Diseases of rabbits

Surveillance Vol.21 No.4 1994
Diseases of rabbits
The rabbit population of New Zealand can be
divided into four main groups; ,wild rabbits,
laboratory rabbits, domestic pets and breeder
units. While this articlediscussessomeof the
major diseases endemic in the rfilbbitpopulation of New Zealand and mentions briefly
some important exotic diseases, it should be
borne in mind that factors such as genetic
variation in resistance, population density
and environment can alter the prevalence
and clinical presentation of disease among
these groups.
Among breeder units, laboratory and
pet rabbits pasteurellosis, ’snuffles’ and
ear mite infestation are common complaints. Older pet rabbits may present
with a variety of tumours iind kidney
problems. The ‘enteritis complex’ may
cause significant losses in breeder units
and factorssuch as environment,hygiene
and management practice play an important part in determining the frequency of stress-related conditions. Little is
documented about the prevalence of diseases among wild rabbits in New Zealand.
10 Surveillance 2 1 (4)
Endemic bacterial diseases
Pasteurellosis: This is probably the
most important and frustrating bacterial
disease within laboratoqr and breeder
units. Asymptomatic carriers and shedders are common, making the disease
difficult to eliminate once introduced.
Pasteurella multocida may reside in the
nares, tympanic bullae, conjunctiva, vagina and lungs where only a minimal
immune response is elicited
A number of differentsyndromesmay
be seen, depending upon factors such as
the age of the rabbit, immune status and
previous exposure. Acuteenzooticpneumonia is common among young rabbits
whereas conditions ranging from peracute septicaemiato chronic abscessation
and suppuration may be seen in older
rabbits?
Transmission may be by direct contact, aerosol or fomites. Ihvironmental
factors such as elevated levels of ammonia, temperature fluctuations,drafts and
poor sanitation may predispose to infection. Respiratoryinfections may be complicated by Bordetella bronchiseptica.
Staphylococcosis:Although subclinical nasal infections due to this organism
are uncommon, carrier states can exist.
A variety of syndromes may be seen,
including purulent rhinitis, conjunctivitis and tympanitis,abscessationand mastitis (‘bluebreast’). Transmissionmay be
by direct contact or fomites. Aerosols are
also possible?
Clostridial diseases: Clostridia are
present in low numbers in the normal
intestinal flora of the rabbit. Disease is
the result of an abnormal proliferation of
Clostridium spiroforme, C. dificile or, rarely, C. perfringens type A? Three main
syndromes can be seen:
Enterotoxaemia. This usually occurs
in weanling fryers (4-to-8 weeks of
age) and is thought to be associated
with a decrease in passively acquired
immunity, rapid body growth and
microbial population of the intestine.
Clinical signs include acute, profuse,
green/brown watery diarrhoea,bloat,
fever, polydipsia, anorexia, fetid
odour and faecal soiling.In adult rabbits the disease is usually associated
with factorswhich have caused alterations in the gut flora, such as high
caloric diets, stress, antibiotics (e.g.
clindamycin, lincomycin, ampicillin,
amoxacillin,erythromycin and cephalothin) or does returning to full feed
immediately after kindling.
The young doe syndrome. This is
seen in both primiparous and multiparous does. Sudden death occurs
when kits are between 1 and 4 weeks
of age. A few days before death the
doe may go off feed and be seen salivating profusely. Similar signs may
be seen with septicaemia resulting
from staphylococcal mastitis?
The toxic milk syndrome. This may
result in sudden deatlh in young rab-
bits during the first three days postpartum and is thought to be caused by
low iimounts of clostridia or clostridial toxin passing via the milk into the
neonatal gut.
Yersiniosis: Occasional infections
with Y. pseudotuberculosis occur in breeder units and wild rabbit populations. A
higher prevalenceis found in the autumn
and winter? Diarrhoea, lymphadenitis
or, infre’quently,septicaemiamay be seen.
The major route of infection in breeder
and laboratory units is considered to be
greens and grass contaminated with faeces from birds and wild rodents.
Salmonellosis: This is not a common
disease. Salmonella Typhimurium, S. enteriditis and (rarely)S. pullorum havebeen
implicated. Clinical manifestations include sudden death, septicaemia, diarrhoea and abortion. Chronic shedders
are possible.
Colibacillosis: Escherichia coli is not a
normal inhabitant of the intestine of
healthy rabbits. If present, it is usually
for a lirnited period between 2 weeks of
age and 1 week after weaning. Mild to
severe diarrhoea may be seen, primarily
in sucking and weanling rabbits.
