Biegunka związana z antybiotykami
Patofizjologia i mechanizm

Biegunka związana z antybiotykami (AAD) dotyka 5-35% pacjentów leczonych antybiotykami i wynika głównie z zaburzenia mikrobioty jelitowej, co prowadzi do zmniejszenia produkcji krótkołańcuchowych kwasów tłuszczowych (SCFA) nawet o 50% oraz zaburzeń metabolizmu węglowodanów i kwasów żółciowych. Mechanizmy patogenetyczne obejmują biegunkę osmotyczną (nagromadzenie niestrawionych węglowodanów) oraz biegunkę sekrecyjną (działanie niemetabolizowanych kwasów żółciowych). Ponadto niektóre antybiotyki, np. erytromycyna i klawulanian, mogą bezpośrednio drażnić błonę śluzową jelita lub stymulować perystaltykę. Spośród patogenów oportunistycznych, Clostridioides difficile odpowiada za 15-25% przypadków AAD, produkując toksyny A i B, które uszkadzają nabłonek jelitowy i wywołują stan zapalny. Szczep hiperpatogenny NAP1/BI/027 wiąże się z cięższym przebiegiem choroby. Inne patogeny to m.in. Clostridium perfringens (2-8% przypadków), Staphylococcus aureus, Klebsiella oxytoca oraz rzadziej Salmonella spp. Ryzyko AAD wzrasta przy stosowaniu cefalosporyn 3. generacji, penicylin szerokowidmowych (amoksycylina, ampicylina), klindamycyny i fluorochinolonów oraz przy terapii trwającej ponad 3 dni. Czynniki ryzyka obejmują wiek ≥65 lat, wcześniejsze AAD, choroby współistniejące, długi pobyt w szpitalu, stosowanie inhibitorów pompy protonowej i chemioterapię.

Biegunka związana z antybiotykami – Patogeneza

Biegunka związana z antybiotykami (ang. Antibiotic-Associated Diarrhea, AAD) stanowi powszechne powikłanie związane ze stosowaniem leków przeciwbakteryjnych, które dotyka od 5% do 35% pacjentów przyjmujących antybiotyki.12 Patogeneza AAD jest złożona i obejmuje kilka mechanizmów, które prowadzą do zaburzenia homeostazy przewodu pokarmowego.

Zaburzenie mikrobioty jelitowej

Głównym mechanizmem wywołującym biegunkę związaną z antybiotykami jest zaburzenie równowagi mikrobioty jelitowej.34 W zdrowym jelicie występuje wiele gatunków bakterii, które utrzymują naturalną równowagę ekologiczną. Antybiotyki mogą drastycznie zmienić tę równowagę poprzez zabijanie dużej liczby prawidłowych bakterii jelitowych.5 To zaburzenie naturalnej mikroflory prowadzi do:

  • Zmniejszenia mechanizmu oporności kolonizacyjnej, która chroni przed patogenami6
  • Zaburzeń w metabolizmie węglowodanów jelitowych7
  • Zmian w metabolizmie kwasów żółciowych8
  • Obniżenia produkcji krótkołańcuchowych kwasów tłuszczowych (SCFA)910

11

Badania sugerują, że zaburzenie mikrobioty jelitowej wywołane antybiotykami prowadzi do znacznego (nawet o 50%) zmniejszenia produkcji krótkołańcuchowych kwasów tłuszczowych i związanego z tym zmniejszenia Na-zależnej absorpcji płynów, co skutkuje biegunką.12

Mechanizmy osmotyczne i sekrecyjne

Biegunka związana z antybiotykami może mieć charakter osmotyczny lub sekrecyjny, w zależności od mechanizmu patogenetycznego:

  • Biegunka osmotyczna: Gdy bakterie anaerobowe mikroflory jelitowej zostają zniszczone przez antybiotyki, ich funkcja rozkładania wielkocząsteczkowych węglowodanów do przyswajalnych krótkołańcuchowych kwasów tłuszczowych zostaje zaburzona. Prowadzi to do gromadzenia się niestrawionych węglowodanów w okrężnicy, które wywołują biegunkę osmotyczną.1314
  • Biegunka sekrecyjna: Zaburzenia mikroflory bakteryjnej powodują również, że niemetabolizowane dihydroksylowe kwasy żółciowe, które są silnymi czynnikami sekrecyjnymi, prowadzą do rozwoju biegunki sekrecyjnej w okrężnicy.15

