key: cord-0040241-uxwgd2mc
authors: O'Rourke, Dorcas P.
title: Disease Problems of Guinea Pigs
date: 2009-05-18
journal: Ferrets, Rabbits, and Rodents
DOI: 10.1016/b0-72-169377-6/50026-5
sha: 1b8ec6ebc2e21fb9e38ab5741562e923c8feb5c3
doc_id: 40241
cord_uid: uxwgd2mc

nan

8 mg/kg. 60 Cefazolin at 50 mg/kg IM, SC is well tolerated; however, to be effective against Bordetella (a common guinea pig pathogen) at this dose, it would need to be administered every 30 minutes. Higher doses of cefazolin cause irritation at the injection site and death. 19 Whenever antibiotics are used to treat a guinea pig, the animal should also receive a Lactobacillus supplement during treatment and for 5 days beyond termination of antibiotic administration. 10 

Salmonella typhimurium and Salmonella enteritidis are the most common causes of bacterial enteritis in guinea pigs. Transmission is by fecal contamination of feed. Animals that are stressed, particularly weanlings, pregnant sows, aged animals, and those with nutritional deficiencies, are particularly susceptible. 26 Signs include scruffy hair coat, weight loss, weakness, conjunctivitis, and abortion. Diarrhea may or may not be present. At necropsy, the spleen and liver are enlarged, and yellow necrotic foci may be present in the viscera. 10 Diagnosis is made by culture and sensitivity testing of a fecal sample. Treatment includes appropriate antibiotic and fluid therapy, keeping in mind that the affected animal could become an asymptomatic carrier. The disease can be prevented by keeping the environment clean, storing food in airtight containers, and thoroughly washing all fresh fruits and vegetables that are offered to guinea pigs. Salmonellosis is a zoonotic disease.

Other causes of bacterial diarrhea in guinea pigs include Yersinia pseudotuberculosis, Clostridium perfringens, Escherichia coli, Pseudomonas aeruginosa, and Listeria monocytogenes. Like Salmonella, these are contracted through fecal contamination of food. Y. pseudotuberculosis can cause abscesses of the intestine and of regional lymph nodes. E. coli causes wasting, depression, and death in weanlings. Intestines may contain yellow fluid. 27 Antibiotic treatment is based on culture and sensitivity analysis. Supportive therapy is also indicated. Tyzzer's disease, caused by Clostridium piliforme (formerly Bacillus piliformis), has been reported in guinea pigs. The organism is transmitted by the fecaloral route, and young, stressed animals are particularly affected. Signs of Tyzzer's disease include diarrhea, an unthrifty appearance, and acute death. 35 In one case, dependent subcutaneous edema and excessive serous fluid were reported. 54 Lesions observed at necropsy include intestinal inflammation and focal hepatic necrosis. Because C. piliforme is an intracellular bacterium, it will not grow on routine culture media. Definitive diagnosis is made at necropsy by identification of the organisms on hematoxylin and eosin-or silver-stained sections of intestine or liver. Treatment has been unrewarding. This disease can be prevented by good husbandry practices and stress reduction, particularly at weaning.

Protozoal diarrhea in guinea pigs is caused by Cryptosporidium wrairi, which affects the small intestine. Transmission is by the fecal-oral route. Weanlings and immunosuppressed animals are most susceptible, 26 although immunocompetent adults can be affected. 9 Signs include failure to gain weight, weight loss, diarrhea, and death. 23 Immunocompetent guinea pigs recover within 4 weeks and are resistant to reinfection. 49 The organisms can be seen on fecal examination or identified histopathologically on the brush border of mucosal epithelial cells. No treatment has proved effective. Oocysts of C. wrairi can be destroyed in the environment with a 5% ammonia solution, freezing to below 32∞F (0∞C), or heating to above 149∞F (65∞C). 26 Cryptosporidiosis is a potentially zoonotic disease.

Guinea pigs are hosts to Eimeria caviae, Balantidium caviae (a protozoan), and Paraspidodera uncinata (a roundworm). In rare cases, E. caviae causes diarrhea, and P. uncinata can cause bronchoalveolar eosinophilia 11 ; otherwise, these organisms cause no clinical disease.

