Made available in DSpace on 2015-07-22T20:49:40Z (GMT). No. of bitstreams: 0 Previous issue date: 2010-06-30 / Introdução: Apesar de relatos sobre a Atenção Integrada às Doenças Prevalentes na Infância (AIDPI) melhorar a assistência à saúde da criança até cinco anos, não são identificados estudos direcionados ao componente peri-neonatal dessa estratégia. Objetivo: avaliar, após a capacitação em AIDPI Neonatal, o conhecimento e a percepção de médicos e enfermeiros quanto à assistência à gestante e à criança do nascimento até os dois meses de vida, e sua aplicabilidade prática em uma região da Amazônia. Método: estudo de coorte constituída de 31 médicos e 61 enfermeiros provenientes de 24 municípios, que participaram de sete capacitações em seis Pólos Regionais de Saúde no interior do Pará, Amazônia, realizado de abr/2006 a dez/2008. O estudo foi conduzido em duas fases, consistindo a 1ª fase na aplicação presencial de cinco questionários antes (T1) e imediatamente após 24 horas (T2) de capacitação em AIDPI Neonatal, conforme diretrizes da OPAS em 2007, adaptadas ao nosso meio. A 2ª fase compreendeu a aplicação presencial dos mesmos questionários aos 92 profissionais, em média 16 (14-20) meses após a 1ª fase (T3). Os questionários abordaram dados demográficos dos profissionais em T1, o conhecimento sobre assistência à gestante, reanimação neonatal, puericultura e doenças até dois meses em T1, T2 e T3, além da avaliação da capacitação em T2 e da percepção das condições de assistência no município e no local de prática clínica em T1 e T3. Para estimar as diferenças entre os tempos e as categorias profissionais foram criados escores de zero (inadequação completa) a 100 (adequaçãocompleta) comparados por meio da análise de variância com medidas repetidas. Resultados: os 92 profissionais caracterizaram-se por ser do sexo feminino (83%), nascidos (74%) e graduados (79%) no Pará, atender crianças duas ou mais vezes por semana (86%) e possuir pós-graduação (63%). Os médicos eram graduados há 17 (1-35) anos e os enfermeiros há nove (0-31) anos (p<0,001). Os primeiros relataram maior atuação em pediatria, e qualificação específica, com residência ou especialização, do que os últimos. Observou-se variação do conhecimento de acordo com o tempo (T1, T2 e T3) e a profissão (médicos>enfermeiros: p<0,001). Entre T1 e T2 constatou-se acréscimo deconhecimento dos profissionais sobre a assistência à gestante (p=0,026), reanimação neonatal (p<0,001), puericultura (p<0,001) e doenças até dois meses (p<0,01). Tal conhecimento perdurou, no mínimo, após 16 meses da capacitação nas áreas de reanimação neonatal (p=0,028) e doenças até dois meses (p<0,001). A capacitação teve avaliação positiva dos profissionais (94%) que perceberam melhora na prática clínica no seu local de trabalho (p<0,001), porém sem relato de alteração nas condições de saúde do município (p=0,066) entre T1 e T3. Conclusão: os médicos e enfermeiros apresentaram acréscimo, no mínimo por 16 meses, no conhecimento sobre a assistência à gestante e à criança até dois meses, além de perceberem melhora em sua condição de prática clínica após a capacitação em AIDPI Neonatal. Essa capacitação pode servir de modelo a ser aplicado em outras regiões com semelhante contexto epidemiológico / Objective: to assess knowledge and perception of professionals about care of pregnant women and children to two months of life, after training in Neonatal Integrated Management of Childhood Illness (IMCI), and its practical applicability in the Amazon Region. Method: a cohort study comprising 92 professionals who participated in seven Neonatal IMCI training courses in Para, from April/2006 to December/2008. Five questionnaires were applied face-to-face before (T1) and 24h (T2) after training in Neonatal IMCI (PAHO, 2007), and 16 (14-20) months after training (T3). Scores ranging from zero (complete inappropriateness) to 100 (complete appropriateness) were compared by ANOVA with repeated measures. Results: Time since graduation was 17y (1-35) for physicians and 9y (0-31) for nurses (p<0.001). Variation of knowledge was observed according to time and profession (physicians>nurses: p<0.001). Between T1 and T2, enhanced knowledge was verified in care of pregnant women (p=0.026), neonatal resuscitation (p<0.001), neonatal and infant care (p<0.001) and diseases up to two months (p<0.01). Such knowledge was observed at least for 16 months in neonatal resuscitation (p=0.028) and diseases up to two months (p<0.001). The capacity-building was positively evaluated by professionals (94%), who perceived improvement in clinical practice (p<0.001), without report of change in health conditions of the city (p=0.066) between T1 and T3. Conclusion: Training in Neonatal IMCI enhanced knowledge about care of pregnant women and infants up to two months, in addition to acknowledging better clinical practice for physicians and nurses. This training can be a model to be applied in other regions with similar epidemiological context. / TEDE / BV UNIFESP: Teses e dissertações