Badania wykazały, że patogeneza biegunki poantybiotykowej nie związanej z C. difficile ma charakter głównie sekrecyjny, podczas gdy biegunka wywołana przez C. difficile ma charakter zarówno inwazyjny, jak i sekrecyjny.16

Bezpośredni wpływ antybiotyków na jelito

Niektóre antybiotyki mogą wywierać bezpośredni efekt toksyczny i farmakologiczny na przewód pokarmowy, niezależnie od zmian w mikrobiomie:

  • Działanie na receptory motyliny: Niektóre antybiotyki, takie jak erytromycyna, są agonistami receptorów motyliny i mogą bezpośrednio stymulować perystaltykę jelit.17
  • Działanie drażniące: Bezpośrednie działanie toksyczne niektórych antybiotyków (np. klawulanianu) na błonę śluzową jelita może prowadzić do zwiększonej sekrecji, podrażnienia i zaburzonych wzorców motoryki.1819

Zakażenia patogenami oportunistycznymi

Utrata normalnej mikroflory jelitowej umożliwia nadmierny wzrost bakterii patogennych. W przeciwieństwie do powszechnej opinii, tylko 10-20% wszystkich przypadków biegunki związanej z antybiotykami jest spowodowanych zakażeniem Clostridioides difficile.20 Jednak istnieje kilka innych patogenów oportunistycznych, które mogą przyczyniać się do AAD:

Clostridioides difficile

Clostridioides difficile jest najlepiej zbadanym patogenem odpowiedzialnym za AAD, powodującym 15-25% przypadków biegunki związanej z antybiotykami i jest związany z najcięższymi postaciami choroby.21 C. difficile wytwarza dwie główne toksyny: toksynę A (enterotoksyna) i toksynę B (cytotoksyna), które odgrywają kluczową rolę w patofizjologii zakażenia.2223

Mechanizm działania toksyn obejmuje:

  • Wiązanie się z receptorami na komórkach nabłonka jelitowego
  • Internalizację i lokalizację w mitochondriach
  • Zatrzymanie produkcji ATP i generowanie reaktywnych form tlenu
  • Inaktywację białek z rodziny Rho GTPaz
  • Depolimeryzację aktyny
  • Uszkodzenie połączeń międzykomórkowych nabłonka jelitowego
  • Wywoływanie intensywnej odpowiedzi sekrecyjnej, stanu zapalnego i martwicy nabłonka okrężnicy2425

Szczególnie niebezpieczny jest hiperpatogenny szczep NAP1/BI/027, który produkuje znacznie więcej toksyn niż inne szczepy i jest związany z cięższym przebiegiem zakażenia, w tym toksycznym rozdęciem okrężnicy, niewydolnością nerek i leukocytozą.2627

Inne patogeny odpowiedzialne za AAD

Oprócz C. difficile, istnieje kilka innych patogenów, które mogą powodować biegunkę związaną z antybiotykami:

  • Clostridium perfringens: Wytwarzający enterotoksynę C. perfringens typu A (obecnie nazywany C. perfringens typu F) jest uważany za ważny czynnik przyczynowy AAD, odpowiadający za około 2-8% przypadków.2829
  • Staphylococcus aureus: Enterotoksyczne szczepy S. aureus mogą wywoływać biegunkę po leczeniu antybiotykami. AAD wywołane przez S. aureus zostało zidentyfikowane jako przyczyna biegunki u pacjentów hospitalizowanych.3031
  • Klebsiella oxytoca: Gram-ujemna fakultatywnie tlenowa enterobakteria K. oxytoca jest czynnikiem wywołującym krwotoczne zapalenie okrężnicy związane z antybiotykami (AAHC).3233
  • Grzyby Candida: Rola grzybów Candida w AAD jest kontrowersyjna. Chociaż nadmierny wzrost Candida był długo postulowany jako przyczyna AAD, ostatnie badania wskazują, że podwyższone miano Candida w kale jest raczej wynikiem leczenia antybiotykami lub samej biegunki, a nie jej przyczyną.3435
  • Salmonella: Rzadko, zakażenie Salmonella spp. może rozwinąć się po leczeniu antybiotykami.3637

Warto zauważyć, że tylko około 40% przypadków AAD można przypisać wyżej wymienionym patogenom, co oznacza, że większość przypadków AAD pozostaje bez ustalonej etiologii mikrobowej.38

Czynniki ryzyka i czasowy przebieg AAD

Antybiotyki związane z wysokim ryzykiem AAD

Chociaż praktycznie każdy antybiotyk może wywołać biegunkę, niektóre są szczególnie często związane z AAD:

