scholarly journals Mycobacterium ulceransin Mosquitoes and March flies captured from endemic areas of Northern Queensland, Australia

2018 ◽  
Author(s):  
Avishek Singh ◽  
William John Hannan McBride ◽  
Brenda Govan ◽  
Mark Pearson ◽  
Scott A. Ritchie
Keyword(s):  
Causative Agent ◽  
Buruli Ulcer ◽  
Mycobacterial Infection ◽  
Blood Feeding ◽  
Mycobacterium Ulcerans ◽  
Mechanical Transmission ◽  
Environmental Reservoir ◽  
Nontuberculous Mycobacterial Infection ◽  
Mode Of Transmission ◽  
Endemic Areas

AbstractMycobacterium ulceransis the causative agent of Buruli ulcer (BU). This nontuberculous mycobacterial infection has been reported in over 33 countries worldwide. In Australia, the majority of cases of BU have been recorded in coastal Victoria and the Mossman-Daintree areas of north Queensland. Mosquitoes have been postulated as a vector ofM. ulceransin Victoria, however the specific mode of transmission of this disease is still far from being well understood. In the current study, we trapped and analysed 16,900 (allocated to 845 pools) mosquitoes and 296 March flies from the endemic areas of north Queensland to examine for the presence ofM. ulceransDNA by polymerase chain reaction. Seven of 845 pools of mosquitoes were positive on screening using the IS2404 PCR target but only one pool was positive for presence ofM. ulceransafter confirmatory testing. None of the March fly samples were positive for the presence ofM. ulcerans.M. ulceranswas detected on proboscises of deliberately exposed mosquitoes.Author SummaryThe causative agent of Buruli ulcer is Mycobacterium ulcerans. This destructive skin disease is characterized by extensive and painless necrosis of skin and underlying tissues usually on extremities of body due to production of toxin named mycolactone. The disease is prevalent in Africa and coastal Australia. The exact mode of transmission and potential environmental reservoir for the pathogen still remain obscure. Aquatic and biting insects have been identified as important niche in transmission and maintenance of pathogen in the environment. In this study we screened mosquitoes and march flies captured from endemic areas of northern Queensland for the presence ofM. ulcerans.In addition, we conducted artificial blood feeding experiment to identify the role of mosquitoes in transmission of this pathogen. We found one pool of mosquito out of 845 pools positive forM. ulceransand none of the March fly samples were positive. This could indicate a low burden of the bacteria in the environment coinciding with a comparatively low number of human cases ofM. ulceransinfection seen during the trapping period of the study. Evidence to support mechanical transmission via mosquito proboscises was found.

scholarly journals Mycobacterium ulceranslow infectious dose and atypical mechanical transmission support insect bites and puncturing injuries in the spread of Buruli ulcer

2016 ◽  
Author(s):  
John R. Wallace ◽  
Kirstie M. Mangas ◽  
Jessica L. Porter ◽  
Renee Marcsisin ◽  
Sacha J. Pidot ◽  
...  
Keyword(s):  
Causative Agent ◽  
Disease Transmission ◽  
Buruli Ulcer ◽  
Blood Feeding ◽  
Mycobacterium Ulcerans ◽  
World Health ◽  
Mechanical Transmission ◽  
Needle Puncture ◽  
Infectious Dose ◽  
Ulcer Disease

