Buruli ulcer (BU), the second most common mycobacterial disease in West Africa, is a necrotizing skin disease that can lead to high morbidity in affected patients. The disease is caused by Mycobacterium ulcerans (MU), whose major virulence factor is mycolactone. Although early infection can be treated with antibiotics, an effective preventative strategy is challenging due to unknown reservoir(s) and unresolved mode(s) of transmission. Further, disease occurrence in remote locations with limited access to health facilities further complicates disease burden and associated costs. We discuss here MU transmission hypotheses and investigations into environmental reservoirs and discuss successes and challenges of studying MU and Buruli ulcer across human, animal, and environmental interfaces. We argue that a One Health approach is needed to advance the understanding of MU transmission and designing management scenarios that prevent and respond to epidemics. Although previous work has provided significant insights into risk factors, epidemiology and clinical perspectives of disease, understanding the bacterial ecology, environmental niches and role of mycolactone in natural environments and during infection of the human host remains equally important to better understanding and preventing this mysterious disease.
Histoplasmosis, a fungal infection caused by Histoplasma capsulatum (H. capsulatum), acquired from contaminated soil with droppings of chicken or birds and found to be distributed in many parts of the world. The prevalence of histoplasmosis has not well studied in Nepal. The common symptoms of acute and epidemic histoplasmosis include high fever, cough, and asthenia and weight loss. Most of the infections associated with histoplasmosis are asymptomatic. People with compromised immune systems such as HIV/AIDS (PLWHA), cancer, and organ transplant recipients are at risk of developing this disease. In this review, we have summarised the current status of histoplasmosis in Nepal and molecular techniques available for its identification. To date, the significant outbreak is not reported in Nepal, but the risk of infection for the vulnerable population cannot be undermined. Appropriate preventive measures and treatment on time can reduce the burden of this fungal disease. Further, this review is also focused on molecular identification of H. capsulatum. Hence, careful considerations by concerned stakeholders for national surveillance programs and the treatment of patients on time after proper diagnosis is highly recommended.
Buruli ulcer is a neglected tropical disease caused by the environmental pathogen, Mycobacterium ulcerans whose major virulence factor is mycolactone, a lipid cytotoxic molecule. Buruli ulcer has high morbidity, particularly in rural West Africa where the disease is endemic. Data have shown that infected lesions of Buruli ulcer patients can be colonized by quorum sensing bacteria such as Staphylococcus aureus, S. epidermidis, and Pseudomonas aeruginosa, but without typical pathology associated with those pathogens’ colonization. M. ulcerans pathogenesis may not only be an individual act but may also be dependent on synergistic or antagonistic mechanisms within a polymicrobial network. Furthermore, co-colonization by these pathogens may promote delayed wound healing, especially after the initiation of antibiotic therapy. Hence, it is important to understand the interaction of M. ulcerans with other bacteria encountered during skin infection. We added mycolactone to S. aureus and incubated for 3, 6 and 24 h. At each timepoint, S. aureus growth and hemolytic activity was measured, and RNA was isolated to measure virulence gene expression through qPCR and RNASeq analyses. Results showed that mycolactone reduced S. aureus hemolytic activity, suppressed hla promoter activity, and attenuated virulence genes, but did not affect S. aureus growth. RNASeq data showed mycolactone greatly impacted S. aureus metabolism. These data are relevant and significant as mycolactone and S. aureus sensing and response at the transcriptional, translational and regulation levels will provide insight into biological mechanisms of interspecific interactions that may play a role in regulation of responses such as effects between M. ulcerans, mycolactone, and S. aureus virulence that will be useful for treatment and prevention.
Antimicrobial resistance is natural phenomenon that occurs when microorganisms are exposed to antibiotic drugs. Under the selective pressure of antibiotics, susceptible bacteria are killed or inhibited, while bacteria that are naturally (or intrinsically) resistant or that have acquired antibiotic-resistant traits have a greater chance to survive and multiply. Many alarming facts regarding antimicrobial resistance have accumulated, particularly over the last few years some of which includes an increase in global resistance rates in many bacterial species responsible for both community- and healthcare-related infections, emergence and dissemination of new mechanisms of resistance, rapid increase in multi-resistance, propensity to use last line therapy to treat nosocomial and community acquired infections, reuse of old drugs with poor efficacy profile and uncertain pharmacokinetics/pharmacodynamics characteristics due to lack of alternative drugs, high morbidity and mortality attributable to multi-resistant bacteria in critically ill patients and serious financial consequences of bacterial resistance. Various steps that health care practitioners and facilities can pursue to reduce antibiotic resistance such as adopting an antibiotic stewardship program, improving diagnosis, tracking and prescribing practices, optimizing therapeutic regimens and preventing infection transmission.
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