There has been one report of a wasting syndrome involving diarrhea, anorexia, rapid weight loss, and acute death in weanling guinea pigs. Coronavirus-like particles were identified in the feces with the use of transmission electron microscopy; no other organisms were isolated. 28

Guinea pigs have hypsodontic (open-rooted) incisors, premolars, and molars that grow continuously; therefore, overgrowth of any of these teeth is possible. Although there is a strong genetic predisposition to malocclusion, diet, trauma, or infection may also play a role. 26 Maxillary premolars and molars overgrow laterally, abrading the cheeks, and mandibular teeth overgrow medially, abrading the tongue and occluding the oropharynx. 10 Overgrown incisors can be identified on physical examination ( Fig. 24-1 ). Because premolar malocclusion usually goes unnoticed until the animal appears anorectic, prehends but cannot swallow food, and loses weight, an evaluation of cheek teeth should always be an integral component of a physical examination. Excess salivation (slobbers), wetting of chin and forepaws, and secondary moist dermatitis are also signs of malocclusion. 26 Malocclusion can be diagnosed by careful oral examination. Because the oral cavity of the guinea pig is narrow and large buccal folds are present, this examination is facilitated by first anesthetizing the animal with isoflurane. Gauze strips looped over the incisors can be used to open the mouth, and a vaginal speculum or otoscope can be used to carefully check the premolars and molars. The teeth can be trimmed with a dental drill, pediatric rongeurs, or a specially designed file. Use care if rongeurs are used to avoid splitting the teeth. Trimming needs to be repeated routinely (usually every 4 to 6 weeks) for the remainder of the animal's life. Vitamin C can be added to the diet of guinea pigs at 15 to 25 mg/day to prevent decreased collagen formation and subsequent tooth movement in the socket. 10 The disease can be prevented by not breeding affected animals and by feeding a proper diet (see Chapter 34) .

Pneumonia is probably the most significant disease in guinea pigs, particularly in damp or humid environments. Guinea pigs are very susceptible to respiratory disease caused by Bordetella bronchiseptica and Streptococcus pneumoniae. Bordetella, a gramnegative rod, is commonly carried by rabbits, dogs, and nonhuman primates. Rabbits and guinea pigs are mutual sources of infection of Bordetella. 8 Streptococcus, a gram-positive coccus, is also transmitted by asymptomatic carriers of many species. Stress increases susceptibility to disease, and young guinea pigs are most often affected. The organisms are transmitted by direct contact, by aerosolization, and on fomites. 26 Signs include inappetence, nasal and ocular discharge, and dyspnea. Bordetella causes a purulent bronchopneumonia with consolidation of lung lobes and exudate in the tympanic bullae. Metritis and abortions have also been described. Streptococcus causes a fibrinopurulent pleuritis and pericarditis in addition to bronchopneumonia. 26 Torticollis and abortions may also occur with Streptococcus. The combination of S. pneumoniae infection and vitamin C deficiency has resulted in septic arthritis. 57 Diagnosis of bacterial pneumonia is made by culture and sensitivity analysis of exudate. Bordetella antibodies can be detected by enzyme-linked immunosorbent assay (ELISA) or by indirect immunofluorescence; however, culture and sensitivity studies should be used to confirm active cases. 58 Radiographs may reveal consolidated lung lobes or an opacity in the tympanic bullae. Antibiotics commonly used to treat bacterial pneumonia in guinea pigs are chloramphenicol palmitate (30-50 mg/kg PO q12h ¥ 7-21 days) and trimethoprim-sulfa (30-50 mg/kg PO q12h ¥ 7 days), and enrofloxacin (5-10 mg/kg q12h ¥ 7-21 days). A combination therapy using enrofloxacin and doxycycline (2.5 mg/kg PO q12h) for 7-21 days has also been effective. Long-term therapy (4-6 weeks) with any of these antimicrobial agents may be necessary. Trovafloxacin, a new quinolone, is effective against S. pneumoniae and was used successfully to treat experimentally induced Legionnaires' disease in guinea pigs. 40 Lactobacillus should be given during antibiotic treatment and for approximately 5 days afterward. Supportive care, such as lactated Ringer's solution, oxygen therapy, and vitamin C, can also be given. Good husbandry, avoidance of stress, and separation of guinea pigs from dogs and rabbits will help control pneumonia.

Other bacteria of clinical significance include Haemophilus species and Streptobacillus moniliformis. Haemophilus has been recovered from the respiratory tract of guinea pigs and rabbits; it can cause subcutaneous abscesses and is easily transmitted to rats. 7 S. moniliformis is usually implicated in cervical lymphadenitis and has caused granulomatous pneumonia in guinea pigs. 31

A necrotizing bronchopneumonia has been described in guinea pigs. The incubation period is 5 to 10 days, and stressed animals are predisposed to developing disease. Morbidity is low, but mortality is high, and affected animals usually die acutely. Lesions include necrotizing, exfoliative bronchiolitis. Sloughed epithelium contains large, round to ovoid, basophilic intranuclear inclusions. An adenovirus is thought to be responsible for this disease. 15, 17, 25, 32 

Bronchogenic pulmonary adenoma is a common tumor found in guinea pigs. In one study, it occurred in approximately 30% of animals older than 3 years. This condition is sometimes misdiagnosed as pneumonia.