AbstractAddressing the transmission enigma of the neglected disease Buruli ulcer (BU) is a World Health Organization priority. In Australia, we have observed an association between mosquitoes harboring the causative agent,Mycobacterium ulcerans, and BU. Here we tested a contaminated skin model of BU transmission by dipping the tails from healthy mice in cultures of the causative agent,Mycobacterium ulcerans. Tails were exposed to mosquito (Aedes notoscriptusandAedes aegypti) blood feeding or punctured with sterile needles. Two of 11 of mice withM. ulceranscontaminated tails exposed to feedingA. notoscriptusmosquitoes developed BU. Eighteen of 20 mice subjected to contaminated tail needle puncture developed BU. Mouse tails coated only in bacteria did not develop disease. We observed a low infectious dose-50 of four colony-forming units and a median incubation time of 12 weeks, consistent with data from human infections. We have uncovered a highly efficient and biologically plausible atypical transmission mode of BU via natural or anthropogenic skin punctures.Author summaryBuruli ulcer is a neglected tropical disease caused by infection withMycobacterium ulcerans. Unfortunately, how people contract this disease is not well understood. Here we show for the first time using experimental infections in mice that a very low dose ofM. ulceransdelivered beneath the skin by a minor injury caused by a blood-feeding insect (mosquito) or a needle puncture is sufficient to cause Buruli ulcer. This research provides important laboratory evidence to advance our understanding of Buruli ulcer disease transmission.

scholarly journals The changing epidemiology worldwide ofMycobacterium ulcerans

2018 ◽  
Vol 147 ◽  
Author(s):  
D. P. O'Brien ◽  
I. Jeanne ◽  
K. Blasdell ◽  
M. Avumegah ◽  
E. Athan
Keyword(s):  
Mycobacterial Infection ◽  
Mycobacterium Ulcerans ◽  
Health Interventions ◽  
World Health ◽  
Transmission Mechanisms ◽  
Current State ◽  
The World ◽  
Environmental Reservoir ◽  
Endemic Areas ◽  
Health Organization

AbstractMycobacterium ulceransis recognised as the third most common mycobacterial infection worldwide. It causes necrotising infections of skin and soft tissue and is classified as a neglected tropical disease by the World Health Organization (WHO). However, despite extensive research, the environmental reservoir of the organism and mode of transmission of the infection to humans remain unknown. This limits the ability to design and implement public health interventions to effectively and consistently prevent the spread and reduce the incidence of this disease. In recent years, the epidemiology of the disease has changed. In most endemic regions of the world, the number of cases reported to the WHO are reducing, with a 64% reduction in cases reported worldwide in the last 9 years. Conversely, in a smaller number of countries including Australia and Nigeria, reported cases are increasing at a rapid rate, new endemic areas continue to appear, and in Australia cases are becoming more severe. The reasons for this changing epidemiology are unknown. We review the epidemiology ofM. ulceransdisease worldwide, and document recent changes. We also outline and discuss the current state of knowledge on the ecology ofM. ulcerans, possible transmission mechanisms to humans and what may be enabling the spread ofM. ulceransinto new endemic areas.

scholarly journals Community-based geographical distribution of Mycobacterium ulcerans VNTR-genotypes from the environment and humans in the Nyong valley, Cameroon

2021 ◽  
Vol 49 (1) ◽  
Author(s):  
Francis Zeukeng ◽  
Anthony Ablordey ◽  
Solange E. Kakou-Ngazoa ◽  
Stephen Mbigha Ghogomu ◽  
David N’golo Coulibaly ◽  
...  
Keyword(s):  
Environmental Samples ◽  
Tandem Repeats ◽  
Buruli Ulcer ◽  
Variable Number ◽  
Mycobacterium Ulcerans ◽  
Community Based ◽  
Human Samples ◽  
Route Of Transmission ◽  
Mode Of Transmission ◽  
Animal Reservoirs

