| < 10%); mortality was high among affected rabbits. In rabbits from Tennessee, we have seen some sporadic cases and others associated with epizootics of diarrheal disease. Dr. James Fox at MIT has been consulted regarding cases in Massachusetts and Michigan, and I've heard of cases in Missouri. 3. Clinical: Moon et al. reported fulminating diarrhea, sometimes with mucus and blood, among weanlings, but many were found dead without observed diarrhea. Our cases have been in sucklings to young adults. Some of them have had fulminating diarrhea, but most have had less severe signs. 4. Pathology: The pattern described by Moon et al. is multifocal to diffuse, suppurative and superficially necrotizing cecocolitis. We have seen a few cases like this; most were associated with the epizootic of rotavirus infection we reported. Organisms were demonstrable in Warthin-Starry-stained sections within epithelial cells in areas of degeneration and necrosis. We also have seen a different pattern, not previously reported in rabbits, in which there is multifocal to diffuse, mild to moderate hyperplasia of mucosal epithelium in the small intestine, cecum, and colon, with numerous organisms demonstrable within the apical cytoplasm of epithelial cells in Warthin-Starry-stained sections. Dr. Fox found that these organisms react with monoclonal antibody against "omega" antigen of intracellular Campylobacter-like organisms extracted from intestines of pigs with proliferative ileitis and with polyclonal antisera against the pig organisms, as do the intracellular bacteria in proliferative ileitis of hamsters and proliferative colitis of ferrets. Organisms in the Moon et al. report had morphologic features of Campylobacter sp.; our findings have been similar. Umemura et al. describe "histiocytic enteritis," in which the distal small intestine was thickened with accumulations of macrophages in the lamina propria and the epithelial cells contained Campylobacter-like bacteria. They didn't mention epithelial hyperplasia in their description, but it is evident in the illustration. A few of our rabbits had similar lesions, with "omega" antigen in macrophages, so it seems likely that "histiocytic enteritis" is the same disease. 5. Diagnosis: Lesions, demonstration of organism (Warthin-Starry, immunofluorescence), rule out other causes. Use cautionCampylobacter has been isolated from rabbits without disease. We have not been able to isolate the causative organism from any of our cases. 6. Control: Specific measures not known. 7. References: Blaser MJ. Campylobacter enteritis. In Infectious Diarrheal Disease: Current Concepts and Laboratory Procedures, ed. Ellner PD, Marcel Dekker Inc., New York, 1984, pp. 1-12. Caldwell MB, Walker RI. 1986. Adult rabbit model for Campylobacter enteritis. Am J Pathol 122:573-576. Fox JG, Lawson GHK. 1988. Campylobacter-like omega intracellular antigen in proliferative colitis of ferrets. Lab Anim Sci 38:34-36. Lawson GHK, Rowland AC, MacIntyre N. 1985. Demonstration of a new intracellular antigen in porcine intestinal adenomatosis and hamster proliferative ileitis. Vet Microbiol 10:303-313. McOrist S, Boid R, Lawson GH. 1989. Antigenic analysis of Campylobacter species and an intracellular Campylobacter-like organism associated with porcine proliferative enteropathies. Infect Immun 57:957-962. McOrist S et al. 1987. Monoclonal antibodies to intracellular campylobacter-like organisms of the porcine proliferative enteropathies. Vet Rec 121:421-422. McOrist S et al. 1989. Early lesions of proliferative enteritis in pigs and hamsters. Vet Pathol 26:260-264. McOrist S, Lawson GH. 1987. Possible relationship of proliferative enteritis in pigs and hamsters. Vet Microbiol 15:293-302. Moon HW et al. 1974. Intraepithelial vibrio associated with acute typhlitis of young rabbits. Vet Pathol 11:313-326. Prescott JF, Bruin-Mosch CW. 1981. Carriage of Campylobacter jejuni in healthy and diarrheic animals. Am J Vet Res 42:164-165. Schoeb TR, Fox JG. Proliferative enteritis associated with intraepithelial Campylobacter-like bacteria in rabbits (Oryctolagus cuniculus). Vet Pathol, in press. Stills HF Jr, Hook RR Jr, Sprouse RF. 1987. Utilization of monoclonal antibodies to evaluate the involvement of Campylobacter jejuni in proliferative ileitis in Syrian hamsters (Mesocricetus auratus). Infect Immun 55:2240-2246. Stills HF Jr, Hook RR Jr. 1989. Experimental production of proliferative ileitis in Syrian hamsters (Mesocricetus auratus) by using an ileal homogenate free of Campylobacter jejuni. Infect Immun 57:191-195. Umemura T et al. 1982. Histiocytic enteritis of rabbits. Vet Pathol 19:326-328. Mucoid Enteropathy 1. Cause: Unknown. Pathologic features suggest it is an enterotoxin-induced secretory diarrhea, and some evidence suggests that ME is infectious and transmissible, but no consistent association with any particular organism has been found. Some experimental results suggest that ME may be related to reduced intestinal motility. Lelkes proposes that ME results from imbalances in cecal microflora. It is uncertain even that ME is a distinct disease. However, there is a syndrome or set of signs and lesions that until further information becomes available can be recognized as ME (see below). 2. Epizootiology: Unknown. ME is widely distributed in U.S. One of the most common causes of mortality in production colonies. 3. Clinical: Anorexia, polydipsia, subnormal temperature, depression, mucinous or fluid diarrhea. Usually in weanling (7-10 weeks old) rabbits. 4. Pathology: Distention of the stomach and small intestine with fluid and gas. The cecum can be impacted with pasty or dry contents. The colon characteristically contains casts of clear gelatinous mucus. Microscopically there may be increased mucus secretion (goblet cell hyperplasia) but there is no inflammation. 5. Diagnosis: Signs and lesions. 6. Control: Unknown. Antibiotics may reduce mortality. 7. References: Lelkes L. 1987. A review of rabbit enteric diseases: A new perspective. J Appl Rabbit Res 10:55-61. McLeod CG, Katz W. 1986. Opportunistic bacteria isolated from the caecum of rabbits with mucoid enteritis. Br Vet J 142:177-188. Toofanian F. 1985. Intestinal disaccharidase and alkaline phosphatase activities in experimental rabbit mucoid enteropathy. Lab Anim Sci 35:624-626. Toofanian F, Targowski S. 1983. Experimental production of rabbit mucoid enteritis. Am J Vet Res 44:705-708. Toofanian F, Targowski S. 1986. Stimulation of colonic goblet cells by cecal filtrates from rabbits with experimental mucoid enteropathy. Lab Anim Sci 36:157-160. Toofanian F, Hamar DW. 1986. Cecal short chain fatty acids in experimental rabbit mucoid enteropathy. Am J Vet Res 47:2423-2425. van Kruiningen HJ, Williams CB. 1972. Mucoid enteritis of rabbits. Comparison to cholera and cystic fibrosis. Vet Pathol 9:53-77. Vetesi F, Kutas F. 1973. Mucoid enteritis in the rabbit associated with E. coli. Changes in water, electrolyte, and acid-base balance. Acta Vet Acad Sci Hung 23:381-388. Yersiniosis 1. Agent: Yersinia pseudotuberculosis (possibly also Y. enterocolitica). 2. Epizootiology: An uncommon disease, transmitted by fecal contamination and ingestion, therefore probably would not be seen in well managed rabbitry. Potentially zoonotic. 