Cases reported "Pneumonia, Pneumocystis"

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1/29. Autoimmune enteropathy with distinct mucosal features in T-cell activation deficiency: the contribution of T cells to the mucosal lesion.

    BACKGROUND: Autoimmune enteropathy is normally characterised by crypt hyperplastic villous atrophy with enterocyte autoantibodies, activation of mucosal lymphocytes and increased epithelial HLA-DR. This case involved a severely affected Portuguese infant who was found to have lymphocyte activation deficiency and demonstrated correspondingly distinct mucosal features. methods: A female infant of nonconsanguineous parents was treated for vomiting and diarrhoea, first with milk exclusion and then with parenteral nutrition. lymphocyte subsets and immunoglobulin concentrations were normal, but in vitro testing showed no activation in response to phytohaemagglutinin, candida, or purified protein derivative, although the response to interleukin (IL)-2 was intact. interleukin-2 deficiency was excluded. Analysis of jejunal biopsy specimens revealed only mild villous blunting with absent goblet cells, normal epithelial proliferation, and no crypt hyperplasia. The dense infiltrate of CD8 and CD4 T lymphocytes showed normal CD2 and CD3 expression but no activation or proliferation markers. HLA-DR was not increased on epithelium or lymphocytes. Thus, in addition to in vitro evidence for lymphocyte activation deficiency, the mucosal specimens showed no evidence of in situ T-cell activation. RESULTS: After development of overwhelming septicaemia, the patient died at 18 months, just before a planned bone marrow transplant. CONCLUSIONS: These findings confirm significant heterogeneity within autoimmune enteropathy. Formal immune function testing should be performed in all affected infants to identify T-cell activation deficiencies. The distinct mucosal findings suggest that activated T cells usually induce the crypt hyperplastic villous atrophy characteristic of classic autoimmune enteropathy.
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2/29. Unsuspected pneumocystis carinii pneumonia at presentation of severe primary immunodeficiency.

    BACKGROUND: pneumocystis carinii is an important pathogen in immunodeficiency but may be an unrecognised cause of respiratory compromise. OBJECTIVES: To ascertain the incidence of P carinii pneumonia (PCP) at presentation of severe combined immunodeficiency (SCID), whether it had been diagnosed, and the effect of treatment on outcome. SETTING: The supraregional paediatric bone marrow transplant unit for primary immunodeficiencies at Newcastle General Hospital. methods: Retrospective case note review of infants referred with a diagnosis of SCID from 1992 to 1998. RESULTS: Ten of 50 infants had PCP at presentation; only one was diagnosed before transfer. Eight were diagnosed by bronchoalveolar lavage and two by lung biopsy. In only one was P carinii identified in nasopharyngeal secretions. Five required ventilation for respiratory failure but all were successfully treated with co-trimoxazole and methylprednisolone with or without nebulised budesonide. Nine survived to bone marrow transplantation and four are long term survivors after bone marrow transplantation; no deaths were related to PCP. CONCLUSIONS: PCP is a common presenting feature of SCID but is rarely recognised. bronchoalveolar lavage or lung biopsy are needed for diagnosis. Treatment with co-trimoxazole is highly successful.
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3/29. Abnormal pulmonary accumulation of indium-111 chloride in pneumocystis carinii pneumonia as detected by bone marrow scintigraphy.

    PURPOSE: Unusual pulmonary uptake of In-111 chloride in a patient with pneumocystis carinii pneumonia and autoimmune hepatitis is described. METHOD: In-111 chloride bone marrow scintigraphy was performed to evaluate the bone marrow activity associated with pancytopenia in a 56-year-old woman with autoimmune hepatitis. RESULTS: An In-111 chloride bone marrow scan showed increased pulmonary uptake predominantly in both upper lung fields. P. carinii pneumonia was seen to be developing as an immunocompromised complication after treatment for autoimmune hepatitis. CONCLUSION: When In-111 chloride bone marrow scintigraphy shows increased uptake in the lungs of immunocompromised patients, a combined opportunistic inflammatory disease such as P. carinii pneumonia should be considered in the diagnosis.
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4/29. Nodular granulomatous pneumocystis carinii pneumonia in a bone marrow transplant recipient. Case report.

    We report a case of nodular granulomatous pneumocystis carinii pneumonia following bone marrow transplantation. The patient was a 40-year-old man who had undergone bone marrow transplantation for myeloblastic acute leukemia. He presented with fever, dyspnea and bilateral diffuse nodular infiltration of the lungs. bronchoalveolar lavage was negative. Open lung biopsy was performed. Histological examination revealed a granulomatous reaction with central necrosis surrounded by epithelioid and giant cells. Toluidine blue and Gomori-Grocott stains identified a few P. carinii. Mycobacterial and fungal cultures were negative. A granulomatous reaction is rarely observed and almost only in hiv-infected patients. To our knowledge this is the first description in a bone marrow transplant recipient.
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5/29. Surfactant protein D and KL-6 as serologic indicators of pneumocystis carinii pneumonia in a child with acute lymphoblastic leukemia.

    pneumocystis carinii pneumonia (PCP) in immunocompromised patients is one of the important causes of morbidity and mortality. serum levels of surfactant protein D (SP-D) and KL-6 are useful biomarkers for understanding some pulmonary inflammatory responses in patients with idiopathic pulmonary fibrosis (IPF). We present a child with PCP following bone marrow transplantation (BMT) for acute lymphoblastic leukemia (ALL), for whom both SP-D and KL-6 in sera were simultaneously measured through the clinical course of PCP. Both serum levels of SP-D and KL-6 were rapidly elevated reflecting some inflammatory processes in the lung that chest X-ray films and CT scans showed as ground-glass attenuations. He died due to respiratory failure 40 days after PCP developed. A combination of the assays for SP-D and KL-6 in sera may be helpful in predicting the treatment results for PCP.
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6/29. pneumocystis carinii pneumonia, pulmonary tuberculosis and visceral leishmaniasis in an adult hiv negative patient.

