Coccidiosis in dogs Diagnosis Epidemiology Control

Coccidiosis in dogs Diagnosis Epidemiology Control Cystoisospora canis; Cystoisospora ohioensis-like; Cystoisospora burrowsi; Cystoisospora neorivolta; Life history;
Coccidiosis in dogs Diagnosis Epidemiology Control

- This paper reviews the biology of Cystoisospora infections in dogs, including taxonomy, diagnosis, epidemiology, and treatment.

- . canis, C. ohioensis, and C. ohioensis-like coccidia are compared.
- Drugs containing toltrazuril were found most efficacious for treating canine coccidiosis.
Abstract Until 1970, coccidian parasites of dogs were considered to have a direct fecal-oral life cycle like Eimeria in poultry. They were thought to be non-host specific and infect both dogs and cats.
Studies conducted in 1970 revealed that dog coccidia was host-specific and had transport or paratenic hosts that were infected with an encysted stage containing a single organism, the monozoic tissue cyst. There are still considerable confusion and uncertainties concerning the life cycles and pathogenicity of coccidian parasites of dogs. The present paper reviews the history, taxonomy, life cycles, pathogenicity, epidemiology, diagnosis, and treatment of conventional coccidian parasites previously called Isospora spp., currently designated Cystoisospora spp. that infect canines.

1. Introduction and history
Although coccidian parasites have been known in cat and dog feces for more than a century until 1970 little was known regarding their clinical or public health significance. Until the report of Wenyon (1923), only one species of coccidia was thought to be present in the feces of cats and dogs. Wenyon (1923, 1926) reviewed earlier literature and concluded that Grassi (1879) probably named Coccidiumrivolta first from the cat, andStiles(1891) namedCoccidium bigemina first from the dog. (1906) transferred these parasites to
the genus Isospora. Wenyon (1926) believed that there were two “races” of I. bigemina, the small race developed in intestinal Villar enterocytes whereas the large race was in the lamina propria.

Wenyon (1923) made the first distinction that there were at least three species of coccidia in cats and dogs, based on the oocyst size: (a) large oocyst size, ~40 µm long; (b) medium oocyst size, ~25 µm long; and (c) small oocyst size, ~10-12 µm long. Wenyon (1923) named the coccidia with large oocysts as Isospora files.

The coccidian species with large and medium-sized oocysts of dogs and cats
The I. bigemina (Coccidium bigemina of Stiles) turned out to be a mixture of numerous species of Sarcocystis, Toxoplasma, Besnoitia, Neospora, and Hammondia

Nemeséri (1959, 1960) first separated coccidia with large-sized oocysts from dogs

from those found in cats and named the dog parasite Isospora cranes and partially described its endogenous stages.

(1975) separated the coccidia with medium
sized oocysts and retained the name I. rivolta for the parasite in cat feces and named the dog parasite Isospora ohioensis. Subsequent studies revealed that there were two other

I. ohioensis-like species in dogs and they were named Isospora burrowsi and Isospora
neorivolta Until the discovery of the life cycle of Toxoplasma gondii, coccidia were considered to have a direct fecal-oral cycle.

(1972a) found extra-intestinal stages of I rivolta in cats and mice.
An encysted stage (tissue cyst) of I. rivolta was found in rodents. Based on these observations,
proposed new genera, Cystoisospora, and Levineia for Isospora species of cats and dogs but Levineia were considered a synonym of Cystoisospora based on the priority of publication conclusion based on molecular phylogeny.

During the last 50 years, much has been learned of coccidiosis in dogs. However, there is still controversy concerning the species and pathogenicity of coccidiosis in dogs. 

The objective of the present review is to summarize the biology of dog coccidia, including
taxonomy, life cycle, prevalence, pathogenicity, diagnosis, and control. 
Life cycle Its life cycle has been studied in detail in newborn dogs fed oocysts or tissues of infected mice. Newborn dogs and littermates were used as controls to minimize extraneous coccidial infections. For the oocyst-induced infections, eight dogs were euthanized 6-120 h after feeding Clinical coccidiosis Before the recognition of enteric viral pathogens of dogs and effective immunization against distemper virus infection in the 1960s, coccidiosis was considered a common disease affecting as many as 50% of dogs the account was given by Perry (1952) who listed individual case histories of 56 dogs presented in the past five years at the Small Animal Clinic at the Tuskegee Institute School of Veterinary Medicine that opened in 1947. In the last 50 years, there are only a few reports of clinical coccidiosis in dogs.

. Depression, weakness, loss of appetite, diarrhea, dehydration were the common clinical
signs and positive response to anticoccidial therapy was considered to support the diagnosis
(Randhawa et al., 1997). Concurrent infections with other pathogens complicated the diagnosis (Gal et al., 2007). In a clinic in Brazil, 66 cases of coccidiosis were diagnosed between 1972 and 1978 (Correa et al., 1983). These cases occurred throughout the year and clinical signs persisted 1-15 days. Abdominal pain (100%), vomiting (25%), diarrhea (90%), and anorexia (80%) were present in 97% of cases. Neurological, respiratory, circulatory disturbances were seen in more than 50% of cases. Therefore, it is uncertain if all clinical signs were due to coccidiosis. Coccidiosis was considered the sole disease in 51% of cases, and in the remaining 49% concurrent infections or other maladies were noted including canine distemper virus infection in 7%, hookworms in
32%, Dipylidium caninum infections in 4%, and organic insecticide poisoning in 6% (Correa et
al., 1983). Olson (1985) provided a detailed clinical history of 3 dogs with coccidiosis; the dogs were 3, 5, and 22 months old and repeated fecal examinations were needed for diagnosis of C. ohioensis infection. All three dogs responded to anti-coccidial therapy. Retrospectively, 21 other cases of clinical coccidiosis were diagnosed in years from 1969-1980 at his institution and C.
ohioensis was the most common cause (18 of 21 cases) and C. canis was diagnosed in 5 cases
(Olson, 1985).
An outbreak of coccidiosis associated with C. ohioensis in puppies housed in a kennel was
reported by Oduye and Bobade (1979). The dogs were reported to have hemorrhagic diarrhea with
abdominal pain and dehydration. However, the pups were mongrels and positive response to
anticoccidial therapy was the main diagnostic criterion.
By far the most striking case with a definitive diagnosis of clinical coccidiosis due to C.
the ohioensis-like organism was in a 10 weeks-old Chihuahua pup with a history of weight loss. The pup had yellow pasty feces and died despite sulfaguanidine therapy for two days. Severe enteritis was associated with asexual and sexual stages of the C. ohioensis-like

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