3. Clinical: Chronic weight loss with or without diarrhea, perhaps palpable abdominal masses. 4. Pathology: Most consistently, enlargement and caseous necrosis of mesenteric lymph nodes. Caseous necrotizing lesions can also occur in Peyer's patches, appendix, liver, spleen, lungs, kidneys, peripheral nodes, bones, heart, etc. 5. Diagnosis: Lesions, culture. 6. Control: Prevent access of vermin to rabbitry. 7. Reference: Pai CH et al. 1980. Experimental Yersinia enterocolitica enteritis in rabbits. Infect Immun 28:238-244. Pasteurellosis 1. Etiology and pathogenesis: Pasteurella multocida, a short gram-negative bipolar bacillus, is the causative organism. Isolates may produce smooth, rough, or mucoid colonies; those producing mucoid ones are thought to be the most pathogenic. Various serotypes exist which may vary in virulence. Some recent evidence suggests that virulence may be related to adherence to respiratory epithelium and may not be due, as previously suggested, to ability to resist phagocytosis and killing by neutrophils. Commonly isolated serotypes include 12:A, 3:D, and 3:A (somatic:capsular antigens). Several organisms other than P. multocida have been isolated from pyogenic respiratory lesions in rabbits, particularly Bordetella bronchiseptica and Staphylococcus aureus. However, only P. multocida causes significant disease experimentally. Still, other factors must be involved because the response to experimental inoculation varies considerably. These factors remain to be elucidated, but likely possibilities include variation in organism virulence and factors affecting host resistance, such as concurrent disease and stress associated with experimentation, parturition and lactation, shipping, bad weather, and so forth. Further, clinically normal rabbits can harbor the organism in the nasal passages, and the extent to which the respiratory tract and other organs are affected also is probably affected by many variables. Currently, it is generally thought that the major route of infection is via the upper respiratory tract from which infection may spread distally to the lungs, to the eyes via the nasolacrimal duct or from the front paws contaminated with nasal exudate, to the middle ears via the auditory tubes, and into the blood resulting in acute death or in localization in other organs. P. pneumotropica has been isolated from "Pasteurella-free" rabbits. It did not cause any disease. 2. Epizootiology: Infection is essentially ubiquitous among conventional colonies. Prevalence of infection within colonies varies widely but can be 70% or more. Transmission is primarily by contact or aerosol, although venereal transmission also can occur. Asymptomatic carriers are important as disseminators of infection. 3. Clinical: Respiratory signs predominate: Mucopurulent nasal discharge, sneezing, coughing, or "snuffling." In a few cases in which otitis extends into the inner ear, torticollis or "wryneck" may occur. Sterility in does and orchitis or balanoposthitis are major manifestations of genital infection. Most deaths result from septicemia and pneumonia. Usually these animals are found dead; premonitory signs are seldom observed. Subcutaneous abscesses and mucopurulent conjunctivitis also occur. 4. Pathology: Chronic suppurative rhinitis, in some cases with grossly visible exudate. Pneumonia is usually typical airway-centered fibrinopurulent bronchopneumonia, sometimes accompanied by pleuritis. In otitis media, exudate usually is visible grossly. Abscesses are typical and not microscopically distinctive. They can occur in the subcutis, lungs, brain, heart, muscle, testicles, uterus, and other organs. Chronic suppurative endometritis with pyometra can occur. Rabbits dying of sep- ticemia may have no lesions or only a few petechiae. 5. Diagnosis: In live rabbits, by culture of nasal swabs. Diagnoses in necropsy cases are made by culturing affected organs and by demonstration of appropriate lesions. Septicemia is difficult to diagnose. The blood, bone marrow, spleen, and liver may be cultured, but Pasteurella septicemia probably is blamed for the deaths of many rabbits that actually are due to other, unknown causes. 6. Control: Good barrier technique, begin colony with Cesarean-derived SPF stock. 7. References: Al-Lebban ZS, Corbeil LB, Coles EH. 1988. Rabbit pasteurellosis: induced disease and vaccination. Am J Vet Res 49:312-316. Cary CJ et al. 1984. Serological analysis of five serotypes of Pasteurella multocida of rabbit origin by use of an enzyme-linked immunosorbent assay with lipopolysaccaride as antigen. J Clin Microbiol 20:191-194. Deeb BJ et al. 1989. Field trial of a live streptomycin dependent Pasteurella multocida serotype A:12 vaccine in rabbits. Lab Anim Sci 39:229-233. DiGiacomo RF et al. 1983. Natural history of infection with Pasteurella multocida in rabbits. J Am Vet Med Assoc 183:1172. DiGiacomo RF et al. 1987. Safety and efficacy of a streptomycin dependent live Pasteurella multocida vaccine in rabbits. Lab Anim Sci 37:187-190. DiGiacomo RF et al. 1989. Atrophic rhinitis in New Zealand white rabbits infected with Pasteurella multocida. Am J Vet Res 50:1460-1465. Glass LS, Beasley JN. 1989. Infection with and antibody response to Pasteurella multocida and Bordetella bronchiseptica in immature rabbits. Lab Anim Sci 39:406-410. Hofing EL et al. 1979. In vitro killing of Pasteurella multocida: The effect of rabbit granulocyte and specific antibody source. Am J Vet Res 40:679-683. Holmes HT et al. 1986. Serologic methods for detection of Pasteurella multocida infections in nasal culture negative rabbits. Lab Anim Sci 36:640-645. Hwang EJ et al. 1986. Characterization of an antigen purified from type 3 strains of Pasteurella multocida and its use for an enzyme-linked immunosorbent assay. Lab Anim Sci 36:633-639. Jones SM, Carrington SD. 1988. Pasteurella dacryocystitis in rabbits. Vet Rec 122:514-515. Kirchner BK et al. 1983. Pasteurella pneumotropica in rabbits from a "Pasteurella-free" production colony. Lab Anim Sci 33:461-462. Klaassen JM et al. 1985. Enzyme linked immunosorbent assay for immunoglobulin G antibody to Pasteurella multocida in rabbits. J Clin Microbiol 21:617-621. Kunstyr I, Naumann S. 1985. Head tilt in rabbits caused by pasteurellosis and encephalitozoonosis. Lab Anim 19:208-213. Liebenberg SP, Badger VM. 1984. Suppurative osteomyelitis in the foot of a rabbit. J Am Vet Med Assoc 185:1382. Lu YS, et al. 1983. Capsular and somatic serotypes of Pasteurella multocida isolates recovered from healthy and diseased rabbits in Texas. J Clin Microbiol 18:292-295. Lu YS et al. 1987. A potassium thiocyanate extract vaccine prepared from Pasteurella multocida 3:A protects rabbits against homologous challenge. Infect Immun 55:2967-2976. Lu YS et al. 1988. Distribution of a monoclonal antibody-recognized protective protein immunogen on the outer membranes of Pasteurella multocida rabbit isolates. J Clin Microbiol 26:1326-1330. Lukas VS et al. An enzyme linked immunosorbent assay to detect serum IgG to Pasteurella multocida in naturally and experimentally infected rabbits. Lab Anim Sci 37:60-64. Manning PJ et al. 1986. Pasteurellosis in laboratory rabbits: characterization of lipopolysaccharides of Pasteurella multocida by polyacrylamide gel electrophoresis, immunoblot techniques, and enzyme linked immunosorbent assay. Infect Immun 