Background: In 1996 the seroprevalence of schistosomiasis in expatriates and travelers who had contact with Lake Malawi, a fresh water source thought to be schistosomiasis-free, was measured at 32%. Clinicians in Arusha, Tanzania, questioned the prevalence of Schistosoma infection in expatriates living in the Arusha region, and how schistosomiasis might relate to symptoms of chronic fatigue in Arusha expatriates.Method: We performed a cross-sectional survey of 80 expatriates living in the Arusha region of Tanzania to determine the seroprevalence of schistosome infection. Whole blood was analyzed by the Falcon assay screening test-enzyme-linked immunosorbent assay (FAST-ELISA) for the presence of species-specific Schistosoma mansoni and Schistosoma haematobium antibodies to microsomal antigens of adult Schistosoma worms, followed by confirmatory enzyme-linked immunoelectrotransfer blot (Western blot). Volunteers answered a questionnaire which included length of residence in Arusha, risk factors, symptoms, and previous diagnosis of schistosomiasis.Results: Of the 80 expatriates sampled, 8 (10%) were positive for schistosomiasis (6 to S. mansoni only, 1 to S. haematobium, 1 to both species). Significant risk factors, elicited by questionnaire, included longer residence in the Arusha region (p = .020), history of fatigue (p = .010) and myalgias (p = .047), and previous diagnosis of schistosomiasis by stool or urine ova (p = .0007).Conclusion: The lower seroprevalence of schistosomiasis in Arusha expatriates, compared with expatriates and travelers to Lake Malawi, suggests a regional variation of rate of schistosomiasis infection. Although a history of fatigue and myalgias was related to seropositivity, there is no strong evidence that schistosomiasis infection is the cause of chronic fatigue in Arusha expatriates.

The immunologic responses that mediate viral clearance of and recovery from hantavirus cardiopulmonary syndrome (HCPS) due to Sin Nombre (SN) virus are unknown. Serial serum samples from 26 patients with acute SN virus infection were tested for IgG, IgA, and IgM reactivity to recombinant viral nucleocapsid (N) and glycoprotein G1 antigens by a novel strip immunoblot assay. The titers of antibodies capable of neutralizing SN virus in vitro also were determined for each sample. At admission, patients with severe disease had lower titers of IgG antibodies to SN virus N antigen (P<.033) and lower neutralizing antibody titers (P<3.4x10-5), compared with patients with mild disease. These data suggest that a strong neutralizing antibody response may be a predictor of effective clearance of and recovery from SN virus infection and raise the possibility that passive immunotherapy may be useful in HCPS.

Hantavirus pulmonary syndrome (HPS) is a severe cardiopulmonary illness resulting in death in approximately 45% of cases. The most frequently recognized etiologic agent of HPS in North America, Sin Nombre virus (SNV), is transmitted to humans from its primary rodent reservoir, Peromyscus maniculatus (deer mouse), by direct contact with infected rodents, rodent droppings, or nests or through inhalation of aerosolized virus particles from mouse urine and feces. Sporadic cases occur throughout the United States and Canada, but the potential for spread from rodents to humans in 1998 probably has increased because of increased rodent population densities in some regions of the country. This report describes three cases of HPS that occurred in the southwestern United States with onsets of illness during April 15-28, 1998, and recommends methods to avoid exposure to rodents inside and around human dwellings.

Hantavirus pulmonary syndrome is an acute pneumonitis with a high mortality rate that is caused by a newly recognized hantavirus. Four Corners virus (also known as Muerto Canyon virus and Sin Nombre virus) is enzootic among deer mice (Peromyscus maniculatus). Incidental transmission to humans can result in a disease characterized by rapidly progressive respiratory insufficiency, diffuse noncardiogenic pulmonary edema, vascular volume contraction with hemoconcentration, lactic acidosis, depressed cardiac output, and cardiac dysrhythmias preterminally. The onset of pulmonary edema is preceded by a prodrome of fever and severe myalgias. Characteristic laboratory abnormalities include thrombocytopenia, leukocytosis with prevalent immature myeloid cells, and the presence of immunoblastic lymphocytes in the peripheral blood. Agent-specific diagnosis is based on the detection of Four Corners virus-specific antibodies in serum by Western blot assays and the detection of Four Corners virus RNA in peripheral blood mononuclear cells by the reverse transcriptase-polymerase chain reaction. Effective treatment depends on the rapid institution of intensive care support.

