Tularemia in Man from a Domestic Rural Water Supply

Jellison, William L.; Epler, Deane C.; Kuhns, Edith; Kohls, Glen M.

doi:10.2307/4587477

Cited by 30 publications

(26 citation statements)

References 2 publications

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“…However, although we have shown preliminary evidence for the survival of F. tularensis in amoebal cysts, the potential for its survival under various types of adverse conditions in these cysts still needs to be systematically examined. The close connection of tularemia with water (30) and the isolation of the bacterium from water samples used for domestic purposes, as well as from natural water systems, as the causal agent of outbreaks of the disease (14,20,21,32) support the hypothesis that amoebae may have a role in the natural transmission of F. tularensis.…”

Section: Discussionmentioning

confidence: 91%

Survival and Growth ofFrancisella tularensisinAcanthamoeba castellanii

Abd

Johansson

Golovliov

et al. 2003

Appl Environ Microbiol

309

269

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Francisella tularensis is a highly infectious, facultative intracellular bacterium which causes epidemics of tularemia in both humans and mammals at regular intervals. The natural reservoir of the bacterium is largely unknown, although it has been speculated that protozoa may harbor it. To test this hypothesis, Acanthamoeba castellanii was cocultured with a strain of F. tularensis engineered to produce green fluorescent protein (GFP) in a nutrient-rich medium. GFP fluorescence within A. castellanii was then monitored by flow cytometry and fluorescence microscopy. In addition, extracellular bacteria were distinguished from intracellular bacteria by targeting with monoclonal antibodies. Electron microscopy was used to determine the intracellular location of F. tularensis in A. castellanii, and viable counts were obtained for both extracellular and intracellular bacteria. The results showed that many F. tularensis cells were located intracellularly in A. castellanii cells. The bacteria multiplied within intracellular vacuoles and eventually killed many of the host cells. F. tularensis was found in intact trophozoites, excreted vesicles, and cysts. Furthermore, F. tularensis grew faster in cocultures with A. castellanii than it did when grown alone in the same medium. This increase in growth was accompanied by a decrease in the number of A. castellanii cells. The interaction between F. tularensis and amoebae demonstrated in this study indicates that ubiquitous protozoa might be an important environmental reservoir for F. tularensis.

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Section: Discussionmentioning

confidence: 91%

Survival and Growth ofFrancisella tularensisinAcanthamoeba castellanii

Abd

Johansson

Golovliov

et al. 2003

Appl Environ Microbiol

309

269

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“…in water sources is likely given the existence of waterborne cases of tularemia [5][6][7][9][10][11] and the observed acquisition of F. tularensis subsp. holarctica (Type B) during the aquatic life cycle of the mosquito vector [15,16].…”

Section: Discussionmentioning

confidence: 99%

Enhanced survival but not amplification of Francisella spp. in the presence of free-living amoebae

Buse

Schaefer

Rice

2016

Acta Microbiologica et Immunologica Hungarica

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Transmission of Francisella tularensis, the etiologic agent of tularemia, has been associated with various water sources. Survival of many waterborne pathogens within free-living amoeba (FLA) is well documented; however, the role of amoebae in the environmental persistence of F. tularensis is unclear. In this study, axenic FLA cultures of Acanthamoeba castellanii, Acanthamoeba polyphaga, and Vermamoeba vermiformis were each inoculated with virulent strains of F. tularensis (Types A and B), the attenuated live vaccine strain, and Francisella novicida. Experimental parameters included low and high multiplicity of infection and incubation temperatures of 25 and 30°C for 0-10 days. Francisella spp. survival was enhanced by the presence of FLA; however, bacterial growth and protozoa infectivity were not observed. In contrast, coinfections of A. polyphaga and Legionella pneumophila, used as an amoeba pathogen control, resulted in bacterial proliferation, cytopathic effects, and amoebal lysis. Collectively, even though short-term incubation with FLA was beneficial, the long-term effects on Francisella survival are unknown, especially given the expenditure of available amoebal derived nutrients and the fastidious nature of Francisella spp. These factors have clear implications for the role of FLA in Francisella environmental persistence.

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“…In fact, natural outbreaks of food-and waterborne tularemia, mainly caused by the type B strain F. tularensis, have occurred recently in Europe, Russia, and the United States (15,20,24,29), and gastrointestinal tularemia is a recognized, although rare, clinical form of F. tularensis infection (18). Experimentally, oral administration of 10 10 CFU of virulent type A F. tularensis, strain SCHU S4, to human volunteers resulted in enlarged painful cervical lymph nodes, and all recipients required prompt antibiotic therapy to prevent further morbidity (18).…”

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confidence: 99%

Mouse Model of Oral Infection with Virulent Type A Francisella tularensis

et al. 2007

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Francisella tularensis is a gram-negative facultative intracellular pathogen and the causative agent of tularemia. Little is known about the immunopathogenesis of oral infection with this pathogen. Here, for the first time, we examined the susceptibility of mice to intragastric inoculation with virulent type A F. tularensis and characterized the course of infection and the associated host responses. Both immunocompetent and immunodeficient mice were relatively susceptible to intragastric inoculation of type A F. tularensis with a 50% lethal dose (LD 50 ) of 10 6 organisms, which was 100,000-fold higher than the LD 100 for intradermal or respiratory routes of infection. Mice deficient in gamma interferon or tumor necrosis factor receptors 1 and 2 were more susceptible than wild-type controls to oral infection with a high dose of the pathogen. After oral inoculation, F. tularensis appeared first in the mesenteric lymph nodes (MLN) and then rapidly spread to the livers and spleens, where the organism multiplied to high numbers and induced marked neutrophilic infiltration and severe tissue necrosis. Infected mice showed rapid increases in tissue cytokine mRNA expression, which peaked in the MLN at 2 days postinfection (dpi) and in the liver and spleen at 3 dpi. The levels of gamma interferon, interleukin-1␤ (IL-1␤), IL-6, tumor necrosis factor alpha, macrophage inflammatory protein 1␣, KC, interferon-inducible protein 10, and monocyte chemotactic protein 1 were elevated from day 2 postinoculation onward. Moreover, mice intradermally immunized with the live vaccine strain of F. tularensis showed little survival advantage over naive mice after oral challenge with type A F. tularensis. These results suggest that type A F. tularensis is an effective oral pathogen that can cause fatal systemic infection and could pose a public health concern, particularly to immunocompromised individuals, if ingested in contaminated water and food.

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Tularemia in Man from a Domestic Rural Water Supply

Cited by 30 publications

References 2 publications

Survival and Growth ofFrancisella tularensisinAcanthamoeba castellanii

Survival and Growth ofFrancisella tularensisinAcanthamoeba castellanii

Enhanced survival but not amplification of Francisella spp. in the presence of free-living amoebae

Mouse Model of Oral Infection with Virulent Type A Francisella tularensis

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