Coccidial oocysts from cat feces. ( A ) Unsporulated oocysts of Isospora felis . Unstained. ( B ) Sporocyst of Sarcocystis sp ( arrow ) and an oocyst of Cryptosporidium sp ( arrowhead ). Unstained. ( C ) Numerous unsporulated oocysts of Toxoplasma gond ii. Unstained. 

Contexts in source publication

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... the high prevalence of serum antibodies in cats worldwide, the prevalence of T. gondii oocysts (Fig. 4C) in feces is very low. In general, less than 1% of cats shed oocysts on any given day. 68 Because cats usually shed T. gondii oocysts for only 1 to 2 weeks after their first exposure, oocysts are rarely found on routine fecal examina- tion. Moreover, cats usually are not clinically ill and do not have diarrhea during the period of ...

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... host (the cat), and only the asexual cycle occurs in nonfeline hosts. The host that excretes the oocyst is called the definitive host, and those hosts wherein only the asexual cycle occurs are called intermediate hosts. A representative coccidian life cycle is best described as follows. Oocysts are passed unsporulated in feces ( Fig. 3 A–C; Fig. 4 ; Fig. 10 C). After exposure to warm (20 C) environmental temperatures and moisture, oocysts sporulate, forming 2 sporocysts. Within each sporocyst are 4 sporozoites ( Fig. 3 D; Fig. 10 D). The sporozoites are banana-shaped and are the infective stage. The sporozoites can survive environmental exposure inside the oocysts for many months. After the ingestion of sporulated oocysts by cats or dogs, sporozoites excyst in the intestinal lumen, and the sporozoites initiate the formation of schizonts or meronts. During schizogony or merogony, the sporozoite nucleus divides into 2, 3, or more nuclei, depending on the parasite and the stage of the cycle. After nuclear division, each nucleus is surrounded by cytoplasm, forming a merozoite ( Fig. 5 B, D; Fig. 6 A; Fig. 7 B–D; Fig. 9 B). The number of merozoites within a schizont varies from 2 (see Fig. 7 B) to several hundred, depending on the stage of the cycle and the species of coccidia. Merozoites are released from the schizont when the infected host cell ruptures. The number of schizogonic cycles varies with the parasitic species. First-generation merozoites repeat the asexual cycle and form second-generation schizonts, or transform into male (micro) and female (macro) gamonts. The microgamont divides into many tiny microgametes ( Fig. 5 C; Fig. 7 F; Fig. 9 D). A microgamete fertilizes a macrogamete ( Fig. 7 E; Fig. 9 C), and an oocyst wall is formed around the zygote (see Fig. 5 D). The life cycle is completed when unsporulated oocysts are excreted in feces. Members of the genus Isospora , the most commonly recognized coccidians infecting dogs or cats, are species specific for the definitive host. At least 4 species, I. canis , I. ohioensis , I. burrowsi , and I. neorivolta , infect dogs, and 2 species, I. felis and I. rivolta , infect cats. The life cycle of Isospora infecting dogs and cats is similar to the basic coccidian intestinal cycle, except an asexual cycle can also occur in the definitive or intermediate host. On ingestion by definitive or suitable paratenic (intermediate) hosts, oocysts excyst in the presence of bile, and free sporozoites invade the intestine. Some sporozoites penetrate the intestinal wall and enter mesenteric lymph nodes or other extraintestinal tissues, where they form enlarging monozoic cysts (see Fig. 8 ). If no replication occurs, the term paratenic host, rather than intermediate host, is used. Monozoic cysts of Isospora may remain in extraintestinal tissues of paratenic hosts for the life of the host. Ingestion of monozoic cysts in paratenic hosts leads to intestinal infection in the definitive dog and cat host. The life cycle after the ingestion of paratenic host is the same as after the ingestion of sporulated oocysts from feces. The significance of the paratenic host in the life cycle of dogs and cats is unknown because the direct fecal-oral cycle is very efficient. Enzootic infections are frequently found in catteries or kennels where animals are congregated. 24–27 Clinical signs are most apparent in neonates. Diarrhea with weight loss and dehydration and, rarely, hemorrhage is the primary sign attributed to coccidiosis in dogs and cats. Anorexia, vomiting, mental depression, and ultimately death may be seen in severely affected animals. Intestinal coccidiosis may be manifest clinically when dogs or cats are shipped or weaned, or experience a change in ownership. Diarrhea might result from the extraintestinal stages of Isospora returning to the intestines. Pathogenesis of intestinal coccidiosis of cats and dogs is not well understood because clinical disease has not been reliably produced in experimentally infected animals, and clinical signs are not correlated with the number of oocysts found in feces. Little is known of the viru- lence of the different strains of these parasites. 