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Query: UMLS:C0032285 (pneumonia)
54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adenovirus pneumonia is uncommon but its severe infection has a mortality as high as 10%, and survivors may have residual airway damages, manifested by bronchiectasis, bronchiolitis obliterans, or pulmonary fibrosis. We report a case of adenovirus pneumonia demonstrating fatal respiratory distress. Adenovirus was isolated from pharyngeal specimens using cell culture and typed as serotype 3 by a combination of polymerase chain reaction (PCR) and restriction fragment length polymorphism analysis. The patient characteristically showed hypercytokinemia, characterized by increased levels of lactate dehydrogenase, ferritin, and several cytokines including interferon-gamma and interleukin-6. We treated the patient with pulse methylprednisolne therapy (25 mg/kg/day, for 3 days), resulting in the rapid amelioration of respiratory distress. This is the first report describing the treatment of pulse methylprednisolone therapy in fatal adenovirus pneumonia. During the clinical course, serum Krebs von den Lungen-6 (KL-6), which is a marker for the activity of diffuse interstitial lung disease, was elevated, suggesting that serum KL-6 could be available as a marker of pulmonary prognosis in viral pneumonia.
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PMID:Pulse methylprednisolone therapy in type 3 adenovirus pneumonia with hypercytokinemia. 1663 25

Legionella pneumophila has been recognized as an important cause of community- and hospital-acquired pneumonia. This study evaluates the interrelationship between that patients group with Legionnaires disease (LD) and the possible factors that may predispose hosts to acquire this infection. Likewise, we search for preliminary biochemical and immunologic evidences that could help physicians to differentiate between LD and other pneumonias. We analyzed biochemical parameters and immunoglobulin levels in 61 LD patients and a control group (n = 30) who were non-Legionella pneumonia diagnosed. We observed statistically significant differences in LD patients versus control group in serum sodium, albumin, gamma-band, IgG levels, (P < .01) and for total proteins, aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) (P < .05). Our study shows a trend between the presence of LD and immunoglobulin deficiencies in the group studied. Deficit in IgG or IgG plus IgM, during the exposure period, may predispose individuals to suffer legionellosis (P < .05). Overall, hypoalbuminemia, hyponatremia, and high AST and LDH levels can represent a useful prognostic marker in patients with severe pulmonary infection suspected to be legionellosis.
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PMID:Biochemical and immunologic features of an outbreak of Legionnaires disease: comparative study between community-acquired pneumonias. 1665 Sep 55

Posttransplant lymphoproliferative disorder (PTLD) is a serious complication after solid organ transplantation. An elevated serum lactate dehydrogenase (LDH) is a marker of PTLD activity. We report the case of a 58-year-old female renal transplant patient with a prior history of extranodal PTLD, which developed 19 years after a second transplant. She was successfully treated with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) and maintained subsequently on sirolimus and prednisone. She presented 3 years later with fever, dyspnea, cough, lung infiltrates and elevated serum LDH concerning for recurrence of PTLD. Bronchoscopy revealed Pneumocystis carinii (jiroveci) pneumonia. The patient was treated with trimethoprim-sulfamethoxazole, but developed nausea and was converted to dapsone. The patient was readmitted 4 weeks later with increasing dyspnea and hypoxemia and found to have a methemoglobin level of 16%. Dapsone was discontinued with resolution of all symptoms. We discuss the diagnostic and clinical challenges in this complex case.
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PMID:Didactic lessons from the serum lactate dehydrogenase posttransplant: a clinical vignette. 1829 52

Influenza A/H5N1 infection has become the major emerging infectious disease of global concern again since late 2003. A history of exposure to dead or sick poultry or wild birds occurs in over 60% of cases of human H5N1 infection. The incubation period of avian-to-human transmission is generally between 2 and 5 days and the median duration of symptoms before hospitalization is about 4.5 days. The clinical spectrum has ranged from asymptomatic infection or mild influenza-like illness to severe pneumonia and multi-organ failure. Fever > 38 degrees C, cough and dyspnoea are the major symptoms on presentation, whereas gastrointestinal symptoms such as watery diarrhoea, vomiting and abdominal pain are common early in the course of the disease. In contrast, upper respiratory tract symptoms are less prominent in human H5N1 infection when compared to seasonal influenza. Laboratory features of human H5N1 infection include leucopoenia, especially lymphopenia, elevated amino-transaminases, thrombocytopenia, prolonged prothrombin time and activated partial thromboplastin time, increased D-Dimer, increased serum lactate dehydrogenase and creatinine phospho-kinase, and hypoalbuminemia. A low absolute lymphocyte count on admission is associated with more severe disease and death. Radiographic abnormalities include multi-focal airspace consolidation, interstitial infiltrates, patchy or lobar involvement, with rapid progression to bilateral and diffuse ground-glass opacities consistent with ARDS. However, none of the clinical, laboratory and radiographic features are specific to H5N1 infection. A detailed exposure history needs to be elicited, including any close contact with sick or dead poultry, wild birds, other severely ill persons, travel to an area with A/H5N1 activity or work in laboratory handling samples possibly containing A/H5N1 virus.
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PMID:Review of clinical symptoms and spectrum in humans with influenza A/H5N1 infection. 1836 21

