Toxoplasmosis and Infectious Mononucleosis

Remington, Jack S.; Barnett, Charles G.; Meikel, Maureen; Lunde, Milford N.

doi:10.1001/archinte.1962.03620230190026

Cited by 42 publications

(4 citation statements)

References 31 publications

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“…It has been estimated to cause 3 to 7% of clinically significant lymphadenopathy (McCabe et al, 1987). Toxoplasmosis is part of the diagnostic considerations of a case of “mononucleosis” syndrome accounting for 1 to 2% of such cases (Remington et al,1962). The majority of patients have either Cytomegalovirus (CMV) or Epstein-Barr virus infections.…”

Section: Clinical Manifestations Of T Gondii Infectionmentioning

confidence: 99%

Toxoplasmosis: A history of clinical observations

Weiss

Dubey

2009

International Journal for Parasitology

694

473

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It has been 100 years since Toxoplasma gondii was initially described in Tunis by Nicolle and Manceaux (1908) in the tissues of the gundi (Ctenodoactylus gundi) and in Brazil by Splendore (1908) in the tissues of a rabbit. Toxoplasma gondii is a ubiquitous, Apicomplexan parasite of warmblooded animals that can cause several clinical syndromes including encephalitis, chorioretinitis, congenital infection and neonatal mortality. Fifteen years after the description of T. gondii by Nicolle and Manceaux a fatal case of toxoplasmosis in a child was reported by Janků. In 1939 Wolf, Cowen and Paige were the first to conclusively identify T. gondii as a cause of human disease. This review examines the clinical manifestations of infection with T. gondii and the history of the discovery of these manifestations.

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Section: Clinical Manifestations Of T Gondii Infectionmentioning

confidence: 99%

Toxoplasmosis: A history of clinical observations

Weiss

Dubey

2009

International Journal for Parasitology

694

473

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“…Heterologous immuno suppressive serums were used to compensate for the relatively advanced immunological capability of the newborn primate and because immuno suppression may facilitate the induction of lymphoreticular system dis orders [32], Interestingly, the changes were observed in monkeys inoculated with Rauscher virus rather than in the monkeys inoculated with EBV. Previous studies in humans with a mononucleosis-like syndrome have revealed evidence of infection with cytomegalovirus, rubella virus, adeno-virus, toxoplasma, and other agents [33][34][35][36][37]. It is, therefore, not surprising that a virus other than EBV is capable, in the subhuman primate, of producing hematological changes similar to those associated with infectious mono nucleosis.…”

Section: Discussionmentioning

confidence: 99%

Hematological and Serological Effects of Rauscher Leukemia Virus and Epstein-Barr Virus on Immunosuppressed Newborn Subhuman Primates

Cohen¹,

Bernstein²,

Levine³

1974

Oncology

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Newborn immunosuppressed rhesus monkeys were inoculated with cells containing Rauscher leukemia virus. Two animals developed a mononucleosis-like hematologic picture with monocytosis in the peripheral blood smear and monocyte percentages up to five times increased. Antibody levels against Epstein-Barr virus (EBV) were measured because of the possible role of this agent in mononucleosis. Due to passive transfer of antibodies from the mothers, the titer against EBV was elevated at birth in all monkeys. However, the levels gradually fell and did not rise during or after the monocytosis associated with Rauscher virus inoculation. The Paul-Bunnell-Davidsohn heterophile test remained negative. Other immunosuppressed primates were inoculated with cells containing EBV. The EBV produced serological but not hematological changes.

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“…For this reason, the skin test is useful in the diagnosis of chronic toxoplasmosis in man. A positive skin reaction virtually excludes any possibility of recent infection (26,27). In experiments with guinea pigs, Frenkel (15) -was able to demonstrate a state of DH 1 month after infection.…”

Section: Discussionmentioning

confidence: 99%

In Vivo and In Vitro Studies of Delayed-Type Hypersensitivity to Toxoplasma gondii in Guinea Pigs

1971

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Delayed-type hypersensitivity develops late in the course of human toxoplasmosis, and a positive skin test is of some value for implicating chronic or eliminating acute forms of toxoplasmosis as a cause of disease. Toxoplasma-infected guinea pigs were studied to determine the onset and development of delayed-type hypersensitivity. Both the toxoplasmin skin test and the in vitro macrophage migration inhibition technique indicated that delayed hypersensitivity to toxoplasma antigen existed as early as 1 week after infection. The mechanism responsible for the observed inhibition of macrophage migration in vitro appeared to be an inhibitory factor(s) released from sensitized lymphoid cells in the presence of antigen.

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Toxoplasmosis and Infectious Mononucleosis

Cited by 42 publications

References 31 publications

Toxoplasmosis: A history of clinical observations

Toxoplasmosis: A history of clinical observations

Hematological and Serological Effects of Rauscher Leukemia Virus and Epstein-Barr Virus on Immunosuppressed Newborn Subhuman Primates

In Vivo and In Vitro Studies of Delayed-Type Hypersensitivity to Toxoplasma gondii in Guinea Pigs

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