Podcasts about Staphylococcus

Dr. Don and Professor Ben talk about the risks of licking someone else's ear wax off your finger Dr. Don - not risky

Small hospitals bring unique stewardship challenges, but also unique opportunities. Dr. Tina Khadem and Dr. Ashley Cubillos join host Dr. Whitney Buckel to discuss the realities of antimicrobial stewardship in small and critical access hospitals. From navigating competing priorities and limited resources, to building strong provider relationships in close-knit communities, we have you covered! Join us as we unpack real-world strategies, challenge common perceptions, and highlight the practical pearls you can apply in your own setting. References: Implementation of Core Elements at Small and Critical Access Hospitals: https://www.cdc.gov/antibiotic-use/media/pdfs/core-elements-small-critical-508.pdf Stenehjem E, Hyun DY, Septimus E, Yu KC, Meyer M, Raj D, Srinivasan A. Antibiotic Stewardship in Small Hospitals: Barriers and Potential Solutions. Clin Infect Dis. 2017 Aug 15;65(4):691-696. Veillette JJ, May SS, Gabrellas AD, Gelman SS, Albritton J, Lyons MD, Stenehjem EA, Webb BJ, Dalto JD, Throneberry SK, Stanfield V, Grisel NA, Vento TJ. A Fully Integrated Infectious Diseases and Antimicrobial Stewardship Telehealth Service Improves Staphylococcus aureus Bacteremia Bundle Adherence and Outcomes in 16 Small Community Hospitals. Open Forum Infect Dis. 2022 Oct 14;9(11):ofac549. Cubillos AL, Fortier K, Hoang A. P-920. Impact of Positive Blood Culture Antimicrobial Stewardship on Staphylococcus aureus Bloodstream Infection Management across Critical Access, Small, and Medium Community Hospitals. Open Forum Infect Dis. 2026 Jan 11;13(Suppl 1):ofaf695.1126. Smith LM, Ahern JW. Establishing Antibiotic Stewardship Programs in Rural Hospitals to Decrease Fluoroquinolone Prescribing: The Vermont Experience. Infect Prev Pract. 2021 Jan 21;3(1):100121. Kassamali-Escobar Z, et al. Antimicrob Steward Healthc Epidemiol 2024. doi: 10.1017/ash.2024.458. Imlay H, Ciarkowski CE, Bryson-Cahn C, et al Infect Control Hosp Epidemiol 2025. 46: 150–155, doi: 10.1017/ice.2024.206 Ciarkowski CE, Imlay HN, Bryson-Cahn C, et al. Infect Control Hosp Epidemiol 2025. 46: 143–149, doi: 10.1017/ice.2024.171 Stenehjem E, et al. JAMA Netw Open. 2023;6(5):e2313011. doi:10.1001/jamanetworkopen.2023.13011 Learn more about the Society of Infectious Diseases Pharmacists: https://sidp.org/About Instagram: @SIDPharm (https://www.instagram.com/sidpharm/) or @breakpointspodcast_sidp (https://www.instagram.com/breakpointspodcast_sidp/)https://www.instagram.com/breakpointspodcast_sidp/?hl=en Facebook: https://www.facebook.com/sidprx LinkedIn: https://www.linkedin.com/company/sidp/ SIDP welcomes pharmacists and non-pharmacist members with an interest in infectious diseases, learn how to join here: https://sidp.org/Become-a-Member Listen to Breakpoints on iTunes, Overcast, Spotify, Listen Notes, Player FM, Pocket Casts, Stitcher, Google Play, TuneIn, Blubrry, RadioPublic, or by using our RSS feed: https://sidp.pinecast.co/

Henry Miller describes a "tour de force" at MIT where AI is used to discover new molecules to fight antibiotic resistance. This technology identifies structures that kill pathogens like staphylococcus and gonorrhea. (14/16)1750

The ESCMID Global Late Breakers series returns to Communicable! Five CMI Communications editors – Marc Bonten, Josh Davis, Angela Huttner, Anne-Grete Märtson, and Erin McCreary – handpicked five late-breaking trials presented at ESCMID Global 2026 to summarise their  findings and discuss whether the results will change their practice. This is part one of the two-part series. Trials presented are listed below and links to their respective sessions can be watched and rewatched on the ESCMID Global Virtual Platform. Links to corresponding publications, if available, and mentioned related articles are provided as well. The FAST trial (Late-breaking research from JAMA)Banerjee R, et al. Fast Antimicrobial Susceptibility Testing for Gram-Negative Bacteremia. The FAST Randomized Clinical Trial, doi: 10.1001/jama.2026.5487 Srinivasan A. A Multinational Trial of Rapid Antimicrobial Susceptibility Testing. Is FASTer Better?, doi: 10.1001/jama.2026.5504The CEFMEC trial (Poster session)Hayakawa K, et al. Effectiveness of cefmetazole versus meropenem for invasive urinary tract infections caused by extended-spectrum β-lactamase-producing Escherichia coli, Antimicrob Agents Chemother 2023, doi: 10.1128/aac.00510-23The COBRA trial (Late-breaking trials in surgical infection prevention)Overdevest AG, et al. Antibiotic treatment for 1 day versus 4-7 days in patients with acute cholangitis after adequate endoscopic biliary drainage (COBRA): study protocol for a randomized controlled trial. Trials, doi: 10.1186/s13063-026-09524-7The DOTS trial, a secondary analysis (Late-breaking research from JAMA)Lodise, TP, et al. Pharmacokinetics of Dalbavancin in Complicated Staphylococcus aureus Bacteremia: A Secondary Analysis of the DOTS Randomized Clinical Trial, JAMA 2026, doi: 10.1001/jamanetworkopen.2026.11652 Walls G, et al. Patient-reported Perceptions, Experiences, and Preferences Around Intravenous and Oral Antibiotics for the Treatment of Staphylococcus aureus Bacteremia: A Descriptive Qualitative Study, Clin Infect Dis 2026, doi: 10.1093/cid/ciaf522Turner  NA , et al.  Dalbavancin for treatment of Staphylococcus aureus bacteremia: the DOTS randomized clinical trial. JAMA 2025, doi: 10.1001/jama.2025.12543 Maribavir for clinically significant cytomegalovirus infection in hematopoietic cell transplantation: a real-world retrospective international study of the Infectious Disease Working Party of EBMT (Late-breaking research from The Lancet)Paviglianiti A, et al. Maribavir for clinically significant cytomegalovirus infection in haematopoietic cell transplant recipients in Europe: a real-world multicentre retrospective registry study. Lancet 2026. doi: 10.1016/S1473-3099(26)00144-1

O jipe Perseverance encontra possíveis bioassinaturas na superfície de uma rocha e dá mais um motivo para que a missão de retorno de amostras de Marte não seja cancelada. As análises sobre a habitabilidade marciana é uma vertente dos estudos na área, que buscam responder: quais são as condições encontradas no planeta hoje e como ele já deve ter sido no passado? O episódio faz parte de um conjunto de reportagens sobre A busca por vida extraterrestre e se essa estaria esquentando. A série é desenvolvida por Danilo Albergaria, bolsista do Programa Mídia Ciência, da FAPESP. Este episódio contou com a participação de Gabriel Gonçalves Silva (pós-doutorando na UNISINOS), Fernanda Jamel (doutoranda – USP e MIT), Roberta Vincenzi (pós-doutoranda no IO-USP) e Isabella Gaião (doutoranda – USP). [Introdução] Danilo: No primeiro episódio da série que trata da astrobiologia, aqui no podcast Oxigênio, a gente falou da alegação de detecção de uma possível bioassinatura num planeta fora do sistema solar. Uma bioassinatura é um sinal produzido por seres vivos – um possível vestígio de atividade biológica. Mas essa notícia de um potencial sinal de vida num exoplaneta não foi a única ocasião em que uma possível bioassinatura em um ambiente extraterrestre gerou manchetes no ano passado. Em setembro de 2025, a NASA anunciou um resultado que foi descrito pela agência aeroespacial americana como: “pode bem ser o sinal mais claro de vida que já encontramos em Marte”. A novidade foi um estudo publicado na revista Nature que apontou a existência de uma “potencial bioassinatura” numa rocha marciana – sim, uma pedra em Marte, coletada e analisada pelo jipe Perseverance, da NASA. A rocha marciana tem algumas características que aqui na Terra são encontradas em rochas que exibem rastros deixados por micróbios. Mas ainda não dá para saber se essas características encontradas na pedra marciana tiveram origem em atividade biológica ou se foram formadas por processos naturais sem o envolvimento de seres vivos. Os equipamentos do jipe, por melhores que sejam, não conseguem produzir resultados claros o suficiente para que os cientistas tirem essa dúvida. Para distinguir se os sinais encontrados são biogênicos (ou seja, foram originados por atividade biológica) ou se são abióticos (ou seja, sem o envolvimento de seres vivos), é preciso trazer as amostras para a Terra.  Eu sou Danilo Albergaria, jornalista e historiador pesquisando a comunicação da astrobiologia, essa área que estuda a origem, a evolução e a distribuição da vida no universo. Neste episódio, vou conversar com quatro cientistas associados ao Laboratório de Astrobiologia da Universidade de São Paulo para entender um pouco melhor de quê se trata essa possível bioassinatura e o que sabemos sobre se Marte pode ou não pode oferecer condições para a existência de vida, ou se já pode em algum momento do passado distante.  [Vinheta] Danilo: Vamos começar pelo que a gente sabe sobre esses resultados anunciados com grande entusiasmo pela NASA no ano passado. O jipe Perseverance está em Marte desde 2021 explorando a região de uma cratera chamada Jezero. A gente sabe que Marte teve água líquida em sua superfície há mais de 3,5 bilhões de anos, e essa cratera já foi um lago nesse passado remoto. Só para vocês terem uma ideia dessa região marciana, para atravessar essa cratera, de borda a borda, é preciso percorrer 45 quilômetros, pouco mais do que a distância entre Campinas e Jundiaí ou de Jundiaí a São Paulo. Em uma parte da borda da cratera existem marcas características de um delta de um rio que desaguava ali. Foi nas margens do leito desse rio, medindo 400 metros de margem a margem, que o jipe encontrou algumas rochas interessantes em julho de 2024. Em uma delas, o Perseverance identificou compostos orgânicos, moléculas compostas de carbono, e o mais importante: marcas que foram apelidadas de “pintas de leopardo”, que são manchas mais claras do que o restante da rocha, circundadas por linhas bem mais escuras. A rocha é formada principalmente de argila e lodo, materiais que costumam preservar rastros de vida microbiana, e fazem da rocha algo tipicamente encontrado no fundo de rios. Essas marcas, as “pintas de leopardo”, são compostas de fosfato de ferro e sulfeto de ferro. Aqui na Terra, esses compostos são associados a rastros químicos causados por reações produzidas por microrganismos em rochas. Essas foram as pistas analisadas para ver se as manchas poderiam ter sido geradas por micróbios há bilhões de anos. O Gabriel Gonçalves Silva é pós-doutorando na UNISINOS, químico associado ao Laboratório de Astrobiologia da USP, e estuda geobiologia. Eu pedi para ele me explicar por que esses sinais foram considerados possíveis vestígios de vida microbiana passada em Marte neste último estudo feito pelos pesquisadores da NASA. Gabriel: Eles analisaram uma amostra que se chama de mudstone, que seria algo como uma rocha formada de uma antiga lama. Marte é muito rico em ferro e foi observado principalmente nessa rocha pequenos pontinhos que eles observaram com mais detalhes e nele foi encontrado o ferro que a gente chama de ferro mais reduzido, que é o ferro 2+, que é interessante porque contrapõe ao ferro que a gente encontra mais em Marte, que é o ferro 3+, que é aquele que tem a cor de ferrugem. E não só essas manchinhas apresentavam principalmente um mineral, que é a vivianita, que é um fosfato de ferro II e a greigita, que é um sulfeto de ferro II. O ferro II na Terra, por exemplo, pode ser formado por processos na ausência de vida ou na presença de microrganismos. Eles conseguiram observar que não havia nessas rochas nenhum indício de grandes mudanças de pH nem de temperatura, mas junto da vivianita e da greigita tinha matéria orgânica. Na Terra, a gente sabe que a matéria orgânica pode acoplar reações onde a oxidação da matéria orgânica resulta na redução do ferro e aí, pela presença de sulfeto e do fosfato, a formação desses minerais. Porém, eles observaram que, por mais que a vivianita possa se formar em condições de temperatura, pressão e pH próximos do que nós consideramos normais, geralmente a formação de sulfeto de ferro dependeria de uma temperatura mais alta, então não só a oxidação da matéria orgânica, levando à redução do ferro, necessitaria de outros elementos para a formação desse mineral, desse sulfeto de ferro II. E graças a observações da composição ali da rocha, ausência de fosfato de alumínio, ausência de outros componentes, eles perceberam que não houve nem aquecimento, nem uma mudança drástica de pH durante esse processo de formação desses minerais. Isso faz com que a causa mais provável para a formação desses minerais, pelo menos se a gente pensasse na Terra, seria a ação da vida como nós conhecemos. Danilo: Vamos entender um pouco mais da química envolvida na produção das “pintas de leopardo”. Algumas bactérias formam minerais usando e transformando compostos químicos, como diferentes tipos de óxidos de ferro, formados por ligações entre ferro e oxigênio. O chamado ferro II (um íon de ferro) é muito importante para atividade biológica porque se liga facilmente ao oxigênio – por exemplo, ele é fundamental para o transporte do oxigênio no nosso sangue por meio da hemoglobina. A Fernanda Jamel, doutoranda no AstroLab da USP e que fez parte de suas pesquisas atuais no MIT (o Massachusetts Institute of Technology, nos EUA), explica a química da formação dos minerais encontrados na rocha marciana como possível explicação biológica, comparando com o que acontece na Terra. Fernanda: Aqui a gente tem formação de vivianita com bactérias que usam o ferro III, o óxido de ferro III, e transforma em ferro II. Por isso que a gente fala que é a redução de ferro. Então, quando as bactérias fazem isso, ela libera o ferro II no ambiente ao redor e aquilo ali vai formando camadas, vai se ligando com o que tem ali, e vai formando camadas que vão se mineralizando. A greigita também, da mesma forma, só que seria bactérias redutoras de sulfato, elas usam o sulfato como receptor de elétrons, o SO4, e elas produzem H2S, que é sulfeto de hidrogênio. E aí esse sulfeto reage com o ferro II disponível no sedimento. Depois vão formando essa combinação de sulfeto de ferro que vai se formando em greigita também dessa mesma forma, no sentido de que isso vai se expandindo: vem de um núcleo e vai se expandindo ao redor.” “É difícil dizer que existe um padrão exatamente igual a esse que a gente encontrou em Marte, mas esses nódulos que se formaram são condizentes com formações que a gente encontra aqui.” Danilo: Além dos compostos orgânicos, os instrumentos do Perseverance também identificaram, na região em que a rocha foi encontrada, alguns compostos químicos ricos em enxofre, ferro oxidado ou ferrugem, e fósforo. Se micróbios existiram ali, esses compostos podem ter fornecido fontes de energia para o metabolismo desses microrganismos, reforçando a hipótese de origem biológica para os vestígios. Porém, o fato de que esses vestígios podem ter sido formados por vida microbiana não quer dizer que dê para descartar outros processos que não envolvam seres vivos – também chamados de processos abióticos. Os próprios autores do artigo que avalia a possível origem biológica das “pintas de leopardo” propõem alguns processos abióticos como explicações alternativas. Até agora, as alternativas abióticas, sem o envolvimento da vida, não parecem muito promissoras para explicar as marcas nas rochas, mas ainda não dá para descartá-las. Talvez estejam faltando algumas peças do quebra-cabeças para uma explicação abiótica convincente. O Gabriel de novo vai nos ajudar a entender isso. Gabriel:  Eles tentaram investigar o máximo possível de reações na ausência de vida, e nenhuma que nós conhecemos hoje poderia sustentar esse tipo de reação. Isso não quer dizer que a vida é sempre necessária para que essas reações aconteçam. A gente pode estar ignorando alguma coisa. Pode não estar percebendo alguma coisa. Podem existir reações que a gente não estudou hoje e que poderia estar fomentando essa formação desses minerais na ausência de vida, ou até mesmo as grandes escalas – a gente está falando aí de bilhões de anos – poderiam permitir que houvesse a formação desses minerais na ausência de vida. Mas de tudo que a gente conhece hoje, essa condição de formação de fosfato de ferro II, formação de sulfeto de ferro II acoplado à presença de matéria orgânica, como nós conhecemos, seria mais bem explicado pela ação da vida. Então eles fizeram um estudo muito minucioso de várias hipóteses. E a que melhor responde hoje é a ação da vida, em contrapartida a reações abióticas, sem a presença de vida.  Danilo: É justamente pela possibilidade de que as “pintas de leopardo” tenham sido formadas por mecanismos abióticos, sem o envolvimento de seres vivos, que os sinais são classificados de “potenciais bioassinaturas”. Ou seja, podem ter sido, como podem não ter sido causados por seres vivos. Para que uma potencial bioassinatura seja considerada um sinal de vida inequívoco, é preciso estabelecer com segurança a sua origem biológica e descartar os mecanismos plausíveis que não envolvam processos biológicos em sua formação – ou seja, é preciso eliminar essas hipóteses abióticas alternativas. É uma barra bem alta, difícil de ser alcançada. Para complicar, os instrumentos a bordo do Perseverance são versões miniaturizadas, simplificadas, de ferramentas que se usa em laboratórios terrestres para buscar bioassinaturas de vida do passado remoto da Terra, como o espectroscópio Raman. Gabriel: Para quem tem um olho um pouco mais treinado nessas questões científicas, quando a gente observa, por exemplo, no próprio artigo, os espectros Raman que foram publicados, a gente leva um pouco de susto, porque a gente vê que são dados muito ruidosos, que isso tem a ver com a forma com que a amostra é tratada lá no espaço. O laser não é tão preciso. O aumento não é tão grande. Você tem a grande influência da iluminação natural. Isso faz com que o espectro fique extremamente ruidoso e dificulta a análise daquilo que se espera estar sendo estudado. Se esse material pudesse ser trazido para a Terra num ambiente muito mais controlado, a gente poderia trabalhar com lasers com focos muito menores, ou seja, na escala de micrômetros, com uma precisão muito grande do que está sendo selecionado para ser estudado. E aí a gente tem alternativas: trocar lasers, trocar aparatos para garantir que o ruído seja minimizado e outros efeitos que atrapalham possam ser minimizados. [música]  Danilo: Da forma como eu e o Gabriel falamos, pode parecer que o Perseverance é um aparelho meio limitado, mas a verdade é que o jipe é uma grande realização da engenharia. O Gabriel me explicou que os engenheiros e cientistas da NASA bolaram soluções muito criativas para poder, por exemplo, em um único espectro separar a fluorescência de raio-X, que permite saber a composição elementar do material analisado, da difração de raio-X, que dá uma informação da estrutura cristalográfica dos minerais – ou seja, permite ver a organização interna dos átomos nas amostras. Apesar da criatividade, esses mini-aparelhos que o jipe carrega nem de longe se comparam com os dos laboratórios aqui na Terra. Por exemplo, o espectroscópio Raman que o Gabriel mencionou e que tem lá no AstroLab, ocupa boa parte de uma sala ao lado do laboratório, enquanto que as dimensões do SHERLOC, o instrumento que inclui o Raman no Perseverance, tem 26cm de comprimento por 20cm de largura (isso porque o SHERLOC carrega ainda outros instrumentos, como a câmera WATSON… sim, os cientistas são bons em dar nomes para os aparelhos… Elementar). Se der para trazer essas amostras para o nosso planeta, daria para trabalhar com radiação síncrotron, por exemplo, que consegue focar e fazer esse tipo de análise em escalas nanométricas. E também fazer a observação de microscopia eletrônica, onde a gente vai ver a estrutura daquela amostra com aumentos entre mil e dez mil vezes. Por isso, o jipe vem colhendo amostras que poderão, no futuro, ser trazidas para cá e analisadas em laboratório. É a única maneira de eliminar algumas incertezas e filtrar as hipóteses da origem das possíveis bioassinaturas. A missão de retorno dessas amostras estava em desenvolvimento pela NASA, mas extrapolou as estimativas de custo iniciais, chegando a 11 bilhões de dólares, e agora está cancelada devido aos cortes profundos no orçamento da NASA propostos pelo governo de Donald Trump. Mas um detalhe mostra que o caro, em ciência, é quase sempre barato quando comparado com gastos militares. Os 11 bilhões previstos para o desenvolvimento de toda a missão de retorno de amostra são os mesmos 11 bilhões que os Estados Unidos gastaram só nos primeiros seis dias de ataques ao Irã entre fevereiro e março deste ano.  [música] Danilo: Com os cortes no orçamento, a situação atual da NASA é complicada, para dizer o mínimo, por isso ainda não dá para saber quando e se vamos um dia analisar as tais “pintas de leopardo” em laboratório e distinguir se elas são biogênicas ou se foram formadas por processos abióticos. Mas dá para saber muita coisa sobre as condições que Marte oferece – e não oferece – para a existência da vida, além das condições que o planeta enferrujado já deve ter oferecido a possíveis seres vivos num passado muito distante. A Isabella Gaião e a Roberta Vincenzi, pesquisadoras associadas ao Laboratório de Astrobiologia da USP, vão me ajudar a entender melhor se Marte é ou já foi habitável um dia. Elas estudam um mesmo microrganismo, a bactéria Staphylococcus nepalensis. O micróbio é adaptado a ambientes hipersalinos, repletos de sal, como as lagoas de Araruama, no estado do Rio de Janeiro, onde elas encontraram essa espécie de bactéria em meio a outros microrganismos que sobrevivem a concentrações de sal nocivas à maior parte dos seres vivos. A superfície de Marte está cheia de sais que são nocivos à vida, como sulfato de magnésio e o perclorato de magnésio. Esses sais são muito mais nocivos do que o cloreto de sódio que predomina nos oceanos terrestres. A Roberta explicou porque esses sais são tão prejudiciais à vida. Roberta: Os principais danos dos percloratos, na verdade, são dois. Eles são muito oxidantes, mas hoje, e essa era uma das principais preocupações na época da descoberta desses sais lá, mas hoje, do que a gente entende, aparentemente, se você pega a parte termodinâmica do negócio, não é tão relevante o fato de eles serem oxidantes, mas eles são extremamente caotrópicos. E esse vai ser um conceito bastante importante para a gente entender os problemas da vida nessas soluções, porque um agente caotrópico é aquele agente que tem o potencial de desestabilizar macromoléculas. Macromoléculas são basicamente tudo que a vida precisa para existir, como proteínas, lipídios, material genético. Então, se você tem agentes caotrópicos em uma solução, essas moléculas que precisam se manter em determinada forma vão ter dificuldade de permanecer assim. E a gente sabe que a forma dessas macromoléculas hoje estão intimamente ligadas à função que elas exercem. Então, quando a gente tem esses agentes caotrópicos, é basicamente uma função de desestabilizar a vida como a gente conhece ali. E esses sais são extremamente caotrópicos. Danilo: A Isabella também me ajudou a entender como a caotropicidade desses sais pode desestruturar o arranjo de grandes moléculas orgânicas, como as proteínas. Isabella: Basicamente um agente caotrópico é qualquer coisa química que desestruture macromoléculas. Aí o que seriam macromoléculas? Qualquer molécula importante para a vida. Então a vida é baseada em células. Células têm principalmente proteínas, que é o arranjado de várias moléculas orgânicas ali e que elas se rearranjam de uma forma 3D. Então, a forma 3D de uma proteína é muito importante para ela executar a função. E função de proteína é tudo. Tudo que envolve uma célula funcionar, você precisa de uma proteína ali trabalhando para ela funcionar. E para essa proteína funcionar, ela tem que estar na forminha dela 3D, ela não pode ser uma linha, ela tem que ter três dimensões. E agentes caotrópicos vão quebrar esse 3D. E se você quebra esse 3D e ela fica, por exemplo, linear, uma proteína, aí ela não tem mais função. Se ela não tem função, a célula não funciona. Se uma célula não funciona, a vida por si não funciona.  Danilo: Como a Roberta já tinha mencionado, os percloratos da superfície marciana desestruturam a química da vida não só por serem caotrópicos, mas também por serem oxidantes. Roberta: Porque quando a gente fala que um composto ele é muito oxidante ou muito oxidativo, significa que ele reage muito fácil com outras coisas ao redor. Então, aquela estrutura que a Isabela falou, que precisa ser mantida, dessas proteínas, para que elas funcionem, quando você tem algo que é muito reativo ao redor… Isso também, ela vai reagir com esse agente oxidativo, que no caso é esse sal, e quando ela reage assim, todas as outras ligações que ela tem para manter essa estrutura específica, para ela funcionar, podem se desorganizar também, e isso vai prejudicar a função, seja das proteínas, como também dos lipídios, por exemplo, que são aquelas gorduras que constroem a membrana biológica das células, que é muito importante para manter um ambiente interno, mas também os próprios materiais genéticos, o DNA e o RNA, que são essenciais pra manter e passar a informação da vida como a gente a conhece. Danilo: a bactéria que a Roberta e a Isabella estudam gosta de alta concentração de sal. É, por isso, considerada um extremófilo, uma espécie adaptada a condições extremas em que a maioria dos seres vivos terrestres não teria condição de sobreviver. Extremófilos que se dão bem com alta concentração de sal são chamados de halófilos. Os halófilos são importantes para entender a possibilidade da existência de vida hoje em Marte. Caso a vida tenha um dia existido no planeta vermelho, ela poderia, talvez, ter se adaptado para sobreviver em bolsões de água debaixo da superfície, algo que provavelmente existe segundo os modelos mais aceitos da estrutura de Marte. Isabella: Mas existem locais na Terra em que de alguma forma a água evaporou demais e concentrou muito sal, então a gente tem um aumento dessa concentração comparado com o mar. E existem principalmente microrganismos nesses ambientes que se adaptaram e desenvolveram para esse tipo de ambiente. Então eles têm uma resposta ao sal, NaCl, cloreto de sódio, diferente dos que vivem no mar, por exemplo. Então eles resistem a concentrações maiores. Roberta: E isso seria interessante porque, como a gente falou, qualquer tipo de água líquida presente em Marte seria o que a gente chamaria de uma salmoura. Então, teria uma concentração alta de sal dissolvida nesses ambientes. Portanto, qualquer tipo de vida presente ali deveria ser capaz de lidar com isso, ou seja, a gente poderia chamar de halófilo. Danilo: esses bolsões subterrâneos de água têm a vantagem de estarem protegidos da alta radiação ultravioleta que castiga a superfície marciana. O nó é que deve haver outras barreiras para a sobrevivência de microrganismos nesses bolsões. A Roberta começa explicando isso e a Isabella depois completa a explicação. Roberta: Porque é possível. Se a gente tem água líquida, as reações são possíveis. Mas a gente vai ter diversas outras características. …desses ambientes que continuam sendo problemáticos. Um deles é, por exemplo, a própria disponibilidade de água que você vai ter numa solução aquosa com muita concentração de sal. Quando você tem uma solução com muita concentração de sal, as moléculas de água estão ligadas ao íon. Então, ela não está disponível para reação. Apesar da água estar líquida, você tem muito mais dificuldade de a reação acontecer. E a gente precisa de reação para que a vida aconteça. Isabella: Ela acabou de introduzir um termo extremamente importante, que ela só não deu o nome, mas é extremamente importante para esse tipo de pesquisa, que é a atividade da água. É o quanto de água está disponível para a vida reagir, para as reações acontecerem e a vida conseguir acontecer. Hoje, é meio arbitrário, esse número vai de zero a um, é um número, enfim, mas a gente sabe que a vida consegue sobreviver até 0,6 de atividade da água. Abaixo disso, não. E aí, quanto maior a atividade da água, ou seja, mais próximo de um, mais água disponível tem. Quanto menor, mais água está retida. Ela está ali, mas ela está se fazendo ligação com outro grupo químico, no caso, o que ela falou, são os sais. Então, os sais estão ligando com aquela água, ela não está disponível para a reação. Então, quanto mais sal, mais você tem a diminuição da atividade da água e menor chance de ter água disponível ali para a vida poder fazer reações químicas. Danilo: Então, no índice de 0 a 1 de atividade da água, a vida consegue existir se este índice estiver acima de 0.6, aproximadamente. O índice estimado de atividade da água nos aquíferos subterrâneos em Marte é 0.57 – ou seja, a bola bate na trave, mas não entra. [música de transição] Danilo: A atividade da água no passado remoto de Marte era, provavelmente, muito acima do mínimo requerido para a existência de vida. Se a superfície de Marte parece hoje inabitável, há mais de 3,5 bilhões de anos o planeta pode ter oferecido condições mais amenas à vida, especialmente a microbiana. O Gabriel publicou recentemente, como primeiro autor e junto com outra pesquisadora do AstroLab – a Ana Paula Schiavo, uma especialista em microrganismos halófilos – um estudo na conceituada revista internacional Astrobiology. Eles exploraram como o lago que existia na cratera Jezero há mais de 3,5 bilhões de anos pode ter sido habitável, pois deve ter sido rico em um íon de ferro capaz de proteger microrganismos da radiação ultravioleta. Ele mesmo explicou esse trabalho interessantíssimo para este podcast. Gabriel: Cada vez mais a gente descobre que Marte é muito mais heterogêneo do que a gente pensa como uma coisa uniforme. Existiam lagos onde você tinha pH muito baixo, que a gente tem uma ideia disso, principalmente por esses depósitos, como sulfatos de magnésio ou sulfatos de ferro, como mineral jarosita, detectado por satélites que orbitam Marte. A presença de jarosita demonstra que essa água, em algum momento, era extremamente abundante de ferro III e extremamente ácida, condições onde a gente possui vida aqui na Terra. Então a gente queria demonstrar que Marte tinha semelhanças com a Terra mas tinha algumas características também que eram um pouco diferentes. E poxa, Marte também estava recebendo uma grande quantidade de radiação do Sol, e eu falo principalmente da radiação ultravioleta, que é aquela que a camada de ozônio protege hoje em dia. Mas ainda assim, a gente tem um pouco de ultravioleta que chega por isso que a gente precisa passar protetor solar. E a gente pensou no ferro como também um protetor solar. Já havia estudos que demonstravam que o próprio solo marciano, por ser muito rico em ferro (por isso, aquela cor de ferrugem) ele já é capaz de proteger fisicamente organismos que eventualmente poderiam estar presentes ali no planeta. A gente queria poder quantificar essa proteção, principalmente nesses lagos.  Danilo: Usando algumas leis químicas que já são bem conhecidas, os pesquisadores do AstroLab desenvolveram um modelo matemático para tentar estimar qual seria o efeito protetivo do ferro em solução nos lagos que existiam no passado remoto de Marte. Pela composição das rochas encontradas no que era o fundo, o assoalho desses lagos, já sabia que eles poderiam ser ricos em ferro. Os pesquisadores do AstroLab fizeram experimentos em laboratório testando o quanto microrganismos poderiam sobreviver com diferentes taxas de radiação ultravioleta e soluções com mais e menos íons de ferro. Eles compararam os resultados dos experimentos com o modelo matemático e viram que o modelo era capaz de prever com uma boa precisão qual seria o efeito protetivo do ferro contra o ultravioleta.  Gabriel: E aí, com isso, a gente pôde modelar como esses lagos poderiam proteger a vida, pelo menos a vida como nós a conhecemos. Aí, claro, a gente tem que assumir várias questões. Por exemplo, a gente não sabe quais eram as concentrações de ferro nesse ambiente. Se existia vida ou não, qual seria a resistência dessa vida naturalmente ao ultravioleta, mas usando exemplos da Terra, a gente conseguiu demonstrar que lagos com pouco ferro, em algumas profundidades relativamente rasas na casa de alguns centímetros, até alguns poucos metros, esse ferro já seria capaz de proteger a vida como nós conhecemos. Então esses lagos marcianos poderiam estar protegidos dessa ação do ultravioleta do Sol. Mesmo não tendo uma camada de proteção de camada de ozônio, ainda assim a vida como nós conhecemos poderia se desenvolver nesse tipo de ambiente que a gente sabe que existiu no passado marciano. Danilo: Se o ouvinte quiser saber um pouco mais sobre esse estudo, pode dar uma olhada na matéria que eu publiquei na Folha de S. Paulo no final do ano passado, com o título “Novo modelo simula condições de habitabilidade de antigos lagos de Marte”. Vamos deixar o link da matéria e do artigo do Gabriel na descrição do episódio. [música de transição] Danilo: A gente viu que a superfície de Marte é inóspita para a vida como a gente a conhece, mas resta alguma esperança de que os aquíferos subterrâneos marcianos sejam habitáveis. Agora, para encontrar água embaixo da superfície, em grande quantidade e com potencial para ser habitável, a gente vai ter que ir para bem mais longe, lá na vizinhança dos planetas gigantes gasosos. No próximo episódio o assunto vai ser as luas de Júpiter e Saturno que têm grandes oceanos debaixo de uma espessa camada de gelo. Essas luas geladas têm se tornado o assunto mais quente da astrobiologia quando se trata da procura por condições e ingredientes para a vida no sistema solar. O roteiro, pesquisa, produção e narração foram feitos por mim, Danilo Albergaria; a revisão do roteiro foi feita pela Simone Pallone. Os entrevistados foram o Gabriel Gonçalves Silva, a Fernanda Jamel, a Roberta Vincenzi e a Isabella Gaião. A edição do episódio foi da Carolaine Cabral. As músicas são do Blue Dot Sessions,  são Creative Commons. E esse podcast foi produzido com o apoio da Fapesp, por meio da bolsa Mídia Ciência, com o projeto Pontes interdisciplinares para a compreensão da vida no universo, o Núcleo de Apoio à Pesquisa e Inovação em Astrobiologia e o Laboratório de Astrobiologia da USP.

