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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute chest syndrome (ACS) is an important cause of morbidity and mortality in sickle cell disease (SCD). Previous studies reported conflicting pictures of ACS making therapeutic interventions difficult. The Cooperative Study of Sickle Cell Disease prospectively followed 3,751 patients enrolled from birth to 66 years of age for ACS. Data on presenting signs and symptoms, laboratory findings, and hospital course were collected. There were 1,722 ACS episodes in 939 patients. Young children (age 2 to 4 years) presented with fever and cough, a negative physical exam, and rarely had pain. Adults were often afebrile and complained of shortness of breath, chills, and severe pain. Upper lobe disease was more common in children; multilobe and lower lobe disease affected adults more often. Severe hypoxia occurred in 18% of adults tested and could not be predicted by examination or laboratory findings. Bacteremia was documented in 3.5% of episodes, but was strongly influenced by age (14% of infants and 1.8% of patients > 10 years). ACS was most common in winter with children having the most striking increase. Transfusion was used less frequently, but earlier in children. Young children were hospitalized for 5.4 days versus 9 days for adults. Fifty percent of adults had a pain event in the 2 weeks preceding ACS and children were more likely to have febrile events. The death rate was four times higher in adults than in children. Fatal cases generally developed rapid pulmonary failure and one third were associated with bacteremia. Age has a striking effect on the clinical picture of ACS. In children, ACS was milder and more likely due to infection, whereas in adults ACS was severe, associated with pain and had a higher mortality rate.
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PMID:Acute chest syndrome in sickle cell disease: clinical presentation and course. Cooperative Study of Sickle Cell Disease. 905 64

We reviewed 71 consecutive patients with Streptococcus pneumoniae bacteremia. The patients were analyzed by age, sex, ethnic background, and clinical presentation. Laboratory data reviewed included a CBC count, electrolyte levels, liver function studies, chest radiograph, HIV status, a sputum culture and Gram's stain, and sensitivities for the S pneumoniae isolated. Modalities of therapy, response to treatment, and ultimate outcome were examined. Many of the patients with pneumococcal bacteremia did not have cough, fever, or chills. HIV positivity was a risk factor for pneumococcal infection although it was not associated with increased mortality. Mortality correlated with elderly status, leukopenia, and lack of fever. Many patients had symptoms suggestive of atypical pneumonia including myalgia and mental status change. Hyponatremia and hyperbilirubinemia were commonly noted.
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PMID:Streptococcus pneumoniae bacteremia in a community hospital. 974 94

Inflammation with infiltrations of eosinophils and mast cells into the walls of airways is considered to increase airway hyperresponsiveness (AHR), which in turn characterizes asthma. We present a child with AHR in whom the clinical course of asthma was related to eosinophilic bronchitis. Our patient was admitted at age 6 months with bronchiolitis and at age 4 years with asthma. Inhaled corticosteroids were begun at age 7 years. At age 8 he developed a meningeal sarcoma. While on chemotherapy, his asthma symptoms resolved and he no longer required prophylactic asthma treatment. After 14 months off all chemotherapy, he again had mild episodic asthma. While receiving chemotherapy for malignancy, he had an admission with a coagulase negative staphylococcal bacteremia. During sputum induction with 4.5% saline, he developed cough, wheeze, and a 20% reduction in peak expiratory flow (220 to 180 L/min) that reversed after treatment with salbutamol. The sputum cell count was 1.7 x 10(6)/ml with 1.1 x 10(6) being neutrophils. Two weeks later and prior to the induction of the second sputum, a 21% increase in FEV1 was recorded after bronchodilator inhalation (82% to 99% of predicted). The second sputum contained 2.7 x 10(6)/ml cells with 1.6 x 10(6)/ml neutrophils. Neither eosinophils nor mast cells were identified in the sputum. A third sputum obtained 14 months after the cessation of chemotherapy showed a sputum cell count of 16 x 10(6)/ml, with 11.6 x 10(6) neutrophils and 0.4 x 10(6) eosinophils; no mast cells were detected. A reversible 15% reduction in FEV1 was detected on hypertonic saline challenge testing. This boy had persistent airway hyperreactivity and reversible airways obstruction on three occasions during and following chemotherapy. When he developed asthma symptoms, his sputum contained neutrophils and eosinophils; while on chemotherapy his sputum did not contain eosinophils and he was symptom-free and off all asthma therapy. One can speculate that chemotherapy for malignancy can induce a remission in asthma symptoms but not AHR, and remission in symptoms is associated with a lack of eosinophilic or mast cell infiltrates in the sputum.
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PMID:Chemotherapy for malignancy induces a remission in asthma symptoms and airway inflammation but not airway hyperresponsiveness. 971 Feb 82

