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Toxoplasmosis: Health Implications, Pathology, Clinical Manifestations, Treatment And Prevention

Updated on March 31, 2014

How To Diagnose Toxoplasmosis

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A General Clinical Overview Of Toxoplasmosis

Infection by the protozoon Toxoplasma gondii causes toxoplasmosis. This parasite undergoes its full lifecycle only in cats and other canine hosts but it affects many mammals, birds and reptiles. The parasite was first discovered in 1908 in a North African rodent- the gondii. Toxoplasma gondii is a crescent-shaped organism 4 to 6 X 2u in size demonstrably by Giemsa on Wright stain. It is seen intraellularly in endothelial cells, monocytes or tissue cells. It may be seen fress in tissues and tissue fluids.

Human infection is acquired by ingesting the oocytes passed in Cat’s feces or contaminated meat of animals and birds. Toxoplasma gondii may be found in the mil of infected animals. Transplancental transmission to the fetus from the mother occurs if she gets infection during early pregnancy. At times, the maternal infection may be silent. Other rarer modes of transmission include inoculation of infected material into skin, blood transfusion and entry through the respiratory tract. The disease is worldwide in distribution and limited serological surveys indicate that it is prevalent in India.

Pathology: The congenital form occurs in 3 to 5% of babies of infected mothers. If the fetus is affected heavily transplacentally during pregnancy, abortion or stillbirth may result. If the fetus is affected in late pregnancy, the baby is normal at birth but symptoms develop after a few months. Lesions are seen widespread in the CNS, eyes, heart, lungs and adrenals. The parasite disappears from all tissues except the CNS and retina. Brain and Spinal cord show extensive areas of necrosis, cyst formation and patchy calcification. Retina shows choroidoretinitis.

In the acquired form, the parasite gets disseminated through the blood and lymphatics from the intestinal epithelium. Lymph nodes and spleen are commonly affected. Other tissues such as the liver, lungs, skeletal muscles, myocardium, meninges and brain may also be involved.

How Toxoplasmosis Is Transmitted From Cats

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Clinical Presentations Of Toxoplasmosis

Congenital toxoplasmosis presents predominantly with neurological involvement. The child develops chronic encephalomeningomyelitis which results in hydrocephalus, microcephaly, convulsions, tremors, focal paralysis and contractures. Eye lesions include microphthalmia, nystagmus, blindness and bilateral choroidoretinitis. In cases with meningoencephalitis, cerebroaspinal fluid is xanthochromic with rise in protein and mononuclear cells but with normal sugar. Toxoplasma gondii may be demonstrable. Other manifestations such as hepatosplenomegaly with jaundice, thrombocytopenic purpura, lymphadenopathy and rashes have been described. Unlike congenital toxollasmosis, acquired toxoplamosis may be symptomless in the vast majority, detectable only by serological tests.

Diagnosis: Strong clinical suspicion is necessary for recognizing the condition. Since the manifestations are protean, toxoplasmosis should be considered in the differential diagnosis of a wide range of clinical abnormalities. Demonstration of T. gondii in the CSF, lymph gland aspirate, or in biopsy specimens, confirms the diagnosis. The organism can be recovered by inoculating the infective material into laboratory animals like mice, hamsters and guinea pigs.

Symptomatic cases may occur in two forms- acute and chronic. The acute form presents frequently with fever, aches and pains, cough, pneumonitis, profound malaise and maculopapular rash. Rarely, jaundice, myocarditis and meningo-encephalitis may develop. In the chronic form, there is generalized painful lymphadenopathy which is more marked in the cervical region, lymphocytosis with atypical lymphocytes in peripheral blood, hepatomegaly and rarely unilateral choroidoretinitis. In persons with latent infection or those who have undergone remission, depression of immune status of the individual results in recrudescence.

The dye test: This is a simple test, which can be undertaken in many laboratories. Toxoplasma gondii is stained by alkaline methylene blue, but if it is mixed with serum containing antibodies, the parasite does not take up the stain. This phenomenon forms the basis of the dye test. Presence of antibodies in the serum gives evidence of past infection. Rising titires are suggestive of active infection.

In addition to dye test, complement fixation test, neutralizing antibody test, indirect hemagglutination test and ELISA test are also available. Toxoplasmin skin test is an intradermal test using toxoplasma antigen. Erythema and induration developing after 48 to 72 is suggestive of infection but not activity of the disease. In some communities, 10 to 20% of apparently healthy persons give positive skin test.

Course and prognosis: The lymphatic form tends to be mild and chronic which runs over several months, but is ultimately self-limiting. Congenital toxoplamosis and acquired neurological lesions are associated with high mortality and morbidity.

Treatment: The organism is susceptible to a combination of purimethamine (Daraprim), 25mg/day and sulphadiazine 1g every 6 hours for 14 days. Pyrimethamine is a folate-antagonist and therefore, megaloblastic anemia may develop during prolonged therapy. In children, the dose of pyrimethamine is 2mg/Kg. Since the drug is teratogenic, it is contraindicated in Pregnancy. Tetracycline and spiramycin are also effective and these can be combined with the standard resistant cases. Spiramycin has been used alone with reports of cure. In ocular toxoplamosis, oral corticosteroid therapy given in addition to pyrimethamine-sulphadiazine is beneficial.

© 2014 Funom Theophilus Makama

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