La BPCO se traduit rapidement par l'apparition d'une susceptibilité aux infections liées aux atteintes des mécanismes de défense du poumon. Les travaux antérieurs de l’équipe montrent qu'une altération de la réponse IL-17/IL-22 et de la fonction des cellules dendritiques (DC) participe au développement de l’exacerbation de la BPCO par les bactéries. Les mécanismes responsables de ce défaut de réponse ne sont pas élucidés. Au cours de cette thèse, nous nous sommes intéressés aux points suivants :1-Mécanismes cellulaires responsables du défaut de production d'IL-17 et d'IL-22 au cours de l'infection.Les cellules présentatrices d'antigène (APC) et en particulier, les DC jouent un rôle essentiel dans la réponse antimicrobienne, par leur fonction de phagocytes et par l’activation et la polarisation de cellules immunitaires innées et adaptatives. Sur des modèles murins d’exacerbation de la BPCO par Streptococcus pneumoniae ou Haemophilus influenzae non typable (NTHi), nous avons réalisé des tris de macrophages, DC et monocytes inflammatoires du poumon par cytométrie en flux. Ces analyses montrent que les cellules APC pulmonaires présentent des altérations fonctionnelles aboutissant à une limitation de leur capacité à polariser la réponse Th17 de Lymphocytes T CD4+. Une analyse transcriptomique est également effectuée sur les ARN des APC triées afin de préciser les altérations fonctionnelles de ces cellules par rapport aux souris contrôles.2-Rôle des cytokines IL-20 dans la susceptibilité à l'infection et l'exacerbation de la BPCO Myles et al ont montré en 2013 que les cytokines IL-20 (IL-19, IL-20 et IL-24) jouent un rôle délétère dans la réponse immunitaire cutanée contre Staphylococcus aureus par un mécanisme impliquant une inhibition indirecte d’IL-17 produite par les cellules T. La fonction des DC peut être affecté par l'environnement cytokinique. Comme les cytokines IL-20 sont surexprimées chez les souris BPCO, notre objectif a été de définir leur rôle au cours de l'exacerbation de la BPCO et l'impact de ces cytokines sur les DC dans ce contexte.Dans notre modèle d’exacerbation de la BPCO, nous avons bloqué cette voie en neutralisant l'IL-20RB qui est commune aux 2 récepteurs de ces cytokines afin d’étudier leur impact sur l'exacerbation et sur la réponse immune associée, notamment la réponse IL-17/IL-22. En parallèle, nous avons analysé la modulation de la fonction des DC humaines par ces cytokines dans un contexte d'infection bactérienne. Nos résultats montrent que le traitement avec l'anticorps bloquant anti-IL-20RB permet de bloquer le développement de l'exacerbation de la BPCO en diminuant la charge bactérienne et l'inflammation associée. Cet effet est associé à une diminution importante de la mobilisation des DC dans le poumon mais sans affecter sur la réponse IL-17/IL-22. In vitro, les cytokines IL-20 sont produites par les DC dans un contexte infectieux. De plus, ces cytokines sont capables de diminuer l'activation des ces cellules par les bactéries et de réduire leur capacité à activer les Lymphocytes T dans ce contexte.3-Capacité d'un immunostimulant à restaurer la réponse IL-17/IL-22, et à limiter le développement de l'exacerbation.L’utilisation d’immunostimulant dont la flagelline (agoniste du TLR-5, principale composante du flagelle bactérien) est souvent proposé comment pouvant promouvoir la réponse immunitaire des muqueuses et en particulier la réponse IL-17/IL-22. Nous avons analysé la capacité de cet agoniste du TLR-5 à améliorer la réponse à S. pneumoniae et NTHi dans notre modèle d’exacerbation de la BPCO.Le traitement par la flagelline permet de limiter les conséquences de l'infection bactérienne chez les souris BPCO en diminuant l'inflammation et les lésions pulmonaires associées. L'effet de ce ligand de TLR est au moins en partie dépendant de la production d'IL-22._A terme, ces données permettent d'envisager de nouvelles options thérapeutiques pour le traitement des exacerbations de la BPCO. / Patients with COPD often presented a susceptibility to respiratory infections. Previous works in our lab have showed that a defect of IL-17/IL-22 response and an altered dendritic cell (DC) function is involved in COPD exacerbation with bacteria. However, the mechanism responsible for this defect is not elucidated yet. In order to better