Urinary tract calculi are common in guinea pigs. In aged boars, congealed ejaculum can form proteinaceous urethral obstructions, resulting in urethritis. Females older than 3 years of age appear to be predisposed to cystitis and cystic calculi. 41 In one report, calcium oxalate uroliths were diagnosed in a number of guinea pigs with Streptococcus pyogenes cystitis. The bacteria formed nidi around which calcium was deposited, resulting in stone formation. 39 Signs of urolithiasis include anorexia, hematuria, dysuria, and a huddled, hunched posture. 48 Lesions include hemorrhage or congestion of bladder mucosa, hemorrhagic exudate within the bladder, and calculi adherent to the bladder wall. 41 S. pyogenes causes hyperemia of bladder mucosa and yellowish-gray deposits within the lumen. 39 Uroliths can sometimes be palpated; however, definitive diagnosis is most often made by radiography. Urinary acidifiers usually are not indicated because guinea pigs cannot easily remove an acid load. 26 Although potassium citrate is sometimes used to help prevent the formation of calculi, the efficacy of this drug has not been proven. In guinea pigs with urethral calculi, retrograde flushing might relieve the obstruction. If this procedure fails or if cystic or ureteral calculi are present, surgery should be considered. Isoflurane or sevoflurane is the anesthetic of choice for guinea pigs. Supportive care for urinary calculi includes antibiotic and fluid therapy.

Chronic interstitial nephritis is commonly found at necropsy in guinea pigs older than 3 years of age. It has also been reported in guinea pigs with diabetes mellitus and hyperglycemia. Animals affected by staphylococcal pododermatitis may develop chronic renal amyloidosis and nephritis as sequelae. 26 Secondary interstitial nephritis can be prevented by proper diet, caging, and good sanitation, which reduce susceptibility to pododermatitis.

Guinea pigs may harbor Klossiella cobayae, a renal coccidian. The organism lives in the epithelial cells lining the renal tubules. Sporocysts are shed in the urine. No clinical disease results from infection, and treatment is generally not recommended. 35 Sulfadimethoxine or trimethoprim-sulfa may be effective in treating renal parasitism.

Cystic rete ovarii have been identified in 76% of female guinea pigs between 18 months and 5 years of age, most commonly in animals age 2 to 4 years. 30 Cysts develop spontaneously, range in diameter from 0.5 to 7 cm, and increase in size as the animal ages. They may be single or multilocular, and they are usually filled with clear fluid (Fig. 24-2) . In most cases, both ovaries are affected; however, if a single ovary is affected, it is usually the right one. 30 Testosterone can stimulate ovarian epithelial cell growth, resulting in cyst formation. 47 Affected animals present with abdominal distention, and occasionally with anorexia, fatigue, and depression. 6, 30 If cysts are functional, bilateral symmetric hair loss can be seen in the flank region ( Fig.  24-3) . The most consistent sign of cysts in breeding sows is a decline in fertility after 15 months of age.

Diagnosis of an ovarian cyst is made by ultrasonography. A 6or 10-MHz mechanical sector transducer oriented in the sagittal plane yields diagnostic real-time images. Treatment consists of ovariohysterectomy. 6 Other problems associated with cystic rete ovarii include leiomyomas, 16 cystic endometrial hyperplasia, and endometritis. 30 Ovarian and uterine neoplasms can be induced by exposure to estradiol, diethylstilbestrol, or testosterone. 43, 46 

Wet, soiled bedding combined with inguinal sebaceous secretions can become adhered to the penis, scrotum, or vulva, resulting in secondary infection or obstruction of urination and defecation. The condition can be corrected by gently soaking the affected part in a dilute chlorhexidine solution and carefully removing the debris. If indicated, systemic antibiotics can be given. This condition is easily prevented by appropriate sanitation and good husbandry practices.

