I. Antibiotic-Induced Enterotoxemia
/ Hemorrhagic Typhlitis
II. Cryptosporidiosis
III. Endoparasites
IV. Hypovitaminosis C (Scurvy)
V. Salmonellosis
VI. Tyzzer's Disease
A. Etiology: Guinea pigs normally have an anaerobic gram-positive
intestinal flora, which can be upset and overcome by enterotoxin-producing
bacteria. This anaerobic bacterial overgrowth can rapidly produce
enterocolitis, septicemia, and death. Hence many things (such as
diet change, stress, prolonged antibiotic therapy) that alter the enteric
microflora can potentially initiate this syndrome. Antibiotics that
have been implicated include penicillin, erythromycin, lincomycin, chlortetracycline,
oxytetracycline, bacitracin, dihydrostreptomycin, cefazolin, cephalexin,
cephalothin, ampicillin, clindamycin & gentamycin. Specific organisms
implicated in the overgrowth and subsequent toxemic pathogenesis include
Clostridium
difficile, C. perfringens, C. spiroforme and several coliforms.
Diarrhea may or may not be present. Enterotoxemia may include anorexia,
rapid weight loss, dehydration, depression, and/or acute death. A
large, distended cecum containing blood and liquid contents with hemorrhagic
serosal and mucosal surfaces is characteristic (Photo A.). Microscopic
lesions include extensive vascular congestion, submucosal hemorrhage and
edema, and sloughing of the absorptive epithelium throughout the GI tract
(photo B). Diagnosis is based upon a history of antibiotic administration,
necropsy findings, and the isolation of an offending organism or toxin.
Treatment is heroic and includes fluids and supportive care. Control
of this syndrome relies on the careful and discriminate use of broad-spectrum
antibiotics in the guinea pig. Some safer antibiotics that have been
used in guinea pigs are chloramphenicol, enrofloxacin and trimethriprim
and sulfamerazine.
A. Etiology: A major protozoan parasite in the Guinea pig is Cryptosporidium wrairi.
B. Clinical signs: Intestinal colonization by this organism may
cause weight loss in adults and diarrhea and/or poor growth rates in weanlings
and juveniles. 
C. Pathology: The organism is most common in the ileum where flattened
and irregular villi along with a granulomatous infiltrate in the lamina
propria and absorptive epithelium are the main pathologic features. Parasites
can be visualized in parasitophorous vacuoles (arrows) at the apical portion
of infected enterocytes. 
D. Diagnosis: Fresh mucosal scrapings of the ileum with observation of the mature schizonts (4 micrometers in diameter) by phase contrast microscopy or by light microscopic exam of IFA stained wet mount preps (commercial kits are available) provides the most rapid method of diagnosis. Histopathologic exam of intestinal biopsies or PCR of mucosal scrapings are other methods for diagnosis of this condition.
E. Treatment: Outbreaks of clinical disease can be partially controlled by the addition of 0.2% sulfamethazine to the water supply.
Public Health Significance: Cryptosporidium wrairi appears to be species specific.
A. Nonpathogenic protozoa frequently observed in Guinea pigs include
the enteric coccidian (Eimeria caviae), and Balantidium caviae,
a large ciliate of the cecum and colon (see photo). 
B. The metazoan parasite commonly associated with guinea pigs is Paraspidodera uncinata, a roundworm which resides in the cecum (A.). Typical roundworm ova ( B.) can be demonstrated by fecal floatation techniques. Piperazine has been reported to be an effective treatment. Ivermectin (.3-.5 mg/kg; SQ) may also be used, but efficacy studies are lacking.
C. Encephalitozoon cuniculi has been reported as a spontaneous infection in Guinea pigs. The incidence of infection is unknown. Lesions in the brain and kidneys are similar to those reported in rabbits. Diagnostic tests for Guinea pigs are the same as for rabbits, and include serologic assays for detection of antibody to E. cuniculi and histopathologic demonstratioin of spores in infected tissues.
IV. Hypovitaminosis C (Scurvy)
A. Etiology: Guinea pigs lack the hepatic enzyme 1-gulonolactone oxidase, which is essential for the conversion of glucose to ascorbic acid. Vitamin C is involved in many biochemical processes in the body including the synthesis of collagen and of intracellular ground substance. If vitamin C is not supplemented in the diet or if the animal is anorexic, scorbutic lesions will rapidly develop.
B. Clinical signs: Scurvy is characterized by frequent vocalizations, weakness, anorexia, diarrhea, flaky to ulcerative skin lesions, stiffness, reluctance to move, petechia of the mucous membranes, subcutaneous hemorrhages and death in two to three weeks due to starvation or secondary infection. Other nonspecific but suspicious signs may include rough hair coat, delayed wound healing, teeth grinding, inactivity, stillbirths, and chronic disease.
C. Pathology: Necropsy findings may include fascial and
articular cartilage hemorrhages, petechial and ecchymotic bleeding on periosteum,
muscle, and gingiva. 
D. Diagnosis: A diagnosis can be made by dietary history, gross pathology, and serum ascorbate levels.
E. Treatment: Severely affected animals can be treated with 25-50 mg vitamin C IP s.i.d. until improvement is noted. Guinea pigs can then be given oral supplemental levels until the animal has recovered.
F. Control: Daily requirement of ascorbic acid is 15 mg/day, and this amount can be provided through supplemental feeding of a handful of cabbage or kale, a green pepper, a quarter of an orange, etc. Pregnant females should receive 30 mg/day. Vitamin C supplemented pellet research diets have an average shelf life of 6 months from the milling date when stored in a cool, dry place; shelf life can be prolonged by storage in a freezer. Commercial pet diets may have a shorter storage life of about 90 days after milling. If the vitamin is to be supplied in the water, a new solution at a dose of 200 to 400 mg/l drinking water should be mixed fresh daily due to instability of the vitamin in the presence of light and chlorine.
Salmonella enterica serovar Typhimurium has been shown to infect guinea pigs. Acute deaths are occasionally seen in very young, very old, or stressed animals; diarrhea is not characteristic of the clinical picture, but nonspecific depression, anorexia, weight loss and unthriftiness are commonly noted. Abortion storms have been reported. No lesions are apparent in acute cases, but carriers and chronically infected animals may have enlarged livers, spleens, and lymph nodes containing small white necrotic foci. Identification of both acute cases and carriers depends on isolation of a Salmonella sp. from feces or mesenteric lymph nodes. No treatment is recommended. Animals that are culture positive for Salmonella should be removed from the facility. Elimination of a colony is recommended if numerous carriers are identified.
Public Health Significance: Humans ingesting Salmonella - contaminated food or water experience a transient diarrhea. Children or immunosuppressed adults are susceptible to more serious clinical disease from Salmonella infection. Exposed personnel must be advised of any apparent risks.
Clostridium piliforme, a spore-forming, obligate intracellular
bacteria, has been shown to cause disease in immunocompromised guinea pigs.
Clinical signs, pathologic effects, and diagnostic procedures applicable
to this disease are the same as for other rodent species. Control
of outbreaks is by strict sanitation, good husbandry, and reduction of
environmental stress.
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