An 82-year-old man was admitted with a 1-week history of chilling fever and dry cough. Laboratory tests revealed pancytopenia and elevated levels of C-reactive protein and lactic dehydrogenase (LDH). Screening for infectious diseases was negative. A bone marrow biopsy showed aspecific findings. The combination of pancytopenia, persistent fever, elevated LDH and hepatomegaly (demonstrated by ultrasound examination of the abdomen) was suggestive of the haemophagocytic syndrome. This was confirmed by very high levels of ferritin and soluble interleukin-2 receptor in the blood. In addition, re-examination of the bone marrow showed several haemophagocytic histiocytes. A polymerase chain reaction for Epstein-Barr virus (EBV) revealed a very high viral load. Since the patient had a history of an increased level of anti-EBV immunoglobulin-G, this was explained by a reactivation of the EBV infection. On the sixth day in hospital the patient developed signs of bilateral pneumonia and subsequent multiple organ failure. Despite intensive treatment the patient died. Autopsy revealed no haematological or other malignancies, but did show haemophagocytosis in many organs. It was then concluded that the patient had a virus-associated haemophagocytic syndrome, due to a reactivation of EBV, for which no underlying cause was found.
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PMID:[Clinical reasoning and decision-making in practice. A patient with fever and pancytopenia]. 1878 29

Severe acute respiratory syndrome (SARS) is a recently emerged infectious disease with significant morbidity and mortality. An epidemic in 2003 affected 8,098 patients in 29 countries with 774 deaths. The aetiological agent is a new coronavirus spread by droplet transmission. Clinical and general laboratory manifestations included fever, chills, rigor, myalgia, malaise, diarrhoea, cough, dyspnoea, pneumonia, lymphopenia, neutrophilia, thrombocytopenia, and elevated serum lactate dehydrogenase (LD), alanine aminotransferase (ALT) and creatine kinase (CK) activities. Treatment has been empirical; initial potent antibiotic cover, followed by simultaneous ribavirin and corticosteroids, with or without pulse high-dose methylprednisolone, have been used. The postulated disease progression comprises (1) active viral infection, (2) hyperactive immune response, and (3) recovery or pulmonary destruction and death. We investigated serum LD isoenzymes and blood lymphocyte subsets of SARS patients, and found LD1 activity as the best biochemical prognostic indicator for death, while CD3+, CD4+, CD8+ and natural killer cell counts were promising predictors for intensive care unit (ICU) admission. Plasma cytokine and chemokine profiles showed markedly elevated Th1 cytokine interferon (IFN)-gamma, inflammatory cytokines interleukin (IL)-1beta, IL-6 and IL-12, neutrophil chemokine IL-8, monocyte chemoattractant protein-1 (MCP-1), and Th1 chemokine IFN-gamma-inducible protein-10 (IP-10) for at least two weeks after disease onset, but there was no significant elevation of inflammatory cytokine tumor necrosis factor (TNF)-alpha and anti-inflammatory cytokine IL-10. Corticosteroid reduced IL-8, MCP-1 and IP-10 concentrations from 5-8 days after treatment. Measurement of biochemical markers of bone metabolism demonstrated significant but transient increase in bone resorption from Day 28-44 after onset of fever, when pulse steroid was most frequently given. With tapering down of steroid therapy, there was a decrease in bone resorption marker together with an increase in bone formation markers round Day 50, suggesting that some of the bone loss might be reversed. Our research studies on the chemical pathology and clinical immunology of SARS should have implications for the pathophysiology and therapy of this potentially lethal infection.
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PMID:Severe acute respiratory syndrome: clinical and laboratory manifestations. 1845 12