  • Wysokie ryzyko: Cefalosporyny (szczególnie 3. generacji), penicyliny szerokowidmowe (szczególnie ampicylina i amoksycylina), klindamycyna, fluorochinolony3940
  • Umiarkowane ryzyko: Makrolidy, kotrimoksazol41
  • Niskie ryzyko: Aminoglikozydy pozajelitowe, tetracykliny, metronidazol, wankomycyna, rifampicyna, rifaksymina42

Najwyższe wskaźniki AAD obserwuje się przy stosowaniu amoksycyliny, amoksycyliny z kwasem klawulanowym (Augmentin) i cefixime.43

Ryzyko rozwoju biegunki związanej z antybiotykami ponad dwukrotnie wzrasta przy stosowaniu antybiotykoterapii dłuższej niż trzy dni.44

Czynniki ryzyka hostitelskie

Oprócz ekspozycji na antybiotyki, istnieją czynniki związane z gospodarzem, które predysponują do rozwoju AAD:

  • Zaawansowany wiek (≥65 lat)45
  • Wcześniejsza historia AAD46
  • Choroby współistniejące i ciężkie choroby podstawowe47
  • Zaburzona odpowiedź immunologiczna na toksyny C. difficile48
  • Dłuższy pobyt w szpitalu49
  • Stosowanie inhibitorów pompy protonowej5051
  • Chemioterapia52
  • Karmienie przez zgłębnik5354

Czasowy przebieg biegunki związanej z antybiotykami

AAD może wystąpić na różnych etapach w odniesieniu do stosowania antybiotyków:

  • Zazwyczaj pojawia się w trakcie leczenia antybiotykami, jednak może wystąpić nawet do 2 miesięcy po zakończeniu terapii5556
  • Biegunka spowodowana przez C. difficile zazwyczaj rozpoczyna się w ciągu 5-10 dni od rozpoczęcia antybiotykoterapii, ale może wystąpić już pierwszego dnia lub nawet do 2 miesięcy później57
  • Większość przypadków zakażenia C. difficile występuje między 4 a 9 dniem antybiotykoterapii58
  • Niebakteryjne przyczyny AAD zwykle występują w ciągu 48-72 godzin od rozpoczęcia antybiotykoterapii, mają tendencję do łagodniejszego przebiegu i zwykle ustępują samoistnie59

Specyficzne mechanizmy patogenezy zakażenia C. difficile

Zakażenie C. difficile (CDI) stanowi najpoważniejszą postać biegunki związanej z antybiotykami. Patogeneza tego zakażenia obejmuje sekwencję wydarzeń, które prowadzą do kolonizacji jelita i produkcji toksyn:

Kolonizacja i produkcja toksyn

Proces patogenezy zakażenia C. difficile można podzielić na następujące etapy:

  1. Zaburzenie prawidłowej mikroflory okrężnicy spowodowane antybiotykami, co obniża oporność kolonizacyjną60
  2. Kolonizacja C. difficile następuje zwykle poprzez spożycie odporne na ciepło formy przetrwalnikowej, która przekształca się w formę wegetatywną w okrężnicy61
  3. Produkcja toksyn: Patogenne szczepy C. difficile wytwarzają dwie główne toksyny (A i B)62
  4. Działanie toksyn na nabłonek jelitowy: Toksyny wiążą się z receptorami na komórkach jelitowych, powodując ich internalizację i lokalizację w mitochondriach63
  5. Inaktywacja białek Rho: Toksyny A i B są glukozylotransferazami, które dezaktywują białka z rodziny Rho GTPaz, co prowadzi do depolimeryzacji aktyny64
  6. Przerwanie bariery nabłonkowej: Prowadzi to do zwiększonej przepuszczalności śluzówki, odpowiedzi sekrecyjnej i stanu zapalnego65
  7. Tworzenie pseudobłon: W miarę pogarszania się zapalenia okrężnicy pojawiają się ogniskowe owrzodzenia, a nagromadzenie ropnej i martwiczej pozostałości tworzy charakterystyczne pseudobłony – oddzielne żółto-białe płytki, które łatwo się odrywają6667

Rola locus patogenności C. difficile

Patogenność C. difficile jest kodowana w specyficznym locus patogenności, które zawiera pięć genów (TcdA-E):

  • TcdA: Gen kodujący toksynę A
  • TcdB: Gen kodujący toksynę B
  • TcdD: Gen kodujący pozytywny regulator transkrypcji toksyn
  • TcdC: Gen kodujący negatywny regulator produkcji toksyn
  • TcdE: Gen kodujący toksynę naruszającą błonę bakteryjną68

