Guinea pigs, like chinchillas, are hystricognath rodents. They belong to the family Cavidae containing 14 species of animals commonly known as cavies and Patagonian hares (or maras). Four digits on the forepaw and 3 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. Several researchers have analyzed guinea pig calls and distinguish 7–11 distinct sound patterns.
In South America, wild cavies inhabit rocky areas, savannas, forest edges, and swamps from Columbia and Venezuela south-ward to Brazil and northern Argentina. They live in groups of up to 10 individuals and inhabit burrows. 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 and was 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 as 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.
Lymphocytes are the predominant WBC in guinea pigs and comprise 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 occur 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 the unusual reproductive physiology characteristic of hystricomorph rodents. Female guinea pigs (sows) have a pregnancy of 68 days (range 59–72 days) and an average estrous cycle length of 17 days (range 13–25 days). They have a vaginal closure membrane that 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 are born fully furred and 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 around 3 mo and females at 2 mo. Guinea pigs live 6–8 yr.
As a species, guinea pigs are adaptable to a range of climates, but 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 after any significant change in their location, feed, or husbandry. The effect of environmental changes on guinea pigs is minimized when 2 animals are kept together. If a sick guinea pig must be kept in hospital, housing a cagemate with the sick animal reduces stress.
Socially, guinea pigs live in family units centered around a dominant male. Mature males, and especially strangers, will fight. Aggression is generally not encountered if 2 males are brought up together from a young age or if a group of guinea pigs is made up of only nonbreeding females. Social problems are diminished with castration and ovariohysterectomy, but learned behavior in adult males may still make them antisocial after castration.
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. However, they are generally good eaters.
Guinea pigs produce 2 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. When food is limited, however, 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. Ears should be examined for discharges or inflammation and eyes for discharges or conjunctivitis. The submandibular area should be examined for swellings.
Guinea pigs lack obviously accessible peripheral veins. The lateral saphenous vein and the cephalic vein are useful for drawing small amounts of blood. For large amounts of blood, the anterior vena cava can be used with the guinea pig under anesthesia. This technique requires practice. If performed incorrectly, there is a risk of death associated with intrathoracic, pericardial, or pulmonary hemorrhage.
Guinea pigs are highly sensitive to many common antibiotics, so they should be used cautiously when treating infectious diseases (see Rodents: Geriatric Disorders). Streptococcus equi zooepidemicus (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. The primary clinical sign is a large, unilateral swelling in the neck. The affected animal is often in good flesh and shows no other signs of disease. Treatment is surgical removal of the affected lymph nodes and chloramphenicol (50 mg/kg, PO, bid for 14 days). The differential diagnosis should always include cavian leukemia. Streptococcus has a narrow antibiotic sensitivity to many antimicrobials known to cause antibiotic-associated dysbacteriosis (eg, ampicillin, amoxicillin, and erythromycin). Streptococci are generally sensitive to chloramphenicol, which can be given systemically to guinea pigs.
S pneumoniae may be carried in the nares as an inapparent infection. Predisposing factors for 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 include 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 radio-density of the affected tympanic bulla may be seen on radiographs. Because of limited antimicrobial sensitivity, chloramphenicol (50 mg/kg, PO, bid) is the recommended treatment. A major differential diagnosis for streptococcal pneumonia is Bordetella bronchiseptica infection.
Rabbits may harbor B bronchiseptica in their respiratory tracts without developing disease. However, this organism is highly pathogenic in guinea pigs and causes pneumonia, conjunctivitis, otitis media, abortions, and stillbirths. The clinical signs include anorexia, inappetence, nasal and ocular discharge, dyspnea, and often sudden death (this can also happen with S pneumoniae and S equi zooepidemicus infection). The history should include whether rabbits and guinea pigs are kept together as pets. Separate housing or keeping only one species should be recommended. Treatment is ciprofloxacin (10–20 mg/kg, bid).
