Parasites of Guinea Pigs

Those who have had intimate contact with guinea pigs understand that they are not just simple caged pets. They have a personality and language all their own. "Popcorning", stretching, nose-touching, squealing, and teeth chattering are just a few behaviors that guinea pigs display that to the astute person is a form of communication. If a trusting relationship is established with a guinea pig, it can be just as rewarding and fulfilling as a relationship with traditional pets such as cats and dogs. However, just like cats and dogs, these small creatures too can be plagued by endo- and ecto-parasites. The trend in guinea pig ownership makes it important for practicing veterinarians to have some knowledge of how to identify and treat these parasites if they should happen to be faced with them. The following includes some common and not so common parasites of guinea pigs. While it is not completely comprehensive of all possible parasites guinea pigs can become infected with, it provides a baseline for where to start.

1. Endoparasites
1.1. Gastrointestinal Tract Parasites
1.1.1. Protozoans
        Eimeria caviae
        Toxoplasma gondii
        Cryptosporidium wrairi
        Balantidium coli
        Giardia
1.1.2. Nematodes
        Paraspidodera uncinata
1.1.3. Trematodes
        Fasciola hepatica
        Fasciola gigantica
1.2. Urinary Tract
1.2.1. Protozoans
        Encephalitozoon cuniculi
        Klossiella cobayae
1.3. Nervous System
1.3.1. Nematodes
        Baylisascaris procyonis
1.4. Respiratory Tract
1.4.1. Nematodes
        Trichinella spiralis

2. Ectoparasites
2.1. Mites
        Chirodiscoides caviae
        Demodex caviae
        Mycoptes musculinus
        Trixacarus caviae
        Sarcoptes scabiei
        Notoedres muris
2.2. Lice
        Gliricola porcelli
        Gyropus ovalis
2.3. Fleas and Ticks
        Ctenocephalides felis
        Nosopsyllus fasciatus
        Dermacentor

1. Endoparasites

1.1. Gastrointestinal Tract Parasites

1.1.1. Protozoans

Eimeria caviae

Etiology and Pathogenesis - Eimeria caviae is a coccidian parasite of the gastrointestinal tract belonging to the subphylum Apicomplexa. The life history includes ingestion of feces containing infective, sporulated oocysts, where sporozoites are released, invade the gastrointestinal epithelium, and become trophozoites enclosed in a parasitophorous vacuole within the host cell. These trophozoites grow in size and become schizonts, which produce first-generation merozoites. These merozoites breakout of their resident cell and invade other surrounding intact epithelial cells to become second-generation merozoites. Completion of schizogony results in a merozoite, which again invades an intact surrounding epithelial cell to become a male or female gametocyte. The gametocytes mature into macrogametes (female) and microgametes (male). The micorgametes breakout of the host cell and search for the macrogametes still enclosed within the host cell. When located, the micorgamete fertilizes the macrogamete to produce a zygote, which eventually forms a wall and becomes an oocyst. The oocyst is passed in the feces (Fig. 1) and sporulates to become an infective oocyst [1].

Figure 1. Eimeria oocyst with typical centrol sporoplasm.

Clinical Signs - Weanlings tend to be susceptible to E. caviae and present with clinical signs of lethargy, anorexia, and pasty diarrhea of 4 to 5 days duration with possible subsequent constipation. The prepatent period is 10 days and an infective oocyst is produced within 48 hours of passage of feces. Necropsy reveals an edematous, congestive, hemorrhagic, thickened proximal colon and cecal wall containing white plaques [2]. The large intestine contains fluid and fetid digesta, which may or may not be mixed with blood [3]. Histology reveals epithelial hyperplasia of the colon, sloughing of enterocytes, edema and congestion of the lamina propria [2], and infiltration of polymorphonuclear and mononuclear cells [3]. The histologic lesions result from the invasive nature of schizogony, which involves destruction of the enterocytes upon the various stages of the organism breaking free from these cells (Fig. 2) [2].

Figure 2. Eimeria caviae in the intestine of a guinea pig.

Diagnosis - The most conventional approach to diagnosing E. caviae is to identify the oocysts through fecal floatation or to identify the organism through mucosal scrapings or histology. Other differential diagnoses for the clinical signs of E. caviae include pantothenic acid or vitamin C deficiency, cryptosporidiosis, bacterial enteropathies, or coronavirus [2].

Treatment and Prevention - Guinea pigs infected with E. caviae show decreased mortality when treated with sulfadimethoxine 25 - 50 mg/kg q 24 h for 10 - 14 days PO [4,8]. Infection can be reduced and/or prevented by reducing stress, maintaining sanitary conditions, and providing a wholesome feed with adequate levels of vitamin C [2].

