Disseminated Infection Due to Rapidly Growing Mycobacteria in Immunocompetent Hosts Presenting with Chronic Lymphadenopathy: A Previously Unrecognized Clinical Entity

Chetchotisakd, Ploenchan; Mootsikapun, Piroon; Anunnatsiri, Siriluck; Jirarattanapochai, Kunya; Choonhakarn, Charoen; Chaiprasert, Angkana; Ubol, Preyawis Na; Wheat, L. Joseph; Davis, Tyler

doi:10.1086/313589

Cited by 83 publications

(55 citation statements)

References 59 publications

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“…Similarly, reports of patients with hemosiderosis suggest that impairment of phagocytic cells may be important (286,363). Case reports of melioidosis and previous or subsequent mycobacterial infection (Mycobacterium tuberculosis, Mycobacterium terrae, or Mycobacterium leprae) may reflect a common host susceptibility to these intracellular pathogens (56,89,362,417).…”

Section: Risk Factorsmentioning

confidence: 99%

Melioidosis: Epidemiology, Pathophysiology, and Management

2005

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Melioidosis, caused by the gram-negative saprophyte Burkholderia pseudomallei, is a disease of public health importance in southeast Asia and northern Australia that is associated with high case-fatality rates in animals and humans. It has the potential for epidemic spread to areas where it is not endemic, and sporadic case reports elsewhere in the world suggest that as-yet-unrecognized foci of infection may exist. Environmental determinants of this infection, apart from a close association with rainfall, are yet to be elucidated. The sequencing of the genome of a strain of B. pseudomallei has recently been completed and will help in the further identification of virulence factors. The presence of specific risk factors for infection, such as diabetes, suggests that functional neutrophil defects are important in the pathogenesis of melioidosis; other studies have defined virulence factors (including a type III secretion system) that allow evasion of killing mechanisms by phagocytes. There is a possible role for cell-mediated immunity, but repeated environmental exposure does not elicit protective humoral or cellular immunity. A vaccine is under development, but economic constraints may make vaccination an unrealistic option for many regions of endemicity. Disease manifestations are protean, and no inexpensive, practical, and accurate rapid diagnostic tests are commercially available; diagnosis relies on culture of the organism. Despite the introduction of ceftazidime- and carbapenem-based intravenous treatments, melioidosis is still associated with a significant mortality attributable to severe sepsis and its complications. A long course of oral eradication therapy is required to prevent relapse. Studies exploring the role of preventative measures, earlier clinical identification, and better management of severe sepsis are required to reduce the burden of this disease

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Section: Risk Factorsmentioning

confidence: 99%

Melioidosis: Epidemiology, Pathophysiology, and Management

2005

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“…Most patients also had serious infections with pathogens other than the RGM (36). The duration of symptoms in the 16 patients persisted from 1 month to 5 years, with a mean of 15.6 months, before diagnosis of the RGM was established.…”

Section: Disseminated Cutaneous Diseasementioning

confidence: 99%

Clinical and Taxonomic Status of Pathogenic Nonpigmented or Late-Pigmenting Rapidly Growing Mycobacteria

2002

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The history, taxonomy, geographic distribution, clinical disease, and therapy of the pathogenic nonpigmented or late-pigmenting rapidly growing mycobacteria (RGM) are reviewed. Community-acquired disease and health care-associated disease are highlighted for each species. The latter grouping includes health care-associated outbreaks and pseudo-outbreaks as well as sporadic disease cases. Treatment recommendations for each species and type of disease are also described. Special emphasis is on the Mycobacterium fortuitum group, including M. fortuitum, M. peregrinum, and the unnamed third biovariant complex with its recent taxonomic changes and newly recognized species (including M. septicum, M. mageritense, and proposed species M. houstonense and M. bonickei). The clinical and taxonomic status of M. chelonae, M. abscessus, and M. mucogenicum is also detailed, along with that of the closely related new species, M. immunogenum. Additionally, newly recognized species, M. wolinskyi and M. goodii, as well as M. smegmatis sensu stricto, are included in a discussion of the M. smegmatis group. Laboratory diagnosis of RGM using phenotypic methods such as biochemical testing and high-performance liquid chromatography and molecular methods of diagnosis are also discussed. The latter includes PCR-restriction fragment length polymorphism analysis, hybridization, ribotyping, and sequence analysis. Susceptibility testing and antibiotic susceptibility patterns of the RGM are also annotated, along with the current recommendations from the National Committee for Clinical Laboratory Standards (NCCLS) for mycobacterial susceptibility testing

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“…[25][26][27] Th us, natural disaster survivors may be at increased risk for NTM lung infections resulting from inhalation or aspiration of contaminated water, soil, or NTM-infected amoebae. 7 Hoefsloot et al 28 [33][34][35] indicating that the tsunami-related infections were likely due to organisms already present in the environment.…”

mentioning

confidence: 99%