
B. Transmission: Blood sucking arthropods (squirrel flea, deerfly, mosquitoes, lice, and woodticks) may serve as mechanical or biological vectors. Transmission may occur by direct contact, ingestion, or aerosol (rare). The incidence of infection in domestic rabbits is rare.
C. Clinical Signs: Depression, anorexia, ataxia, and death are the nonspecific signs associated with this disease.
D. Gross Pathology: Widespread visceral congestion, splenomegaly,
consolidated and congested lungs, and multiple pinpoint white foci on the
liver and spleen are characteristic lesions.
E. Diagnosis: Necropsy findings, and bacterial isolation are
recommended diagnostic measures.
F. Treatment: There is no treatment.
G. Control: Elimination or control of vectors and wild mammal populations will prevent exposure.
Public Health Significance: Man is susceptible to infection.
Transmission can occur by ingestion of contaminated water, penetration
of unbroken skin or contamination of cutaneous wounds, tick bites, or by
aerosolization of the organism in dust, feces, or when skinning wild rabbits.
Human tularemia is manifest by cutaneous lesions, septicemia, and/or meningitis.
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