Toxoplasmosis and Neosporosis: More than Muscles
World Small Animal Veterinary Association World Congress Proceedings, 2003
Craig E. Greene
University of Georgia
Athens, GA, USA

Toxoplasmosis

Etiology. The cat is the definitive host of this disease caused by Toxoplasma gondii. Cats become infected most commonly through ingestion of bradyzoites in infected tissues. They only shed oocysts following ingestion of infected meat for a maximum period of two weeks, although the parasite remains encysted in their muscle for life. Reshedding of oocysts does not occur under most circumstances.

Clinical Signs. Clinical signs in the acute disease are varied depending on the tissue of encystment. Fever, lymphadenomegaly, hyperesthesia and uveitis have been seen. Cats concurrently infected with feline immunodeficiency virus have persistent and unresponsive infections. Congenital infections in cats were thought to be uncommon; however now it has been documented that they occur probably via transplacental or lactational transmission. Neonates are most severely affected and still births or neonatal death are common. In older cats with disseminated disease, infection of the lungs, CNS or muscle, hepatic, cardiac and ocular tissues are most common. In older or chronically infected animals, the clinical signs may be more insidious. CNS or ocular signs are most common in chronic reactivated infections associated with stress or immunosuppression.

Clinical signs in dogs can also involve the respiratory, neuromuscular or GI systems. Reactivated infections may be more chronic while disseminated disease involving parenchymal organs such as the lung and liver can be more rapid and fatal. Myocardial involvement may be more insidious and lead to arrhythmias or eventual myocardial failure. Chronic polymyositis is a syndrome observed in dogs with reactivated infections. Neurologic dysfunction is also seen with chronic infections and the signs observed depend on the location of the inflammation within the CNS.

Diagnosis. Hematologic and biochemical abnormalities are usually nonspecific. Hypoalbuminemia may be observed in the acute infections and hyperglobulinemia in more chronic infections.

Increased hepatic transaminases or creatine kinase activities are found in animals with acute hepatic or muscle necrosis.

Tachyzoites are rarely detected in tissues and body fluids during acute illness. Radiographic findings may indicate an alveolar to interstitial infiltrate in the lung fields. Intestines or mesenteric nodes may be enlarged. Detection of oocysts in the feces of cats is an inaccurate means of confirming a diagnosis. The prevalence of oocysts is low and the excretion interval l4 days or less. Only some cats develop diarrhea during the period of oocyst shedding.

Assays for IgG and IgM antibodies have allowed demonstration of multisystemic infection in cats and for determining their public health risk. Once infected, animals harbor Toxoplasma cysts for their life. Young kittens acquire maternal antibody in colostrum which can persist for up to 12 weeks. Serologic testing shows exposure to Toxoplasma is prevalent worldwide and increases with the age of the animal. A number of serologic assays are available; however, none by itself is definitive. Agglutination, IFA, and ELISA assays are most commonly used. Documentation of a positive agglutination or IgM titer generally indicates active or recent infection and may correlate with the period of oocyst shedding in cats. A change in IgG titer with paired sera can also be used. A single increased IgG titer can be associated with chronic or reactivated infections. A positive IgG titer in cats actually confirms their acute infection period has passed and that they are of little risk of shedding oocysts. For ocular or CNS infections, measurement of ratios of serum to aqueous humor or CSF levels has been used.

Organism detection is definitive for infection by Toxoplasma. Cytologic identification can be helpful but very insensitive. PCR has been used to verify the presence of T. gondii in biologic specimens.

Treatment. Treatment of cats involves the use of oral clindamycin daily at a dose of 25 to 50 mg/kg. The daily dose in dogs is 10 to 40 mg/kg /day, usually divided into two doses. Drugs used to treat toxoplasmosis suppress the replication of the parasite; however, may not completely sterilize the tissues. Clinical signs of improvement usually begin within 24 to 48 hours. Other effective drugs include antifolates such as sulfonamides, pyrimethamine, and trimethoprim-sulfonamide combinations.

