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Query: UMLS:C0023241 (Legionella)
 6,990 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous investigations have shown that Legionella pneumophila converts from virulence to avirulence after passage on supplemented Mueller-Hinton (SMH) agar and may convert back to virulence after passage in guinea pigs. However, there is no additional information concerning the apparent interconversion of virulent and avirulent derivatives of L. pneumophila cultures. We investigated the stability of a parental virulent culture and its avirulent derivatives and the growth and viability of these cultures on charcoal-yeast extract (CYE) and SMH agars. Avirulent derivatives of a highly virulent L. pneumophila culture were obtained by passage of the virulent parent culture on SMH agar. The only time a virulent L. pneumophila culture was recoverable from an avirulent culture was when the avirulent culture was derived from a saline suspension of a virulent culture which had been passaged only five times on SMH agar. When an avirulent culture was derived from a virulent culture passaged 25 times on SMH agar or from an isolated colony which grew on a SMH agar plate, we were unable to recover a virulent culture after successive passage through guinea pigs. These results suggest that the conversion process which occurs between virulent and avirulent forms of L. pneumophila is a one-way phenomenon from virulence to avirulence and that stable avirulent derivatives can be isolated. Furthermore, our findings suggest that SMH agar acts as a selective medium for the growth of avirulent L. pneumophila, and growth on SMH agar may be a phenotypic marker for avirulence. Virulent cells, although unable to grow on SMH agar, may remain viable for several passages on SMH agar and propagate when inoculated into guinea pigs.
Infect Immun 1988 Dec
PMID:Virulence conversion of Legionella pneumophila: a one-way phenomenon. 318 73

From January 1983 until December 1985, 35 cases of sporadic nosocomial legionella pneumonia, all caused by Legionella pneumophila, were diagnosed in a university hospital. L. pneumophila serogroup (SG) 1 was cultured from 12 of the 35 cases and compared to corresponding L. pneumophila SG 1 isolates from water outlets in the patients' immediate environment by subtyping with monoclonal antibodies. The corresponding environmental isolates were identical to 9 out of 12 (75%) of those from the cases. However, even in the remaining three cases identical subtypes were found distributed throughout the hospital water supply. From the hospital water supply four different subtypes of L. pneumophila SG 1 were isolated, three of which were implicated in legionella pneumonia. Of 453 water samples taken during the study 298 (65.8%) were positive for legionellae. Species of Legionella other than L. pneumophila have not been isolated. This may explain the exclusiveness of L. pneumophila as the legionella pneumonia-causing agent. Our results suggest that the water supply system was the source of infection.
Epidemiol Infect 1988 Dec
PMID:Nosocomial legionella pneumonia: demonstration of potable water as the source of infection. 321 93

Guinea-pigs were exposed for 14 days to an aerosol of titanium dioxide (TiO2) dust to produce macrophage blockade. Groups of the animals were later infected by aerosol with Legionella pneumophila. Histological and ultrastructural studies showed that TiO2 dust alone was inert and non-fibrogenic and even at 6 weeks induced no pathological lesions in the lungs, apart from accumulation of macrophages in interalveolar septa. The macrophage blockade by TiO2 did not alter the animals' susceptibility to Legionnaires' disease nor increase mortality. The blockade was effective in the early stages of the infection and limited multiplication of L. pneumophila in the lungs. Later blood monocytes were recruited into the lungs, where they phagocytosed Legionellae, resulting in lung counts comparable to those of TiO2-free control animals.
Br J Exp Pathol 1988 Dec
PMID:Effects of inhaled titanium dioxide dust on the lung and on the course of experimental Legionnaires' disease. 321 83