Toxoplasma gondii

Etiology and Pathogenesis - Toxoplasma gondii is an enteric coccidian parasite of the subphylum Apicomplexa that is capable of infecting guinea pigs. Noninfective oocysts containing a single sporont are passed in the feces of cats (Fig. 3). Infective oocysts develop within 1 to 5 days provided external factors are favorable to the oocyst. This process involves the formation of two sporocysts, both of which contain four sporozoites. Upon ingestion of these infective oocysts, guinea pigs become paratenic hosts in which the parasites grow and divide, but do not undergo development. Sporozoites released from the ruptured oocyst in the intestine invade the enterocytes and mesenteric lymph nodes, multiply, and develop into tachyzoites. Rupture of the enterocytes releases the tachyzoites into systemic circulation where they invade cells and tissues all over the body. Some tachyzoites settle in the brain, striated muscles, and liver and become encysted as bradyzoites. The formation of bradyzoites may be another means of transmission via cannibalism of infected guinea pigs. Cats ingest the paratenic hosts where the sexual phase of the life cycle is completed resulting in the shedding of oocysts in the feces [1].

Figure 3. Oocsyt of Toxoplasma gondii.

A study was performed by Flori et al., in which the possibility of maternofetal transmission of T. gondii infection was demonstrated. The study involved the infection of female guinea pigs with various strains of T. gondii at various days of gestation. One set of female guinea pigs was infected IP with 100 tachyzoites of the RH strain or 100 cysts of the PRU strain. Another set of female guinea pigs was infected orally with 100 cysts of the 76K or PRU strains. This resulted in stillborn or nonviable newborns believed to have suffered from congenital toxoplasmosis while the others were euthanized at 15 days of age. All guinea pig organs were examined for T. gondii using nested and real-time quantitative polymerase chain reaction (PCR). The percentage of maternofetal transmission for RH was 54%, 76K was 86%, and PRU was 84%. These results indicate transplacental transmission of T. gondii in guinea pigs, which can most likely be attributed to the presence of their hemomonochorial placenta [5].

Clinical Signs - Infection of guinea pigs with T. gondii is generally asymptomatic although some animals may develop multifocal hepatitis and pneumonitis [3]. Other clinical signs include vulvar bleeding, abortion, and encephalitis [2]. Cysts develop in the tissues of chronically infective asymptomatic carrier guinea pigs [3].

Diagnosis - Diagnosis includes histology of the brain, striated muscles, and liver. Antibodies to the tachyzoites are generated when they rupture from the enterocytes. These antibodies can be detected using various serological tests [2].

Treatment and Prevention - Guinea pigs infected with T. gondii can be treated with a combination of sulphadiazine and pyrimethamine as a suppressive treatment early in infection [4].

Cryptosporidium wrairi

Etiology and Pathogenesis - Cryptosporidium is another enteric coccidian parasite of the subphylum Apicomplexa that is capable of infecting guinea pigs [1]. The species that commonly infects guinea pigs is C. wrairi, which is found primarily in the small intestine of these animals [6]. The life cycle begins with ingestion of infective oocysts contained within feces (Fig. 4). Four sporozoites are released from the oocysts into the gastrointestinal tract and invade the microvillous border of the distal small intestine [1]. Oocysts enter the microvillous border via phagocytosis by M cells found within Peyer’s patches of the ileum [7]. The sporozoites are contained within a parasitophorous vacuole within these cells where they undergo schizogony, gametogony, fertilization, and sporogony resulting in the release of infective oocysts into the feces [1].

Figure 4. Oocysts of Cryptosporidium in a sugar flotation.

C. wrari differs from other Sporozoa in that it contains vacuoles with membranous lamellae that perform the functions of mitochondria thereby lacking mitochondria altogether. The golgi complex does not resemble those seen in mammalian cells, but does perform the same functions such as protein synthesis. The microgemetes of C. wrairi lack flagella and the merozoites lack subpellicular tubules, both indicating that C. wrairi may be less motile that other coccidians. C. wrairi also differs in that it does not contain microspores within its life cycle, which is believed to be attributed to its ability to obtain nutrients through endocytosis of nutrients within the vacuolated area between the parasite and the host cell rather than through ingestive microspores [19].

