Guinea pigs, like chinchillas, are hystricognath rodents. They belong to the family Cavidae, which contains 14 species of animals commonly known as cavies and Patagonian hares (or maras). Four digits on the forepaw and three on the hindfoot characterize Cavidae.
Guinea pigs have a stocky build, large head, short legs, and unfurred, short ears. Head and body length is 200–400 mm, there is no external tail, and weight is 500–1,500 g.
In South America, wild cavies inhabit rocky areas, savannas, forest edges, and swamps from Columbia and Venezuela southward to Brazil and northern Argentina. They live in groups of up to 10 individuals and inhabit burrows that they or other animals dig. They are most active at night, when they forage for a variety of plant materials. Domestication of the guinea pig began at least by 900 BCE and may have begun as early as 5,000 BCE.
The American Cavy Breeders Association recognizes 13 breeds that it divides into groups or varieties. The most common breed is the American cavy, known originally as the English cavy. Self cavies are a group of solid-colored animals (eg, black, cream, red, lilac, beige, saffron, and chocolate). Nonselfs are a group made up of the coated breeds, the marked breeds, and the ticked or agouti breeds. The coated cavies include the Abyssinian, Rex, Longhaired varieties (Peruvians, Silkies, Shelties, Coronets, and Texels), Crested, Teddy, and Satins. The short, wire-haired Abyssinian may look unhealthy because its coat is arranged in whorls or rosettes, giving it a ruffled, untidy appearance. An undercoat and projecting guard hairs make up the normal fur coat of a cavy. The Rex has short guard hairs that do not appear above the level of the undercoat, the Satin breeds have an abnormal hair fiber that produces a sheen, and the Teddy breeds have a kinked or bent hair shaft that causes the coat to stand erect over the entire body. The marked group contains Dalmatian, tortoise shell, and Himalayan varieties. The term “variety” describes a color (eg, steel grey, tortoiseshell) that is not yet a recognized breed.
Guinea pigs have between 7 and 11 distinct sound patterns, or calls. Although different researchers have given different names to each unique sound, there is general agreement on at least 7 sounds.
Lymphocytes are the predominant WBC in guinea pigs and range from 45%–80% of the WBC count. Many small lymphocytes are similar in size to erythrocytes. Large lymphocytes contain Kurloff bodies, large intracytoplasmic mucopolysaccharide inclusion bodies. Kurloff bodies are seen under normal conditions in guinea pigs and are estrogen dependent. Pregnant females may have 2%–5% lymphocytes with Kurloff bodies in their peripheral blood; they are present in large numbers in adult females, and numbers fluctuate with the stage of estrous cycle. There are few Kurloff bodies in adult males, and they are rarely seen in newborns.
Like chinchillas, guinea pigs share unusual reproductive physiologic characteristics of hystricomorph rodents. Female guinea pigs (or sows) have a pregnancy of 68 days (range 59–72 days) and an average estrous cycle length of 17 days (range 13–25 days). The vaginal closure membrane is open at estrus and parturition but sealed during anestrus and pregnancy. Guinea pigs have an average of 4 young per litter, with a range of 1–13. The young (of both species) are born precocial, meaning they are born fully furred, with eyes open, and overall well developed. Young guinea pigs usually nurse for 21 days, although they can survive on solid food alone after 5 days. Guinea pigs have only a single pair of inguinal nipples.
Male guinea pigs have pronounced penile styles or spicules on the glans penis. Young male guinea pigs reach puberty at 2–3 months of age and females at 2 months. Guinea pigs live 6–8 years.
As a species, guinea pigs are extremely adaptable to a great range of climates, although as individuals they are highly susceptible to variations in local temperature and humidity. Guinea pigs are nervous animals and may refuse to drink or eat for a period after any significant change in their location, feed, or husbandry. The effect of environmental changes on guinea pigs is minimal or nonexistent when two animals are kept together. If a sick guinea pig must be kept in hospital, housing a cagemate with the sick animal reduces stress.
Guinea pigs live in family units centered on an alpha male. Mature males, and especially strangers, will fight. However, two males raised together from a young age or a group of nonbreeding females do not develop dominance problems. Social problems are diminished with castration and ovariohysterectomy, but learned behavior in adult males after castration may still make them antisocial.
