Surveillance Vol.21 No.4 1994

Diseases of rabbits

The rabbit population of New Zealand can be Endemic bacterial diseases bits during the first three days post- divided into four main groups; ,wild rabbits, partum and is thought to be caused by laboratory rabbits, domestic pets and breeder Pasteurellosis: This is probably the low iimounts of clostridia or clostrid- units. While this articlediscussessomeof the most important and frustrating bacterial ial toxin passing via the milk into the major diseases endemic in the rfilbbitpopula- disease within laboratoqr and breeder neonatal gut. tion of New Zealand and mentions briefly units. Asymptomatic carriers and shed- Yersiniosis: Occasional infections some important exotic diseases, it should be ders are common, making the disease with Y. pseudotuberculosis occur in breed- borne in mind that factors such as genetic difficult to eliminate once introduced. er units and wild rabbit populations. A variation in resistance, population density Pasteurella multocida may reside in the higher prevalenceis found in the autumn and environment can alter the prevalence nares, tympanic bullae, conjunctiva, va- and winter? Diarrhoea, lymphadenitis and clinical presentation of disease among gina and lungs where only a minimal or, infre’quently,septicaemia may be seen. these groups. immune response is elicited The major route of infection in breeder Among breeder units, laboratory and A number of different syndromesmay and laboratory units is considered to be pet rabbits pasteurellosis, ’snuffles’ and be seen, depending upon factors such as greens and grass contaminated with fae- ear mite infestation are common com- the age of the rabbit, immune status and ces from birds and wild rodents. plaints. Older pet rabbits may present previous exposure. Acuteenzooticpneu- Salmonellosis: This is not a common with a variety of tumours iind kidney monia is common among young rabbits disease. Salmonella Typhimurium, S. en- problems. The ‘enteritis complex’ may whereas conditions ranging from pera- teriditis and (rarely)S. pullorum havebeen cause significant losses in breeder units cute septicaemia to chronic abscessation implicated. Clinical manifestations in- and factorssuch as environment, hygiene and suppuration may be seen in older clude sudden death, septicaemia, diar- and management practice play an im- rabbits? rhoea and abortion. Chronic shedders portant part in determining the frequen- Transmission may be by direct con- are possible. cy of stress-related conditions. Little is tact, aerosol or fomites. Ihvironmental Coli bacillosis: Escherichia coli is not a documented about the prevalence of dis- factors such as elevated levels of ammo- normal inhabitant of the intestine of eases among wild rabbits in New Zea- nia, temperature fluctuations, drafts and healthy rabbits. If present, it is usually land. poor sanitation may predispose to infec- for a lirnited period between 2 weeks of tion. Respiratoryinfections may be com- age and 1 week after weaning. Mild to plicated by Bordetella bronchiseptica. severe diarrhoea may be seen, primarily Staphylococcosis:Although subclin- in sucking and weanling rabbits. ical nasal infections due to this organism Listeriosis: Infection with Listeria are uncommon, carrier states can exist. monocytogenes is uncommon. The organ- A variety of syndromes may be seen, ism may cause septicaemia and has a including purulent rhinitis, conjunctivi- predilection for the gravid uterus, caus- tis and tympanitis,abscessation and mas- ing a necrosuppurative myometritis and titis (‘blue breast’). Transmissionmay be foetal death. Involvement of the central by direct contact or fomites. Aerosols are nervous system is rare.3 also possible? Necrobacillosis (Schmorl’s disease): Clostridial diseases: Clostridia are Fusobacterium necrophorum is present in present in low numbers in the normal thedigestive tract of normal rabbits. Clin- intestinal flora of the rabbit. Disease is ical signs associated with this disease the result of an abnormal proliferation of include abscessation and ulceration of Clostridium spiroforme, C. dificile or, rare- the skin, usually with involvement of the ly, C. perfringens type A? Three main head, neck and lips and occasionally the syndromes can be seen: underlying muscle. The angle of the jaw Enterotoxaemia. This usually occurs is a cornmon site of infection and maxil- in weanling fryers (4-to-8 weeks of lary osteomyelitis has been reported. age) and is