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G a s t ro i n t e s t i n a l D i s e a s e i n
Guinea Pigs and Rabbits
Julie DeCubellis, DVM, MSa,
Jennifer Graham, DVM, DABVP (Avian/Exotic Companion Mammal), DACZMa,b,*

KEYWORDS
 Gastrointestinal disease  Rabbit  Guinea pig  Stasis  Enteritis  GDV
 Liver torsion

KEY POINTS
 Dental disease is a commonly encountered problem in guinea pigs and rabbits.
 Even minor changes in the diet or digestive process can lead to significant gastrointestinal
(GI) disease in guinea pigs and rabbits.
 Diarrheal disease is common and frequently results from alterations in intestinal microflora
balance.
 Several cases of dilatation have been documented in guinea pigs.
 Rabbits secrete higher levels of gastric acid and pepsin than do rats and guinea pigs, likely
contributing to their higher incidence of gastric ulceration.
 Signs of lead toxicity in rabbits include neurologic presentations, such as seizures, torti-
collis, and blindness, but more common signs may be nonspecific and include anemia,
anorexia, loss of body condition, and GI stasis.
 One of the authors has documented 16 cases of liver torsion in rabbits at a single referral
institution in 5 years.

DENTAL DISEASE, GASTROINTESTINAL STASIS, AND DYSBIOSIS IN GUINEA PIGS AND

RABBITS

Dental disease is a commonly encountered problem in guinea pigs and rabbits. Guinea
pig and rabbit teeth are elodont (continuously growing/erupting), aradicular (open
rooted), and hypsodont (long-crowned) and contain incisors and cheek teeth (premo-
lars and molars). With insufficient wear, particularly from low-fiber, low-abrasion diets,

The authors have nothing to disclose.

a
Department of Zoological Companion Animal Medicine, Cummings School of Veterinary
Medicine, Tufts University, 200 Westboro Road, North Grafton, MA 01536, USA; b Department
of Comparative Medicine, University of Washington School of Medicine, 1959 Northeast Pacific
Street, Seattle, WA 98195, USA
* Corresponding author. Department of Zoological Companion Animal Medicine, Cummings
School of Veterinary Medicine, Tufts University, 200 Westboro Road, North Grafton, MA
01536, USA.
E-mail address: [Link]@[Link]

Vet Clin Exot Anim 16 (2013) 421–435

[Link] [Link]
1094-9194/13/$ – see front matter Ó 2013 Elsevier Inc. All rights reserved.
422 DeCubellis & Graham

molar crowns elongate and alter the slope of the occlusal plane, eventually creating
sharp points that inhibit closure, often resulting in secondary incisor elongation.1
Malocclusion also results from diets deficient in vitamin C in guinea pigs because it
is critical for gingival health and anchoring of teeth. Trauma, infection, and genetics
are also implicated. Dental disease can lead to oral ulcerations, infection, abscess
formation, and tongue entrapment in guinea pigs. Guinea pigs are more sensitive to
subtle occlusal changes than rabbits, and even mild disease can lead to anorexia
and malnutrition.2 Buccal ulcerations generally form along the upper arcades and
lingual ulcerations along the lower arcades in rabbits. Congenital deformities can
also result in malocclusion and produce dental disease at several months of age. In
rabbits with mandibular prognathism, most commonly seen in dwarf rabbits, misalign-
ment causes overgrowth of unopposed incisors, with upper incisors curving inward
and upward toward the roof of the mouth and lower incisors curving outward and
upward, sometimes into the upper lip or nose.1,3,4
Clinical signs of primary dental disease include anorexia, dysphagia, excessive sali-
vation and drooling, weight loss, emaciation, and changes in fecal appearance and
quantity. The presence of facial masses, excessive swelling, exophthalmos, and puru-
lent nasal discharge suggests secondary infection/abscess formation. Animals with
anorexia or dysphagia from a systemic disease, or with ocular disease restricting
feeding, can develop secondary dental disease.4 Diagnosis requires a routine physical
examination, including thorough oral examination of the incisors, cheek teeth, periapical
structures, bone, tongue, and oral mucosa. Complete dental examinations require
extraoral radiographic studies from multiple projections (lateral, obliques, ventrodorsal,
and rostrocaudal) using high-definition (mammography) film5 as well as a thorough
examination with patients under anesthesia, assisted by oral endoscopy, when avail-
able.6 Diagnosis of periapical disease and abscess can be aided by CT, when available.7
Dental correction involves shortening of overgrown teeth, restoring the occlusal
plane, extracting any diseased teeth, and treating abscessation. Dental procedures8
and anesthetic and analgesic considerations4,8,9 have recently been reviewed.
Surgical treatment must be combined with medical therapy to manage pain, restore
health (hydration, diet correction, and vitamin C supplementation for guinea pigs),
and minimize infection as well as the risk of postoperative GI stasis.2 Long-term
management of dental disease includes providing a high-fiber diet with Timothy grass
hay (ad lib),10 adequate vitamin C for guinea pigs (10–30 mg/d), and regular rechecks
with tooth trimming as needed.
Guinea pigs are less prone than rabbits to develop periapical infections and osteo-
myelitis, although they frequently present with more advanced disease and poor prog-
nosis.11 Periapical infection, abscessation and/or osteomyelitis of the surrounding
bones are common sequelae in rabbits with dental disease. Treatment typically
requires extraction, opening and excising an entire abscess capsule, careful débride-
ment of bone, marsupialization with secondary closure, and packing the surgical site.
Antibiotic therapy should be based on culture and sensitivity results and can include
combinations of oral and/or injectable agents as well as impregnated beads.11