53:460-463. Manning PJ. 1982. Serology of Pasteurella multocida in laboratory rabbits: A review. Lab Anim Sci 32:666-671. Manning PJ. 1984. Naturally occurring pasteurellosis in laboratory rabbits: Chemical and serological studies of whole cells and lipopolysaccharides of Pasteurella multocida. Infect Immun 44:502-507. Murray KA et al. 1985. Acute meningoencephalomyelitis in a rabbit infected with Pasteurella multocida. Lab Anim Sci 35:169-171. Nakagawa M et al. 1986. Bacteriological and serological studies on Pasteurella multocida infection in rabbits. Jikken Dobutsu 35:463-469. Percy DH et al. 1984. Characterization of Pasteurella multocida isolated from rabbits in Canada. Can J Comp Med 48:162-165. Percy DH et al. 1985. Pasteurella multocida infection in the domestic rabbit: immunization with a streptomycin dependent mutant. Can J Comp Med 49:227-230. Percy DH et al. 1986. Experimental pneumonia in rabbits inoculated with strains of Pasteurella multocida. Can J Vet Res 50:36-41. Rimler RB, Brogden KA. 1986. Pasteurella multocida isolated from rabbits and swine: Serologic types and toxin production. Am J Vet Res 47:730. Ringler DH et al. 1985. Protection of rabbits against experimental pasteurellosis by vaccination with a potassium thiocyanate extract of Pasteurella multocida. Infect Immun 49:498-504. Rush HG et al. 1981. Resistance of Pasteurella multocida to rabbit neutrophil phagocytosis and killing. Am J Vet Res 47:1760-1768. Scharf RA et al. 1981. A modified barrier system for maintenance of Pasteurella-free rabbits. Lab Anim Sci 31:513-515. Scher S et al. 1969. The establishment of a specific pathogen-free rabbit breeding colony. I. Procedure for establishment and maintenance. Lab Anim Sci 19:610-799. Sokkar SM et al. 1987. Pathogenesis of Pasteurella multocida in experimentally infected rabbits. Arch Exp Veterinarmed 41:516-521. Ward GM. 1973. Development of a Pasteurella-free rabbit colony. Lab Anim Sci 23:671-674. Welch WD et al. 1987. Pharmacokinetics of penicillin G in serum and nasal washings of Pasteurella multocida free and infected rabbits. Lab Anim Sci 37:65-68. Staphylococcosis 1. Agent: Staphylococcus aureus. 2. Epizootiology: S. aureus is very widespread and is carried in the upper respiratory tracts of many animals and people. Transmission readily occurs via fomites, contact, and aerosol. 3. Clinical: Subcutaneous and mammary gland abscesses and necrotizing dermatitis are most common. Septicemic rabbits are usually just found dead. Lesions can be chronic and exudative, but extensive necrotizing lesions leading to death also occur. In very young rabbits, outbreaks of exudative staphylococcal dermatitis can cause high morbidity and mortality. 4. Pathology: Suppurative to necrotizing dermatitis and mastitis. Rabbits dead of peracute septicemia will probably have no lesions, but those surviving a few days can develop multifocal suppurative lesions in the heart, kidneys, lungs, liver, spleen, testicles, epididymides, joints, and bones. 5. Diagnosis: Culture. 6. Control: Difficult to exclude from colony. Can treat with antibiotics but some will die of enteric complications of therapy. Autogenous bacterin may help control. 7. References: Adlam C et al. 1977. Natural and experimental staphylococcal mastitis in rabbits. J Comp Pathol 86:581-593. Carolan MG. 1986. Staphylococcosis in rabbits [letter]. Vet Rec 119:412. Cohen JO. 1987. Veterinary medicine today: Staphylococcosis. J Am Vet Med Assoc 190:151-153. Devriese LA. 1984. A simplified system for biotyping Staphylococcus aureus strains isolated from animal species. J Appl Bacteriol 56:215-220. Millichamp NJ, Collins BR. 1986. Blepharoconjunctivitis associated with Staphylococcus aureus in a rabbit. J Am Vet Med Assoc 189:1153-1154. Okerman L et al. 1984. Cutaneous staphylococcosis in rabbits. Vet Rec 114:313-315. Snyder SB et al. 1976. Disseminated staphyloccal disease in laboratory rabbits (Oryctolagus cuniculus). Lab Anim Sci 26:86-89. Tularemia 1. Agent: Francisella tularensis (gram-negative and aerobic). 2. Epizootiology: Although numerous species, including laboratory rabbits, are susceptible, from a practical standpoint the disease is important mostly as a zoonotic hazard associated with wild rabbits (Sylvilagus spp.) and hares (Lepus spp.). Direct contact and wound entry or penetration of intact skin are most common means of transmission to man, but transmission by inhalation or ingestion also occurs. Among wild animals, infection is spread primarily by blood-sucking or biting arthropods, which may be merely mechanical or true biological vectors. Human infections also have resulted from tick bites. 3. Clinical: Affected animals usually are found dead; signs when observed are nonspecific. In man, fever and lymphadenopathy with or without abscess or phlegmon at initial site. Can be fatal if untreated, but responds well to antibiotics. 4. Pathology: Multifocal necrotizing and suppurative lesions in many organs: liver, spleen, lungs, lymph nodes, bone marrow, et al. 5. Diagnosis: Lesions, culture. 6. Control: Prevent vectors from entering colony. Use care when dressing wild rabbits. 7. References: Evans ME et al. 1985. Tularemia: A 30-year experience with 88 cases. Medicine (Baltimore) 64:251-269. Gordon JR et al. 1983. Tularemia transmitted by ticks (Dermacentor andersoni) in Saskatchewan. Can J Comp Med 47:408-411. Morner T et al. 1988. Infections with Francisella tularensis biovar palaearctica in hares (Lepus timidus, Lepus europaeus) from Sweden. J Wildl Dis 24:422-433. Rohrbach BW. 1988. Zoonosis update. Tularemia. J Am Vet Med Assoc 193:428-432. Treponematosis 1. Agent: Treponema cuniculi, a spirochete. 2. Epizootiology: Disease is rare, although serologic evidence indicates that infection may be rather more common than disease. Transmission is by contact during breeding. 3. Clinical: Lesions usually are on the genitalia but can also affect the anus and the skin of the perineum. A few rabbits develop lesions on the face. Lesions begin as reddened swellings which exude serum, become crusty and ulcerated, and eventually become dry and scaly and heal, with mild scarring. The course is usually several weeks. Affected rabbits are otherwise healthy. Females are reported to be less severely affected than males. 4. Pathology: Epidermal acanthosis and hyperkeratosis with dermal infiltration by lymphocytes and plasma cells, or ulceration with chronic suppurative reaction; there may be dermal or subcutaneous focal granulomas with necrotic centers. Spirochetes demonstrable in skin with Warthin-Starry stain. 5. Diagnosis: Lesion morphology, Warthin-Starry stain, dark field microscopy, serologic tests for syphilis including VDRL (Venereal Disease Research Laboratory), RPR (rapid plasma reagin), and FTA-ABS (fluorescent treponemal antibody-absorbed) tests. FTA-ABS antibodies appear to be the most persistent after treatment. 6. Control: No unusual measures needed. Treat with penicillin (lesions can still take 1 to 4 weeks to heal completely). 