The susceptibility of coliform bacteria and bacterial pathogens to free chlorine residuals was determined before and after incubation with amoebae and ciliate protozoa. Viability of bacteria was quantified to determine their resistance to free chlorine residuals when ingested by laboratory strains of Acanthamoeba castellanii and Tetrahymena pyriformis. Cocultures of bacteria and protozoa were incubated to facilitate ingestion of the bacteria and then were chlorinated, neutralized, and sonicated to release intracellular bacteria. Qualitative susceptibility of protozoan strains to free chlorine was also assessed. Protozoa were shown to survive and grow after exposure to levels of free chlorine residuals that killed free-living bacteria. Ingested coliforms Escherichia coli, Citrobacter freundii, Enterobacter agglomerans, Enterobacter cloacae, Klebsiella pneumoniae, and Klebsiella oxytoca and bacterial pathogens Salmonella typhimurium, Yersinia enterocolitica, Shigella sonnei, Legionella gormanii, and Campylobacter jejuni had increased resistance to free chlorine residuals. Bacteria could be cultured from within treated protozoans well after the time required for 99% inactivation of free-living cells. All bacterial pathogens were greater than 50-fold more resistant to free chlorine when ingested by T. pyriformis. Escherichia coli ingested by a Cyclidium sp., a ciliate isolated from a drinking water reservoir, were also shown to be more resistant to free chlorine. The mechanism that increased resistance appeared to be survival within protozoan cells. This study indicates that bacteria can survive ingestion by protozoa. This bacterium-protozoan association provides bacteria with increased resistance to free chlorine residuals which can lead to persistence of bacteria in chlorine-treated water. We propose that resistance to digestion by predatory protozoa was an evolutionary precursor of pathogenicity in bacteria and that today it is a mechanism for survival of fastidious bacteria in dilute and inhospitable aquatic environments.
Appl Environ Microbiol 1988 Dec
PMID:Survival of coliforms and bacterial pathogens within protozoa during chlorination. 322 66

Direct effects of antimicrobial agents on macrophages functions are not well precised. However, antimicrobials can enhance phagocytosis of bacteria by macrophages in vitro, at subinhibitory concentrations. This enhancement is related to the antibiotic effect. It is dependent of the nature of the antimicrobial agent, of the experimental procedure and some discrepancies appeared in the results. The precise mechanism, effect on the bacterial wall, or on the bacterial protein synthesis is uncertain. The third type of interaction concerns the intracellular penetration and activity of antimicrobial agents within macrophages. In a human monocyte-derived macrophage model, the intracellular growth of Legionella pneumophila was inhibited by erythromycin, rifampicin and fluoroquinolones at concentrations clearly lower than their MICs; doxycycline and cotrimoxazole were inhibitory at concentrations closed to their MICs. Cefoxitin was not inhibitory even at high concentrations despite a low MIC value. This confirms the good intracellular activity of macrolides and fluoroquinolones and the low intracellular activity of beta-lactams.
Pathol Biol (Paris) 1987 Dec
PMID:[Interactions between macrophages and anti-infective agents]. 332 8

This article reviews the classification and identification of the 23 described species, the 11 unnamed species, and the 49 serogroups presently known in the family Legionellaceae and the genus Legionella. The events leading to the isolation and classification of the first species, Legionella pneumophila, are summarized; these include the outbreak of legionnaires' disease at the 1976 American Legion Convention in Philadelphia, the five outbreaks preceding the Philadelphia outbreak, and the isolation of three Legionella species before 1976. The phenotypic characteristics of legionellae are described, including growth requirements, isolation media, biochemical tests, cellular fatty acids, quinones, and the guanine-plus-cytosine (G + C) content of DNA. Identification of legionellae by serology, monoclonal antibodies, and gene probes is described. Each species is listed with an explanation of its name, the source, location of its isolation, its involvement, if any, in human disease, its type strain, and the person who isolated it. The basis of taxonomy by DNA hybridization at the species level and evidence consistent with all species in a single genus and family are described. Problems with identification of legionellae at the species level and with their classification, especially at the genus level, are discussed.
Semin Respir Infect 1987 Dec
PMID:Classification of the legionellae. 332 89

