Chronic pulmonary histoplasmosis.

Chronic pulmonary histoplasmosis is best regarded as an opportunist or saprophytic infection of abnormal pulmonary spaces by a fungus of very low human pathogenicity. Tissue disease results from host immune response to dispersions of soluble antigen from these focal sources. There are two distinct types of clinical and radiological response. One is an acute or subacute illness manifested by often large segmental pneumonic lesions which tend to heal and are designated as early lesions. The other, usually developing as a complication of the first, is a chronic disease marked by persistent cavitation, low gard chronic illness, and a tendency to promote pulmonary fibrosis and often progressive pulmonary insufficiency. The early lesion is a segmental interstitial pneumonitis with central areas of infarct-like necrosis often adjacent to bullous disease and often outlining prominent emphysematous spaces which appear as radiolucencies. These radiological findings are further characterized by early clearing of the interstitial components, infarct-like contraction of the necrotic zones, obliteration of much of the contained emphysematous and bullous spaces, and healing attended by considerable loss of lung volume. Symptoms are variable but tend to be mild. Malaise, fatigability, low-grade fever, aching chest pain and mild cough lasting a few days to a few weeks are usual. Symptoms are ameliorated by rest. Rest and diminished activity are recommended as treatment. Under these circumstances, 80% of early lesions heal completely and probably most of these would heal spontaneously. Any subsequent course of the disease depends on whether or nor large air spaces, adjacent to or contained within the area of pneumonitis, become infected and persist as cavities. This occurs in 20% of early lesions. Once established, an infected cavity tends to persist and to be attended by symptoms of chronic bronchitis with chronic cough and sputum, fatigability, anorexia, and weight loss. Persisting thickwalled cavities often induce gradual development of pulmonary fibrosis, particulary in the lung bases, apparently from aspiration of antigenic material. This and the accelerated obstructive bronchopulmonary disease often lead to progressive pulmonary insufficiency. The use of amphotericin B is recommended for all persistent thick-walled cavities and in some circumstances surgical resection may be indicated.

An improved method for examination of cerebrospinal fluid cells.

A new collection technique allows cytologic examination up to 2 weeks after lumbar puncture without loss of cells or morphologic detail. Cerebrospinal fluid (CSF) was allowed to flow directly from a lumbar puncture needle into a solution of Carbowax in ethanol and was then processed with a cytocentrifuge. Two groups of patients were studied -- those undergoing spinal anesthesia and those having myelography for low back pain. Lymphocytes, polymorphonuclear neutrophils, and ependymal cells were regularly found in the CSF; a definite difference was found in the quantity and cell types in the two patient populations. The proposed method may be sensitive enough to aid in the identification of other neurologic diseases with low cell counts.

The development of the Minnesota Multiphasic Personality Inventory.

The Minnesota Multiphasic Personality Inventory (MMPI) was constructed at the University of Minnesota before and during World War II. In its developmental phase, the MMPI was conceptualized as an efficient way of detecting psychiatric disturbance. The test's construction was made possible by atypical cooperation between psychologists and psychiatrists, within the context of a crisis in the U.S. public mental health care system. The MMPI was designed to meet the diagnostic needs of psychiatrists. As such, it represented the operationalization of medical hegemony. However, the interpretation of the MMPI shifted significantly after the war, reflecting organizational reform in clinical psychology and changing professional relationships between psychologists and psychiatrists.

Schistosoma mansoni infection in mice depleted of thymus-dependent lymphocytes. I. Eosinophilia and immunologic responses to a schistosomal egg preparation.

Chronic murine schistosomiasis is characterized by a host cell-mediated immune response to schistosomal egg antigens. This response is manifested in vitro by lymphocyte blastogenic reactivity to a soluble schistosomal egg antigen preparation (SEA) and in vivo by delayed dermal hypersensitivity to SEA. In addition, mice develop reaginic, agglutinating, and early dermal reactive antibodies to SEA and a characteristic pattern of peripheral blood eosinophilia. In this study, depletion of thymus-dependent lymphocytes abolished the anti-SEA lymphocyte blastogenic response and delayed dermal reactivity, reaginic antibody response and the major peak of peripheral blood eosinophilia, which in normal mice occurs at the same time as SEA-induced blastogenesis. Antibodies mediating the early dermal reaction to SEA and agglutinins for SEA-coated particles were not inhibited by T-lymphocyte depletion. The experimental group did not develop the normally observed granulomatous response, but rather suffered focal hepatic and mucosal liquefactive necrosis, bacteremia and accelerated mortality.

Schistosoma mansoni infection in mice depleted of thymus-dependent lymphocytes. II. Pathology and altered pathogenesis.

Murine schistosomiasis mansoni is a more rapidly fatal disease in hosts deprived of their cell-mediated immune capabilities. Analysis of the histopathology of the disease under these circumstances indicates that rather than the hepatic granulomata characteristic of the normal infection, the host develops zones of liquefactive necrosis in the liver and intestinal mucosa. These lesions are associated with severe parenchymal cell destruction. Such hepatic and mucosal damage, with subsequent toxemia and septicemia, is presumed central to the altered course of the disease.

Gamma heavy chain disease--presenting as pancytopenia and splenomegaly.

A patient with gamma heavy chain disease (Franklin's disease) was discovered during evaluation for pancytopenia and splenomegaly. Lymphadenopathy, palatal edema, and infiltration of the bone marrow palatal edema, and infiltration of the bone marrow with abnormal cells were all absent. Serum and urine protein electrophoresis demonstrated a monoclonal protein migrating in the beta region. Immunoelectrophoresis showed that it reacted with antibodies against the Fc fragment of IgG heavy chains (gamma chains) but not with antibodies against kappa and lambda but not with antibodies against kappa and lambda light chains of Fab fragments. In the first year after detection of the disease, the patient had acute cholecystitis and disseminated herpes zoster. Sixteen months after diagnosis he died of overwhelming pneumonia caused by Pseudomonas aeruginosa and lebsiella neumoniae. A striking feature of his illness was his asymptomatic presentation, with pancytophenia and splenomegaly the only indication of this disease.