GASTROINTESTINAL HYPOMOTILITY AND STASIS

GI stasis is a common problem in guinea pigs and rabbits. The GI tract is specialized
for its high-fiber herbivorous diet; even minor changes in the diet or digestive process
can lead to significant GI disease. GI stasis has a multifactorial etiology. In animals
receiving an adequate diet, GI stasis can result from reduced intake secondary to
one of several or a combination of factors causing anorexia, including dental disease,
 GI Diseases in Guinea Pigs and Rabbits 423

dysphagia, pain, anxiety, environmental changes, infection, dysbiosis, neoplasia,

chronic disease, drug effects (anesthetics, anticholinergics, opioids, and antibiotics),
obstruction/foreign bodies, and accidental or forced restriction (preoperative fasting).
Restricted water intake and activity also impair adequate processing of dietary fiber
and promote stasis. In addition to reducing intake, chronic stress causes increased
catecholamine signaling, acting on the enteric nervous system to impair intestinal
motility. Once initiated, dysmotility leads to reduced colonic transit, with decreased
fecal output, increased dehydration of intestinal contents, dehydration of gastric
contents with trichobezoar formation, impaired cecal fermentation, and disruption of
the enteric microflora, creating a cycle of further anorexia and worsening stasis.12,13
In severe cases, stasis leads to partial or complete obstruction or accumulation of
gas within the GI tract (bloat) that can be a life-threatening emergency (discussed
later). Clinical signs of GI stasis can include decreased or absent fecal material,
anorexia, bruxism, pain with abdominal palpation, decreased GI sounds, dehydration,
abdominal distension, gastric tympany, and respiratory or cardiovascular compro-
mise.14 Severely ill rabbits progress to hypovolemic shock with reduced blood pres-
sure and altered mentation.
Diagnosis requires a thorough history, physical examination, and abdominal
imaging (radiographs and/or ultrasound). Radiographic studies of the abdomen in
2 views are essential for examining gastric contents, colonic fecal contents, and,
most importantly, severe gas/fluid accumulation suggestive of obstruction, which
constitutes a surgical emergency.15 Trichobezoars are an uncommon cause of stasis
in guinea pigs but also require surgical intervention.16 Laboratory studies (complete
blood cell count, biochemistry, and urinalysis) can be helpful for determination of an
underlying cause of anorexia, but most have only nonspecific findings of dehydration
or possibly elevated hepatic enzymes from developing hepatic lipidosis.17
Routine GI stasis is treated with comprehensive supportive care (aggressive fluid
hydration, pain management, and assisted nutrition) best performed in a hospital
setting for close monitoring. Animals should be kept warm in a dark, quiet place to
minimize stress. Fluid replacement is achieved with warmed fluids (25–35 mL/kg every
8 hours) and can be given orally or subcutaneously [SC]), although animals with severe
dehydration require more aggressive intravenous (IV) fluids. Anxiety can be minimized
with injectable midazolam (0.25–0.5 mg/kg IV/intramuscular [IM]) and pain controlled
with analgesics, such as buprenorphine (0.01–0.05 mg/kg, IM or SC every 4–6 hours),
which can later be transitioned to meloxicam after adequate hydration (0.2 mg/kg IM/
SC/by mouth every 24 hours in guinea pigs and 0.2–1 mg/kg IM/SC/by mouth every 24
hours in rabbits). Once obstruction has been ruled out, prokinetic agents, including
metoclopramide (0.5 mg/kg SC/by mouth every 8–12 hours) and/or cisapride (0.5
mg/kg by mouth every 8–12 hours) can be used. Simethicone (20 mg/kg by mouth
every 8–12 hours) can be used to reduce gas distension and ranitidine (2 mg/kg IV
every 24 hours, 2–5 mg/kg by mouth every 12 hours) used in cases with prolonged
anorexia where gastric ulceration is likely. Nutritional support is essential and can
be performed by syringe feeding (15 mL/kg every 8 hours) of an herbivore critical
care formulation. Prolonged nutritional support can be provided by nasogastric
tube. Antibiotics should only be used in cases complicated by enterotoxemia and
bacterial enteritis.17–19

