Rapidly Expanding Lung Abscess Caused by Legionella pneumophila in Immunocompromised Patients: A Report of Two Cases.

Miyara, Takayuki; Tokashiki, Kaori; Shimoji, T; Tamaki, Kazunori; Koide, Michio; Saitô, Atsushi

doi:10.2169/internalmedicine.41.133

Cited by 22 publications

(11 citation statements)

References 12 publications

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“…120 Risk factors for Legionella spp. 121,123 In vitro data from mice demonstrating that TNF-a is critical for clearing macrophage infection with Legionella further supports the hypothesis of an increased risk of L. pneumophila infection among patients treated with anti-TNF-a antagonists. 121,122 Besides corticosteroids, it has been shown that combined immunosuppression or use of anti-TNF-a antagonists in patients with IBD and rheumatoid arthritis has been associated with an increased risk of Legionella pneumonia.…”

Section: Legionellosismentioning

confidence: 71%

Opportunistic Infections Due to Inflammatory Bowel Disease Therapy

Dave

Purohit

Razonable

et al. 2014

Inflammatory Bowel Diseases

116

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The use of biological agents and immunomodulators for inflammatory bowel disease (IBD) has remarkably improved disease management in the current era but at the same time has increased the risk of infectious complications. Patients with IBD on corticosteroids, immunomodulators, and biological agents are considered immunocompromised and are at risk for opportunistic infections. These are infections caused by organisms that take advantage of a weakened immune system, and cause disease, when they ordinarily would cause mild illness or no disease in an immunocompetent host. Risk factors for opportunistic infections include malnutrition, older age, congenital immunodeficiency, HIV infection, chronic diseases, and use of corticosteroids, immunomodulators, and anti-tumor necrosis factor alpha therapy. Apart from immunosuppressive medications and older age, there is only indirect evidence for above risk factors contributing directly to opportunistic infection risk in patients with IBD. Opportunistic infections in patients with IBD include viral infections (herpes viruses, human papillomavirus, influenza virus, and JC virus), bacterial infections (tuberculosis, nocardiosis, Clostridium difficile infection, pneumococcal infection, legionellosis, and listeriosis), fungal infections (histoplasmosis, cryptococcosis, Pneumocystis jirovecii infection, aspergillosis, and candidiasis), and parasite infections (Strongyloides stercoralis). Although these infections lead to high morbidity and mortality, only a minority of patients with IBD develop opportunistic infections. Currently, we lack a test to accurately predict patients at risk of opportunistic infection, and future research needs to focus on biomarkers or predictive models for risk stratification. Until such a test is developed, we need to screen, prevent, diagnose, and treat opportunistic infections in all patients with IBD in a timely manner.

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Section: Legionellosismentioning

confidence: 71%

Opportunistic Infections Due to Inflammatory Bowel Disease Therapy

Dave

Purohit

Razonable

et al. 2014

Inflammatory Bowel Diseases

116

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“…Human disease occurs when aerosolized L. pneumophila is inhaled from man-made or natural freshwater reservoirs harboring the bacteria. L. pneumophila poses a significant worldwide public health problem, particularly for individuals with compromised immune systems (19,38,40). Eradication of the pathogen from freshwater, industrial settings has proven difficult, since L. pneumophila thrives in environments that exclude antibacterial agents, such as biofilms and the intracellular compartments of protozoa (8,46,47).…”

mentioning

confidence: 99%

Evidence for Acquisition ofLegionellaType IV Secretion Substrates via Interdomain Horizontal Gene Transfer

Felipe

Pampou

Jovanovic³

et al. 2005

J Bacteriol

259

316

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Intracellular pathogens exploit host cell functions to create a replication niche inside eukaryotic cells. The causative agent of Legionnaires' disease, the ␥-proteobacterium Legionella pneumophila, resides and replicates within a modified vacuole of protozoan and mammalian cells. L. pneumophila translocates effector proteins into host cells through the Icm-Dot complex, a specialized type IVB secretion system that is required for intracellular growth. To find out if some effector proteins may have been acquired through interdomain horizontal gene transfer (HGT), we performed a bioinformatic screen that searched for eukaryotic motifs in all open reading frames of the L. pneumophila Philadelphia-1 genome. We found 44 uncharacterized genes with many distinct eukaryotic motifs. Most of these genes contain G؉C biases compared to other L. pneumophila genes, supporting the theory that they were acquired through HGT. Furthermore, we found that several of them are expressed and up-regulated in stationary phase in an RpoS-dependent manner. In addition, at least seven of these gene products are translocated into host cells via the Icm-Dot complex, confirming their role in the intracellular environment. Reminiscent of the case with most Icm-Dot substrates, most of the strains containing mutations in these genes grew comparably to the parent strain intracellularly. Our findings suggest that in L. pneumophila, interdomain HGT may have been a major mechanism for the acquisition of determinants of infection.The ␥-proteobacterium Legionella pneumophila is an opportunistic human pathogen that multiplies within alveolar macrophages and causes the nosocomial and community-acquired pneumonia known as Legionnaires' disease (18,25,48). Human disease occurs when aerosolized L. pneumophila is inhaled from man-made or natural freshwater reservoirs harboring the bacteria. L. pneumophila poses a significant worldwide public health problem, particularly for individuals with compromised immune systems (19,38,40). Eradication of the pathogen from freshwater, industrial settings has proven difficult, since L. pneumophila thrives in environments that exclude antibacterial agents, such as biofilms and the intracellular compartments of protozoa (8,46,47).In order to create a replicative niche inside eukaryotic cells suitable for replication, L. pneumophila is believed to modulate host cell functions by the delivery of effector proteins through a type IVB secretion system known as the Icm-Dot complex (52, 59). Effector proteins presumably regulate several pathways in the host, including up-regulation of phagocytosis (23), delay in phagosome-lysosome fusion (24), recruitment of ARF1 to the phagosome (43), acquisition of endoplasmic reticulum-derived vesicles (29), and nonlytic egress from the host cell (11).Several laboratories found Icm-Dot substrates through genetic screens and bioinformatic approaches (3,7,11,13,36,43,44,57). Most of the known effector proteins are not individually required for intracellular multiplication, since knocking out th...

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“…To our knowledge, this is the first report on E. faecium causing pulmonary infection (abscesses) as a single pathogen since a mixture of pulmonary pathogens including E. faecium has been documented so far [3]. Undoubtedly, both profound immunosupression with antithymocyte globulin and urinary leak contributed to this condition in our patient.…”

mentioning

confidence: 66%