define these mechanisms and to develop new therapeutic approaches against COPD exacerbation, we focused on the following points during this PhD project:1-Cellular mechanisms responsible of the defect of IL-17 and IL-22 production during infection in COPD.Antigen presenting cells (APC) particularly, DC are essential in antimicrobial immune response since they are professional phagocytes able to engulf and kill bacteria, but also by their essential role in the polarization of innate and adaptive immune responses. We worked on COPD exacerbation mice model infected with Streptococcus pneumoniae or Nontypeable Haemophilus influenzae (NTHi). APC including macrophages, DC and inflammatory monocytes were sorted by flow cytometry for phenotype and functional analysis. We found an altered function of these lung APC showing limited capacity of Th17 polarization. Transcriptional analysis on total RNA from sorted APC is performed to decipher the mechanisms involved in this functional alteration regarding to control mice.2-The role of IL-20 cytokines in the susceptibility to infection during COPD exacerbation.Myles et al showed in 2013 that IL-20 cytokines (IL-19, IL-20 and IL-24) are deleterious in skin immune response against Staphylococcus aureus. Indeed, these IL-20 cytokines indirectly inhibited IL-17 produced by T cells. The function of DC is also controlled by the presence of cytokines in the microenvironment. Because IL-20 cytokines are overexpressed in COPD, we aimed to determine their role during COPD exacerbation and the impact on DC.We used IL-20RB (common subunits of the 2 receptors) neutralizing antibodies to blocked IL-20 cytokines in COPD exacerbation mice model. We analyzed the impact of this treatment on the immune response, more particularly IL-17/IL-22 response. In addition, we analyzed the modulation of human monocyte derived DC (MDDC) function by IL-20 cytokines in the context of bacterial infection.Our results shows that treatment with IL-20 RB neutralizing antibodies limited COPD exacerbation by reducing the bacterial burden and the associated inflammatory response. This process was associated to reduced number of DC in the lung without impacting IL-17 and IL-22 production. In vitro, MDDC produced IL-20 cytokines upon bacterial infection. Additionally, these cytokines impaired MDDC activation following bacterial infection, which was associated to a reduced capacity of MDDC to activate T lymphocytes.3-The possibility to restore IL-17 and IL-22 response with immuno-stimulants in order to limit the development of COPD exacerbation.Flagellin (a TLR-5 agonist, the main component of bacterial flagellum) is an immuno-stimulant often used to promote mucosal immune response. This activity is related to its ability to promote IL-17 and IL-22 production. In this PhD work, we analyzed the capacity of this TLR-5 agonist to improve the immune response during S. pneumoniae and NTHi infection in COPD exacerbation mice model.Flagellin treatment reduced the bacterial burden and limited the consequences of bacterial infection in COPD mice, by lowering the inflammation and the associated lung remodeling. We also found that the immunomodulatory effect of flagellin was at least partially IL-22 dependent.Finally, these data allow to identify new therapeutic tools potentially useful for the treatment of COPD exacerbations.

Charles University First Medical Faculty Study programme: History of Medicine Summary of dissertation The Spanish Flu Pandemic 1918/19 with particular reference to the Bohemian Lands and Central European relations Dr. med. univ. Harald Salfellner Prague, 2017 Summary Towards the end of the First World War, in 1918 and 1919, humanity faced a previously unparalleled flu pandemic; within a few months, more people had been killed than in all the battles of the 1914-18 war put together. The precise number of victims is unknown but is today generally reckoned at between 20 and 50 million. The whole world was affected by the Spanish flu, with the exception of a few remote islands, and Europe, already bled to death by industrialised warfare, was particularly hard hit. In summer 1918, the pandemic reached Bohemia in an early, relatively benign wave. A few weeks later, thousands were struck down in Prague in a second and far more deadly phase of the illness. In October 1918, as the First Czechoslovakian Republic arose from the ashes of the multiethnic Austrian state, and the masses celebrated in the cities, thousands of feverish patients were coughing behind drawn curtains, and facing an uncertain fate. In the USA, the flu pandemic - the greatest health disaster of the 20th century - has been the subject of many...