Hantaviruses are parasites of small mammals, predominantly peridomestic and commensal rodents. They have a worldwide distribution. Hantavirus-related illness occurs in rural areas where humans come into contact with rodents. In most cases human infection is manifested by one of a variety of acute illnesses involving hemorrhagic fever and renal disease. In May 1993, a cluster of patients with an acute pulmonary disease with high mortality was noted in the Four Corners region of the southwestern United States. Serologic and genetic studies indicated that the etiologic agent was a novel hantavirus. The uncertainty engendered by the emergence of a new disease with high mortality forced a rapid response by state and federal agencies and by the University of New Mexico Medical Center, Albuquerque, where most patients from this region were referred. Considerable progress has been made in identifying infected cases on clinical and laboratory grounds and in ensuring that appropriate supportive care is made available to patients as soon as they are suspected of having hantaviral infection. Cases of hantavirus pulmonary syndrome--both new and retrospectively diagnosed--are still being recognized throughout the western United States. Many important questions remain unanswered.

The reluctance of students in health professions to care for AIDS patients is partially based on the perceived risk of transmission of HIV from patient contact. We hypothesize that fear of contagion is due to lack of knowledge and deep‐rooted attitudes and emotions existing even in areas of low HIV seroprevalence. We tested this hypothesis on medical, nursing, and medical technology students. Using a questionnaire that yielded four scales, results showed only 58% of students were knowledgeable, 81% were fearful of contagion, 57% were homophobic, and 8% had death anxiety. Lack of knowledge was correlated with fear of contagion (p < .05), whereas homophobia was weakly associated (p = .08). We conclude that this perceived risk of infection is a result of lack of knowledge, disbelief of the facts, and the interplay of personal values and emotions. Alternative educational methods are needed to increase students’ knowledge and to encourage students to examine their personal feelings and attitudes.

The hemolytic-uremic syndrome (HUS) following dysentery caused by S. dysenteriae Type 1, characterized by microangiopathic hemolytic anemia and acute renal insufficiency, is clinically similar but not identical to the idiopathic HUS. We studied renal necropsy specimens of nine children who died of HUS following shigellosis by light and immunofluorescent microscopy and compared them to 12 controls: six cases with severe shigellosis without HUS, and six with pneumonia or sepsis. Eight of nine HUS cases showed cortical necrosis, extensive glomerular thrombosis or arterial thrombosis. Cases without HUS showed only scattered glomerular fibrin thrombin and widening of the mesangium. Among seven HUS cases studied by immunofluorescent microscopy, three demonstrated deposition of glomerular IgM and complement (C3) and one of the three had IgG and IgA as well; four cases had neither immunoglobulin or complement deposits. Among nine controls, two demonstrated IgM and three IgG, but none had C3. Both HUS and non-HUS cases had fibrin deposition. In the three HUS cases studied by electron microscopy intracapillary material (fibrin and platelets) was seen in all three, and sparse electron-dense deposits in mesangial matrix in one. The data indicate that the renal histopathology in the HUS following shigellosis consistently presents as a severe thrombotic microangiopathy, but lacks the characteristic endothelial and mesangial lesions of idiopathic HUS. The infrequent demonstration of glomerular immunoglobulin deposition fails to support an immunoglobulin-mediated pathogenesis.

Reporte de investigacion -- Universidad de Costa Rica, Instituto de Investigaciones en Salud. 1978