Pregnancy toxemia (pregnancy ketosis) is most commonly seen in primiparous, obese sows during the final 2 weeks of gestation and the first week after delivery. Although pregnancy is a contributing factor, toxemia is not limited to females; boars are also susceptible to this disorder. Obesity and fasting are the most critical predisposing conditions. Dietary alterations, environmental changes, and other stressors also play a role in precipitating this disease. 18, 35 Onset of signs is abrupt. The guinea pig becomes anorectic, quits drinking, and within 24 hours is prostrate and dyspneic. Convulsions and death can occur within 2 to 5 days. Clinically, the animal is hypoglycemic (less than 60 mg/dL), ketonemic, proteinuric, and aciduric (pH 5-6; normal pH = 9). The liver is enlarged and fatty, and the stomach is empty. In pregnant sows, the heavy, gravid uterus may compress its own vascular supply, resulting in ischemia, thromboplastin release, and disseminated intravascular coagulopathy. 26, 35 Treatment of pregnancy toxemia is usually unrewarding. Keep the guinea pig warm, give fluids intravenously or, if necessary, intraperitoneally, and administer glucose intravenously or by mouth. If the animal is in shock, it also can be treated with corticosteroids and calcium gluconate. Stress of treatment, combined with anorexia and an empty stomach, may lead to a fatal enteritis. 26 The prognosis for recovery from pregnancy toxemia is guarded to grave.

Prevention is the preferred method of dealing with pregnancy toxemia. All guinea pigs should be kept on a good-quality diet, and care should be taken to prevent obesity. Feeding fresh vegetables will condition animals to a varied diet and lessen the chance of refusal when new foods are offered. Fresh water should always be available ad libitum, and environmental, physical, and social stresses should be avoided, particularly during late pregnancy.

Dystocia is common in guinea pigs. In female guinea pigs, during the last week of pregnancy, relaxin (a hormone released from the pituitary and endometrium) causes the fibrocartilage of the pubic symphysis to disintegrate, resulting in a 3-cm separation. 10, 24 If a sow is not bred for the first time before she reaches 7 to 8 months of age, her pelvic symphysis will permanently fuse in close apposition, preventing passage of the fetuses during parturition ( Fig. 24-4) . Obesity, large fetuses, and uterine inertia can also cause dystocia.

In guinea pigs, pups are normally delivered within a 30minute period, with a resting period of approximately 5 minutes between pups. Signs of dystocia include unproductive contractions and straining. Animals may present with depression and may have a bloody or greenish-brown vulvar discharge. Diagnosis is based on history and signs. If the pelvic symphysis is wide enough and the problem is uterine inertia, 0.2 to 3 IU/kg of oxytocin can be given intramuscularly to stimulate contractions. 18 If pups are manually extracted, the fetal membranes must be rapidly removed. 10 If oxytocin fails to stimulate contractions, or if the pubic symphysis is less than 20 to 25 mm dilated, immediate cesarean section is indicated. 18 The female can be given buprenorphine (0.05 mg/kg SC q8-12h), followed by isoflurane or sevoflurane via mask induction and maintenance. A standard ventral midline approach is used. The uterus is exteriorized and incised longitudinally. Once the pups are removed, they should be cleaned off and stimulated to breathe immediately. The uterus is closed with an inverted suture pattern. The linea is closed with absorbable suture and the skin with nonabsorbable suture, using a simple interrupted pattern for both closure locations (see Chapter 27) . Guinea pigs do not tolerate the stress of anesthesia and surgery well; prognosis is guarded to poor. 18 Dystocia is best prevented by breeding guinea pigs before 6 months of age and by preventing obesity.

Mastitis in guinea pigs is caused by E. coli or Pasteurella, Klebsiella, Staphylococcus, Streptococcus, and Pseudomonas species. Wet, dirty cages and trauma caused by nursing pups predispose sows to infection. Organisms enter via the teat canal or through bite wounds on the teats. Clinically, the glands are initially swollen, red, and warm; later, they can become cool and cyanotic. The milk is often bloody. Infection can spread systemically and result in the death of both mother and pups. Guinea pigs with mastitis can be treated with systemic antibiotics, particularly chloramphenicol palmitate, trimethoprim-sulfa, and enrofloxacin. Hot packs can be applied to the affected glands. The environment should be cleaned, and the pups may be weaned early. If necessary, the mammary glands can be resected. 26

Most mammary gland tumors guinea pigs are benign fibroadenomas. Approximately 30% are adenocarcinomas, which are locally invasive but rarely metastasize. 10, 35 If tumors are excised, make a wide excision that includes a large amount of normal tissue. Local lymph nodes should also be removed.