15 Intestinal coccidial infection in dogs and cats is diagnosed by identification of the oocysts with any of the fecal flotation methods commonly used to diagnose parasitic infections. In dogs, only I. canis can be identified with certainty by oocyst size and shape (see Fig. 3 A, B). The oocysts of the other 3 species of Isospora , namely I ohioensis , I. burrowsi , and I neorivota , may overlap in size, and their distinction is not clinically important. The 2 species of Isospora occurring in cats can be readily distinguished by oocyst size. Although oocysts of these Isospora are passed unsporulated in freshly excreted feces, they sporulate partially by the time fecal examination is made. Partially sporulated oocysts contain 2 sporocysts without sporozoites. Isospora species may sporulate within 8 hours of excretion, and these Isospora are highly infectious. In cats, I. felis oocysts are twice the size of I. rivolta . In extreme cases epithelial casts may be found in feces, and schizonts, merozoites, and partially formed oocysts can be found in smears made in normal saline (not water). The primary goal of treatment of Isospora spp infections is to resolve diarrhea in puppies and kittens. 24 Whereas controlled data are generally not available for most protocols listed in Table 3 , there is anecdotal evidence that administration of drugs can lessen morbidity and mortality, and lessen oocyst shedding. Supportive care such as fluid therapy for correction of dehydration should be administered as indicated. The majority of the drugs listed in Table 3 have only a coccidiostatic effect on the organisms and so infection may not be cleared. In addition to the potential for gastrointestinal irritation, some sulfa drugs have other significant side effects including induction of keratoconjunctivitis sicca, cholestasis, hepatocellular necrosis, and thrombocytopenia. 28,29 The activity of ponazuril, diclazuril, and toltrazuril against api- complexans has been studied recently. 30–35 These drugs are currently preferred for the treatment of Isospora spp infection by many clinicians. Ponazuril is available in the United States as a treatment for Sarcocystis neurona infection in horses (Marquis Paste, Bayer Animal Health). This product can be purchased by veterinarians and diluted for use in puppies or kittens. Most compounding pharmacies alternatively will provide appropriate concentrations of ponazuril for use in small animals by prescription. Depending on the protocol used, infection may or may not be eliminated in all puppies or kittens. In addition, repeated infection with Isospora spp can occur. Thus, it is unclear whether there is value in repeating diagnostic testing after success- ful treatment of clinical disease. Treatment of all other ‘‘in-contact’’ dogs or cats may lessen the likelihood of repeat infection, but also increases expense to the owner and increases the risk for drug-associated side effects. Isospora spp are very resistant to routine disinfectants used in small animal practice. If there is a problem with recurrent coccidiosis in a kennel or cattery, potential transport hosts should be controlled, and the treatment of all animals combined with careful environmental cleaning as well as steam cleaning of surfaces may be indicated. In shelters with recurrent problems with coccidiosis, it is recommended that ponazuril be used prophylactically by administering a dose to all puppies or kittens at 2 to 3 weeks of age (. sheltermedicine.com/portal/is_parasite_control.shtml). Diarrhea associated with Isospora spp infections is generally self-limited or rapidly responsive to drug therapy. Thus, puppies and kittens with persistent diarrhea and Isospora spp oocyst shedding should be evaluated thoroughly for other coinfections or diseases that could potentiate Isospora spp associated disease. Coccidiosis tends to be a problem in areas of poor sanitation. The fecal shedding of large numbers of environmentally resistant oocysts makes infection likely under such conditions. Animals should be housed so as to prevent contamination of food and water bowls by oocyst-laden soil or infected feces. Feces should be removed daily and incinerated. Oocysts survive freezing temperatures. Runs, cages, food utensils, and other implements should be disinfected by steam cleaning or immersion in boiling water or by 10% ammonia solution. Animals should have limited access to intermediate hosts and should not be fed uncooked meat. Insect control is essential in animal quarters and food storage areas because cockroaches and flies may serve as mechanical vectors of oocysts. Coccidiostatic drugs can be given to infected bitches before or soon after whelping to control the spread of infection to puppies. ...

