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Neurologic disease occurs frequently in patients infected with the human immunodeficiency virus (HIV), and a large body of literature now exists detailing the various infections, neoplasms, and other conditions that can affect the central nervous system (CNS) or the peripheral nervous system in children and adults with AIDS, persistent generalized lymphadenopathy, or (in some cases) only serologic evidence of retroviral infection. Although certain opportunistic infections (toxoplasmosis, cryptococcosis, progressive multifocal leukoencephalopathy, and herpesviral infections) and CNS lymphomas often produce CNS disease in patients with AIDS, it is now clear that many cases of neurologic disease are caused by a group of disorders thought to be related to direct CNS infection by the AIDS retrovirus. Disease of the peripheral nervous system is also being increasingly recognized; some cases probably have an autoimmune basis.

The authors compared a group of 197 women with different ascertained forms of toxoplasmosis and a group of 72 women with negative serological reactions on toxoplasmosis and hereby they revealed that the consumption of insufficiently heated meats as well as the contact with animals (rearing and digestion embowelling or drawing of coat) play an eminent part. As test animals above all cats were used. The results of the two groups were compared and a significant difference between them was ascertained for the consumption of the insufficiently heated meat as well as for the contact with the animals. The women with toxoplasmosis more frequently consumed insufficiently heated meat and had more contact with cats and other animals.

Pericarditis caused by toxoplasma infection is exceptional: 16 cases only have been published since 1943. The authors report a case of Hodgkin's disease associated with, and revealed by, toxoplasmic pleuro-pericarditis, and they review the literature on this complication of toxoplasmosis. Since the infection can be cured and since pericarditis may become chronic and constrictive if untreated, toxoplasmosis should be envisaged and confirmed or infirmed by serological tests in all patients presenting with pericarditis of uncertain origin. Provided it has not reached the chronic stage, toxoplasmic pericarditis responds well to the conventional treatment with pyrimethamine and sulfonamides.

Although opportunistic infections after allogeneic bone marrow transplantation are common, cerebral toxoplasmosis has only been reported once. We report a case of lethal cerebral toxoplasmosis in a patient with acute leukemia who had been submitted to intensive cytotoxic therapy and allogeneic marrow rescue. The clinical course was characterized by an unusually sudden neurological onset. It was remarkable that, in this case, toxoplasma serology remained repeatedly negative. The autopsy revealed that the infection also involved the myocardium. Serological data and pathology findings are presented.

A retrovirus designated HTLV-III has been recovered from patients with AIDS and patients with pre-AIDS syndrome. This virus, which appears to be the cause of AIDS, attacks and suppresses T-helper lymphocytes, rendering the host susceptible to a variety of serious protozoal, fungal, mycobacterial, bacterial and viral infections, as well as neoplasms. Pneumocystis carinii and cytomegalovirus are frequent causes of pulmonary infiltrates in AIDS.

About 2 cases reports, the authors stress on the principal characteristics of neurotoxoplasmosis : neurologic and/or febrile symptoms in a immuno-compromised patient with predominantly a deficient cellular mediated immunity. Cerebrospinal fluid, electroencephalographic and tomodensitometric abnormalities. Importance of serology in the survey of high-risk patients. Bad prognosis of acute clinical pictures. Potential regression of subacute and chronic forms.

Sera from 1,050 persons, 69 cats, 18 goats, 23 bovines, 2 monkeys, and 1 dog from 7 villages in South Kalimantan were tested for indirect hemagglutination Toxoplasma gondii antibodies. A seroepidemiologic study with the methylene blue dye test was conducted 1 year later at one village among 25 families and their cats. Toxoplasma antibody prevalence in man in different villages varied from 9.7% to 51.0%. Forty-one percent of the cats and 61% of the goats also had positive titers. None of the bovines was positive. The epidemiologic study indicated that, in spite of the presence of many infected cats in the village, goat meat was a significant source of Toxoplasma infection for man in this population.

In immunocompromised patients with cerebral toxoplasmosis, the tachyzoite forms rather than cystic and bradyzoite forms of the protozoon are commonly seen. These tachyzoites are minute, scattered among cellular debris, sometimes lodged inside macrophages and neutrophils, and difficult to visualize by light microscopy, even with special stains. Immunodiagnostic tests may be falsely negative due to inability of the host to produce appropriate antibodies. Isolation of the organism is dangerous because Toxoplasma gondii is highly infective. In this situation, transmission electron microscopy (EM) may be a diagnostic tool of choice. It demonstrates the fine definitive features of the protozoon and can be expedited to give results in five hours. Further evaluation of EM for diagnosing possible toxoplasmosis in immunocompromised patients is indicated.

