Les protéines de la membrane externe de Leqionella pneumophila sérogroupes 1 à 8 ont été préparées, à partir d'un lysat bactérien, par solubilisation sélective au lauryl sarcosinate de sodium. Les protéines ainsi obtenues ont été séparées par électrophorèse sur gel de polyacrylamide en présence de dodécyl sulfate de sodium (SDS-PAGE) et transférées sur des feuilles de nitrocellulose. Des antisérums de lapin dirigés contre chacun des 8 sérogroupes de L. pneumophila ont été obtenus en immunisant chaque animal avec des bactéries vivantes. Les protéines tranfé- rées ont été révélées avec ces antisérums et des immunoglobulines de porc anti-immunoglobulines de lapins marquées à la peroxidase. Des déterminants antigéniques communs aux 8 sérogroupes ont été trouvés dans au moins 2 antigènes de la membrane externe (29 Kd et 45 Kd). Cependant, des expériences d'absorptions croisées ont révélé que ces antigènes auraient des déterminants antigéniques différents selon le sérogroupe. Ces résultats ne sont pas incompatibles avec ce que l'on connaît des protéines de la membrane externe des autres bactéries. Toutefois, certains indices nous laissent croire que notre préparation de protéines a pu être contaminée avec du lipopolysaccharide. Ceci expliquerait pourquoi les relations antigéniques observées avec les bandes de 29 et 45 Kd correspondent bien avec celles observées par immunofluorescence. / Montréal Trigonix inc. 2018

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A dissertation submitted to the Faculty of Medicine of the University of the Witwatersrand. Johannesburg. for the Degree of Master of Science in Medicine Johannesburg 1994 / South African gold-miners work under stressful conditions and live in communal hostels. Respiratory infections are common in these workers and several cases of Legionnaires' Disease have previously been diagnosed in workers at a gold mine on the East Rand. The prevalence of antibodies and the rate of seroconversion within a period of six months, to C. pneumoniae and L. paeumopbils, both common causes of atypical pneumonia, was studied in relation to several risk factors including age, smoking habits, previous underground experience and past exposure to dust and humidity in the environment. Factory workers from a rural area in Natal and hospitalised patients with community acquired pneumonia were tested for comparison. Water samples were collected from several areas at the mine, including both surface and underground samples" Antibodies to C. pneumoniae were present in 66% of the mine workers, compared to 50% of pneumonia patients and 22% of factory workers, a statistically significant difference (P<O.OOl), Seroconversion was demonstrated ill 17% of the mine workers within a period of six months working underground, and in 22% of pneumonia patients, with convalescent stage sera taken 1-6 weeks after onset of symptoms. None of the risk factors studied influenced the prevalence of C. pneumoniae antibodies in the mine workers, but a significant association between the presence of respiratory symptoms in the six month period and seroconversicn was demonstrated (P<O.025). Using heat- killed antigens, antibodies to L. paeumopbile serogroups 1-4 were demonstrated in 36% of the mine workers, in 16% of the pneumonia patients and in 10% of factory workers (P<O.OOl). Seroconversion occurred in 18% of mine workers and in 14% of pneumonia patients. An association could not be demonstrated between any (if the risk factors studied and the prevalence of antibodies or the rate of seroconversion to L. pneumophila in the mine workers. No legionellae were cultured from the water samples, and the presence of these organsims in chlorinated water from both surface and underground samples could not be confirmed.

Bibliography: leaves 246-304. Describes experiments aimed at characterising the potential virilant factors of Legionella longbeachae sg 1, an important human pathogen which is responsible for nearly half of all clinical cases of Legionella related pneumonia reported each year.

Legionella pneumophila (Lp.), the causative agent of Legionnaires’ disease, has been well known for infecting and replicating inside airway macrophages. Previous results from our laboratory indicated that Lp. attaches to non-polarized lung epithelial cells by binding and activating E-cadherin and β1-integrin. However, in the polarized alveolar epithelia these receptors are segregated from the apical cell surface by tight junctions (TJs). Our results showed that Lp. behaves as an opportunistic pathogen that efficiently targets disrupted, but not integrated epithelial cell monolayer. In such conditions, Lp. can reach its host-cell receptors and consequently invade and replicate intracellularly, producing large amount of bacterial progeny. These results and clinical evidence suggest the contribution of damaged airway epithelia to Legionellosis by providing a replication reservoir for the bacteria.