Guinea pigs are susceptible to ringworm. Young animals are more susceptible because of their incompletely developed immune systems and lower amounts of fungistatic fatty acids in their sebum. 51 The dermatophyte most frequently isolated is Trichophyton mentagrophytes, although Microsporum canis has also been identified. Animals may be asymptomatic carriers; disease usually occurs secondary to overcrowding, poor husbandry, and other stressors. The organism is easily transmitted by direct contact and fomites. Lesions in the guinea pig are pruritic and consist of focal circular areas of alopecia with crusts. Lesions are usually seen first on the face, forehead, and ears and later spread over the back and down the limbs. 10 Diagnosis is made by plucking or scraping hairs and crusts from the periphery of the lesion and placing these on dermatophyte test medium (DTM) or another appropriate culture medium. Ringworm can be treated topically with miconazole (q24h ¥ 2-4 weeks). 26 Butenafine has been used effectively as a 1% cream applied topically (q24h ¥ 10-20 days). 1 Fluconazole can be administered at 16 mg/kg PO q24h ¥ 14 days. 37 Griseofulvin pediatric solution (25 mg/100 g PO q10 days ¥ three treatments) has proved effective, 10 but griseofulvin is more commonly given at 25 mg/kg PO q24h ¥ 14-28 days. Because it is teratogenic, this drug should not be given to pregnant animals. 10 Ringworm is a potentially zoonotic disease.

Guinea pigs are susceptible to infestation by mites (Trixacarus caviae, Chirodiscoides caviae), lice (Gliricola porcelli, Gyropus ovalis), and fleas (Ctenocephalides felis). Of these, Trixacarus, the sarcoptid mite, is the most significant pathogen (Fig. 24-5) . Trixacarus is a burrowing mite that can also transiently infest humans. Signs of Trixacarus infestation include intense pruritus with excoriations and secondary infection. In some animals, pruritus is so severe that it may cause seizures. Lesions are seen on the thighs and back and can extend over the shoulders and neck. 50 Yellowish crusts can cover the affected skin. Microscopically, orthokeratotic hyperkeratosis, eosinophilic microabscesses, and necrotic areas can be seen. Cross-sections of mites may be present in the stratum corneum. 20 Hematologic changes associated with Trixacarus infestation are leukocytosis, monocytosis, eosinophilia, and basophilia. 44 Chirodiscoides is a nonburrowing fur mite that is much less of a problem than Trixacarus. Chirodiscoides can cause lesions on the perineal and hip area, but infestation is usually asymptomatic. Gliricola and Gyropus are debris-feeding lice that attach to the hair shafts (both adults and eggs). Alopecia, crusts, and a rough hair coat are seen with lice infestations. 50 All of these parasites are transmitted by direct contact.

Diagnosis of an ectoparasitic infection is made by skin scraping (mites), by plucking or combing hairs to look for eggs and adults (lice), or by visual identification (fleas). Potassium hydroxide digestion of skin scrapings may be necessary to visualize Trixacarus. 20 Trixacarus is effectively treated with ivermectin (0.5-0.8 mg/kg SC, repeat in 7 days). Lice and Chirodiscoides also are treated with ivermectin (0.3 mg/kg SC, PO, repeat in 10 days). 50 Fleas can be treated with pyrethrin-based cat flea powder. Selamectin (6 mg/kg; Revolution, Pfizer, Exton, PA) is a topical parasiticide that has also been effective in guinea pigs. Treatment of any ectoparasite should be accompanied by thorough and repeated cleaning of the environment to prevent reinfestation.

Cervical lymphadenitis (lumps) is a disease that commonly affects guinea pigs (Fig. 24-6) . It is caused predominantly by Streptococcus zooepidemicus, Lancefield's group C, a gram-positive coccus. Occasionally, S. moniliformis is also involved. 35 S. zooepidemicus is normally present in the conjunctiva and nasal cavity of guinea pigs. If the animal's oral mucosa becomes abraded from malocclusion, dietary roughage (hay stems), or biting, bacteria invade the cervical lymph nodes and cause abscessation. Animals with intact nasal and conjunctival mucosa can also develop disease. 36 Stress increases susceptibility to infection. 26 Clinically, the guinea pig presents with pus-filled ventral cervical masses. Occasionally, bacteria spread systemically, resulting in septicemia or necrotizing bronchopneumonia. 31 Diagnosis is based on clinical signs and results of impression smears, Gram stains of the pus, and culture and sensitivity testing. Treatment consists of surgically excising the abscess (preferably) or draining of the abscess and copious flushing of the wound. A systemic antibiotic should be administered. This condition can be prevented by keeping the guinea pig on a good diet and in a clean, stress-free environment. S. moniliformis is a potentially zoonotic disease. 31

Although guinea pigs are social animals, group housing can lead to bite wounds that occasionally abscess. Treatment consists of draining and irrigating the wound with saline solution 2 and administering appropriate systemic antibiotics, based on results of sensitivity testing. 

