A complicated case of cholecystitis, listeriosis and HIV/AIDS

Barnet and Chase Farm NHS Trust, Chase Farm Hospital, The Ridgeway, Enfield, Middlesex, UK.
Case Reports 01/2011; 2011. DOI: 10.1136/bcr.08.2010.3292
Source: PubMed


A 37-year-old woman of Tanzanian origin presented with symptoms of cholecystitis, sepsis and oral candidiasis. Subsequent investigation found listeriosis and HIV infection. Effective use of the appropriate antibiotics and surgical management to remove the source of sepsis lead to a good recovery from the acute illness. The patient was subsequently transferred to a tertiary centre for specialist care of her underlying chronic condition of HIV/AIDS. Her case demonstrates a previously unreported association of HIV, Listeria and cholecystitis.

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    ABSTRACT: Listeriosis usually manifests at the extremes of age, during pregnancy or among immunocompromised individuals as an acute meningoencephalitis with or without associated septicemia. Localized infections are rare. We investigated the incidence of Listeria monocytogenes cholecystitis using the data of the Listeria reference laboratory of the University of Würzburg/FRG. Out of 467 culture proven L.m-infections in the years 1986 and 1987, two cases were localized infections of the gall bladder. Although studies of the microbiology of gallbladder infections have not demonstrated the recovery of Listeria monocytogenes as a pathogen in acute or chronic cases of cholecystitis, these two cases substantiate the existence of this rare form of listeriosis as an entity and support the theory of the importance of the gastrointestinal tract in the pathogenesis of Listeria infections.
    Zeitschrift für Gastroenterologie 04/1989; 27(3):145-7. · 1.05 Impact Factor
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    ABSTRACT: For many years the Gram-positive facultatively intracellular food-borne pathogen Listeria monocytogenes has been used as a model organism for the study of intracellular parasitism. Whilst the basic mechanisms of cellular pathogenesis have been elucidated by a series of elegant studies, recent research has begun to focus upon the gastrointestinal (GI) phase of L. monocytogenes infection. Epidemiological studies of outbreaks of human disease now demonstrate that the pathogen can cause gastroenteritis in the absence of invasive disease and associated mortality. Furthermore, the pathogen has the ability to colonize the gallbladder in infected mice and this may function as a significant focus of infection during pathogenesis. The ability of the pathogen to survive within the various microenvironments of the GI tract is essential for the causation of food-borne infection. Survival of the pathogen within gastric acid requires the glutamate decarboxylase (GAD) system. In addition, the carnitine uptake system, OpuC is essential for adaptation within the murine GI tract and subsequent invasive disease. Survival of bile salts both in vitro and in vivo requires a number of mechanisms including bile salt hydrolase (Bsh) and the recently described bile exclusion system, BilE (previously OpuB). Finally a number of these systems (including Bsh, OpuC and BilE) are regulated by both the alternative stress sigma factor, Sigma B and by the regulator of virulence gene expression, PrfA.
    Journal of Applied Microbiology 02/2005; 98(6):1345-53. DOI:10.1111/j.1365-2672.2005.02559.x · 2.48 Impact Factor
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    ABSTRACT: The bacterium Listeria monocytogenes can cause a life-threatening systemic illness in humans. Despite decades of progress in animal models of listeriosis, much remains unknown about the processes of infection and colonization. Here, we report that L. monocytogenes can replicate in the murine gall bladder and provide evidence that its replication there is extracellular and intraluminal. In vivo bioluminescence imaging was employed to determine the location of the infection over time in live animals, revealing strong signals from the gall bladder over a period of several days, in diseased as well as asymptomatic animals. The data suggest that L. monocytogenes may be carried in the human gall bladder.
    Science 03/2004; 303(5659):851-3. DOI:10.1126/science.1092712 · 33.61 Impact Factor

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