7. References: Cunliffe-Beamer T, Fox RR. 1981. Venereal spirochetosis of rabbits: Eradication. Lab Anim Sci 31:379-381. DiGiacomo RF et al. 1983. Treponema paraluis-cuniculi infection in a commercial rabbitry. Epidemiology and serodiagnosis. Lab Anim Sci 33:562-566. DiGiacomo RF et al. 1984. Clinical course and treatment of venereal spirochaetosis in New Zealand white rabbits. Br J Vener Dis 60:214-218. DiGiacomo RF et al. 1985. Chronicity of infection with Treponema paraluis cuniculi in New Zealand white rabbits. Genitourin Med 61:156-164. Gaertner DJ, Barthold SW. 1989. Diagnostic exercise: nasal mass in a rabbit. Lab Anim Sci 39:440-441. Miscellaneous bacterial conditions 1. Listeriosis Agent: Listeria monocytogenes, a small gram-positive bacillus. Listeriosis is sporadic and rarely recognized today. Transmission is poorly understood. The organism survives well in the environment, and there is some evidence for ingestion as common route; therefore, many opportunities for ingestion of contaminated feed probably occur. Clinical signs include death or abortion. Listeriosis is a septicemic disease, with cervical and mesenteric lymphadenitis, multifocal necrotizing and suppurative hepatitis, splenitis, adrenal adenitis, etc. In pregnant does, suppurative endometritis results in placentitis, abortion, and fetal or neonatal septicemia, as in other species. Watson GL, Evans MG. 1985. Listeriosis in a rabbit. Vet Pathol 22:191-193. 2. Necrobacillosis Agent: Fusobacterium necrophorum, a gram-negative anaerobe and common intestinal commensal. Disease is sporadic and usually results from fecal contamination of wounds, thus it usually occurs in situations of poor sanitation. Lesions are most commonly on the face (perhaps because of coprophagy) and feet. They are necrotizing and fetid and often ulcerative, although they may be deep, even in underlying bone. Visceral dissemination occurs in some cases. The primary characteristic of the lesions is caseous necrosis. Garibaldi BA, Moyer C, Fox JG. 1990. Diagnostic exercise: mandibular swelling in a rabbit. Lab Anim Sci 40:77-78. Nakajima Y et al. 1987. The effects of Escherichia coli endotoxin as a trigger for hepatic infection of rabbits with Fusobacterium necrophorum. J Comp Pathol 97:207-215. 3. Sylvatic plague Agent: Yersinia pestis. Not a disease of laboratory rabbits, but occasionally affects wild rabbits, and human infections have been acquired from handling wild rabbits. Transmitted naturally by arthropods, especially fleas, but people can acquire from contact with carcasses. In man, disease can be septicemic, pneumonic, or localized with lymphadenopathy. Diagnosis is by culture. 4. Cilia-associated respiratory (CAR) bacillus Rabbits are susceptible to natural and experimental infection. The prevalence of CAR bacillus in rabbits is not known. We have seen several cases here. In some, the bronchi had mild lesions similar to those observed in rats; in others, the organisms were evident only in the larynges and were associated with mild suppurative laryngitis. Lukas VS, Ruehl WW, Hamm TE Jr. 1987. An enzyme-linked immunosorbent assay to detect serum IgG in rabbits naturally exposed to cilia-associated respiratory bacillus. (Abstract) Lab Anim Sci 37:533. MacKenzie WF, Magill LS, Hulse M. 1981. A filamentous bacterium associated with respiratory disease in wild rats. Vet Pathol 18:836-839. Matsushita S et al. 1989. Transmission experiments of cilia-associated respiratory bacillus in mice, rabbits and guineapigs. Lab Anim 23:96-102. Waggie KS, Spencer TH, Allen AM. 1987. Cilia associated respiratory (CAR) bacillus infection in New Zealand White rabbits. (Abstract) Lab Anim Sci 37:533. 5. Other Srivastava KK et al. 1986. Characterization of a Haemophilus sp. isolated from a rabbit with conjunctivitis. Lab Anim Sci 36:291-293. Zarnke RL, Schlater L. 1988. Actinobacillosis in free-ranging snowshoe hares (Lepus americanus) from Alaska. J Wildl Dis 24:176-177. Mycotic diseases Fungal diseases in rabbits are uncommon to rare. Dermatophytosis should be a differential diagnosis in dermatitis. Frame SR, Mehdi NA, Turek JJ. 1989. Naturally occurring mucocutaneous histoplasmosis in a rabbit. J Comp Pathol 101:351-354. Matsui T et al. 1985. Pulmonary aspergillosis in apparently healthy young rabbits. Vet Pathol 22:200-205. Vogstberger LM et al. 1986. Spontaneous dermatophytosis due to Microsporum canis in rabbits. Lab Anim Sci 36:294-297. Encephalitozoonosis 1. Agent: Encephalitozoon cuniculi (Microsporida). The organism has been confused with Nosema sp., from which it cannot be distinguished by ordinary light microscopy, but there are distinctive ultrastructural and antigenic differences between the two. 2. Epizootiology: Natural mode of transmission not proven, but probably is via ingestion of infective spores passed in urine. Transplacental transmission also can occur. 3. Clinical: For practical purposes, none, although some older reports mention various neurological signs. 4. Pathology: Most common finding is scarring in the kidney, visible as multiple 1-2 mm pale slightly depressed areas in the capsular surface. These are confluent with radially oriented linear areas of chronic tubulointerstitial nephritis. Early lesions are granulomatous and necrotizing; older ones are fibrotic and contain many plasma cells. Gross lesions are not visible in the brain, but many, if not most, infected rabbits have some degree of multifocal granulomatous encephalitis, with mononuclear perivascular cuffing and leptomeningitis near affected areas. Lesions can occur anywhere in the brain but usually are most numerous in the cerebrum. Other organs are rarely if ever affected. Organisms are gram-positive and can be demonstrated with tissue gram stains, although they are difficult to find in many cases. 5. Diagnosis: Lesions, gram stain, serologic tests. 6. Control: Difficult, but can be done by cesarean derivation with intensive monitoring. 7. References: Ansbacher L, Nichols MF, Hahn AW. 1988. The influence of Encephalitozoon cuniculi on neural tissue responses to implanted biomaterials in the rabbit. Lab Anim Sci 38:689-695. Beckwith C et al. 1988. Dot enzyme-linked immunosorbent assay (dot ELISA) for antibodies to Encephalitozoon cuniculi. Lab Anim Sci 38:573-576. Bywater JE, Kellett. 1978. Encephalitozoon cuniculi antibodies in a specific-pathogen- free rabbit unit. Infect Immun 21:360-364. Bywater JE, Kellett. 1978. The eradication of Encephalitozoon cuniculi from a specific pathogen-free rabbit colony. Lab Anim Sci 28:402-404. Cox JC. 1977. Altered immune responsiveness associated with Encephalitozoon cuniculi infection in rabbits. Infect Immun 15:393-395. Cox JC et al. 1972. Presumptive diagnosis of Nosema cuniculi in rabbits by immunofluorescence. Res Vet Sci 13:595-597. Cox JC et al. 1977. Application of immunofluorescence to the establishment of an Encephalitozoon cuniculi-free rabbit colony. Lab Anim Sci 27:204-209. Cox JC, Gallichio HA. 1977. An evaluation of indirect immunofluorescence in the serological diagnosis of Nosema cuniculi infection. Res Vet Sci 22:50-52. Didier ES, Shadduck JA. 1988. Modulated immune responsiveness associated with experimental Encephalitozoon cuniculi infection in BABL/c mice. Lab Anim Sci 38:680- 688. Flatt RE, Jackson SJ. 1970. Renal nosematosis in young rabbits. Pathol Vet 7:492-497. Goodman DG, Garner FM. 1972. A comparison of methods for detecting Nosema cuniculi in rabbit urine. Lab Anim Sci 22:568-572. Howell JMcC, Edington N. 1968. The production of rabbits free from lesions associated with Encephalitozoon cuniculi. Lab Anim 2:143-146. Hunt RD et