Clinical Signs - Clinical signs are most commonly seen in animals less than 300 gm or 16 weeks of age [2,20]. Diarrhea is a common clinical sign, but is of decreased severity in guinea pigs compared to other animals infected with various species of Cryptosporidium due to the presence of a well-developed cecum that is able to counteract the hypersecretory and malabsorptive effects of these organisms through reabsoption [7]. Other clinical signs of C. wrairi may include weight loss, potbellied appearance, rectal prolapse, and death. Grossly, hyperemia of the small intestine and serosal edema of the cecal wall may be observed [20]. Histologically, basophilic, round to oval, 1 - 4 µm, C. wrairi may be observed within or on the intestinal epithelial cells from the duodenum to the cecum [2,20]. Necrosis and sloughing [20] induces the cells on the tips of villi to become flattened and cuboidal. In addition, infiltration of lymphocytes, neutrophils, and eosinophils into the lamina propria, increased crypt depth (cd), decreased villous height (vh) and decreased vh/cd ratio in the ileum and jejunum, and decreased villous height and vh/cd ratio in the duodenum is observed. The presence of necrotizing enteritis in the cecum indicates that C. wrairi infections cause a change in the intestinal bacterial flora similar to the way antibiotics do in guinea pigs [7]. Infected guinea pigs recover within 4 weeks and are resistant to reinfection [8].

Diagnosis - Guinea pigs develop antibody titers to C. wrairi that steadily increases for 2 weeks and lasts for 8 weeks post-infection. Serological tests can be used to detect these antibodies [7]. Mucosal scrapings can help identify the organisms using a phase contrast microscope or stained section. The bodies of these organisms are located in the brush border epithelium and in the anterior ileum and appear basophilic, round to oval, with a diameter of 1 to 4 µm [2]. The organisms can also be identified through fecal samples [8].

Treatment and Prevention - There has been no real successful treatment identified for Cryptosporidium infections of any species. Prevention is the best way to control outbreaks. The oocysts can be destroyed using 5% ammonia solution, freezing to below 0°C, or heating to above 65°C [8].

Balantidium coli

Etiology and Pathogenesis - Balantidium coli is a ciliated protozoan of the subphylum Ciliophora [1]. It is indigenous to the cecum of guinea pigs [2]. In the intestine the organism is of the trophozoite form. It is covered by cilia and contains a peristome, macro- and micro-nuclei, two contractile vacuoles, and many food vacuoles. It reproduces by transverse fission to produce cysts that are passed in the feces (Fig. 5) [1]. B. coli, as it is known in the guinea pig, is normally a nonpathogenic protozoan, however, the trophozoites may become opportunistic when the normal intestinal flora is disrupted by a bacterial enteropathy [2].

Figure 5. Cyst of Balantidium coli.

Diagnosis - B. coli can be identified by its trophozoites from diarrhea in direct fecal smears or by its cysts from normal feces in fecal flotation [1]. The trophozoites may also be identified in intestinal lesions and ingesta [2].

Treatment and Prevention - Opportunism by B. coli can be prevented when treating bacterial infections of guinea pigs by using probiotics such as Bene-bactm Pet Gel (Pet-Ag, Inc., Hampshire, IL).

Giardia

Etiology and Pathogenesis - Giardia is a parasitic mucosoflagellate belonging to the subphylum Sarcomastigophora [1]. Different species of Giardia have been isolated from the intestine of guinea pigs [9,10]. Guinea pigs become infected by eating infective cysts containing two trophozoites in the feces of infected guinea pigs or other domestic animals. In the intestine, the two trophozoites are released and attach to the mucosa of the small intestine via a sucking disc. The trophozoites have a characteristic teardrop shape containing two nuclei within each cell (Fig. 6). They then rapidly multiply on the mucosa of the small intestine and form infective cysts prior to being passed in the feces [1].

Figure 6. Trophozoite of Giardia lamblia.

Clinical Signs - Infection with Giardia may or may not produce diarrhea due to intestinal malabsorption [1]. Histopathology reveals inflammation of the intestine as well as cystic enlargement of the crypts of the duodenum and jejunum [9].

Diagnosis - Giardia can be diagnosed through the identification of trophozoites in direct smears from diarrhea. Cysts can be identified using zinc sulfate with a specific gravity of 1.18. Histopathology of the intestinal mucosa will also reveal infections of Giardia [1].

Treatment and Prevention - Giardia in guinea pigs can be treated with fenbendazole 20 mg/kg q 24 h for 5 days PO or metronidazole 20 - 40 mg/kg q 12 h PO [1,8]. Prevention of infection involves maintaining sanitary food and water reserves. Giardia cysts can be killed with Lysol (2% to 5%), Sterinol (1%), or sodium hypochlorite (1%) [1].