Patients with systemic lupus erythematosus (SLE) have increased susceptibility to infection by Pneumocystis carinii, but this condition has rarely been reported in Taiwan. Here, we describe two cases of patients with SLE who developed Pneumocystis carinii pneumonia (PCP). The first patient was a 39-year-old woman presenting with fever and dyspnea that had lasted 2 weeks. Chest roentgenography disclosed bilateral interstitial and alveolar infiltrates. The second patient was a 22-year-old woman presenting with a 4-day history of malaise, cough, dyspnea, and fever. She had concomitant Mycobacterium tuberculosis infection. Both patients had been treated with varying doses of corticosteroids and/or cytotoxic drugs within 4 months before presentation. Diagnosis was established based on the findings of bronchoalveolar lavage (BAL) and transbronchial lung biopsy (TBLB). Both patients received trimethoprim-sulfamethoxazole (20 mg.kg-1.d-1 trimethoprim), but finally died of nosocomial septicemia (Acinetobacter baumanni and Pseudomonas aeruginosa bacteremia in one, P. aeruginosa bacteremia in the other). These two cases demonstrate that PCP should be included in the differential diagnosis of patients with SLE presenting with pneumonic processes. In addition, a second opportunistic pathogen should be suspected. Bronchoscopic examination should be performed if the diagnosis is not clear and should include TBLB and BAL.
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PMID:Pneumocystis carinii pneumonia in systemic lupus erythematosus: a report of two cases. 1176 Mar 77

Coagulase negative staphylococci (CoNS) are a main cause of catheter related infections (CRI). Earlier studies (1994-1996) revealed a high incidence of CRI (6 per 1000 catheter days) among neutropenic hemato-oncologic patients in the Erasmus MC Hematology Department (Rotterdam, The Netherlands). This was mainly explained by expansion of two methicillin resistant Staphylococcus epidermidis (MRSE) clones (Nouwen et al., J. Clin. Microbiol. 36 (1998) 2696-2702). In a new, 16-bed unit in the same institution, we investigated the effect of strict clinical isolation measures on the incidence of CRI. During two 6-month screening periods (period I: April 1998-December 1998 and period II: April 1999-October 1999) all patients receiving a central venous catheter were prospectively monitored for the development of CRI. During period I every visitor of the cubicles had to wear hair caps, masks, gowns and gloves. During period II these procedures were abolished, but hands were cleansed using alcohol and masks were worn during both periods in case of coughing and sneezing. All CoNS strains isolated from blood cultures were genetically classifies by pulsed field gel electrophoresis (PFGE). The incidence of CRI during period I was 13.0 per 1000 catheter days, in comparison to 9.6 in period II (P=0.84). During this latter period, 19 CRI were diagnosed, 14 catheter related bacteremia episodes (CRB) and five local infections. Seventy-two percent (n=9) of CRB were due to a CoNS. The mean catheter survival until appearance of a CRI increased from 43 days during period I to 78 days in period II (P=0.39). The mean catheter survival until infection related removal was increased from 43 days to 133 days (P=0.12). During period I less experienced intervention radiologists introduced the catheters, which may have limited the efficacy of the strict hygiene measures. Thus, abolishing strict isolation precautions had no negative effect on the incidence of CRI. After genotyping of 38 MRSE strains isolated from blood and central venous catheter cultures of 12 patients in period II, eight PFGE types were found. Three types were found in more than one patient, but based on epidemiological data patient-to-patient spread could not be proven. No genotypic identity between patient and personnel CoNS isolates was shown and the two major clonal types that were present between 1994 and 1996 were not encountered. However, from December 1998 onwards new MRSE clones could be identified (types E and J). In conclusion, despite a constant rate of CRI and implementation of optimal patient care, clonal spread of MRSE strains was not prevented by strict hygiene measures.
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PMID:Strict infection control measures do not prevent clonal spread of coagulase negative staphylococci colonizing central venous catheters in neutropenic hemato-oncologic patients. 1312 49

A 46-year-old man was admitted to our hospital, because of cough and exertional dyspnea. We diagnosed small cell lung cancer, clinically staged as T2N3M0, limited disease. Radiation therapy was performed at first to relieve the severe stenosis of the proximal airway, followed by anti-cancer chemotherapy. Fever developed on the fifth day of chemotherapy, and he was successfully treated with intravenous antibiotics. A blood culture yielded Helicobacter cinaedi on the seventh day of incubation. H. cinaedi bacteremia occurred again during the second course of chemotherapy. The same bacteria were also found in his intestinal contents, with no gastrointestinal symptoms. We assume that the bacteria found in the blood was derived from his own intestinal contents. When bacteremia occurs in lung cancer patients during chemotherapy, an uncommon strain such as H. cinaedi is a possible causative agent.
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PMID:[A case of recurrent Helicobacter cinaedi-associated bacteremia in a small cell lung cancer patient during chemotherapy]. 1731 23