This episode reviews four recently published studies about the impact of doxycycline post-exposure prophylaxis (doxy PEP) on Neisseria gonorrhoeae isolates with tetracycline resistance, Staphylococcus aureus, Group A streptococcus, and syphilis. View episode transcript and references at www.std.uw.edu.This podcast is dedicated to an STD [sexually transmitted disease] review for health care professionals who are interested in remaining up-to-date on the diagnosis, management, and prevention of STDs and STIs. Editor and host Dr. Meena Ramchandani is an Assistant Professor of Medicine at the University of Washington (UW), Program Director of the UW Infectious Diseases Fellowship Program, and Associate Editor of the National STD Curriculum.  

Send us Fan MailIn this episode of Skin Anarchy, Dr. Ekta Yadav sits down with Oliver Liu of Hypothesis to unpack one of the most misunderstood areas in skincare today: the microbiome. While the term has become a marketing staple, this conversation reveals just how early we still are in understanding the microbial ecosystems that shape skin health—and why most current treatments fail to reflect that complexity.Oliver reframes common conditions like acne and eczema as problems of imbalance, not simple bacterial overgrowth. In eczema, a weakened barrier, immune dysregulation, and the presence of Staphylococcus aureus create a self-reinforcing cycle of inflammation and irritation. In acne, it's not the presence of bacteria that drives breakouts—but which strains dominate. This shift challenges the long-standing idea that eliminating bacteria altogether is the solution.That insight exposes a deeper flaw in traditional treatments. Broad-spectrum approaches like benzoyl peroxide and antibiotics remove both harmful and beneficial microbes, often leading to temporary relief followed by recurrence, increased sensitivity, and long-term imbalance.The conversation then turns to a new model: precision skincare. Inspired by naturally occurring enzymes, Oliver explains how targeted approaches can selectively eliminate harmful bacteria without disrupting the surrounding ecosystem—preserving balance while addressing the root cause.This episode ultimately reframes skincare as ecosystem management, not correction.Listen to the full episode to hear Oliver break down the science of the microbiome and why the future of skincare lies in precision, not force.Shop HypothesisDon't forget to subscribe to Skin Anarchy on Apple Podcasts, Spotify, or your preferred platform.Reach out to us through email with any questions.Sign up for our newsletter!Shop all our episodes and products mentioned through our ShopMy Shelf!*This is a sponsored collaborationSupport the show

The trajectory of the success for a dairy cow begins with mammary development, long before lactation begins.  Dr. Benjamin Enger, Associate Professor for The Ohio State University in Wooster, has worked with his team for years to best understand how infection can change the development and if the timing of infection impacts that response. He was specifically interested in Staphylococcus aureus (SA), a common contagious pathogen in dairy farms. To study this, 21 bred heifers at three stages (6.5, 7.5 and 8.5 months) of pregnancy were inoculated, and tissue samples were collected 21 days later to determine the damage done. In this edition, there is much discussion about the physiology of mammary gland development and how different stages of pregnancy impacts progress towards lactation. Understanding the development of the mammary, will likely illuminate the importance of seemingly meniscal management steps. Analyzing your farm's data could hold the key to eliminating what might be the source of this devastating pathogen. Listen in today to learn more! Topics of discussion 1:40      Introduction of Dr. Ben Enger   3:08      Project set up 3:47      Knowledge gained in projects leading up to this hypothesis 6:53      What is mammary epithelial cells (MEC) and stromal cells 10:18    How did Staph Aureus (SA) impact amount of MEC and stromal cells in infected quarters 13:21     Cellular changes in heifers 6.5 vs 8.5 months pregnant 17:00     Cellular differences between the edge tissue vs the center (pic p4) 18:40    Duration of impact as the result of SA infection in pregnant heifers   20:54     How does SA get into calves prior to freshening? 22:53    Did you observe immunotolerance in the pregnant heifers? 25:53    What do you want ‘boots on the ground' dairymen to know about your project  27:26    Experimental increase of milk using blanket therapy to heifers precalving 28:17    Examine first test SCC in first calf heifers 27:20     What do you want ‘boots on the ground' dairymen to know about your project                 Featured Articles: Impact of Staphylococcus aureus intramammary infection on cellular proliferation and apoptosis on developing mammary glands of pregnant dairy heifers Supporting article: Impact of intramammary infections on mammary gland development in pregnant dairy heifers during late gestation #2xAg2030; #journalofdairyscience; #openaccess; #MODAIRY; #SA; #staphaureus ; #SA; #mammary; #mammarydevelopment; #heifer; #milk; #dairysciencedigest; #ReaganBluel

Academic SummaryResearchers investigated whether birch tar—a well-known adhesive used by Neanderthals—possessed medicinal properties that could have supported prehistoric healthcare. By recreating Middle Palaeolithic production methods, the study demonstrated that birch tar has selective antibacterial effects against Staphylococcus aureus, a bacterium notorious for causing wound and skin infections. The antibacterial efficacy was found to be independent of the extraction method used, suggesting that medicinal benefits were an inherent affordance of the material's production for tool-making. These scientific results mirror the traditional ecological knowledge of Indigenous communities, such as the Mi'kmaq, who use birch bark oil (maskwio'mi) as a traditional skin remedy. Ultimately, this research provides explicit data supporting the existence of a "structure of care" in the Pleistocene, where complex pyrotechnology served both technological and life-saving medicinal needs#NeanderthalMedicine #BirchTar #PrehistoricScience #AncientAntibiotics #Archaeology #EvolutionaryBiology #STEM #IndigenousKnowledge #TheCatalyst #HistoryUncoveredFormal CitationSiemssen T, Oludare A, Schemmel M, Puschmann J, Bierenstiel M. Antibacterial properties of experimentally produced birch tar and its medicinal affordances in the Pleistocene. PLoS One. 2026;21(3):e0343618. doi:10.1371/journal.pone.0343618.Medical & Legal DisclaimerThis content is for informational and educational purposes only and does not constitute medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. This research involves experimental and historical recreations and should not be attempted at home. Alchepharma,Ralph Turchiano,citation,research,study,Neanderthal medicine,birch tar,birch bark oil,maskwio'mi,Staphylococcus aureus,Pleistocene healthcare,Middle Palaeolithic technology,ancient antibiotics,prehistoric adhesive,Betula pendula,Betula pubescens,wound care history,Indigenous medicine,antimicrobial properties,Kirby-Bauer assay,zone of inhibition,Gram-positive bacteria,prehistoric chemistry,pyrotechnology,ancient pharmacy,STEM educationNARRATOR: Ralph TurchianoANALYSIS: Gemini

In this episode, a fascinating new bacteriophage, JS1. While most contractile phages (which inject DNA like a spring-loaded syringe) are rigid and straight, JS1 sports a curved, flexible tail that may help it navigate the complex "canyons and valleys" of the bacterial cell wall. Watch this episode: https://youtu.be/eDGta8xc4_0 Guests: Sabrina Suhani, Ph.D., Graduate Student, Monash University, Australia Trevor Lithgow, Ph.D., Professor, Monash University's Biomedical Discovery Institute. Links:  Staphylococcus species infected by a bacteriophage with a tail that is both curved and contractile This episode of Editors in Conversation is brought to you by mBio® and hosted by mBio Editor in Chief, Marvin Whiteley, Ph.D.  Visit journals.asm.org/journal/mbio to read articles and/or submit a manuscript. Receive up to 50% off fees when you publish in mBio® or any of the ASM journals by becoming an ASM member. Sign up at asm.org/joinasm.