1.1.2. Nematodes

Paraspidodera uncinata

Etiology and Pathogenesis - Paraspidodera unicinata is a heterakoid nematode that inhabits the cecum, but does not become invasive through penetration of the cecal and colonic mucosa. It is capable of infecting both domestic [2] and wild [11] guinea pigs. The life cycle takes approximately 51 to 66 days to complete and eggs become infectious 3 to 5 days prior to passage through the feces [2].

Clinical Signs - Clinical signs associated with P. unicinata infections include weight loss, incapacitation, and diarrhea [2].

Diagnosis - Ellipsoidal eggs of P. uncinata can be identified in fecal samples [2].

Treatment and Prevention - Guinea pigs infected with P. uncinata can be treated by feeding 1 g of phenothiazine per 20 g of molasses guinea pig feed [4]. Inhibiting exposure of healthy guinea pigs to feces from infected guinea pigs and maintaining a sanitary environment is the best way to control infestations [2].

Miscellaneous Nematodes

Other nematodes that have been identified in wild guinea pigs and rarely in domestic guinea pigs include Capillaria hepatica, Graphidioides mazzai, and Trichuris gracilis [11].

1.1.3. Trematodes

Fasciola hepatica and Fasciola gigantica

Etiology and Pathogenesis - Fasciola hepatica and Fasciola gigantica are parasitic trematodes of the liver and bile ducts belonging to the order Digenea. The eggs (Fig. 7) are passed in the feces and upon contact with water a larva, called the miracidium, will develop inside the operculated egg.

Figure 7. Egg of Fasciola.

A fully developed miracidium will emerge from the egg through the operculum within 2 to 4 weeks and searches for a snail host. It enters the snail’s body and becomes a sporocyst within the gonads and digestive gland, the snail equivalent to the liver. The mother sporocyst contains multiple germinal balls, which develop into a redia. Fully developed rediae emerge from the mother sporocyst into the tissue of the snail. The redia also contains germinal balls, which develop into second-generation rediae. The second-generation redia develops into third-generation larvae known as cercariae. Cercariae contain a tail for swimming and emerge from the redia into the snail’s tissues, exit the body, and is deposited into the water. It loses its tail and becomes an infective metacercaria that encysts on vegetation. Upon ingestion of the infected vegetation by a host, the metacercaria becomes a marita and bores its way to the liver and then the bile ducts where it matures into an adult (Fig. 8) and begins laying eggs, which are passed in the host’s feces. The entire life cycle takes approximately 3 to 4 months [1]. Guinea pigs may become infected with F. hepatica [11,12] and F. gigantica [2] when they eat leafy vegetables containing encysted metacercaria.

Figure 8. Adult Fasciola hepatica.

Clinical Signs - Acute fluke disease is caused by maritas boring their way through the liver parenchyma and an associated inflammatory reaction (Fig. 9). Clinical signs of acute fluke disease include abdominal pain, debilitation, and death. Necropsy reveals blood-tinged exudate in the abdominal cavity, hepatomegaly, and a liver covered with fibrin and filled with maritas. Chronic fluke disease results from the presence of adult flukes in the bile ducts. Clinical signs associated with chronic fluke disease include loss of body condition, weakness, anorexia, hypoproteinemia leading to edema, and death. Necropsy reveals thickened bile ducts filled adult flukes [1].

Figure 9. Necropsy of rabbit with marita’s in the liver.

Diagnosis - A diagnosis of infection with F. hepatica and F. gigantica includes identification of eggs in the feces, maritas in the liver, and adult flukes in the bile duct.

Treatment and Prevention - Treatment includes administration of albendazole or clorsulon (Curatrem) [1]. Infections of guinea pigs can be prevented by thoroughly washing vegetables before providing them.

1.2. Urinary Tract Parasites

1.2.1. Protozoans

Encephalitozoon cuniculi

Etiology and Pathogenesis - Encephalitozoon cuniculi is an intracellular microsporidian [12], which recently has been classified as a fungus rather than a parasite [1]. Infective spores can be transmitted through inhalation or ingestion of urine, through possible transplacental transmission [2], or carnivorism. Spores are distributed to target tissues via the systemic circulation by an unknown mechanism. Sporoplasm is incorporated into the host cell cyctoplasm via a polar filament. Sporogony and merogony occur in vacuoles within the cytoplasm of endothelial cells, peritoneal macrophages, oligodendrocytes, and renal tubular epithelial cells. The infected host cell degenerates thereby releasing mature spores, which can then infect other viable neighboring cells. The life cycle is completed when spores released from degenerated renal tubular epithelial cells are voided in the urine [12].

