Many species of coccidia infect the intestinal tract of cats and dogs. All species appear to be host-specific. Cats have species of Hammondia, Isospora, Besnoitia, Toxoplasma, and Sarcocystis. Dogs have species of Hammondia, Isospora, and Sarcocystis. Neither dogs nor cats have Eimeria.
Although some species are widespread, clinical disease is uncommon and usually mild. There is some controversy over the occurrence of clinical disease and, when it apparently occurs, other causes need to be eliminated or considered as partly associated with the problem.
Hammondia spp has an obligatory two-host life cycle with cats or dogs as final hosts and rodents or ruminants as intermediate hosts, respectively. Hammondia oocysts are indistinguishable from those of Toxoplasma and Besnoitia but are nonpathogenic in either host ( see also Besnoitiosis, Sarcocystosis, and Toxoplasmosis.)
Etiology and Pathogenesis of Coccidiosis of Cats and Dogs
The most common coccidia of cats and dogs are Isospora spp. Two species infect cats: I felis and I rivolta; both can be identified easily by oocyst size and shape.
Four species infect dogs: I burrowsi, I canis, I neorivolta, and I ohioensis. In dogs, only I canis can be identified by the oocyst structure; the other three Isospora spp overlap in dimensions and can be differentiated only by endogenous developmental characteristics.
When clinical coccidiosis is present it is often related to intercurrent infections, immunosuppression, or stress.
In dogs, the prepatent period is about 3 weeks. Most infection in dogs and cats is a direct life cycle involving the ingestion of oocysts in the feces once infective. Sporulation can occur in 6 hours in warm, moist, and oxygenated conditions but usually takes 7–10 days. Isospora spp have the potential for producing very large numbers of oocysts within a short period.
There is an indirect life cycle, especially with Isospora spp in cats and dogs, which can facultatively infect other mammals and also the definitive host’s own tissues and produce an encysted form (cystozoite) that can later become activated to infect the cat or dog. Thus, cystozoites of I felis are found in lymph nodes and abdominal viscera in paratenic hosts such as mice and rats and infective stages are released in the cat’s intestines. Cystozoite reactivation in cat tissues in stressed kittens or immunosuppressed cats may be important in causing disease in these specific hosts. However, this cycle is usually considered to maintain the life cycle but not sufficient to cause disease in most animals.
There is some controversy over pathogenicity. Heavy infections leading to intestinal damage can produce decreased nutrient absorption, loss of fluid and electrolytes, and, with some Isospora spp, hemorrhage. High fecal shedding of oocysts is associated with clinical signs of disease, especially in kittens.
Epidemiology of Coccidiosis of Cats and Dogs
Coccidiosis is uncommon in young kittens or puppies. It usually occurs in young animals in facilities with a high population and potential contamination. Illness may become a problem in breeding or boarding catteries and kennels.
Almost every cat eventually becomes infected with I felis. In dogs, mainly puppies are infected. Most cats and dogs are infected at a young age, and when clinical signs occur, they occur in kittens and puppies (4–12 weeks) and very occasionally in debilitated or immunocompromised adult dogs. In kittens, illness occurs primarily during weaning stress. In puppies, clinical signs develop about 2 weeks after infection. After oocyst exposure, immunity is good, especially in cats.
Clinical Findings of Coccidiosis of Cats and Dogs
Most infections in cats and dogs are without clinical signs. The most prominent clinical sign is diarrhea in several animals. Acute cases are associated with some diarrhea. In kittens with severe cases of I felis and I rivolta infection, there can be diarrhea (mucoid or watery); occasionally, later on, bloody diarrhea occurs in kittens, and, possibly, anorexia, dehydration, abdominal distress, and weight loss. Rarely, anemia, respiratory and nervous signs occur. In puppies with severe cases with high oocyst counts, associated signs can occur. Both I canis and I ohioensis may cause bloody diarrhea and poor growth. IIsospora burrowsi may not cause clinical disease. Isospora neorivolta occasionally causes diarrhea.