Salmonella infections were formerly common in guinea pigs, especially in research colonies. With present standards of husbandry, rodent control, and good quality feed, the disease rarely occurs. It is most likely to be seen when groups of guinea pigs are kept outside, and wild rodents have access to their pelleted feed. All ages of guinea pigs are susceptible, but disease is more often observed in younger 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, intermittent shedding of organisms may occur. Diagnosis is accomplished by isolating the organism from blood, ocular secretions, lymph nodes, or spleen. Due to zoonotic considerations and the potential for a carrier state, treatment is not recommended.
Chronic dermatitis (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 cause and probably enters the foot through a skin wound. Awns and straw in the bedding can also cause foot punctures. The inflammation can progress to osteoarthritis and systemic amyloidosis secondary to chronic staphylococcal infection. Surgical treatment is often unsuccessful as there is rarely an abscess to be excised or drained but rather a diffuse cellulitis that infiltrates surrounding tissue; cutting the tissue only results in severe bleeding. Treatment involves removing the affected guinea pig to a clean cage with dry, soft bedding and topical or parenteral administration of antibiotics. Unfortunately, the condition rarely responds 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 animals 4–8 wk of age. 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, yellowish 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 diagnosis. The most sensitive and reliable method of diagnosis is PCR testing. Antichlamydial therapy with tetracycline is the treatment of choice and usually results in complete recovery. Guinea pigs develop short-lived immunity to C caviae infection.
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 disease. Serologic surveys indicate that guinea pigs develop antibodies to pathogenic viruses of mice and rats but do not develop disease.
Mange, caused by the sarcoptid mite Trixacarus caviae is a common disease. The clinical signs are dramatic: intense pruritus, widespread alopecia, and hyperkeratosis. Transmission of T caviae occurs through direct animal-to-animal contact, from sow to weanlings during feeding, and through contact with infested cage material such as bedding. The ectoparasite may be capable of existing subclinically, becoming active with stressors (eg, shipping, 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 can be controlled by diazepam (1–2 mg/kg, IM, as needed). The presumptive diagnosis should be confirmed with several skin scrapings, which usually reveal a massive T caviae infestation. Treatment options include ivermectin (200 μg/kg repeated at 10- to 14-day intervals or 300 μg/kg, SC, repeated 3 times at 3-day intervals) or spot-on dermal treatments with a topical solution of 10% imidacloprid and 1% moxidectin (every 30 days for 3 applications). The guinea pig should also have a whole body washing with fipronil.
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 (12 mg/kg) administered twice at 2-wk 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 is associated with Trichophyton mentagrophytes mentagrophytes. Lesions typically begin as broken hairs and circular, scaly alopecia initially occurring at the tip of the nose, which spread 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 and represents an important potential zoonosis. Historically, guinea pigs have been an important cause of ringworm in humans.
Metabolic and Nutritional Disorders
Guinea pigs of all ages depend on 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, ~½ of the initial vitamin C may be oxidized and lost 90 days after the diet has been mixed and stored above 22°C. Water in an open container may lose up to 50% of its vitamin C in 24 hr. Aqueous solutions of vitamin C deteriorate more rapidly in metal, hard water, or heat and are more stable in neutral to alkaline solutions.
Clinical signs of hypovitaminosis C include diarrhea, alopecia, joint pain, and a thin, unkempt appearance. Petechiae on mucous membranes are not always seen, although hematuria may be present. Guinea pigs show signs of vitamin C deficiency within 2 wk if it is withheld. Serum hypercholesterolemia (>60 mg/dL) and hypertriglyceridemia (>30 mg/dL) are observed in vitamin C-deficient guinea pigs after an overnight fast. Guinea pigs need ~10 mg vitamin C/kg body wt daily for maintenance and 30 mg vitamin C/kg body wt daily during pregnancy. Vegetables high in vitamin C include red or green peppers, tomatoes, spinach, and asparagus.
Metastatic calcification occurs most often in guinea pigs >1 yr old. Clinically, animals present with muscle stiffness and failure to thrive. Mineralization may be confined to soft tissues around elbows and ribs or may be more widespread, involving the lungs, heart, aorta, liver, kidneys, uterus, and sclera. Dietary factors such as 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.