Listeriosis: Infection with Listeria
monocytogenes is uncommon. The organism may cause septicaemia and has a
predilection for the gravid uterus, causing a necrosuppurative myometritis and
foetal death. Involvement of the central
nervous system is rare.3
Necrobacillosis (Schmorl’s disease):
Fusobacterium necrophorum is present in
thedigestive tract of normal rabbits. Clinical signs associated with this disease
include abscessation and ulceration of
the skin, usually with involvement of the
head, neck and lips and occasionally the
underlying muscle. The angle of the jaw
is a cornmon site of infection and maxillary osteomyelitis has been reported.
Transmission is via contact with open
wounds, especially during coprophagy.
Pseudomonas infection: Pseudomonas
aeuginclsa may cause diarrhoea, splenomegaly, moist dermatitis and septicaemia.
Menin,gitis and pulmonary abscesses
have allso been reported.
Tuberculosis: There has only been
one documented case of mycobacterial
infection caused by Mycobacterium bovis
in rabbits in New Zealand. The affected
rabbit ‘was in poor condition and lesions
were found in the prescapular lymph
node, Ilung, liver and kidney. Chronic
granulomatous lesions were seen on histological examination and M . bovis was
cultured.5 Infection was thought to be
the result of a bite wound from an infected cat. The low incidence of tuberculosis
in wild rabbits is thought to be due to
their behaviour.6
Tyzzer‘s disease: Thisdisease,caused
by Bacillus piliformis, is most commonly
seen in 6-to-12-week-old rabbits. It causes a ‘triad’ of lesions, characterised by
necrosiis, involving the intestine,liver and
heart. Clinical signs may vary greatly
Surveillance Vol.21 No.4 1994
from non-specific illness to acute, profuse, watery diarrhoea, dehydration and
rapid death. Predisposing factors include stress, poor sanitation, overcrowding and sulphonamide therapy. This
organism is difficult to culture, but the
diseasehas been diagnosed on characteristic histological findings in other species.
Endemic viral diseases
Papovavirus: The Shope (papilloma)
virus primarily affects wild rabbits and
produces wart-like lesions in the skin,
but never the oral cavity. The oral papillomatosis virus affects non-keratinised
surfaces and produces solitary growths
which eventually regress.
Coronavirus: Infection may result in
a fatal enteritis in 340-8 week-old rabbits, 'pleural effusion disease' and rabbit
cardiomyopathy.
Rotavirus: Infection may produce a
mild to severe diarrhoea with high morbidity and varying mortality in weaning
rabbits.
Endemic parasites
Helminths: These parasites generally do not produce clinical disease in rabbits. Nematodes include Obeliscoides cuniculi (stomach worm), Trichostrongylus
calcaratus and Cittotaenia variabilis (tape
worm) found in the small intestine, Passalurisambiguus (pinworm)and Trichuris
leporus (whip worm) found in the caecum and large intestine.
Rabbits are alsothe intermediate hosts
for Taenia pisiformis and T. serialis. The
former is common in wild rabbits and
heavy infestations may produce weight
loss, lethargyand abdominal di~tention.3,~
Endemic protozoan diseases
Hepatic coccidiosis: Hepatic coccidiosis affectsrabbitsand wild lagomorphs.
It is caused by Eimeria stiedae. The disease
usually affects weanling rabbits (540-8
weeks of age) and is characterized by
anorexia, ill thrift, weight loss and an
enlarged abdomen. Grossly white spots
may be seen over the liver and histologically there is bile duct hyperplasia,which
in severe cases may resemble neoplasia.
In young, naive rabbits death may occur
before oocysts appear in the faeces. Immunity develops in animals which survive and carrier states can exist. Rabbits
are not reinfected through coprophagy.
Intestinal coccidiosis: Approximately 96% of rabbits shed coccidial
oocysts, but disease is rare? Several
Eimeria species have been documented
which vary in pathogenicity and occupy
the small or large intestine, or both. The
disease is mainly a problem when young
or old rabbitsare exposed to new coccidial
species. Clinically intestinal coccidiosis
presents as failure to gain weight or
weight loss, soft, watery faeces and severe dehydration. Mortality varies with
the species of Eimeria involved, immune
status of the host and amount of
inoculum?