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... with severe respiratory or CNS signs. Anterior or posterior uveitis involving one or both eyes is common. Iritis, iridocyclitis, or chorior- etinitis can occur alone or concomitantly. Aqueous flare, keratic precipitate, lens luxa- tion, glaucoma, and retinal detachment are common manifestations of uveitis. Chorioretinitis may occur in both tapetal and nontapetal areas. Ocular toxoplasmosis occurs in some cats without polysystemic clinical signs of disease. Clinical signs may be localized in respiratory, neuromuscular, or gastrointestinal systems, or may be caused by generalized infection. 8,36,37,62–66 The neurologic form of toxoplasmosis may last for several weeks without involvement of other systems, whereas severe disease involving the lungs and liver may kill dogs within a week. Generalized toxoplasmosis is seen mostly in dogs younger than 1 year and is characterized by fever, tonsillitis, dyspnea, diarrhea, and vomiting. Icterus usually results from extensive hepatic necrosis. Myocardial involvement is usually subclinical, although arrhythmias and heart failure may develop as predominant findings in some older dogs. The most dramatic clinical signs in older dogs have been associated with neural and muscular systems. Neurologic signs depend on the site of lesion in the cerebrum, cerebellum, or spinal cord. Seizures, cranial nerve deficits, tremors, ataxia, and paresis or paralysis may be seen. Dogs with myositis may initially show abnormal gait, muscle wasting, or stiffness. Paraparesis and tetraparesis may rapidly progress to lower motor neuron paralysis. Canine toxoplasmosis is clinically similar to Neospora caninum infection, which was previously confused with toxoplasmosis (see neosporosis later). Although these diseases are similar, toxoplasmosis seems to be more prevalent in cats and neosporosis in dogs. There are only a few reports of ocular lesions associated with toxoplasmosis in dogs. Retinitis, anterior uveitis, iridocyclitis, ciliary epithelium hyperplasia, optic nerve neuritis, and keratoconjuctivitis have been noted. Severe keratoconjuctivitis was recently reported in a dog on prolonged topical corticosteroid therapy. 67 Clinical signs, serum chemistry, cytology, radiology, fecal examination, and serology can aid diagnosis. 8,37,42,44,51,52,54,56 Routine hematologic and biochemical parameters may be abnormal in cats and dogs with acute systemic toxoplasmosis. Nonregener- ative anemia, neutrophilic leukocytosis, lymphocytosis, monocytosis, and eosinophilia are most commonly observed. Leukopenia of severely affected cats may persist until death, and is usually characterized by an absolute lymphopenia and neutropenia with an inappropriate left shift, eosinopenia, and monocytopenia. Biochemical abnormalities during the acute phase of illness include hypoproteine- mia and hypoalbuminemia. Hyperglobulinemia has been detected in some cats with chronic toxoplasmosis. Marked increases in serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) have been noted in animals with acute hepatic and muscle necrosis. Dogs generally have increased serum alkaline phosphatase activity with hepatic necrosis, but this occurs less frequently in cats. Serum creatine kinase activity is also increased in cases of muscle necrosis. Serum bilirubin levels have been increased in animals with acute hepatic necrosis, especially cats that develop cholangiohepatitis or hepatic lipidosis. Cats or dogs that develop pancreatitis may show increased serum amylase and lipase activities. Cats often show proteinuria and bilirubinuria. Cats with pancreatitis may have reduced serum total calcium with normal serum albumin concentrations. Tachyzoites may be detected in various tissues and body fluids by cytology during acute illness. Tachyzoites are rarely found in blood, cerebrospinal fluid (CSF), fine- needle aspirates, and transtracheal or bronchoalveolar washings, but are more common in the peritoneal and thoracic fluids of animals developing thoracic effusions or ascites. Inflammatory changes are usually noted in body fluids. In suspected feline toxoplasmosis of the nervous system, CSF protein levels were within reference ranges to a maximum of 149 mg/dL, and nucleated cells were a maximum of 28 cells/mL. Lymphocytes predominate, but a mixture of cells may be found. Thoracic radiographic findings, especially in cats with acute disease, consist of a diffuse interstitial to alveolar pattern with a mottled lobar distribution. Diffuse symmetric homogeneous increased density due to alveolar coalescence has been noted in severely affected animals. Mild pleural effusion can be present. Abdominal radiographic findings may consist of masses in the intestines or mesenteric lymph nodes or homogeneous increased density as a result of effusion. Loss of contrast in the right abdominal quadrant can indicate pancreatitis. Despite the high prevalence of serum antibodies in cats worldwide, the prevalence