This Biotech CEO is Working on Making The Impossible Possible & Helping Us Fight Bad Bacteria. Meet Dr. Deborah Birx (Armata Pharmaceuticals -ARMP)GuestCEO Full Name: Dr. Deborah Birx CEO, Armata Pharmaceuticals Company Name: Armata Pharmaceuticals, Inc.Website: http://www.armatapharma.com/Ticker: $ARMP (NYSE American)Dr. Deborah Birx Bio: Deborah L. Birx, M.D., was appointed Chief Executive Officer on July 10, 2023. Prior to joining Armata, Dr. Birx served as a member of Innoviva's Board of Directors from March 2021 until July 2023.Dr. Birx is a world-renowned medical expert and leader who most recently served as the response coordinator of the White House Coronavirus Task Force. Previously, she served as Ambassador-at-Large, when she assumed the role of the Coordinator of the United States Government Activities to Combat HIV/AIDS and U.S. Special Representative for Global Health Diplomacy. Dr. Birx also served as the U.S. Global AIDS Coordinator where she oversaw the President's Emergency Plan for AIDS Relief (PEPFAR) at the CDC and as the Director of the U.S. Military HIV Research Program (USMHRP) at the Walter Reed Army Institute of Research.From 1980 until 2008, Dr. Birx served in the United States Army, retiring with the rank of colonel. Dr. Birx has published over 230 manuscripts in peer-reviewed journals, authored nearly a dozen chapters in scientific publications, as well as developed and patented vaccines. She received her medical degree from the Hershey School of Medicine, Pennsylvania State University, and beginning in 1980, she trained in internal medicine and basic and clinical immunology at the Walter Reed Army Medical Center and the National Institutes of Health. Dr. Birx is board certified in internal medicine, allergy and immunology, and diagnostic and clinical laboratory immunology.Company Bio: Armata is a late clinical-stage biotechnology company focused on the development of high-purity pathogen-specific bacteriophage therapeutics for the treatment of antibiotic-resistant and difficult-to-treat bacterial infections using its proprietary bacteriophage-based technology. Armata is developing and advancing a broad pipeline of natural and synthetic phage candidates, including clinical candidates for Pseudomonas aeruginosa, Staphylococcus aureus, and other important pathogens. Armata is committed to advancing phage therapy with drug development expertise that spans bench to clinic including in-house phage-specific current Good Manufacturing Practices manufacturing to support full commercialization

 In this episode of The Moos Room, Brad shares insights from a recent study at the University of Minnesota Morris dairy focused on reducing mastitis and improving behavior in first-lactation heifers. The research tested a simple, low-labor strategy: bringing heifers into the parlor once per week for three weeks before calving, gently acclimating them, and applying a 1% iodine teat dip. Results showed that trained heifers were calmer, easier to milk, and significantly less likely to kick during milking, improving both animal welfare and milker safety. While overall clinical mastitis rates did not differ, the treatment notably reduced Staphylococcus aureus infections, with untrained heifers having five times greater odds of infection shortly after calving. The episode highlights how small, proactive management steps before calving can break the cycle of stress, poor behavior, and disease—offering a practical approach to improving transition success in dairy heifers. Questions, comments, scathing rebuttals? -> themoosroom@umn.edu or call 612-624-3610 and leave us a message!Linkedin -> The Moos RoomTwitter -> @UMNmoosroom and @UMNFarmSafetyFacebook -> @UMNDairyYouTube -> UMN Beef and Dairy and UMN Farm Safety and HealthInstagram -> @UMNWCROCDairyExtension WebsiteAgriAmerica Podcast Directory 

This is the first episode of the 'Quarterly catchup' series, in which CMI Communications editors discuss important and useful articles that have come out in the last 3 months to understand their results and potential clinical impact. In this inaugural episode of 'Quarterly catchup', Emily McDonald (Canada), Thomas Tängdén (Sweden) and Navaneeth Narayanan (USA) convene to discuss clinical microbiology and infectious diseases studies published in the first quarter of 2026 [1-6]. From Wolbachia-infected mosquitoes reducing dengue infection to exploration of antibiotic combination therapies against multidrug-resistant organisms, our hosts summarize six articles they found the most interesting, and discuss whether they can and should change clinical practice.   This episode was peer reviewed by Connor Prosty of McGill University, Montréal, Canada.  ReferencesLim JT, et al. Dengue suppression by Male Wolbachia-Infected mosquitoes. NEJM 2026. doi: https://doi.org/10.1056/NEJMoa2503304 Escrihuela-Vida F, et al. Adjunctive Fosfomycin for the Treatment of Staphylococcus aureus Bacteremia: A Pooled Post Hoc Analysis of Individual Participant Data From 2 Randomized Trial. Clin Infect Dis 2026. doi: https://doi.org/10.1093/cid/ciaf387 Baldanzi G, et al. Antibiotic use and gut microbiome composition links from individual-level prescription data of 14,979 individuals. Nat Med 2026. doi: https://doi.org/10.1038/s41591-026-04284-y.Quentin Vallé, et al. Evaluating the antibacterial activity of ceftazidime/avibactam and aztreonam combinations against multidrug-resistant Stenotrophomonas maltophilia complex isolates in a hollow fibre infection model.  Clin Microbiol Infect 2026. doi: https://doi.org/10.1016/j.cmi.2026.02.010 Rana AI, et al. Cabotegravir plus Rilpivirine for Persons with HIV and Adherence Challenges. NEJM 2026. doi: https://doi.org/10.1056/NEJMoa2508228 Donovan J, et al. Genotype-stratified adjunctive dexamethasone for tuberculous meningitis in HIV-negative adults: a randomized controlled phase 3 trial. Nat Med 2026. doi: https://doi.org/10.1038/s41591-025-04138-z Further readingThwaite GE, et al. Dexamethasone for the Treatment of Tuberculous Meningitis in Adolescents and Adults. NEJM 2004. doi: https://doi.org/10.1056/NEJMoa040573 Behrmann LV. “The specimen is never wrong”: the pathologist behind Wolbachia. CMI Communications, 2026. doi: https://doi.org/10.1016/j.cmicom.2026.105185                

This episode features Dr. Maria Teresa García-Romero, MD MPH from the National Institute of Pediatrics in Mexico City, talking about the skin microbiome and how it relates to atopic dermatitis. The skin microbiome varies widely at different sites on the body, but in general, increased diversity is associated with healthy skin. In atopic dermatitis, Staphylococcus aureus becomes abundant and skin microbiome diversity decreases, correlating with inflammatory responses. Treatments have the effect of reducing Staphylococcus aureus. These bacteria are now established to have a role in the pathophysiology of the disease. The caution with antibiotic treatment is that a systematic review and meta-analysis from Dr. García-Romero's group found Staphylococcus aureus isolates from people with atopic dermatitis had suboptimal susceptibility to commonly used antimicrobials, especially in lower middle-income and upper middle-income countries. Mechanistically, Staphylococcus aureus decrease natural antimicrobial molecules in the skin, stimulate the innate immune response, and likely reduce beneficial bacteria. New treatments are urgently needed because atopic dermatitis is very prevalent (affecting 20-30% of the population), with far-reaching effects in children's and families' lives. Two ingested probiotics are commercially available for atopic dermatitis, backed by clinical data, whereas topical probiotic treatments require further research. Episode abbreviations and links: Paper showing how treatments for atopic dermatitis help the skin microbiome more closely resemble healthy controls: The Skin Microbiome of Patients With Atopic Dermatitis Normalizes Gradually During Treatment Systematic Review and Meta-Analysis looking at susceptibility of atopic-dermatis associated Staphylococcus aureus to antibiotics in different regions of the world: Global Antimicrobial Susceptibility Patterns of Staphylococcus aureus in Atopic Dermatitis About Dr. Maria Teresa García-Romero: Dr. Maria Teresa García-Romero is a medical doctor graduated from Tec de Monterrey School of Medicine, magna cum laude. She has a Specialty in Dermatology and Diploma in Medical Mycology from UNAM, Mexico City. Dr. García-Romero completed a Fellowship in Pediatric Dermatology at the University of Toronto, and a Master's degree in Public Health and Quantitative methods of research at Harvard University Chan School of Public Health. She has received meritorious awards including the Mexican Foundation for Health (FUNSALUD), Harvard University Presidential Award, Society for Pediatric Dermatology Fellow Award, among others; and funding for research projects by prestigious international organizations such as MIT (Massachusetts Institute for Technology) seed funds and EB Research Partnership. She is currently an attending physician in the Dermatology Department of the National Institute of Pediatrics in Mexico City and a member of the National System of Researchers level II. She has more than 150 articles published in national and international magazines, supervised multiple postgraduate theses and has presented in multiple forums worldwide. Dr. García-Romero is a member of the Editorial Committee of JAMA Dermatology, Pediatric Dermatology and other high impact journals. Her research interests include the skin microbiome, atopic dermatitis, vascular anomalies and autoimmune disease.

In this episode, we are going to take a closer look at Vancomycin, one of the most widely used antibiotics in the hospital setting and a medication that pharmacists frequently monitor. Vancomycin is a glycopeptide antibiotic primarily used to treat serious gram-positive infections, including those caused by Methicillin-resistant Staphylococcus aureus (MRSA). Its mechanism of action involves inhibiting bacterial cell wall synthesis by binding to the D-alanine–D-alanine portion of peptidoglycan precursors, which ultimately prevents the bacteria from forming a stable cell wall. Clinically, vancomycin is commonly used for infections such as bacteremia, endocarditis, osteomyelitis, and severe skin and soft tissue infections when resistant gram-positive organisms are suspected. One of the most important aspects of vancomycin therapy is therapeutic drug monitoring, as maintaining appropriate exposure is critical for both efficacy and safety. Current practice often focuses on achieving target AUC-to-MIC ratios rather than relying solely on trough levels. Pharmacists also play an important role in adjusting doses based on renal function and monitoring for adverse effects. Two key safety concerns with vancomycin are nephrotoxicity and vancomycin infusion-related reactions such as “red man syndrome,” which is characterized by flushing, rash, and hypotension if the medication is infused too rapidly. Throughout this episode, we will review the pharmacology, monitoring parameters, and clinical pearls that healthcare professionals should understand when managing patients receiving vancomycin therapy. Be sure to check out our free Top 200 study guide – a 31 page PDF that is yours for FREE! Support The Podcast and Check Out These Amazing Resources! NAPLEX Study Materials BCPS Study Materials BCACP Study Materials BCGP Study Materials BCMTMS Study Materials Meded101 Guide to Nursing Pharmacology (Amazon Highly Rated) Guide to Drug Food Interactions (Amazon Best Seller) Pharmacy Technician Study Guide by Meded101

On episode #102 of the Infectious Disease Puscast, Daniel and Sara review the infectious disease literature for the weeks of 2/26 – 3/11/26. Host: Daniel Griffin and Sarah Dong Subscribe (free): Apple Podcasts, RSS, email Become a patron of Puscast! Links for this episode Viral Measles Outbreak — New Mexico, 2025 (CDC: MMWR) Epidemiology of HMPV and Other Respiratory Viral Infections Among Outpatients, 2016–2022 (OFID) Notes from the Field: Congenital Rubella Syndrome — Florida, 2025 (CDC: MMWR) Long-term efficacy and safety of the single-dose tetravalent Butantan dengue vaccine (Nature Medicine) Bacterial Clinical Outcomes in Hypervirulent Carbapenem-Resistant Klebsiella pneumoniae Infection: A Cohort Study (JID) Duration of therapy for Pseudomonas aeruginosa bacteremia – a post hoc subgroup analysis from the BALANCE randomized controlled trial (CID) Diagnostic Yield of Tongue Swab- Compared to Sputum-Based Molecular Testing for Tuberculosis in Four High-Burden Countries (CID) WHO recommends near point-of-care tests, tongue swabs, and sputum poolingfor TB diagnosis (WHO) Respiratory virus co-infection is a risk factor for adverse outcomes during Staphylococcus aureus bacteraemia (OFID) Balance Versus Bias: Correcting Misinformation About the 2025 ATS Community-Acquired Pneumonia Guidelines (CID) Fungal The Last of US Season 2 (YouTube) Immunomodulation in the Treatment of Disseminated Coccidioidomycosis (CID) Parasitic Comparison of six weeks doxycycline versus six weeks rifampicin or three weeks of the combination of doxycycline plus rifampicin in the treatment of onchocerciasis: a randomized, placebo-controlled, double-blind, phase 2 trial (OFID) Cutaneous Larva Migrans Within the United States Military Health System – Clinical Presentation and Association with Autochthonous Spread or International Travel (OFID) Miscellaneous Distinct prophage infections in colorectal cancer-associated Bacteroides fragilis (Communications Medicine) Rounding Styles on Inpatient Infectious Disease Consult Services: Impact on Education and Patient-Care Delivery (OFID) Possible quality indicators for clinical infectious diseases consultations – results from a hybrid Delphi-nominal group approach and scenario study (CMI: Clinical Microbiology and Infections) Music is by Ronald Jenkees Information on this podcast should not be considered as medical advice.

The latest Georgia Tech Research Podcast episode for the Agricultural Technology Research Program (ATRP) focuses on the Georgia Tech Diggle Lab (www.thedigglelab.com). This episode discusses cross-campus collaboration between GTRI's ATRP and GT's Diggle Lab.  The Lab's director is Dr. Steve Diggle (hence, the name).  The Diggle Lab is based in the Center for Microbial Dynamics and Infection (part of the School of Biological Sciences) at Georgia Tech.  Its primary objective is to gain a deeper understanding of microbial interactions and social behaviors, with a focus on their impact on virulence, antimicrobial resistance (AMR), and the development of therapeutic strategies. A prominent project is an investigation of the antibiotic-resistant superbug, Pseudomonas aeruginosa, which the Centers for Disease Control and Prevention (CDC) has classified as a "critical threat" in health care environments. GTRI and the Diggle Lab collaborated on research focused on bio-based wound dressings and antibiotic resistance. The collaboration has led to has developed piacens, protein-based antimicrobial structures that target specific bacteria without causing resistance.  The lab also explored ancient biotics, recreating a 1,000-year-old recipe that effectively treated Staphylococcus aureus. The collaboration aims to address antibiotic resistance and biofilm issues in poultry and industrial settings, leveraging piacens' precision and stability.

Na segunda parte do episódio sobre endocardite, William e Jordan recebem novamente a ⁠Dra. Cely Saad Abboud⁠ para discutir o manejo terapêutico da doença, com foco prático em profilaxia, antibioticoterapia e decisão cirúrgica.O episódio aborda as recomendações atuais para profilaxia em procedimentos odontológicos e pacientes de alto risco, como portadores de valva protética, história prévia de endocardite e cardiopatias congênitas, além da lógica por trás das mudanças nos guidelines ao longo dos anos. São discutidos os esquemas terapêuticos para endocardite em válvula nativa e prótese valvar, precoce e tardia, incluindo tratamento empírico na hemocultura negativa, terapias direcionadas para Staphylococcus aureus, estreptococos e enterococos, duração do tratamento, terapia combinada, toxicidades e abordagem da endocardite fúngica.A conversa aprofunda ainda o conceito de Endocarditis Team, os critérios de indicação cirúrgica como falência cardíaca, infecção não controlada e prevenção de embolização, além da evidência atual sobre terapia oral com base no estudo POET.Um episódio essencial para infectologistas, cardiologistas e intensivistas que atuam no manejo de pacientes graves com infecção cardiovascular.

Four years after our original antibiotic myth-busting episode (Ep 60), we're back with Dr Riati Scarborough to talk antibiotic prescribing habits. This time we're joined by fellow stewardship expert Dr Laura Hardefeldt, and this time we're asking the harder question: Have we actually changed?The good news? Some prescribing habits are shifting. We're seeing shorter courses and less ‘just in case antibiotic usage. But let's not pat ourselves on the back too quickly. Because some of our most entrenched habits are still alive and well, like how we treat skin disease, and our ongoing love affair with amoxiclav.This episode is a practical, clinically grounded update on what the evidence says in 2026 - and how to make realistic changes without compromising patient care.We cover:Why skin disease remains the single biggest driver of antimicrobial resistance in small animal practice, and what to do about itAmoxicillin vs amoxiclav: when de-escalation is not just safe, but smarterWhy convenience (you know the brand we're talking about right…) is not a clinical indicationTrimethoprim-sulphonamide and the real story on KCS riskDentals, heart murmurs, and what prophylaxis actually looks like in 2026Simple in-clinic stewardship strategies that genuinely shift prescribing behaviourThis isn't about perfection. It's about progress.If you'd like effective antibiotics to still exist in five to ten years…This episode is essential listening.Find out how we can support you in your vet career at ⁠⁠⁠⁠⁠⁠⁠thevetvault.com⁠⁠⁠⁠⁠⁠⁠.⁠Subscribe to our weekly newsletter⁠ ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠here⁠⁠⁠⁠⁠⁠ ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠for Hubert's favourite clinical and non-clinical learnings from the week.Grab one last handful of spots in the Maldives for our surf/dive vet conference with ⁠Vets On Tour⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠. Tips and Timestamps3:03 Progress in prescribing habits including UTI durations and surgical prophylaxis4:55 Skin disease as the biggest problem area in small animal practice7:01 Topical therapy versus systemic antibiotics for skin conditions9:28 Deep pyoderma and the new consensus statement11:00 Gut bacteria as a source of resistant infections12:41 Rise of MRSP, methicillin-resistant Staphylococcus pseudintermedius14:00 Amoxicillin-clavulanate overuse16:47 Vets on Tour conferences advertisement18:08 Pharmacology refresher on amoxicillin, amoxicillin-clavulanate, and cefovecin19:45 Why cefovecin is classified as high importance, vs the convenience argument for cefovecin in cats22:56 Long-acting amoxicillin injections as an alternative24:00 Getting amoxicillin back on the shelf24:53 Communicating antibiotic choices to clients29:32 Dental antibiotics and debunking the heart murmur myth34:07 Subclinical bacteriuria and stopping cultures in asymptomatic patients38:30 Reassessing the dry eye risk of trimethoprim-sulfonamide41:43 Antimicrobial stewardship trial using colour-coded pharmacy shelves

Send me a question or story!Continuing our DERM DRUG series... we are discussing one of the most common class of drugs asked about: antibiotics! Specifically, those used for staphyloccal pyoderma since it is seen almost every day in general practice.A majority of this discussion was developed from the newly updated ISCAID (International Society for Companion Animal Infectious Diseases). These guidelines were updated in 2025 and are open access to the public. You can find them at https://onlinelibrary.wiley.com/doi/10.1111/vde.13342.These guidelines cover duration of treatment, topical therapy and different tiers of systemic antibiotics. Which antibiotics can you feel more comfortable using empirically? Find out on this week's episode of The Derm Vet podcast!00:00 – Intro02:12 – Important Precursors05:37 – First Choice Drugs08:50 – Second Choice Drugs14:39 – Reserved Microbial Drugs21:21 – Overview23:47 – Outro

In this episode of Communicable, Josh Davis (Newcastle, Australia) and Emily McDonald (Montreal, Canada), plus invited guest, Steven Tong (Melbourne, Australia)—all practicing physicians and clinical trialists—assemble to discuss some of their ‘top infectious diseases papers published in 2025'. Bassam Ghanem (Jeddah Lol, Saudi Arabia), whom one might know better as Antibiotic Steward on social media, was also invited to share his favourite publications of 2025.Six papers that were most consistently picked by the panel are presented, explaining why they were picked and how they have shifted paradigms or changed their practice. This episode complements the previous episode, which presented ‘top clinical microbiology papers in 2025', and was peer reviewed by Akshatha Ravindra of Kasturba Medical College, Manipal, India.   ResourcesCLARITY initiative websitePapers presented (in order of presentation) Turner NA, et al. Dalbavancin for Treatment of Staphylococcus aureus Bacteremia. JAMAMeya DB, et al. Trial of High-Dose Oral Rifampin in Adults with Tuberculous Meningitis. NEJMVodstrcil LA, et al. Male-Partner Treatment to Prevent Recurrence of Bacterial Vaginosis. NEJMKreimer A, et al. Noninferiority of One HPV Vaccine Dose to Two Doses. NEJMGuglielmetti L, et al. Oral Regimens for Rifampin-Resistant, Fluoroquinolone-Susceptible Tuberculosis. NEJMRoss JDC et al, Oral gepotidacin for the treatment of uncomplicated urogenital gonorrhoea (EAGLE-1). Lancet  ‘One liners' (in order of presentation)Burdet C et al. Cloxacillin versus cefazolin for meticillin-susceptible Staphylococcus aureus bacteraemia (CloCeBa). LancetLemiale V et al, Adjunctive corticosteroids in non-AIDS patients with severe Pneumocystis jirovecii pneumonia (PIC). Lancet Respir MedLuetkemeyer AF et al, Doxycycline to prevent bacterial sexually transmitted infections in the USA. Lancet Inf DisEyting M, et al. A natural experiment on the effect of herpes zoster vaccination on dementia. NatureXie M, et al. The effect of shingles vaccination at different stages of the dementia disease course. CellPomirchy M, et al. Herpes Zoster Vaccination and Dementia Occurrence. JAMADurbin AP et al, Daily Mosnodenvir as Dengue Prophylaxis in a Controlled Human Infection Model. NEJMHook EW et al, One Dose versus Three Doses of Benzathine Penicillin G in Early Syphilis. NEJMOpdam MAA et al, Continuation versus temporary interruption of immunomodulatory agents during infections in patients with inflammatory rheumatic diseases. Clin Infect DisArundel C et al, Negative pressure wound therapy versus usual care in patients with surgical wound healing by secondary intention in the UK (SWHSI-2). LancetHonourable mentionsChaccour C, et al. Ivermectin to Control Malaria. NEJMLucinde RK, et al. A Pragmatic Trial of Glucocorticoids for Community-Acquired Pneumonia. NEJMMorel J, et al. Effect of a 1-month methotrexate delay on pneumococcal vaccine immunogenicity and disease control in patients with early rheumatoid arthritis (VACIMRA). Lancet RheumatolHaukoos J, et al. Hepatitis C Screening in Emergency Departments. JAMAMajor Extremity Trauma Research Consortium (METRC). Oral vs Intravenous Antibiotics for Fracture-Related Infections: The POvIV Randomized Clinical Trial, JAMA SurgAnderson CS, et al. Influenza vaccination to improve outcomes for patients with acute heart failure (PANDA II). LancetSt Peter SD, et al. Appendicectomy versus antibiotics for acute uncomplicated appendicitis in children. LancetPan CQ, et al. Tenofovir and Hepatitis B Virus Transmission During Pregnancy. JAMAGohil SK, et al. Improving Empiric Antibiotic Selection for Patients Hospitalized With Abdominal Infection. JAMA SurgRelated podcast episodesCommunicable E44: Top clinical microbiology papers in 2025 https://share.transistor.fm/s/6e5c26aeCommunicable E29: Bacterial vaginosis & male partners, https://share.transistor.fm/s/3de4f5c3 Communicable E28: Late-breaker trials at ESCMID Global: Should they change your practice? - part 2, https://share.transistor.fm/s/4f044e8c Communicable E20: Tuberculosis today https://share.transistor.fm/s/9858900e 

