(“coccidia”; formerly Isospora spp.) Species of veterinary importance include Cystoisospora canis, C. ohioensis, C. neorivolta, and C. burrowsi in dogs, and C. felis and C. rivolta in cats; these species are not zoonotic.
Host range: Dogs and cats serve as definitive hosts. A wide range of mammalian paratenic hots (mice, rats, cows, etc.) can carry an encysted form of this parasite that is infective for the cat or dog upon consumption.
Geographic range: Csytoisospora spp. are found worldwide where dogs and cats are present.
Life cycle: Dogs and cats are infected by ingestion of sporulated oocysts or encysted stages in paratenic host tissues. Sporozoites that are released from oocysts invade intestinal epithelial cells where they develop through several asexual and sexual stages. Oocysts are released in feces and undergo sporulation in the environment.
Diagnosis: Oocysts can be observed by microscopy after fecal flotation. Clinical disease is more frequent in young animals housed in stressful and/or crowded environments.
Management: Cats usually eliminate infection naturally without treatment. Trimethoprim-sulfonamide or toltrazuril is recommended for clinically affected cats. In kennels, prophylaxis (amprolium) and sanitation must be prioritized. In severe cases, sulfonamides or toltrazuril coupled with supportive fluid therapy should be used as treatment of choice. Consumption of raw meat should be avoided.
T. gondii is the causative agent of toxoplasmosis and one of the most important zoonotic parasites.
Host range: Cats are the only definitive host.
However, T. gondii is capable of infecting a broad range of warm-blooded paratenic hosts (humans, livestock, companion animals and wildlife).
Geographic distribution: Worldwide.
Life cycle: Transmission occurs by three routes: (1) Ingesting meat from a paratenic host carrying bradyzoite tissue cysts, (2) Ingesting sporulated oocysts (fecal-oral), and (3) transplacental and transmammary transmission. Asexual and sexual development occurs in the intestine, and oocysts are shed in the feces, sporulating in 1-5 days. Infected cats shed oocysts for just 1-2 weeks, which minimizes the risk of direct zoonotic transmission from cats. However, millions of oocysts are produced during this period, resulting in significant environmental contamination. Extraintestinal replication of T. gondii can lead to disseminated toxoplasmosis in dogs and sometimes cats.
Diagnosis: Oocysts can be observed by microscopy after fecal flotation. Antibody assays are useful to detect current and past exposure to T. gondii in cats, but most cats are seronegative at the time of oocyst shedding. Cats with intestinal infection are typically asymptomatic.
Management: There is no approved treatment for toxoplasmosis in cats or dogs. Several medications including clindamycin hydrochloride, pyrimethamine and trimethoprim-sulfonamide can be used in cases of disseminated toxoplasmosis. Prevention protocols should emphasize avoidance of hunting by cats, elimination of raw or undercooked meat or viscera from the diet, and daily cleaning of litterboxes to remove oocysts before they have a chance to fully sporulate.
Species of interest include Sarcocystis cruzi, S. tenella, S. wenzeli, S. camelicanis and S. neurona in dogs and at least 11 named species in cats.
Host range: A variety of vertebrate animals serve as intermediate or definitive hosts for Sarcocystis spp., with specific predator/prey (definitive host/intermediate host) pairings identified for each species.
Geographic range: Worldwide. Especially common in areas where livestock is raised or where companion animals have contact with wildlife.
Life cycle: Cats and dogs are infected by ingesting tissue cysts (sarcocysts) in intermediate host tissues. Sexual replication occurs in the intestine and infective sporocysts are shed in the feces. Sporocysts ingested by intermediate hosts release sporozoites that replicate asexually in vascular endothelia and eventually muscle fibers.
Diagnosis: Sporocysts can be observed by microscopy after fecal flotation. Infections are typically asymptomatic.
Management: Infections in dogs and cats are typically asymptomatic. Rarely, acute myositis, hepatitis, and neurological complications have been reported in dogs, potentially leading to death. Experimental treatment with clindamycin and decoquinate can be useful in dogs presenting with extraintestinal infection. Dogs and cats should not be fed raw meat or offal.
Species of interest include C. canis in dogs and C. felis in cats. Human cryptosporidiosis is predominantly caused by C. hominis and C. parvum; zoonotic infections by C. canis and C. felis have only been reported in immunocompromised individuals.
Host range: A wide variety of vertebrate hosts. However, most Cryptosporidium spp. are highly adapted to specific hosts.