thought to be associated Transmission is via contact with open with a decrease in passively acquired wounds, especially during coprophagy. immunity, rapid body growth and Pseudomonas infection: Pseudomonas microbial population of the intestine. aeuginclsa may cause diarrhoea, splenom- Clinical signs include acute, profuse, egaly, moist dermatitis and septicaemia. green/brown watery diarrhoea,bloat, Menin,gitis and pulmonary abscesses fever, polydipsia, anorexia, fetid have allso been reported. odour and faecal soiling.In adult rab- Tuberculosis: There has only been bits the disease is usually associated one documented case of mycobacterial with factors which have caused alter- infection caused by Mycobacterium bovis ations in the gut flora, such as high in rabbits in New Zealand. The affected caloric diets, stress, antibiotics (e.g. rabbit ‘was in poor condition and lesions clindamycin, lincomycin, ampicillin, were found in the prescapular lymph amoxacillin, erythromycin and cepha- node, Ilung, liver and kidney. Chronic lothin) or does returning to full feed granulomatous lesions were seen on his- immediately after kindling. tological examination and M. bovis was The young doe syndrome. This is cultured.5 Infection was thought to be seen in both primiparous and mul- the result of a bite wound from an infect- tiparous does. Sudden death occurs ed cat. The low incidence of tuberculosis when kits are between 1 and 4 weeks in wild rabbits is thought to be due to of age. A few days before death the their behaviour.6 doe may go off feed and be seen sali- Tyzzer‘s disease: This disease, caused vating profusely. Similar signs may by Bacillus piliformis, is most commonly be seen with septicaemia resulting seen in 6-to-12-week-old rabbits. It caus- from staphylococcal mastitis? es a ‘triad’ of lesions, characterised by The toxic milk syndrome. This may necrosiis, involving the intestine,liver and result in sudden deatlh in young rab- heart. Clinical signs may vary greatly 10 Surveillance 2 1 (4) Surveillance Vol.21 No.4 1994

from non-specific illness to acute, pro- status of the host and amount of ing of teeth and bloated abdomen. Fae- fuse, watery diarrhoea, dehydration and inoculum? ces may consistof clear jelly-like material rapid death. Predisposing factors in- Encephalitozoonosis: Infection with (older animals), be watery or contain clude stress, poor sanitation, overcrowd- Encephalitazoon cuniculi (Nosema cuniculi) blood (younger rabbits). ing and sulphonamide therapy. This is usually asymptomatic. Spores liberat- Other miscellaneous conditions in- organism is difficult to culture, but the ed from ruptured intestinal cells infect clude vitamin B toxicosis, pregnancy tox- disease has been diagnosed on character- renal tubular epithelium and endotheli- aemia/fatty liver, hair balls (related to istic histological findings in other spe- um of capillaries in the central nervous long hair coats and lack of roughage), cies. system. Organisms are shed in the urine arterial calcification, splay leg (the inabil- (and possibly also cross the placenta). ity to adduct one or both hind legs, pos- Occasionallyneurological signsand poly- sibly hereditary and seen from a few Endemic viral diseases uria may be observed. On histological days of age to a few months. Muscles Papovavirus: The Shope (papilloma) examination granulomatous lesionsmay may be functional or paralysed), maloc- virus primarily affects wild rabbits and be seen in the brain and kidney. This clusion (possibly familial), sore hocks produces wart-like lesions in the skin, organism may be a threat to immuno- (trauma related, ulcerative pododerma- but never the oral cavity. The oral papil- suppressed human contacts? titis), broken back (often the result of lomatosis virus affects non-keratinised Toxoplasmosis: This conditionisrare. incorrect restraint), 'slobbers' (wet dew- surfaces and produces solitary growths Infection may be inapparent or clinical lap), hypovitaminosis E (associatedwith which eventually regress. signs may vary with the tissue affected. stillbirth, neonatal death, degeneration Retarded growth, tremors and paresis and necrosis of skeletaland cardiac mus- Coronavirus: Infection may result in have been noted. Toxoplasma and Nosema cle), heat stress (may cause infertility), a fatal enteritis in 340-8 week-old rab- may be differentiated on the basis of their uterine adenocarcinoma (up to 60%inci- bits, 'pleural effusion disease' and rabbit staining