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We report a case of a 39-year-old West African man with unknown human immunodeficiency virus status diagnosed with gastric toxoplasmosis as the presenting manifestation of acquired immunodeficiency syndrome. Toxoplasma gondii is common in severely immunosuppressed patients and most frequently involves the central nervous system, followed by the eye, myocardium and skeletal muscle, lungs, bone marrow, and peripheral blood. For unclear reasons, gastrointestinal involvement is exceedingly rare and occurs in the context of severe immunosuppression and disseminated disease. To our knowledge, this is the first report in the English literature of a patient with isolated, manifest gastric toxoplasmosis without evidence of concomitant cerebral or extracerebral involvement. It is important for both the clinician and the pathologist to maintain a high index of suspicion for toxoplasmosis in immunosuppressed patients presenting with nonspecific symptoms of gastritis and radiologic and endoscopic presence of thickened gastric folds with or without ulceration.

Objective: Owing to the increasing number of patients with acquired immunodeficiency syndrome and immunosuppressed transplant patients, disseminated Toxoplasma gondii has emerged as a potentially fatal pathogen. Common presentations include encephalitis, pneumonia, and myocarditis. The objective of this report is to describe the clinical course, histologic features, and outcome in two immunocompromised patients with disseminated toxoplasmosis presenting with parasitemia and panniculitis., Materials and Methods: Two cases of disseminated toxoplasmosis presenting with parasitemia (patient 1) and panniculitis (patient 2) were retrieved from the clinical, surgical, and autopsy pathology archives of Vanderbilt University Medical Center, Nashville, Tenn. The histology and diagnostic approaches used are reported. Charts were reviewed for primary diagnosis, therapy protocols, clinical presentation of infection, and outcome., Results: Patient 1 developed a clinically unexplained sepsis syndrome shortly after heart transplantation; T gondii parasitemia was diagnosed by examination of peripheral blood smears. The diagnosis was confirmed at autopsy. Patient 2 was a child undergoing induction chemotherapy for lymphoma who developed rapidly progressive neurologic deterioration accompanied by a maculopapular skin rash; T gondii panniculitis was diagnosed retrospectively when histologic examination was combined with immunohistochemistry. Autopsies performed in both cases confirmed widely disseminated infection., Conclusions: Disseminated toxoplasmosis should be considered in the differential diagnosis of immunocompromised patients with culture-negative sepsis syndrome, particularly if combined with neurologic, respiratory, or unexplained skin lesions. Examination of Wright's-stained peripheral blood smears or antitoxoplasma immunoperoxidase studies of skin biopsies may be diagnostic and allow rapid initiation of antibiotic therapy. Autopsy findings contributed to both of our cases by documenting the wide-spread heavy parasite burden and demonstrating numerous diagnostic T gondii cyst forms.

We describe a variety of toxoplasmic lesions in seven patients with the acquired immunodeficiency syndrome. The first patient had multiple small-intestinal ulcers associated with Toxoplasma tachyzoites and high antibody titers; he died of disseminated histoplasmosis. The second patient, who died of tuberculosis, also had an inactive chronic Toxoplasma infection, with tissue cysts in the brain that were associated with glial nodules. A third patient died of Toxoplasma encephalitis, manifested by multiple foci of necrosis associated with Toxoplasma tachyzoites, cysts, and hypertrophic arteritis. A fourth patient had been treated for toxoplasmic encephalitis with co-trimoxozol (trimethoprim-sulfamethoxazole combination) for 3 to 4 days and showed degenerating tachyzoites associated with necrotic areas. A fifth patient, treated for toxoplasmic encephalitis with co-trimoxazol for 14 days, had necrotic lesions associated with Toxoplasma antigen and a few cysts. A sixth patient with encephalitis and Toxoplasma tachyzoites and young cysts in the biopsy showed healed brain lesions after 22 days of treatment. A seventh patient, diagnosed radiologically and serologically with Toxoplasma encephalitis, was treated for 7 months; his ring-enhancing lesions subsided, and he died of a central nervous system lymphoma. Toxoplasma could not be isolated from the brain, although toxoplasmic DNA was detected in the brain and heart by polymerase chain reaction. The pathogenesis of the range of these lesions, their diagnosis, and the possibility of terminating Toxoplasma infection by prolonged chemotherapy are discussed.

Encephalitis due to the protozoan Toxoplasma gondii has emerged as a common cause of central nervous system disease in patients with acquired immunodeficiency syndrome. Extraneural disease is less common and more difficult to diagnose. We report a case of widely disseminated toxoplasmosis that presented as acute gastrointestinal and pulmonary disease in a patient without a prior diagnosis of acquired immunodeficiency syndrome. The diagnosis of toxoplasmosis was made only at autopsy. Antemortem diagnosis of disseminated T gondii infection requires a high degree of clinical suspicion and the prompt utilization of appropriate diagnostic testing. Since toxoplasmosis is a potentially treatable opportunistic infection, diagnosis allows the swift institution of anti-Toxoplasma therapy.