Abstract Background Genotyping is a powerful tool for investigating outbreaks of infectious diseases and it can provide useful information such as identifying the source and route of transmission, and circulating strains involved in the outbreak. Genotyping techniques based on variable number of tandem repeats (VNTR) are instrumental in detecting heterogeneity in Mycobacterium ulcerans (MU) and also for discriminating MU from other mycobacteria species. Here, we describe and map the distribution of MU genotypes in Buruli ulcer (BU) endemic communities of the Nyong valley in Cameroon. We also tested the hypothesis of whether the suspected animal reservoirs of BU that share the human microhabitat are shedding contaminated fecal matters and saliva into their surrounding environments. Methods Environmental samples from suspected MU-risk factors and lesion swabs from human patients were sampled in BU-endemic communities and tested for the presence of MU by qPCR targeting three independent sequences (IS2404, IS2606, KR-B). Positive samples to MU were further genotyped by VNTR with confirmation by sequencing of four loci (MIRU1, Locus 6, ST1, Locus 19). Results MU was detected in environmental samples including water bodies (23%), biofilms (14%), detritus (10%), and in human patients (73%). MU genotypes D, W, and C were found both in environmental and human samples. The micro geo-distribution of MU genotypes from communities showed that genotype D is found both in environmental and human samples, while genotypes W and C are specific to environmental samples and human lesions, respectively. No obvious focal grouping of MU genotypes was observed at the community scale. An additional survey in the human microhabitat suggests that domestic and wild animals do not shed MU in their saliva and feces in sampled communities. Conclusions VNTR typing uncovered different MU genotypes circulating in the endemic communities of the Akonolinga district. A MU environmental genotype was found in patients, yet the mechanism of contamination remains to be investigated; and recovering MU in culture from the environment remains key priority to enable a better understanding of the mode of transmission of BU. We also conclude that excretions from suspected animals are unlikely to be major sources of MU in the Nyong Valley in Cameroon.

scholarly journals Delays in Patient Presentation and Diagnosis for Buruli Ulcer (Mycobacterium ulcerans Infection) in Victoria, Australia, 2011–2017

2019 ◽  
Vol 4 (3) ◽  
pp. 100
Author(s):  
Shaun P. Coutts ◽  
Colleen L. Lau ◽  
Emma J. Field ◽  
Michael J. Loftus ◽  
Ee Laine Tay
Keyword(s):  
Multivariable Analysis ◽  
Buruli Ulcer ◽  
Mycobacterium Ulcerans ◽  
Control Measures ◽  
Diagnosis Delay ◽  
The Public ◽  
Endemic Areas ◽  
Significant Change ◽  
Transmission Pathways ◽  
And Control

Uncertainty regarding transmission pathways and control measures makes prompt presentation and diagnosis for Buruli ulcer critical. To examine presentation and diagnosis delays in Victoria, Australia, we conducted a retrospective study of 703 cases notified between 2011 and 2017, classified as residing in an endemic (Mornington Peninsula; Bellarine Peninsula; South-east Bayside and Frankston) or non-endemic area. Overall median presentation delay was 30 days (IQR 14–60 days), with no significant change over the study period (p = 0.11). There were significant differences in median presentation delay between areas of residence (p = 0.02), but no significant change over the study period within any area. Overall median diagnosis delay was 10 days (IQR 0–40 days), with no significant change over the study period (p = 0.13). There were significant differences in median diagnosis delay between areas (p < 0.001), but a significant decrease over time only on the Mornington Peninsula (p < 0.001). On multivariable analysis, being aged <15 or >65 years; having non-ulcerative disease; and residing in the Bellarine Peninsula or South-East Bayside (compared to non-endemic areas) were significantly associated with shorter presentation delay. Residing in the Bellarine or Mornington Peninsula and being notified later in the study period were significantly associated with shorter diagnosis delay. To reduce presentation and diagnosis delays, awareness of Buruli ulcer must be raised with the public and medical professionals, particularly those based outside established endemic areas.

scholarly journals Subtractive Hybridization Reveals a Type I Polyketide Synthase Locus Specific to Mycobacterium ulcerans

2003 ◽  
Vol 185 (23) ◽  
pp. 6870-6882 ◽  
Author(s):  
Grant A. Jenkin ◽  
Timothy P. Stinear ◽  
Paul D. R. Johnson ◽  
John K. Davies
Keyword(s):  
Genetic Basis ◽  
Polyketide Synthase ◽  
Buruli Ulcer ◽  
Subtractive Hybridization ◽  
Mycobacterial Infection ◽  
Mycobacterium Ulcerans ◽  
Suppressive Subtractive Hybridization ◽  
Type I ◽  
The Third ◽  
Close Genetic Relationship