Since corticosteroids were introduced, a steadily increasing number of opportunistic pathogens have been causing major disease in both systemically and locally compromised hosts. In ocular disease, the most common cause of compromise (and of infection with such opportunistic pathogens as the herpeviruses, many gram-negative bacteria, numerous fungi and Toxoplasma) is the topical use of corticosteroids and antibiotic-corticosteroid preparations. To avoid the damaging and sometimes blinding results of opportunistic infection, the use of these preparations should be carefully restricted.

Infectious complications are the cause of death in the overwhelming majority of patients with the acquired immunodeficiency syndrome (AIDS). These infectious complications are outstanding in severity and number. Infecting organisms are mainly those which take advantage of defective T-cell function. Many cause latent infections which can reactivate and cause disease in AIDS patients because of immunosuppression. Serological diagnosis of infections in AIDS patients is complicated because of the defect in B-cell function; rising antibody titers are not observed in most patients with infectious complications. The natural history of AIDS is one of repeated infections leading to a fatal outcome. However, treatment for most of the bacterial, fungal, and parasitic infections is effective. Treatment of some of these infections must be prolonged indefinitely because of the tendency to relapse.

To determine the prevalence of infection with Toxoplasma gondii in the Fars Province of Iran, sera from 300 patients hospitalised at the Pahlavi University Medical Centre in Shiraz were tested. There were 157 males and 143 females, with a mean age of 39 years (range 10--80 years). The indirect immunofluorescent antibody technique was used and titres of 1:16 and above were considered positive. Eighty eight patients of whom 50 were male and 38 female (mean age 41 years, range 14--80 years) had positive sera. Of these 88 patients, 35 (40%), 25 (28%), 17 (19%), 5 (6%) and 6 (7%) had antibody titres of 1:16, 1:32, 1:64, 1:128 and 1:256 respectively. One hundred and twenty three of the 212 patients with negative sera (58%) had contact with cats. A similar proportion of patients with positive sera [51 of 88 (58%)] also had contact with cats. It is concluded that a substantial proportion of our patients (29%) show serological evidence of infection with Toxoplasma gondii. A significant correlation between exposure to cats and the consumption of improperly cooked meat on the one hand and seropositivity on the other, could not be demonstrated. There was no significant increase in the incidence of seropositivity with increasing age (P = 0.35).

A 47-year-old patient with AIDS and cerebral toxoplasmosis was treated with sulfadiazine pyrimethamine for 5 days. After developing a severe rash his regimen was changed to clindamycin 600 mg q 6 h intravenously and pyrimethamine 25 mg daily, given for 37 days. This resulted in improvement of clinical symptoms and complete resolution of CT scan abnormalities. Clindamycin combined with pyrimethamine may be a useful alternative therapy for cerebral toxoplasmosis in patients who can not tolerate sulfonamides.

Pneumocystis carinii and Toxoplasma gondii are the commonest protozoans causing infections in patients with acquired immunodeficiency syndrome (AIDS). P. carinii is almost exclusively a pulmonary pathogen and caused the commonest serious infection experienced by AIDS patients. The clinical findings are those of progressive pneumonia. Diagnosis requires microscopic examination of lower respiratory secretions or lung tissue. Pentamidine or combinations of trimethoprim and sulfamethoxazole are equally effective (85% recovery), but about one-half of patients thus treated experience severe toxicity. T. gondii infections occur primarily in the brain; patients present with focal seizures or neurologic deficit and have focal abnormalities as assessed by computed tomography. Serologic tests for toxoplasmosis are rarely diagnostic in AIDS patients, and most patients are treated empirically with a combination of pyrimethamine and sulfonamide. Less invasive diagnostic tests and better chemotherapeutic agents are required for both pneumocystosis and toxoplasmosis.