Clinical Signs - There are no known clinical signs of E. cuniculi infection in guinea pigs [2]. This exacerbates transmission because infected guinea pigs will continue to be used in breeding programs. Gross lesions are also relatively uncommon in guinea pigs, but may include renal lesions consisting of multiple, 2 to 4 mm, grey to white cortical foci that are flat or indented. Histologic examination involves mainly the kidney and brain. Renal lesions include granulomatous interstitial infiltrate with fibrosis and tubular epithelial repair due to the invasion of merozoites and sporozoites in the renal tubular epithelial cells. Lesions within the brain may include multifocal necrosis, granulomas with perivascular lymphoplasmacytic cuffs, or lymphocytic meningitis [12].

Diagnosis - E. cuniculi spores can be identified in lesions within the kidney and the brain (Fig. 10). Spores appear gram positive when stained with Goodpasteur carbol fuschin and are birefringent and emit an apple-green color when viewed under polarized light. These two criteria help distinguish E. cuniculi infections from other granulomatous encephalitis inducing organisms such as Listeria monocytogenesand Toxoplasma gondii. Serologic tests to detect antibodies include indirect ELISA, indirect fluorescent antibody, and India-ink immunoreaction assay [12].

Figure 10. Encephalitozoon in kidney tubules.

Treatment and Prevention - There is no known drug treatment for E. cuniculi infection. Screening using serological tests and subsequent culling of seropositive animals is the key to eradicating this disease within colonies of guinea pigs. Only confirmed seronegative guinea pigs should be purchased. Proper sanitation should be maintained using quaternary ammonium solutions, oxidizing compounds, and amphoteric surfactants to kill infective spores. Cesarean section and foster rearing practices can be used to block transmission from dam to neonates [12].

Klossiella cobayae

Etiology and Pathogenesis - Klossiella cobayae is a coccidian parasite [1] of the guinea pig kidney [2] belonging to the subphylum Apicomplexa. The life cycle of these parasites is not very well defined [1]. Sporozoites are released into the gut upon ingestion of oocysts in urine and find their way to the kidney via the systemic circulation. The sporozoites become first generation schizonts, containing 8 to 12 merozoites, having a predilection for the endothelial cells of the glomerulus. These schizonts may also enter the cells of the proximal convoluted tubule through the systemic circulation or by rupture of the endothelial cells of the glomerulus where they become second generation schizonts containing as many as 100 merozoites. Gametogony and sporogony take place in the cells of the Loop of Henle producing oocysts that are passed in the urine [2].

Clinical Signs - Clinical or gross signs are generally not associated with infections by K. cobayae. Occasionally the kidney surface may appear mottled due to enlargement of the glomerular endothelial cells. Histology reveals the organism in different cells of the kidney and infiltration of inflammatory cells (Fig. 11) [2].

Figure 11. Klossiella cobayae in the kidney of a guinea pig.

Diagnosis -  K. cobayae infections are confirmed by identification of the various asexual and sexual stages in histologic sections of the kidney [1].

Treatment and Prevention - Prevention of infection includes maintaining proper sanitation and preventing the exposure of healthy guinea pigs to the urine of infected guinea pigs [2].

1.3. Nervous System Parasites

1.3.1. Nematodes

Baylisascaris procyonis

Etiology and Pathogenesis - Baylisascaris procyonis is a parasitic worm belonging to the order Ascaridida that normal infects raccoons in North America. It is has been known to cause visceral larva migrans in numerous hosts including guinea pigs. Characteristics of the worm include their ability to continue to grow as they migrate and a tendency to invade the central nervous system of intermediate hosts. The ability to grow within the brain renders these worms very pathogenic leading to death with only 1 to 3 worms [1]. Larvae also produce enzymes and toxic waste products during migrations, which may lead to destruction of surrounding tissue. Guinea pigs become infected by exposure to husbandry items such as feed, water, or bedding contaminated by raccoon feces [13].

Clinical Signs - A research facility reported guinea pigs infected with B. procyonis exhibiting signs of progressive neurologic disease including lethargy, head tilt, and ataxia. The signs progressed to anorexia, stupor, hyperexcitability, lateral recumbency, inability to rise, and opisthotonos. Gross necropsy lesions included thin animals with very little ingesta in the gastrointestinal tract. Histologic lesions involved the white matter of the cerebral peduncles and folia, midbrain, hypothalamus, and cerebrum. Lesions included eosinophilic granulomatous inflammation, multifocal neutrophilic infiltrates, perivascular lymphoid cuffing, and malacia. Larvae were observed in areas of lesions and in healthy tissue of the brain (Fig. 12). Histology of the intestine revealed uninucleate low columnar cells, thin microvillous border, cytoplasmic granules. Eosinophilic granulomatous inflammation and larvae induced granulomas were observed in the lungs [13].