Geographic distribution: Worldwide.
Life cycle: Cats and dogs get infected by ingestion of oocysts present in the environment (water, food or fomites). The parasites undergo asexual and sexual reproduction in the small intestine, releasing sporulated oocysts into the feces. Oocysts are immediately infectious when shed. They may survive in the environment for extended periods of time.
Diagnosis: Presence of Cryptosporidium spp. can be detected by: (1) acid-fast stain or fluorescent antibody tests on fecal smears, (2) Sheather’s sugar centrifugal flotation, (3) ELISA for detecting fecal antigen, and (4) PCR assay, which also allows for genotyping and subtyping. Infected animals exhibit a self-limiting diarrhea.
Management: Extra-label treatment of highly diarrheic animals has shown some success. Paromomycin and azithromycin are currently used for both dogs and cats, while tylosin is only recommended for cats. Environmental decontamination requires heat treatment (over 70°C) or ammonia-based disinfectants.
Giardia duodenalis (formerly G. intestinalis and G. lamblia) is molecularly classified into several assemblages, which vary in their infectivity for animals and humans. Dogs have mainly assemblages C, D, and A1, while cat isolates fall mainly into assemblages F and A1. Assemblages A1, A2, and B are infectious to people.
Host range: The total number of Giardia strains and host infectivity ranges is unknown. Canine assemblages (C, D) are not known to infect cats, and feline (F) assemblages are not known to infect dogs. Transmission of Giardia from pets to humans appears to be rare, and is of most concern in households with immunocompromised people.
Geographic distribution: Worldwide.
Life cycle: Cats and dogs are infected by ingestion of cysts present in the environment (water, food or fomites) or through self-grooming. Cysts release trophozoites that reside on the mucosal surface of the small intestine. Trophozoites replicate by binary fission and will ultimately encyst prior to being released in the feces as infectious cysts.
Diagnosis: Presence of Giardia spp. can be detected by different complementary methods: (1) direct smear of diarrheic stools revealing motile trophozoites, (2) 33% ZnSO4 centrifugal flotation demonstrating cysts, (3) Fecal ELISA for antigen, and (4) PCR assay. Due to intermittent shedding, it may be necessary to perform tests over multiple days to confirm infection. Infected animals may or may not exhibit diarrhea.
Management: Asymptomatic dogs and cats do not require treatment. Treatment is recommended for pets living with or in frequent contact with immunocompromised people; in these cases, genotyping to determine if the Giardia belongs to an assemblage infectious to people may bring owners peace of mind. In the absence of an approved treatment, fenbendazole (with or without metronidazole) is commonly used as extra-label therapy. Treatment should be combined with disinfection of surfaces as well as shampooing of the animals to remove fecal debris containing cysts. A second, longer course of treatment may be necessary for infections that are not successfully cleared the first time.
Species of interest include L. infantum, L. mexicana, L. donovani, and L. braziliensis in dogs. Leishmania spp. has been infrequently reported in cats. L. infantum is an important zoonotic agent and dogs are considered the primary reservoir host.
Host range: Vertebrate hosts include a wide variety of mammals e.g. rodents, dogs, foxes and humans. Insect hosts (vectors for transmission) are mainly small blood-sucking sandflies.
Geographic distribution: L. infantum has an almost global distribution, being endemic in the Mediterranean basin, the Balkans, much of Asia, Africa and Central and South America. Canine leishmaniasis is currently documented in foxhounds from many kennels in the U.S. and Canada.
Life cycle: In addition to classical vector-mediated transmission, L. infantum can be transmitted directly from dog to dog, either vertically (i.e. transplacental) or horizontally (through blood and secretions). Dog-to-dog transmission is believed to be the route of infection in North American foxhound kennels.
Diagnosis: Diagnosis should be guided by clinical signs in combination with antibody tests (indirect fluorescent antibody assay, direct agglutination assay, and enzyme immunoassay). Presence of Leishmania parasites can be confirmed by Wright-Giemsa staining or in vitro culture of biopsies from target organs (spleen, liver, lymph nodes, etc.). PCR assays are also available. Not all dogs develop clinical disease. Signs, when present, may include regional alopecia and dermatitis, cachexia, epistaxis, conjunctivitis, lameness, diarrhea, etc.
Management: Leishmanicidal drugs used in dogs include pentavalent antimonials, allopurinol, and sometimes miltefosine. However, no drug is able to consistently cure canine leishmaniasis and relapses are very common.
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- LeishVet guidelines for the practical management