[Pneumocyctic carinii pneumonia. Diagnosis and therapy].
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Biomedical subjects
Publications and source records attributed to S Kernbaum.
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Bacterial infections are the most common cause of death in patients with malignant blood diseases. After recalling the main bacteria responsible and the factors which predispose patients to infection, the authors consider various forms of treatment, including antibiotic therapy, transfusions of white blood cells, gammaglobulins, etc., and prophlyactic measures, such as antibiotics by mouth, isolation in a sterile ward, etc., which have been proposed for some years. During renal grafts, infective complications are also very frequenct. Their prevention is essential for on this, to a large extent, depends the success of the transplantation.
Hyperosmolalities comparable to those of the renal medulla did not altered the clumping of C. albicans by human serum but diminished ingestion and evenmore the killing of C. albicans by human polymorphonuclear leukocytes (PMN).
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Cases of systemic infections caused by C. albicans are increasing in number and the kidney appears to be involved more often than any other tissue. The renal medulla is especially susceptible to infection by C. albicans and by bacteria - Previous works has showed that this is essentially due to hyperosmolality and to inactivation of the complement system. Polymorphs are one of the main host defense mechanisms against C. albicans and the authors have studied their power of phagocytosis against Candida and fongicidal activity in serum depleted in C3 and C4. Both are found to be normal.
A young woman aged 23 showed the clinical feature of relapsing polychondritis. This disease included recurrent inflammation of right ear, nasal rib and larynx cartilages. She had also arthritis of ankle and wrist. She never had aphtosis before her cartilaginous disease. Buccal and genital erosions similar to aphtae occurred before each recurrent attack of cartilage inflammation. In one instance aseptic vesiculo-pustular and erythema nodosum like lesions occurred. This case raises the question of whether this is a never reported association of two diseases or relapsing polychondritis may have dermatological symptoms bordering aphtosis. The latter hypothesis is supported: firstly by the fact that skin symptoms of aphtosis had been reported separately in cases of relapsing polychondritis (buccal aphtae, pustular eruption, erythema nodosum, recurrent thrombophlebitis); secondly by a case very similar to our (Thivolet, see text) showing a typical feature of relapsing polychondritis with a complete dermatological aspect of aphtosis.
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Human neutrophils incubated with 8 immunosuppressive agents ingest and kill normally C. albicans and C. pseudotropicalis. It agrees with previous studies of living microorganism phagocytosis. The decreased resistance to infection of patients treated with immunosuppressive agents seems not to be due to impaired granulocyte phagocytosis.
Pneumocystis carinii (P.c.) pneumonia was induced in 40 rats by a prolonged corticosteroid treatment (group 1); 40 healthy rats of equal weight constituted the control group (group 2); 9 rats received the same corticosteroid treatment as group 1, together with trimethoprim-sulfamethoxazole (TMP-SFZ) in order to prevent P.c. multiplication (group 3). We could distinguish the respiratory effects induced by corticosteroids from those caused by P.c. pneumonia (group 3 vs group 1). For six weeks the blood leukocyte count, the weight of the spleen and the thymus and the pulmonary status were monitored. Blood gases and acid-base status were measured in conscious rats. There was no pulmonary oedema. The infected P.c. rats had a low PaCO2 and a slight disturbance of blood oxygenation, exemplified by A-aDO2 of 30 mmHg, compared with 17.5 mmHg in control rats and 17 mmHg in TMP-SFZ treated rats. P.c. infected rats had a lymphocyte depletion induced by corticosteroids. They did not exhibit respiratory distress. P.c. pneumonia alone in rats did not cause frank hypoxemia.