Postmortem Lesions
In cats with I felis, lesions usually occur in the small intestine and cecum but are minimal. Histologic examination in cats shows asexual stages in the epithelial cells of both surface and crypt cells. Infection with I rivolta takes place in the small intestine. Histologically, both asexual and sexual stages are present in the small intestine surface and crypt epithelial cells. In dogs with I canis, the infection is mainly in the caudal part of the small intestine. For I burrowsi, all stages occur in the aborad small intestine.
For I neorivolta, the asexual stages occur in the aborad half of the small intestine and the sexual stages occur in the ileum and cecum. For I ohioensis, initially the asexual and sexual stages are present in the aborad half of the small intestine but then also progress to the ileum, cecum, and colon. Reddening and mucus production of the jejunal surface occur in heavy infections. Histologic examination shows the various stages of I canis occur in the subepithelial layer, with hemorrhage as the parasite emerges from that position. Also, in severe infections, there is villous atrophy and excessive mucus production. For I burrowsi, the stages are seen at the epithelial tips and lamina propria. For I neorivolta, the asexual stages are in the lamina propria near the villi tips, and the gametocytes occur in the lamina propria and surface epithelium. For I ohioensis, the various stages of the parasite may appear at the epithelial cells of the villous tips in the small intestine. In the ileum, cecum, and colon, the cells lining the whole villus and crypts can be invaded, leading to inflamed crypts, shedding of the villous tips, flattening of the epithelial cells, and villous atrophy.
Diagnosis
A fecal sample is examined for oocysts using fecal flotation (saturated salt or sucrose solutions). Speciation should be undertaken, and in puppies this may require artificial sporulation of the oocysts with potassium dichromate.
Differential diagnoses including bacterial infection (Campylobacter spp, Clostridium spp, Escherichia coli, Salmonella spp, etc) can be detected by culture. For viruses (coronavirus, parvovirus, rotavirus, etc), usually fecal tests or blood tests are used. Cryptosporidia fecal examination is used to for detection of cryptosporidial oocysts. helminth eggs should be present; however, helminths are unlikely to cause diarrhea in the age group affected by coccidiosis.
Treatment
In almost all kittens and puppies, infection is spontaneously eliminated, making treatment unnecessary. Those affected must be kept warm and hydrated. In such cases, supportive fluid therapy and nutritional support may be required if dehydrated. All queening and whelping areas and rearing pens must be kept scrupulously clean.
No specific treatments are licensed in most countries.
Trimethoprim-sulfonamide (30–60 mg/kg per day for 6 days; halve dose for small dogs) can be used in clinically infected patients. Sulfonamides, such as sulfadimethoxine (50 mg/kg the first day and 25 mg/kg per day for 1–3 weeks thereafter or 50 mg/kg until 2–3 days after clinical signs resolve), can be used in severe cases. They are licensed in the US, but they are not licensed in many countries. Toxicity is reported occasionally.
Triazine antiprotozoals, including diclazuril and toltrazuril, may be effective. They have been used in very few dogs, but diclazuril (5 mg/kg, PO, once) is reported effective in cats. Ponazuril (20 to 50 mg/kg, PO, for 2 to 5 days) is reported to be used in dogs and cats, but it is unlicensed in most countries.
Control and Prevention of Coccidiosis of Cats and Dogs
Scrupulous hygiene is required in kittening and whelping areas. Preemptive fecal testing of cats in late pregnancy can be helpful where infections have previously occurred. Sanitation is important, especially in catteries and kennels, or where large numbers of animals are housed. Feces should be removed frequently. Fecal contamination of feed and water should be prevented. Runs, cages, and utensils should be disinfected daily. Raw meat should not be fed. Insect control should be established. Effective rodent control is required.
Infective oocysts can survive for many months in the environment and are resistant to most commonly used disinfectants. Chlorine disinfectants are effective (test check to see if too corrosive to surfaces). Some ammonia-based disinfectants kill oocysts but cannot be used while animals are present. Steam cleaning is effective. After thorough cleaning, a fallow period is recommended before further occupation. Preventive medication is usually not necessary. However, in cattery or kennel conditions, prophylactic medicines may be used. Amprolium, although not approved, is used for puppies as a drench often adding flavors to help disguise the taste. It is reported effective. Triazine antiprotozoals (diclazuril and toltrazuril) have been used orally in catteries and kennels, especially shelter premises, but as an extralabel use.