Guinea pigs require a constant source of water that must be changed daily. They dirty their water bowls or sipper tubes with food when they drink. They do not lick sipper tubes without training, defecate indiscriminately, and are prone to sit in and soil their food bowls and sleeping areas. Guinea pigs are neophobic, ie, afraid of new things, especially with regard to food and water. Any changes in appearance, taste, texture, etc, can put guinea pigs off feed or water. Guinea pigs develop food preferences early in life and may not recognize new food items as food if introduced later. This is why it is important to expose young guinea pigs to a variety of foods, especially a variety of vegetables, early in life.
Guinea pigs produce two types of fecal pellets: one nitrogen-rich intended for cecotrophy, and one nitrogen-poor delivered as fecal pellets. When food is continually available, ~40% of the feces are reingested, and 90% of this coprophagy occurs at night. However, when food is limited, guinea pigs ingest feces during parts of the day when food is unavailable.
Guinea pigs are easy to hold and restrain. Although they do not bite, very young guinea pigs may nip. Healthy guinea pigs feel “dense” and are alert. Fatigue, lack of interest in surroundings, and light body weight are often general signs of illness. Sick guinea pigs may show evidence of weight loss, hunched posture, abnormal gait, drawn-in abdomen, scruffy fur, or labored breathing. They may be lethargic or unresponsive to stimulation. Respiratory and GI conditions are most commonly encountered; thus, ocular or nasal discharges or diarrhea may be present. Feet should be examined for sores or broken nails. Teeth may sometimes overgrow and should be checked. However, the mouth is small, and examination of the oral cavity is difficult. A nasal speculum attached to an otoscope handle is an invaluable tool for examination of the cheek teeth in an awake guinea pig. Ears and eyes should be examined for discharges or inflammation, and the submandibular area should be examined for swellings.
Venipuncture can be difficult in guinea pigs because of the lack of obviously accessible peripheral veins. The lateral saphenous vein and the cephalic vein are useful to draw small amounts of blood. For large amounts of blood, the anterior vena cava can be used while the guinea pig is under anesthesia. This technique requires practice because, if performed incorrectly, there is a risk of death associated with intrathoracic, pericardial, or pulmonary hemorrhage.
Streptococcus equi subsp zooepidemicus (previously S zooepidemicus) may be carried in the nasopharynx as a latent infection. Abrasions of the oral cavity (eg, molar malocclusion) allow bacteria to be transported to draining lymph nodes of the head and neck, causing suppurative lymphadenitis. Clinically, guinea pigs present with large, unilateral swellings in the neck. The affected animal is often in good flesh and shows no other signs of disease. The differential diagnosis should always include cavian leukemia. Treatment is surgical excision of the affected lymph nodes and systemic antibiotic treatment. Bacterial culture and antibiotic sensitivity should always be recommended. Streptococci are generally sensitive to chloramphenicol (50 mg/kg, PO, twice a day), and this antibiotic is “safe” to give systemically to guinea pigs. Alternative “safe” antibiotics are azithromycin (15–30 mg/kg/day, PO; discontinue if soft feces result) and fluoroquinolones; however, bacterial resistance to these antibiotics is now frequently seen.
Streptococcus pneumoniae may be carried in the nares as an inapparent infection. Predisposing factors for development of bacterial pneumonia are changes in environmental temperature, humidity, or ventilation. This always occurs in winter in guinea pigs kept outside. The young, old, and pregnant are the most susceptible. Clinical signs of pneumonia are dyspnea, wheezy breathing, sneezing, nasal discharge, and coughing. The affected guinea pig becomes depressed and anorectic. S pneumoniae infections are nearly always associated with middle ear infection and head tilt. Increased radiodensity of the affected tympanic bulla may be seen on radiographs. Because of limited antimicrobial sensitivity, chloramphenicol (50 mg/kg, PO, twice a day) is the recommended treatment. A major differential diagnosis for pneumonia is Bordetella bronchiseptica infection.
