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

Pulmonary infection due to the filariform larvae of Strongloides stercoralis may occur in immunocompromised patients residing in endemic areas of the United States. Such infection usually presents as dyspnea with a cough that sometimes results in bloody sputum. Although the chest roentgenogram often reveals a patchy bilateral alveolar infiltrate, acute respiratory distress is unusual. We report a patient who experienced severe exacerbation of his underlying obstructive lung disease that was associated with chest infiltrates and recovery of S stercoralis from his sputum. Although initial improvement was accomplished with Thiobendazole treatment, a re-exacerbation occurred when antiparasitic therapy was completed. The persistence of his infection is correlated to factors that are commonly employed in the treatment of COPD but may be overlooked as predisposing causes of hyperinfection with S stercoralis.
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PMID:Exacerbation of chronic obstructive pulmonary disease due to hyperinfection with Strongyloides stercoralis. 234 69

Sixty-five cases of pleural empyema (50 boys and 15 girls) were seen between January 1983 and June 1986. Fifty-three of these 65 children were below 10 years of age. Pulmonary infection was the commonest underlying cause. Cough with or without expectoration (98%) and fever (95%) were the commonest symptoms followed by breathlessness (85%) and chest pain (83%). Staphylococcus aureus was isolated from pus and blood in 61% and 18% of cases, respectively, while pseudomonas was grown in 8% and 3%. Most of the children (88%) were treated with antibiotics and tube thoracostomy drainage. Decortication was needed in 12% of cases. There were four deaths in this study. The overall success rate was 94%.
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PMID:Management of Empyema thoracis in children--a study of 65 cases. 244 45

We describe two cases of pulmonary infection due to Mycobacterium xenopi (M. xenopi). Both cases were men, ages 61 and 54 yr. In the first patient, lung infection due to M. xenopi occurred after gastrectomy. The second patient had an inactive M. tuberculosis infection. Both had pulmonary symptoms including cough, sputum and fever. Each chest X-ray showed an infiltrative shadow with a cavity in a unilateral, upper lobe. Isolates from both patients were studied not only by microbiological characteristics but also by DNA-DNA hybridization. All isolates were susceptible to streptomycin and kanamycin. In the first case, the patient had initially received rifampicin, isoniazid and ethambutol despite in vitro susceptibility patterns, however, there was no response and a new infiltrative shadow appeared in the contralateral lobe. With a multiple drug regimen based on in vitro susceptibility, clinical and roentgenographic improvements were achieved. The second patient showed a favorable response to the initial chemotherapy. Pulmonary infection due to M. xenopi can generally be successfully treated with drugs to which the organisms show in vitro sensitivity. We also reviewed the other two cases reported in Japan.
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PMID:Pulmonary infection due to Mycobacterium xenopi. 800 Jan 3

Pulmonary infections can mimic or occasionally co-exist with pulmonary neoplasms. In order to determine the frequency and nature of these infections, we conducted a retrospective analysis, covering a 3-year period, of patients who were referred to our center with presumed lung cancer but turned out to have pulmonary infection instead. The overwhelming majority of patients (93.3%) referred to "rule out" lung cancer were documented as having a neoplastic process, and only 1.3% had an infection. Fungal infections (histoplasmosis, cryptococcosis, coccidiomycosis) accounted for 46%, mycobacteria for 27%, bacteria for 22%, and parasitic lesions (dirofilariasis) for 5% of these infections. The most common clinical manifestations were cough and chest pain, and the most common radiographic finding was a solitary pulmonary nodule. There were no specific clinical or radiographic features predictive of either infection or neoplastic disease. All patients responded to specific anti-infective therapy with or without surgical excision. Our data indicate that pulmonary infections mimic neoplasms very infrequently. However, establishing a specific diagnosis is critical, since the management and outcome of these two processes are entirely different.
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PMID:Pulmonary infections mimicking cancer: a retrospective, three-year review. 906 6

Reported here is a case of microsporidiasis that occurred in an acute myeloblastic leukemia (AML)-M3 patient who underwent chemotherapy. Fever, cough, expectorate and dyspnea were observed during the therapy. Since this case was considered as adult respiratory distress syndrome due to the chest X-ray and arterial blood gas findings, the male patient was bounded to a mechanical ventilator. As coagulation tests showed compatible findings with disseminate intravascular coagulation (DIC), it was thought to be a case of sepsis originating from the lungs and DIC. Pseudomonas aeruginosa and Staphylococcus aureus were found in the sputum of the patient. Although he was given combined antibiotic therapy, there was no reduction in the fever. A bronchoalveolar lavage (BAL) sample was taken and Microsporidia sp. was found upon staining with Giemsa. The patient died due to sepsis and DIC just before receiving therapy for microsporidiasis. Pulmonary infection with Microsporidia, although classically occurring in patients with HIV infection, may occur rarely in leukemia patients, especially if previously treated with systemic immune suppression. This case reinforces the need to consider Microsporidia as a possible pathogen in immunocompromised patients with pulmonary infections.
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PMID:A case of pulmonary Microsporidiasis in an acute myeloblastic leukemia (AML) - M3 patient. 1261 89