Indiana University-Purdue University Indianapolis (IUPUI) / Haemophilus ducreyi is the causative agent of the genital ulcer disease chancroid, which has been shown to facilitate the transmission of HIV. H. ducreyi is likely exposed to multiple sources of antimicrobial peptides in vivo. APs are small, cationic molecules with both bactericidal and immunomodulatory functions. Because H. ducreyi is able to establish and maintain an infection in an environment rich with antimicrobial peptides, we hypothesized that the bacterium was resistant to the bactericidal effects of these peptides. Using a 96-well AP bactericidal assay, we examined H. ducreyi susceptibility to eight human APs likely to be encountered at the site of infection, including the α-defensins human neutrophil peptide-1, human neutrophil peptide-2, human neutrophil peptide-3, and human defensin 5, the β-defensins human β defensin-2, human beta defensin-3, and human beta defensin-4, and the human cathelicidin, LL-37. H. ducreyi survival was compared to the survival of Escherichia coli ML35, a strain known to be susceptible to several antimicrobial peptides. H. ducreyi was significantly more resistant than E. coli ML35 to the bactericidal effects of all peptides tested. Furthermore, we found that representative class I and class II strains of H. ducreyi were each resistant to APs of each functional category, indicating that resistance to antimicrobial peptides could represent a conserved method of pathogenesis for H. ducreyi as a species. The H. ducreyi genome contains a homolog for the Sap influx transporter. To study the role of the H. ducreyi Sap transporter in AP resistance, we generated an isogenic sapA mutant and used the 96-well AP bactericidal assay to compare the AP susceptibility profiles of wild-type H. ducreyi, the sapA mutant and the sapA trans-complement to α-defensins, β-defensins, and LL-37. We observed a 25% decrease in the survival of the sapA mutant when it was exposed to LL-37. These findings suggest that the H. ducreyi Sap transporter plays a role in H. ducreyi resistance to LL-37, but it is likely that other AP resistance mechanisms co-exist within the bacterium.

"March 2004" / Includes bibliographical references (leaves 213-272) / xxiii, 272 leaves ; ill. (some col.), plates ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.)--University of Adelaide, Dept. of Paediatrics, 2004

<p>Acute otitis media (AOM) is a common disease in childhood and is one of the most common causes for outpatient antibiotic treatment. The major aetiological agents of AOM have varied over the decades. Now the three most common pathogens are <i>Streptococcus pneumoniae</i>, <i>Haemophilus influenzae</i> and <i>Moraxella catarrhalis</i>. The resistance patterns of these organisms have also varied from the beginning of the antibiotic era to the situation we have today with an increasing incidence of penicillin-resistant <i>S. pneumoniae</i> and a moderate to high frequency of beta-lactamase production in <i>H. influenzae</i> and <i>M. catarrhalis</i>. In Sweden we have continued to use the Scandinavian treatment policy of penicillins as the first-line antibiotic treatment of AOM, which has been implemented with good results in the past. The question is if this policy will continue to have acceptable treatment results.</p><p>In order to investigate aspects of treatment, protection and structural changes in AOM, an animal model was used.</p><p>Amoxicillin treatment of AOM caused by <i>H. influenzae</i> was studied. Amoxicillin treatment was shown to shorten the duration of the infection and to reduce the morphological changes normally observed after an untreated AOM. The influence of antibiotic treatment on recurrent AOM was evaluated. Amoxicillin treatment did not lead to less protection against reinfection. Abstaining from antibiotics did not improve the levels of serum IgG antibodies. The IgG levels were significantly higher in treated animals after rechallenge. AOM caused by <i>H</i>. <i>influenzae</i> with a non-beta-lactamase-mediated resistance to beta-lactams was investigated and it was observed that during amoxicillin treatment the chromosomal changes mediating resistance were possibly advantageous for the bacterium. In cultures from children with