Rabbits may harbor B bronchiseptica in their respiratory tracts without developing disease. However, this organism is an aggressive pathogen in guinea pigs, causing pneumonia, conjunctivitis, otitis media, abortions, and stillbirths. Clinical signs include anorexia, inappetence, nasal and ocular discharge, dyspnea, and often sudden death (this could also include S pneumoniae and S equi zooepidemicus infections). Rabbits and guinea pigs should not be housed together as pets. Treatment is ciprofloxacin (10–20 mg/kg, PO, twice a day). B bronchiseptica possesses a beta-lactamase and is resistant to many penicillins and cephalosporins and mostly resistant to trimethoprim-sulfamethoxazole. Most isolates are sensitive to doxycycline (2.5–5 mg/kg, PO, twice a day) and fluoroquinolones (marbofloxacin, 4 mg/kg/day, PO; ciprofloxacin, 10–20 mg/kg, PO, twice a day; enrofloxacin, 5–10 mg/kg, PO, twice a day for 14 days).
Salmonella infections were historically common in guinea pigs in research colonies. With present standards of husbandry, rodent control, and good quality feed, the disease rarely occurs. It is most likely seen when guinea pigs are kept outside and wild rodents have access to their feed. Disease is more often seen in young or stressed animals. Infection may be subclinical, and diarrhea is rarely present. Clinical signs include conjunctivitis, fever, lethargy, anorexia, rough fur, palpable hepatosplenomegaly, cervical lymphadenitis, and abortion in pregnant sows. Mortality is often high in epizootic outbreaks. If animals recover, organisms may be shed intermittently. Diagnosis is accomplished by isolating the organism from blood, ocular secretions, lymph nodes, or spleen. Because of zoonotic considerations and the potential for a carrier state, treatment is not recommended.
Chronic pododermatitis (especially of the forepaws) is a common condition usually seen in obese guinea pigs housed on wire or abrasive floors. Poor sanitation is also a predisposing factor. The feet are swollen and hairless with ulcers and scabs 1–3 cm in diameter on the plantar surface. Staphylococcus aureus is the usual causative agent and probably enters the foot through a cutaneous wound. Awns and straw in the bedding can also cause foot punctures. The inflammation can progress to osteoarthritis and/or osteomyelitis and systemic amyloidosis secondary to chronic staphylococcal infection. Surgical treatment is often unsuccessful, because there is rarely an abscess to be excised or drained but rather a diffuse cellulitis that infiltrates surrounding tissue. Treatment involves housing the affected guinea pig on clean, dry, soft bedding; topical or parenteral administration of antibiotics; and foot bandages as needed. Unfortunately, the condition may not respond to therapy.
Chlamydial conjunctivitis is one of the most common causes of infectious conjunctivitis in guinea pigs. It is caused by Chlamydia caviae, an obligate intracellular bacterium. Clinical disease usually is found in young animals 4–8 weeks old. Rhinitis, lower respiratory tract disease, and abortion can also occur. Concurrent bacterial infections can contribute to the respiratory signs. C caviae can rapidly spread through a breeding or research colony. The organism infects primarily the mucosal epithelium of the conjunctiva and, less frequently, the genital tract of guinea pigs. Asymptomatic infection can occur, but clinical disease most often results in mild inflammatory conjunctivitis with a slight, yellow-white discharge, conjunctival hyperemia, chemosis, and even severe conjunctivitis with profuse, purulent ocular exudate. Demonstration of intracytoplasmic inclusion bodies in Giemsa-stained conjunctival epithelial cells often confirms the diagnosis. The most sensitive and reliable method of diagnosis of chlamydiosis is PCR testing. Antichlamydial therapy with doxycycline (5 mg/kg, PO, twice a day for 10 days) is the treatment of choice and usually results in complete recovery. Guinea pigs develop short-lived immunity to C caviae and, after a short period, may be susceptible to reinfection.
Adenovirus is species-specific for guinea pigs and may cause a primary respiratory pneumonia. The asymptomatic carrier state is thought to be common, but prevalence is unknown. Clinical disease, while rare, can be initiated by stress or inhalation anesthesia and occurs more often in immunocompromised, young, or aged animals. Morbidity is low, but animals usually die suddenly without clinical signs.
Other naturally occurring viral infections of guinea pigs such as cytomegalovirus and parainfluenza rarely cause detectable clinical disease. Serologic surveys indicate that guinea pigs will develop antibodies to rat and mouse pathogenic viruses but do not develop disease.