The study of outbreaks of Legionella pneumophila has been essential in understanding the organism, the disease, and its pathogenesis. Early epidemics defined the clinical spectrum: Pontiac fever is an acute, self-limited, febrile illness with an attack rate of 95% to 100% and an incubation period of 36 hours. In contrast, legionnaires' disease is a life-threatening bronchopneumonia with an attack rate of 2% to 7% and an incubation period of two to ten days. Three times as many males as females are affected with legionnaires' disease, and age, cigarette smoking, and chronic medical disease (particularly immunosuppression) appear to be separate risk factors. Furthermore, L pneumophila is responsible for approximately 1% to 3% of community-acquired pneumonias, 13% of those acquired in the hospital and as many as 26% of atypical pneumonias. Diverse environmental reservoirs have been identified, including cooling systems, potable or domestic water systems, respiratory therapy devices, industrial coolants, and whirlpool spas. Hot water temperature, stagnant water, sediment, and the presence of other microorganisms are important factors in the amplification of the Legionellaceae. Although airborne transmission has been widely suggested, aspiration may be an important mode in certain patients. Regional and national surveillance may identify common sources and allow the introduction of early control measures. The latter have included primarily pulse and continuous hyperchlorination and super-heating hot water systems to 50 to 60 degrees C. Experimental data suggest that ozone and UV light may be useful in the future. Additionally, cooling towers and evaporative condensers have been decontaminated and maintained with a variety of biocides. The prevention of outbreaks requires thoughtful planning, redesign, and good engineering practices.
Semin Respir Infect 1987 Dec
PMID:The epidemiology of Legionella pneumophila infections. 332 90

Infection with members of the genus Legionella can produce a wide spectrum of disease ranging from a self-limiting febrile illness to life-threatening pneumonia. The primary site of infection in the pneumonic form of the disease appears to be the lung, but dissemination to other organs is possible. Infection results in an intense alveolitis with infiltration by large numbers of mixed inflammatory cells. The legionellae are facultative intracellular pathogens which multiply within host phagocytic cells, primarily alveolar macrophages, and disrupt the bactericidal mechanisms of these cells. The role of the polymorphonuclear leukocyte is less clearly understood. Many members of the genus produce a number of toxins which may be responsible for some of the pulmonary and extrapulmonary manifestations of disease.
Semin Respir Infect 1987 Dec
PMID:Pathogenesis and pathology of legionellosis. 332 91

Legionnaires' disease is an illness with protean manifestations that are due to infection with Legionella pneumophila. It occurs both in epidemic and sporadic form and usually presents as an atypical pneumonia. Relative bradycardia, abnormal liver function test results, and a patient presenting with an atypical pneumonia should alert the clinician to the possibility of Legionella. The presence of systemic involvement, specifically neurological, gastrointestinal, and renal abnormalities, should further suggest the diagnosis. Patients may demonstrate multiple extrapulmonary manifestations of legionnaires' disease, sometimes without pneumonia. Several methods are available to aid the clinician in making the diagnosis of legionnaires' disease, and the use of all tests will increase the overall sensitivity.
Semin Respir Infect 1987 Dec
PMID:Clinical and laboratory aspects of Legionnaire's disease. 332 92

Legionnaires' disease can be diagnosed by culture, by direct detection of the bacterium or its products by using immunologic means, with a DNA probe, and by serologic means. Culture diagnosis is the most specific and sensitive test. Legionellae can be isolated from sputum samples by using selective techniques. Antibody detection is more suited for epidemiologic purposes than for use in individual cases. Immunofluorescent microscopy is a useful and rapid means of diagnosis. Alternative rapid and specific tests are urinary antigen detection and the use of a DNA probe. Culture must always be performed for optimal sensitivity and for epidemiologic purposes.
Semin Respir Infect 1987 Dec
PMID:The laboratory diagnosis of Legionnaires' disease. 332 93


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