Encephalitozoonosis: Infection with
Encephalitazoon cuniculi (Nosema cuniculi)
is usually asymptomatic. Spores liberated from ruptured intestinal cells infect
renal tubular epithelium and endothelium of capillaries in the central nervous
system. Organisms are shed in the urine
(and possibly also cross the placenta).
Occasionallyneurological signsand polyuria may be observed. On histological
examination granulomatous lesionsmay
be seen in the brain and kidney. This
organism may be a threat to immunosuppressed human contacts?
Toxoplasmosis: Thisconditionisrare.
Infection may be inapparent or clinical
signs may vary with the tissue affected.
Retarded growth, tremors and paresis
have been noted. Toxoplasma and Nosema
may be differentiatedon the basis of their
staining characteristics.
Sarcosporidiosis: Sarcocystis cuniculi
is rare in laboratory rabbits but may be a
differentialdiagnosis in hind limb paralysis.
Mites
Ear mites: Infestation with Psoroptes
cuniculi tends to start low in the ear and
causes pruritus, scale and crusting.
Fur mites: Cheyletiella parasitivorax
are present on 15% to 60% of rabbits,
usually located over the scapulae and
back, and are usually asymptomatic.
Fungi: Clinical infections are rarely
seen. Trichophyton mentagrophytes, Candida albicans and Microsporum canis have
been isolated from the skin and Aspergillus has been occasionally associatedwith
deep myco~es.~
Miscellaneous conditions
Mucoid enteropathy: This condition
is one of the most important causes of
mortality in weanling rabbits, although
adults are also affected. The disease is
characterised by marked hyperplasia of
goblet cells, thought to be caused by the
action of a secretogogue produced by an
unknown bacteria. Clinically there is
gel-like mucoid faeces, abdominal distention, hunched posture, teeth grinding
and weight loss. Stress, low and high
fibre diets (< 6% and > 20%); caecal
maldigestion and feeding monensin may
contribute to the di~ease.~,
Enteropathy in young rabbits: Several factorsare thought to be responsible
for disease, including diet, stress, genetics, gut dysfunction, microbes and the
immune status of the rabbit. Enteropathies appear to be linked closely with
hypomotility which results in retention
of digesta and substrate, pH and microbial changes. Rabbits 3-to-4-weeks-old
are most susceptible due to the naive
state of their gut and the low gastric
activity in the post-weaning period favouring passage and colonization by
potential pathogens.
Clinical signsincludeanorexia, weight
loss, depression, rough hair coat, grind-
ing of teeth and bloated abdomen. Faeces may consistof clear jelly-likematerial
(older animals), be watery or contain
blood (younger rabbits).
Other miscellaneous conditions include vitamin B toxicosis, pregnancy toxaemia/fatty liver, hair balls (related to
long hair coats and lack of roughage),
arterial calcification,splay leg (theinability to adduct one or both hind legs, possibly hereditary and seen from a few
days of age to a few months. Muscles
may be functional or paralysed), malocclusion (possibly familial), sore hocks
(trauma related, ulcerative pododermatitis), broken back (often the result of
incorrect restraint), 'slobbers' (wet dewlap), hypovitaminosis E (associatedwith
stillbirth, neonatal death, degeneration
and necrosis of skeletaland cardiacmuscle), heat stress (may cause infertility),
uterine adenocarcinoma (up to 60%incidence in does over 4years of age): 'bloody
urine' (very rare. In most cases this turns
out to be a porphyrin-pigmented, basic
urine or sanguineous vaginal discharge
from tumours or abortion). If true haematuria is present differentials include
cystitis, urolithlasis and leptospirosis.
Exotic bacterial diseases
There a number of important diseases
which do not occur in New Zealand.
Included amongst the bacterial diseases
are;
Tularaemia: Infection with Francisella tularensis is common in wild rabbits in
the Americas, most European countries,
Russia, the Middle East, and China and
Japan. However, it is rare in outdoor
domestic colonies. It causes a peracute
septicaemia. Animals are usually found
dead. Transmission can occur via arthropods and cutaneous, intestinaland respiratory routes. This organism is highly
infectious and can affect otherwise
healthy animals.
Spirochaetosis (rabbit syphilis):
Treponema cuniculi is transmitted by direct contact, especially during mating.