Mange, caused by the sarcoptid mite Trixacarus caviae, is common in guinea pigs. The clinical signs are dramatic: intense pruritus, widespread alopecia, and hyperkeratosis. T caviae is transmitted through direct animal-to-animal contact from sow to weanlings during feeding, and through contact with infested cage material such as bedding. The mites may be capable of existing subclinically, becoming active with stressors (such as shipping or pregnancy), immunosuppression, or other underlying diseases. In affected animals that exhibit hematologic changes such as heterophilia, monocytosis, eosinophilia, and basophilia, vigorous scratching may trigger convulsive seizures. The seizures are controlled by diazepam (1–2 mg/kg, IM, as needed). The clinical presumptive diagnosis should be confirmed with several skin scrapings, usually revealing a massive T caviae infestation. Treatment involves ivermectin (0.4–0.5 mg/kg, SC, repeated 2–3 times at intervals of 7–10 days), or spot-on dermal treatment with either selamectin (15 mg/kg for <800 g body weight; 30 mg/kg for >800 g body weight). The guinea pig should also have a whole body washing with fipronil repeated twice at intervals of 7–10 days. Fipronil should not be used when open skin wounds are present.
Other ectoparasitic diseases are infrequent in guinea pigs. Infestation with the fur mite Chirodiscoides caviae may result in pruritus and alopecia along the posterior trunk of the body, while underlying skin is relatively unaffected. Subclinical cases may be asymptomatic. Treatment is with selamectin (15 mg/kg for <800 g body weight, 30 mg/kg for >800 g body weight) administered twice at 2-week intervals.
Lice infestation with either Gyropus ovalis or Gliricola porcelli is usually asymptomatic but in severe cases may lead to pruritus, alopecia, and flaky skin surfaces around the neck and ears. Lice may be observed directly on hair shafts with a magnifying glass. A single application of 0.05 mL of a topical solution containing 10% imidacloprid and 1% moxidectin is an effective treatment for lice infestations in guinea pigs. Prevention is aimed at improving sanitary conditions in the animal’s environment.
Dermatophytosis is common in guinea pigs, and natural infection is always associated with Trichophyton mentagrophytes var mentagrophytes. Lesions typically begin as broken hairs and circular, scaly alopecia initially occurring at the tip of the nose, which spreads to the periocular, forehead, and pinnal areas. In severe cases, the dorsal sacrolumbar area is also affected, but the limbs and ventrum are usually spared. Pruritus is usually minimal or absent. Some animals have more inflammatory lesions characterized by erythema, follicular papules, pustules, crusts, pruritus, and occasional scarring. High temperature and humidity may contribute to a more severe infection.
T mentagrophytes can be isolated from the skin and fur in up to 15% of clinically normal guinea pigs. Guinea pigs can be tested for dermatophytes by using a new toothbrush to comb all parts of the hair coat and impress the bristles onto dermatophyte test medium (DTM) in several sites. In a healthy animal, dermatophytosis is generally a self-limiting disease, with full resolution after development of an appropriate cell-mediated immune response. In immunocompetent animals, this usually takes 100 days. Nevertheless, treatment is recommended because it will accelerate resolution of lesions caused by dermatophytes, thereby minimizing the time course of the infection and minimizing the potential for spread to other animals or people. Whenever possible, curing the infection in the pet, while simultaneously decontaminating the environment, is desirable. Environmental control should be performed every 14 days with enilconazole (0.2%) or concentrated chlorine laundry bleach (1:10) solutions.
Treatment is systemic therapy with or without topical treatment. Spot-on treatment products should not be used alone, because they may predispose individuals to chronic subclinical infection. Rather, whole-body shampooing, dipping, or rinsing with topical antifungal agents in conjunction with systemic therapy is preferred. For topical therapy, either enilconazole (0.2% at a dilution of 1:70) or miconazole shampoo (with or without chlorhexidine), once or twice weekly, can be used. Enilconazole is licensed for use as an environmental disinfectant and is used off-label in treatment of dermatophytosis. Systemic therapy is either itraconazole (10 mg/kg/day, PO) or terbinafine (30–40 mg/kg/day, PO) for 4–8 weeks. Lesions may resolve in 2–3 weeks, but antifungal therapy should be continued until two DTM cultures are negative, with a 2-week interval between cultures. Often, dermatophyte infections of the skin require 2–3 months of therapy.