A 51-year-old man complaining of cough and bloody sputum, was admitted to our hospital because of antibiotic-resistant chronic pneumonia in the right upper lobe. Initially, bronchoscopic examination and sputum culture revealed no evidence of malignancy or any specific infection, either pathologically or microbiologically. However, pathological examination of a solid body expectorated with sputum revealed typical sulfur granules, indicating pulmonary actinomycosis. Two actinomyceses named Actinomyces odontolyticus and Actinomyces meyeri were detected later. Pulmonary infection caused by these types of actinomyceses is rare, and the diagnostic procedure seemed to be unusual.
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PMID:[A case of pulmonary actinomycosis, who expectorated sulfur granules, caused by Actinomyces odontolyticus and Actinomyces meyeri]. 1596 70

Pulmonary infection and respiratory failure are frequently encountered in the early stage of acute spinal cord injury (SCI) and are thought of as the chief causes of death. Unfortunately, there is little knowledge concerned with the pathogenesis of pulmonary infection, respiratory failure and other pathological changes in the lung in the early stage of SCI. Pulmonary embolism, respiratory muscle dysfunction, poor expectoration caused by position, and decreased ability to cough up respiratory secretions were the main causes. These explanations may be beyond criticism in high-level paraplegia in SCI, but are unconvincing in lower SCI such as in low-thoracic cord injury where the phenomenon of pneumonia and respiratory dysfunction remains. There might be some more important factors that lead to pulmonary infection and respiratory failure in the early stage of SCI. In SCI rats, pulmonary edema and hemorrhage were occurred in the early stage of SCI while the other organs were almost normal. And the location of lung edema and hemorrhage were the same as that of pulmonary infection. The purpose of this paper is to propose pathological changes in the lung and possible causes for pulmonary infection and respiratory failure. We hypothesize that pulmonary edema and hemorrhage in the early stage of SCI might be the chief factor contributing to pulmonary infection and respiratory failure in lower SCI.
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PMID:Pulmonary edema and hemorrhage, possible causes of pulmonary infection and respiratory failure in the early stage of lower spinal cord injury. 2268 46

Diffuse alveolar hemorrhage (DAH) represents a syndrome that can complicate many clinical conditions and may be life-threatening, requiring prompt treatment. It is recognized by the signs of acute- or subacute-onset cough, hemoptysis, diffuse radiographic pulmonary infiltrates, anemia, and hypoxemic respiratory distress. DAH is characterized by the accumulation of intra-alveolar red blood cells originating most frequently from the alveolar capillaries. It must be distinguished from localized pulmonary hemorrhage, which is most commonly due to chronic bronchitis, bronchiectasis, tumor, or localized infection. Hemoptysis, the major sign of DAH, may develop suddenly or over a period of days to weeks; this sign may also be initially absent, in which case diagnostic suspicion is established after sequential bronchoalveolar lavage reveals worsening red blood cell counts. The causes of DAH can be divided into infectious and noninfectious, the latter of which may affect immunocompetent or immunodeficient patients. Pulmonary infections are rarely reported in association with DAH, but they should be considered in the diagnostic workup because of the obvious therapeutic implications. In immunocompromised patients, the main infectious diseases that cause DAH are cytomegalovirus, adenovirus, invasive aspergillosis, Mycoplasma, Legionella, and Strongyloides. In immunocompetent patients, the infectious diseases that most frequently cause DAH are influenza A (H1N1), dengue, leptospirosis, malaria, and Staphylococcus aureus infection. Based on a search of the PubMed and Scopus databases, we review the infectious diseases that may cause DAH in immunocompetent patients.
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PMID:Infectious diseases causing diffuse alveolar hemorrhage in immunocompetent patients: a state-of-the-art review. 2312 13

Bronchiectasis is a disorder of persistent lung inflammation and recurrent infection, defined by a common pathological end point: irreversible bronchial dilatation arrived at through diverse etiologies. This suggests an interplay between immunogenetic susceptibility, immune dysregulation, bacterial infection, and lung damage. The damaged epithelium impairs mucus removal and facilitates bacterial infection with increased cough, sputum production, and airflow obstruction. Lung infection is caused by respiratory bacterial and fungal pathogens, including Pseudomonas aeruginosa, Haemophilus, Aspergillus fumigatus, and nontuberculous mycobacteria. Recent studies have highlighted the relationship between the lung microbiota and microbial-pathogen niches. Disease may result from environments favoring interleukin-17-driven neutrophilia. Bronchiectasis may present in autoimmune disease, as well as conditions of immune dysregulation, such as combined variable immune deficiency, transporter associated with antigen processing-deficiency syndrome, and hyperimmunoglobulin E syndrome. Differences in prevalence across geography and ethnicity implicate an etiological mix of genetics and environment underpinning susceptibility.
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PMID:Bronchiectasis: Current Concepts in Pathogenesis, Immunology, and Microbiology. 2698 Jan 62