al. 1972. Encephalitozoonosis: Evidence for vertical transmission. J Infect Dis 126:212-214. Kellett BS, Bywater JEC. 1978. A modified india-ink immunoreaction for the detection of encephalitozoonosis. Lab Anim 12:59-60. Kunstyr I et al. 1986. Humoral antibody response of rabbits to experimental infection with Encephalitozoon cuniculi. Vet Parasitol 21:223-232. Kunstyr I, Naumann S. 1985. Head tilt in rabbits caused by pasteurellosis and encephalitozoonosis. Lab Anim 19:208-213. Pakes SP et al. 1972. A diagnostic skin test for encephalitozoonosis (nosematosis) in rabbits. Lab Anim Sci 22:870-877. Pakes SP et al. 1984. Comparison of tests for the diagnosis of spontaneous encephalitozoonosis in rabbits. Lab Anim Sci 34:356-359. Pang VF, Shadduck JA. 1985. Susceptibility of cats, sheep, and swine to a rabbit isolate of Encephalitozoon cuniculi. Am J Vet Res 46:1071-1077. Pye D, Cox JC. 1977. Isolation of Encephalitozoon cuniculi from urine samples. Lab Anim 11:233-234. Waller T. 1977. The india-ink immunoreaction: a method for the rapid diagnosis of encephalitozoonosis. Lab Anim 11:93-97. Waller T, Bergquist NR. 1982. Rapid simultaneous diagnosis of toxoplasmosis and encephalitozoonosis by carbon immunoassay. Lab Anim Sci 32:515-517. Wosu NJ et al. 1977. Diagnosis of encephalitozoonosis in experimentally infected rabbits by intradermal and immunofluorescence tests. Lab Anim Sci 27:210-216. Wosu NJ et al. 1977. Diagnosis of experimental encephalitozoonosis in rabbits by complement fixation. J Infect Dis 135:944-948. Hepatic Coccidiosis 1. Agent: Eimeria stiedae. 2. Epizootiology: Common in conventional rabbits. Transmitted by fecal-oral route. 3. Clinical: Usually none. Severely affected rabbits can lose weight, become debilitated, develop hepatomegaly and icterus. 4. Pathology: Yellow-white or yellow-tan nodules from a few mm to 1-2 cm in diameter in the liver; these are bile ducts chronically inflamed and dilated with bile and exudate. Microscopic: chronic proliferative cholangitis and cholecystitis, with numerous schizonts, microgametes, macrogametes, and developing oocysts in the epithelial cells; also, oocysts in the lumen. 5. Diagnosis: Fecal examination; lesions. 6. Control: Good barrier technique (must start with clean stock); can be controlled with sulfonamide treatment but not recommended. 7. References: Gomez Bautista M et al. 1986. The levels of total protein and protein fractions in the serum of rabbits infected with Eimeria stiedae. Ann Parasitol Hum Comp 61:393-400. Gomez Bautista M et al. 1987. The effect of the host's age on the pathology of Eimeria stiedae infection in rabbits. Vet Parasitol 24:47-57. Joyner LP et al. 1983. Eimeria stiedae in rabbits. The demonstra-tion of responses to chemotherapy. Res Vet Sci 34:64-67. Pakandl M. 1986. Efficacy of salinomycin, monensin and lasalocid against spontaneous Eimeria infection in rabbits. Folia Parasitol (Praha) 33:195-198. Patterson LT. 1987. Rabbit coccidiosis. Vet Hum Toxicol 29(Suppl 1):73-79. Peeters JE, Geeroms R. 1986. Efficacy of toltrazuril against intestinal and hepatic coccidiosis in rabbits. Vet Parasitol 22:21-35. Intestinal Coccidiosis 1. Agents: Eimeria spp. At least 10 spp., but only 3 or 4 are significant pathogens, e.g., E. magna, E. irresidua, E. intestinalis. 2. Epizootiology: Transmission is by fecal-oral route; oocysts must sporulate to become infective. Common among conventional rabbits. 3. Clinical: Varies from none to profuse watery, even bloody, diarrhea and death, depending on susceptibility of host (young or not previously exposed are more susceptible), species of causative organism, and inoculating dose. Mild or no signs are more common. Our experience has been that although infection is common in conventional rabbits, we never have seen a case in which enteric coccidiosis caused death. 4. Pathology: Most Eimeria species in rabbits affect one or more segments of small intestine; a few affect cecum or colon also. Parasitized enterocytes are lost resulting in superficially necrotizing enteritis. Severity of epithelial destruction and degree of inflammatory response vary considerably. 5. Diagnosis: Fecal examination; histopathology. 6. Control: Sanitation; barrier technique. Sulfonamides control but not recommended. 7. References: Gregory MW, Catchpole J. 1986. Coccidiosis in rabbits: The pathology of Eimeria flavescens infection. Int J Parasitol 16:131-145. Ogunbiyi AO, Uche EM. 1981. Intussusception in a rabbit (Oryctolagus cuniculus) associated with coccidiosis. Lab Anim 15:129. Pakandl M. 1988. Description of Eimeria vejdovskyi sp.n. and redescription of Eimeria media Kessel, 1929 from the rabbit. Folia Parasitol (Praha) 35:1-9. Peeters JE et al. 1984. Clinical and pathological changes after Eimeria intestinalis infection in rabbits. Zentralbl Veterinarmed [B] 731:9-24. Peeters JE, Geeroms R. 1989. Efficacy of diclazuril against robenidine resistant Eimeria magna in rabbits. Vet Rec 124:589-590. San Martin-Nunez BV, Ordonez-Escudero D, Alunda JM. 1988. Preventive treatment of rabbit coccidiosis with alpha-difluoromethylornithine. Vet Parasitol 30:1-10. Varga I. 1982. Large scale management systems and parasite populations: Coccidia in rabbits. Vet Parasitol 11:69-84. Miscellaneous Protozoa 1. Cryptosporidium cuniculus. Frequency of infection not known. Probably transmitted via fecal-oral route. No clinical signs known; reported only from apparently healthy rabbits. Pathogenic in other species, however. No histologic lesions; organisms attached to enterocytes of small intestine. Inman LR, Takeuchi A. 1979. Spontaneous cryptosporidiosis in an adult female rabbit. Vet Pathol 16:89-95. Rehg JE et al. 1979. Cryptosporidium cuniculus in the rabbit (Oryctolagus cuniculus). Lab Anim Sci 29:656-660. Ryan MJ et al. 1986. Cryptosporidium in a wild cottontail rabbit (Sylvilagus floridanus). J Wildl Dis 22:267. 2. Toxoplasma gondii. Transmitted by ingestion of infective oocysts from cat feces; also transplacentally. Rare today in domestic rabbits. Clinically, fever, usually without specific signs but sometimes neurologic signs, death in a few days. Multifocal necrosis of lymph nodes, spleen, liver, lungs, heart, brain, with vasculitis; organisms parasitize endothelial cells. Chronic lesions may be granulomatous or proliferative ("reticuloendothelial" hyperplasia). Ise Y et al. 1985. Detection of circulating antigens in sera of rabbits infected with Toxoplasma gondii. Infect Immun 48:269-272. 3. Sarcocystis cuniculi. Life cycle not definitely known, but rabbit is intermediate host. Definitive host is probably cat. Transmission is by ingestion of infective oocysts. No clinical disease. Lesions: sarcocysts in skeletal and cardiac muscle. These are grossly visible as fine pale streaks. There is usually no inflammatory response but in some cases eosinophilic myositis and myocarditis may result. Psoroptic Mange (Otoacariasis) 1. Agent: Psoroptes cuniculi. 2. Epizootiology: Common among conventional rabbits. Transmitted via contact. 3. Clinical: Ears are painful and itch intensely; affected rabbits shake heads and scratch ears. Inner surface of pinna covered with brown, scaly, fetid material. Skin beneath is raw, mites are grossly visible. 4. Pathology: Chronic erosive and proliferative eosinophilic dermatitis. Mites are non- burrowing and thus are found only in exudate, not in tissue. 