characteristics. dence in does over 4years of age): 'bloody cardiomyopathy. Sarcosporidiosis: Sarcocystis cuniculi urine' (very rare. In most cases this turns Rotavirus: Infection may produce a is rare in laboratory rabbits but may be a out to be a porphyrin-pigmented, basic mild to severe diarrhoea with high mor- differential diagnosis in hind limb paral- urine or sanguineous vaginal discharge bidity and varying mortality in weaning ysis. from tumours or abortion). If true hae- rabbits. maturia is present differentials include cystitis, urolithlasis and leptospirosis. Mites Endemic parasites Ear mites: Infestation with Psoroptes Exotic bacterial diseases Helminths: These parasites general- cuniculi tends to start low in the ear and There a number of important diseases ly do not produce clinical disease in rab- causes pruritus, scale and crusting. bits. Nematodes include Obeliscoides cu- which do not occur in New Zealand. Fur mites: Cheyletiella parasitivorax Included amongst the bacterial diseases niculi (stomach worm), Trichostrongylus are present on 15% to 60% of rabbits, calcaratus and Cittotaenia variabilis (tape are; usually located over the scapulae and Tularaemia: Infection with Francisel- worm) found in the small intestine, Pas- back, and are usually asymptomatic. (pinworm)and la tularensis is common in wild rabbits in salurisambiguus Trichuris Fungi: Clinical infections are rarely leporus (whip worm) found in the cae- the Americas, most European countries, seen. Trichophyton mentagrophytes, Cand- cum and large intestine. Russia, the Middle East, and China and ida albicans and Microsporum canis have Japan. However, it is rare in outdoor Rabbits are also the intermediate hosts been isolated from the skin and Aspergil- for Taenia pisiformis and T. serialis. The domestic colonies. It causes a peracute lus has been occasionally associatedwith septicaemia. Animals are usually found former is common in wild rabbits and deep myco~es.~ heavy infestations may produce weight dead. Transmission can occur via arthro- loss, lethargyand abdominal di~tention.3,~ pods and cutaneous, intestinal and respi- Miscellaneous conditions ratory routes. This organism is highly infectious and can affect otherwise Endemic protozoan diseases Mucoid enteropathy: This condition healthy animals. is one of the most important causes of Spirochaetosis (rabbit syphilis): Hepatic coccidiosis: Hepatic coccid- mortality in weanling rabbits, although Treponema cuniculi is transmitted by di- iosis affects rabbits and wild lagomorphs. adults are also affected. The disease is rect contact, especially during mating. It is caused by Eimeria stiedae. The disease characterised by marked hyperplasia of Clinical disease is characterizedby vesic- usually affects weanling rabbits (540-8 goblet cells, thought to be caused by the ular swelling, hyperaemia and scaling weeks of age) and is characterized by action of a secretogogue produced by an followed by the development of mac- anorexia, ill thrift, weight loss and an unknown bacteria. Clinically there is ules, papules, erosions, ulcers and crusts enlarged abdomen. Grossly white spots gel-like mucoid faeces, abdominal dis- on external genitalia, perineal areas, the may be seen over the liver and histolog- tention, hunched posture, teeth grinding nose, eyelids and lips. Regression after ically there is bile duct hyperplasia,which and weight loss. Stress, low and high several weeks is common. This disease in severe cases may resemble neoplasia. fibre diets (< 6% and > 20%); caecal may be present in New Zealand. Past In young, naive rabbits death may occur maldigestion and feeding monensin may records from a laboratory animal unit before oocysts appear in the faeces. Im- contribute to the di~ease.~, suggests that a spirochaetalorganism has munity develops in animals which sur- Enteropathy in young rabbits: Sev- been isolated from a rabbit with lesions vive and carrier states can exist. Rabbits eral factors are thought to be responsible around the vent.I0 are not reinfected through coprophagy. for disease, including diet, stress, genet- Intestinal coccidiosis: Approxi- ics, gut dysfunction, microbes and the Exotic viral diseases mately 96% of rabbits shed coccidial immune status of the rabbit. Enteropa- oocysts, but disease is rare? Several thies appear to be linked closely with Viral haemorrhagic disease (VHD): Eimeria species have been documented hypomotility which results in retention Also known as rabbit haemorrhagic