Sera from 1661 persons in 12 age groups from 0 to 79 years were titrated for toxoplasma antibodies in the indirect immunofluorescence test. The sera were collected from patients with symptoms suggestive of acute, mainly respiratory, viral infections. After the first year of life, the prevalence of antibodies started to rise, reaching 59% between 40 and 79 years of age. From the prevalence of antibodies in different age groups the annual infection risk, i.e, the risk of a non-immune person acquiring toxoplasma infection, was estimated for successive age periods. The estimated annual infection risk increased from 0 . 5% in early childhood to 3% during adolescence and early adult life. Approximately 70--80% of females entered the age of reproduction without evidence of seroimmunity to toxoplasma. The risk of primary infection during pregnancy was estimated from the age distribution of parturient women in The Netherlands in 1975 and the age-specific incidence of primary infections, i.e. the incidence in the total population of susceptible and immune persons. This incidence of primary infection decreased from 1 . 62% per 9 months at the age of 17 1/2--20 years to 0 . 37% at the age of 37--45 years. The incidence of primary infections in pregnant women was estimated to be 1 . 25%.

With reference to a case of malignant toxoplasmosis in a patient with angioimmunoblastic lymphadenopathy, the following features are recalled: in compromised hosts, clinical manifestations of malignant toxoplasmosis are highly variable, with neurologic signs and fever being predominant; the occurrence of lesions of the fundus, such as chorioretinitis, is an essential clue to the diagnosis; serologic tests for toxoplasmosis should be performed routinely at each stage of the disease in order to ascertain seroconversion through comparison with baseline results.

A survey of the literature of neurological manifestations associated with the acquired immune deficiency syndrome (AIDS) shows a broad disease spectrum affecting approximately one third of the patients in large hospital series. The complications include focal cerebral lesions caused by abscesses, lymphomas, leucoencephalopathy or infarcts as well as encephalitis, meningitis and myelitis. Most opportunistic infections of the central nervous system presumably are caused by toxoplasma gondii, cytomegalovirus and cryptococcus neoformans. One tenth of all patients have neurological disease as their initial symptom of AIDS. The diagnosis should always be considered in patients at risk and in males with an unusual neurological history or with a peculiar CT scan of the brain. Besides the opportunistic complications of AIDS, LAV/HTLV-III itself probably attacks the nervous system and gives rise to concomitant lesions of the long tracts of the spinal cord with ataxia, paresis and spasticity and to subacute encephalopathy and peripheral nerve abnormalities as well.

During the period from 1981 through 1984, 14 immunocompromised homosexual males with intermediate or high-grade non-Hodgkin's lymphoma were seen at University of Texas M.D. Anderson Hospital and Tumor Institute. Six patients had diffuse large-cell lymphoma, seven had diffuse undifferentiated lymphoma, and one had unclassifiable lymphoma that suggested large-cell lymphoma. Eight patients had the acquired immunodeficiency syndrome (AIDS) and five had the AIDS-related complex. Kaposi's sarcoma was initially present in four patients and developed later in two others. The patients with diffuse large-cell lymphoma were characterized by more severely altered immune parameters, multicentric brain mass lesions, pretherapy opportunistic infections, lower performance status, poor response to therapy, and death in all within six months. The undifferentiated lymphoma group had preceding generalized reactive lymphadenopathy, less severe immune dysfunction, and excellent response to combination chemotherapy, with survival time greater than 19 months in three patients. Twelve of the patients had extranodal sites of lymphoma at presentation. There is a definite trend for the development of aggressive non-Hodgkin's lymphomas with unusual sites of extranodal involvement in immunocompromised homosexual males, with the potential for good tolerance to combination chemotherapy and improved survival in the subgroup without severe concomitant opportunistic infections.

A patient is described who was thought to have developed a malignant lymphoma of the brain after renal transplantation. The correct diagnosis was toxoplasmosis.

The neuropathological features are presented of an autopsy series of 43 renal transplant recipients. Inflammatory CNS lesions were found in 18 cases and were attributable to secondary CNS involvement in bacterial or fungal septicaemia (8 cases) or in localized extraneural infections (5 cases). Mixed bacterial-fungal infection and bacterial-fungal-viral triple infection were seen in one case each. Isolated toxoplasmic granulomas were observed in two cases. No tissue changes typical of CNS viral infections, including cytomegaly, were found except for small glial nodules in the brain stem in 7 cases. Massive intracerebral haemorrhages were seen in 2 cases after haemodialysis; subdural haematoma occurred once. Non-specific changes including brain oedema and diffuse glial poliodystrophy were found in many cases; vascular lesions and purpura occurred only seldom. A meningocerebellar malignant lymphoma, probably of metastatic origin was found in one case. Clinico-pathological correlation was poor in 5 cases; this is considered to be due to immunosuppressive therapy, which may mask either clinical expression of severe CNS lesions or morphological expression of viral encephalitis.