5. Diagnosis: Appearance is characteristic; mites easily identified microscopically. 6. Control: Barrier technique. Can treat with mineral oil with or without acaricide, but cannot eliminate from colony. 7. References: Pandey VS. 1989. Effect of ivermectin on the ear mange mite, Psoroptes cuniculi, of rabbits. Br Vet J 145:54-56. Rafferty DE, Gray JS. 1987. The feeding behaviour of Psoroptes spp. mites on rabbits and sheep. J Parasitol 73:901-906. Stewart GA, Fisher WF. 1986. Cross reactivity between the house dust mite Dermatophagoides pteronyssinus and the mange mites Psoroptes cuniculi and P. ovis. I. Demonstration of antibodies to the house dust mite allergen Dpt 12 in sera from P. cuniculi infested rabbits. J Allergy Clin Immunol 78:293-299. Wright, FC, Riner JC. 1985. Comparative efficiency of injection routes and doses of ivermectin against Psoroptes in rabbits. Am J Vet Res 46:752-754. Sarcoptic Mange 1. Agents: Sarcoptes scabei and Notoedres cati. 2. Epizootiology: Worldwide distribution. Uncommon today in domestic rabbits. Zoonotic. 3. Clinical: Lesions are pruritic, variably alopecic, and crusty or oozing; usually on the muzzle at first then spreading over the face and head. 4. Pathology: Chronic dermatitis with acanthosis, burrowing mites in epidermis. Self-trauma can result in ulcerated areas with suppurative inflammation. 5. Diagnosis: Skin scraping, histopathology. 6. Control: Barrier technique. 7. References: Arlian LG et al. 1988. Effects of S. scabiei var. canis (Acari: Sarcoptidae) on blood indexes of parasitized rabbits. J Med Entomol 25:360-369. Lin SL et al. 1984. Diagnostic exercise. Sarcoptic mange in a rabbit. Lab Anim Sci 34:353-355. Fur Mites 1. Agent: Cheyletiella parasitovorax. 2. Epizootiology: Transmitted by contact. Not common today. 3. Clinical: None with light infestation, but if severe may have alopecia with red, scaly skin, not pruritic, mainly on trunk over scapulae. 4. Pathology: Dermatitis with hyperkeratosis. Mite is non-burrowing. 5. Diagnosis: Skin scraping. Differentiate from Listrophorus gibbus, another fur mite which is considered non-pathogenic. 6. Control: Topical treatments work; good barrier better. Helminth Parasites 1. Nematodes: Many spp. are known in wild rabbits, including Obeliscoides cuniculi, Nematodirus leporis, et al. (Trichostrongylidae, found in the stomach); Protostrongylus boughtoni (Metastrongylidae, bronchi); Passaluris ambiguus et al. (Oxyuridae, cecum and colon); Trichuris leporis (Trichuridae, cecum and colon); and Dirofilaria scapiceps (Filaridae, subcutis). Recently, a filariid of wild (Sylvilagus) rabbits in Louisiana was described: Brugia lepori. Of these, only Passaluris ambiguus is found in domestic rabbits with any frequency, and it is considered non-pathogenic. Larvae of the racoon ascarid Baylisascaris procyonis can cause visceral larval migrans with necrotizing and eosinophilic encephalitis. Duwel D, Brech K. 1981. Control of oxyuriasis in rabbits by fenbendazole. Lab Anim 15:101-105. Eberhard ML. 1984. Brugia lepori sp. n. (Filaroidea: Onchocerdidae) from rabbits (Sylvilagus aquaticus, S. floridanus) in Louisiana. J Parasitol 70:576-579. Kazacos KR et al. 1983. Fatal cerebrospinal disease caused by Baylisascaris procyonis in domestic rabbits. J Am Vet Med Assoc 183:967-971. Kazacos KR, Kazacos EA. 1988. Diagnostic exercise: Neuromuscular condition in rabbits. Lab Anim Sci 38:187-189. Watkins AR et al. 1984. The effects of single and multiple doses of thiabendazole on growing and arrested stages of the rabbit stomach worm Obeliscoides cuniculi. Vet Parasitol 16:295-302. 2. Cestodes: Wild rabbits frequently harbor Cittotaenia spp. and Raillietina spp. These are very rarely found in domestic rabbits. Domestic rabbits raised under poor husbandry conditions, however, commonly harbor larvae of the dog tapeworm Taenia pisiformis as cysticerci in the mesentery and liver and of T. serialis as coenuri in the skeletal muscles. Others have been reported. Tenora F, Beranek L, Stanek M. Larvocysts of the cestode T. polyacantha (Leucart, 1856) parasitizing Oryctolagus cuniculus. Folia Parasitol (Praha) 1988; 35:21-22 3. Trematodes: Hasstilesia tricolor is common in wild rabbits but has not been reported in domestic rabbits. Miscellaneous Parasites 1. Linguatula serrata A pentastomid. Rabbits are intermediate hosts and are infected by ingesting ova coughed up or defecated by definitive host (Canidae such as dog, fox, etc. and rarely sheep and man). Common in wild rabbits but rare in domestic rabbits. No disease; usually discovered at necropsy as incidental finding. Encysted nymphs found in abdominal and thoracic viscera. About 5 mm long. 2. Haemaphysalis leporis-palustris Only tick of significance in domestic rabbits; numerous other species affect wild rabbits. All can be vectors of tularemia, probably other bacterial diseases such as staphylococcosis, and of rickettsial diseases such as Rocky Mountain spotted fever and borelliosis. H. leporis-palustris occurs throughout North America. A three-host tick; larvae and nymphs commonly attach to birds, and adults spend only short time on rabbits, so not commonly seen. Sometimes abscesses at attachment site, but usually none. Anderson JF et al. 1989. Antigenically variable Borrelia burgdorferi isolated from cottontail rabbits and Ixodes dentatus in rural and urban areas. J Clin Microbiol 27:13-20. Ciceroni L et al. 1988. Rickettsiae of the spotted fever group associated with the host-parasite system Oryctolagus cuniculi/Rhipicephalus pusillus. Zentralbl Bakteriol Mikrobiol Hyg [A] 269:211-217. Lane RS, Burgdorfer W. 1988. Spirochetes in mammals and ticks (Acari: Ixodidae) from a focus of Lyme borreliosis in California. J Wildl Dis 24:1-9. 3. Haemodipsus ventricosus Louse, order Anoplura. Transmitted by contact. Present only under conditions of poor husbandry. Potential disease vector. No disease in in light infestations, anemia if heavy. 4. Cuterebra spp. Adult flies lay eggs around rabbit burrows or housing, larvae penetrate skin and develop. Larvae encyst in subcutis; cysts communicate with skin surface. Commonly called "warbles". Baird CR. 1983. Biology of Cuterebra lepusculi Townsend (Diptera: Cuterebridae) in cottontail rabbits in Idaho. J Wildl Dis 19:214-218. 