Pododermatitis (bumblefoot) is commonly seen in guinea pigs. Typically, the disease is found in obese animals that are housed on wire-bottom cages or with abrasive bedding. Areas of hyperkeratosis develop on the palmar and plantar surfaces of the feet. These ulcerate, permitting secondary invasion by Staphylococcus aureus. 35 Infection can extend deep into the tissues of the feet, traveling up tendons and into bone, resulting in osteomyelitis. Guinea pigs with pododermatitis are in significant pain, vocalize frequently, and are reluctant to walk. Diagnosis is based on clinical signs and identification of lesions. Radiography may be useful in identifying osteomyelitis. Treatment consists of appropriate systemic antibiotics, surgical debridement of lesions, chlorhexidine foot soaks, wound bandaging, and appropriate analgesic therapy. As with pododermatitis in most species, the prognosis is guarded. The disease is best prevented by keeping the environment clean dry; housing the animals on soft, nonabrasive bedding; and avoiding obesity.

The most common skin tumor in guinea pigs is the trichofolliculoma, a benign basal cell epithelioma. Trichofolliculomas appear as solid or cystic masses, most commonly over the lumbosacral area (Figs. 24-7 and 24-8). 10, 35 They are easily removed surgically.

Alopecia resulting from noninfectious causes is quite common in guinea pigs. Included in this group are barbering, endocrine alopecias, and vitamin deficiencies. Barbering is recognized by close examination of the area of hair loss. In barbering, broken hair shafts are present, and the underlying skin is not inflamed or pruritic. 35 Alopecia over the flank areas indicates self-barbering, which can occur secondary to boredom. Providing hay, other roughage, or chew toys may alleviate this problem. In group-housed guinea pigs, the dominant animal often barbers subordinates. Guinea pig sows in late gestation can experience transient endocrine alopecia. 22 Partial alopecia has been documented in weanlings. 35 Supplementation of the diet with hay has been demonstrated to reduce trichophagia. 22

Guinea pigs possess a mutated gene for L-gulono-g-lactone oxidase and cannot produce this enzyme. Therefore, they cannot convert glucose to ascorbic acid and are incapable of endogenous synthesis of vitamin C. 38 For this reason, guinea pigs require 15 to 25 mg/day vitamin C added to their diet; pregnant animals require 30 mg/day. 26 Ascorbic acid is necessary for collagen synthesis; lack of dietary vitamin C results in defective type IV collagen, laminin, and elastin, which compromises blood vessel integrity and results in joint and gingival hemorrhages. 34 Collagen also is necessary to anchor teeth tightly in their sockets; without it, teeth loosen and malocclusion occurs. In addition, vitamin C is necessary for appropriate retention of vitamin E. 33 Signs of vitamin C deficiency include rough hair coat, anorexia, diarrhea, teeth grinding, vocalizing from pain, delayed wound healing, lameness, and increased susceptibility to bacterial infections. 35 Radiographically, long bone epiphyses and costochondral junctions of the ribs are enlarged. Pathologic fractures may also be evident. Young, growing animals are more susceptible to scurvy, and clinical disease can develop after as little as 2 weeks of ascorbic acid deprivation. 10 Diagnosis of vitamin C deficiency is based on history, clinical signs, and radiographic lesions. Serum ascorbic acid levels can be used to confirm the diagnosis. Treatment should be initiated with parenteral ascorbic acid at a dose of 50 mg/day IP, IM, or SC. Once response is noted, vitamin C may be administered orally at the same dosage. After recovery, vitamin C should be supplemented daily in the diet. Fresh, good-quality guinea pig (not rabbit) chow provides adequate vitamin C if used within 90 days of the milling date (see Chapter 23) . Fresh cabbage, kale, and oranges also provide a source of vitamin C: 100 g of kale contains 125 mg vitamin C, and 50 g of cabbage contains 30 mg vitamin C. 26 Vitamin C tablets can be added to the drinking water at a concentration of 200 to 400 mg/L 35 ; medicated water should be replaced daily. 

Spontaneous osteoarthritis has been described in guinea pigs. Osteoarthritis of the knee in guinea pigs mimics the disease in humans both morphologically and epidemiologically. Obesity is a predisposing factor. 4 Spontaneous cartilage degeneration and osteoarthrosis of the femorotibial joint of young guinea pigs has been described. 5 No cause has been identified, and the disease does not appear to be widespread.

A combination of fentanyl and droperidol has been documented to cause muscle necrosis at the injection site in guinea pigs. 26 Ketamine and diazepam have also been implicated in nerve damage and self-mutilation distal to the injection site in guinea pigs.