Legionella pneumophila (Lp) is the pathogen responsible for Legionnaires disease. Lp invades and survives in human macrophages to form an intracellular compartment, called the Legionella containing vacuole (LCV). Within the LCV, Lp avoids degradation and replicates, before killing its host and releasing its virulent progeny. Lp is pleomorphic, exhibiting a combination of short rod phenotypes and filaments. Filamentous Lp has been reported in patient samples, but current studies of Lp virulence are exclusively focused on rods. Our results show that filamentous Lp can invade and replicate in human and murine macrophages. Filaments are phagocytosed gradually into tubular phagocytic cups. Interestingly, the formation of the LCV starts at this stage of phagocytosis, and LCV markers were detected before the sealing of the phagosome occurred. We present evidence that the filamentous morphology acts cooperatively with Lp effectors to subvert the microbicidal activities of the macrophage, contributing to the survival of Lp.

Legionella pneumophila (Lp) is the pathogen responsible for Legionnaires disease. Lp invades and survives in human macrophages to form an intracellular compartment, called the Legionella containing vacuole (LCV). Within the LCV, Lp avoids degradation and replicates, before killing its host and releasing its virulent progeny. Lp is pleomorphic, exhibiting a combination of short rod phenotypes and filaments. Filamentous Lp has been reported in patient samples, but current studies of Lp virulence are exclusively focused on rods. Our results show that filamentous Lp can invade and replicate in human and murine macrophages. Filaments are phagocytosed gradually into tubular phagocytic cups. Interestingly, the formation of the LCV starts at this stage of phagocytosis, and LCV markers were detected before the sealing of the phagosome occurred. We present evidence that the filamentous morphology acts cooperatively with Lp effectors to subvert the microbicidal activities of the macrophage, contributing to the survival of Lp.

Legionella pneumophila (Lp.), the causative agent of Legionnaires’ disease, has been well known for infecting and replicating inside airway macrophages. Previous results from our laboratory indicated that Lp. attaches to non-polarized lung epithelial cells by binding and activating E-cadherin and β1-integrin. However, in the polarized alveolar epithelia these receptors are segregated from the apical cell surface by tight junctions (TJs). Our results showed that Lp. behaves as an opportunistic pathogen that efficiently targets disrupted, but not integrated epithelial cell monolayer. In such conditions, Lp. can reach its host-cell receptors and consequently invade and replicate intracellularly, producing large amount of bacterial progeny. These results and clinical evidence suggest the contribution of damaged airway epithelia to Legionellosis by providing a replication reservoir for the bacteria.

Legionellabakterien orsakar den så kallade legionärssjukan vilken är en form av lunginflammation med hög dödlighet. Bakterien lever i färskvatten och finns naturligt i våra sjöar och vattendrag. Enligt Smittskyddsinstitutet trivs Legionellabakterien i temperaturintervallet 20°C till 42°C med en optimal tillväxt vid 35°C, bakterien lever dock redan från 0°C. Vi har i denna undersökning försökt utreda om legionella kan vara en risk ombord i fartyg. Eftersom tester för förekomsten av legionellabakterier inte ingår i de krav som ställs på dricksvattenkvaliteten ombord, har vi kontaktat fem rederier för att fråga om de har utfört några utökade tester där legionella ingår. Av dessa fem rederier hade tre aldrig testat sitt dricksvatten för legionella och två hade testat och påträffat legionella. Då många av de komponenter som ingår i dricksvattenförsörjningen var placerade i maskinrummet där en omgivningstemperatur mellan 20°C - 42°C var vanligt förekommande, och det faktum att dricksvattensystemen ombord ofta var långa med många tappställen som kunde ge upphov till stillastående vatten, kunde det konstateras att legionella mycket väl kan vara en risk ombord. / The Legionella bacteria cause the so called Legionnaires' disease which is a form of pneumonia with high mortality. The bacterium lives naturally in freshwater lakes and other freshwater sources. According to Smittskyddsinstitutet the bacteria thrives in the temperature interval 20°C - 42°C with an optimal growth at 35°C. However, the bacteria can live in temperatures down to 0°C. In this study we have tried to determine if legionella could be a risk onboard ships. Since testing for legionella bacterium is not required according to regulations, we decided to contact five shipping companies in order to establish if they have ever taken any tests for legionella. Three of those shipping companies had never tested for legionella the other two had tested and found legionella in their drinking water system. Since many components included in the drinking water system were placed in the engine room where the ambient air temperature usually is between 20°C - 42°C, and the fact that the drinking water system often includes long piping’s and many consumers which can lead to standing water, we could conclude that legionella very well could be a risk onboard.