5. Cediopsylla simplex and Odontopsyllus multispinosus Fleas; numerous species can affect rabbits but these are the only ones found with any frequency on domestic rabbits. Reportedly common, but not often found as only a few fleas generally infest each rabbit. Potential disease vectors. Usually no clinical signs, possibly some scratching or dermatitis. Neoplasms 1. Oryctolagus cuniculus. Accumulation of good data is hampered by the longer generation time and life span of the domestic rabbit compared to the mouse, and by the lack of old rabbits. Most are killed before 2 years old (normal life span is 7-8 years) so few rabbits reach a tumor-prone age. However, as in mice, some strains have a greater than usual incidence of certain tumors. Survey of Reported Tumors: a. Common: Uterine adenocarcinoma, lymphosarcoma, embryonal nephroma, and biliary adenoma and carcinoma, mammary intraductal papilloma and carcinoma (in older, > 3 yrs, female rabbits). (Though not tumors, adrenal cortical hyperplastic nodules are common and could be confused with tumors.). b. Uncommon: leiomyoma and leiomyosarcoma, vaginal squamous cell carcinoma. c. Rare or very rare: Ovarian, testicular, stomach, intestine, lung, CNS, urinary bladder, skin, bone, endocrine. (i) Uterine adenocarcinoma is the most common tumor of Oryctolagus cuniculus. Reproductive problems precede clinical appearance (palpable uterine nodules) by 6-10 months, and include decreased fertility and litter size, and more stillbirths, dystocia, and other difficulties. Tumors are usually multiple. The growth rate varies considerably but a typical mass could reach 5 cm in diameter by 6 months or so; many metastasize (mostly to the lung) and cause death in 12-24 months. Thus, they are slowly developing but inexorable. Gross lesions tend to be poorly demarcated pale lumps in the uterus, and somewhat more discrete, round, sometimes confluent or umbilicated nodules in the lungs. These are characterized histologically by a tubular and papillary adenocarcinoma pattern with abundant fibrous or myoid stroma. In the uterus, any of several endometrial abnormalities usually precedes the appearance of carcinoma: Adenomyosis (internal endometriosis), endometritis, pyometra, hyperplasia or atrophy. Which, if any, of these may be regarded as "precancerous" is unknown. Etiologic factors other than age remain obscure. There is apparently no relationship to parity. There may be a breed (hereditary) predisposition, but some random bred colonies also have high incidence. Some believe that "endocrine disturbances", particularly hyperestrogenism, are important. This remains to be substantiated experimentally, but some such general effect may indeed exist; mammary gland hyperplasia, adenosis, cysts, and tumors commonly accompany uterine adenocarcinoma. The high spontaneous incidence of this tumor gives it potential value as an experimental model. Elsinghorst TA et al. 1984. Comparative pathology of endometrial carcinoma. Vet Q 6:200-208. Hughes JR et al. 1981. Cystic mammary disease in a rabbit. J Am Vet Med Assoc 178:138-139. Lansdown AB et al. 1980. Endometrial adenocarcinoma in a young rabbit. Vet Rec 107:353. (ii) Lymphosarcoma: In contrast to other species, reported features of rabbit lymphosarcoma are rather uniform. Juveniles and young adults (8-18 months) are most commonly affected. Clinical findings include palpable abdominal masses, peripheral lymph node enlargement, anemia, and visible invasion of the ciliary body and anterior chamber of the eye. Four gross lesions are nearly constant: pale confluent renal cortical nodules, hepatomegaly usually without discrete nodules but with lobular accentuation, splenomegaly, and enlargement of any or all lymph nodes. Lymphoid tissue in the gastrointestinal tract is commonly affected and may ulcerate; peribronchial lymphoid tissue is affected less frequently. Ovaries and adrenals can be completely destroyed. The cells resemble large lymphoblasts. In the liver they accumulate periportally and in the kidney they are mostly interstitial with little destruction of nephrons. Interestingly, there is evidence that in certain strains at least, susceptibility is conferred by an autosomal recessive gene. This gene also apparently is responsible for a disease resembling that of NZB mice, except that it is sometimes accompanied by thymomas. (Thymomas are ordinarily sporadic and usually incidental findings, though thymic hyperplasia is not uncommon.) A rare Hodgkins'- like type has been described. Cloyd GG, Johnson GR. 1978. Lymphosarcoma with lymphoblastic leukemia in a New Zealand white rabbit. Lab Anim Sci 28:66-69. Fiume JW et al. 1980. Lymphoblastic leukemia in a rabbit: a case report. Lab Anim 14:49-51. (iii) Biliary adenoma and adenocarcinoma. Adenomas of the intrahepatic ducts are single or multiple, well demarcated, and often cystic. Most have considerable fibrous or myxoid stroma. They usually are an incidental PM finding. (iv) Embryonal nephroma. All reported ones were benign and were usually incidental findings. They have been found in old as well as young rabbits and apparently are very slow growing. They are single or multiple, white, projecting, discrete cortical nodules in either or both kidneys. Microscopically they resemble the human and porcine counterpart but contain no cartilage, muscle, or other mesenchymal elements as do many Wilm's tumors, which can be highly malignant. Thus, the rabbit tumor is of little value as a model. Polycythemia can accompany these tumors. Wardrop HJ et al. 1982. Nephroblastoma with secondary polycythemia in a New Zealand white rabbit. Lab Anim Sci 32:280-282. Lipman NS et al. 1985. Polycythemia in a New Zealand White rabbit with an embryonal nephroma. J Am Vet Med Assoc 187:1255-1256. (v) Mammary carcinoma is more common in multiparous females 3 years of age or more. Resembling mammary tumors in women in many ways, carcinomas are frequently preceded by cystic hyperplasia and adenomas. Papillomas appear in cystic ducts and become progressively more aggressive and invasive with time. Widespread metastases may occur. Some believe endocrine disturbances to be of etiologic importance. There is no evidence for a rabbit mammary retrovirus. (vi) Oral papillomas are fairly common in some areas of the U.S. They are caused by DNA virus of the genus Papillomavirus, as is the Shope papilloma of Sylvilagus spp; however the viruses are antigenically distinct, and the oral papilloma does not become malignant as the Shope papilloma can. Oral papilloma occurs naturally only in Oryctolagus spp., although Sylvilagus sp. can be experimentally infected. Following a latent period of 2-4 weeks after inoculation, papillomas appear, typically on the ventrum of the tongue. They grow slowly over 3-9 months reaching a maximum height of 4-6 mm. A cell-mediated response eventually occurs, resulting in sloughing of the tumors. Basophilic intranuclear inclusions are reportedly found in affected epithelium. 2. Sylvilagus sp. The only well known tumors of wild rabbits are the Shope tumors. A very few others have been reported including cases of lymphosarcoma resembling that of Oryctolagus sp. 3. Lepus sp. Very little is known of neoplasms in hares. They presently seem similar to those in rabbits with the following exceptions: myeloid leukemia, ovarian teratomas, and hare fibromas (caused by a distinct virus of the myxoma-fibroma group of poxviruses) in European hares. Miscellaneous referencesneoplasms: Altman NH et al. 1978. Trichoepithelioma in a rabbit. Vet Pathol 15:671-672. Bishop L. 1978. Intracranial teratoma in a domestic rabbit. Vet Pathol 15:525-530. Brown PJ, Stafford RA. 1989. A testicular seminoma in a rabbit. J Comp Pathol 100:353-355. Hoover JP et al. 1986. Osteogenic sarcoma with subcutaneous involvement in a rabbit. J Am Vet Med Assoc 189:1156-1157. Lichtensteiger CA, Leathers CW. 1987. Peritoneal mesothelioma in a rabbit. Vet Pathol 24:464-466. Pletcher JM, Murphy JC. 1984. Spontaneous malignant hemangioendothelioma in two rabbits. Vet Pathol 21:542-544. Walberg JA. 1981. Osteogenic sarcoma with metastasis in a rabbit (Oryctolagus cuniculus). Lab Anim Sci 31:407-408. Zwicker GM, Killinger JM. 1985. Interstitial cell tumors in a young adult New Zealand white rabbit. Toxicol Pathol 13:232-235. Ulcerative Pododermatitis ("Sore Hocks") 1. Cause: Trauma and bacterial infection (commonly Staph. aureus). Wire bottoms may traumatize feet especially if rabbits are large and heavy, if cage is poorly constructed, or if sanitation is poor. 2. Clinical: Crusty or exuding ulcers on plantar aspect of metatarsus, sometimes on front feet also. Affected rabbits can appear healthy but some can lose appetite, lose weight, and eventually die. 3. Treatment: Topical ointments with antibiotics, can put flat surface in cage or put rabbit in solid-bottom cage with soft bedding, but creates sanitation problems. Vertebral Fracture and Luxation ("Broken Back") 1. Cause: Trauma due to improper handling. 