The risk of acquiring toxoplasmosis is present in soil contaminated by cat feces and in raw or undercooked meats. Although difficult, restricting of hunting can help reduce the exposure of cats to infection. Cats have such a brief (2 week) oocyst shedding phase which can be terminated or suppressed with drug therapy. Caution should be used in preparing foodstuffs that are eaten raw by placing them on surfaces that were exposed to undercooked meat.

Neosporosis

Etiology. Neospora caninum is a closely-related protozoan that has been confused with T. gondii because of the resemblance of its tachyzoites and tissue cysts. Dogs appear to be the definitive hosts of this parasite, and herbivores, especially cattle are intermediate hosts. In dogs, tachyzoites are found within neural and muscle tissues of chronically infected animals but dissemination to many organs may occur in the acute illness. Within neural tissue, the organism exists within cysts that may rupture eliciting a granulomatous inflammatory response. The predominant clinical sign in the intermediate herbivore host is abortion. Natural infections have not been found in cats but they can be infected experimentally.

In the definitive dog host, initial infection can be by carnivorism, but once a reproductively intact female is infected, the predominant route of infection is transplacental. Chronically infected bitches transmit the organism to their offspring and sequential litters may be affected.

Purebred dogs have been noticeably more prevalent in reported cases and certain breeds predominate. This may relate to reduced host immunity from inbreeding and maintenance in the breed by transplacental spread. While some pups show signs early, others may be subclinically affected with reactivation of infection later in life.

Clinical Signs. Neural and muscular signs predominate but any parenchymal tissue may become inflamed. Young pups often develop ascending paralysis manifest by muscle rigidity. Laboratory abnormalities include increases in serum muscle enzymes and CSF pleocytosis with mixed inflammatory cell types. Adult dogs also are affected, and as with toxoplasmosis, any tissue can be infected resulting in inflammation. Most infections involve muscle or nervous tissues. Multifocal CNS involvement, polymyositis, myocarditis, dermatitis, pneumonia, peripheral neuritis or multifocal dissemination have been observed.

Diagnosis. Hematologic and biochemical abnormalities are nonspecific. Increased muscle enzymes activities, and increased hepatic transaminase activities have been observed. CSF abnormalities include pleocytosis with a mixed inflammatory pattern. EMG abnormalities include spontaneous discharges and high frequency discharges characteristic of myopathy or peripheral neuropathy.

Serologic testing is often used to demonstrate serum antibodies to N. caninum IFA titers can vary between laboratories; however, in general, titers above 1:200 are considered positive. Antibodies to T. gondii do not cross-react with N. caninum at lower dilutions. N. caninum may be found in CSF or tissue aspirates and muscle or tissue biopsies of some dogs. Biopsy of affected muscle may yield a definitive diagnosis where organisms are detected. Although N. caninum tachyzoites are similar to those of T. gondii by light microscopy, the former have thicker walls. Nonsuppurative encephalomyelitis, polyradiculoneuritis, ganglionitis, myositis, and myofibrosis are the predominant histologic findings. Tissue cysts are present only in central or peripheral neural tissues, while tachyzoites are present in many tissues.

Treatment. Drugs used for therapy of toxoplasmosis should be tried early in the course of illness. Clindamycin, sulfadiazine, pyrimethamine alone or in combinations have been used to treat canine neosporosis. The dosages are the same used to treat toxoplasmosis. All pups in an affected litter should be treated as soon as possible. Unlike toxoplasmosis, there is no known public health risk to neosporosis. Dogs should be given limited access to offal from herbivores and they should never be fed raw or uncooked meat. Once the infection has been detected in a litter, the bitch and all subsequent litters should be presumed infected. Serologic testing of these related animals should be done. Furthermore, early treatment of future offspring can be attempted. Because of the effects of antifolates on replicating cells, this cannot be done for the first 2 weeks during the neonatal period without some possible risk.

Speaker Information
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Craig E. Greene
University of Georgia
Athens, GA, USA


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