Chitin promotes<i>Mycobacterium ulcerans</i>growth

Sanhueza, Daniel; Chevillon, Christine; Colwell, Rita R.; Babonneau, Jérèmie; Marion, Estelle; Marsollier, Laurent; Guégan, Jean‐François

doi:10.1093/femsec/fiw067

Cited by 19 publications

(28 citation statements)

References 27 publications

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“…M. ulcerans was reported to grow in Middlebrook 7H9 broth, Middlebrook 7H10, and Middlebrook 7H11 agar media with oleic acid-albumin-dextrose-catalase (OADC) enrichment and Löwenstein-Jensen (LJ) medium. The addition of chitin to 7H9 Middlebrook broth was indirectly shown to increase the growth of one strain of M. ulcerans (100). Interestingly, the five available M. ulcerans genomes encoded a GH18 family member, compatible with a putative chitinase activity.…”

Section: Ulcerans the Agent Of Buruli Ulcermentioning

confidence: 99%

Buruli Ulcer, a Prototype for Ecosystem-Related Infection, Caused by Mycobacterium ulcerans

et al. 2018

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Buruli ulcer is a noncontagious disabling cutaneous and subcutaneous mycobacteriosis reported by 33 countries in Africa, Asia, Oceania, and South America. The causative agent, , derives from by genomic reduction and acquisition of a plasmid-borne, nonribosomal cytotoxin mycolactone, the major virulence factor. -specific sequences have been readily detected in aquatic environments in food chains involving small mammals. Skin contamination combined with any type of puncture, including insect bites, is the most plausible route of transmission, and skin temperature of<30°C significantly correlates with the topography of lesions. After 30 years of emergence and increasing prevalence between 1970 and 2010, mainly in Africa, factors related to ongoing decreasing prevalence in the same countries remain unexplained. Rapid diagnosis, including laboratory confirmation at the point of care, is mandatory in order to reduce delays in effective treatment. Parenteral and potentially toxic streptomycin-rifampin is to be replaced by oral clarithromycin or fluoroquinolone combined with rifampin. In the absence of proven effective primary prevention, avoiding skin contamination by means of clothing can be implemented in areas of endemicity. Buruli ulcer is a prototype of ecosystem pathology, illustrating the impact of human activities on the environment as a source for emerging tropical infectious diseases.

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Section: Ulcerans the Agent Of Buruli Ulcermentioning

confidence: 99%

Buruli Ulcer, a Prototype for Ecosystem-Related Infection, Caused by Mycobacterium ulcerans

et al. 2018

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“…Although MU DNA can be found in the whole aquatic community, these results suggest that low trophic level organisms (for example, filter feeders and scavengers) might acquire the bacterium from sediments, mud, detritus, plant and algae biofilms where MU preferentially flourish 21, 23, 24, 25 and even from chitinous remains. 26 However, because low trophic level organisms show greater bacterial loads, the passive transmission of MU by contact with intermediate (for example, taxa Baetidae, Caenidae, Leptophlebiidae and Corixidae) and higher (for example, Tanypodinae and Coenagrionidae) trophic level organisms, increasing contact rates with humans through daily activities (for example, swimming, bathing and fishing), appears to be more likely than (for instance) its bio-accumulation by specific aquatic insects, as has previously been proposed. 6, 27 …”

Section: Introductionmentioning

confidence: 99%

Global and local environmental changes as drivers of Buruli ulcer emergence

Combe

Velvin

Morris

et al. 2017

Emerging Microbes & Infections

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Many emerging infectious diseases are caused by generalist pathogens that infect and transmit via multiple host species with multiple dissemination routes, thus confounding the understanding of pathogen transmission pathways from wildlife reservoirs to humans. The emergence of these pathogens in human populations has frequently been associated with global changes, such as socio-economic, climate or biodiversity modifications, by allowing generalist pathogens to invade and persist in new ecological niches, infect new host species, and thus change the nature of transmission pathways. Using the case of Buruli ulcer disease, we review how land-use changes, climatic patterns and biodiversity alterations contribute to disease emergence in many parts of the world. Here we clearly show that Mycobacterium ulcerans is an environmental pathogen characterized by multi-host transmission dynamics and that its infectious pathways to humans rely on the local effects of global environmental changes. We show that the interplay between habitat changes (for example, deforestation and agricultural land-use changes) and climatic patterns (for example, rainfall events), applied in a local context, can lead to abiotic environmental changes and functional changes in local biodiversity that favor the pathogen's prevalence in the environment and may explain disease emergence.

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“…As an example, it has been shown that the incorporation of chitin into the Middlebrook 7H9 broth enhances the growth of M . ulcerans [ 37 ]. Accordingly, our study points towards a possible association of M .…”

Section: Discussionmentioning

confidence: 99%

“…It is used here in the context of unique carbon metabolisms such as chitinase exhibited by M . ulcerans [ 37 ].…”

Section: Introductionmentioning

confidence: 99%

High-Throughput Carbon Substrate Profiling of Mycobacterium ulcerans Suggests Potential Environmental Reservoirs

et al. 2017

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BackgroundMycobacterium ulcerans is a close derivative of Mycobacterium marinum and the agent of Buruli ulcer in some tropical countries. Epidemiological and environmental studies pointed towards stagnant water ecosystems as potential sources of M. ulcerans, yet the ultimate reservoirs remain elusive. We hypothesized that carbon substrate determination may help elucidating the spectrum of potential reservoirs.Methodology/Principal findingsIn a first step, high-throughput phenotype microarray Biolog was used to profile carbon substrates in one M. marinum and five M. ulcerans strains. A total of 131/190 (69%) carbon substrates were metabolized by at least one M. ulcerans strain, including 28/190 (15%) carbon substrates metabolized by all five M. ulcerans strains of which 21 substrates were also metabolized by M. marinum. In a second step, 131 carbon substrates were investigated, through a bibliographical search, for their known environmental sources including plants, fruits and vegetables, bacteria, algae, fungi, nematodes, mollusks, mammals, insects and the inanimate environment. This analysis yielded significant association of M. ulcerans with bacteria (p = 0.000), fungi (p = 0.001), algae (p = 0.003) and mollusks (p = 0.007). In a third step, the Medline database was cross-searched for bacteria, fungi, mollusks and algae as potential sources of carbon substrates metabolized by all tested M. ulcerans; it indicated that 57% of M. ulcerans substrates were associated with bacteria, 18% with alga, 11% with mollusks and 7% with fungi.ConclusionsThis first report of high-throughput carbon substrate utilization by M. ulcerans would help designing media to isolate and grow this pathogen. Furthermore, the presented data suggest that potential M. ulcerans environmental reservoirs might be related to micro-habitats where bacteria, fungi, algae and mollusks are abundant. This should be followed by targeted investigations in Buruli ulcer endemic regions.

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Chitin promotesMycobacterium ulceransgrowth

Cited by 19 publications

References 27 publications

Buruli Ulcer, a Prototype for Ecosystem-Related Infection, Caused by Mycobacterium ulcerans

Buruli Ulcer, a Prototype for Ecosystem-Related Infection, Caused by Mycobacterium ulcerans

Global and local environmental changes as drivers of Buruli ulcer emergence

High-Throughput Carbon Substrate Profiling of Mycobacterium ulcerans Suggests Potential Environmental Reservoirs

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