Dysbiosis and Antibiotic-associated Enterotoxemia

Diarrheal disease is common and frequently results from alterations in the intestinal
microflora balance,20 or dysbiosis, ranging from mild changes causing soft stools, to
pathogenic bacterial overgrowth with more significant enteritis, to life-threatening
424 DeCubellis & Graham

enterotoxemia. The gut flora is sensitive to any type of environmental change. Frequent
causes of dysbiosis include poor diet, hypomotility, stress, toxins, and antibiotic use.
Low-fiber, high-carbohydrate diets are the primary risk factor for several reasons:
(1) formation of dense masses that prohibit adequate digestion and sterilization by
the low pH gastric juice and enzymes; (2) reduced hindgut motility (discussed previ-
ously), delaying clearance of luminal bacteria and fermentation byproducts, causing
an altered cecal pH and fermentation environment that favors the growth of pathogenic
species; and (3) carbohydrate-rich diets that provide a readily available source of
luminal glucose for opportunistic organisms, such as Escherichia coli and Clostridium
spp.12,21 Systemic illness and stress, also acting to reduce motility, can precipitate
dysbiosis. Indiscriminate antibiotic use, particularly with narrow-spectrum agents
that selectively target beneficial gram-positive bacteria (penicillins, amoxicillin  clav-
ulanic acid, cephalosporins, ampicillin, clindamycin, and lincomycin), creates optimal
conditions for overgrowth of pathogenic species. Chloramphenicol, trimethoprim/
sulfas, and fluoroquinolones are least likely to damage the microflora, and there is
a decreased risk with parenteral versus oral administration.14,22
Overgrowth of C spiroforme in rabbits causes an often-fatal enterotoxemia due to
elaboration of bacterial toxin. Although adults with dysbiosis can develop enterotox-
emia, weanlings are most susceptible due to their poorly established flora and high
gastric pH. Newborns can also develop toxemia from toxin secreted into the milk of
infected mothers.12 Recently, it has been demonstrated that C spiroforme toxin (binary
actin-ADP-ribosylating, iota-like toxin) gains access to enterocytes via the lipolysis-
stimulated lipoprotein receptor, which is also used by the C difficile transferase and
C perfringes iota toxins, causing a secretory diarrhea.23,24 In acute infections, rabbits
develop watery diarrhea, possibly with blood, that soils the perineum and legs. They
become anorexic and decline over 2 to 4 days into a moribund state with hypovolemic
shock, leading to death. On necropsy, the cecum, the primary reservoir for bacterial
growth, is often covered with petechial and ecchymotic hemorrhage that can spread
into the appendix and proximal colon. The mucosa can also contain hemorrhage, thick
mucus, gas, or pseudomembranes.25
In young rabbits (7–14 weeks of age), bacterial dysbiosis and resultant cecal hyper-
acidity can lead to the proliferation of enteric goblet cells with voluminous mucus
production, causing a mucoid enteritis.26 Although the exact cause is unclear, the
disease is predominantly found in intense breeding colonies and is uncommon in
pet rabbits. Affected animals have anorexia and develop lethargy, weight loss, and
cecal impaction.25
Clinical symptoms of antibiotic associated enterotoxemia begin 1 to 5 days after
antibiotic administration, and include anorexia, dehydration, and hypothermia; diar-
rhea may or may not be present. Diagnosis is based on clinical history and clinical
signs and can be confirmed with polymerase chain reaction or ELISA-based commer-
cial tests for C difficile toxin. Treatment of dysbiosis/enteritis/enterotoxemia involves
aggressive supportive care and correction of hypomotility. Correction of dehydration
and nutritional deficiencies are critical, as is providing a warm, safe environment with
adequate analgesia. For cases of enteritis caused by bacterial overgrowth, fecal
bacterial culture and sensitivity can be helpful to guide antiobiotic therapy with
broad-spectrum agents, including trimethoprim-sulfamethoxazole (30 mg/kg by
mouth every 12 hours) or enrofloxacin (15 mg/kg by mouth every 24 hours). For enter-
otoxemia, a dual approach of metronidazole (20 mg/kg every 12 hours) and cholestyr-
amine (2 g/20 mL water every 24 hours by gavage) can be used to treat Clostridium
infection and bind its toxin, although C spiroforme has widespread intrinsic and
acquired antimicrobial resistance.27,28 Chloramphenicol (50 mg/kg by mouth every
 GI Diseases in Guinea Pigs and Rabbits 425

8 hours) can be used to attempt to suppress Clostridial overgrowth.14,22 Preventing

dysbiosis with a high-fiber diet and reducing stress is key to prevention. Attempts
to correct the dysbiosis have anecdotal success, including transfaunation and
commercial probiotics containing Lactobacillus spp, although controlled studies to
document their utility are lacking.29 Exterotoxemia is best avoided by judicious antibi-
otic use in guinea pigs and rabbits.