Pneumocystis jirovecii is a common cause of life-threatening pneumonia among immunocompromised patients. Using 400 fresh bronchoalveolar lavage samples, we compared prospectively routine direct immunofluorescence assay (DFA) and a real-time PCR assay, performed on a LightCycler system, for the detection of P. jirovecii. Among the 66 PCR positive samples, 31 were positive by DFA. No patient was found as having the pattern "PCR--ve/DFA+ve". The semi-quantification of the P. jirovecii DNA was represented by the cycle threshold (Ct). Using DFA as the gold standard, the sensitivity of the PCR was 100% for Ct > or = 28 and the specificity was 100% for Ct < 22. Between these two points, the results could be discrepant. The patients of the "22 < or = Ct < 28" group presented more frequently with a radiological interstitial syndrome than the "Ct > or = 28" group, and presented less frequently with HIV-infection and elevated lactate dehydrogenase (LDH) assay than in the "Ct < 22" group. A negative PCR allowed us to exclude the P. jirovecii pneumonia. The real-time PCR assay seems to be an accurate diagnosis method and could replace the DFA. The semi-quantitative results should be helpful to distinguish colonized, subclinically infected and P. jirovecii pneumonia patients.
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PMID:Accuracy of a routine real-time PCR assay for the diagnosis of Pneumocystis jirovecii pneumonia. 1860 98

Mycoplasma hyopneumoniae is an important pathogen of pigs causing enzootic pneumonia of swine. The pathogen remains largely enigmatic as far as the host-pathogen interactions are concerned. In the present study, the protein profiles of two strains of M. hyopneumoniae were compared by two-dimensional gel electrophoresis and mass spectrometry. The results indicate that the major adhesin P97, the 50-kDa protein derived from P159 adhesin, and the 43-kDa cleavage product of P102 are expressed at much higher levels in the pathogenic strain 232. In contrast, the avirulent strain J switches its focus to metabolism and expresses more glyceraldehyde 3-phosphate dehydrogenase in gluconeogenesis and lactate dehydrogenase, pyruvate dehydrogenase, and phosphate acetyltransferase in the pyruvate metabolism pathway. We speculate that the avirulent strain may have developed better capabilities to cope with the rich environment during repeated inoculations. Simultaneously, the capability to infect host cells may become less important so that the adhesion-related protein genes are down-regulated.
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PMID:Proteomic comparative analysis of pathogenic strain 232 and avirulent strain J of Mycoplasma hyopneumoniae. 1926 78

Multiple organ damage in severe acute respiratory syndrome (SARS) patients is common; however, the pathogenesis remains controversial. This study was to determine whether the damage was correlated with expression of the SARS coronavirus receptor, angiotensin converting enzyme 2 (ACE2), in different organs, especially in the endocrine tissues of the pancreas, and to elucidate the pathogenesis of glucose intolerance in SARS patients. The effect of clinical variables on survival was estimated in 135 SARS patients who died, 385 hospitalized SARS patients who survived, and 19 patients with non-SARS pneumonia. A total of 39 SARS patients who had no previous diabetes and received no steroid treatment were compared to 39 matched healthy siblings during a 3-year follow-up period. The pattern of SARS coronavirus receptor-ACE2 proteins in different human organs was also studied. Significant elevations in oxygen saturation, serum creatinine, lactate dehydrogenase, creatine kinase MB isoenzyme, and fasting plasma glucose (FPG), but not in alanine transaminase were predictors for death. Abundant ACE2 immunostaining was found in lung, kidney, heart, and islets of pancreas, but not in hepatocytes. Twenty of the 39 followed-up patients were diabetic during hospitalization. After 3 years, only two of these patients had diabetes. Compared with their non-SARS siblings, these patients exhibited no significant differences in FPG, postprandial glucose (PPG), and insulin levels. The organ involvements of SARS correlated with organ expression of ACE2. The localization of ACE2 expression in the endocrine part of the pancreas suggests that SARS coronavirus enters islets using ACE2 as its receptor and damages islets causing acute diabetes.
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PMID:Binding of SARS coronavirus to its receptor damages islets and causes acute diabetes. 1933 47

Human herpesvirus 6 (HHV-6) infection can induce unusual complications in transplant patients, such as interstitial pneumonitis, encephalitis and marrow aplasia. We describe the clinical course of HHV-6 infection in a girl with renal transplantation. She presented with diarrhea and poor feeding on day 36 post-transplantation (Tx), after a 5-day steroid pulse for clinical signs of acute rejection. A week later she developed fever and had elevated plasma creatinine and lactic dehydrogenase levels, but a physical examination did not reveal any anomalies with respect to suggest rash, pneumonitis, encephalitis or lymphadenopathy. Two weeks later, the patient developed anemia and leucopenia. HHV-6 was the only pathogen detected by the PCR assay of the serum and marrow aspiration. The patient had a successful recovery without specific treatment. This case report highlights the wide spectrum of complications resulting from HHV-6 infection in immunosuppressed patients.
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PMID:HHV-6 infection in a pediatric kidney transplant patient. 1958 81


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