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

With the expanding knowledge of rhinovirus transmission and rhinovirus chemistry, the outlook for control of infections with these agents has brightened considerably. Although rhinoviruses are probably the world's leading cause of respiratory illness, they are surprisingly reluctant transmitters, infecting only about 50% of susceptibles in family-like settings. Current research suggests that rhinoviruses are spread chiefly by aerosol, rather than by fomites or personal contact. It has been possible to interrupt rhinovirus transmission completely by careful use of virucidal facial tissues, which, presumably, smothered aerosols generated by coughing, sneezing and nose blowing. Accordingly, it may be feasible to control rhinovirus (and perhaps other virus) dissemination by appropriate air handling and filtration systems in combination with careful nasal sanitation. Anti-rhinovirus drug development is also moving forward. Although there are over 100 rhinovirus serotypes, it has been found that most rhinoviruses attach to a single cell receptor by a single binding site on the virus. Also, the structure of the rhinovirus capsid is now known at the atomic level. These two pieces of knowledge about basic viral architecture appear to open new vistas for reasoned synthesis of antiviral drugs, and some promising compounds are now under investigation. Even interferon has been demonstrated useful in a family setting. On several research fronts, there are good grounds for optimism about control of rhinovirus colds.
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PMID:Transmission and control of rhinovirus colds. 244 13

Medical records, radiographs, and bronchial cytologic abnormalities of 65 cats with bronchial disease were reviewed. Bronchial disease was defined as abnormality of the lower airways to the exclusion of disease originating or mainly involving the alveoli, interstitium, vasculature, or pleura. Cats with bronchial disease were more likely to be female and older. Siamese cats were overrepresented and had more chronic disease. In order of frequency, the following clinical signs were reported: coughing, dyspnea, occasional sneezing, wheezing, and vomiting. Radiography revealed prominent bronchial markings, with some cats having collapse of the middle lobe of the right lung (n = 7), overinflation of the lungs (n = 9), or aerophagia (n = 13). Of 65 bronchial washes, 58 were considered exudative, with the predominant cell type being eosinophil in 24%, neutrophil in 33%, macrophage in 22%, and mixed population of cells in 21%. Cultures for bacteria were considered positive in 24% of the cats. Circulating eosinophilia was not helpful in predicting the predominant cell type in bronchial cytologic exudates. Hyperproteinemia without dehydration was present in a third of the cats, indicating an immunologic response. Half the cats had resolution of clinical signs, whereas half the cats required continuing medication with bronchodilators, antimicrobial agents, or corticosteroids.
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PMID:Clinical, radiographic, and bronchial cytologic features of cats with bronchial disease: 65 cases (1980-1986). 247 Jul 10

Toxicosis caused by Anabaena spiroides was diagnosed in 7 of 26 finishing hogs in a farrow-to-finish operation in Kentucky. Several sick pigs in the herd had the following clinical signs: vomiting, dull appearance, lethargy, anorexia, muscle tremors, frothing at the mouth, coughing, sneezing, dyspnea, and bloody diarrhea. Of the 7 dead pigs, 2 were necropsied. Tissue speciments and stomach contents were obtained for microscopic, microbiologic, and toxicologic evaluations. In addition, vomitus from sick pigs and pond water samples were collected for laboratory analysis. Direct microscopic examination of pond water, vomitus, and stomach contents revealed nearly pure A spiroides, a toxic blue-green algae. The possible involvement of bacterial toxins in these pigs was not established; however, the laboratory and field data suggested that the clinical signs and death losses were attributable to the consumption of pond water mixed with the bloom of the alga, A spiroides.
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PMID:Blue-green algae (Anabaena spiroides) toxicosis in pigs. 250 12

Case report on a 39-year-old man who for five years suffered from a recurrent, firm, crepitant swelling in the medial canthal region after coughing and sneezing. The swelling could be eliminated by digital compression. During a severe bout of sneezing a walnut-sized swelling suddenly occurred which could not be eliminated by compression. Echographic and intraoperative findings confirmed the diagnosis of a large, diverticulous pneumatocele that had compressed the lacrimal sac to such an extent that the entrapped air could not escape. Endoscopy of the nose revealed a wide nasolacrimal ostium, without a Hasner's valve. It was thus possible for air to flow back into the lacrimal drainage system from the nasal cavity.
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PMID:[Compression pneumatocele of the lacrimal sac]. 250 83

Ara-T-resistant strain of pseudorabies virus (PRV) was inoculated intranasally into six 2-week-old gnotobiotic pigs. Five inoculated pigs were sneezing and coughing. In pigs 1 to 4 killed on postinoculation days (PID) 3, 5, 7, and 9, respectively, PRV antigen was detected in respiratory epithelial cells, and pigs had severe pneumonitis. In pigs 5 and 6 killed on PID 11 and 13, respectively, PRV antigen was localized in macrophages in alveoli and necrotizing nodules. Immunoglobulin-containing cells (IgG, IgM, and IgA) were detected first in pneumonic lesions in pig 4 killed on PID 9. Detection of immunoglobulin-containing cells was coincident with pulmonary inflammation and regeneration of pneumonic lesions. The number of IgG-containing cells was greater than that of IgM- and IgA-containing cells. Corresponding to transient viral multiplication, IgG-, IgM-, and IgA-containing cells were demonstrated first in lymphatic tissues in pig 1 killed on PID 3 and their number was 5 to 10 times more than those in control pigs 7 and 8. Seemingly, PRV replication in lymphatic tissues stimulated the proliferative response of specific immunoglobulin-producing cells, and the appearance of immunoglobulin-containing cells in the lungs was associated with clearance of PRV and regeneration of pneumonic lesions.
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PMID:Immunohistologic study of pulmonary and lymphatic tissues from gnotobiotic pigs inoculated with ara-T-resistant strain of pseudorabies virus. 255 33