Guinea pigs of all ages require a dietary source of vitamin C. The stability of vitamin C in diets varies with composition of the diet, storage temperature, and humidity. The feed content of vitamin C is reduced by dampness, heat, and light. In fortified diets, approximately half of the initial vitamin C may be oxidized and lost 90 days after the diet has been mixed and stored at temperatures >22°C (71.6°F). Water in an open container may lose up to 50% of its vitamin C content in 24 hours. Aqueous solutions of vitamin C will more rapidly deteriorate in metal, hard water, or heat and are more stable in neutral to alkaline solutions.
Clinical signs of hypovitaminosis C include diarrhea, alopecia, and pain (from joints); animals are thin and unkempt. Petechiae on mucous membranes are not always seen, although hematuria may be present. Guinea pigs will show signs of vitamin C deficiency within 2 weeks if it is not provided. Serum hypercholesterolemia (>60 mg/dL) and hypertriglyceridemia (>30 mg/dL) is seen in vitamin C–deficient guinea pigs after an overnight fast. Guinea pigs need ~10 mg vitamin C/kg body weight daily for maintenance and 30 mg vitamin C/kg body weight daily for pregnancy. Vegetables high in vitamin C include red or green capsicums, tomatoes, spinach, and asparagus.
Metastatic calcification occurs most often in guinea pigs >1 year old. Clinically, animals present with muscle stiffness and failure to thrive. Mineralization may be confined to soft tissues around elbows and ribs. Mineral deposition may also be more widespread, involving lungs, heart, aorta, liver, kidneys, uterus, and sclera. Dietary factors such as a low-magnesium and high-phosphorus diet, and high calcium and/or high vitamin D intake have been implicated. Feeding commercial, high-quality guinea pig diets has reduced the incidence seen in laboratory colonies.
Two other, similar syndromes in guinea pigs affect either the skeletal muscles (muscular dystrophy) or the myocardium and skeletal muscles (muscular degeneration and mineralization). These two conditions are associated with a vitamin E/selenium deficiency. A separate, incidental finding of multifocal mineralization of individual muscle fibers may be seen in major muscles of hindlimbs. Affected animals are often asymptomatic.
Spontaneous diabetes mellitus is common in guinea pigs. The clinical manifestations are mild or variable. Guinea pigs show polydipsia and weight loss while maintaining a good appetite. Hematology and urinalysis show glycosuria, hyperglycemia, and high serum triglyceride levels; ketonemia and ketonuria are not seen. Exogenous insulin is not required for survival.
Multiple cysts are often present on ovaries of females >1 year old. The cysts contain clear, serous fluid and may reach 2–4 cm in diameter. Cysts may be unilateral or bilateral. Clinically, ovarian cysts are associated with reduced reproductive performance, cystic endometrial hyperplasia, mucometra, endometritis, and alopecia. Radiography and ultrasonography should be performed, especially if an abdominal mass is palpable. Diagnosis of the disease by plain radiography is difficult because of the similar opacity of ovarian cysts and abdominal neoplasms. Abdominal ultrasound allows differentiation by imaging the inner structure of the ovarian cyst. Treatment is laparotomy and surgical removal of the ovary and cyst. Differential diagnoses include splenic, uterine, and ovarian tumors.
Although the clinical signs are similar, there are two recognized forms of pregnancy toxemia: the fasting/metabolic form and the toxic form. Both occur in late pregnancy. Affected sows show depression, acidosis, ketosis, proteinuria, ketonuria, and a lowered urinary pH (from ~9 to 5–6).
Metabolic pregnancy toxemia occurs in obese sows, especially females in their first or second pregnancy. The disease is caused by a reduced carbohydrate intake and mobilization of fat as a source of energy. Changes in feeding routine and stress may precipitate the crisis. Clinically, the sow stops eating and is initially depressed, then becomes comatose and usually dies within 5–6 days. Treatment is rarely successful in advanced cases. Aggressive treatment is necessary and involves administration of 5% glucose solution either IV or SC and/or propylene glycol orally, nutritional supplementation, and cesarean section. Sows in late pregnancy can be given water within which a small amount of glucose has been dissolved as a preventive measure.
The circulatory or preeclampsia form of pregnancy toxemia is due to uteroplacental ischemia. The gravid uterus compresses the aorta, resulting in significant reduction of blood flow to the uterine vessels. Placental necrosis, hemorrhage, ketosis, and death follow. If suspected, emergency cesarean section and/or ovariohysterectomy are required to save the sow’s life.