AOM, there is sometimes growth of several bacteria. The possibility of a sheltering effect of beta-lactamase-producing <i>H. influenzae</i> on a penicillin-sensitive <i>S. pneumoniae</i> in a mixed infection was investigated, and amoxicillin was shown to eradicate the pneumococci from the middle ear despite the presence of beta-lactamase. An increasingly cultured bacterium in nasopharynx and in AOM is <i>M. catarrhalis</i>. It is now beta-lactamase-producing in almost 100% of cases and is thus not eradicated by penicillins. An animal model of AOM caused by beta-lactamase-producing <i>M. catarrhalis</i> was established to study the course of this infection with the possibility of evaluating aspects of virulence between AOM pathogens. The AOM observed was a self-limiting disease.</p><p>The results obtained in this study in a rat model support the continuing use of penicillins as first-line drugs in the treatment of AOM. Penicillins are not sufficient to treat all causative agents, but the majority of pathogens including the most virulent bacteria are eradicated from the middle ear. </p>

DNA mismatch repair ensures faithful transmission of genetic material from parents to progeny, which is required for the survival of the organism. The studies on E. coli MMR proteins have formed the basis for the study of the MMR system in eukaryotic organisms, because the functions of MMR proteins believed to be been conserved. In organisms that harbor MutH protein, it is known that MutH acts as a monomer which nicks the unmethylated daughter strand and is activated in a MutS-MutL- dependent manner. The cleavage specificity of MutH is very stringent. Till recently, it was not clear as to how MutH distinguishes hemimethylated DNA from fully or unmethylated DNA. The co-crystal structures of MutH-DNA complexes revealed that Y212, R184 and P185 were in close proximity to the methyl-adenine. Clustal-W sequence alignment of MutH with Sau3AI showed that Sau3AI has PCT residues instead of L183, R184, and P185. A triple mutant MutH-L183P-R184C-P185T was found to cleave both unmethylated and methylated DNA. The nicking endonuclease activity of the LRP→ PCT triple mutant was enhanced in the presence of Haemophilus influenzae MutL. The mutL gene of Neisseria gonorrhoeae was cloned and the gene product purified. It was shown that the homodimeric Neisseria gonorrhoeae MutL (NgoL) protein displays an endonuclease activity that incises covalently closed circular DNA in the presence of manganese or magnesium or calcium ions unlike human MutLα which shows endonuclease activity only in the presence of manganese. Further more the C-terminal domain of Neisseria gonorrhoeae MutL (NgoL-CTD) consisting of amino acids 460 to 658 also exhibits Mn2+ dependent endonuclease activity. Sedimentation velocity, sedimentation equilibrium and dynamic light scattering experiments show NgoL-CTD to be a dimer. By in vitro comparison of wild-type and a mutant NgoL-CTD protein, it was shown that the latter protein exhibits highly reduced endonuclease activity. Surface plasmon resonance spectroscopy was used to determine the kinetics of DNA binding by NgoL. The DNA binding was carried out in absence of metal ions. Interaction studies with NgoL with ssDNA in SPR spectroscopy revealed a KD value of 4.7 × 10–8 M. While the human MutLα endonuclease activity was shown to be stimulated by ATP, ATP inhibits NgoL endonuclease activity. By in vitro comparison of wild-type and a mutant NgoL-CTD protein, it was shown that the latter protein exhibits highly reduced endonuclease activity. NgoL ATPase activity was enhanced in the presence of DNA. The fact that NgoL ATPase activity is stimulated ~ 2.5-fold by dsDNA and ~ 2-fold by ssDNA is a further evidence for the interaction between NgoL and DNA. The results presented above show that NgoL harbors a nicking endonuclease activity which is present in the C-terminal domain. NgoL and NgoL-CTD are dimers in solution and DMHA(X)2E(X)4E motif present in the CTD is required for the nicking endonuclease activity. These results suggest that DNA mismatch repair mechanism in N. gonorrhoeae is different from that in E. coli. In the absence of MutH homolog, N. gonorrhoeae is able to repair the DNA by virtue of MutL nicking endonuclease activity.

