Active Toxoplasmosis Research Articles

Photocoagulation of Active Toxoplasmic Retinochoroiditis

Active, recurrent, protracted toxoplasmic retinochoroiditis that had been unresponsive to intensive medical therapy with pyrimethamine, sulfamethoxypyridazine, intramuscular folicic acid, or clindamycin and corticosteroids, was treated with photocoagulation in five eyes. Four eyes healed rapidly within a few weeks. In one patient's eye, lens and vitreous opacities prevented adequate treatment with the red III intensity level of the xenon are photocoagulator. Subsequent surgical diathermy and cryocoagulation resulted in prompt healing of the lesion. Noninvasive photocoagulation of active toxoplasmosis retinochoroiditis is recommended in protracted cases if the media are clear, the macula is threatened, or there are severe complications from systemic medications.

Dermatomyositis and toxoplasmosis

In a patient with childhood dermatomyositis, high toxoplasma antibodies were found at the time of diagnosis. A direct immunofluorescence technique demonstrated active toxoplasmosis in the muscle biopsy. The response to treatment and follow-up in this patient suggest that toxoplasmosis could have caused the dermatomyositis.

Detection of circulating antigen during acute infections with Toxoplasma gondii by enzyme-linked immunosorbent assay.

The serodiagnosis of toxoplasmosis is usually based on demonstration of antibodies by means of different serological methods. However, for confirmation of active toxoplasmosis, examination of paired sera is still needed. In this study a description is given of a sensitive enzyme method (enzyme-linked immunosorbent assay) with which it is possible to detect circulating antigens during the acute stage of mouse and human toxoplasmosis. Preliminary investigations of human sera suggested that circulating antigens are only found during a short period (active phase) of the toxoplasma infection and that they can be found in cases of fresh infections as well as during reinfections. The possible clinical relevance is discussed.

Therapy of Toxoplasmosis Uveitis

At the present time the combination of pyrimethamine (Daraprim), sulfa and sys­ temic steroids appears to be the most effective treatment for the granulomatous uveitis attributed to toxoplasmosis infection. This is based on animal experimental data and human clinical data interpreted as showing (1) pyrimethamine or sulfa alone are thera­ peutic, ( 2 ) pyrimethamine and sulfa together have a synergistic effect against toxoplas­ mosis infections, ( 3 ) steroids enhance the therapeutic effect of pyrimethamine and sulfa and (4 ) the combination of pyrimeth­ amine, sulfa, and systemic steroids is supe­ rior to any other form of treatment reported thus far . 1 7 This paper is a report of therapy with pyrimethamine, sulfa and systemic steroids in a series of patients diagnosed as having active toxoplasmosis chorioretinitis.

Toxoplasmosis found by recovery of toxoplasma gondii from excised maxillary gland.

Toxoplasmosis as a disease of man was first observed by Janku in 1923. Since that time this protozoal disease has been found with increasing frequency, especially among infants. The causative organism was first established in 1939. The disease in infants is usually manifested as a form of encephalitis with such features as hydrocephalus or microcephaly, chorioretinitis, microthalmos, and intracerebral calcification. Cases of active toxoplasmosis among adults, confirmed by isolation of the causative organism, have been relatively few in number, approximately a dozen, and often have proved fatal. These cases have usually been manifested by a prolonged remittent fever with such features as pneumonitis, encephalitis, myocarditis, and maculopapular rash, and have borne little resemblance to the disease in infants. Toxoplasmosis of the newborn is apparently contracted from the mother, who acquires the infection during pregnancy and who, while usually free of symptoms pointing toward the disease, nevertheless, gives srologie evidence of

Experimental congenital toxoplasmosis. III. Toxoplasmosis in the offspring of mice infected by the vaginal route. Incidence and manifestations of the disease.

A study has been made of congenital toxoplasmosis in the offspring of mice infected with Toxoplasma by the vaginal route during pregnancy. Some of the young mice were retarded in postnatal development, and some became ill or died in the 2nd to 4th weeks of life while the majority remained symptom-free in spite of the presence of toxoplasmic lesions of varying degrees of severity. Congenital toxoplasmosis developed only in offspring whose mothers had been infected on the 7th to 9th day of pregnancy. Infection of the offspring without active toxoplasmosis in the mother was not observed. The highest incidence of congenital infection (57.6 per cent) was obtained by giving 2 vaginal instillations of Toxoplasma-infected mouse brain on the 8th and 9th days of pregnancy. Mice infected before the 7th day developed placental toxoplasmosis but rarely delivered viable young. When the mother was infected after the 9th day, the offspring were normal. When congenital toxoplasmosis occurred in a litter, a majority or all of the individual offspring were usually infected. Although pathologic changes were not present in the suckling mice at birth, and did not appear before the 9th postnatal day, reasons are stated for excluding the possibility of postnatal contact or milk-borne infection. It cannot be assumed from the experimental disease that the vagina is a portal of entry of Toxoplasma in human congenital toxoplasmosis. Any route of infection leading to a maternal parasitemia during pregnancy might result in toxoplasmosis of the placenta and transmission of the disease to the offspring before birth. Unlike the restricted time interval effective in the mouse, there is a long period during the later months of pregnancy in the human being in which transplacental passage of the infection may occur. When transmission to the fetus takes place shortly before parturition, evidence of disease in the human infant, as in the mouse, may not become manifest until several weeks postpartum, and the prenatal origin of the infection may not be apparent. When the fetus becomes infected well before parturition, symptoms of congenital toxoplasmosis may be present at birth. The asymptomatic character of the infection in many of the young mice would appear to have a counterpart in certain instances of human congenital toxoplasmosis.

The Complement Fixation Reaction in Toxoplasmic Infection

A frozen and thawed extract of toxoplasma-infected rabbit brain (but not similar extracts of certain other heavily parasitized tissues) yielded an antigen which fixed complement specifically in the presence of immune sera from experimentally infected rhesus monkeys but not rabbits, dogs, and cats. This complement fixing antibody appeared within 1 to 4 weeks after inoculation, but unlike the neutralizing antibody disappeared again in most monkeys, sometimes as early as 2 months. A certain number of human beings who were known or suspected to have experienced toxoplasmic infection also gave positive complement fixation reactions. However, twenty selected individuals whose sera had neutralizing antibodies against toxo-plasma gave negative complement fixation reactions, but in none of these was there evidence of recent or active infection. While a positive complement fixation reaction does not in all cases indicate active or even recent infection, it is believed that this test may have its greatest usefulness in the rapid diagnosis of active toxoplasmosis.