ABSTRACT Mycobacterium ulcerans causes Buruli ulcer, the third most prevalent mycobacterial infection of immunocompetent humans after tuberculosis and leprosy. Recent work has shown that the production by M. ulcerans of mycolactone, a novel polyketide, may partly explain the pathogenesis of Buruli ulcer. To search for the genetic basis of virulence in M. ulcerans, we took advantage of the close genetic relationship between M. ulcerans and Mycobacterium marinum by performing genomic suppressive subtractive hybridization of M. ulcerans with M. marinum. We identified several DNA fragments specific to M. ulcerans, in particular, a type I polyketide synthase locus with a highly repetitive modular arrangement. We postulate that this locus is responsible for the synthesis of mycolactone in M. ulcerans.

scholarly journals Antimycobacterial activity of medicinal plants against the causative agent of buruli ulcer: Mycobacterium ulcerans

2016 ◽  
Vol 5 ◽  
pp. S105 ◽  
Author(s):  
R. Keumoe ◽  
M.S. Nguembou ◽  
F.P.V. Tsouh ◽  
D.V.F. Donkeng ◽  
D. Dize ◽  
...  
Keyword(s):  
Medicinal Plants ◽  
Causative Agent ◽  
Buruli Ulcer ◽  
Antimycobacterial Activity ◽  
Mycobacterium Ulcerans

scholarly journals Snapshot fecal survey of domestic animals in rural Ghana forMycobacterium ulcerans

PeerJ ◽  
2016 ◽  
Vol 4 ◽  
pp. e2065 ◽  
Author(s):  
Nicholas J. Tobias ◽  
Nana Ama Ammisah ◽  
Evans K. Ahortor ◽  
John R. Wallace ◽  
Anthony Ablordey ◽  
...  
Keyword(s):  
Gastrointestinal Tract ◽  
Buruli Ulcer ◽  
Domestic Animals ◽  
Mycobacterium Ulcerans ◽  
Animal Reservoir ◽  
Rural Ghana ◽  
Reservoir Species ◽  
Mode Of Transmission ◽  
High Concentrations ◽  
Negative Controls

Identifying the source reservoirs ofMycobacterium ulceransis key to understanding the mode of transmission of this pathogen and controlling the spread of Buruli ulcer (BU). In Australia, the native possum can harborM. ulceransin its gastrointestinal tract and shed high concentrations of the bacteria in its feces. To date, an analogous animal reservoir in Africa has not been identified. Here we tested the hypothesis that common domestic animals in BU endemic villages of Ghana are reservoir species analogous to the Australian possum. Using linear-transects at 10-meter intervals, we performed systematic fecal surveys across four BU endemic villages and one non-endemic village in the Asante Akim North District of Ghana. One hundred and eighty fecal specimens from a single survey event were collected and analyzed by qPCR for theM. ulceransdiagnostic DNA targets IS2404and KR-B. Positive and negative controls performed as expected but all 180 test samples were negative. This structured snapshot survey suggests that common domestic animals living in and around humans do not shedM. ulceransin their feces. We conclude that, unlike the Australian native possum, domestic animals in rural Ghana are unlikely to be major reservoirs ofM. ulcerans.

scholarly journals Mycobacterium ulcerans Population Genomics To Inform on the Spread of Buruli Ulcer across Central Africa

mSphere ◽  
2019 ◽  
Vol 4 (1) ◽  
Author(s):  
Koen Vandelannoote ◽  
Delphin Mavinga Phanzu ◽  
Kapay Kibadi ◽  
Miriam Eddyani ◽  
Conor J. Meehan ◽  
...  
Keyword(s):  
Disease Control ◽  
Population Genomics ◽  
Demographic History ◽  
Buruli Ulcer ◽  
Central Africa ◽  
Mycobacterium Ulcerans ◽  
Evolutionary Trajectory ◽  
Content Type ◽  
Mode Of Transmission ◽  
The Impact