Guinea pigs have a high perinatal mortality. Dystocia and stillbirths are related to large fetuses, subclinical ketosis, and fusion of the symphysis pubis. If females are first bred after 6 months of age, the symphysis pubis often fuses and does not separate during parturition. Many stillbirths are often seen in primiparous females. Pregnancy lasts 59–72 days (average 63 days). If a female strains continually for >20 minutes or young do not appear after 2 hours of intermittent straining, dystocia may be occurring. Careful examination of the cervix is necessary to assess how much separation of the symphysis pubis is present. There should be at least the width of the index finger to permit passage of the fetus. If adequate separation has occurred, oxytocin (1–2 units, IM) can be given. If the fetus is stuck, or parturition does not begin within 15 minutes of giving oxytocin, performing a cesarean section is necessary. The uterus should be opened close to the bifurcation of the horns. The guinea pig has a bicornuate uterus with one cervix.
Spontaneous tumors are relatively uncommon in guinea pigs and are usually seen in animals >3 years old. Trichofolliculoma, a benign tumor of the hair follicle epithelium, is the most common skin tumor of guinea pigs. The tumor presents as a slow-growing, oval mass varying in diameter from 0.5–7 cm and located predominantly in the subcutis of the dorsal lumbar or sacral region, or in the lateral femoral and lateral thoracic area. Males are affected twice as frequently as females. The average age of affected animals is 3 years. Epidermoid cysts arising from hair follicles are often associated with these tumors or may arise independently. Ulcerating tumors and ruptured cysts discharge caseous material. Treatment of trichofolliculomas and epidermoid cysts is surgical excision.
Tumors of the reproductive tract represent 25% of spontaneous tumors in guinea pigs. Most are ovarian and uterine tumors, although mammary adenocarcinoma is seen in both male and female guinea pigs. The prevalence of mammary tumors in males is higher than in other species.
The lethal sensitivity of guinea pigs to antibiotic therapy cannot be overemphasized. Antibiotics reported to cause enterotoxemia are penicillin, ampicillin (amoxicillin), bacitracin, erythromycin, spiramycin, streptomycin, lincomycin, clindamycin, vancomycin, and tetracycline. Topical antibiotics have also caused fatal enterotoxemia. The following therapeutic dosages of antibiotics have been used clinically in guinea pigs (see Table: Antibiotic Dosages for Use in Guinea Pigs).
Trimethoprim-sulfamethoxazole, chloramphenicol, and enrofloxacin can be used in guinea pigs. Narrow-spectrum antibiotics with antibacterial activity against gram-positive bacteria should be avoided; the cause of death is a decreased gram-positive bacterial flora and increased gram-negative flora, with related bacteremia/septicemia. Paradoxically, clostridial overgrowth (Clostridium difficile) has also been identified. C difficile is a pathogenic organism, not normally recoverable from intestinal contents.
Antibiotic Dosages for Use in Guinea Pigs
Treatment for antibiotic toxicity is primarily supportive. The antibiotics should be stopped immediately, fluid therapy (IV or intraosseous) administered, and analgesics provided to prevent abdominal discomfort. High-fiber diets should be syringe-fed to prevent ileus. Cholestyramine (1 g in 10 mL water, three times a day, for 5–10 days), an ion exchange resin, has been used experimentally to bind clostridial toxins in clindamycin-induced enterotoxemia. If the enterotoxemia is severe, the condition is life-threatening and the prognosis guarded.
Urolithiasis is a common problem in older guinea pigs, especially females, because of the proximity of the urethral orifice to the anus and the high risk of infection with fecal contaminants such as E coli. However, it may be seen in guinea pigs of both sexes and all ages. Clinical signs include dysuria, vocalizing when attempting to urinate, and occasionally hematuria. Diagnosis is by abdominal radiology. The calculi are radiopaque and usually composed of calcium carbonate or calcium phosphate; calculi can also be composed of calcium oxalate. Obstructive urolithiasis, hydroureter, hydronephrosis, and possible concurrent septicemia can develop if the problem is not treated.
In addition to sex and age, diet may be related to urolithiasis. Foods high in calcium, eg, alfalfa hay, may result in a high dietary calcium:phosphorus ratio. Urinary ascorbate, if present at a high concentration, increases stone formation in guinea pigs given high-calcium or high-oxalate diets. This may be both beneficial and deleterious, ie, needing to give enough vitamin C to prevent scurvy but not increase stone formation.