Clinical disease is characterizedby vesicular swelling, hyperaemia and scaling
followed by the development of macules, papules, erosions,ulcers and crusts
on external genitalia, perineal areas, the
nose, eyelids and lips. Regression after
several weeks is common. This disease
may be present in New Zealand. Past
records from a laboratory animal unit
suggests that a spirochaetalorganism has
been isolated from a rabbit with lesions
around the vent.I0
Exotic viral diseases
Viral haemorrhagic disease (VHD):
Also known as rabbit haemorrhagic disease (RHD) and haemorrhagic tracheopneumonia, this disease first occurred in
China in 1984. It has sincebeen reported
in Korea, about 17 European countries,
Egypt, Lebanon, Tunisia and Mexico.
Three clinical forms of the disease have
been documented. These tend to affect
rabbits over 8 weeks of age." They are;
sudden death
Surveillance2 1(4) 19
Surveillance Vol.21 No.4 1994
acutedepression,anorexia, dyspnoea,
inco-ordination and convulsions (often accompanied by foamy haemorrhages from the nostrils)
depression and anorexia with recovery and immunity. Infection may be
by inhalation, ingestion or abrasions.
Mortalities may be close to 100%with
30%- 80%morbidity. Histologically
there is a severe necrotising hepatitis
with haemorrhage and thrombi in
many organs. Disseminated intravascular coagulation is a common
complication of the disease.
It is now generally agreed that viral
haemorrhagicdisease is caused by a calicivirus.12 Transmission can occur by
contactwith secretionsor excretionsfrom
infected animals or indirectly by attending persons or equipment. There is no
evidence for transmission by other rodents or insects. A vaccine is available
which gives 6 months protection.
Myxomatosis: This disease, caused
by Leporipoxvirus, is rare in laboratory
rabbits, but endemic in the wild in most
countrieswhererabbitsarefound. Young
rabbits are more susceptible although
adults with intercurrent disease are at
increased risk and pregnant does may
abort. Clinical signs vary considerably
due to variations in virulence between
strains of virus and the development of
resistance in rabbit populations. Virulent strains such as the Californian strain
produce a 'sleepy eyed' rabbit characterized by mild lethargy, red eyes, swollen
lids and a watery ocular discharge. If
death does not occur at this stage then
hyperaemia and swelling extend to the
lips, face, ears and ano-genital areas.
Cutaneous haemorrhages may also be
seen. Histologically there is extensive
epithelial proliferation with hyperkeratinisation and ballooning of cells in the
stratum granulosum. Large eosinophilic
intracytoplasmic inclusion bodies are
present within the stratum germinativum. There is a depletion of lymphoid
tissue in the spleen and necrosis of lymphatic tissue in several organs.
The European and South American
strains produce mucinous skin tumours
(myxoma nodules) within the dermis?
Transmission may be by direct contact
and arthropods (rabbit flea, mosquito,
black fly and mites). Attenuated vaccines are available.
Pox virus: Rabbit pox, caused by an
orthopoxvirus, is a rare, generalised disease with cutaneous lesions. Oculonasal
discharge, fever, enlarged lymph nodes
and typical pox lesionsmay be seen in the
skin. Spread is via direct contact.
Introduction of disease
Exotic disease could enter New Zealand through, for example, the importation of live rabbits, rabbit products and
biologicals. Domestic rabbits have been
imported from counties such as Australia, Canada, Denmark, th.eRepublicof
Ireland, United Kingdom and the United
20 Surveillance 21(4)
States of America. No post-arrival quarantine is required althoughtlhe exporting
country and/or property must be free of
certain diseases and rabbits must be certified as free of contagious disease and
external parasites within48hours of their
departure.
Outbreaks of viral haernorrhagic disease have recently been linked to frozen
rabbit
Although New Zealand
no longer imports rabbit meat from China,where the disease is endemic, Angora
This could be a
fibre is still imp~rted.'~
potential source of infection if imports
are improperly treated, since the virus
has been known to survive for more than
3 months in the dry state at ambient
temperatures.I6
Myxomatosis was introduced to New
Zealand in the early 1950s but failed to
establish due to the absence of a suitable
vector. Tularaemia is prevalent in the
Americas, Europe and Asia. AlthoughF.
tularensis is killed rapidly by heat and
disinfection, it may survivefor monthsin
a moist environment. It is of importance
due to its highly infectious nature, wide
host-range (including humans) and ability to be transmitted by biting arthropods
or infected tissues.