of T. gondii oocysts ( Fig. 4 C) in feces is very low. In general, less than 1% of cats shed oocysts on any given day. 68 Because cats usually shed T. gondii oocysts for only 1 to 2 weeks after their first exposure, oocysts are rarely found on routine fecal examination. Moreover, cats usually are not clinically ill and do not have diarrhea during the period of oocyst shedding. Although cats are considered immune to reshedding of oocysts, they may shed a few oocysts after rechallenge with different strains more than 6 years later. Clinical pharmacological doses of corticosteriods do not reactivate shedding of oocysts. T. gondii oocysts in feline feces are morphometrically indistinguishable from oocysts of Hammondia hammondi and Besnoitia spp (see Table 1 ), which also occur in cats. Oocysts of these coccidians can be differentiated only by sporulation and subsequent animal inoculation. If 10- to 12- m m sized oocysts are found, they should be considered to be T. gondii until proved otherwise. Further inoculations should be attempted only in a diagnostic laboratory with competence in this procedure because of the infectious nature of the organism. Because of their small size, oocysts of T. gondii are best demonstrated by centrifugation using Sheather sugar solution. Five to 10 g of feces are mixed with water to a liquid consistency, and the mixture is strained with gauze. Two parts Sheather sugar solution (500 g sugar, 300 mL water, and 6.5 g melted phenol crystals) are added to one part fecal suspension and centrifuged in a capped centrifuge tube. Care should be taken not to fill the tube to the top, to prevent spills or aerosols. After centrifugation at 1000 g for 10 minutes, remove 1 to 2 drops from the meniscus with a dropper, place on a microscope slide, cover with a coverslip, and examine at low-power ( Â 100) magnification. T. gondii oocysts are about one- fourth the size of I. felis oocysts and one-eighth the size of eggs of Toxocara cati (the common roundworm of the cat). Once infected, animals harbor toxoplasmic tissue cysts for life. IgG in kittens born to chronically infected queens is transferred in colostrum and persists for 8 to 12 weeks after birth. Serologic surveys indicate that T. gondii infections are prevalent worldwide. Approximately 30% of cats and dogs in the United States have T. gondii antibodies. The prevalence of seropositivity increases with age of the cat or dog because of the chance of exposure rather than susceptibility. Multiple serologic tests for the detection of antibodies have been used in the diagnosis of toxoplasmosis. The use of these tests in cats has been reviewed. 37 No single serologic assay exists that can definitively confirm toxoplasmosis. The magnitude of titer is not associated with severity of clinical signs. The measurement of serum antibodies in healthy cats cannot predict the oocyst-shedding period. In general, for as- sessing human health risk, serologic test results from healthy cats can be interpreted as follows. (1) A seronegative cat is not likely currently shedding oocysts but will likely shed oocysts if exposed; this cat poses the greatest public health risk. (2) A seropositive cat is probably not currently shedding oocysts and is less likely to shed oocysts if reexposed or immunosuppressed. It is still recommended that potential exposure to oocysts be minimized. Because antibodies occur in the serum of both healthy and diseased cats, results of these serologic tests do not independently prove clinical toxoplasmosis. Antibodies of the IgM class are commonly detected in the serum or aqueous humor of clinically ill or FIV-infected cats, but not healthy cats, and they may be a better marker of clinical disease than IgG or IgA. T. gondii IgM is occasionally detected in the serum of cats with chronic or reactivated infection, and does not always correlate with recent exposure. A tentative antemortem diagnosis of clinical toxoplasmosis in dogs or cats can be based on the following combination of serology and clinical parameters: (1) serologic evidence of recent or active infection consisting of high IgM titers, or fourfold or greater, increasing or decreasing, IgG or other antibody titers (after treatment or recovery); (2) exclusion of other causes of the clinical syndrome; (3) beneficial clinical response to an anti- Toxoplasma drug. Treatment of T. gondii infection is indicated to decrease oocyst shedding in acutely infected cats, and to control the signs of clinical toxoplasmosis in dogs and cats. Multiple drugs have been administered to cats to shorten the oocyst shedding period. 37 As discussed, ingestion of bradyzoites results in an enteroepithelial cycle that generally only lasts days, so duration of drug therapy can be short. The drugs most commonly available are listed in Table 4 . It is difficult to induce clinical toxoplasmosis in dogs or cats without concurrent immune suppression, so controlled studies on the effect of treatments are lacking. Based on studies ...