Acute otitis media (AOM) is a common disease in childhood and is one of the most common causes for outpatient antibiotic treatment. The major aetiological agents of AOM have varied over the decades. Now the three most common pathogens are Streptococcus pneumoniae, Haemophilus influenzae and Moraxella catarrhalis. The resistance patterns of these organisms have also varied from the beginning of the antibiotic era to the situation we have today with an increasing incidence of penicillin-resistant S. pneumoniae and a moderate to high frequency of beta-lactamase production in H. influenzae and M. catarrhalis. In Sweden we have continued to use the Scandinavian treatment policy of penicillins as the first-line antibiotic treatment of AOM, which has been implemented with good results in the past. The question is if this policy will continue to have acceptable treatment results. In order to investigate aspects of treatment, protection and structural changes in AOM, an animal model was used. Amoxicillin treatment of AOM caused by H. influenzae was studied. Amoxicillin treatment was shown to shorten the duration of the infection and to reduce the morphological changes normally observed after an untreated AOM. The influence of antibiotic treatment on recurrent AOM was evaluated. Amoxicillin treatment did not lead to less protection against reinfection. Abstaining from antibiotics did not improve the levels of serum IgG antibodies. The IgG levels were significantly higher in treated animals after rechallenge. AOM caused by H. influenzae with a non-beta-lactamase-mediated resistance to beta-lactams was investigated and it was observed that during amoxicillin treatment the chromosomal changes mediating resistance were possibly advantageous for the bacterium. In cultures from children with AOM, there is sometimes growth of several bacteria. The possibility of a sheltering effect of beta-lactamase-producing H. influenzae on a penicillin-sensitive S. pneumoniae in a mixed infection was investigated, and amoxicillin was shown to eradicate the pneumococci from the middle ear despite the presence of beta-lactamase. An increasingly cultured bacterium in nasopharynx and in AOM is M. catarrhalis. It is now beta-lactamase-producing in almost 100% of cases and is thus not eradicated by penicillins. An animal model of AOM caused by beta-lactamase-producing M. catarrhalis was established to study the course of this infection with the possibility of evaluating aspects of virulence between AOM pathogens. The AOM observed was a self-limiting disease. The results obtained in this study in a rat model support the continuing use of penicillins as first-line drugs in the treatment of AOM. Penicillins are not sufficient to treat all causative agents, but the majority of pathogens including the most virulent bacteria are eradicated from the middle ear.

Haemophilus influenzae is a pathogenic Gram-negative bacterium that colonizes the upper respiratory tract of humans and can cause otitis media, upper and lower respiratory infections, and meningitis. Factors important for H. influenzae to colonize humans and cause disease are not fully understood. Different bacterial pathogens are armed with virulence mechanisms unique to their specific strategies for interacting with their hosts. Many of the proteins mediating these interactions are secreted and contain disulfide bonds required for function or stability. I postulated that identifying the set of secreted proteins in H. influenzae that require periplasmic disulfide bonds would provide better understanding of this bacterium's pathogenic mechanisms. In this thesis, the periplasmic disulfide bond oxidoreductase protein, DsbA, was found to be essential for colonization and virulence of H. influenzae. Mutants of dsbA were also found to be sensitive to the bactericidal effects of serum. However, the DsbA-dependent proteins important for pathogenesis of this organism have not been previously identified. To find them, putative targets of the periplasmic disulfide bond pathway were identified and examined for factors which might be important for mediating critical virulence aspects. By doing so, novel virulence factors were discovered including those important for heme and zinc acquisition, as well as resistance to complement. Overall, the work presented here provides insight into requirements for H. influenzae to survive within various host environments.

Yaws is a skin debilitating disease caused by Treponema pallidum subspecies pertenue with most cases reported in children. World Health Organization (WHO) aims at total eradication of this disease through mass treatment of suspected cases followed by an intensive follow-up program. However, effective diagnosis is pivotal in the successful implementation of this control program. Recombinase polymerase amplification (RPA), an isothermal nucleic acid amplification technique offers a wider range of differentiation of pathogens including those isolated from chronic skin ulcers with similar characteristics such as Haemophilus ducreyi (H. ducreyi). We have developed a RPA assay for the simultaneous detection of Treponema pallidum (T. pallidum) and H. ducreyi (TPHD-RPA). The assay demonstrated no cross-reaction with other pathogens and enable detection of T. pallidum and H. ducreyi within 15 min at 42 °C. The RPA assay was validated with 49 clinical samples from individuals confirmed to have yaws by serological tests. Comparing the developed assay with commercial multiplex real-time PCR, the assay demonstrated 94% and 95% sensitivity for T. pallidum and H. ducreyi, respectively and 100% specificity. This simple novel TPHD-RPA assay enables the rapid detection of both T. pallidum and H. ducreyi in yaws-like lesions. This test could support the yaws eradication efforts by ensuring reliable diagnosis, to enable monitoring of program success and planning of follow-up interventions at the community level.