Vital Signs
Lenore Manderson, Elizabeth Cartwright, Anita Hardon in The Routledge Handbook of Medical Anthropology, 2016
Globally, gender hierarchies continue to disadvantage women. Women still lack the autonomy to make their own decisions about their health. The photograph by Mark Nichter, the preface to Chapter 8, depicts a woman using a cell phone to gain her husband’s permission to proceed with treatment for a chronic ulcer, and to explain to him the costs that might be involved. The woman has Buruli ulcer, an infectious bacterial infection which, untreated, will cause certain disfigurement and debility. Yet it is possible that the cost will be ‘too high’ from her husband’s point of view. Women continue too, worldwide, to have less access to: food and so have compromised nutritional status; preventive health technologies such as bed nets to protect against malaria; transport to medical services; and the right to receive care if the provider is male. The majority of people subject to sexual assault and intimate partner violence are women. Women continue to receive less education and receive lower remuneration for their work, and so, more often than men, they live with their children in poverty. In these respects, the social impact of gender is clear. But we know far less of how sex shapes the onset and course of many diseases biologically, and so our capacity as anthropologists to tease out the synergies of the biological and social is necessarily fragmentary.
BCG and Other Vaccines
Lloyd N. Friedman, Martin Dedicoat, Peter D. O. Davies in Clinical Tuberculosis, 2020
Vaccination with BCG may confer protection against non-tuberculous mycobacterial species due to cross-reactivity with conserved, often immunodominant, antigens.58 The estimates of protective efficacy against leprosy, caused by Mycobacterium leprae, vary from 20% to 90%.45,59 Although one meta-analysis determined an overall BCG-vaccine protective effect of 41% (95% CI 16–66) for trials and 60% (95% CI 51–70) for observational studies,60 another analysis reported just 26% (95% CI 14–37) and suggested that protection had been overestimated in observational studies.61 Cross-protection of BCG against Buruli ulcer disease has been reported in some studies62,63 but not in others.64,65 Murine studies have demonstrated a protective effect of BCG against infection with Mycobacterium avium and Mycobacterium kansasii.66 A study of neonates in the Czech Republic found that M. avium intracellulare complex-associated lymphadenitis was lower in BCG-vaccinated compared with unvaccinated children.38
Lipid-Based Nanocarriers for the Treatment of Infected Skin Lesions
Andreia Ascenso, Sandra Simões, Helena Ribeiro in Carrier-Mediated Dermal Delivery, 2017
The mycobacteria species that may cause localized infections of the skin and subcutaneous tissue are M. chelonae, M. fortuitum, M. abscessus, M. marinum, and M. ulcerans. Rapid growth of M. chelonae, M. fortuitum, or M. abscessus may occur due to localized drainage or abscess formation at the site of puncture wounds, open traumatic injuries or fractures, surgical wound infections, post- injection abscesses [5]. Occasionally, these infections may also spread to lymphatics [6]. M. marinum represents one of the most frequent cutaneous atypical mycobacterial infections. The usual source is water from lakes, swimming pools, or aquariums [6]. Buruli ulcer (BU), caused by M. ulcerans, is the third most widespread mycobacterial infection in the world after tuberculosis and leprae being the least understood. It has been recently recognized by the World Health Organization (WHO) as an emerging disease [7,8]. The causative organism is from the family of bacteria which causes tuberculosis and leprae; however, BU has received less attention than these diseases. BU has been reported in over 30 countries with tropical and subtropical climates affecting mainly poor rural communities in Africa, North America (Mexico), South America, Southeast Asia, and Oceania. Currently, Bellarine Peninsula in Victoria is known to be the highest endemic area in Australia [9]. In light of this emerging disease able to cause great human suffering, this review will focus on current therapies used, drawbacks associated, and new alternative lipid nanocarriers for fighting this mycobacterial skin infection.
State-of-the-art treatment strategies for nontuberculous mycobacteria infections
Published in Expert Opinion on Pharmacotherapy, 2020
Maria-Carmen Muñoz-Egea, Nerea Carrasco-Antón, Jaime Esteban
Buruli ulcer is caused by M. ulcerans. Surgery still remains crucial for the cure of this condition in severe ulcers [53], although the combination of rifampin and a quinolone or clarithromycin for 8 weeks has shown promising results [71].
Reconstructive surgery for sequellae of Mycobacterium ulcerans infection (Buruli ulcer) of the upper limb
Published in Journal of Plastic Surgery and Hand Surgery, 2021
W. M. Calonge, P. Meredith, K. A. Kouakou-Adonis, C. K. Yao, K. M. N’da Assie, H. Asse
Buruli ulcer (BU), is a necrotizing skin condition caused by Mycobacterium ulcerans.It is the third most common mycobacterial infection worldwide, though in some areas its prevalence seems to have overrun those of tuberculosis and leprosy [1–3].
Pharmacologic management of Mycobacterium ulcerans infection
Published in Expert Review of Clinical Pharmacology, 2020
Tjip S Van Der Werf, Yves T Barogui, Paul J Converse, Richard O Phillips, Ymkje Stienstra
Antimicrobial treatment has brought many advantages for patients with Buruli ulcer, but some questions have remained unanswered. Clinical studies can only address relatively simple questions; and although randomized trials provide the highest level of evidence to guide therapy, in clinical practice, many decisions require individualized decisions. For some infections, like community-acquired pneumonia, duration of antimicrobial treatment can be safely individualized and indeed stopped after fulfilling criteria to achieve clinical stability [161]. For many infections, like tuberculosis, no robust biomarker or decision rule have been developed that can be used to individualize treatment duration. For tuberculosis, notably for patients with drug-resistant forms of tuberculosis, individualized treatment has primarily focused on the selection of drugs. The concept of tailoring treatment according to pharmacokinetic/pharmacodynamic (PK) modeling combined with susceptibility testing [90,162,163], using drug susceptibility essays for each individual drug in the treatment schedule, combined with adjusting dosing based on drug exposure measurements, i.e., therapeutic drug monitoring [164] holds promise for tuberculosis, but may not necessarily be the way forward for Buruli ulcer individualized treatment. One problem with this approach is, that phenotypic in vitro drug susceptibility testing using solid or liquid culture media with steady single drug concentrations below the breakpoint hardly reflects what happens in infectious foci in patients harboring the pathogen under study; the hollow fiber infection model mimics these variable drug concentrations in the bloodstream over time with continued nutritional, pCO2, and PO2 conditions as happens in the bloodstream of patients [100]. Even modeling drug concentrations in the bloodstream of patients may still differ from what happens at the site of infection – and at least in tuberculosis, some of these assumptions prove wrong [165]. Indeed, typically, blood drug concentrations in patients vary following ingestion, with resorption, distribution, and elimination following a curve of rising and falling concentrations over time. This is especially important for micro-organisms with slow replication like mycobacteria, where drug concentrations tend to fall over time due to chemical instability [103,166]. Despite these considerations, telacebec, for example, showed an impressive activity in the mouse footpad model, confirming the in vitro data [91,107]. Use of auto – or bioluminescent strains of M. ulcerans may have the potential to reduce and refine animal experimentation [127].