[Origin, course and prevention of mass occurence of interstitial pneumonia in infant homes].
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Pentamidine isethionate and sulfadoxine plus pyrimethamine are excellent therapeutic agents in experimental and hypoergic, hypoimmune pneumocystosis as well as in focal interstitial plasma cell pneumonia (IPCP) in infants. Their effectiveness is seriously limited in cases in which either a diffuse massive plasma cell exudate has been established or in adults in whom the phagocytic and resorptive facility is depressed. Infantile pneumocystosis leading to IPCP can be completely prevented by proper feeding and care of the patient or prophylactic drug therapy with sulfadoxine-pyrimethamine. Similar measures should be taken for adult patients at risk in hospitals where pneumocystosis is frequent or when pneumocystosis has been recently diagnosed.
Forty years ago, Pneumocystis carinii was identified by Czech researchers J. Vanĕk and O. Jírovec as the causative agent of interstitial plasma cell pneumonia in infants. At present, it is the commonest pulmonary pathogen in AIDS patients. This review summarizes the experience and latest data on the etiopathogenesis, pathology, clinical presentation, diagnosis and therapy of P. carinii pneumonia.
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Orphanage epidemics of interstitial plasma cell pneumonia (IPCP) occur among premature infants whose passive immunity due to maternally transferred antibodies has lost its effectiveness before the infants' humoral immune systems have reached sufficient maturity to respond effectively to Pneumocystis carinii. IPCP occurs also among mature newborns receiving substandard care in understaffed and crowded orphanages. Infantile diarrhea in these institutions leads to marasmus and deficient immune response in infants 3-4 months after birth. The P. carinii organisms in the alveoli elicit a plasma cell response in the interstitial tissues of the lung, which may be so massive that it interferes with respiration and leads to death by asphyxiation. Such observations at the Shiraz Orphanage are discussed.
Four cases of lymphomatoid granulomatosis were studied. One case, previously reported, has had a prolonged remission of 8 years' duration. In one case, the course was rapid and progressive, and the patient died 2 months after the onset of the disease. In two other patients, the disease appears to be arrested effectively, both clinically and radiographically, by administration of corticosteroids. In the fatal case, postmortem examination revealed a typical angiocentric and destructive polymorphous lymphoreticular infiltrate in the lungs, kidneys, and adrenal glands. The diagnosis was made on specimens obtained from three patients by open thoracotomy. An adequate specimen is mandatory for diagnosis and thoractomy is indicated. To be considered in the differential diagnosis are Wegener's granulomatosis, the limited form of Wegener's granulomatosis, lymphoma, allergic granulomatosis, lymphocytic interstitial pneumonia, plasma cell granuloma, and infectious granuloma.
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Lymphoid tissue is a normal component of the lung. The various lymphoproliferative diseases affect the lung parenchyma. The purpose of this article is to classify various lymphoproliferative diseases and to understand their computed tomography features of pulmonary involvement. The examples include follicular bronchiolitis, lymphocytic interstitial pneumonia, plasma cell granuloma, Castleman disease, lymphomatoid granulomatosis, and mucosa-associated lymphoid tissue lymphoma. Pathologic correlation is helpful for understanding imaging findings and their pathophysiology.
The opportunistic fungus Pneumocystis is the etiologic agent of an interstitial plasma cell pneumonia that primarily afflicts immunocompromised individuals. Like other fungi Pneumocystis maintains a H(+) plasma membrane gradient to drive nutrient uptake and regulates intracellular pH by ATP-dependent proton efflux. Previously, we identified a Pneumocystis gene, PCA1, whose predicted protein product was homologous to fungal proton pumps. In this study, we show by functional complementation in a Saccharomyces strain whose endogenous PMA1 proton pump activity is repressed that the Pneumocystis PCA1 encodes a H(+)-ATPase. The properties of PCA1 characterized in this system closely resemble those of yeast PMA1. Yeast expressing PCA1 grow at low pH and are able to acidify the external media. Maximal enzyme activity (V(max)) and efficiency of substrate utilization (K(m)) in plasma membranes were nearly identical for PCA1 and PMA1. PCA1 contains an inhibitory COOH-terminal domain; removal of the final 40 amino acids significantly increased V(max) and growth at pH 6.5. PCA1 activity was inhibited by proton pump inhibitors omeprazole and lansoprazole, but was unaffected by H(+)/K(+)-ATPase inhibitor SCH28080. Thus, H(+) homeostasis in Pneumocystis is likely regulated as in other fungi. This work also establishes a system for screening PCA1 inhibitors to identify new anti-Pneumocystis agents.
Two hundred and twelve determinations of IgA, IgG, and IgM were performed in 50 infants during an epidemic of interstitial plasma cell pneumonia. Criteria for diagnosis are discussed. The immunoglobulin levels in pneumocystic, non-pneumocystic, and normal American infants are compared. An analysis of the findings in individual cases reveals a time-related immunoglobulin response, which helps to elucidate the pathogenicity of the disease.
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Explore the source record for details and available documents.