Treatment of rabbit diseases
When selecting therapeutic agents
consideration should be given to factors
such as age, sex, diet, breeding status of
the rabbits and the influence of these
compounds on any experimentalprotocol in which the rabbit is involved. It is
also important to determine whether the
drug is registered for use in rabbits and if
there is a withholdingperiod specified in
animals used in meat production. Further, some drugs which are relatively
safe and efficacious in other species may
be toxic to rabbits or suppress an active
clinical infection to a chronic, subclinical
carrier state.
Fatal reactions to antibiotics are a
major concern in the therapy of rabbit
disease, either through a direct toxic effect, e.g. streptomycinand dihydrostreptomycin, or indirectly through altering
the intestinal flora and producing enterotoxaemia, e.g. penicillin and cephalosporins.'
Lincomycin is contraindicated in rabbits and ampicillin, amoxacillin, erythromycin, cephalexin and procaine penicillin
should be avoided. Care should also be
taken to avoid precipitation when administering drugs via drinking water as
this may lower the amount of antibiotic
available to the rabbit and lead to bacterial resistance.
Informationof therapeutic agents and
treatment protocols for various rabbit
diseases are referenced.'
Acknowledgements
I would like to thank Mrs G Absolon,
Dr J Jones, Mr J E Onnsby and Dr J
Schofield for useful discussions.
References
1
4
7
8
9
10
11
12
13
14
15
16
Harkness, JE, 1990: Rabbits and rodents.
Laboratory Animal Science. Refresher Course
for Veterinarians Proceedings 142. Post
Graduate Committee in Veterinary Science.
University of Sydney.
Harlcness,JE, Wagner, JE, 1983: TheBiology
and Medicine of Rabbits and Rodents. 2nd
edition. Lea & Febiger. Philadelphia.
Lipscomb, TP, 1989: Pathology of the laboratory rabbit : In Pathology of Laboratory
Animals. Course in Continuing Education.
Sponsored by the American Registry of Pathology, Armed Forces Institute of Pathology. Maryland, United States of America.
Mackintosh, CG, Henderson, T, 1984: Potenc.ial wildlife sources of Yersinia
pseudotuberculosis for farmed red deer
(Cewus elaphus). New Zealand Veterinary
Journal 32: 208-210.
Gill, JW,
Jackon, R, 1993: Tuberculosis in a
rabbit: A case revisited. New Zealand Veterinary Journal 41: 147.
Allen, GM, 1991 : Otheranimals as sources of
TB infection. Proceedings from a Symposium on Tuberculosis, Palmerston North.
Veterinary Continuing Education. Massey
University: 197-201.
Jones, JM, 1992: Diseases of Rabbits. Clinical Studies IIa: 95.401. Massey University.
Margileth, AM, Strano, AJ, Chandra, R,
Neafie, R, Blum, M, McCully, RM, 1973:
Disseminated nosematosis in an
immunologically compromised infant. Archives of Pathology 95: 145-150.
Lelkes, L, Chang, C-L. 1987: Microbial
dysbiosisinrabbitmucoidenteropathy. Laboratory Animal Science 97: 757-764.
Onnsby, JE. Personal communication.
Du, N, 1990: Rabbit haemorrhagic disease
(RHD) - A new disease and its viral etiology.
Deutsche Tierarztliche-Wochenschrifr 9 7
114-1 16.
Fuller, HE, Chasey, D, Lucas, MH, Gibbens,
JC, 1993: Rabbit haemorrhagic disease in the
United Kingdom. The Veterinary Record
133: 611-613.
Greg, DA, House, C, Meyer, R, Beminger,
M, 1991: Cited by Plassiart, G, Guelfi, J-F,
Ganiere, J-P, Wang, 8, Andre-Fontaine, G,
Wlyers, M, 1992: Haematological parameters
and visceral lesions relationships in rabbit
viral haemomhagic disease. Journal of Veterinary Medicine B 3 9 443-453.
Morisse, JP, Le Gall, G , Bouilletot, E, 1991,
cikd by Fuller, HE, Chasey, D, Lucas, M H,
Gibbens, J C, 1993: Rabbit haemorrhagic
disease in the United Kingdom. The Veterinary Record 133: 61 1-613.
Mulqueen, K. Personal communication.
Snud, B, Valicek, L, Rodack, L, Stephanek,
S, Jurak, E, 1991, cited by Fuller, E, Chasey,
D, Lucas, M H, Gibbens, J C, 1993: Rabbit
haemorrhagic disease in the United Kingdom. The Veterinary Record 18 133: 61 1613.
Wendy .L Townsend
Batchelar Animal Health Laboratory