David Jernigan 0:15Hello! Dr. Deb 0:16Hi there, sorry for all the confusion. David Jernigan 0:19Oh, no worries, you gotta love it, right? Dr. Deb 0:21Oh, I can’t hear you. David Jernigan 0:23No way, let’s see, my mic must be turned off? Dr. Deb 0:27Hang on, I think it’s me. Let’s see…Okay, let’s try now. David Jernigan 0:40Okay, can you hear me? Dr. Deb 0:42Yep, I can hear you now. David Jernigan 0:43Excellent, excellent. And, how are you today? Dr. Deb 0:48I am good, thank you. How about yourself? David Jernigan 0:50I’m good. Well, it’s good to finally meet you and get this thing rolling. Dr. Deb 0:56Yes, yes, I’m so sorry about that. David Jernigan 0:58That’s alright, that’s alright.So… Dr. Deb 1:01Yeah, go ahead. David Jernigan 1:03So, tell me about yourself before we get going. Dr. Deb 1:06Yeah, so I am a nurse practitioner. I’m also a naturopath. I have a practice here in Wisconsin. I’ve been treating Lyme for about 20 years, so I’m really excited to have this conversation and learn what you’re doing, because it’s so exciting and new. David Jernigan 1:21Well, thank you. Dr. Deb 1:22Yeah, so we treat a lot of chronic illness patients, do some anti-aging regenerative things as well, so… David Jernigan 1:30Yeah, I went to your website and saw you guys are killing it, looks like. Dr. Deb 1:35Yeah. David Jernigan 1:35Got a lot of good staff, it looks like. Dr. Deb 1:37Yeah, we’ve got great staff, great patients, busy practice. We have 5 practitioners, so we have about 15,000 patients in our practice right now. David Jernigan 1:46Well, excellent. Yeah. Excellent. Yeah, yeah.So, I’m excited for this discussion. Dr. Deb 1:53Good, me too. So I pre-recorded our intro, so we can just kind of dive right in, and I’ll just ask you to kind of introduce yourself a little bit, tell us a little bit about yourself, and, and then we can just dive right into it. David Jernigan 2:08All right. I’m Dr. David Jernigan, and I own the Biologic Center for Optimum Health in… Franklin, Tennessee, and I’ve been in practice for over 30 years. I shook Willie Bergdurfer’s hand, if anybody knows who that is. It’s kind of infamous now with some of the revelations that have happened about Lyme being a bioweapon and weaponized. But, you know, I’ve been doing this, probably longer than almost anybody that’s still in the business in the natural realm. It chose me. I did not choose Lyme. Matter of fact, there were many times in my career that I was like. You know, cancer’s easier because of the fact that everybody agrees, you know, what we’re dealing with. And in the 90s, it was a whole different reality, where nobody actually understood that you could have Lyme disease and not be coming from New England.You know, so I had actually the first documented case of a Lyme disease, CDC positive.Patient that had never left the state of Kansas before. So they couldn’t say that it wasn’t in Kansas, and so she had actually been, pregnant with… twin boys, and they were born CDC-positive as well, and so it is transmitted across the placenta we know.So, I, you know, the history of how I did all this was, in the 90s, probably 1996, probably, somewhere in there, 97. With this woman, you know, I… if you go into Robin’s pathology books from back then. Which we all used, medical doctors and everybody else studying. you know, there was basically a paragraph about Lyme disease, and on the national board tests, as you recall, it was probably like, what causes, or what is, bullseye rash associated with? And you’d had to guess Lyme disease, of course. Dr. Deb 4:07Female. David Jernigan 4:08But that was, you know, considered to be more a New England illness, and you would never see it anywhere else. But here was this woman. I knew… nothing about Lyme beyond what we had gotten taught in college, which was, like I say, next to nothing. And she would not let me stop feeding me information. I mean, you gotta remember, the internet wasn’t even hardly in existence in those years. I mean, it was brand new. It was supposed to be this information highway, and So I started purchasing, like a lot of doctors do even now, they start purchasing every kind of new supplement that’s supposed to work for bacteria. There was no product in those days that actually was Lyme-specific. I mean, nobody was really dealing with it naturally. It was always a pharmaceutical situation. Dr. Deb 5:04And a very short course at that. David Jernigan 5:06Yeah, 2 weeks of doxy and you’re cured, whether your symptoms are gone or not, which… she’d had the 2 weeks of doxy, and her symptoms and her son’s symptoms were not gone. And so, I absolutely just purchased everything I could find. Nothing would work. I mean, I could name names of products, and you would recognize them, because they’re still out there today. Dr. Deb 5:28Which is. David Jernigan 5:30Kind of a… A sad thing that natural medicine is still riding on these things that have the most marketing. Dr. Deb 5:37As opposed to sometimes the things that actually have the documented research. David Jernigan 5:42Behind it, and I am a doctor of chiropractic medicine, and I specialized all these years in chronic, incurable illnesses of all types. That may sound odd to a lot of people, but doctors of chiropractic medicine are trained just like a GP typically would be. The medical schools, as I understand it, got together, decades ago and said, wow, if all we did was… Crank out general practitioners for the next 10 years, we wouldn’t have still enough general practitioners to supply the demand. Dr. Deb 6:17Right. Everybody in medicine, in medical schools, wanted to be a specialist, because that’s where the money was, and it was… David Jernigan 6:24Easier, kind of, also, to… you know, just focus on one part of the body, and specialize in that. Dr. Deb 6:31Expert in that one area. David Jernigan 6:32So we all now have the same training. We all go through pre-med. We got a bachelor’s degree, I got my bachelor’s degree in nutrition, and through, Park University in Parkville, Missouri. And so, you know, when I ran out of options to purchase, I just used a technology that I developed, which was an advancement upon other technologies, but I called it bioresonance scanning. And I coined the term back in the 90s. It was a way to kind ofKind of like a sensitive test, you know, like you might. Dr. Deb 7:09I wouldn’t. David Jernigan 7:09Of applied kinesiology, then clinical kinesiology, then chiro plus kinesiology, then, you know, you can just keep going with all the advancements that were made. Well, this was an advancement upon those things, so… I developed… I was the first in… in… my known world of doctors to develop a way to detect adjunctively, obviously we can’t say it’s a primary diagnosis. Adjunctively detect the presence of a given specimen. So we could say, thus saith my test. It’s highly likely you have Borrelia burgdurferi. And, but I had to have the specimen on hand to be able to match what I call frequency matching to the specimen. Brand new concept in those days. And so I was able to detect whether or not my treatments were successful or not. This is something even now that’s really difficult for doctors, because antibody tests, even the most advanced ones, it’s still an antibody test. It’s still an immune response to an infection.And accurately, you know, some doctors will slam those tests, saying, well. That doesn’t mean you actually have the infection, that just means your body has seen it before, which is a correct statement, kind of. So being able to detect the presence, and even where in the body these infections are was a way huge advancement in the 90s, for sure it’s kind of funny, I think about a conference I went to, and cuz… I’m kind of jumping ahead. Because I ended up developing my own formula, just for this woman and her children, and it worked. And I was like, wow! Their symptoms were gone, all the blood tests came back negative. In those days, we were using the iGenX. Western blot, eventually. And the, what was called a Lyme urine antigen test. I don’t know if you remember that, because it… Only decades later did I meet, the owner of iGenX, Nick Harris. Dr. Deb 9:17Person. And I was like, whatever happened to the Luwat test? Because I took it off the market after a while. He said, honestly, we lost the antigen and couldn’t find it again. Oh, no. David Jernigan 9:27And so… but that was a brilliant test. It was the actual gold standard in those days. Again, the world… it can’t be understated how different the world was in the 90s. Dr. Deb 9:40Yeah. David Jernigan 9:41Towards natural medicine, even. Dr. Deb 9:44Oh, yeah. We think… we think it’s bad now, but, like, when I started, too, I started in the early 2000s, like, we were all hiding under the radar, like, you didn’t market, we would have never been on social media, we didn’t run ads, we didn’t do any. David Jernigan 10:00Right. Dr. Deb 10:01Because the medical boards were coming for us. David Jernigan 10:04Came after me. Dr. Deb 10:05Because I had the word Lime on my page, my website. David Jernigan 10:10You know, not saying that I treat Lyme. Dr. Deb 10:13Hmm? David Jernigan 10:13Yes Dr. Deb 10:15Just talking about mind. David Jernigan 10:16And it’s funny, because, once I had this formula, it was something… and I trained in Germany, in anthroposophical medicine, and they’ve been trained in herbal… making herbal extracts, making homeopathic remedies in the anthroposophical methodology, and I trained with the Hahnemann versions of homeopathy, which is just slightly different. Yeah. And, so I was well-versed with making some of my own formulas by that time. And so, it was really something that I wrote on the bottle, you know, and I had to call it something, so I called it Borreligin, which is still in existence, and it’s still a phenomenal herbal remedy right now. And to my knowledge, it’s the only frequency-matched herbal formula. Maybe still out there. Because unless you knew how to do my testing, the bioresonent scanning, there was no way to actually do frequency matching. Matter of fact, as a really famous herbalist attacked me online, saying, oh, none of these herbs will kill anything. And I’m like, that wasn’t what I was saying. I was saying, back in those days, I was saying, well, if… what would the body need to address these infections?You know, not, like, what’s gonna kill the infections for the body. Dr. Deb 11:38Right. David Jernigan 11:39Right? So it was a phenomenal way, but the LUAT test was amazing because what you’d do is you would give your treatment, like an MD would give an antibiotic for a week, ahead of time. Trying to increase the number of dead spirochetes showing up in your urine one day out of 3 days urine catch. So you’d wake up in the morning, you’d collect your urine 3 days in a row, and any one of those being positive is a positive. But it was a brilliant test because it wasn’t an antibody test. They were literally counting the number of dead pieces of Lyme bacteria in your urine. I mean, it was pretty irrefutable. So I had a grand slam on the… the Western blot on patients, and I’d also have a grand slam on the LUAT, and their medical doctors would say, oh, that doctor in the lab are probably in cahoots change some lab. Dr. Deb 12:38Of course. David Jernigan 12:39That come in. And I still see that today. You know, it’s like, oh my gosh, the better the tests are getting. There’s still a bias if you do your own research. Well, if you happen to be a doctor who loves research. And you’re a clinician, so you actually treat patients who’s gonna write the research study? Well, of course, the doctor who did the study, well, he’s biased, and I’m like, I still can’t influence lab tests. Well, lab tests aren’t everything. People scream over the internet at me. It’s like, well, a negative lab test doesn’t mean anything. I was like… I get that with the old Western blot testing. Dr. Deb 13:16Right. David Jernigan 13:16The more sensitive tests, which are very close to 100%, Sensitivity, and 100% specificity. So, meaning, like, they can… if you have the infection, they’re gonna find it. Dr. Deb 13:30They’ll find it, yeah. David Jernigan 13:31And if they… if you have the infection, they’re going to be able to tell you exactly 100% correctly what kind of infection it is. Back in those days, you couldn’t, you could just count the dead pieces, which was… Dr. Deb 13:43Yeah. David Jernigan 13:43Significant, but It’s funny, because when medicine does that, you know, mainstream medicine that’s backed by all the nice foundations who donate millions of dollars towards the research. Their negative tests are significant, but if you fund your own, Yours isn’t that significant. Dr. Deb 14:04Right, or what if we call something a seronegative autoimmune disease, like lupus or rheumatoid arthritis, because none of the tests are positive, but you have all the symptoms. Here, let me give you this $100,000 a year drug. David Jernigan 14:19Yeah. Dr. Deb 14:19And instead of looking for what might actually be causing the symptoms. That’s all okay, but what we do is not okay. David Jernigan 14:27Right. Yeah, it’s a double standard, and it’s getting better. I want to do… tell the world it is getting better. Some of the dinosaurs are retiring. Dr. Deb 14:36No. David Jernigan 14:37Way for people who are… Are more open-minded to new ideas. But, getting back to that woman, she… that formula that I made just for her and her son, I… She went online. Dr. Deb 14:54Which, I had never been on a news group. David Jernigan 14:58Not even sure I knew what one was, you know? Imagine, I’m kind of that dinosaur that… Cell phones were, like, these really big things with a big antenna sticking out of it, and… Dr. Deb 15:09Nope. David Jernigan 15:10So I thought I was pretty hot stuff, just that I actually had a computer software program that was running my front desk. And even then, it was an Apple IIe computer. Dr. Deb 15:21Right. David Jernigan 15:22Probably be pretty valuable right now if I’d kept it, but… Dr. Deb 15:25Mmm… David Jernigan 15:26It being an antique. But, suddenly people were calling my clinic, because the lady with the twin boys that was well was telling people on these research, I mean, these Lyme disease forums and boards online. And, I started going, oh my gosh, you know, as a doctor, it’s one thing to treat a person in your clinic, it’s a different thing to have your clinic name on the label. Like, we all do, Even now, and you’re supposed to write everything that’s on the label, and… all these guidelines, and I’m like, wow, I need to split this off. I mean, I def… I definitely want to help people, and this is… I was pretty excited about the results we were getting. Pre-treat… Pre-treatment and post-treatment. And, so… that’s where I developed, my nutraceutical business in the 90s called Journey Good Nutraceuticals. My advice to anybody thinking about doing the same thing, don’t put your last name on it. Dr. Deb 16:25– David Jernigan 16:25You know, because anytime negative anything comes out, there goes the Jernigan name, you know, the herbal, you know, there’s just all these, and especially nowadays, with all the bots that are just designed to slam natural medicine. Dr. Deb 16:38Yeah. David Jernigan 16:39And that is out there in a… and just ugly people. Dr. Deb 16:42Or should we just say, people with a different opinion? How’s that? David Jernigan 16:46Yeah. That are being less than supportive. Dr. Deb 16:49But. David Jernigan 16:51It was amazing, because by 1999, I presented my research, my first research, I’d never done research. This is what I would… I would say to a lot of people who go, my doctor did… I don’t know, my doctor doesn’t know what you’re doing, my doctor… I was like going, you know, most doctors don’t do research. They don’t publish anything. Their opinion is their opinion, but they don’t back it up in peer review, right? And so that’s what I always tried to do, was back it up in peer review and publish. And so, in 1999, I presented at the International Tick-Borne Diseases Conference in New York City. I’m telling you, it was like the country boy going to the city, you know, I got my… I got my suit on, and I looked all right, and my booth was wonderful, and all these different things, and it was just a big wake-up call.Because what we had demonstrated… let’s get back to the… and this was what I demonstrated with that first study. was that… A positive LUAC test, that Lyme urine antigen test for my Gen X, was a score of 32. Meaning, one of those 3 mornings urine had 32 pieces in the amount of urine they checked of deadline bacteria spirochetes. Okay? Okay. With antibiotic challenges, a highly positive was a score of 45. Dr. Deb 18:19Wow when I would give one dropper 3 times a day for a week. David Jernigan 18:24Ahead of time, and then do the person’s LUAT test, We were getting scores 100, 200… And at that point, we only had a couple, but we had a couple that were greater than 400. Yeah, dead pieces, where the lab just quits counting. They just said, somewhere over 400, right? Dr. Deb 18:45Yeah. David Jernigan 18:46Which, when the medical system at the conference, you know, I was the only natural doctor in the world that was… had any kind of proof of anything naturally that could outperform antibiotics. Can you imagine? Dr. Deb 18:59Yeah. And… David Jernigan 19:01They were just, oh my gosh, incredulous. They’re like, I’ve given the most… one guy came up to me, and to my face, and he goes, I’ve given the most aggressive antibiotic protocols And I’ve only seen one patient over 100. I was like, that makes this pretty significant, doesn’t it? But, it didn’t just, like, make us take off, because guess what? In Lyme world, if a pharmaceutical antibiotic made you feel horrible. That meant it was working. Dr. Deb 19:28That’s right. We used to, back in the day, if you didn’t herx. And had that horrible die-off reaction, for those of you who don’t know what a herx is, but if we didn’t make you herx, we weren’t doing our job right. David Jernigan 19:40You’re looking for your patients to feel horrible, and sometimes to the level of committing suicide. Dr. Deb 19:46Yes. David Jernigan 19:47So bad. Dr. Deb 19:48Yes. David Jernigan 19:49And I was the first doctor, I think, in the world to start screaming and hollering and saying, stop using the worsening of your patient’s symptoms as a guide to good treatment, because they’re… I wasn’t seeing it with my formulas. Because I was doing a comprehensive program of care. I think I was also one of the first doctors to say, we need to detoxify these people as we’re doing this. And you would sit there and say, well, sure you were. I was like, well, remember, there wasn’t a lot of communication. There wasn’t anybody on the internet saying, do this, do that. And, It was, it was interesting in those days. It was, how do you… How do you help the world heal from these things? That they don’t know they have. So later, I actually had a beautiful booth at a health… a big health expo in Texas, I remember, and I was like, you know, you spend a lot of money on the booth, and… Dr. Deb 20:43Yup. David Jernigan 20:43And you’re thinking about it because you’re funding the whole thing, you say, wow, if I only sell one case, I’ll at least cover my cost. Dr. Deb 20:51Yep. Yeah, you’re great. David Jernigan 20:52And I had this beautiful banner of, like, a blown-up tick’s mouth under microscope. You know those beautiful pictures of, like, all the barbs sticking out, and how they anchor themselves in your skin, and… And, thousand people walking by my booth, and they’re just like, keep walking, because they didn’t know they had Lyme. There was, like, and they had MS, maybe, but they don’t have Lyme, and so they just would keep walking. Nobody even knew. Why would I go to a conference in Texas? And I’m trying to say, no, guys, it’s everywhere. Dr. Deb 21:24Yeah. David Jernigan 21:24And… and everybody, you know, yes, you probably have this, you know, kind of thing. If you’re… if you… are chronically ill, almost, of any kind of way. You know, kind of trying to tell people this was… Again, in Robin’s pathology textbooks, one of the few things that it did tell you about Lyme was that it was called the Great… the New Great Imitator. Because it would imitate up to 200 or more different illnesses. So, it’s been an interesting journey, of… educating people, writing articles, but it was interesting, the lady who I first fixed, Laboratory verified, everything like that, symptoms went away, all that kind of fun stuff. Her children were fine, they’ve been fine for years now. When she went on the newsboards in the Lyme disease support groups, It created a war. Oh my goodness, it was like, how dare you? And, say that something natural might actually help, right? Dr. Deb 22:30Right, exactly. David Jernigan 22:32And, I even had… A… one of those first calls to… with a marketing company at one point, way a long time ago. And the lady got on the phone, the owner of the marketing company goes, I would have blood on my hands if I actually took your clinic on. Yeah, you can’t treat Lyme disease, and… Even the big, big associations that are out there are still largely that way. I mean, they’re getting better, but it’s just like… you know, a lot of the times, it’s herbs are good. Herbs will help. Good, you know, but they’re safe. So, it’s still a challenge to… to… present in mainstream Lyme communities, even. Because there’s this… Fear of doing anything outside of antibiotics. Dr. Deb 23:32Yeah, so let me ask you this. From your perspective. Why do you think so many chronic infections exist these days, like Lyme and the co-infections, Babesia, Bartonella, mold illness? And we talked a little bit about herbs and why they, antibiotics and things like that fail, but let’s talk a little bit about that. David Jernigan 23:53So, it’s fascinating. When I trained in Germany, they said that we, as humanity, has moved away from what they called the inflammatory diseases. You know, in the old days, it was. Lots of high fevers, purulent, pus-generating bacterial infections. And I said, as a society, we have… Dr. Deb 24:14Have shifted from those to what they call cold sclerotic diseases, which are your… David Jernigan 24:21Cancers, your diabetes, your atherosclerosis, your… and they said, we’re starting to see what used to only be geriatric diseases in our children. That’s how bad it’s gotten. We have suppressed fevers, we don’t… we don’t respect the wisdom of the human body. So, you know, the doctors say, step aside, body, I will fix this infection for you with this antibiotic. And so, what we’ve done with the, overuse of antibiotics, and this isn’t me just talking from a natural perspective, this is… Right, it’s everybody around the world is acknowledging. I’ll show you… I could show you a, a presentation, if we can do a screen-sharing situation. Yeah. About the antibiotic situation in the world, because it’s really concerning. But what I would say, and kind of like an advancement forward, is we are seeing mutated bacteria. You know, they talked about… do you remember when they found the Iceman, you know, the… You know, the prehistoric guy that’s… In the eyes, and he had Lyme bacteria. I was like, he had spirochetes, maybe. Dr. Deb 25:33Yeah. David Jernigan 25:33That isn’t a modified, mutated version. That’s just maybe the… Lyme… you know, Borrelia… call it Borrelia something, you know, it’s a spirochete, but what we’re dealing with today. Even under strep or staph, as you know, you know, Pseudomonas aeruginosa, you name it, whatever kind of infection a person has is not the same bacteria that your grandparents dealt with. Dr. Deb 26:01That’s right. David Jernigan 26:32It’s a much mutated, stronger, more resistant to treatment type of thing. So, I think that’s one reason. I think the, It’s great that we’re seeing, you know, Secretary Robert F. Kennedy Jr. bringing awareness to things that Like it or not, yeah, seed oils do create inflammation, and everyone in the natural realm, as you know. Has been trying to say this for probably how long? Dr. Deb 26:35Yeah, 25, 30 years. 20 years each. David Jernigan 26:48Yes. You know, thank goodness for people like Sally Fallon and her beautiful book, Nourishing Traditions, that started you know, Dr. Bernard Jensen’s books way back in the day, Dr. Christopher’s books way back in the day. Dr. Deb 26:48Damn. David Jernigan 26:49You know, all of them were way ahead of their time, saying, by the way, your margarine is only missing one ingredient from being axle grease. Dr. Deb 26:58Yeah. David Jernigan 26:58I think that was Dr. Jensen saying that at one point, probably 50, 60 years ago, I don’t know. Dr. Deb 27:03Yep. David Jernigan 27:04So, we’ve created this monster. We, we live in a very controlled environment, you know, of 72, 74 degrees at all times, we don’t sweat, we don’t have to work that hard, typically. You know, most of us aren’t out there like our ancestors were, so that’s making us more and more… Move towards the cold sclerotic diseases, of which even Lyme disease is, you know, which… Yes, it has inflammation, yes, but as a presentation, it’s very often associated with some of these Cold sclerotic diseases of mankind that we see now. Dr. Deb 27:46You have it. David Jernigan 27:47Yeah. Dr. Deb 27:48So, tell me, what is phage therapy? David Jernigan 27:52Well, may I show you a cool video? Dr. Deb 27:55Yeah, I’d love that. David Jernigan 27:56I did not make this video, this is just one of my favorites, because it’s from the National Institute of Health. Let’s see if I can just… Click the share screen thing. And get that to pop up. That’s not what I’m looking for, but it’s gonna be soon. Let’s go here… Alright, can you see that? Dr. Deb 28:18Yeah. David Jernigan 28:19Okay. Modern medicine faces a serious problem. Thanks in part to overuse and misuse of antibiotics, many bacteria are gaining resistance to our most common cures. Researchers are probing possible alternatives to antibiotics, including phages. So, bacteriophages, or we like to call them phages for short, are naturally occurring viruses that infect and kill bacteria. The basic structure consists of a head, a sheath, and tail fibers. The tail fibers are what mediate attachment to the bacterial cell. The DNA stored in the head will then travel down the sheath and be injected inside the cell. Once inside the cell, the phage will hijack the cellular machinery to make many copies of itself. Lastly, the newly assembled phages burst forth from the bacterium, which resets their phage life cycle and kills the bacterium in the process. Someday, healthcare providers may be able to treat MRSA and other stubborn bacterial infections using a mixture of phages, or a phage cocktail process would be first to identify what the pathogen is that’s causing the infection. So the bacterium is isolated and is characterized. And then there’s a need to select a phage in a process known as screening of phage that are either present in a repository or in a so-called phage library. That allows for many of the phages to be evaluated for effectiveness against that isolated I don’t know, bacterium. Phages were first discovered over 100 years ago by a French-Canadian named Felice Derrell. They initially gained popularity in Eastern Europe, however, Western countries largely abandoned phages in favor of antibiotics, which were better understood and easier to produce in large quantities. Now, with bacteria like these gaining resistance to antibiotics, phage research is gaining momentum in the United States once again. NIAID recently partnered with other government agencies to host a phage workshop, where researchers from NIH, FTA, the commercial sector, and academia gathered to discuss recent progress. NIH… So… That is… That is what phage therapy in… is. in what I call conventional phage. Let’s see, how do I get out of the share screen? Hope you already don’t see it. Dr. Deb 30:58Yep, at the top, there should just be a button. David Jernigan 31:00I don’t. Dr. Deb 31:00Stop sharing, yeah. David Jernigan 31:01So… Conventional phage therapy, as you just saw, is a lot like what it is that we’re doing, only the difference is they’re taking wild phages from the environment. They’re finding phages anywhere there’s, like, a lot of bacteria. And then they isolate those phages, and like he said, the gentleman at the very end said we put them in a library, and so there are banks of phages that they can actually now use, and One of the largest banks that I know of has about 700 different bacteriophages, or phages. In their bank that they can pull from. Dr. Deb 31:43Wow. Do you want to take a guess? David Jernigan 31:46How many bacteriophages they’ve identified are in the human gut, on average? Dr. Deb 31:52Oh my god, there’s gotta be more… David Jernigan 31:53Kinds, different kinds of phages, how many? Dr. Deb 31:56There’s gotta be millions. David Jernigan 31:57Well… In population, there’s… humongous numbers, numbers probably well beyond the trillions, okay? Hundreds of trillions, quadrillions, maybe, even. But in the gut, a recent peer-reviewed journal article said that there were 32,242 different types of bacteriophages that live naturally in your intestines, your gut. Dr. Deb 32:25Boom. David Jernigan 32:2632,000. Okay, so… If you read any article on phage therapy that’s in peer review, almost every single one in the very first paragraph, they use the same sentence. They go, Phages are ubiquitous in nature. They’re ubiquitous in nature. So my brain, when I find… when all this finally clicked together, and when we clicked together 5 years into my research, I could not get it to work for 5 years. I just kept going. But that sentence really got me going. I was, like, going, you know. If you look at what ubiquitous means, it says if Phages were the size of grains of sand. Like sand on the beach. They would completely cover the earth and be 50 miles deep. How crazy is that? Dr. Deb 33:24Wow. David Jernigan 33:25That’s how many phages are on the planet. There’s so many… they outnumber every species collectively on the planet. So, it’s an impossibility in my mind. I went, huh, it’s an impossibility that… You catching a, a sterile Bacteria, it’s almost an impossibility. Since the beginning of time, phages have been needing to use a reproductive host. And it’s very specific, so every kind of bacteria has its own kind of phage it uses as a reproductive host. Because phages are… and this is a clarification I want to make for people. just like in the old days, we were talking about the 90s, I talked to a veterinarian that had gotten in trouble with the veterinary board in her state. Dr. Deb 34:14Back in the old days. David Jernigan 34:16Because she gave dogs probiotics. And the board thought she was giving the dogs an infection so that she could treat them and make money off of the subsequent infection. Dr. Deb 34:28Oh my god. David Jernigan 34:29Nobody actually had heard of good, friendly bacteria in the veterinary world, I guess she said she had gotten in trouble, and she had to defend herself, that, no, I’m giving friendly, benevolent, beneficial bacteria. Okay, to these animals, and getting good results.So, phages… Are friendly, benevolent, beneficial viruses. That live in your body, but they only will infect a certain type of bacteria. So… What that means is if you have staff.Aureus, you know, Staphylococcus aureus bacteria. That bacteria has its own kind of phage that infects it called a staph aureus phage. E. coli has an E. coli phage. Each type of E. coli has its own phage, so Borrelia burgdurferi has its own Borrelia burgdurferi type of phage, whereas Borrelia miyamotoi alright? Or any of the other Borrelia species, or the Bartonella species, or the… you just keep going, and Moses has its own type of phage that only will infect that type of bacteria. So that’s… You know, when you realize, wow, why are we going to the environment Was my thought. Dr. Deb 35:54Yeah. David Jernigan 34:55Trying to find wild phages and put them into your body, and hopefully they go and do what you want them to do. What if we could trigger the phages themselves that live in your body to, instead of just farming that bacteria that it uses as a host, because what I mean by farming is the phages will only kill 40% of that population of bacteria a day. Dr. Deb 36:20Wow. David Jernigan 36:20And then they send out a signal to all the other phages saying, stop killing! Dr. Deb 36:24It’s like. David Jernigan 36:2560% of the bacteria population left to be breeding stock. It’s kind of like the farmer, the rancher, who… he doesn’t send his whole herd to the butcher. Dr. Deb 36:35Right. David Jernigan 36:36Just to, you know, he keeps his breeding stock. He sends the rest, right? So, the phages will kill 40% of the population every day, just in their reproduction process. Because once there’s so many, as you saw in the video, once the phage lands on top of the bacteria, injects its genetic material into the bacteria, that bacteria genetic engine starts cranking out up to 5,200 phages per bacteria. Dr. Deb 37:06I don’t know who counted all those… David Jernigan 37:08Inside of a bacteria, but some scientists peer-reviewed it and put it out there. that ruptures, and it literally looks like a grenade goes off inside of the bacteria. I wish I’d remembered to bring that video of a phage killing a bacteria, but it just goes, oof. And it’s just a cloud of dust. So, you’re breaking apart a lot of those different toxins and things. So… That’s… That was the impetus to me creating what I did. That and the fact that I looked it up, and I found out that phages will sometimes go… Crazy. I don’t know how to say it. Wiping out 100% of their host. And it could be a trigger, like change in the body’s pH levels, it could be electromagnetically done, you know, like, there’s been documentation of… I think it was, 50 Hz, electricity. Triggering one kind of phage to go… Crazy and annihilate its host population. There’s other ways, but I was, like, going, none of those fit me, you know? It’s not like I’m gonna shock somebody with a… Jumper cable or something to try to get phages to… to do that kind of thing. But the fact that it could be done, they can be triggered, they can switch and suddenly go crazy against their population. But what happens when they kill 100% of their host? The phages themselves die within 4 days. Dr. Deb 38:45Hmm. Because they can’t keep reproducing. David Jernigan 38:47There’s nothing to reproduce them, yeah. Dr. Deb 38:49Yeah. Especially… unless they’re a polyvalent phage, that means a phage that can segue and use. David Jernigan 38:54One or two other kinds of bacteria. To, as a reproductive host. But a lot of phages, if not the majority, are monovalent, which means they have one host that they like to use. And so… Borrelia, so… my study that I ended up doing, and I published the results in 2021, And it’s a small study, but it’s right in there at the high end, believe it or not, of phage research. Most phage research is less than 30 people. In the study. But, we did 26 people.And after one month of doing the phage induction that I invented, which only… Appears to only, induce or stimulate the types of phages that will do the job in your body. I don’t care what kind of phage it is. I don’t care if it’s a Borrelia phage, it may be a polyvalent phage that normally doesn’t use the Borrelia burgdurferi as its number one. Host, but it can. To go and kill that infection. And the fascinating thing is, there was a brand new test that came out at the same time I came out with the idea, literally the same weekend they presented. Dr. Deb 40:1511. David Jernigan 40:15ILADS conference in Boston in 2019. It was called the Felix Borrelia phage Test. So the Felix Borrelia phage test. Because Borrelia are often intracellular, right, they’re buried down in the tissue, they’re not often in the blood that much. And therefore, doing a blood test isn’t really that accurate. But you remember how there’s, like, potentially as many as 5,200 phages of that type erupt from each bacteria when it breaks apart. It’s way easier to detect those phages, because they’re now circulating, those 52, as you saw in the video. 5,200 different phages are now seeking out another Borrelia that they can infect. And so, while they’re out in circulation, that’s easy to find in the bloodstream. So, 77% of the people, so 20 out of 26, were tested after a 2-week period. After only a 4-day round of treatment. Because according to my testing, remember, I can actually test adjunctively to see if I can find any signatures for those kinds of bacteria. And I couldn’t after 4 days, so we discontinued treatment and waited Beyond the 4 days that would allow the phages themselves to die, so we waited about a week and a half.And redid the test. And 77%, so that 20 out of 26 of the people, were completely negative. Dr. Deb 41:50Wow. David Jernigan 41:52Which, you go, well, it’s just a blood test. Well, no, we actually had people that were getting better, like, they’d never gotten better before. We had one woman who was wheelchair-bound, and in two weeks was able to walk, and even ultimately wanted to work for my clinic. I’m just, like, going… Dr. Deb 42:07I didn’t want to write about all that. I wanted to write about the phages. I was like… David Jernigan 42:12article, I probably should have put some of those stories, because, Critics would say, well, you got rid of the infection, maybe, but… Did you fix the Lyme disease? Well, that’s… there’s two factors here that every doctor needs to understand. There’s the infection in chronic illness, there’s the infection, and then there’s the damage that’s been done. Because sometimes I have these people that would come in and say, well, Dr. Jernigan, it didn’t work for me, I’m still in the wheelchair. And I’m like, no, it worked. Repeat lab test over months says it’s gone, it’s gone, it’s gone. It’s like, we would follow, and 88% of the people we followed long-term were still negative, which is amazing to me. Dr. Deb 42:56And then they have to repair the damage. David Jernigan 42:59It’s the damages why you still have your symptoms. And that’s where the doctor has to get busy, right? Dr. Deb 43:06Right David Jernigan 43:06They were told erroneously by their doctor that originally treated them that they’d be well, they’d get out of the wheelchair, if he could actually kill all these infections. Dr. Deb 43:15It’s not true. David Jernigan 43:16Unless it’s caught early. So I love the analogy, and I’ve said it a thousand times.that Lyme disease and chronic infections are much like having termites in the wood of your house. If you find the termites early, then yeah, killing the infection, life goes back to normal, the storm comes and your house doesn’t fall down. But if it’s 20 years later. Killing the termites is still a grand idea. Right. But you have the damage in the wood that needs to be repaired as well. All the systems… when I talk about damage to the wood, I mean, like. All the bioregulatory aspects of the body, how it regulates itself, all the biochemical pathways, the metabolic pathways we all know about, getting the toxins that have been lodged in there for many years, stopping the inflammatory things that have been running crazy. Dealing with all those cytokines that are just running rampant through the body, creating this whole MCAS situation. Which are largely… Dr. Deb 44:21Coming from your body’s own immune cells called macrophages, which are not even… David Jernigan 44:26It’s not… a virus at all, it’s part of the immune system, it’s like a Pac-Man, and research shows that especially in spirochetes. There is no toxin. Now, I wrote 4 books. I think I wrote the very first book on the natural treatment of people with Lyme disease back in the 90s. Why did I write that? Not because I wanted to be famous, it’s a tiny book, actually, the first one was.I was just trying to help people get out of this idea that you will be well when you kill all the bugs. I was saying, it’s… you need to be doing this. If you can’t come to my clinic, at least do this. Try to find somebody that will do this for you. And that ultimately led to a bigger book.as I kept learning more, and I was like, going, well, okay, now at least do this amount of stuff. And you need to make sure your doctor is handling this, this, this, and this. And so, the third book was, like, 500 and something pages long. And then the fourth book was 500 and something pages long, and now they’re all obsolete with the whole phage thing, because this just rewrites everything. Dr. Deb 45:34Yeah. David Jernigan 45:34It’s pretty fascinating. Dr. Deb 45:37Do you think the war on bugs, mentality created more chronic illness than it solved? David Jernigan 45:44Because of the tools that doctors had to use, yes. We’re a minority, we’re still a minority, you and I. Dr. Deb 45:54Yep. Our doctoring… David Jernigan 45:56Methods I never had, and you’d never… maybe you did, but I’d never had the ability to grab a prescription pad and write out a prescription. I had to figure out, how do I get… and this was… and still my guiding thing, is like, how do I identify, number one, everything that can be found that’s gone wrong in the human body. And what do I need to provide that body? Like, the body is the carpenter. That has to do the repair, has to regenerate, has to do everything, has to get… everything fixed right? We can’t fix anything. If you have a paper cut, there isn’t a doctor on the planet that can make that go away. Dr. Deb 46:38Right. David Jernigan 46:39Of their own power, much less chronic illnesses. So, all the treatments are like the screws, saws, hammers, you know the carpenter must be able to use. So a lot of the time, doctors are just throwing an entire Home Depot on top of the carpenter. In the form of, like, bags of supplements, you know, hundreds of supplements, I’ve seen patients walk in my door with two suitcasefuls. And they were taking 70 bottles, 65 to 70 bottles of supplements, and I’d be just like, wow, your carpenter who’s been working for 24 hours a day, 7 days a week. He’s exhausted. There’s chaos everywhere, you don’t know where to. Dr. Deb 47:22Starting. David Jernigan 47:22He goes, you want me to do what with all this stuff? Dr. Deb 47:25Yep, I’ve seen the same thing. People… thousands, you know, several thousand dollars a month on supplements, and not any better. But they’re afraid to give up their supplements, too, because they don’t want to go backwards, either, and… there’s got to be a better way on both sides, the conventional side and the alternative side, although you and I don’t say it’s alternative, that’s the way medicine should be, but… David Jernigan 47:48Right. Dr. Deb 47:49We have to have a good balance on both sides. David Jernigan 47:52And I will say, too, in defense of doctors using a lot of supplements, I do use a lot of supplements. Dr. Deb 47:57Yeah, I do too. David Jernigan 47:58but I want to synergize what I’m giving the patient so that the carpenter isn’t overwhelmed and can actually get the job done. Like, everything has to work harmoniously together, so it’s not that… It’s not the number of supplements, and why would you need a lot of supplements? Well, because every system in your body is Messed up. My kind of clientele for 30 years. Our clientele, yours and mine. Dr. Deb 48:25Yeah. David Jernigan 48:26They have been sick, For decades, many of them. Dr. Deb 48:31Yeah. David Jernigan 48:31And if they went into a hospital, they honestly need every department. They need endocrinology, they need their kidney doctor, they need their… They’re a cardiologists, they need a neurologist, they need a rheumatologist. I mean, because none of those doctors are gonna deal with everything. They’re just gonna deal with one piece of the puzzle. And if they did get the benefit of all the different departments they need, yeah, they’d go out with a garbage bag full of stuff, too. Dr. Deb 48:57Hey, wood. David Jernigan 48:58Only, they’re not synergized. They don’t work together. You’re creating this chemistry set of who knows how much poison. And I want to tell your listeners, and I mean, you probably say this to your patients as well. There is a law of pharmacy that I learned eons ago, and it applies to natural medicine, too. Dr. Deb 49:21Yep. David Jernigan 49:22But the law says every drug’s primary side effect Is its primary action. So, if you listen to TV, you can see this on commercials. I love… I love listening to these commercials, because I’m like, wow. let’s… let’s… I don’t want to say I’ve named Brandon. I don’t know if that’s…Inappropriate to name a name brand, but let’s just say you have a pharmaceutical that is for sleep. After they show you this beautiful scene of the person restfully sleeping and everything like that, they tell you the truth. It’s like, this may cause sleepiness… I mean, sleeplessness. Dr. Deb 50:04Yeah. David Jernigan 50:04Found insomnia. Dr. Deb 50:06And headaches, and diarrhea. David Jernigan 50:08All the other things, and if it’s an antidepressant, what does the commercial do after it finishes showing you little bunny foo-foo, jumping through a green, happy people? They tell you, this may create depression, severe depression, and suicidal tendencies, which is the ultimate depression. So, I want everyone to understand you need to figure out what your doctor’s tools are that they’re asking you to take, and they’re wanting you to take it forever, generally in mainstream medicine, right? In the hospitals and everything. They don’t say, hey, your heart has this condition, take this medicine for 3 months, after which time you can get off. Dr. Deb 50:48Yep. David Jernigan 50:49not fixing it, right? So… That, on a timeline, there is a point, if it was truly even fixing anything. That you… it’s done what it should do, and you should get off, even if it’s a natural product. It’s just like. Dr. Deb 51:03Right David Jernigan 51:03It’s done what it should do, and you should get off, but instead. you go through the tree… the correction and out the other side, and that’s where it starts manifesting a lot of the same problems that it had. So, anti-inflammatories, painkillers, imagine the number one side effects are pain inflammation. So, the doctor says, well. If you say, hey, I’m having more pain, what does he do? He ups the dosage. And if he… if that doesn’t work, if you’re still in a lot of pain, which he would be, he changes it to a more powerful thing, right? But it starts the cycle all over again. So when you ask me, it’s like, why are we having so much chronic illness? It’s because of the whole philosophy. is the treatment philosophy of mainstream medicine that despises what you and I do. Because we’re… our philosophy from the start is the biggest thing. It’s like… We’re striving for cure. That dirty four-letter word, cure, we’re not even supposed to use it. And yet, if you look it up in Stedman’s Medical Dictionary, it just means a restoration of health. Remission. Everyone’s like, oh, I’m in remission. I’m like, remission is a drug term. It’s a medical term. Again, look it up in a medical dictionary. It is a pharmaceutical term for a temporary pause Or a reduction of your symptom, but because it’s just… symptom suppression, it will come back. It’s… remission is great, I suppose, in… At the end of, like, where you’ve exhausted everything, because I can’t fix everything, I don’t know about you. Dr. Deb 52:41No, I can’t either, yeah. David Jernigan 52:43you know, on my phone consults, I try to always remind people, as much as I get excited about my technologies gosh, I see so much opportunity to fix you. I always try to go, please understand, I’m gonna tell you what most doctors may not tell you on a phone consultation. I can’t fix everything. Dr. Deb 53:03Yeah. David Jernigan 53:03For all of my tricks, I can’t fix everything. Not tricks, but you know, all my technologies, and all my inventions. Phages, too. They are a tool. You know, antibiotics. I think I wrote a blog one time, it should be on my website somewhere, that says, Antibiotics do not… fix… neurological disease, or… I don’t know, something like that. You know, you’re using the wrong tool. I mean, it does what it does. Dr. Deb 53:32Yeah, you’re using a hammer to do what a screwdriver needs to. David Jernigan 53:35Yeah, you know, it’s like it’s… And yet, you can probably tell her… that you’ve had patients, too, that they go, Dr. Jernigan. My throat was so sore, and as soon as I swallowed that antibiotic. I felt better, and I’m, like, going… How long did it take? Oh, it was immediate! I was like, dude, the gel cap didn’t even have time to dissolve, I mean… Dr. Deb 53:58SIBO. David Jernigan 54:00But, it’s not going to repair the tissues that were all raw. kind of stuff. So, I mean, that ulceration of your throat that’s happening, the inflammation, there’s no anti-inflammatory effect of these things. So, I digress a little bit, but phages, too… I wrote an article that’s on the website, that’s setting healthy expectations for phages, because they want… we can see some amazing things happen, things that in my 30 years, I wish I had all my career to do over again, now having this tool. It’s just that much fun. I… when doctors around the country now are starting to use our inducent formulas, there’s, 13 of them now, formulas. For different broad-spectrum illness presentations. I tell them all the same thing, I was like, you are gonna have so much fun. Dr. Deb 54:53That’s exciting. Women. David Jernigan 54:54Winning is fun, you know? I was like. You know, mainstream medicine may never accept this, I don’t know. I feel a real huge burden, though, to do my best to follow a, very scientific methodology. I’ve published as much as I can publish at this time by myself. I never took money from the… the sources that are out there, because what do they do? They always come… money comes with strings. Dr. Deb 55:22Yes, it does. David Jernigan 55:23I don’t trust… I don’t trust… I mean, if you listen to the, roundtable that Our Secretary Robert F. Kennedy Jr. Dr. Deb 55:35Yeah. David Jernigan 55:36On Lyme disease last week the first couple of speakers were, like, pretty legit. I mean, all of them were legit, but I mean, they were, like, senators and congressmen or something like that, I think. And then you have… RFK Jr. himself, who’s legit. Yeah they were fessing up to the fact that, yes, they were suppressing anything to do with Lyme. Dr. Deb 56:00Yeah. David Jernigan 56:00Our… our highest levels of, marbled halls and pillars and… of medicine were doing everything the way I thought they were. They were suppressing me. I was like, how can you ignore the best formulas ever, and still, I think Borreligen, and now, induced native phage therapy are still, I believe, I don’t… I’ve never seen it, I could be wrong. The only natural things that have been documented in a medical methodology. Dr. Deb 56:34Hmm in the natural realm. I mean, all the herbs that we talk about. David Jernigan 56:39You know, there’s one that was really famous for a while, and it said, we gave… so many patients. This product, and other nutritional supplements. And at the end, X number of them were… dramatically better. That’s not research. Dr. Deb 56:57Right. That’s observation. David Jernigan 56:59The trick there was we gave this one thing, and then we gave high-dose proteolytic enzymes, we gave high dose this, we gave high dose that, but at the end of the study, we’re going to point back at the thing we’re trying to sell you as being what did it. Dr. Deb 57:12Which is what we do in all research, pretty much. David Jernigan 57:15Well… Dr. Deb 57:16tried to… David Jernigan 57:17Good guys, I hope. Dr. Deb 57:18Do the way we want, right? In… in conventional… David Jernigan 57:22Yeah. Dr. Deb 57:22Fantastic David Jernigan 57:23Very often, yeah, in conventional medicine, definitely. Yeah. And, it’s kind of scary, isn’t it, how many pharmaceuticals are slamming us with, because they’re… Dr. Deb 57:33Okay. David Jernigan 57:34There’s a new one on TV every day, and there’s. Dr. Deb 57:36Every day, yes. David Jernigan 57:37It’s like, who comes up with these names? They’re just horrible. Dr. Deb 57:40Yeah, you can’t pronounce them. David Jernigan 57:41I want to be a marketing company and come up with some Zimbabwehika, or something that actually they go with, and I’m like, I just made a million bucks coming up with it. I’ll be glad when that’s not on the TV anymore, which… Oh, me too. Me too. Dr. Deb 57:54Dr. Jaredgen, this was really wonderful. What do you want to leave our listeners with? David Jernigan 58:00Well, you know, everyone’s calling for a new treatment. Dr. Deb 58:05Yeah. You bet. David Jernigan 58:08I have done everything I can do to get it out there, scientifically, in peer review, so that if you want to look up my name. Dr. Deb 58:16I published an open access journal so that you didn’t have to buy the articles. Like, PubMed, you have to be a member. If you want to look at a lot of the research, you have to buy the articles. David Jernigan 58:26I’ve done everything open access so that people had access to the information. I honestly created induced native phage therapy to fix my own wife. I mean, I… I was… I used to think I could actually fix almost anything. Gave me enough time. And, I could not fix her. You know, the first 10 years, she was bedridden. Dr. Deb 58:49Wow. David Jernigan 58:50People go, oh, it’s easy for you, Dr. Jernigan, you’re a doctor. Dr. Deb 58:54Oh yeah, right? Yeah. David Jernigan 58:56Oh my gosh, how many tears have been shed, and how much heartache, and how much of this and that. I mean, 90% of our marriage, she was in, bed, just missing Christmas. All the horror stories you hear in the Lime world, that was her, and I could not get her completely well. And, she’s a very discerning woman. I say that in all my podcasts, because it’s. Dr. Deb 59:19Just… David Jernigan 59:16Amazing. It’s like, every husband, I think, should want a wife that’s… Always, right? Not that you surrender your own opinion, but it’s like, it’s… it was literally, I don’t know what, 6 months before the ILADS conference in Boston in 2029… in 2019 that She said, are you going to the ILADS conference this year? And I’m like, I’ve been going for, like, 15, 20 years, however long it’s been going on, and I was like, I’m not gonna go to this one. And, 3 days before the conference, she says, I think you should go. And I go, okay. Like I say, she’s generally right. And that… I bought a Scientific American magazine at the newsstand in the Nashville airport. Started reading a story about phages in that that copped that edition of the Scientific American, and It was a good article, but it wasn’t super meaty, you know. very deep on those, but I just was stimulated. Something about being at elevation. Dr. Deb 1:00:02Yeah. Your own mountains, I don’t know, I get all inspired. David Jernigan 1:00:25And I wrote in the margins and highlighted this and that until it was, like, ultimately, I spent the entire conference hammering this out. And it worked. And it’s been working, it’s just amazing. It’s… We’re over 200 different infections that we’ve… we’ve clinically or laboratory-wise documented. There’s a new test for my GenX called the CEPCR Lyme Panel. like, culture. 64 different types of infections, and I believe right now the latest count is something like 10 for 10 were completely negative. Dr. Deb 1:01:03Wow. David Jernigan 1:01:03These chronically infected people. And so, that hadn’t been published anywhere. So, in my published article, remember I was talking about that 20 out of the 26 were tested as negative for the infection? That doesn’t mean they’re cured, okay? Remember, they’re chronically damaged. That’s how we need to look at it. Dr. Deb 1:01:23funny David Jernigan 1:01:24damaged. You’re not just chronically infected. And, but with 30-day treatment.24 out of the 26 were tested as negative. Dr. Deb Muth 1:01:34That’s amazing. David Jernigan 1:01:35So 92% of the people were negative.Okay? The chances of that happening, when you run it through statistical analysis.The chances… when you compare the results to the sensitivity percentages, you know, the 100% specificity and 92% sensitivity of the…Of the lab testIt’s a 4.5 nonillion to 1 chance that it was a fluke. Isn’t that amazing? Now, nearly… I’m not even sure how many zeros that is, but it’s a lot. Dr. Deb Muth 1:02:08That’s is awesome. David Jernigan 1:02:09Like, if I just said, well, it’s a one in a million chance it was a fluke.Okay.So, lab tests don’t lie. You’re not done, necessarily, just because you got rid of the infections. Now that formula for Lyme has grown to be 90-plusmicrobes targeted in the one formula. So, we figured out we can actually target individually, but collectively, almost like an antibiotic that’s laser-guided to only go after the bad guys that we targeted.So, all the Borrelia types are targeted, all the Babesias, for,the Bartonellas, the anaplasmosis, you name it, mycoplasma types are all targeted in that one formula, because I said.Took my collective 30 years of experience and 15,000 patients.that I would typically see as co-infections and put them into that one formula, so…When we get these tests coming back that are testing for 64, it’s because of that.So, there’s a lot of coolnesses that I could actually keep going and going. Dr. Deb Muth 1:03:15That’s exciting. David Jernigan 1:03:15I love this topic, but I thank you for letting me come on. Dr. Deb Muth 1:03:18Thank you for joining us. How can people find you? David Jernigan 1:03:22Two ways. There’s the Phagen Corp company that is now manufacturing my formulas.That is P-H-A-G-E-N-C-O-R-P dot com. Practitioners can go there, and there’s a practitioner side of the website that’s very beefy with science, and… and all the formulas that were used, what’s inside of all the formulas, meaning what microbes are targeted by each one. Like, there’s a GI formula, there’s a UTI formula, there’s a SIRS formula, there’s a Lyme formula, there’s a central nervous system type infection formula, there’s… And we can keep going, you know, SIBO, SIFO formula, mold formula… I mean, we’ve discovered so many things that I could just keep going for hours, and… Dr. Deb Muth 1:04:05Yeah. David Jernigan 1:04:06About the discoveries, from where it started in its humble beginnings, To now, so… There’s another way, if you wanted to see our clinic website, is Biologics, with an X, so B-I-O-L-O-G-I-X, Center, C-E-N-T-E-R dot com. And, if somebody thinks they want to be a patient and experience this at our clinic, typically we don’t take just Easy stuff. All we see is chronic.Chronic cases from all over the world. Something like 96% of our patients come from other states and countries. And typically, I’ve been close to 90% for my whole career.About 30-something percent come from other countries in that, so… we’ve gotten really good and learned a lot in having to deal with what nobody else knows what to do with. But if you do want to do that, you can contact us. And, if you… If you don’t get the answers from my patient care staff, then I do free consultations. With the people that are thinking about, whether we can help them or not. Dr. Deb Muth 1:05:13Well, that’s excellent. For those of you who are driving or don’t have any way of writing things down, don’t worry about it, we’ve got you. We will have all of his contact information in our show notes, so you will be able to reach out to him. Thank you again for joining me. This has been an amazing conversation. David Jernigan 1:05:30Thank you, I appreciate you having me on. It was a lot of fun. The post Episode 252 – Induced Native Phage Therapy (INPT) & advanced natural therapies first appeared on Let's Talk Wellness Now.

