Search for: All records

Despite the clinical relevance of major tuberculous pathogens to domestic animals and humans, the understanding of mycobacterial transmission modes, pathways, and interactions in their natural habitats remains very limited. The reason for this is primarily because ecological and evolutionary concepts have not yet been widely applied to the understanding of these bacteria. Most existing research on mycobacterial transmission is not founded on hypothesis testing but rather tends to accept the most recent explanation and turn it into a canonical fact. In this comparative review, we discuss plausible alternative hypotheses against a null hypothesis of environmental origin to intensify research on mycobacterial pathogens and their capacity to spread in the context of global change. We highlight a major bias in perceptions of mycobacterial infection transmission, with most work concentrating only on the contagious stage of tuberculous clones. We suggest broadening the field to include research on environmental non-tuberculous mycobacteria and their life histories. A deeper understanding of mycobacterial ecology and evolution is more important now than ever, considering the vast diversity of known and unknown mycobacterial species in natural ecosystems. Infectious disease medicine, veterinary science, and public health surveillance should take a more integrative disease ecology approach to enhance the development of new approaches for control of these animal and human pathogens. 

Despite recent interest in land-use and land-cover (LULC) change effects on emerging infectious diseases (EIDs), the debate on global potential health threats remains polarizing. These depend on diverse LULC changes, different types of infectious disease systems, and spatio-temporal scales of studies. Here, using both a bibliometric and scoping review method, we summarize the reliability and availability of published relevant studies on LULC effects on mycobacteria, an important group of infectious bacteria that affect humans and both wild and domestic animals. We make connections of LULC with environmental changes (e.g. soils) that likely lead to an increased risk of mycobacteria spillover to human and other animal populations. An important feature of our review is a focus on research from the richest countries of the world, though some studies have been done in Africa, Asia and South America. Geographically, regions experiencing important LULC transformations, such as many tropical regions of Meso- and South America and Southeast Asia, have been given little or no attention in this important topic. Research onMycobacterium bovis,and to a larger extent onM. ulcerans,constitutes convincing illustrations of the importance of acknowledging shifts in spatio-temporal scales, from local to global and inter-annual to decadal ones, when evaluating responses of mycobacteria to LULC changes. However, studies on other pathogenic mycobacteria remain very much confined to local and dispersed scales. To date, the role of LULC change effects has not been adequately studied for many human and animal pathogens, and more research and attention to this issue is clearly needed. This review provides a comprehensive set of data on the updates of LULC change and their impact on animal and human mycobacterial infections. It also proposes several research recommendations, in particular to better understand the emergence of mycobacteria in context, by multiplying study sites in different regions of the world and in adopting an ecosystem-based perspective, in order to encourage interdisciplinary research better linking environmental microbiology, veterinary science and medical research. 

ABSTRACT Mycobacterium ulceranspseudoshottsiiis a mycolactone‐producing bacterium previously isolated from Striped Bass (Morone saxatilis(Walbaum)) from Chesapeake Bay and adjacent waters of the Atlantic Coast of North America. We report the first molecular detection of this pathogen in the native Gulf strain ofMorone saxatiliscollected from the Pearl River, Mississippi (USA). Molecular identification was conducted using a novel PCR assay targeting the parA‐625 intergenic spacer of the virulence‐associated pMUM plasmid. The isolate was unambiguously assigned toM. u. pseudoshottsiibased on diagnostic single nucleotide polymorphisms (SNPs) and phylogenetic analysis. This report expands the known range ofM. u. pseudoshottsiito include Gulf Coast watersheds and highlights the need for enhanced surveillance in wild and aquacultured fish populations of the southern United States. 

ABSTRACT Buruli ulcer disease is a neglected tropical disease caused by the environmental pathogen Mycobacterium ulcerans . The M. ulcerans major virulence factor is mycolactone, a lipid cytotoxic compound whose genes are carried on a plasmid. Although an exact reservoir and mode(s) of transmission are unknown, data provide evidence of both. First, Buruli ulcer incidence and M. ulcerans presence have been linked to slow-moving water with low oxygen. M. ulcerans has also been suggested to be sensitive to UV due to termination in crtI , encoding a phytoene dehydrogenase, required for carotenoid production. Further, M. ulcerans has been shown to cause disease following puncture but not when introduced to open abrasion sites, suggesting that puncture is necessary for transmission and pathology. Despite these findings, the function and modulation of mycolactone and other genes in response to dynamic abiotic conditions such as UV, temperature, and oxygen have not been shown. In this study, we investigated modulation of mycolactone and other genes on exposure to changing UV and oxygen microenvironmental conditions. Mycolactone expression was downregulated on exposure to the single stress high temperature and did not change significantly with exposure to UV; however, it was upregulated when exposed to microaerophilic conditions. Mycolactone expression was downregulated under combined stresses of high temperature and low oxygen, but there was upregulation of several stress response genes. Taken together, results suggest that temperature shapes M. ulcerans metabolic response more so than UV exposure or oxygen requirements. These data help to define the environmental niche of M. ulcerans and metabolic responses during initial human infection. IMPORTANCE Buruli ulcer is a debilitating skin disease caused by the environmental pathogen Mycobacterium ulcerans . M. ulcerans produces a toxic compound, mycolactone, which leads to tissue necrosis and ulceration. Barriers to preventing Buruli ulcer include an incomplete understanding of M. ulcerans reservoirs, how the pathogen is transmitted, and under what circumstances mycolactone and other M. ulcerans genes are expressed and produced in its natural environment and in the host. We conducted a study to investigate M. ulcerans gene expression under several individual or combined abiotic conditions. Our data showed that mycolactone expression was downregulated under combined stresses of high temperature and low oxygen but there was upregulation of several stress response genes. These data are among only a few studies measuring modulation of mycolactone and other M. ulcerans genes that could be involved in pathogen fitness in its natural environment and virulence while within the host. 

ABSTRACT Understanding the interactions of ecosystems, humans and pathogens is important for disease risk estimation. This is particularly true for neglected and newly emerging diseases where modes and efficiencies of transmission leading to epidemics are not well understood. Using a model for other emerging diseases, the neglected tropical skin disease Buruli ulcer (BU), we systematically review the literature on transmission of the etiologic agent, Mycobacterium ulcerans (MU), within a One Health/EcoHealth framework and against Hill's nine criteria and Koch's postulates for making strong inference in disease systems. Using this strong inference approach, we advocate a null hypothesis for MU transmission and other understudied disease systems. The null should be tested against alternative vector or host roles in pathogen transmission to better inform disease management. We propose a re-evaluation of what is necessary to identify and confirm hosts, reservoirs and vectors associated with environmental pathogen replication, dispersal and transmission; critically review alternative environmental sources of MU that may be important for transmission, including invertebrate and vertebrate species, plants and biofilms on aquatic substrates; and conclude with placing BU within the context of other neglected and emerging infectious diseases with intricate ecological relationships that lead to disease in humans, wildlife and domestic animals.