    This is a case report of a 29 year old male with pneumocystis pneumonia and tuberculosis, and who was initially suspected of having hiv infection, based on risk factor analyses, but was subsequently shown to be hiv negative. The patient arrived at the hospital with fever, cough, weight loss, loss of appetite, pallor, and arthralgia. In addition, he was jaundiced and had cervical lymphadenopathy and mild heptosplenomegaly. He had interstitial infiltrates of the lung, sputum smears positive for mycobacterium tuberculosis and pneumocystis carinii, and stool tests were positive for strongyloides stercoralis and schistosoma mansoni. He was diagnosed as having AIDS, and was treated for tuberculosis, pneumocystosis, and strongyloidiasis with a good response. The patient did not receive anti-retroviral therapy, pending outcome of the hiv tests. A month later, he was re-examined and found to have worsening hepatosplenomegaly, pancytopenia, fever, and continued weight loss. At this time, it was determined that his hiv ELISA antibody tests were negative. A bone marrow aspirate was done and revealed amastigotes of leishmania, and a bone marrow culture was positive for Leishmania species. He was treated with pentavalent antimony, 20 mg daily for 20 days, with complete remission of symptoms and weight gain. This case demonstrates that immunosuppression from leishmaniasis and tuberculosis may lead to pneumocystosis, and be misdiagnosed as hiv infection. The occurrence of opportunistic infections in severely ill patients without hiv must always be considered and alternate causes of immunosuppression sought.
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7/29. hypercalcemia in a renal transplant recipient suffering with pneumocystis carinii pneumonia.

    hypercalcemia occurs frequently after renal transplantation. Preexisting hyperparathyroidism is the most common cause of post-transplantation hypercalcemia. We describe a renal transplant recipient infected with pneumocystis carinii pneumonia (PCP) who developed hypercalcemia, elevated 1,25-dihydroxyvitamin D, and suppressed parathyroid hormone levels. This phenomenon mimics the extrarenal production of 1,25-dihydroxyvitamin D by activated alveolar macrophages in granulomatous diseases with hypercalcemia. To the best of our knowledge, this is the first report of 1,25-dihydroxyvitamin D-mediated hypercalcemia caused by PCP in a renal transplant recipient. This entity should be included in the differential diagnosis for renal transplant recipients with hypercalcemia, especially in patients who develop lung infections.
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8/29. pneumocystis carinii pneumonitis in haemophagocytic lymphohistiocytosis.

    We report on a 10-y-old boy who developed pneumocystis carinii pneumonitis (PCP) as the dominant symptom at the onset of haemophagocytic lymphohistiocytosis (HLH). PCP is a common infection in patients with combined primary immunodeficiencies or acquired immunodeficiency syndrome but it has rarely been observed at the onset of HLH. Typically, HLH presents as a febrile syndrome associated with cytopenia and hepatosplenomegaly. Repeated bone marrow aspirates, spleen or lymph node biopsies are sometimes required to reveal haemophagocytosis. Because of the significant immunosuppression during treatment of HLH, prophylaxis of PCP with co-trimoxazole is recommended. However, de-arranged immune response in HLH renders the patients susceptible to opportunistic infections, even before the introduction of immunosuppressants. Conclusion: We suggest that in patients with unclear respiratory symptoms, it is worth considering a differential diagnosis of HLH.
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9/29. Elective bone marrow transplantation in a child with X-linked hyper-IgM syndrome presenting with acute respiratory distress syndrome.

    We describe a 10-month-old boy diagnosed with X-linked hyper-IgM syndrome (XHIM) after suffering from life-threatening acute respiratory distress syndrome (ARDS) caused by pneumocystis carinii pneumonia (PCP), although his previous clinical history and first level laboratory tests investigating immunological function did not indicate immunodeficiency. When the patient's overall condition was good, elective bone marrow transplantation from an HLA-matched older brother was performed successfully. We describe how correct diagnosis and successful treatment were made possible thanks to the involvement of a network of specialists.
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10/29. Granulomatous pneumocystis carinii pneumonia complicating hematopoietic cell transplantation.

    pneumocystis carinii pneunonia (PCP) is associated with a wide spectrum of clinical and histopathological presentations. While granulomatous PCP uncommonly occurs in AIDS patients, it is extremely rare in other non-AIDS immunocompromised patients. We identified three patients who developed granulomatous PCP after bone marrow or blood stem cell transplantation. In all cases, fiberoptic bronchoscopy with bronchoalveolar lavage was non-diagnostic, and an open lung biopsy was required for diagnosis. All patients were successfully treated with trimethoprim-sulfamethoxazole. The histological appearance varied from an ill-defined granulomatous pneumonia to well-formed necrotizing granulomas. The typical intraalveolar eosinophilic frothy exudate was absent. Often sparsely distributed, the organisms were detected by GMS and immunohistochemical stains for P. carinii. No other pathogens were identified by additional histochemical stains or by microbiological cultures. awareness of this unusual granulomatous tissue response to P. carinii and initiation of specific treatment can lead to successful resolution of this potentially lethal infection.
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