dis- which vary in pathogenicity and occupy of digesta and substrate, pH and micro- ease (RHD) and haemorrhagic tracheop- the small or large intestine, or both. The bial changes. Rabbits 3-to-4-weeks-old neumonia, this disease first occurred in disease is mainly a problem when young are most susceptible due to the naive China in 1984. It has since been reported or old rabbits are exposed to new coccidial state of their gut and the low gastric in Korea, about 17 European countries, species. Clinically intestinal coccidiosis activity in the post-weaning period fa- Egypt, Lebanon, Tunisia and Mexico. presents as failure to gain weight or vouring passage and colonization by Three clinical forms of the disease have weight loss, soft, watery faeces and se- potential pathogens. been documented. These tend to affect vere dehydration. Mortality varies with Clinical signsinclude anorexia, weight rabbits over 8 weeks of age." They are; the species of Eimeria involved, immune loss, depression, rough hair coat, grind- sudden death Surveillance 2 1 (4) 19 Surveillance Vol.21 No.4 1994

acutedepression, anorexia, dyspnoea, States of America. No post-arrival quar- References inco-ordination and convulsions (of- antine is required although tlhe exporting ten accompanied by foamy haemor- country and/or property must be free of 1 Harkness, JE, 1990: Rabbits and rodents. rhages from the nostrils) certain diseases and rabbits must be cer- Laboratory Animal Science. Refresher Course for Veterinarians Proceedings 142. Post depression and anorexia with recov- tified as free of contagious disease and Graduate Committee in Veterinary Science. ery and immunity. Infection may be external parasites within48 hours of their University of Sydney. by inhalation, ingestion or abrasions. departure. Harlcness,JE, Wagner, JE, 1983: TheBiology Mortalities may be close to 100%with Outbreaks of viral haernorrhagic dis- and Medicine of Rabbits and Rodents. 2nd 30%- 80% morbidity. Histologically ease have recently been linked to frozen edition. Lea & Febiger. Philadelphia. there is a severe necrotising hepatitis Lipscomb, TP, 1989: Pathology of the labo- rabbit Although New Zealand ratory rabbit : In Pathology of Laboratory with haemorrhage and thrombi in no longer imports rabbit meat from Chi- Animals. Course in Continuing Education. many organs. Disseminated intra- na,where the disease is endemic, Angora Sponsored by the American Registry of Pa- vascular coagulation is a common fibre is still imp~rted.'~This could be a thology, Armed Forces Institute of Pathol- complication of the disease. potential source of infection if imports ogy. Maryland, United States of America. are improperly treated, since the virus 4 Mackintosh, CG, Henderson, T, 1984: Po- It is now generally agreed that viral has been known to survive for more than tenc.ial wildlife sources of Yersinia haemorrhagicdisease is caused by a cal- 3 months in the dry state at ambient pseudotuberculosis for farmed red deer icivirus.12 Transmission can occur by temperatures.I6 (Cewus elaphus). New Zealand Veterinary contact with secretionsor excretions from Journal 32: 208-210. Myxomatosis was introduced to New Gill, JW,Jackon, R, 1993: Tuberculosis in a infected animals or indirectly by attend- rabbit: A case revisited. New Zealand Veteri- ing persons or equipment. There is no Zealand in the early 1950s but failed to establish due to the absence of a suitable nary Journal 41: 147. evidence for transmission by other ro- Allen, GM, 1991 : Otheranimals as sources of dents or insects. A vaccine is available vector. Tularaemia is prevalent in the TB infection. Proceedings from a Sympo- which gives 6 months protection. Americas, Europe and Asia. Although F. sium on Tuberculosis, Palmerston North. tularensis is killed rapidly by heat and Veterinary Continuing Education. Massey Myxomatosis: This disease, caused disinfection, it may survive for monthsin by Leporipoxvirus, is rare in laboratory University: 197-201. a moist environment. It is of importance 7 Jones, JM, 1992: Diseases of Rabbits. Clini- rabbits, but endemic in the wild in most due to its highly infectious nature, wide cal Studies IIa: 95.401. Massey University. countrieswhererabbitsare found. Young host-range (including humans) and abil- 8 Margileth, AM, Strano, AJ, Chandra, R, rabbits are more susceptible although ity to be transmitted by biting arthropods Neafie, R, Blum, M, McCully, RM, 1973: adults with intercurrent disease are at or infected