Hiperpatogenne szczepy, takie jak NAP1/BI/027, często mają mutacje w genie TcdC, co prowadzi do zwiększonej produkcji toksyn i zwiększonej wirulencji.69

Nowe spojrzenie na patogenezę AAD

Mikrobiom jelitowy a podatność na AAD

Ostatnie badania sugerują, że skład mikrobioty jelitowej przed rozpoczęciem antybiotykoterapii może wpływać na podatność na rozwój AAD. Badania wykazały, że poziom bakterii z rodziny Ruminococcaceae w kale pacjentów, którzy rozwinęli biegunkę po leczeniu amoksycyliną z kwasem klawulanowym, był znacznie niższy zarówno przed, jak i w trakcie leczenia w porównaniu z pacjentami, którzy nie rozwinęli biegunki. Sugeruje to, że osoby mogą, w zależności od składu mikrobioty jelitowej, być predysponowane do biegunki związanej z antybiotykami.70

Rola probiotyków w zapobieganiu AAD

Probiotyki są żywymi mikroorganizmami, które podawane w odpowiednich ilościach przynoszą korzyści zdrowotne gospodarzowi. Jednym z najczęstszych wskazań do stosowania probiotyków jest zapobieganie biegunce związanej z antybiotykami.71

Mechanizmy, poprzez które probiotyki mogą zapobiegać lub łagodzić AAD, obejmują:

  • Wzmacnianie funkcji bariery jelitowej poprzez zwiększenie wydzielania mucyny i regulację białek połączeń ścisłych72
  • Modulowanie skład mikrobioty jelitowej73
  • Zwiększenie produkcji krótkołańcuchowych kwasów tłuszczowych74
  • Zmiana pH jelitowego, które nie sprzyja namnażaniu się patogenów75
  • Hamowanie wydzielania toksyn bakteryjnych76
  • Skuteczne konkurowanie o składniki odżywcze i miejsca wiązania z bakteriami patogennymi77

Meta-analizy wykazały, że probiotyki znacząco zmniejszają częstość występowania biegunki związanej z antybiotykami u dzieci (zbiorcze RR = 0,42, 95%CI: 0,33-0,53) oraz zakażeń C. difficile (zbiorcze RR = 0,35, 95%CI: 0,13-0,92).78

Transplantacja mikrobioty kałowej

Biorąc pod uwagę, że wszystkie formy AAD reprezentują zaburzenie mikrobioty jelitowej, przywrócenie normalnej mikroflory komensalnej jest atrakcyjnym sposobem leczenia tego schorzenia.79 Transplantacja mikrobioty kałowej (FMT) wykazała się wyjątkową skutecznością w leczeniu nawracających zakażeń C. difficile, z odsetkiem wyleczeń przekraczającym 85%, a w wielu przypadkach nawet 90%.80

Rozwój naszego zrozumienia znaczenia mikrobioty jelitowej oraz wyraźna skuteczność FMT w badaniach klinicznych zwiększyły znaczenie badań nad zakażeniem C. difficile i poszukiwaniem bardziej wyrafinowanych, ukierunkowanych terapii.81

Podsumowanie mechanizmów patogenezy AAD

Biegunka związana z antybiotykami jest wynikiem złożonych interakcji między lekami przeciwbakteryjnymi, mikrobiotą jelitową gospodarza i potencjalnymi patogenami oportunistycznymi. Główne mechanizmy patogenetyczne obejmują:

  1. Zaburzenie mikrobioty jelitowej, prowadzące do zmniejszonej produkcji krótkołańcuchowych kwasów tłuszczowych i zmienionego metabolizmu węglowodanów i kwasów żółciowych
  2. Biegunkę osmotyczną spowodowaną nagromadzeniem niestrawionych węglowodanów
  3. Biegunkę sekrecyjną spowodowaną przez niemetabolizowane kwasy żółciowe
  4. Bezpośrednie działanie drażniące niektórych antybiotyków na błonę śluzową jelita
  5. Nadmierny wzrost patogenów, szczególnie C. difficile, który wytwarza toksyny uszkadzające nabłonek jelitowy
  6. Zakażenia innymi patogenami oportunistycznymi, takimi jak C. perfringens, S. aureus, K. oxytoca i Salmonella