The pathophysiology, clinical manifestations and diagnosis, and pharmacotherapy of allergic rhinitis are reviewed. Allergic rhinitis is an immunologically mediated disease initiated by an antigen-antibody reaction in sensitized persons. Clinical manifestations include nasal obstruction, rhinorrhea, itching of the nose and eyes, coughing, and sneezing and may be perennial or seasonal. Diagnosis is confirmed by challenging the patient with suspected allergens in skin-prick tests. Avoidance of offending allergens is the cornerstone of therapy. Antihistamines and decongestants provides only minimal relief when used alone and are more effective when combined with other agents. Two newer antihistamines, astemizole and terfenadine, lack the sedative and anticholinergic properties of older antihistamines. Intranasal corticosteroids are particularly effective in relieving symptoms; beclomethasone diproprionate and flunisolide do so without producing systemic adverse effects. Cromolyn sodium is effective in relieving nasal symptoms and is the prototype of a new noncorticosteroidal class of compounds termed antiallergy drugs. Drugs under investigation for the treatment of allergic rhinitis include histamine H2-receptor antagonists, nonsteroidal anti-inflammatory agents, anticholinergic agents, and beta-adrenergic receptor agonists. Immunotherapy is a helpful adjunctive treatment. Treatment with drugs may be necessary for those patients with allergic rhinitis who find it difficult or impossible to avoid the offending allergen. The severity of symptoms and the adverse effects of agents should be considered when individual therapeutic plans are being established.
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PMID:Pharmacotherapy of allergic rhinitis. 266 11

Described is an outbreak of nosocomial RSV infection, following the admission of a 20-day-old and 11-day-old newborn with lower respiratory infections, diagnosed as being caused by RSV through detection of viral antigens by direct FAT (fluorescent antibody test) of nasopharyngeal samples. Later on, 5 of the other 20 newborn in patients in the same care unit also showed positive results in direct FAT, for RSV. The clinical manifestations of these patients were mild even in those cases with underlying PHT and cardiac disease and consisted of: cough (5/5), nasal discharge (3/5), poor feeding (1/5), sneezing (1/5), distress (1/5) and irritability (1/5). The rapid diagnosis of RSV though the direct FAT enables us to establish hygienic restrictions and patients isolation to keep the virus from spreading.
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PMID:[Outbreak of respiratory syncytial virus in a neonatal unit]. 267 77

Coughing, sneezing, talking, bed-making, turning pages of books, etc. all generate microbial aerosols which are carried and dispersed by air movements. Inhalation of these particles may cause allergic responses but whether or not infectious disease ensues depends in part on the viability and infectivity of the inhaled microbes and their landing sites. Desiccation is experienced by all airborne microbes; gram-negative bacteria and lipid-containing viruses demonstrate phase changes in their outer phospholipid bilayer membranes owing to concomitant changes in water content and/or temperature. These changes most likely lead to cross-linking reactions of associated protein moieties principally at mid to high relative humidity (RH). For lipid-free viruses these reactions of their surface protein moieties occur most rapidly at low RH. Radiation, oxygen, ozone and its reaction products and various pollutants also decrease viability and infectivity through chemical, physical and biological modification to phospholipid, protein and nucleic acid moieties. The extent of damage and the degree of repair together with the efficacy of host defence mechanisms largely controls whether the causative microbes take hold and spread disease via the airborne route. At least indoors, where desiccation is the predominant stress, the general reversibility of membrane-phase changes by vapour-phase rehydration when coupled with efficacious microbial enzymatic repair mechanisms under genetic control, virtually ensures the spread of disease by the aerobiological pathway.
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PMID:Airborne bacteria and viruses. 269 73

Non-traumatic cerebrospinal-fluid rhinorrhoea is a rare condition. Its insidious onset may occur with a sneezing or coughing episode which may lead to an incorrect diagnosis of allergic rhinitis or vasomotor rhinorrhoea. Two cases that occurred in association with primary empty-sella syndrome are described--in the second case, the fistula arose from the pituitary fossa. The history, incidence, clinical profile, investigation and management of this condition are reviewed.
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PMID:Non-traumatic cerebrospinal-fluid rhinorrhoea in cases of primary empty-sella syndrome. 271 86

The specific features of the spread of S. aureus from carriers indoors were studied. In this study S. aureus cells were most frequently isolated from the floor, less frequently from the walls and furniture and even less frequently from the air. S. aureus were detected on environmental objects as early as 30 minutes after the carrier stayed and breathed in the room. The contamination of environmental objects increased when the carrier spoke loudly and made such respiratory acts as coughing and sneezing. After the carrier left the room the contamination of the environmental objects persisted for at least 14 hours (the term of observation), gradually decreasing. The degree of the contamination of environmental objects was inversely related to the distance of these objects from the carrier. The contamination of the environment was shown to be directly related to the concentration of S. aureus in the nasal cavity of carriers.
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PMID:[Features of contamination of the environment by Staphylococcus aureus carriers]. 272 5


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