tissues. Disseminated nosematosis in an increased risk and pregnant does may immunologically compromised infant. Ar- abort. Clinical signs vary considerably chives of Pathology 95: 145-150. due to variations in virulence between Treatment of rabbit diseases 9 Lelkes, L, Chang, C-L. 1987: Microbial strains of virus and the development of dysbiosis inrabbitmucoidenteropathy. Labo- When selecting therapeutic agents ratory Animal Science resistance in rabbit populations. Viru- 97: 757-764. consideration should be given to factors 10 Onnsby, JE. Personal communication. lent strains such as the Californian strain such as age, sex, diet, breeding status of 11 Du, N, 1990: Rabbit haemorrhagic disease produce a 'sleepy eyed' rabbit character- the rabbits and the influence of these (RHD) - A new disease and its viral etiology. ized by mild lethargy, red eyes, swollen compounds on any experimentalproto- Deutsche Tierarztliche-Wochenschrifr 97 lids and a watery ocular discharge. If 114-1 16. col in which the rabbit is involved. It is death does not occur at this stage then 12 Fuller, HE, Chasey, D, Lucas, MH, Gibbens, also important to determine whether the hyperaemia and swelling extend to the JC, 1993: Rabbit haemorrhagic disease in the drug is registered for use in rabbits and if lips, face, ears and ano-genital areas. United Kingdom. The Veterinary Record there is a withholdingperiod specified in Cutaneous haemorrhages may also be 133: 611-613. animals used in meat production. Fur- 13 seen. Histologically there is extensive Greg, DA, House, C, Meyer, R, Beminger, ther, some drugs which are relatively M, 1991: Cited by Plassiart, G, Guelfi, J-F, epithelial proliferation with hyperkerat- safe and efficacious in other species may Ganiere, J-P, Wang, 8, Andre-Fontaine, G, inisation and ballooning of cells in the be toxic to rabbits or suppress an active Wlyers, M, 1992: Haematological parameters stratum granulosum. Large eosinophilic clinical infection to a chronic, subclinical and visceral lesions relationships in rabbit intracytoplasmic inclusion bodies are viral haemomhagic disease. Journal of Vet- carrier state. present within the stratum germinati- erinary Medicine B 39 443-453. vum. There is a depletion of lymphoid Fatal reactions to antibiotics are a 14 Morisse, JP, Le Gall, G,Bouilletot, E, 1991, tissue in the spleen and necrosis of lym- major concern in the therapy of rabbit cikd by Fuller, HE, Chasey, D, Lucas, M H, phatic tissue in several organs. disease, either through a direct toxic ef- Gibbens, J C, 1993: Rabbit haemorrhagic fect, e.g. streptomycinand dihydrostrep- disease in the United Kingdom. The Veteri- The European and South American nary Record 133: 61 1-613. strains produce mucinous skin tumours tomycin, or indirectly through altering 15 Mulqueen, K. Personal communication. (myxoma nodules) within the dermis? the intestinal flora and producing enter- 16 Snud, B, Valicek, L, Rodack, L, Stephanek, Transmission may be by direct contact otoxaemia, e.g. penicillin and cepha- S, Jurak, E, 1991, cited by Fuller, E, Chasey, and arthropods (rabbit flea, mosquito, losporins.' D, Lucas, M H, Gibbens, J C, 1993: Rabbit haemorrhagic disease in the United King- black fly and mites). Attenuated vac- Lincomycin is contraindicated in rab- cines are available. dom. The Veterinary Record 18 133: 61 1- bits and ampicillin, amoxacillin, erythro- 613. Pox virus: Rabbit pox, caused by an mycin, cephalexin and procaine penicillin orthopoxvirus, is a rare, generalised dis- should be avoided. Care should also be Wendy .L Townsend ease with cutaneous lesions. Oculonasal taken to avoid precipitation when ad- Batchelar Animal Health Laboratory discharge, fever, enlarged lymph nodes ministering drugs via drinking water as and typical pox lesionsmay be seen in the this may lower the amount of antibiotic skin. Spread is via direct contact. available to the rabbit and lead to bacte- rial resistance. Introduction of disease Informationof therapeutic agents and treatment protocols for various rabbit Exotic disease could enter New Zea- diseases are referenced.' land through, for example, the importa- tion of live rabbits, rabbit products and Acknowledgements biologicals. Domestic rabbits have been imported from counties such as Aus- I would like to thank Mrs G Absolon, tralia, Canada, Denmark, th.e Republic of Dr J Jones, Mr J E Onnsby and Dr J Ireland, United Kingdom and the United Schofield for useful discussions. 20 Surveillance 21(4)