Pituitary morphology was studied in 49 autopsied patients with acquired immunodeficiency syndrome. Direct infectious involvement was noted in six adenohypophyses (12%), including five cases by cytomegalovirus and one by Pneumocystis carinii. Two cases with neurohypophysial lesions presumably caused by cytomegalovirus and one questionable case of Toxoplasma gondii were also observed. In all instances these changes were associated with generalized and/or cerebral infection by these same agents. Neither Kaposi's sarcoma nor malignant lymphoma was encountered in the pituitary glands. Acute necrotic foci, presumably due to infarction, were noted in four cases. Four pituitary microadenomas (8%) and four hyperplastic nodules were identified. The incidence of such noninfectious lesions, as well as the prevalence and distribution of the various immunoreactive adenohypophysial cell types, were similar to those seen in the pituitary glands of age-matched male control patients.

A 40-year-old man had disseminated toxoplasmosis preceded by miliary tuberculosis and associated with skin anergy. In previously reported cases of disseminated toxoplasmosis, the three organs most commonly involved were brain, heart, and lungs. The histopathologic picture of toxoplasmal lymphadenopathy was not present in our case or in previously reported cases. Therefore, we believe that the diagnosis of disseminated toxoplasmosis should not be rejected simply because of the likely absence of toxoplasmal lymphadenopathy in biopsy material. The thymus in our case was morphologically abnormal and showed features suggestive of an autoimmune process.

Fourteen cases of toxoplasmosis in subjects at autopsy with acquired immunodeficiency syndrome are reviewed. Death was related to toxoplasmosis in four cases: in three from central nervous system complications and in one case from myocarditis. In six cases the infection was identified outside of the central nervous system and in only two cases was infection disseminated to multiple extracerebral organs. Review of clinical history and laboratory data revealed no specific risk factors or laboratory indicators associated with toxoplasmosis in acquired immunodeficiency syndrome. Though inflammatory cell infiltrates often accompanied disseminated infections, diagnosis could be made with certainty only by finding characteristic Toxoplasma organisms, either as free tachyzoites, pseudocysts, or as true parasitic cysts. We found immunohistochemical staining to have limited usefulness for diagnosis in extracerebral sites. Characteristic Toxoplasma organisms were most readily identified in central nervous system tissues in our acquired immunodeficiency syndrome population, making this the most useful site for diagnosis.

Seven brain biopsies from patients with the acquired immune deficiency syndrome (AIDS) were reviewed. Toxoplasmic encephalitis was diagnosed in five patients, neurotuberculosis in one patient, and no diagnosis was made in the seventh patient. Frozen sections and smears enabled a rapid diagnosis to be made in four patients. Routine histochemical analysis was diagnostic in five patients, and the immunoperoxidase technique for Toxoplasma gondii was required for diagnosis in an additional case. Brain biopsy is a valuable and safe method in the evaluation of mass lesions in patients with AIDS.

Testicular infection due to Toxoplasma gondii in two young men with the acquired immunodeficiency syndrome manifested as a multifocal necrotizing lesion of the testicular parenchyma. At the periphery of the necrotic area were inflammatory infiltrates consisting mainly of eosinophilic leukocytes. The Toxoplasma organisms were mainly found within the necrotic seminiferous tubules, where they were identified with periodic acid-Schiff or May-Grünwald-Giemsa stains and by electron microscopy. The histologic pattern of this orchitis is characteristic and should be suspected in patients with severe disorders of the immune response.

We describe an unusual intranodal vascular proliferation following acute toxoplasmosis in a man. This proliferation is distinct from other benign vasoformative nodal lesions. It could be interpreted as a reactive healing process that might be misdiagnosed as nodal Kaposi's sarcoma. Some criteria to avoid such misdiagnosis are presented.

Two adult patients receiving immunosuppressive therapy experienced toxoplasma cerebritis. In one, the brain findings were typical of this form of the disease in adults, but the clinical features and brain lesions of the other were atypical, and had some resemblance to those seen in congenital toxoplasmosis. It is suggested that two patterns of encephalitis can occur in opportunistic toxoplasma infections, a common form with random foci of gland necrosis associated with numerous intracerebral organisms, and another with vascular lesions and periventricular necrosis. The latter has morphologic features in common with congenital encephalitis, and may also have a similar pathogenesis.

Data on 54 persons who died of acquired immunodeficiency syndrome were reviewed for lesions of the heart. These persons met the criteria of the Centers for Disease Control (Atlanta) for acquired immunodeficiency syndrome. Pathologic changes were seen in 30 patients (55%). Changes were seen in the endocardium (17%), myocardium (83%), and epicardium (3%). The most frequent finding was lymphocytic myocarditis. Six of these were due to Toxoplasma myocarditis. Only one patient succumbed to cardiac arrest.