Figure 12. Baylisascaris procyonis larva in tissue section.

Diagnosis - B. procyonis infections are confirmed by identification of larvae in histologic sections or brain homogenates and accompanying clinical signs [13].

Treatment and Prevention - Prevention of B. procyonis infections involves securing food and bedding supplies from raccoons. The eggs are resistant to sodium hypochlorite and quarternary ammonium solutions, but are heat-sensitive. Therefore, all items capable of withstanding high temperatures such as bedding and cages should be autoclaved [13].

1.4. Respiratory Parasites

1.4.1. Nematodes

Trichinella spiralis

Etiology and Pathogenesis - Trichinella spiralis is a parasitic nematode of the order Enoplida that is capable of infecting guinea pigs. Transmission occurs through the ingestion of meat from infected hosts that contain encysted larvae. First-stage larvae are released from the cysts of the muscle within the digestive tract and invade the mucosa. Sexual maturity is reached 2 days post infection, copulation occurs, the males die, and the females lay prelarvae 5 days post infection. The prelarvae enter the bloodstream via the lymphatics where they are transported to the skeletal muscle. They develop into first-stage larvae within 2 to 3 weeks and encyst as spirals within the muscle [1].

Clinical Signs - Within the bloodstream, migrating prelarvae pass through the lung microvasculature on their way to the skeletal muscle (Fig. 13 and Fig. 14). The lungs respond to this passage in various ways in guinea pigs. Histologically, primary infection by T. spiralis in the lungs results in infiltration of inflammatory cells such as lymphocytes, macrophages, neutrophils, and eosinophils.

Figure 13. Trichinella spiralis larva in histological section of skeletal muscle.

Figure 14. Trichinella spiralis larva in pressed skeletal muscle.

Secondary infection by T. spiralis results in even greater numbers of lymphocytes and eosinophils. However, despite the fact that these inflammatory cells infiltrate the site of infection within the lungs, a very limited effector response results. Only primary infection initiates the production of the superoxide anion from alveolar macrophages. Infection does not result in increased levels of lung phospholipid peroxidation markers indicating that lung damage is not resulting from the production of inflammatory mediators. Inducible nitric oxide synthase is expressed by macrophages, but nitric acid is not produced. It is possible that the prelarvae of T. spiralis interfere with the production of inflammatory mediators by macrophages thereby protecting and prolonging their stay within the guinea pig [14].

Diagnosis - Infection of T. spiralis can be confirmed by histologic identification of prelarvae in the blood or lungs and first-stage larvae encysted in the skeletal muscle [1].

Treatment and Prevention - T. spiralis can be treated with albendazole [1].

2. Ectoparasites

2.1. Mites

Demodex caviae

Etiology and Pathogenesis - Demodex caviae belongs to the suborder Prostigmata. Physical characteristics of this mite include a wormlike shape with short, stubby legs (Fig. 15). They are commonly located in hair follicles and sebaceous glands [1].

Figure 15. Demodex.

Clinical Signs - The presence of D. caviae in guinea pigs does not necessarily result in clinical signs [2]. Clinical signs observed in other domestic animals that may be seen in guinea pigs include alopecia and erythema with or without pruritus [1].

Diagnosis - D. caviae is diagnosed through skin biopsy [15]. For deep burrowing mites such as D. caviae, a scalpel blade can be dipped in mineral oil or glycerin and used to abrade a pinch of skin until blood is observed. The material on the scalpel from the scraping is then applied to a microscope slide and observed for the presence of the mites [1].

Treatment and Prevention - Ivermectin (0.3 - 0.5 mg/kg PO / SQ repeat in 8 to 10 days) is used to treat guinea pigs with D. caviae [8]. Prevention of infestation includes the use of autoclaved, laboratory grade bedding, which should be changed regularly. The cage and other areas where guinea pigs play should be cleaned and rinsed thoroughly with a diluted bleach solution [15].

Chirodiscoides caviae

Etiology and Pathogenesis - Chirodiscoides caviae are hair-clasping mites of guinea pigs belonging to the suborder Astigmata (Fig. 16). Physical features of these mites include one or more pairs of legs, which are flattened, bowed, and modified for hair clasping [1]. These mites remain on the hair shafts and do not burrow into the skin [8]. Transmission is through direct contact with infested cage material such as bedding, from sow to weanling during feeding, and through animal to animal contact, which can include contact with an infested carcass [2].

Figure 16. Chirodiscoides caviae.