ABSTRACT Buruli ulcer is a neglected tropical disease of skin and subcutaneous tissue caused by infection with the pathogen Mycobacterium ulcerans. Many critical issues for disease control, such as understanding the mode of transmission and identifying source reservoirs of M. ulcerans, are still largely unknown. Here, we used genomics to reconstruct in detail the evolutionary trajectory and dynamics of M. ulcerans populations at a central African scale and at smaller geographical village scales. Whole-genome sequencing (WGS) data were analyzed from 179 M. ulcerans strains isolated from all Buruli ulcer foci in the Democratic Republic of the Congo, The Republic of Congo, and Angola that have ever yielded positive M. ulcerans cultures. We used both temporal associations and the study of the mycobacterial demographic history to estimate the contribution of humans as a reservoir in Buruli ulcer transmission. Our phylogeographic analysis revealed one almost exclusively predominant sublineage of M. ulcerans that arose in Central Africa and proliferated in its different regions of endemicity during the Age of Discovery. We observed how the best sampled endemic hot spot, the Songololo territory, became an area of endemicity while the region was being colonized by Belgium (1880s). We furthermore identified temporal parallels between the observed past population fluxes of M. ulcerans from the Songololo territory and the timing of health policy changes toward control of the Buruli ulcer epidemic in that region. These findings suggest that an intervention based on detecting and treating human cases in an area of endemicity might be sufficient to break disease transmission chains, irrespective of other reservoirs of the bacterium. IMPORTANCE Buruli ulcer is a destructive skin and soft tissue infection caused by Mycobacterium ulcerans. The disease is characterized by progressive skin ulceration, which can lead to permanent disfigurement and long-term disability. Currently, the major hurdles facing disease control are incomplete understandings of both the mode of transmission and environmental reservoirs of M. ulcerans. As decades of spasmodic environmental sampling surveys have not brought us much closer to overcoming these hurdles, the Buruli ulcer research community has recently switched to using comparative genomics. The significance of our research is in how we used both temporal associations and the study of the mycobacterial demographic history to estimate the contribution of humans as a reservoir in Buruli ulcer transmission. Our approach shows that it might be possible to use bacterial population genomics to assess the impact of health interventions, providing valuable feedback for managers of disease control programs in areas where health surveillance infrastructure is poor.

scholarly journals Mycobacterium ulcerans low infectious dose and mechanical transmission support insect bites and puncturing injuries in the spread of Buruli ulcer

2017 ◽  
Vol 11 (4) ◽  
pp. e0005553 ◽  
Author(s):  
John R. Wallace ◽  
Kirstie M. Mangas ◽  
Jessica L. Porter ◽  
Renee Marcsisin ◽  
Sacha J. Pidot ◽  
...  
Keyword(s):  
Buruli Ulcer ◽  
Mycobacterium Ulcerans ◽  
Mechanical Transmission ◽  
Infectious Dose ◽  
Insect Bites

scholarly journals Draft Genome Sequence of Mycobacterium ulcerans S4018 Isolated from a Patient with an Active Buruli Ulcer in Benin, Africa

2017 ◽  
Vol 5 (17) ◽  
Author(s):  
Stanimir Kambarev ◽  
Stéphane Corvec ◽  
Annick Chauty ◽  
Estelle Marion ◽  
Laurent Marsollier ◽  
...  
Keyword(s):  
Genome Sequence ◽  
Causative Agent ◽  
Cutaneous Lesion ◽  
Draft Genome ◽  
Buruli Ulcer ◽  
Mycobacterium Ulcerans ◽  
Tropical Disease ◽  
Draft Genome Sequence ◽  
Content Type

ABSTRACT Currently, there are only two publicly available genomes of Mycobacterium ulcerans—the causative agent of the neglected, but devastating, tropical disease Buruli ulcer. Here, we report the draft genome sequence of isolate S4018, recovered from an active cutaneous lesion of a patient with Buruli ulcer in Benin, Africa.

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