Osteomyelitis in children is common enough to miss and serious enough to matter. In this episode of PEM Currents, we review a practical, evidence-based approach to pediatric acute hematogenous osteomyelitis, focusing on diagnostic strategy, imaging decisions including FAST MRI, and modern antibiotic management. Topics include age-based microbiology, empiric and pathogen-directed antibiotic selection with dosing, criteria for early transition to oral therapy, and indications for orthopedic and infectious diseases consultation. Special considerations such as MRSA, Kingella kingae, daycare clustering, and shortened treatment durations are discussed with an emphasis on safe, high-value care. Learning Objectives After listening to this episode, learners will be able to: Identify the key clinical, laboratory, and imaging findings that support the diagnosis of acute hematogenous osteomyelitis in children, including indications for FAST MRI and contrast-enhanced MRI. Select and dose appropriate empiric and pathogen-directed antibiotic regimens for pediatric osteomyelitis based on patient age, illness severity, and local MRSA prevalence, and determine when early transition to oral therapy is appropriate. Determine when consultation with orthopedics and infectious diseases is indicated, and recognize clinical features that warrant prolonged therapy or more conservative management. References Woods CR, Bradley JS, Chatterjee A, et al. Clinical practice guideline by the Pediatric Infectious Diseases Society and the Infectious Diseases Society of America: 2021 guideline on diagnosis and management of acute hematogenous osteomyelitis in pediatrics. J Pediatric Infect Dis Soc. 2021;10(8):801-844. doi:10.1093/jpids/piab027 Woods CR, Bradley JS, Chatterjee A, et al. Clinical practice guideline by the Pediatric Infectious Diseases Society and the Infectious Diseases Society of America: 2023 guideline on diagnosis and management of acute bacterial arthritis in pediatrics. J Pediatric Infect Dis Soc. 2024;13(1):1-59. doi:10.1093/jpids/piad089 Stephan AM, Platt S, Levine DA, et al. A novel risk score to guide the evaluation of acute hematogenous osteomyelitis in children. Pediatrics. 2024;153(1):e2023063153. doi:10.1542/peds.2023-063153 Alhinai Z, Elahi M, Park S, et al. Prediction of adverse outcomes in pediatric acute hematogenous osteomyelitis. Clin Infect Dis. 2020;71(9):e454-e464. doi:10.1093/cid/ciaa211 Burns JD, Upasani VV, Bastrom TP, et al. Age and C-reactive protein associated with improved tissue pathogen identification in children with blood culture-negative osteomyelitis: results from the CORTICES multicenter database. J Pediatr Orthop. 2023;43(8):e603-e607. doi:10.1097/BPO.0000000000002448 Peltola H, Pääkkönen M. Acute osteomyelitis in children. N Engl J Med. 2014;370(4):352-360. doi:10.1056/NEJMra1213956 Transcript This transcript was provided via use of the Descript AI application Welcome to PEM Currents, the Pediatric Emergency Medicine Podcast. As always, I'm your host, Brad Sobolewski, and today we're covering osteomyelitis in children. We're going to talk about diagnosis and imaging, and then spend most of our time where practice variation still exists: antibiotic selection, dosing, duration, and the evidence supporting early transition to oral therapy. We'll also talk about when to involve orthopedics, infectious diseases, and whether daycare outbreaks of osteomyelitis are actually a thing. So what do I mean by pediatric osteomyelitis? In children, osteomyelitis is most commonly acute hematogenous osteomyelitis. That means bacteria seed the bone via the bloodstream. The metaphysis of long bones is particularly vulnerable due to vascular anatomy that favors bacterial deposition. Age matters. In neonates, transphyseal vessels allow infection to cross into joints, increasing the risk of concomitant septic arthritis. In older children, those vessels involute, and infection tends to remain metaphyseal and confined to bone rather than spreading into the joint. For children three months of age and older, empiric therapy must primarily cover Staphylococcus aureus, which remains the dominant pathogen. Other common organisms include group A streptococcus and Streptococcus pneumoniae. In children six to 36 months of age, especially those in daycare, Kingella kingae is an important and often underrecognized pathogen. Kingella infections are typically milder, may present with lower inflammatory markers, and frequently yield negative routine cultures. Kingella is usually susceptible to beta-lactams like cefazolin, but is consistently resistant to vancomycin and often resistant to clindamycin and antistaphylococcal penicillins. This has direct implications for empiric antibiotic selection. Common clinical features of osteomyelitis include fever, localized bone pain, refusal to bear weight, and pain with movement of an adjacent joint. Fever may be absent early, particularly with less virulent organisms like Kingella. A normal white blood cell count does not exclude osteomyelitis. Only about one-third of children present with leukocytosis. CRP and ESR are generally more useful, particularly CRP for monitoring response to therapy. No single CRP cutoff reliably diagnoses or excludes osteomyelitis in children. While CRP is elevated in most cases of acute hematogenous osteomyelitis, the Pediatric Infectious Diseases Society and the Infectious Diseases Society of America note that high-quality data defining diagnostic thresholds are limited. A CRP above 20 milligrams per liter is commonly used to support clinical suspicion, with pooled sensitivity estimates around 80 to 85 percent, but no definitive value mandates the diagnosis. Lower values do not exclude disease, particularly in young children, as CRP is normal in up to 40 percent of Kingella kingae infections. CRP values tend to be higher in Staphylococcus aureus infections, especially MRSA, and higher levels are associated with complications such as abscess, bacteremia, and thrombosis, though specific cutoffs are not absolute. In summary, CRP is most useful for monitoring treatment response. It typically peaks two to four days after therapy initiation and declines rapidly with effective treatment, with a 50 percent reduction within four days seen in the majority of uncomplicated cases. Blood cultures should be obtained in all children with suspected osteomyelitis, ideally before starting antibiotics when feasible. In children, blood cultures alone can sometimes identify the pathogen. Plain radiographs are still recommended early, not because they're sensitive for acute osteomyelitis, but because they help exclude fracture, malignancy, or foreign body and establish a baseline. MRI with and without contrast is the preferred advanced imaging modality. MRI confirms the diagnosis, defines the extent of disease, and identifies complications such as subperiosteal abscess, physeal involvement, and concomitant septic arthritis. MRI findings can also guide the need for surgical consultation. Many pediatric centers now use FAST MRI protocols for suspected osteomyelitis, particularly from the emergency department. FAST MRI uses a limited sequence set, typically fluid-sensitive sequences like STIR or T2 with fat suppression, without contrast. These studies significantly reduce scan time, often avoid the need for sedation, and retain high sensitivity for bone marrow edema and soft tissue inflammation. FAST MRI is particularly useful when the clinical question is binary: is there osteomyelitis or not? It's most appropriate in stable children without high concern for abscess, multifocal disease, or surgical complications. If FAST MRI is positive, a full contrast-enhanced MRI may still be needed to delineate abscesses, growth plate involvement, or adjacent septic arthritis. If FAST MRI is negative but clinical suspicion remains high, further imaging may still be necessary. The Pediatric Infectious Diseases Society and the Infectious Diseases Society of America recommend empiric antibiotic selection based on regional MRSA prevalence, patient age, and illness severity, with definitive therapy guided by culture results and susceptibilities. Empiric therapy should never be delayed in an ill-appearing or septic child. In well-appearing, stable children, antibiotics may be briefly delayed to obtain imaging or tissue sampling, but this requires close inpatient observation. For children three months and older with non–life-threatening disease, empiric therapy hinges on local MRSA rates. In regions with low community-acquired MRSA prevalence, generally under 10 percent, reasonable empiric options include cefazolin, oxacillin, or nafcillin. When MRSA prevalence exceeds 10 to 20 percent, empiric therapy should include an MRSA-active agent. Clindamycin is appropriate when local resistance rates are low, while vancomycin is preferred when clindamycin resistance is common or the child has had significant healthcare exposure. For children with severe disease or sepsis, vancomycin is generally preferred regardless of local MRSA prevalence. Some experts recommend combining vancomycin with oxacillin or nafcillin to ensure optimal coverage for MSSA, group A streptococcus, and MRSA. In toxin-mediated or high-inoculum infections, the addition of clindamycin may be beneficial due to protein synthesis inhibition. Typical IV dosing includes cefazolin 100 to 150 milligrams per kilogram per day divided every eight hours; oxacillin or nafcillin 150 to 200 milligrams per kilogram per day divided every six hours; clindamycin 30 to 40 milligrams per kilogram per day divided every six to eight hours; and vancomycin 15 milligrams per kilogram every six hours for serious infections, with appropriate monitoring. Ceftaroline or daptomycin may be considered in select MRSA cases when first-line agents are unsuitable. For methicillin-susceptible Staphylococcus aureus, first-generation cephalosporins or antistaphylococcal penicillins remain the preferred parenteral agents. For oral therapy, high-dose cephalexin, 75 to 100 milligrams per kilogram per day divided every six hours, is preferred. Clindamycin is an alternative when beta-lactams cannot be used. For clindamycin-susceptible MRSA, clindamycin is the preferred IV and oral agent due to excellent bioavailability and bone penetration, and it avoids the renal toxicity associated with vancomycin. For clindamycin-resistant MRSA, vancomycin or ceftaroline are preferred IV agents. Oral options are limited, and linezolid is generally the preferred oral agent when transition is possible. Daptomycin may be used parenterally in children older than one year without pulmonary involvement, typically with infectious diseases and pharmacy input. Beta-lactams remain the drugs of choice for Kingella kingae, Streptococcus pyogenes, and Streptococcus pneumoniae. Vancomycin has no activity against Kingella, and clindamycin is often ineffective. For Salmonella osteomyelitis, typically seen in children with sickle cell disease, third-generation cephalosporins or fluoroquinolones are used. In underimmunized children under four years, consider Haemophilus influenzae type b, with therapy guided by beta-lactamase production. Doxycycline has not been prospectively studied in pediatric acute hematogenous osteomyelitis. There are theoretical concerns about reduced activity in infected bone and risks related to prolonged therapy. While short courses are safe for certain infections, the longer durations required for osteomyelitis increase the risk of adverse effects. Doxycycline should be considered only when no other active oral option is available, typically in older children, and with infectious diseases consultation. It is not appropriate for routine treatment. Many hospitals automatically consult orthopedics when children are admitted with osteomyelitis, and this is appropriate. Early orthopedic consultation should be viewed as team-based care, not failure of medical management. Consult orthopedics when MRI shows abscess or extensive disease, there is concern for septic arthritis, the child fails to improve within 48 to 72 hours, imaging suggests devitalized bone or growth plate involvement, there is a pathologic fracture, the patient is a neonate, or diagnostic bone sampling or operative drainage is being considered. Routine surgical debridement is not required for uncomplicated cases. Infectious diseases consultation is also often automatic and supported by guidelines. ID is particularly valuable for antibiotic selection, dosing, IV-to-oral transition, duration decisions, bacteremia management, adverse reactions, and salvage regimens. Even in straightforward cases, ID involvement often facilitates shorter IV courses and earlier oral transition. Osteomyelitis is generally not contagious, and clustering is uncommon for Staphylococcus aureus. Kingella kingae is the key exception. It colonizes the oropharynx of young children and spreads via close contact. Clusters of invasive Kingelladisease have been documented in daycare settings. Suspicion should be higher in children six to 36 months from the same daycare, with recent viral illness, mild systemic symptoms, refusal to bear weight, modest CRP elevation, and negative routine cultures unless PCR testing is used. Public health intervention is not typically required, but awareness is critical. There is no minimum required duration of IV therapy for uncomplicated acute hematogenous osteomyelitis. Transition to oral therapy should be based on clinical improvement plus CRP decline. Many children meet criteria within two to six days. Oral antibiotics must be dosed higher than standard outpatient regimens to ensure adequate bone penetration. Common regimens include high-dose cephalexin, clindamycin, or linezolid in select cases. The oral agent should mirror the IV agent that produced clinical improvement. Total duration is typically three to four weeks, and in many cases 15 to 20 days is sufficient. MRSA infections or complicated cases usually require four to six weeks. Early oral transition yields outcomes comparable to prolonged IV therapy with fewer complications. Most treatment-related complications occur during parenteral therapy, largely due to catheter-related issues. Take-home points: osteomyelitis in children is a clinical diagnosis supported by labs and MRI. Empiric antibiotics should be guided by age, illness severity, and local MRSA prevalence. Early transition to high-dose oral therapy is safe and effective when clinical response and CRP support it. Orthopedics and infectious diseases consultation improve care and reduce variation. FAST MRI is changing how we diagnose osteomyelitis. Daycare clustering is uncommon except with Kingella kingae. That's all for this episode. If there are other topics you'd like us to cover, let me know. If you have the time, leave a review on your favorite podcast platform. It helps more people find the show and learn from it. For PEM Currents, this has been Brad Sobolewski. See you next time.    