A 54-year-old man was admitted to our hospital because of intermittent high fever, general malaise, cough and body weight loss after he had been examined and treated at the former hospital for 3 years without a definitive diagnosis and effective therapy. Bacterial examination on admission revealed Streptococcus pyogenes in peripheral blood, bone marrow aspirates and pleural effusion. Furthermore, Mycobacterium avium complex (MAC) was detected in sputum, gastric juice, bone marrow liquid, pleural effusion by acid-fast bacillus culture or polymerase chain reaction (PCR). Biopsy of the neck lymph node showed multiple granulomas and the presence of acid-fast bacilli. Administration of ABPC/SBT and later CLDM resulted in disappearance of Streptococcus pyrogenes after 2 weeks. We suspected of generalized immunodeficiency that might underlie the severe bacteremia/osteomyelitis and disseminated MAC infection. We tested interferon (IFN)-gamma production of peripheral blood mononuclear cells (PBMC) of the patient after phytohemagglutinin (PHA)-stimulation and found that these cells produced no or undetectable levels of IFN-gamma in the presence of autologous plasma while produced almost normal levels of IFN-gamma in the presence of healthy donor's plasma. Since this neutralizing activity was co-purified in the IgG fraction, the immunodeficient state of the patient seemed to be caused by autoantibody to IFN-gamma. As far as we know, this is the first report of a Japanese case of disseminated MAC infection presumably due to autoantibody to IFN-gamma.
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PMID:Disseminated Mycobacterium avium complex infection in a patient with autoantibody to interferon-gamma. 1760 41

Organisms of the genus Gemella can, on occasion, cause serious systemic illness. The present paper reports a successfully treated case of endocarditis in a 12-year-old girl with congenital heart disease caused by species of Gemella. The child presented with cough, fatigue and decreased appetite without fever. Echocardiogram demonstrated marked mitral insufficiency with flail posterior mitral valve leaflet, mitral valve vegetations, and an enlarged left atrium and ventricle. While being treated with vancomycin, the child initially had persistent bacteremia, which resolved after the addition of gentamycin; the course of therapy was completed with penicillin G and gentamycin once antimicrobial susceptibilities were available. Attempts to identify the species of Gemella were unsuccessful in the local laboratory, and at reference laboratories in Canada and the United States. The isolate is undergoing further evaluation to determine its taxonomic status.
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PMID:Gemella species endocarditis in a child. 1815 56

Bordetella holmesii is a rare cause of bacteremia. It occurs mainly in hyposplenic patients, such as those affected by sickle cell anemia. The most frequent clinical signs are not very specific: fever, cephalalgia, cough, dyspnea, vomiting, etc. B. holmesii is frequently isolated from blood cultures. We describe the case of a 26-year-old sickle cell patient, presenting with dry cough and fever caused by a B. holmesii blood stream infection, identified by 16S rRNA gene sequencing. The outcome was favorable with amoxicillin. It is useful to know about B. holmesii, especially for physicians managing sickle cell or hyposplenic patients, because of its variable susceptibility to beta-lactams.
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PMID:[Bordetella holmesii bacteremia in a 26-year-old patient with sickle cell disease]. 1958 32

Community-acquired pneumonia is diagnosed by clinical features (e.g., cough, fever, pleuritic chest pain) and by lung imaging, usually an infiltrate seen on chest radiography. Initial evaluation should determine the need for hospitalization versus outpatient management using validated mortality or severity prediction scores. Selected diagnostic laboratory testing, such as sputum and blood cultures, is indicated for inpatients with severe illness but is rarely useful for outpatients. Initial outpatient therapy should include a macrolide or doxycycline. For outpatients with comorbidities or who have used antibiotics within the previous three months, a respiratory fluoroquinolone (levofloxacin, gemifloxacin, or moxifloxacin), or an oral beta-lactam antibiotic plus a macrolide should be used. Inpatients not admitted to an intensive care unit should receive a respiratory fluoroquinolone, or a beta-lactam antibiotic plus a macrolide. Patients with severe community-acquired pneumonia or who are admitted to the intensive care unit should be treated with a beta-lactam antibiotic, plus azithromycin or a respiratory fluoroquinolone. Those with risk factors for Pseudomonas should be treated with a beta-lactam antibiotic (piperacillin/tazobactam, imipenem/cilastatin, meropenem, doripenem, or cefepime), plus an aminoglycoside and azithromycin or an antipseudomonal fluoroquinolone (levofloxacin or ciprofloxacin). Those with risk factors for methicillin-resistant Staphylococcus aureus should be given vancomycin or linezolid. Hospitalized patients may be switched from intravenous to oral antibiotics after they have clinical improvement and are able to tolerate oral medications, typically in the first three days. Adherence to the Infectious Diseases Society of America/American Thoracic Society guidelines for the management of community-acquired pneumonia has been shown to improve patient outcomes. Physicians should promote pneumococcal and influenza vaccination as a means to prevent community-acquired pneumonia and pneumococcal bacteremia.
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PMID:Diagnosis and management of community-acquired pneumonia in adults. 2166 12


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