There are 2 other, similar syndromes in guinea pigs that affect either the skeletal muscles (muscular dystrophy) or the myocardium and skeletal muscles (muscular degeneration and mineralization). These two conditions are associated with 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 elevated serum triglycerides; ketonemia and ketonuria are not seen. Exogenous insulin is not required for survival.
Multiple cysts are often present on ovaries of females >1 yr old. The cysts contain clear, serious 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 there is a palpable abdominal mass. 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 2 recognized forms of pregnancy toxemia: the fasting/metabolic form and the toxic or circulatory 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 the 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 in 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 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 mo of age, the symphysis pubis has often fused and does not separate during parturition. High rates of stillbirths are often seen in primiparous females. If a female strains continually for >20 min or fails to produce young after 2 hr 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 min 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 1 cervix.
The most common skin tumor of guinea pigs is trichofolliculoma, a benign tumor of the hair follicle epithelium. The tumor presents as a slow-growing, oval mass 0.5–7.0 cm in diameter. Trichofolliculomas are located predominantly in the subcutis of the dorsal lumbar or sacral region or the lateral femoral and thoracic area. Males are affected twice as frequently as females. The average age of affected animals is 3 yr. 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. The majority are ovarian and uterine tumors, although mammary adenocarcinoma occurs in both male and female guinea pigs.
Miscellaneous and Geriatric Disorders
Guinea pigs are highly sensitive to many antibiotics. Antibiotics reported to cause enterotoxemia include penicillin, ampicillin (amoxicillin), bacitracin, erythromycin, spiramycin, streptomycin, lincomycin, clindamycin, vancomycin, and tetracycline. Topical antibiotics have also caused fatal enterotoxemia. Safe therapeutic doses for guinea pigs are available, however (see Rodents: Antibiotic Dosages for Use in Guinea Pigs).
In general, narrow-spectrum antibiotics with antibacterial activity against gram-positive bacteria should be avoided. The cause of death is a decrease in intestinal gram-positive bacteria and an increase in gram-negative bacteria, leading to bacteremia or septicemia. Paradoxically, clostridial overgrowth (Clostridium difficile) has also been identified. C difficile is a pathogenic organism, not normally recoverable from intestinal contents.
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 like Escherichia coli. However, it may be seen in guinea pigs of both sexes and all ages. Clinical signs include dysuria, crying when attempting to urinate, and occasionally hematuria. Diagnosis is by abdominal radiology. The calculi are radio-opaque and usually composed of calcium carbonate or calcium phosphate; calculi can also be composed of calcium oxalate. Obstructive urolithiasis and possible concurrent septicemia can develop if the problem is not treated.
In addition to sex and age, diet may contribute to urolithiasis. Too much alfalfa hay may lead to a high Ca:P ratio in the diet. Urinary ascorbate, if present at a high concentration, increases stone formation in guinea pigs given high-calcium or high-oxalate diets.
Surgical removal is the standard treatment. However, it is often complicated by excessive inflammatory reactions to suture material. Prophylactically, potassium citrate/citric acid can be given as an inhibitor of 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.
The clinical signs and treatment for malocclusion in the guinea pig are almost identical to those in the rabbit, except premolar teeth are more commonly affected (see Rabbits: Dental Malocclusion).
Alopecia develops to a degree in all guinea pigs in late pregnancy (60–70 days) and during nursing. It is due to 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 after parturition or when the sow stops nursing.
Thinning of hair is common in young animals at weaning. It is associated with a period of transition during 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 self-barber. 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 and providing large amounts of fresh hay often prevent boredom and stop the problem.
Bilateral, symmetric alopecia may be seen in older females with ovarian cysts. Other differential diagnoses for alopecia include mite infections and ringworm.
Sebaceous glands are abundant along the dorsal surface of guinea pigs and around the anal orifice. 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 must be periodically cleaned to preclude infections and unpleasant smell. The secretions can be removed with surgical alcohol or a gel hand cleanser.
Last full review/revision July 2011 by Thomas M. Donnelly, BVSc, DACLAM