2. Clinical: Posterior paresis or paralysis. If cord is transected, rabbit will lose bladder and anal sphincter control and will have soiled fur on the hindquarters. If not recognized for several days, may develop decubital ulcers, uremia. 3. Treatment: Usually euthanasia. However, rabbits not having severe cord damage can recover various degrees of limb function over two weeks or so. Moist Dermatitis ("Slobbers," "Wet Dewlap") 1. Cause: Bacterial infection of skin kept chronically wet because of drooling (e.g., due to malocclusion), watering in pans or poor husbandry. 2. Clinical: Exudative, sometimes fetid, dermatitis affecting the folds of the dewlap. 3. Treatment: Remove cause of wetness; topical or systemic antibiotics or both. Buphthalmia 1. Cause: Hereditary, autosomal recessive with incomplete penetrance (not all bu/bu homozygotes are affected). 2. Clinical: Common in NZW rabbits raised for laboratory use. One or both eyes affected; become enlarged and protruding, and corneal opacity, ulceration, and even rupture may result. 3. Pathology: Thought to result from abnormal drainage from anterior chamber. Analogous to glaucoma, but weaker sclera of rabbit permits enlargement which is not characteristic of glaucoma. Also, atrophy of ciliary processes and excavation of optic disc. 4. Diagnosis: Characteristic morphology. Mandibular Prognathism (Malocclusion) 1. Cause: Autosomal recessive (mp/mp) mutation. 2. Clinical: Common in domestic NZW rabbits. Mandibular incisors extend past maxillary incisors so that normal wearing against one another does not occur. Maxillary incisors grow in a curve and may eventually pierce the palate. Mandibular incisors protrude from the mouth. The rabbit may be unable to eat and eventually die of starvation. 3. Treatment: Incisors of affected rabbits must be clipped frequently (they grow 2 to 2.5 mm/week). General References Lelkes L. 1987. A review of rabbit enteric diseases: A new perspective. J Appl Rabbit Res 10:55-61. Weisbroth SH, Flatt RE, Kraus AL (eds). The Biology of the Laboratory Rabbit. Academic Press, New York, 1974. Miscellaneous References Bortolotti A, Castelli D, Bonati M. 1989. Hematology and serum chemistry values of adult, pregnant and newborn New Zealand rabbits (Oryctolagus cuniculus). Lab Anim Sci 39:437-439. Broderson JR. 1989. A retrospective review of lesions associated with the use of Freund's adjuvant. Lab Anim Sci 39:400-405. Brown RL et al. 1969. Ultrastructural pathology of an acute fatal enteritis of captive cottontail rabbits. Search for an etiologic agent. Am J Pathol 57:93-107. Burgess EC, Windberg LA. 1989. Borrelia sp. infection in coyotes, black-tailed jack rabbits and desert cottontails in southern Texas. J Wildl Dis 25:47-51. Fallon MT et al. 1988. Diagnostic exercise: eye lesions in a rabbit. Lab Anim Sci 38:612-613. Filice G, Cereda PM, Varnier OE. 1988. Infection of rabbits with human immunodeficiency virus. Nature 335:366-369. Fox RR et al. 1971. Hereditary cortical cysts in the rabbit. J Heredity 62:105-109. Garibaldi BA, Goad ME. 1988. Hypercalcemia with secondary nephrolithiasis in a rabbit. Lab Anim Sci 38:331-333. Garibaldi BA, Goad ME. 1988. Lipid keratopathy in the Watanabe (WHHL) rabbit. Vet Pathol 25:173-174. Gillett NA et al. 1983. Medical and surgical management of gastric obstruction from a hair ball in the rabbit. J Am Vet Med Assoc 183:1176-1178. Green PW et al. 1984. Spontaneous degenerative spinal disease in the laboratory rabbit. J Orthop Res 2:161-168. Green RA, Baker DC. 1987. Coagulation defects of aflatoxin intoxicated rabbits. Vet Pathol 24:62-70. Hanglow AC et al. 1986. Synovitis associated with serum IgM rheumatoid factor arising spontaneously in 'Old English' rabbits. Ann Rheum Dis 45:331-338. Hill JE et al. 1988. Spontaneous storage-like disease in a rabbit. Vet Pathol 25:91-92. Hinton M. 1981. Kidney disease in the rabbit: A histological survey. Lab Anim 15:263-265. Hofmann JR Jr, Hixson CJ. 1986. Amyloid A protein deposits in a rabbit with pyometra. J Am Vet Med Assoc 189:1155-1186. Leary SL et al. 1984. Experimental and naturally-occurring gastric foreign bodies in laboratory rabbits. Lab Anim Sci 34:58-61. Lee KJ et al. 1978. Hydronephrosis caused by urinary lithiasis in a New Zealand white rabbit (Oryctolagus cuniculus). Vet Pathol. 15:676-678. Machii K et al. 1989. Infection of rabbits with Sendai virus. Lab Anim Sci 39:334-337. Mendlowsky B. 1975. Neuromuscular lesions in restrained rabbits. Vet Pathol 12:378-386. Moore CP et al. 1987. Anterior corneal dystrophy of American Dutch Belted rabbits: Biomicroscopic and histopathologic findings. Vet Pathol 24:28-33. Morrell JM. 1989. Hydrometra in the rabbit. Vet Rec 125:325. Morton D et al. 1986. Histologic alterations in the testes of laboratory rabbits. Vet Pathol 23:214-217. Ngatia TA et al. 1989. Arteriosclerosis and related lesions in rabbits. J Comp Pathol 101:279-286. Pfaffenberger GS, Valencia VB. 1988. Ectoparasites of sympatric cottontails (Sylvilagus audubonii Nelson) and jack rabbits (Lepus californicus Mearns) from the high plains of eastern New Mexico. J Parasitol 74:842-846. Port CD, Dodd DC. 1983. Two cases of corneal epithelial dystrophy in rabbits. Lab Anim Sci 33:587-588. Richter CB, Hendren RL. 1969. The pathology and epidemiology of acute enteritis in captive cottontail rabbits (Sylvilagus floridanus). Vet Pathol 6:159-175. Sebesteny A et al. 1985. Lipid keratopathy and atheromatosis in an SPF laboratory rabbit colony attributable to diet. Lab Anim 19:180-188. Shell LG, Saunders G. 1989. Arteriosclerosis in a rabbit. J Am Vet Med Assoc 194:679-680. Smith CA, Stone DM, Prieur DJ. 1989. Spontaneous profuse superovulation in association with ectopic fetuses in a rabbit. Lab Anim Sci 39:74-77. Stadler J et al. 1983. Use of the New Zealand white rabbit in teratology. Incidence of spontaneous and drug-induced malformations. Food Chem Toxicol 21:631-636. Strohlein DA, Christensen BM. 1983. Metazoan parasites of the eastern cottontail rabbit in western Kentucky. J Wildl Dis 19:20-23. Swartout MS, Gerken DF. 1987. Lead-induced toxicosis in two domestic rabbits. J Am Vet Med Assoc 191-717-719. Van Herck H et al. 1989. Prolapsus vaginae in the IIIVO/JU rabbit. Lab Anim 23:333-336. Weisbroth SH. 1975. Torsion of the caudate lobe of the liver in Oryctolagus cuniculus. Vet Pathol 12:13-15. Wilson RB et al. 1987. Liver lobe torsion in a rabbit. Lab Anim Sci 37:506-507. Yamini B, Stein S. 1989. Abortion, stillbirth, neonatal death, and nutritional myodegeneration in a rabbit breeding colony. J Am Vet Med Assoc 194:561-562. | |
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