Gastrointestinal Disease in the Guinea Pig

Gastric dilation and volvulus
GI stasis can result in the accumulation of gas within the GI tract (bloat), particularly in
the stomach and cecum, prompting a surgical emergency. Gastric dilation-volvulus
(GDV) is a rare, life-threatening complication of this gas accumulation, with such
a high mortality that is frequently diagnosed at necropsy. Although far less common
than in other species (human, canine, and swine), several cases have been docu-
mented in guinea pigs,30–33 many involving breeding females in laboratory colonies.
The authors have had 3 recent cases of GDV in guinea pigs at their institution (Fig. 1).
Clinical signs of gastric dilation are similar to those found with GI stasis, although
more severe symptoms, such as dyspnea, cyanosis, tachycardia, and cardiovascular
shock, may also be present.30 When gastric tympany is present and/or there is
evidence of gastric dilation on imaging, decompression is achieved by passing a large
red rubber tube into the stomach through the oral cavity. A needle used as a trocar can
be passed percutaneously, although this carries a risk of gastric or cecal rupture or
peritonitis. If GDV is suspected, emergent surgical intervention is required to reduce
the volvulus. After surgical intervention, medical management per GI stasis is used.
Simethicone can be used to enhance gas absorption but only after aggressive hydra-
tion to avoid a potential foreign body from dehydrated simethicone.18

Bacterial enteritis
Although dietary factors (low fiber and excess carbohydrates) can cause soft stools in
all guinea pigs, diarrhea from bacterial enteritis is usually seen in weanlings, pregnant
sows, and immunocompromised/chronically stressed adults. The most common cause
is C piliforme (Tyzzer disease), transmitted by fecal-oral route. Infected animals prog-
ress rapidly from onset of lethargy, anorexia, and diarrhea to acute death. Antemortem
diagnosis is generally not possible because C piliforme is an intracellular bacterium that
does not grow in culture. At necropsy, infections are marked by intestinal inflammation

Fig. 1. Lateral radiographic projection of a guinea with a caudally displaced gastric dilata-
tion volvulus. There is also mineralized material in the caudal region suggestive of urolith-
iasis. The owners declined emergency surgery and this guinea pig died within 3 hours of
instituting supportive care measures.
426 DeCubellis & Graham

and patchy hepatic necrosis. Treatment has not proved beneficial, and prevention is
best achieved by good husbandry and stress reduction, especially during weaning.14,34
Salmonellosis from S typhimurium and S enteritidis are less-frequent causes of
bacterial enteritis but are highly lethal with greater than 50% mortality. Transmission
is generally from contaminated food or water, although fecal transmission also occurs.
Infected animals exhibit anorexia, weight loss, light-colored feces with or without diar-
rhea, weakness, depression, and poor grooming. Infected pregnant sows have a high
incidence of abortion. Physical examination frequently reveals hepatosplenomegaly
(with punctate necrotic foci in the viscera at necropsy) and conjunctivitis. Salmonella
can be cultured from the feces. Because infected animals can become asymptomatic
carriers of this zoonotic disease, treatment is not recommended. Preventive measures
include thorough disinfection of the environment and proper storage and washing of
all fresh fruits and vegetables offered.14,35
Other causes of bacterial enteritis include Yersinia pseudotuberculosis, E coli, C per-
fringes, Pseudomonas aeruginosa, Citrobacter freundii, Listeria monocytogenes, and
Lawsonia intracellularis. Y pseudotuberculosis can cause distinct clinical presenta-
tions: an acute, rapidly fatal (28–48 h) septicemic form; a chronic diarrheal disease
with wasting and death within weeks; and a nonfatal infection marked by abscesses
of the head and neck lymph nodes. Y pseudotuberculosis can also cause abscess
formation in the ileum, cecum, mesenteric lymph nodes, liver, and omentum. Treatment
is not advised, because it can induce an asymptomatic carrier state and promote zoo-
notic transmission.22,35 E coli infection/overgrowth is particularly virulent in weanlings
and is marked by anorexia, diarrhea, depression, wasting, and death. At necropsy,
yellow fluid and gas are found in the intestines, and there is often focal hepatic
necrosis.35 L intracellularis is most often found in swine but can also infect rodents,
including guinea pigs. The intracellular organism infects enteric epithelial cells, causing
a proliferative enteropathy marked by diarrhea, wasting, and eventual death.36