A 31-year-old woman with long-standing amyopathic dermatomyositis developed a maculopapular rash resembling erythema multiforme in some areas, accompanied by lymphadenopathy and malaise. An acute infection with Toxoplasma gondii was found to be the cause of clinical symptoms that mimicked an exacerbation of the underlying condition.

Cerebral toxoplasmosis is the most common cause of focal CNS disease complicating AIDS and may afflict 10% to 33% of such patients. We present the clinical, neuroradiological and immunological findings in 5 cases with cerebral toxoplasmosis complicating the acquired immune deficiency syndrome. All patients had focal neurological signs and symptoms; CT scan findings included single or multiple lesions with ring contrast enhancement, mass effect and oedema. CSF analysis showed increased protein levels, decreased glucose levels and pleocytosis; CSF IgG antitoxoplasma antibodies were positive in 4 patients; serum IgG antitoxoplasma antibodies were positive in all patients, while IgM resulted always negative in serum and in CSF. After therapy, in 2 cases CT scans showed small areas of encephalomalacia replacing the abscesses. We think that non-invasive techniques (CT scans, CSF and serum immunochemical tests) together with the finding of a favourable response to therapy may be useful for the diagnosis of cerebral toxoplasmosis, allowing to avoid invasive technique such as cerebral biopsy.

Toxoplasma infection comes from oöcysts in cat faeces and from tissue cysts in the flesh of infected animals. It can also be transferred congenitally by trophozoites. Where cats are common, where social, climatological and geological conditions favour the survival and maturation of oöcysts, and where raw or undercooked meat is rarely eaten infection comes predominantly from oöcysts. Where raw or undercooked meat is commonly eaten and opportunities for contact with cats and their faeces are few, infection comes predominantly from tissue cysts. Infection is very common in all species of mammals and birds throughout the world, but rarely does any harm. Exceptions are when lowered resistance due to disease or cytotoxic or immunosuppressive drugs allow latent infection to become patent and when infection is transmitted congenitally.

A 19-year-old immunosuppressed male patient, after renal transplantation, developed at the 10th postoperative day (p.d.) fever, anemia hepatosplenomegaly and plaquetopenia; this condition deteriorated progressively and was complicated by drowsiness and generalized convulsions which persisted until the death at the 29th p.d. Autopsy revealed acute encephalitis characterized by multiple disseminated small lesions in the brain, containing cysts and trophozoites of Toxoplasma gondii. The diagnosis was not done during life, as occurred with most of previously reported cases, a fact that points to the necessity of preventive controlling measures of these patients before the institution of immunosuppressive measures.

A 45-year-old man with the Acquired Immunodeficiency Syndrome (AIDS) and CNS toxoplasmosis presented with acute renal failure, hematuria, and renal colic shortly after starting treatment with sulfadiazine. Ultrasound examination of his kidneys was suggestive of intraparenchymal crystallization of sulfadiazine. His renal failure and ultrasound findings rapidly resolved with alkaline hydration. On rechallenge with sulfadiazine, he again developed renal insufficiency and ultrasonic findings consistent with stones. The use of sulfadiazine in the treatment of CNS toxoplasmosis in AIDS patients should be monitored carefully with the recognition that this form of crystalline-induced acute renal failure can occur in a dehydrated patient.

We used immunoblotting to ascertain if toxoplasma encephalitis in disease caused by the human immunodeficiency virus (HIV) could be diagnosed by the appearance of characteristic antibodies recognizing specific Toxoplasma antigens. The profile of antibodies to Toxoplasma was examined in human serum and cerebrospinal fluid from patients with chronic and acute toxoplasmosis with or without HIV infection. Many Toxoplasma antigens were recognized by all sera; the majority were presumably surface proteins, as determined by 125I labeling. All sera recognized antigens at 38, 35, 28, and 26 kilodaltons. No specific antibody or pattern of antibodies distinguished between groups of patients. A 120-kilodalton antigen recognized by sera from Atlanta was not, however, seen in most sera from New York. Study of the recognition of the antigens of different strains of Toxoplasma gondii (RH, C56, T100) by the same human sera demonstrated strain-specific antigenic differences. These strain variations may account for the antibody diversity among the patients studied.