Lymphocytic choriomeningitis virus (LCMV) is an arenavirus that causes meningitis and hind limb paralysis in guinea pigs, although it is more commonly reported in mice and hamsters. Lesions include lymphocytic infiltrates in the choroid plexus, ependyma, and meninges. 35 The virus is transmitted through inhalation, ingestion, or direct contact with contaminated urine, saliva, and feces. Biting insects can transmit LCMV, and transplacental transmission also occurs. LCMV can be transmitted to humans. Signs of LCMV infection in humans include headache, vomiting, and fever; fatalities are rare (See Chapter 40).

Conjunctivitis due to Chlamydophila psittaci has been described in guinea pigs. 13 Animals age 1 to 3 weeks are most commonly affected. The mode of transmission is unknown. Signs include conjunctival reddening and serous ocular discharge. Diagnosis is made by the identification of intracytoplasmic inclusions in conjunctival scrapings. 35 Because the disease resolves spontaneously in 2 to 3 weeks, no treatment is recommended. Although C. psittaci is a zoonotic pathogen, no documented cases of transmission from guinea pig to human exist.

Ototoxicity has been reported in guinea pigs after administration of various drugs. Gentamicin can be ototoxic when applied topically. 12 Cortisporin otic suspension (Glaxo Wellcome, Research Triangle Park, NC), which contains neomycin and polymyxin B, is also ototoxic to guinea pigs. 42 Cisplatin administered at 7.5 mg/kg IM twice within 5 days induced ototoxicity in guinea pigs. 45

Spontaneous diabetes mellitus has been described in adult male Abyssinian-Hartley guinea pigs. The diabetes is noninsulindependent and is similar to adult-onset diabetes in humans. Affected animals develop bladder hypertrophy and voiding dysfunction and have a life span of about 5 years. 3 An adult female guinea pig was diagnosed with diabetes mellitus after the animal presented with cystitis and urination of small, frequent amounts. The guinea pig responded to NPH insulin 53 ; Caninsulin (Intervet Canada, Whitby, Ontario) worked best. 52 Diabetes mellitus may be transient, and a correct, low-fat, high-fiber diet is important in treatment and prevention. 29, 52 

Adrenal tumors have been documented in guinea pigs. One case report described an adult male guinea pig that presented with obesity, bilateral alopecia, hepatomegaly, and depression. An adrenal tumor and ureterolith were diagnosed by ultrasound. Both were removed surgically, but the guinea pig died from surgical complications. 21

Guinea pigs are susceptible to heat stress. Guinea pigs housed outdoors can develop heat stress in ambient temperatures as low as 70∞ to 75∞F (21∞ to 24∞C). Guinea pigs suffering from heat stress will salivate profusely in an attempt to thermoregulate. They exhibit shallow, rapid respiration, pale mucous membranes, and elevated rectal temperature. These signs may be followed by coma and death. Treatment is supportive and includes cool water baths and administering corticosteroids and parenteral fluids. Prognosis is very guarded.

Metastatic mineralization in guinea pigs is normally an incidental finding at necropsy. The etiology is unclear and is possibly related to subclinical mineral imbalances and dehydration or oversupplementation of dietary vitamin D 3 or minerals. Although the disease is usually clinically unapparent, it can manifest as muscle stiffness and renal dysfunction. 35 Lesions are seen in animals older than 1 year of age and include mineralization of kidneys, heart, vessels, stomach, and colon. There is no treatment.

Lymphosarcoma is the most common tumor of guinea pigs. The disease is caused by a type C retrovirus. Animals present with a scruffy coat and lymphadenopathy. Hepatomegaly, splenomegaly, and mediastinal masses are occasionally seen. Diagnosis is based on the results of a complete blood count and cytologic examination of aspirates of enlarged nodes or abdominal or pleural fluids. Leukemic animals have a total white blood cell count of 25,000 to 500,000 cells/mm 3 . 10 At necropsy, lymph nodes and visceral organs may be enlarged, with infiltration by proliferating lymphoblasts. The course of the disease is 2 to 5 weeks. Prognosis is poor, although some animals have responded initially to chemotherapy. 35 

Effects of butenafine hydrochloride, a new benzylamine derivative, on experimental dermatophytosis in guinea pigs

Saline wound irrigation reduces the postoperative infection rate in guinea pigs

Bladder dysfunction in the spontaneously diabetic male Abyssinian-Hartley guinea pig

Animal models of arthritis: relevance to human disease

Osteoarthritis in guinea pigs: histopathologic and scanning electron microscopic features