Parasitic disease
GI helminth infections are predominately due to the guinea pig roundworm, Paraspido-
dera uncinata. The nematode develops and resides in the cecum and colon but does
not invade the mucosa. Typical oxyurid eggs are shed in the feces, and ingestion leads
to infection within 3 to 5 days. Infections are often mild and subclinical, although heavy
infections lead to anorexia, diarrhea, weight loss, and poor coat. Treatment is with
ivermectin (0.2 mg/kg SC) and prevention by effective sanitation.22,34
Cryptosporidium wrairi is a protozoan that targets the small intestine epithelial brush
border. Transmission is by ingestion of oocysts from infected food, water, and fomites.
Infections are marked by diarrhea, weight loss, rectal prolapse, potbellied appear-
ance, and a greasy coat. Although immunocompetent animals generally recover within
4 weeks and develop resistance, weanlings, juveniles, and immunosuppressed
animals often have a more severe course with mortality approaching 50%. Oocysts
can be diagnosed on fecal examination, and organisms may be seen on histopa-
thology. Oocysts can be destroyed with 5% ammonia or extremes of temperature.
Cryptosporiodosis is potentially zoonotic.
Eimeria caviae is an intestinal coccidian of guinea pigs that is generally nonpatho-
genic but can cause significant disease in weanlings. Infections are more common
in breeding colonies due to overcrowding, poor husbandry, and concurrent disease.
Watery diarrhea and pasty stools usually start 10 to 13 days postexposure to oocysts
and can last 4 to 5 days. This is accompanied by anorexia and lethargy and is
frequently fatal. Fecal analysis can provide a diagnosis, and treatment with sulphona-
mides is effective when combined with sanitation (10% ammonia kills oocysts) and
 GI Diseases in Guinea Pigs and Rabbits 427

housing improvements.37 Balantidium caviae, Trichomonas caviae, and Giardia duo-

denalis are other generally nonpathogenic protozoans found in guinea pigs.

Fecal impaction
Fecal impaction is predominately identified in older guinea pigs, especially boars. The
exact cause is unknown, but inguinal gland infections, loss of muscle tone, and
reduced coprophagy have all been implicated. Animals present with straining and
have a large, foul-smelling impacted mass of feces and sebaceous secretions within
a large, flaccid vent opening. Therapeutic interventions include dietary changes to
increase fiber, mineral oil, and repeated manual evacuations using a cotton-tipped
applicator. Long-term therapy is generally required.14,22

Hepatic lipidosis
Hepatic lipidosis is a rapidly developing, fatal complication of anorexia, especially in
obese guinea pigs. A pathogenic mobilization and uptake of fatty acids for glucose
generation is a likely cause, although the mechanisms are unclear. Significant hepatic
damage can occur within 48 hours; thus, anorexia for 12 hours or more is an emer-
gency requiring nutritional support.14

Neoplasia
Neoplasms of the GI tract are rare in guinea pigs but can mimic clinical findings of
more common GI disorders. Lymphosarcomas, adenocarcinomas of the stomach
and cecum, and GI stromal tumors have been reported.38

Gastrointestinal Disease in the Rabbit

Gastric ulceration
Rabbits secrete higher levels of gastric acid and pepsin than do rats and guinea pigs,
likely contributing to their higher incidence of gastric ulceration.39 In a review of 1000
rabbit postmortem examinations, Hinton40 reported 7.3% with gastric ulcers. The
majority occurred in the fundus and without significant surrounding reaction, suggest-
ing a stress response to other illness. The link between stress and ulcers can be exper-
imentally demonstrated in rabbits by intraperitoneal injections of epinephrine, because
rabbits serve as a model organism for ulcers.41 Similarly, hypovolemic shock can
induce gastric ulcers in rabbits in a matter of hours.42 In Hinton’s review, 2% of the
rabbits had solitary peptic ulcers, the majority of which were perforated and found
in females dying in the peripartum period.40
Rabbits with gastric ulcers frequently present with anorexia and evidence of pain,
such as bruxism. In more severe or perforated disease there may be clinical signs of
anemia and shock. Physical examination may reveal acute abdomen with peritoneal
signs. Radiographic imaging or ultrasonography is helpful to eliminate other causes,
such as obstruction, neoplasia, or foreign body. Although endoscopy can provide direct
visualization of ulcers, many animals are not sufficiently stable for an anesthetized
procedure.13 Treatment should be aimed at controlling any underlying diseases,
providing hydration and analgesia (discussed previously), mucosal protection with
sucralfate, and acid blockade with ranitidine (2 mg/kg IV every 24 hours or 2–5 mg/kg
by mouth every 12 hours).