Clinical Signs - Infestation with C. caviae is usually asymptomatic, however, heavy infestations cause pruritus and alopecia [2,4]. These mites commonly infest the hindquarters including the perineal and hip areas [2,8].

Diagnosis - Diagnosis of C. caviae involves skin scrapings, skin biopsy, or examination of the hair shafts [2,15].

Treatment and Prevention - C. caviae is treated with dusting of the guinea pig and bedding with carbaryl (5%) powder lightly once per week. Ivermectin (0.3 - 0.5 mg/kg PO / SQ repeat in 8 to 10 per days) can also be used to treat guinea pigs [8]. Prevention of infestation includes the use of autoclaved, laboratory grade bedding, which should be changed regularly. The cage and other areas where guinea pigs play should be cleaned and rinsed thoroughly with a diluted bleach solution [15].

Myocoptes musculinus

Etiology and Pathogenesis - Myocoptes musculinus is another hair-clasping mite belonging to the suborder Astigmata [1] that is capable of infesting guinea pigs (Fig. 17 and Fig. 18) [2]. The third pair of legs belonging to the male and the third and fourth pair of legs belonging to the female are modified for hair-clasping [1]. These mites remain on the hair shafts and do not burrow into the skin [8]. Transmission is through direct contact with infested cage material such as bedding, from sow to weanling during feeding, and through animal to animal contact, which can include contact with an infested carcass [2].

Figure 17. Male of Myocoptes musculinus.

Figure 18. Female of Myocoptes musculinus.

Clinical Signs - Infestation with M. musculinus usually causes a pruritic dermatitis [2].

Diagnosis - Diagnosis of M. musculinus involves skin scrapings, skin biopsy, or examination of the hair shafts [2,15].

Treatment - M. musculinus can be treated by dusting of the guinea pig and bedding with carbaryl (5%) powder lightly once per week. Ivermectin (0.3 - 0.5 mg/kg PO / SQ repeat in 8 to 10 per days) can also be used to treat guinea pigs [8]. Prevention of infestation includes the use of autoclaved, laboratory grade bedding, which should be changed regularly. The cage and other areas where guinea pigs play should be cleaned and rinsed thoroughly with a diluted bleach solution [15].

Trixacarus caviae

Etiology and Pathogenesis - Trixacarus caviae is a highly pathogenic sarcoptid mite of guinea pigs belonging to the order Astigmata [1]. Transmission of this mite is through direct contact with infested cage material such as bedding, from sow to weanling during feeding, and through animal to animal contact, which can include contact with an infested carcass [2]. Newborns can acquire the mite and exhibit clinical signs such as scratching within 72 hours after birth and erythema within 3 to 4 weeks after birth in comparison to the development of clinical signs within 10 to 50 days in mature guinea pigs. T. caviae tends to be confused with other sarcoptid members such as Sarcoptes scabiei and Notoedres cati. Characteristics that differentiate T. caviae from these other species include a smaller female compared to S. scabiei, the anus is on the dorsal surface in the male and on the ventral surface in the female of T. caviae compared to dorsal positioning in both sexes of N. cati and ventral positioning in both sexes of S. scabiei, and T. caviae have simple setae and sharp dorsal spines while S. scabiei contains dorsal cones and spines. Guinea pigs can be carriers of T. caviae and upon stressors such as transport or pregnancy a suppressed immune system can lead to clinical infection [16].

Clinical Signs - Commonly infected areas of the guinea pig infested with T. caviae include the trunk, inner thighs, neck, and shoulders [2]. The hair can be easily removed exposing dry to oily skin with yellow scale and crusts that may be up to 10 cm thick [2,16,17]. The intense pruritus may cause alopecia, self-inflicted wounds, vocalization, infertility, abortion, seizures, and even death [1,2,17]. Histopathology of the skin reveals eosinophilic and lymphocytic infiltration, microabscesses, epidermal hyperplasia, dermal inflammation and spongiosis, and necrosis [2,16]. Necropsy reveals, in addition to skin lesions, wasting, pale liver, and secondary bacterial infection lesions of the skin. Complete blood count reveals leukocytosis including a basophilia [2].

Diagnosis - T. caviae infestation can be identified using skin scrapings dissolved and filtered in 10% potassium hydroxide [2,16] where eggs, fecal material, intermediate stages, and adult mites can be observed within short tunnels in the stratum corneum [17].