Surgical removal of uroliths is standard treatment. However, it is often complicated by severe inflammatory reactions to suture material. Prophylactically, potassium citrate/citric acid can be given to inhibit crystal formation in urine. Citrate is not administered for its urine-acidifying effect as it is in dogs and cats, but because of its ability to bind calcium into water-soluble calcium citrate.
Coronal elongation of the cheek teeth is the most common dental disease of guinea pigs, and it is most commonly caused by inappropriate nutrition (not enough hay or other sources of crude fiber to wear down the crowns). Because of the unique, curved structure of their cheek teeth and associated oblique occlusal plane, diagnosis and treatment of dental disease in guinea pigs is more challenging than in rabbits. Guinea pigs with dental disease present with nonspecific clinical signs, from mild inappetance to anorexia, difficulty chewing and/or swallowing, reduced activity, weight loss, and ptyalism. Diagnosis of dental disease depends on a thorough oral examination, which may need to be performed under sedation/anesthesia. Imaging, either with radiographs or CT, may also be required to fully diagnose the extent of dental disease.
The primary treatment of elongation and malocclusion of cheek teeth in guinea pigs is to reduce crown length, done under general anesthesia. This may require extensive use of an electric burr and also may include removal of maxillary points on the buccal surface (see Dental Malocclusion). Sometimes, extraction of severely diseased and loose cheek teeth may also be necessary. Mandibular overgrowth may become so severe as to cause tongue entrapment, which prevents normal swallowing. For severe or chronic cases, correcting the malocclusion gradually, with multiple procedures performed every 3-4 weeks until normal occlusal surfaces are achieved, may be beneficial or necessary. Treatment of dental disease should always include modification of diet, because soft diets low in crude fiber are usually the inciting cause. Supplemental syringe feeding with Critical Care® should always be added until the patient can eat enough on their own to maintain body condition. Analgesics are also recommended, especially in severe cases when extensive drilling is required or in animals with buccal ulcers from maxillary points.
Alopecia develops to a degree in all guinea pigs in late pregnancy (60–70 days) and during nursing. It results from reduced anabolism of maternal skin associated with fetal growth. Hair loss usually begins on the back and progresses bilaterally on the flanks and ventral abdomen. Nursing guinea pigs may worsen the condition by pulling hair from their mothers. The alopecia resolves slowly either after parturition or when the sow stops nursing.
Thinning hair is common in young animals at weaning. It is associated with a period of transition in which coarse guard hairs of the adult coat are developing and neonatal fur is being lost. Ear chewing and barbering are seen in group-housed guinea pigs that develop a social hierarchy. Often younger animals of lower rank develop hair loss from fur chewing by dominant older members. The hair loss is characterized by an irregular, almost stepwise pattern. Treatment involves separation of the aggressive animal(s).
Single-housed guinea pigs that become bored may inflict self-barbering. In these cases, areas the animal cannot reach such as the head, neck, and anterior shoulders are not affected. Changing the guinea pig’s environment, adding enrichment, and providing large amounts of fresh hay often prevent boredom and stop this vice.
Bilateral, symmetric alopecia may be seen in older females with ovarian cysts. Other differential diagnoses for alopecia are mite infections and dermatophytosis.
Sebaceous glands are abundant along the dorsal surface of guinea pigs and around the anal orifice. The circumanal region contains a large accumulation of sebaceous glands. The sebaceous glands are testosterone dependent, and in adult males, excessive accumulation of sebaceous secretions occurs in the skin around the base of the spine and the folds of the circumanal and genital region. In areas covered by fur, the hair becomes thick, matted, and greasy. These folds can be periodically cleaned with surgical alcohol or a gel hand cleanser to preclude infection and unpleasant smell.
Pet guinea pigs carrying dermatophytes are a zoonotic risk for their owners, especially children, who are often the only affected members of a household. Risk factors for human dermatophytosis are young guinea pigs and recent acquisition of a new guinea pig. When treating ringworm in guinea pigs, environmental treatment should also be recommended to the owners, with special attention given to the bedding and clothing of people in contact with infected or carrier animals. Contagious material may persist in the owner’s clothing and bedding and is a common reason for a pet’s relapse after an initial response.