Dr. Don and Professor Ben talk about the risks of wearing "new" (to you) clothes without washing first. Dr. Don - not risky

Dr. Don and Professor Ben talk about the risks of holding raw chicken at room temperature "all day" before cooking. Dr. Don - risky ☣️ Professor Ben - risky ☣️ Staphylococcosis in Poultry - Poultry - Merck Veterinary Manual Evaluation of the Prevalence of Staphylococcus aureus in Chicken Fillets and Its Bio-Control Using Different Seaweed Extracts - PMC

Dr. Don and Professor Ben talk about the risks of making rare roast beef. Dr. Don - not risky

Dr. Don and Professor Ben talk about the risks of eating hand sliced Prosciutto ham stored at room temperature for months. Dr. Don - not risky

Hello to you listening in Sayville, New York!Coming to you from Whidbey Island, Washington this is Stories From Women Who Walk with 60 Seconds for Motivate Your Monday and your host, Diane Wyzga.The other day I was talking with my longtime friends, colleagues and brainstormers, Tania and Leanne, about times when we set out to achieve X but an unintended, better-than-expected Y happened. You know what I mean: the mystery of unintended consequences that turns out to be amazing!Here's one: The Scottish biologist Alexander Fleming  was working on a project on Staphylococcus bacteria at St. Mary's Hospital in London. He took off on vacation leaving behind an uncovered petri dish of bacteria. When he returned he saw a blue-green mold (like what you might find growing on bread exposed to moisture) growing on the dish and that the Staph bacteria were being killed in the area of the mold. Fleming - knowing a good thing when he saw one - identified the mold as the fungus penicillin notatum, and Shazaam! developed penicillin as an antibiotic. Fleming's unintended discovery of penicillin revolutionized the treatment of infections.Click HERE to learn more about the Discovery and Development of Penicillin 1928-1945Now, as to the moldy bread in your kitchen. Yes, penicillin is an antibiotic produced by a fungus called Penicillium notatum. Yes, this fungus is commonly found on moldy bread. Yes, when the fungus grows on bread, it releases penicillin into the surrounding environment.Let me caution you! Not all moldy bread contains penicillin. Moreover, eating moldy bread is a very big “No! No!” as it can contain harmful substances. Having said that think twice before you toss out what might be an unintended answer to a problem.  Question: When did you set out to achieve X but an unintended Y turned out to be what you were looking for?  What happened next?You're always welcome: "Come for the stories - Stay for the magic!" Speaking of magic, I hope you'll subscribe, share a 5-star rating and nice review on your social media or podcast channel of choice, bring your friends and rellies, and join us! You will have wonderful company as we continue to walk our lives together. Be sure to stop by my Quarter Moon Story Arts website, check out the Communication Services, arrange a no-obligation Discovery Call, and stay current with me as "Wyzga on Words" on Substack.Stories From Women Who Walk Production TeamPodcaster: Diane F Wyzga & Quarter Moon Story ArtsMusic: Mer's Waltz from Crossing the Waters by Steve Schuch & Night Heron MusicALL content and image © 2019 to Present Quarter Moon Story Arts. All rights reserved.  If you found this podcast episode helpful, please consider sharing and attributing it to Diane Wyzga of Stories From Women Who Walk podcast with a link back to the original source.