Treatment and Prevention - T. caviae infestations can be treated with 2.5% lime sulfur solution apply once per week for 4 to 6 weeks [8]. Ivermectin (0.3 - 0.5 mg/kg PO / SQ repeat in 8 to 10 per days) can also be used to treat guinea pigs [2], however, care should be taken due to reports of ivermectin resistance [17]. Guinea pigs can also be bathed in a medicated shampoo to remove the crusty lesions [2]. One report indicates that spray fipronil can be used to treat T. caviae [18]. Prevention of infestation includes the use of autoclaved, laboratory grade bedding, which should be changed regularly. The cage and other areas where guinea pigs play should be cleaned and rinsed thoroughly with a diluted bleach solution [15].

Sarcoptes scabiei and Notoedres muris

Etiology and Pathogenesis - Sarcoptes scabiei and Notoedres muris are both sarcoptid mites belonging to the suborder Astigmata (Fig. 19) [1]. Being that both these mites and other mites in the same suborder look similar, the most important physical feature to help differentiate these mites includes the ventral surface position of the anus in S. scabiei and the dorsal surface position of the anus in N. muris [16]. The female S. scabiei burrows through the epidermis producing tunnels filled with eggs and feces. The pretarsus of S. scabieiand N. muris has a long unsegmented stalk, also known as the pedicel [1].

Figure 19. Female Sarcoptes scabiei.

Clinical Signs - Lesions caused by S. scabiei that occur in other domestic species that are probably consistent in guinea pigs include follicular papules, erythema, crusts, excoriations from self-mutilation, hyperkeratosis, and exfoliation of the epidermis. Clinical signs associated with N. muris infestation is most likely also applicable to guinea pigs include alopecia, hyperkeratosis, pruritus, crusts, lesions from self-mutilation, epidermal hypertrophy, and secondary bacterial infection [1].

Diagnosis - Diagnosis of S. scabiei or N. muris involves skin scrapings, skin biopsy, or examination of the hair shafts [2]. For deep burrowing mites such as S. scabiei, a scalpel blade can be dipped in mineral oil or glycerin and used to abrade a pinch of skin until blood is observed. The material on the scalpel from the scraping is then applied to a microscope slide and observed for the presence of the mites [1].

Treatment and Prevention - Ivermectin (0.3 - 0.5 mg/kg PO / SQ repeat in 8 to 10 per days) can also be used to treat guinea pigs with S. scabiei and N. muris infestations [1,2]. Prevention of infestation includes the use of autoclaved, laboratory grade bedding, which should be changed regularly. The cage and other areas where guinea pigs play should be cleaned and rinsed thoroughly with a diluted bleach solution [15].

2.2. Lice

Gliricola porcelli and Gyropus ovalis

Etiology and Pathogenesis - Gliricola porcelli (Fig. 20 and Fig. 21) and Gyropus ovalis (Fig. 22) are chewing lice belonging to the order Mallophaga and suborder Amblycera. Characteristics of Amblycerans include club-shaped antennae positioned within grooves in the head, four-segmented maxillary palpi, stout mandibles on the ventral side of their heads, and broad heads.

Figure 20. Gliricola porcelli female.

Figure 21. Gliricola porcelli male.

Figure 22. Gyropus ovalis male.

Both species tear pieces of skin until blood pools and feed from these pools [1]. The head and body of G. porcelli is slightly smaller than that of G. ovalis. Guinea pigs acquire these lice through direct contact with other infested guinea pigs or their bedding [2].

Clinical Signs - Clinical signs associated with infestations with G. porcelli or G. ovalis include pruritus, alopecia, and scabbing along the ears and neck (Fig. 23 and Fig. 24) [2].

Figure 23. Gliricola porcelli on a guinea pig.

Figure 24. Gyropus ovalis on a guinea pig.

Diagnosis - G. porcelli or G. ovalis infestations can be diagnosed by observing skin scrapings or hair shafts for adults and eggs. Cooling of the guinea pig body causes the lice to migrate and crawl along the hair shafts [2].

Treatment and Prevention - Treatment of G. porcelli or G. ovalis involves dusting of the guinea pig and bedding with carbaryl (5%) powder lightly once per week, dipping in 2.5% lime sulphur solution once per weeks for 4 to 6 weeks [8], or ivermectin (0.3 - 0.5 mg/kg SQ / SQ repeat 8 to 10 days) [2,8]. Prevention of infestation includes the use of autoclaved, laboratory grade bedding, which should be changed regularly. The cage and other areas where guinea pigs play should be cleaned and rinsed thoroughly with a diluted bleach solution [15].

2.3. Fleas and Ticks

It has been reported that guinea pigs rarely become infested with the cat flea (Fig. 25), Ctenocephalides felis, the northern rat flea, Nosopsyllus fasciatus, and ticks of the genus Dermacentor [2].

Figure 25. Ctenocephalides on a guinea pig.