Cecal impaction
Altered cecocolonic motility, as well as diets high in fine-particle indigestible fiber
(such as psyllium), can cause dehydration and compaction of cecal and colonic
contents into hard lumps, or cecoliths. Cecoliths are the most common cause of
lower intestinal obstruction, most frequently in the sacculated colon. Frequently,
428 DeCubellis & Graham

this is a chronic problem and rabbits have a history of anorexia, abdominal pain, and
failure to thrive. Many are also positive for Encephalitozoon cuniculi, suggesting
a possible link.12
Clinical presentation correlates with severity of the obstruction and ranges from
anorexia and abdominal pain to moribund animals requiring emergent attention.
Cecoliths are readily palpable on physical examination, and abdominal imaging is
helpful to gauge intestinal obstruction. Treatment involves SC or IV fluid therapy, anal-
gesia (buprenorphine, 0.03–0.05 mg/kg SC/IV every 6–12 hours), and careful enemas
to advance fecal contents without destroying the damaged colonic mucosa. Animals
should initially be fed foods with a high water content supplemented with grass hay for
fiber and can later be supplemented with canned pumpkin (1 tbsp every 12 hours) to
boost water content.12

Dysautonomia
Dysautonomia is a rare idiopathic, progressive loss of autonomic system function. It
was successfully documented in the rabbit after studies of animals with presumed
mucoid enteropathy.43,44 Clinical features are consistent with autonomic dysfunc-
tions, including dry mucous membranes, mydriasis, urinary incontinence, brady-
cardia, proprioceptive deficits, cecal impaction, and loss of anal sphincter tone.
Anorexia and depression are common. A presumptive diagnosis is made by the clin-
ical findings, and radiography is helpful to document megaesophagus, aspiration
pneumonia, and a dilated, impacted colon. Definitive diagnosis requires histologic
documentation of chromolytic degeneration of autonomic neurons. Supportive care
is provided, although the prognosis is poor in rabbits.

Bacterial enteritis
Bacterial enteritis from enteropathogenic E coli can cause large outbreaks in weaning
commercial rabbits but is not reported in pet rabbits. The bacteria attach to cecal and
colonic epithelial cells and cause effacement of the surface microvilli, inhibiting colonic
absorption and causing watery diarrhea. Severity depends on the age of the rabbit and
serotype, although mortality can be more than 50%. On necropsy, the cecal wall may
have characteristic longitudinal, paintbrush hemorrhages. A presumptive diagnosis
is made by isolation of E coli on fecal cultures, although serotyping is not commer-
cially available. Supportive care as well as antimicrobial therapy with trimethoprim-
sulfamethoxazole (30 mg/kg by mouth every 12 hours) or enrofloxacin (10 mg/kg by
mouth every 12 hours) pending culture sensitivity results.45,46
Enteritis caused by C piliforme (Tyzzer disease), a motile gram-variable spore-forming
obligate intracellular bacterium, is found in many species of small mammals, including
rabbits and guinea pigs. Infected animals, in particular weanlings, progress rapidly from
onset of lethargy, anorexia, and watery diarrhea to acute death. Adults may have a more
chronic course. Antemortem diagnosis is generally not possible because C piliforme is
an intracellular bacterium that does not grow in culture. At necropsy, infections are
marked by patchy necrosis in the liver and proximal colon and degenerative lesions
of the myocardium. Treatment has not proved beneficial, and prevention is best
achieved by disinfection (spores are killed with 0.3% sodium hypochlorite solution
or 80 C heat for 30 min), good husbandry, and stress reduction, especially during
weaning.12
Proliferative enteritis caused by L intracellularis, an intracellular, gram-negative,
curved-to-spiraled bacterium, is most often found in swine but can also be found in
rabbits and rodents. The intracellular organism infects enteric epithelial cells, causing
a proliferative enteropathy marked by diarrhea and wasting.36 It is most common in
 GI Diseases in Guinea Pigs and Rabbits 429

weanlings (2–4 months) and can be treated with chloramphenicol (30–50 mg/kg by
mouth/SC every 12 hours for 7–14 days) because macrolide antibiotics, used to treat
L intracellularis in other species, are not recommended for use in rabbits.12

Viral diseases
Oral papillomatosis Rabbit oral papillomatosis virus infection seems restricted to
laboratory rabbits, especially New Zealand white rabbits, causing benign oral papil-
lomas on the ventral surface of the tongue. Rarely, papillomas occur elsewhere in
the mouth, and there is 1 report of a concomitant conjunctival papilloma.47 Papillomas
start as small millimeter-sized sessile lesions and can grow into larger (3–5 mm) clus-
ters of pedunculated papules. The lesions are benign and can persist for as long as
145 days.48