A retrospective review of cranial CT scans obtained over a 4 year period in patients with acquired immunodeficiency syndrome (AIDS) and documented central nervous system (CNS) pathology is presented. The spectrum of diseases and the value of CT in detecting new, recurrent, and superimposed disease processes were determined. Fifty-one AIDS patients with confirmed CNS pathology were identified. Six of them had two coexistent diseases. Opportunistic infections predominated, especially Toxoplasma encephalitis and cryptococcal meningitis, while tumor was seen infrequently. Initial CT was positive in 76% of cases. In contrast to meningeal processes, where it was not very effective, CT was very sensitive in detecting most parenchymal disease processes. Characteristic although not pathognomonic CT patterns were found for certain diseases. Improvement or resolution of CT abnormalities in patients on medical therapy for Toxoplasma encephalitis correlated well with clinical improvement. Recurrence of CT abnormalities correlated well with medical noncompliance. The optimal contrast enhancement technique for detecting CNS pathology and for monitoring the effectiveness of medical therapy was also evaluated by a prospective study in which both immediate (IDD) and 1 hr delayed (DDD) double-dose contrast CT scans were compared. The examination found to be diagnostically superior in 30 of the 41 IDD/DDD studies was the delayed scan. It is recommended that CT be used routinely and with the 1 hr DDD scan to evaluate and follow AIDS patients with neurologic symptoms and/or signs.

Central nervous system toxoplasmosis is a well known disease of immunocompromised patients. Neuropathologic examinations have only rarely demonstrated spinal cord involvement. This report describes a fatal case of toxoplasmosis that presented with a subacute myelopathy. Toxoplasmosis should be considered in immuno-compromised patients, including patients with the acquired immune deficiency syndrome, that develop intramedullary lesions of the spinal cord.

Lymphocyte blastogenic transformation in response to Toxoplasma lysate antigen was markedly impaired in six of eight patients with chronic, latent Toxoplasma gondii infection and treated Hodgkin's disease. None of these patients with serum antibody to T. gondii measured by the Sabin Feldman Dye test and impaired lymphocyte transformation to T. gondii antigens had clinical or serologic evidence of disseminated, active infection with T. gondii. Partial depletion of adherent mononuclear leukocytes improved the impaired lymphocyte transformation of three of six patients; treatment of cultures from all patients with indomethacin improved their blastogenic transformation but culture with normal heterologous serum did not. These studies indicate that lymphocyte blastogenic response to T. gondii antigens is impaired in some patients with chronic, latent T. gondii infection and treated Hodgkin's disease but that this impairment of lymphocyte function is not sufficient to cause reactivation of chronic, latent T. gondii infection.

Opportunistic infections in patients with acquired immunodeficiency syndrome (AIDS) require hematotoxic drugs. Neutropenia and anemia are the major hematologic abnormalities attributed to zidovudine (AZT). Concomitant medications associated with an increased frequency of toxicity are trimethoprim-sulfamethoxazole (cotrimoxazole), sulfadiazine, pyrimethamine, ganciclovir. AZT is stopped during initial treatment then reintroduced at full dosage with cotrimoxazole, at reduced dosage with sulfadiazine + pyrimethamine or ganciclovir.

The radiologic studies of 200 consecutive AIDS patients with neurologic symptoms were evaluated to determine their diagnostic specificity and prognostic value. Of 81 patients with initially normal CT scans, four (5%) later developed progressive neurologic illness. Of 75 patients with CT evidence of diffuse cerebral atrophy, 12 (16%) later developed CT abnormalities or had postmortem CNS disease. CT scans showed mass lesions initially in 44 patients and later in an additional seven patients. Although toxoplasma gondii infection was the most frequent cause of these lesions, the CT characteristics of cerebral toxoplasmosis are too nonspecific to warrant diagnosis without biopsy. Preliminary evidence suggests that MRI may be more sensitive than CT in detecting intracranial disease in patients with AIDS.

Authors report a case of fatal CNS toxoplasmosis in a young homosexual man suffering from Kaposi angio-sarcoma. This paper is principally concerned with CT scan and neuropathological correlations.