Ultrasonic diagnosis of ovarian cysts in ten guinea pigs

Serological relationship of some V-factor dependent Pasteurellaceae (Haemophilus sp.) from guinea pigs and rabbits

Multifactorial analysis of antibiotic sensitivity of Bordetella bronchiseptica isolates from guinea pigs, rabbits and rats

Comparison of the host ranges and antigenicity of Cryptosporidium parvum and Cryptosporidium wrairi from guinea pigs

Common diseases and medical management of rodents and lagomorphs

Bronchoalveolar eosinophilia in guinea pigs harboring inapparent infections of Paraspidodera uncinata

Topical gentamicin and ethacrynic acid: effects on cochlear function

Guinea pig inclusion conjunctivitis (GPIC) in a commercial colony

Incidence and classification of thyroid lesions in 210 guinea pigs

Necrotizing viral bronchopneumonia in guinea pigs

Spontaneous reproductive tract leiomyomas in aged guinea-pigs

Adenovirus pneumonia of guinea pigs

Reproductive disorders in the rabbit and guinea pig

Pharmacokinetics of cefazolin in guinea pigs

Mange induced by Trixacarus caviae in a guinea pig

Ultrasonographic detection of adrenal gland tumor and ureterolithiasis in a guinea pig

Influence of feeding hay on the alopecia of breeding guinea pigs

Cryptosporidiosis in guinea pigs: a retrospective study

Relaxin and its role in pregnancy

Experimental pneumonia virus of mice infection of guinea pigs spontaneously infected with Bordetella bronchiseptica

The Biology and Medicine of Rabbits and Rodents

Diagnostic exercise: depression and anorexia in recently shipped guinea pigs

Coronavirus-like virions associated with a wasting syndrome in guinea pigs

Small mammal endocrinology. Proc Annu Conf Assoc Avian Vet

Reproductive failure associated with cystic rete ovarii in guinea pigs

Isolation of Streptobacillus moniliformis from a guinea pig with granulomatous pneumonia

Adenovirus pneumonia in guinea pigs: an experimental reproduction of the disease

Vitamin C supplementation restores the impaired vitamin E status of guinea pigs fed oxidized frying oil

Vitamin C deficiency in guinea pigs differentially affects the expression of type IV collagen, laminin, and elastin in blood vessels

Biology and diseases of guinea pigs

Cervical lymphadenitis in guinea pigs: infection via intact ocular and nasal mucosa by Streptococcus zooepidemicus

Comparison of the therapeutic efficacy of oral doses of fluconazole and griseofulvin in a guinea pig model of dermatophytosis

Guinea pigs possess a highly mutated gene for L-gulono-g-lactone oxidase, the key enzyme for L-ascorbic acid biosynthesis missing in this species

An outbreak of Streptococcus pyogenes infection associated with calcium oxalate urolithiasis in guinea pigs (Cavia porcellus)

Bacteriological activity of trovafloxacin, a new quinolone, against respiratory tract pathogens

Cystitis and cystic calculi in aged guinea pigs

Effect of Cortisporin otic suspension on cochlear function and efferent activity in the guinea pig

Use of endoscopic and ultrasound techniques in the guinea pig leiomyoma model

Haematological and pathological responses to experimental Trixacarus caviae infection in guinea pigs

Similar pharmacokinetics and differential ototoxicity after administration with cisplatin and transplatin in guinea pigs

Induction of epithelial neoplasms in the ovaries of guinea pigs by estrogenic stimulation

The induction of benign epithelial neoplasms of the ovaries of guinea pigs by testosterone stimulation: a potential animal model

Urolithiasis in a guinea pig

Cryptosporidiosis in immunocompetent guinea pigs

Pruritus in rabbits, rodents, and ferrets

Prevalence of dermatophytes in asymptomatic guinea pigs and rabbits

Vannevel J: Diabetes in the guinea pig: not uncommon

Vannevel J: Diabetes mellitus in a 3-year-old, intact, female guinea pig

Naturally occurring Bacillus piliformis infection (Tyzzer's disease) in guinea pigs

Diseases of Exotic Animals. Philadelphia

Practical Guide to Laboratory Animals

Streptococcus pneumoniae arthritis and osteomyelitis with vitamin C deficiency in guinea pigs

Interlaboratory comparison of enzyme-linked immunosorbent assay (ELISA) and indirect immunofluorescence (IIF) for detection of Bordetella bronchiseptica antibodies in guinea pigs

Clostridium difficile toxin A excites enteric neurons and suppresses sympathetic neurotransmission in the guinea pig

An evaluation of ampicillin pharmacokinetics and toxicity in guinea pigs