Rabbit enteric coronavirus The virus was discovered as a cause of rapidly fatal enteritis
in young (3–10 weeks) laboratory rabbits.49 Infected rabbits develop lethargy, diarrhea,
abdominal swelling, pleural effusion, and cardiomyopathy and invariably die within
24 hours. At necropsy, the intestine is fluid-filled and the villi are effaced. The virus
has hemagglutination activity and can be detected in the feces. A divergent coronavirus
strain has recently been identified in game rabbits in Asia.50
Rotavirus Rotavirus is highly infectious with a high morbidity and variable (generally
low) mortality. Weanling rabbits (2–4 months) are most susceptible, and disease
severity is increased with coinfection with another enteric pathogen.51 Antibodies to
rotavirus are found in laboratory, commercial, and pet rabbits, indicating it can infect
most strains.52 Infection impairs the sodium solute pumps on the enterocyte surface,
impairing reabsorption.53 Rotavirus infections are marked by anorexia, dehydration,
and green-yellow watery diarrhea. The intestines become distended and congested,
with petechial hemorrhages, chronic inflammation, and villous atrophy. Diagnosis
requires virus identification, and treatment is with supportive care.

Rabbit hemorrhagic disease virus This calicivirus of the genus Lagovirus affects only
European rabbits. It was first described in China in 1984 and rapidly spread throughout
Asia, Australia, and New Zealand and into Europe, with rare outbreaks in the United
States and elsewhere.54 Transmission is via direct contact (shed into urine, feces,
and respiratory secretions), fomite contamination, and even by intermediate insect
vectors. The disease occurs in rabbits over 2 months of age, in part due to its binding
to the histo-blood group antigens H, A, and B type 2 oligosaccharides, which are
present on the surface of mature respiratory and intestinal epithelial cells.55 The virus
replicates in the liver, causing severe hepatic necrosis and eventual death from
disseminated intravascular coagulation. The clinical presentation and course varies
from a peracute disease lasting only 12 to 36 hours, followed by sudden death, to
an acute or subacute febrile illness with anorexia, diarrhea (or constipation), neuro-
logic, and other systemic symptoms, lasting a few days to weeks, to a persistent/latent
disease with continued virus shedding.
Laboratory studies demonstrate a worsening lymphopenia and thrombocytopenia,
with eventual prolonged prothrombin and thrombin times. At necropsy, there is exten-
sive hepatic necrosis, splenomegaly, pulmonary hemorrhage, and evidence of
disseminated intravascular coagulation. The virus cannot be cultured; thus, diagnosis
requires molecular testing.54 Rabbit hemorrhagic disease virus is a reportable disease.
Vaccination programs using attenuated vaccines have had mixed results. A recombi-
nant vaccine has recently been developed and should assist prevention in endemic
areas.56 The virus can be inactivated with 0.5% sodium hypochlorite or 1% formalin.
430 DeCubellis & Graham

Parasitic diseases
Coccidiosis Coccidia are the most common parasites of the rabbit GI tract and,
although they cause significant disease in young (<6 months old) rabbits, they can
be incidentally found in fecal studies in adult rabbits. Of the 12 species of the genus
Eimeria, E stiedae is exclusive to the liver, with the rest causing intestinal disease.
Hepatic coccidiosis is ubiquitous in commercial rabbitries and can be fatal in young
rabbits by obstructing liver function. Severe disease is marked by anorexia, diarrhea,
abdominal bloating, and icterus. Biochemical tests confirm hepatic disease, with
aspartate aminotransferase, alanine aminotransferase, bile acids, and total bilirubin
elevations. On necropsy, the liver is studded with nodular, encapsulated abscesses.
Oocysts can be identified in bile or feces.
Intestinal coccidiosis is common in rabbits of all ages and most often associated
with E perforans infection. Subclinical infection is common, and disease severity varies
with age (worse under 6 months), species of Eimeria, parasite burden, and condition of
the rabbit (stress, poor husbandry, and poor diet). Significant disease is marked by
diarrhea with possible mucus or blood, dehydration, and weight loss. Intussusception
is a complication of severe disease. Diagnosis depends on histopathology and/or fecal
identification. Molecular assays have been developed to identify intestinal Eimeria
spp.57 In addition to supportive care, sulfa drugs are most effective at limiting multipli-
cation. Sulfadimethoxine (15 mg/kg by mouth every 12 hours) or trimethoprim-
sulfamethoxazole (30 mg/kg by mouth every 12 hours) can be used for 10 days of
therapy. Recovering rabbits develop lifelong immunity.12

Cryptosporidiosis Cryptosporidium parvum infects the small intestine and causes

a self-limited diarrheal illness (4–5 days duration) in young rabbits (peak, 30–40 days
old). Illness is accompanied by anorexia, depression, and dehydration. The organism
can be identified on histopathology. Other than supportive care, there is no effective
treatment. Recently, reports of rabbit Cryptosporidium spp causing zoonotic disease
in humans have been reported in several countries.58