It's World AMR Awareness Week (WAAW) and we have prepared a special episode in light of that. In this week's Communicable, Navaneeth Narayanan and Thomas Tängdén host Aula Abbara (London, UK), Guido Granata (Rome, Italy) and Tuomas Aro (Helsinki, Finland) to discuss the phenomenon of AMR in conflict and crisis zones. They elaborate on how difficult conditions and austere environments amplify the spread of AMR, drawing on findings from the ongoing conflicts in Ukraine, Gaza, Syria and other regions. Other topics covered include adapting antimicrobial stewardship and infection prevention and control (IPC) practices as well as the need for genuine political will and international collaboration to end conflicts and their exacerbation on AMR.This episode follows the webinar “Beyond the frontlines” organised by ESCMID's AMR Action Subcommittee for WAAW 2025, featuring the same guests, and is available on ESCMID Media. This Communicable episode was peer reviewed by Arjana Zerja of Mother Theresa University Hospital Centre, Tirana, Albania.  Related ESCMID and Communicable mediaESCMID Media, Part 1: Beyond the frontlines - tackling AMR in conflict and crisis zones, webinar Communicable episode 11: Nightmare series, part 2 – how to deal with carbapenemase producers Communicable episode 16: Climate change and infections – effects on clinical practice & sustainabilityResourcesTrainee Association of ESCIMD (TAE) Doctors without Borders (Médecins sans Frontières), Antibiogo, https://www.antibiogo.org/Doctors without Borders (Médecins sans Frontières), Mini-lab, https://fondation.msf.fr/en/projects/mini-lab Further ReadingAbbara A, et al. Unravelling the linkages between conflict and antimicrobial resistance. NPJ Antimicrob Resist. 2025. DOI: 10.1038/s44259-025-00099-yAbbara A, et al. A summary and appraisal of existing evidence of antimicrobial resistance in the Syrian conflict. Int J Infect Dis. 2018. DOI: 10.1016/j.ijid.2018.06.010Abu-Shomar R, et al. Multidrug-resistant Pseudomonas isolated from water at primary health care centers in Gaza, Palestine: a cross-sectional study. IJID Reg. 2025. DOI: 10.1016/j.ijregi.2025.100671Aldbis A, et al. The lived experience of patients with conflict associated injuries whose wounds are affected by antimicrobial resistant organisms: a qualitative study from northwest Syria. Confl Health. 2023. DOI: 10.1186/s13031-023-00501-4Aro T, et al. War on antimicrobial resistance: high carriage rates of multidrug-resistant bacteria among war-injured Ukrainian refugees. Clin Microbiol Infect. 2025. DOI: 10.1016/j.cmi.2025.07.010  Bazzi W, et al. Heavy Metal Toxicity in Armed Conflicts Potentiates AMR in A. baumannii by Selecting for Antibiotic and Heavy Metal Co-resistance Mechanisms. Front Microbiol. 2020. DOI: 10.3389/fmicb.2020.00068 Dewachi O. War Biology and Antimicrobial Resistance: The Case of Gaza, AMR Insights, 2024.Granata G, et al. The impact of armed conflict on the development and global spread of antibiotic resistance: a systematic review. Clin Microbiol Infect. 2024. DOI: 10.1016/j.cmi.2024.03.029 Huang XZ, et al. Molecular analysis of imipenem-resistant Acinetobacter baumannii isolated from US service members wounded in Iraq, 2003-2008. Epidemiol Infect. 2012. DOI: 10.1017/S0950268811002871Hujer KM, et al. Analysis of antibiotic resistance genes in multidrug-resistant Acinetobacter sp. isolates from military and civilian patients treated at the Walter Reed Army Medical Center. Antimicrob Agents Chemother. 2006. DOI: 10.1128/AAC.00778-06Karah N, et al. Teleclinical Microbiology: An Innovative Approach to Providing Web-Enabled Diagnostic Laboratory Services in Syria. Am J Clin Pathol. 2022. DOI: 10.1093/ajcp/aqab160Keen EF 3rd, et al. Evaluation of potential environmental contamination sources for the presence of multidrug-resistant bacteria linked to wound infections in combat casualties. Infect Control Hosp Epidemiol. 2012. DOI: 10.1086/667382Murray CK, et al. Recovery of multidrug-resistant bacteria from combat personnel evacuated from Iraq and Afghanistan at a single military treatment facility. Mil Med. 2009. DOI: 10.7205/milmed-d-03-8008Petersen K, et al. Diversity and clinical impact of Acinetobacter baumannii colonization and infection at a military medical center. J Clin Microbiol. 2011. DOI: 10.1128/JCM.00766-10Scott P, et al. An outbreak of multidrug-resistant Acinetobacter baumannii-calcoaceticus complex infection in the US military health care system associated with military operations in Iraq. Clin Infect Dis. 2007. DOI: 10.1086/518170Sensenig RA, et al. Longitudinal characterization of Acinetobacter baumannii-calcoaceticus complex, Klebsiella pneumoniae, and methicillin-resistant Staphylococcus aureus colonizing and infecting combat casualties. Am J Infect Control. 2012. DOI: 10.1016/j.ajic.2011.03.025World Health Organization. Fourth WHO Global Evidence Review on Health and Migration stresses that equitable access to and appropriate use of antibiotics for refugees and migrants is essential to tackling Antimicrobial Resistance, News, 2022.

Episode 205: Atopic Dermatitis Kara Willbanks (medical student) explains the definition, pathophysiology, and treatment of eczema. Dr. Arreaza adds some input about bleach baths and topical steroids. Written by Kara Willbanks, MSIV, American University of the Caribbean. Comments and edits by Hector Arreaza, MD.You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.October is the Eczema Awareness Month!What Is Atopic Dermatitis? Atopic dermatitis, a form of eczema, is a chronic, relapsing inflammatory skin disorder that often begins in childhood but can affect people of all ages. Other eczematous dermatoses include seborrheic dermatitis, contact dermatitis, juvenile plantar dermatosis, and stasis dermatitis. Atopic dermatitis is one of the most common skin conditions in the developed world, typically affecting up to 20% of children and 5-10% of adults. Patients usually present with severe pruritus (itchiness) and dry, inflamed patches of skin. Common sites include the face and extensor surfaces in infants, and flexural areas — like the elbows and knees — in older children and adults. Atopic dermatitis is often associated with other allergic conditions like asthma and allergic rhinitis — what we call the “atopic triad.” These conditions should also be considered when diagnosing someone with atopic dermatitis. PathophysiologyAtopic dermatitis is believed to occur due to a combination of genetic, immune, and environmental factors. A major component is a defective skin barrier, often linked to mutations in the filaggrin gene. This allows irritants, allergens, and microbes to penetrate the skin more easily, triggering inflammation.Differential DiagnosisAtopic dermatitis can sometimes mimic other skin conditions, so it's important to keep a differential in mind: -Contact dermatitis – triggered by allergens or irritants; often limited to the area of exposure but also tends to be very itchy. -Seborrheic dermatitis – greasy scales, typically on the scalp, eyebrows, and nasolabial folds -Psoriasis – well-demarcated plaques with silvery scales; sometimes found in similar areas of the body as eczema. -Tinea (fungal infections) – ring-shaped lesions with active, scaly borders -Important to note that treatment of tinea with topical steroids can make the rash much worse. -Scabies – intense itching, especially at night, with burrows between fingers. Ruling out these conditions helps guide the right treatment and prevent chronic mismanagement. As a recap our main differential diagnosis: contact dermatitis, seborrheic dermatitis, psoriasis, tinea, and scabies.The treatment cornerstone: Moisturizers The most important daily treatment for atopic dermatitis is regular moisturizing. Moisturizers repair the skin barrier, reduce water loss, and protect against irritants. They should be applied at least twice daily, ideally right after bathing while the skin is still damp (within 3 minutes is most ideal). Use greasy ointments or thick creams rather than lotions — think products with ceramides or glycerin (hydrates and protects skin). It is best to choose ointments or creams without additives, perfumes or fragrances. Greasier ointments are the preferred vessel; however, patient compliance may be less as they may be unpleasant to some.Bleach Baths For patients with frequent skin infections or severe eczema, dilute bleach baths can be a game-changer. How to do it? Use ¼ to ½ cup of household bleach in a full standard bathtub of water (about 40 gallons) and soak for 10 minutes, twice a week. This helps reduce bacterial colonization — particularly Staphylococcus aureus — which commonly worsens eczema. After the bath, pat the skin dry and immediately apply a moisturizer (within 3 minutes). Bleach baths are endorsed by the American Academy of Pediatrics and the American Academy of Dermatology as an adjunctive treatment for atopic dermatitis, especially in patients with moderate to severe disease and frequent bacterial infections, but the evidence for their efficacy is mixed, and further well-designed studies are needed.Medical Treatments-Topical corticosteroids: When moisturizers alone aren't enough, we move to anti-inflammatory therapy. Topical corticosteroids are the first-line treatment for flares. Some studies suggest that a short burst of a high-potency topical corticosteroid to rapidly control active disease, followed by a quick taper in potency, is most effective, whereas others use the lowest-potency agent thought to be needed and adjust upward only if this fails. Common steroids used are hydrocortisone (low potency), triamcinolone (medium potency), or betamethasone (high potency). -High-potency steroids should never be applied to sensitive skin like the face. With short-term use of lower-potency steroids, there is a low likelihood of skin atrophy but use for more than 6 months is linked with greater levels of skin thinning -Wet wrap therapy: Wet wrap therapy improves absorption of topic steroid. Apply a topical steroid, then layer a wet dressing and then a dry dressing over the top of that. This can be beneficial in providing  both relief of symptoms and prevention of itching. In pediatric patients it is called “daddy's socks therapy” because large socks may be used to cover the arms of kids.-Topical calcineurin inhibitors — like tacrolimus — are great alternatives for sensitive areas or for maintenance once inflammation is under control. They may burn upon application which can scare patients away from their use.-PO antihistamines can help with itching, especially at night, but they don't treat inflammation itself.-Systemic therapies, like dupilumab (Dupixent®), an IL-4 receptor antagonist, are reserved for moderate to severe cases unresponsive to topical therapy. This is a great time to refer to your local dermatologist for management! Many of the newer treatments are highly effective but can require more frequent monitoring.Recent Research One recent study is the 2024 Cochrane network meta-analysis comparing effectiveness of topical anti-inflammatory treatments for eczema that was recently published in the AFP Journal in July of 2025.Here are the highlights:-Over 291 RCTs with ~45,846 participants were included. -The analysis ranked potent topical corticosteroids, JAK inhibitors (for example ruxolitinib (Opzelura® 1.5 %), and tacrolimus 0.1 % among the most effective for reducing signs and symptoms of eczema. -In contrast, PDE-4 inhibitors [like crisaborole (Eucrisa®) 2 %] were among the least effective in this comparison. -Regarding side effects: tacrolimus and crisaborole were more likely to cause burning or stinging at the application site; corticosteroids were less likely in the short term to cause local irritation.-Long-term outcomes regarding effectiveness or safety of treatments for eczema were not addressed by the review because they are rarely reported.”-Another insight from this study is considering cost when initiating treatment. Most topical steroids are significantly more cost effective than JAK inhibitors or calcineurin inhibitors so it may be best to start with a cheaper solution in an uninsured patient considering their relative effectiveness. Additional Tips & Lifestyle -Keep baths and showers short and in lukewarm water.-Avoid harsh soaps and detergents — use gentle, fragrance-free cleansers.-Wear soft cotton clothing instead of wool or synthetics.-Identify and avoid triggers — common ones include stress, sweating, allergens, and certain foods (especially in kids).-Ice packs can help reduce itching and relieve any burning sensation.-Keep fingernails short, especially in children, help cause less trauma to the skin from repeated itching. Living with eczema Many celebrities like Kerry Washington, Jessica Simpson, Kelly Rowland, Brad Pitt and Kristen Bell have spoken out about their lives with eczema. They have shared personal stories about how they were diagnosed, what treatment works for them, and the general impact it has had on their lives and mental health. I feel like it can be so important for celebrities to speak out about their lives with certain conditions because it helps to normalize the condition, raise awareness of the struggles, and encourages more open dialogue.It is important to remember that for patients living with eczema, the persistent itch-scratch cycle can be very distressing, causing patients to struggle with their sleep and day-to-day activities. Anxiety and depression are common in patients with eczema so as physicians it is vital to monitor for signs of distress. Support groups can be incredibly helpful for patients [National Eczema Association]If you are interested in providing additional information to your patients or getting this for yourself, you can find more resources on altogethereczema.org or nationaleczema.org. Key Takeaways Atopic dermatitis is chronic but manageable. Moisturizers are the foundation of treatment. Topical steroids and calcineurin inhibitors control inflammation. Bleach baths help reduce bacterial load and flare severity. Always rule out other skin conditions to ensure appropriate management. Atopic dermatitis can be managed by the primary care physician but in certain cases (cases refractory to standard topical treatment, recurrent infections, etc.), a referral to dermatology can be especially helpful.Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! References:Coping with eczema. Allergy & Asthma Network. (2025, May 20). https://allergyasthmanetwork.org/what-is-eczema/coping-with-eczema/.Eichenfield LF, Tom WL, Chamlin SL, et al. Guidelines of care for the management of atopic dermatitis: section 1. Diagnosis and assessment of atopic dermatitis. J Am Acad Dermatol. 2014 Feb;70(2):338-51. doi: 10.1016/j.jaad.2013.10.010. Epub 2013 Nov 27. PMID: 24290431; PMCID: PMC4410183. https://pubmed.ncbi.nlm.nih.gov/24290431/.Yancey, J. R., & Green, S. (2025, July 15). Effectiveness of topical anti-inflammatory drugs for eczema. American Family Physician. https://www.aafp.org/pubs/afp/issues/2025/0700/cochrane-eczema.html.Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

rWotD Episode 3084: RsaOG Welcome to random Wiki of the Day, your journey through Wikipedia's vast and varied content, one random article at a time.The random article for Monday, 13 October 2025, is RsaOG.RsaOG (an acronym for RNA S. aureus Orsay G) is a non-coding RNA that was discovered in the pathogenic bacteria Staphylococcus aureus N315 using a large scale computational screening based on phylogenetic profiling. It was first identified, but not named, in 2005. RsaOG has since been identified in other strains of Staphylococcus aureus under the name of RsaI, it has also been discovered in other members of the Staphylococcus genus (such as Staphylococcus carnosus) but in no other bacteria.The RsaOG gene is conserved in all Staphylococcaceae sequenced genomes, its secondary structure contains two highly conserved unpaired sequences which have the ability to form a pseudoknot. Northern blot experiments show that RsaOG is expressed in several S. aureus strains. Mapping of RsaOG ends indicates a size of 146 nucleotides in S. aureus. RsaOG ncRNA is thought to have trans-acting regulatory functions, possibly on fine tuning toxin production or aiding with invasion.This recording reflects the Wikipedia text as of 01:11 UTC on Monday, 13 October 2025.For the full current version of the article, see RsaOG on Wikipedia.This podcast uses content from Wikipedia under the Creative Commons Attribution-ShareAlike License.Visit our archives at wikioftheday.com and subscribe to stay updated on new episodes.Follow us on Bluesky at @wikioftheday.com.Also check out Curmudgeon's Corner, a current events podcast.Until next time, I'm long-form Patrick.

Long-term care facilities face unique challenges in preventing healthcare-associated infections (HAIs) and managing multidrug-resistant organisms (MDROs). In this episode of The ICHE Podcast, Dr. Loren G. Miller (UCLA), Dr. Lyndsay M. O'Hara (University of Maryland School of Medicine), and Dr. Mary-Claire Roghmann (University of Maryland School of Medicine) share insights from their recent studies on decolonization and enhanced barrier precautions—two promising approaches for reducing infection risk among residents. They explore what the latest research tells us, where evidence gaps remain, and how facilities can apply practical, evidence-based interventions today to improve safety and quality of care. UCI SHIELD Nursing Home Decolonization Toolkit: https://www.ucihealth.org/healthcare-professionals/shield/nursing-home-decolonization-toolkit Enhanced barrier precautions to prevent transmission of *Staphylococcus aureus* and Carbapenem-resistant organisms in nursing home chronic ventilator units: https://www.cambridge.org/core/journals/infection-control-and-hospital-epidemiology/article/abs/enhanced-barrier-precautions-to-prevent-transmission-of-staphylococcus-aureus-and-carbapenemresistant-organisms-in-nursing-home-chronic-ventilator-units/43FBB459BB569B052DEDF87EA57193FB Impact of routine chlorhexidine bathing and nasal iodophor on MDRO colonization and environmental contamination in nursing homes: https://www.cambridge.org/core/journals/infection-control-and-hospital-epidemiology/article/abs/impact-of-routine-chlorhexidine-bathing-and-nasal-iodophor-on-mdro-colonization-and-environmental-contamination-in-nursing-homes/EE2288CCE486EB4822A545BFE6210BA5

Karl Matthews, Ph.D., Professor of Microbial Food Safety at Rutgers University, discusses ways to eliminate pathogens like Salmonella, E. coli O157:H7 and Listeria from fresh fruits and vegetables. He highlights the importance of preventative measures from farm to table, including the use of water antimicrobials, like chlorine, and photosensitizers, like curcumin. Watch this episode: https://youtu.be/6Wkef9RyUVE Ashley's Biggest Takeaways We consume billions of microorganisms in the food that we eat each day. Fresh fruits and vegetables that are not thermally processed are likely to carry a higher microbial load than cooked foods. Many of those microbes are not concerning to human health. However, when pathogens of human health concern are present, the food can become unsafe to eat. Scientists use many methods from pre-harvest through post-harvest to keep food free of human pathogens. Water antimicrobials, such as chlorine, and photodynamic inactivation using photosensitizers, such as curcumin, are 2 preventative measures that Matthews and colleagues are investigating. Curcumin is a natural chemical compound found in the turmeric plant. It is responsible for giving tumeric its yellow color. Curcumin is also a photosensitizer, meaning that it can absorb light energy and transfer it to another molecule to initiate chemical reactions that produce cytotoxic singlet oxygen. Featured Quotes When I look at [what makes fruits and vegetables safe to eat] as far as from a microbiological perspective, it's are they free of pathogens of human health concern? And so, we might think about organisms, such as Salmonella or the Shiga toxin producing E coli or Listeria. There are a number of processes and initiatives that are put into place, from the pre-harvest through post-harvest levels to try to ensure that the product is not contaminated with microorganisms of human health concern. Each day, we're consuming literally billions of microorganisms in the foods that we eat, and particularly the raw fruits and vegetables that we're eating that are not being thermally processed in any fashion by which you might reduce the microbial load. Oftentimes we think about the bacteria that might well be there. But we do know that there's viruses that could be present. There's certain type of protozoa that might be present. Many of us know of norovirus and the concerns associated with that particular pathogen. So, there's a multitude of microorganisms that might well be associated with fresh fruits and vegetables, but there's really a very limited number or types that are actually of concern from a human health standpoint. In my program, we're working on E. coli O157:H7, in particular. It's a certain serotype of E. coli, a diarrheagenic E. coli, what's also known as a Shiga toxin-producing E. coli. We work with Salmonella, and we work with Listeria monocytogenes, but there's other microorganisms, such as Campylobacter, Yersinia, Staphylococcus aureus. All of those types of pathogens can also be associated with foods—and different types of foods, at that—and be of concern to the general public—the consumer. If we look at a lot of the processing of foods that are taking place, not only here in the United States, but globally, many times, what will happen is they're utilizing some type of a water antimicrobial, and I stress that because, oftentimes, these antimicrobials are added to the water to control the microbial load in the water. So, ultimately, you're not basically putting on water and putting on a whole load of microorganisms along with it. And also, you can prevent cross contamination through that. Here in the U.S. and elsewhere, we'll often put additional chlorine into the water. So, let's say we're increasing the chlorine concentration to 20 parts per million, or 50 parts per million, or maybe in poultry processing, they're utilizing peracetic acid. These are 2 common antimicrobials that are being used. What we wanted to do is find out could we utilize some other types of methods that might well control microorganisms on the commodity itself? And that's where we started looking at photodynamic inactivation and coupling that with the use of a photosensitizer. And in this particular case, the photosensitizer we were using was curcumin. The reason for working with curcumin is that it's naturally used in foods as a food dye. It's also used as a flavoring agent, and so forth. So, it's there, and it's being used—not just in the U.S., but [also] globally. And we thought we would try to see if we utilize this compound, could we have an additive effect to it? If you apply certain wavelengths of light, you can inactivate microorganisms, but if you apply that wavelength to something like a photosensitizer type molecule (curcumin), you could generate singlet oxygen molecules. And those singlet oxygen molecules would act like little explosions on the cell membrane and basically blow it apart and, therefore, inactivate the organism. We looked at the ability of this to inactivate Listeria monocytogenes, Salmonella, as well as E. coli O157:H7, so these Shiga toxin-producing E. coli, and what we did indeed find is that it was very effective. We looked at it in comparison to peracetic acid use in the poultry industry, and we found it to be equivalent, at least to treatments that we were utilizing on poultry skin, with inactivation of the microorganisms, such as Listeria, on the poultry skin. So, it is really exciting. Links for This Episode ​​​​​​Preventing Foodborne Outbreaks Starts in the Field. Influences of photosensitizer curcumin on microbial survival and physicochemical properties of chicken during storage.

