Plague is a zoonotic disease caused by Yersinia pestis, and it is endemic in Madagascar. The plague cycle involves wild and commensal rodents and their fleas; humans are an accidental host. Madagascar is the country where plague burden is the highest. Plague re-emerged in Mahajanga, the western coast of Madagascar, in the 1990s and infected populations in the popular and insalubrious zones. Sanitation is considered a primary barrier to infection by excluding pathogens from the environment and reservoirs. Poor housing and hygiene and proximity to rodents and fleas in everyday life are major and unchanged risk factors of plague. The aim of this study was to measure the impact of sanitation on Yersinia pestis bacteria in human and small mammal reservoirs and flea vectors. This study was conducted on 282 households within 14 neighborhoods. Two sessions of sampling were conducted in 2013 and 2016. Small mammals were trapped inside and around houses using live traps. Fleas, blood and spleen were sampled to detect Y. pestis infection and antibodies and determine the level of plague circulation before and after the installation of sanitation in order to assess the impact of sanitation improvement on inhabitant health. Two major types of housing can be described, i.e., formal and informal (traditional), scattered in all the suburbs. Among the small mammals captured, 48.5% were Suncus murinus, and 70% of houses were infested. After sanitation, only 30% of houses remained infested, and most of them were located around the market. Fleas were mostly Xenopsylla cheopis. Before and after intervention, the overall prevalence of fleas was the same (index 4.5) across the 14 suburbs. However, the number of houses with fleas drastically decreased, and the flea index increased significantly in rodent-infested houses. Rodent abundance also decreased from 17.4% to 6.1% before and after intervention, respectively. A serology study highlights that plague is still circulating in Mahajanga, suggesting that small mammals maintain enzootic plague transmission in the city.
Journal Article > EditorialFull Text
Pathogens. 2023 October 19; Volume 12 (Issue 10); 1263.; DOI:10.3390/pathogens12101263
Santos ALS, Rodrigues IA, d’Avila-Levy CM, Sodré CL, Ritmeijer KKD, et al.
Pathogens. 2023 October 19; Volume 12 (Issue 10); 1263.; DOI:10.3390/pathogens12101263
Human African trypanosomiasis (also known as sleeping sickness, with Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense as etiological agents), American trypanosomiasis (also known as Chagas disease, with Trypanosoma cruzi as the etiological agent), and leishmaniasis (including cutaneous, mucocutaneous, and visceral forms, with multiple species belonging to the Leishmania genus as etiological agents) are recognized as neglected tropical diseases (NTDs). These diseases affect marginalized populations and pose a high-impact health problem, primarily in low- or low-to-middle-income countries in Africa, Asia, Latin America, and the Caribbean. Leishmania and Trypanosoma not only infect humans, but they also infect wild and domesticated animals, which serve as reservoirs for these diseases. Relevantly, the movement of people and animals across borders and within countries has become increasingly common in our interconnected world, and this mobility can both facilitate the transmission of diseases and challenge efforts to control outbreaks. Furthermore, climate changes can contribute to the spread of NTDs to areas that were previously unaffected.
Journal Article > ResearchFull Text
Pathogens. 2024 October 22; Volume 13 (Issue 11); 918.; DOI:10.3390/pathogens13110918
Rahelinirina S, Razafiarimanga ZN, Rajerison M, Djedanem M, Handschumacher P, et al.
Pathogens. 2024 October 22; Volume 13 (Issue 11); 918.; DOI:10.3390/pathogens13110918
Journal Article > ReviewFull Text
Pathogens. 2021 December 1; Volume 10 (Issue 12); 1568.; DOI:10.3390/pathogens10121568
Zawedde-Muyanja S, Reuter A, Tovar MA, Hussain H, Loando Mboyo A, et al.
Pathogens. 2021 December 1; Volume 10 (Issue 12); 1568.; DOI:10.3390/pathogens10121568
In this review, we discuss considerations and successful models for providing decentralized diagnosis, treatment, and prevention services for children and adolescents. Key approaches to building decentralized capacity for childhood TB diagnosis in primary care facilities include provider training and increased access to child-focused diagnostic tools and techniques. Treatment of TB disease should be managed close to where patients live; pediatric formulations of both first- and second-line drugs should be widely available; and any hospitalization should be for as brief a period as medically indicated. TB preventive treatment for child and adolescent contacts must be greatly expanded, which will require home visits to identify contacts, building capacity to rule out TB, and adoption of shorter preventive regimens. Decentralization of TB services should involve the private sector, with collaborations outside the TB program in order to reach children and adolescents where they first enter the health care system. The impact of decentralization will be maximized if programs are family-centered and designed around responding to the needs of children and adolescents affected by TB, as well as their families.
Journal Article > ResearchFull Text
Pathogens. 2023 October 13; Volume 12 (Issue 10); 1241.; DOI:10.3390/pathogens12101241
Pean P, Madec Y, Nerrienet E, Borand L, Laureillard D, et al.
Pathogens. 2023 October 13; Volume 12 (Issue 10); 1241.; DOI:10.3390/pathogens12101241
IRIS is a common complication in HIV-infected patients treated for tuberculosis (TB) and cART. Our aim was to evaluate NK cell reconstitution in HIV-infected patients with TB-IRIS compared to those without IRIS. 147 HIV-infected patients with TB from the CAMELIA trial were enrolled. HIV+TB+ patients were followed for 32 weeks. The NK cell repertoire was assessed in whole blood at different time points. As CAMELIA has two arms (early and late cART initiation), we analysed them separately. At enrolment, individuals had low CD4 cell counts (27 cells/mm3) and high plasma viral loads (5.76 and 5.50 log/mL for IRIS and non-IRIS individuals, respectively). Thirty-seven people developed IRIS (in the early and late arms). In the early and late arms, we observed similar proportions of total NK and NK cell subsets in TB-IRIS and non-IRIS individuals during follow-up, except for the CD56dimCD16pos (both arms) and CD56dimCD16neg (late arm only) subsets, which were higher in TB-IRIS and non-IRIS individuals, respectively, after cART. Regarding the repertoire and markers of NK cells, significant differences (lower expression of NKp30, NKG2A (CD159a), NKG2D (CD314) were observed in TB-IRIS compared to non-IRIS individuals after the start of cART. In the late arm, some changes (increased expression of CD69, NKG2C, CD158i) were observed in TB-IRIS compared to non-IRIS individuals, but only before cART initiation (during TB treatment). KIR expression by NK cells (CD158a and CD158i) was similar in both groups. CD69 expression by NK cells decreased in all groups. Expression of the NCR repertoire (NKp30, NKp44, NKp46) has similar kinetics in TB-IRIS subjects compared to non-IRIS subjects regardless of the arm analysed. NK cell reconstitution appeared to be better in TB-IRIS subjects. Although NK cell reconstitution is impaired in HIV infection after cART, as previously reported, it does not appear to be affected by the development of IRIS in HIV and TB-infected individuals.