Nematodes Passalurus ambiguous, the rabbit pinworm, is found in most rabbits, and
even large parasite burdens are not pathogenic. Adult worms reside in the cecum and
colon, and transmission is direct by ingestion of eggs during cecotrophy. Diagnosis is
often routine by identification of worms or eggs in the feces, although identification
should not prompt treatment in most cases. When treatment is necessary, benzimid-
azoles, such as fenbendazole (10–20 mg/kg by mouth, repeated in 10–14 days), are
effective.12

Aflatoxicosis
Aflatoxins produced by the fungi, Aspergillus flavus and Aspergillus parasiticus, cause
liver and biliary damage in rabbits. Rabbits are the most sensitive species to these
toxins and serve as an animal model for aflatoxicosis.59 Outbreaks occur from contam-
inated feed and are accompanied by anorexia, depression, and weight loss, progress-
ing to icterus and death within 3 to 4 days.60 On necropsy, livers are congested with
periportal and ductal fibrosis, sinusoidal dilation, and hepatocyte degenerative
changes. Treatment involves removal of contaminated feed and supportive care.

Neoplasia
GI neoplasms in rabbits include epithelial and smooth muscle tumors. Epithelial
tumors include gastric adenocarcinoma, papilloma of the sacculus rotundus, papil-
lomas of the rectal squamocolumnar junctional mucosa, and metastatic tumors, espe-
cially uterine adenocarcinoma. Smooth muscle tumors include leiomyoma and
 GI Diseases in Guinea Pigs and Rabbits 431

leiomyosarcoma of the stomach and intestines. Clinically, these tumors can present as
intestinal obstruction.61 Biliary tumors, such as bile duct adenoma and carcinoma, are
reported in the rabbit.62

Lead Toxicity
Signs of lead toxicity in rabbits include neurologic presentations, such as seizures, torti-
collis, and blindness, but more common signs may be nonspecific and include anemia,
anorexia, loss of body condition, and GI stasis.63 Lead toxicity should be a differential in
rabbits that chew baseboards or paint in older houses and have nucleated red cells or
basophilic stippling on blood smears. Lead levels greater than 10 mg/dL are diagnostic
for lead poisoning.63 The authors diagnose at least 1 to 2 cases of lead toxicity in rabbits
annually and signs usually involve GI stasis or loose stools (Fig. 2).64 Affected rabbits
can be treated with calcium ethylenediaminetetraacetic acid (30 mg/kg SC every
12 hours for 5–7 days) in addition to supportive care for GI stasis. Debilitated animals
should be hospitalized for more intensive supportive care but stable animals can
be treated at home with SC injections given by the owner. The source of lead should
be determined and eliminated from the rabbit’s environment to prevent further
intoxication.

Colonic Entrapment
Partial colonic entrapment and chronic recurring GI stasis may result from adhesions
after ovariohysterectomy.64 Practitioners should keep this differential in mind if seeing
a recently spayed female rabbit with recurring ileus. A mass effect may be palpated in
the region of adhesions and colonic segments cranial to the area of entrapment may
be dilated. Radiographs and ultrasound can be helpful to assess these patients and
surgical exploratory is indicated in patients with significant disease. Due to the deli-
cate nature of the rabbit intestinal tract, prognosis may be poor if there is significant
accompanying colonic pathology.

Liver Lobe Torsion

One of the authors (JG) has documented 16 cases of liver torsion in rabbits at a single
referral institution in 5 years.64–66 Rabbits with this condition present with nonspecific
signs of GI stasis and some have cranial abdominal pain or an abnormally placed liver
lobe on abdominal palpation. Because signs can be nonspecific, it is advisable to
perform blood work on all rabbits presenting with nonspecific signs of GI stasis. If liver
enzymes are elevated, abdominal ultrasound is recommended. Ultrasound reveals
lack of blood flow in the affected liver lobe on color flow Doppler (Fig. 3) and is diag-
nostic for liver lobe torsion. Prompt surgical removal of the affected lobe is advisable if

Fig. 2. Lateral radiographic projection of a rabbit with lead toxicosis (lead >65 mg/dL;
normal <10 mg/dL). This rabbit presented with a 2-week history of diarrhea that had been
refractory to antibiotic therapy by the referring veterinarian. Note that this radiograph is
consistent with nonspecific GI stasis and no metallic densities are seen on the films.
432 DeCubellis & Graham

Fig. 3. Ultrasound image of a rabbit with a caudate liver lobe torsion. The box surrounds the
torsed lobe and demonstrates a lack of blood flow in the affected liver lobe on color flow
Doppler. Note the surrounding hyperechoic fat, a common finding seen on ultrasound of
liver lobe torsions in rabbits.

the patient is stable for surgery.65 If an owner declines surgery, supportive care
measures alone (fluids, syringe feeding, prokinetic agents, analgesics, and antibiotics,
if indicated) are still indicated. The author (JG) has documented survival in 3 of 6 rabbits
with liver lobe torsion treated with supportive care measures alone.

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