Le “triangle de la mort” désigne une zone du visage comprise entre l'arête du nez et les commissures des lèvres, formant un triangle. Cette appellation spectaculaire vient d'une particularité anatomique : dans cette région, les veines superficielles (veine faciale, veine angulaire) communiquent directement avec des veines profondes de l'orbite (veines ophtalmiques) et, au-delà, avec le sinus caverneux, une grande veine située à la base du crâne. Or ces veines sont dépourvues de valvules efficaces, ce qui autorise un reflux du sang vers le crâne en cas d'inflammation, de pression ou d'infection locales.Concrètement, une lésion cutanée banale du triangle — bouton manipulé, poil incarné, gerçure, furoncle dans le vestibule nasal — peut, très rarement, permettre à des bactéries (souvent Staphylococcus aureus, parfois streptocoques ou anaérobies) de gagner la circulation veineuse puis le sinus caverneux. Cela expose à une thrombose du sinus caverneux (formation d'un caillot infecté), à une méningite ou à un abcès intracrânien. Ces complications restent exceptionnelles à l'ère des antibiotiques, mais leur gravité explique la réputation de cette zone.Les signes d'alarme qui doivent faire consulter en urgence après une infection du nez ou de la lèvre supérieure sont : fièvre, céphalée intense, douleur autour d'un œil, œdème palpébral, rougeur conjonctivale, diplopie (vision double), douleur aux mouvements oculaires, proptose (œil “qui ressort”), diminution de la vision, engourdissement du front ou de la joue (atteinte des nerfs V1/V2), voire paralysie oculomotrice (nerfs III, IV, VI). Le diagnostic repose sur l'examen clinique et l'imagerie (IRM avec angio-IRM ou TDM), et le traitement associe antibiothérapie intraveineuse rapide, prise en charge en milieu spécialisé, parfois anticoagulation selon les cas.Pourquoi le risque augmente-t-il quand on “triture” un bouton ? En pressant, on provoque microtraumatismes et diffusion bactérienne dans des tissus très vascularisés, avec un gradient de pression qui peut favoriser la remontée du sang vers les veines profondes. Le risque est majoré par le diabète, l'immunodépression, une sinusite non traitée ou une infection dentaire maxillaire.Les gestes de prévention sont simples : éviter de percer ou manipuler les lésions dans cette zone ; nettoyer la peau avec une solution douce ; traiter les croûtes/sécheresses nasales (salines isotoniques, baumes adaptés) ; consulter en cas de douleur, fièvre, extension de la rougeur, écoulement purulent nasal, ou atteinte de l'œil. En résumé, le “triangle de la mort” n'est pas une fatalité : c'est le rappel qu'ici, la connexion veineuse directe avec l'intérieur du crâne impose de respecter les règles d'hygiène et de ne pas jouer les dermatologues amateurs. Hébergé par Acast. Visitez acast.com/privacy pour plus d'informations.

Antimicrobial resistance (AMR) continues to grow as a global health threat, making infections harder to treat and leaving fewer options for patients. The need for new antibiotics is an urgent matter — but traditional discovery methods are slow and limited. In this episode of Let's Talk Micro, Luis is joined by Dr. James Collins, professor at MIT and researcher at the Broad Institute, who is leading efforts to apply AI to antibiotic discovery. We discuss how his team used deep learning to uncover promising new compounds, including NG1 and DN1, which showed activity against drug-resistant Neisseria gonorrhoeae and Staphylococcus aureus. We also talk about the challenges of bringing discoveries from computer models to the clinic, and what this approach could mean for the future of the fight against superbugs.   Link to study: https://www.cell.com/cell/abstract/S0092-8674%2825%2900855-4   Check out the website: https://www.letstalkmicro.com/ Questions? Feedback? Send those to letstalkmicro@outlook.com Want to support the podcast? Here's how: Venmo: https://venmo.com/u/letstalkmicro Buy me a Ko-fi: https://ko-fi.com/letstalkmicro  

À l'ère du smartphone et du télétravail, les écouteurs font désormais partie de notre quotidien. Que ce soit pour écouter de la musique, téléphoner ou suivre une visioconférence, ils restent des heures durant dans nos oreilles. Mais ce geste anodin est-il sans risque pour notre santé ? Plus précisément, peut-il favoriser l'apparition d'otites ?La réponse est oui, dans certains cas. Les spécialistes ORL s'accordent sur un point : l'usage prolongé et répété d'écouteurs intra-auriculaires peut créer un environnement propice aux infections, en particulier les otites externes, c'est-à-dire les inflammations du conduit auditif.Une étude publiée en 2008 dans le Journal of Laryngology and Otology (par Leong et al.) a comparé le conduit auditif de deux groupes : un groupe portant régulièrement des écouteurs, et un groupe n'en utilisant jamais. Résultat : les utilisateurs fréquents d'écouteurs présentaient un taux significativement plus élevé de bactéries pathogènes, notamment Staphylococcus aureus et Pseudomonas aeruginosa, des germes souvent impliqués dans les otites externes.Pourquoi ce lien entre écouteurs et otites ? Plusieurs mécanismes sont en cause :1. Obstruction du conduit auditif : les écouteurs, surtout intra-auriculaires, empêchent la bonne ventilation du canal. L'humidité naturelle ne s'évacue pas correctement, créant un terrain chaud et humide, idéal pour la prolifération des bactéries.2. Microtraumatismes : le frottement régulier des embouts ou leur insertion brutale peut irriter la peau du conduit, facilitant l'entrée des agents infectieux.3. Manque d'hygiène : peu d'utilisateurs nettoient leurs écouteurs régulièrement. Or, ces dispositifs sont souvent posés sur des surfaces non stériles ou partagés entre plusieurs personnes. Les germes présents sur les écouteurs peuvent ainsi être introduits dans l'oreille à chaque usage.Les symptômes d'une otite externe liée aux écouteurs sont classiques : douleurs, démangeaisons, rougeur du conduit auditif, voire écoulement. Dans certains cas, l'audition peut temporairement diminuer. Si ces signes apparaissent, il est recommandé d'arrêter immédiatement l'usage des écouteurs et de consulter un médecin.Pour limiter les risques, quelques gestes simples suffisent :Ne pas porter d'écouteurs plus de deux heures d'affilée.Les désinfecter régulièrement avec un chiffon doux imbibé d'alcool à 70 %.Éviter de les partager.Aérer ses oreilles entre deux utilisations.En conclusion, si les écouteurs ne sont pas à l'origine directe de toutes les otites, leur usage excessif et négligent peut en augmenter la probabilité, notamment en cas de mauvaise hygiène. Pour écouter en toute sécurité, mieux vaut penser aussi à… laisser respirer ses oreilles. Hébergé par Acast. Visitez acast.com/privacy pour plus d'informations.

On episode #87 of the Infectious Disease Puscast, Daniel and Sara review the infectious disease literature for the weeks of 7/31/25 – 8/18/25. Host: Daniel Griffin and Sara Dong Subscribe (free): Apple Podcasts, RSS, email Become a patron of Puscast! Links for this episode Viral Adjuvanted recombinant zoster vaccine is effective against herpes zoster ophthalmicus, and is associated with lower risk of acute myocardial infarction and stroke in adults aged ≥50 years (CID) Bacterial Dalbavancin for Treatment of Staphylococcus aureus Bacteremia (JAMA) Propensity-Matched Comparison of Timely vs. Delayed Antibiotic Therapy in Stenotrophomonas maltophilia Pneumoni (OFID) The proportion of Treponema pallidum PCR-positive primary syphilis infections which are seronegative for syphilis (OFID) Cefixime versus benzathine penicillin G for the treatment of early syphilis (Journal of Antimicrobial Chemotherapy) Dalbavancin for Treatment of Staphylococcus aureus Bacteremia (JAMA) Fungal The Last of US Season 2 (YouTube) Parasitic Increasing Length of the Babesia Season in New England in the Climate Change Era (OFID) Ivermectin to Control Malaria (NEJM) Miscellaneous ACIP Recommendations Summary (CDC: Influenza) Relative effectiveness of high-dose versus standard-dose influenza vaccine against hospitalizations and mortality according to frailty score (JID) Music is by Ronald Jenkees Information on this podcast should not be considered as medical advice.

Agradece a este podcast tantas horas de entretenimiento y disfruta de episodios exclusivos como éste. ¡Apóyale en iVoox! En 1928, Alexander Fleming, un bacteriólogo escocés, realizó uno de los descubrimientos médicos más importantes de la historia: la penicilina. Mientras trabajaba en el Hospital St. Mary’s de Londres, Fleming notó que una placa de cultivo de bacterias Staphylococcus aureus había sido contaminada por un moho de color verde. Observó detenidamente lo que había sucedido y advirtió que, alrededor del moho, las bacterias no crecían, lo que indicaba que el moho producía una sustancia que las inhibía. Este moho fue bautizado como Penicillium notatum, y la sustancia, como penicilina. Esto marcó el inicio de la era de los antibióticos. Aunque Fleming publicó sus hallazgos en 1929, no pudo purificar la penicilina ni producirla a gran escala. Fue en la década de 1940 cuando científicos como Ernst Chain y Howard Florey lograron aislar y estabilizar el compuesto, permitiendo su uso médico. La industria farmacéutica estadounidense hizo el resto. Durante la Segunda Guerra Mundial, la penicilina salvó innumerables vidas al tratar infecciones bacterianas en soldados lo que supuso toda una revolución para la medicina. El descubrimiento de Fleming fue accidental, pero su observación meticulosa y su curiosidad científica las bases para un avance que transformó el tratamiento de enfermedades infecciosas. La penicilina no solo redujo la mortalidad por infecciones, sino que también abrió la puerta al desarrollo de otros antibióticos. Escucha el episodio completo en la app de iVoox, o descubre todo el catálogo de iVoox Originals

Agradece a este podcast tantas horas de entretenimiento y disfruta de episodios exclusivos como éste. ¡Apóyale en iVoox! En 1928, Alexander Fleming, un bacteriólogo escocés, realizó uno de los descubrimientos médicos más importantes de la historia: la penicilina. Mientras trabajaba en el Hospital St. Mary’s de Londres, Fleming notó que una placa de cultivo de bacterias Staphylococcus aureus había sido contaminada por un moho de color verde. Observó detenidamente lo que había sucedido y advirtió que, alrededor del moho, las bacterias no crecían, lo que indicaba que el moho producía una sustancia que las inhibía. Este moho fue bautizado como Penicillium notatum, y la sustancia, como penicilina. Esto marcó el inicio de la era de los antibióticos. Aunque Fleming publicó sus hallazgos en 1929, no pudo purificar la penicilina ni producirla a gran escala. Fue en la década de 1940 cuando científicos como Ernst Chain y Howard Florey lograron aislar y estabilizar el compuesto, permitiendo su uso médico. La industria farmacéutica estadounidense hizo el resto. Durante la Segunda Guerra Mundial, la penicilina salvó innumerables vidas al tratar infecciones bacterianas en soldados lo que supuso toda una revolución para la medicina. El descubrimiento de Fleming fue accidental, pero su observación meticulosa y su curiosidad científica las bases para un avance que transformó el tratamiento de enfermedades infecciosas. La penicilina no solo redujo la mortalidad por infecciones, sino que también abrió la puerta al desarrollo de otros antibióticos. · Canal de Telegram: https://t.me/lacontracronica · “Contra la Revolución Francesa”… https://amzn.to/4aF0LpZ · “Hispanos. Breve historia de los pueblos de habla hispana”… https://amzn.to/428js1G · “La ContraHistoria de España. Auge, caída y vuelta a empezar de un país en 28 episodios”… https://amzn.to/3kXcZ6i · “Lutero, Calvino y Trento, la Reforma que no fue”… https://amzn.to/3shKOlK · “La ContraHistoria del comunismo”… https://amzn.to/39QP2KE Apoya La Contra en: · Patreon... https://www.patreon.com/diazvillanueva · iVoox... https://www.ivoox.com/podcast-contracronica_sq_f1267769_1.html · Paypal... https://www.paypal.me/diazvillanueva Sígueme en: · Web... https://diazvillanueva.com · Twitter... https://twitter.com/diazvillanueva · Facebook... https://www.facebook.com/fernandodiazvillanueva1/ · Instagram... https://www.instagram.com/diazvillanueva · Linkedin… https://www.linkedin.com/in/fernando-d%C3%ADaz-villanueva-7303865/ · Flickr... https://www.flickr.com/photos/147276463@N05/?/ · Pinterest... https://www.pinterest.com/fernandodiazvillanueva Encuentra mis libros en: · Amazon... https://www.amazon.es/Fernando-Diaz-Villanueva/e/B00J2ASBXM #FernandoDiazVillanueva #penicilina #fleming Escucha el episodio completo en la app de iVoox, o descubre todo el catálogo de iVoox Originals

Dalbavancin, a long-acting IV lipoglycopeptide, may be an option for the treatment of complicated Staphylococcus aureus bacteremia without requiring long-term IV access. Author Thomas L. Holland, MD, MSc, from Duke University School of Medicine discusses key points of the DOTS randomized clinical trial and more with JAMA Deputy Editor Preeti Malani, MD, MSJ.Related Content: Dalbavancin for Treatment of Staphylococcus aureus BacteremiaManagement of Staphylococcus aureus Bacteremia

Dalbavancin, a long-acting IV lipoglycopeptide, may be an option for the treatment of complicated Staphylococcus aureus bacteremia without requiring long-term IV access. Author Thomas L. Holland, MD, MSc, from Duke University School of Medicine discusses key points of the DOTS randomized clinical trial and more with JAMA Deputy Editor Preeti Malani, MD, MSJ. Related Content: Dalbavancin for Treatment of Staphylococcus aureus Bacteremia Management of Staphylococcus aureus Bacteremia

No episódio de hoje do Check-up Semanal, nosso editor-chefe médico, Ronaldo Gismondi, traz as principais atualizações do último mês sobre Clínica Médica publicadas no Portal Afya.Confira os temas do episódio:- Diretrizes para ajuste de antibioticoterapia em pacientes obesos;- Câncer de sítio primário oculto: ainda vale buscar o local de origem?;- Roteiro estratégico para investigação de diarreia aguda e crônica;- Quando indicar antibióticos na pancreatite aguda;- Ecocardiograma transesofágico na bacteremia por Staphylococcus aureus: sempre necessário?Aperte o play e ouça agora os destaques que impactam a prática clínica na atenção ao paciente adulto!

Cauda Equina Syndrome • Neurosurgical emergency due to compression of cauda equina nerve roots, usually from disc herniation, tumor, or trauma Clinical Presentation Labs, Studies, and Physical Exam Findings Treatment Key Differentiators Epidural Abscess • • Spinal epidural infection commonly caused by Staphylococcus aureus Clinical Presentation Labs, Studies, and Physical Exam Findings Treatment Key Differentiators […] The post 131 Neuro: Spinal Cord issues appeared first on Physician Assistant Exam Review.

On episode #85 of the Infectious Disease Puscast, Daniel and Sara review the infectious disease literature for the weeks of 7/3 – 7/21/25. Hosts: Daniel Griffin and Sara Dong Subscribe (free): Apple Podcasts, RSS, email Become a patron of Puscast! Links for this episode Viral Elimination of HIV Reservoirs Harboring Intact Proviruses (JID) Bacterial Expansion of tetM-Carrying Neisseria gonorrhoeae in the United States, 2018–2024 (NEJM) Study hints doxyPEP use coincides with rise in tetracycline-resistant gonorrhea in US (CIDRAP) Potential Impact of Doxycycline Post-Exposure Prophylaxis on Tetracycline Resistance in Neisseria gonorrhoeae and Colonization With Tetracycline-Resistant Staphylococcus aureus and Group A Streptococcus (CID) Methenamine hippurate asprophylaxis for recurrent urinary tract infections in older women – a triple-blind, randomised, placebo-controlled, phase IV trial (ImpresU). (CMI: Clinical Microbiology and Infection) Diagnosis and Management ofCommunity-acquired Pneumonia(American Journal of Respiratory and Critical Care Medicine) Complicated Urinary Tract Infections (cUTI): Clinical Guidelines for Treatment and Management (IDSA) The impact of an intervention to increase follow-up blood cultures for patients with Staphylococcus aureus bacteriuria (Antimicrobial Stewardship & Healthcare Epidemiology) Fungal The Last of US Season 2 (YouTube) Candida auris Containment Responses in Health Care Facilities that Provide Hemodialysis Services (CDC: MMWR) Candidozyma auris: an emerging threat (Reflections on Infectious Prevention and Control) Effects of postoperative antifungal therapy on the recurrence of Aspergillus infection after pulmonary aspergilloma resection (BMC Infectious Diseases) Triazole-resistant Aspergillus fumigatus in the Netherlands between 1994 and 2022: a genomic and phenotypic study (LANCET: Microbe) Large language models and their performance for the diagnosis of histoplasmosis (PLoS Neglected Tropical Diseases) Parasitic Field evidence of Trypanosoma cruzi infection, diverse host use and invasion of human dwellings by the Chagas disease vector in Florida, USA (PLoS Neglected Tropical Diseases) Music is by Ronald Jenkees Information on this podcast should not be considered as medical advice.

Dr. Don and Professor Ben talk about the risks of making pancakes from old sourdough leftovers. Fedica text: Dr. Don - not risky

Story at-a-glance Your scalp hosts a dense microbial ecosystem that protects against inflammation and disease. When disrupted, it can lead to flaking, itching, thinning hair, and inflammatory scalp conditions like seborrheic dermatitis The scalp microbiome is dominated by key bacteria like Cutibacterium acnes and Staphylococcus epidermidis. These microbes help protect your skin barrier, manage inflammation, and regulate other harmful organisms Scalp dysbiosis can be triggered by overwashing, harsh shampoos, excessive oil production, and even genetic factors like hair density or dandruff-prone skin. These disrupt the balance of good and bad microbes Dandruff is linked to reduced microbial diversity and fungal overgrowth. Studies show healthy scalps have more protective bacteria, while dandruff-prone scalps are overrun with inflammatory microbes like Malassezia restricta and Malassezia globosa Long-term relief comes from restoring beneficial microbes, not just killing fungi. Using microbiome-safe natural products, avoiding daily shampooing, and consuming foods that promote the growth of probiotics, prebiotics, and postbiotics are effective ways to rebalance your scalp naturally

Breakpoints joins forces with CMI Communications' Communicable podcast to discuss the highly anticipated SNAP trial updates presented at ESCMID Global 2025. Hosts Drs. Erin McCreary and Angela Huttner interview SNAP trial investigators, Drs. Joshua Davis and Steven Tong, on results from penicillin-susceptible and methicillin-susceptible Staphylococcus aureus domains. Conflict of Interest for DSMC Members: Conflicts of interest were evaluated when choosing individuals to serve on the SNAP DSMC. Aside from being compensated for their duties on the committee, DSMC members have no ongoing financial relationship that relate to the trial and are not involved in the conduct of the trial in any role other than that of a DSMC member. DSMC members have no intellectual conflict of interest or bias and reviewed SNAP data in a fully objective manner. Each DSMC candidate was well vetted.

Do you keep relapsing after treating candida, SIBO or other conditions? The culprit behind these never-ending cycles may be biofilms. In this episode, I'll explain how biofilms form, help you identify signs that you have them, and recommend the best antibiofilm agents. Tune in!   Learn more about biofilms and improve your gut now! Reach out to our virtual clinic: https://drruscio.com/virtual-clinic/  

Man Says He Visited Heaven, Met Jesus During Near-Death Experience Watch this video at- https://youtu.be/3FQmcCFZ8Ng?si=x4U0Eezqh21CuDDg CBN News 2.28M subscribers 123,685 views May 16, 2024 Randy Kay's "afterlife" experience still leaves him visibly emotional as he recounts details of visiting heaven, meeting Jesus, and returning to share his harrowing journey. Kay, author of the book, "Heaven Stormed: A Heavenly Encounter Reveals Your Assignment in the End Time Outpouring and Tribulation," told CBN News he was once a denier of near-death experience claims — until he faced his own purported heaven journey. He recalled his own afterlife experience, which began with a sore calf. At first, he thought he had strained a muscle, but while working out and going on a bike ride, his calf began to swell. "I was able to make it back home and then went to the doctor to get an anti-inflammatory prescription, and lo and behold, when I pressed my heel into the floor as the doctor had suggested, I collapsed," Kay said. "And I was rushed to the emergency room." It turns out, the pain and swelling were due to seven blood clots that had formed. He then contracted Methicillin-resistant Staphylococcus aureus (MRSA), a drug-resistant bacteria. "The doctor said I was a walking dead man," Kay said. "And then the septic shock which entered into my body caused a traffic jam in my vessels, my vascular system." The chaos landed Kay in a dire situation — one that he believes sent him to heaven. "Everything went dark initially and the next moment of recall, I was looking down on my body," he said. "I was being pulled by this light. I know that sounds cliche, almost, but it's absolutely true." Kay continued, "I was in a kind of very vague, ethereal space initially where I saw these figures in front of me, and they were warring against each other. There's no other way of putting it." After his return from his after-death experience, Kay discerned he was watching spiritual warfare play out. Regardless of what people choose to believe, Kay's physical body was dead at this point, making these memories and claims quite fascinating. "My heart had stopped," he said, noting that hospital records indicate he was clinically dead for 30 minutes and 49 seconds. During that time, Kay believes he was experiencing heaven, noting he was aware that her was himself but suddenly was seeing and visualizing the world quite differently. "I was seeing things, hearing things beyond which I would be able to do otherwise in my body," he said.

In this episode of Skin Anarchy, host Dr. Ekta welcomes Dr. Barbara Paldus, founder of Codex Labs, to explore breakthrough insights into eczema treatment. Dr. Paldus delves into the science behind the skin-gut-brain microbiome axis and explains how addressing both internal and external factors can revolutionize eczema care. Drawing on her recent TED Talk, she reveals that supporting gut health, reducing systemic inflammation, and restoring a balanced skin barrier can yield up to three times the benefits of traditional topical treatments.Dr. Paldus outlines the two main theories behind eczema—whether it starts with a leaky gut or a weakened skin barrier—and emphasizes that true relief comes from a holistic approach. She shares compelling data and real-world results from Codex Labs' innovative products, including the Bia Unscented Soap, Bia Eczema Relief Lotion, and Antü Skin Barrier Support Supplement. These products are designed to soothe, hydrate, and strengthen the skin from within, proving effective even in rigorous clinical trials.The conversation highlights the importance of understanding the genetic and environmental factors that contribute to eczema, from mutations in the filaggrin gene to the role of Staphylococcus aureus. Dr. Paldus also offers practical advice on integrating dietary changes, stress management, and gentle skincare into a comprehensive routine that supports long-term skin health.Tune in to discover how combining cutting-edge science with holistic wellness is paving the way for a new era in eczema treatment and learn why taking care of your skin from the inside out is the future of dermatology.Shop Codex's NEW Bia Eczema Relief Lotion.To learn more about Codex Labs, visit their website and social media. Don't forget to subscribe to Skin Anarchy on Apple Podcasts, Spotify, or your preferred platform. Reach out to us through email with any questions.Shop all our episodes and products mentioned through our ShopMy Shelf! Hosted on Acast. See acast.com/privacy for more information.