Zrozumienie tych mechanizmów jest kluczowe dla opracowania skutecznych strategii zapobiegania i leczenia biegunki związanej z antybiotykami, a także dla zmniejszenia związanego z nią obciążenia klinicznego i ekonomicznego systemów opieki zdrowotnej.8283

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  1. 11.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1 Antibiotics and antibiotic-associated diarrhea: a real-world disproportionality study of the FDA adverse event reporting system from 2004 to 2022 | BMC Pharmacology and Toxicology | Full Text
    https://bmcpharmacoltoxicol.biomedcentral.com/articles/10.1186/s40360-023-00710-w
    Our study aimed to assess the risk signals of antibiotic-associated diarrhea (AAD) caused by various antibiotics using real-world data and provide references for safe clinical applications. […] The excessive use of broad-spectrum antibiotics disrupts the balance of healthy gut bacteria and leads to AAD. Approximately 5%~35% of patients suffer from AAD after receiving antibiotics. […] AAD is frequently caused by various pathogenic bacteria, with Clostridium difficile (CD) being responsible for almost one-third of AAD cases. […] Overuse of some antibiotics can speed up the growth rate of CD, which can influence other bacteria in the gastrointestinal system, leading to inflammation. […] Clostridium difficile infection (CDI) is a major cause of nosocomial infections, particularly in developed countries.
  • #2 Probiotics for the Prevention of Antibiotic-Associated Diarrhea
    https://www.mdpi.com/2227-9032/10/8/1450
    Several communities have started using probiotic-rich fermented foods as therapeutic options with presumed medicinal powers. […] Probiotics have been tested for a number of clinical uses such as the prevention of antibiotic-associated diarrhea (AAD). […] AAD is a common side effect of antibiotic usage, which affects up to 30% of patients. […] The hypothesis behind using probiotics for AAD is that they help normalize an unbalanced flora. […] There are many potential mechanisms by which probiotics support intestinal health such as (i) boosting immunity, (ii) increasing gut barrier integrity, (iii) producing antimicrobial substances, (iv) modulating the gut microbiome, (v) increasing water absorption, and (vi) decreasing opportunistic pathogens. […] Probiotic research for the treatment of AAD is growing due to the increasing prevalence of AAD and the subsequent strain on the healthcare system. AAD is a common side effect of antibiotic usage that affects up to one-third of patients who are treated with antibiotics.
  • #3 Antibiotic-Associated Diarrhea Beyond C. Difficile: A Scoping Review | Published in Journal of Brown Hospital Medicine
    https://bhm.scholasticahq.com/article/39745-antibiotic-associated-diarrhea-beyond-c-difficile-a-scoping-review
    A common complication of antibiotic use is the development of diarrheal illness. The pathogenesis of antibiotic associated diarrhea (AAD) may be mediated through alteration of intestinal microbiota, overgrowth of opportunistic pathogens, and direct drug toxicity on the gut. […] The likely pathogenesis of AAD includes alteration of intestinal microbiota, direct drug toxicity on the gut and development of a superinfection by a pathogenic microbe. […] Although the role of C. difficile in the pathogenesis of AAD has been well studied, there are considerable gaps in our understanding of the pathogenesis of non-CDI AAD due to putative microbial etiologies including C. perfringens, S. aureus, K. oxytoca, and Candida species. Identifying the etiology and understanding the pathogenesis of AAD will help in improving healthcare and in reducing the economic burden.
  • #4 Pathogenesis of antibiotic-associated diarrhea (AAD)—a systematic review
    https://digitalcommons.library.tmc.edu/dissertations/AAI1515607/
    A common complication of antibiotic use is the development of diarrheal illness. The pathogenesis of antibiotic associated diarrhea (AAD) may be mediated through alteration of intestinal microbiota, overgrowth of opportunistic pathogens, and direct drug toxicity on the gut. Alterations in the intestinal microbiota result in metabolic imbalances, loss of colonization resistance and in turn allow proliferation of opportunistic pathogens. Currently less than 33% of AAD cases can be attributable to Clostridium difficile leaving a large number of cases undiagnosed and poorly treated. Although the pathogenesis of Clostridium difficile infection (CDI) has been well documented, the role of other putative microbial etiologies (Clostridium perfringens, Staphylococcus aureus, Klebsiella oxytoca, Candida species) and their pathogenic mechanisms in AAD has been unclear. […] This review provides a comprehensive and systematic approach to the existing data on AAD and includes concise descriptions of the pathogenesis of CDI and non-CDI AAD in the form of figures.
  • #5 Antibiotic-Associated Diarrhea – Harvard Health
    https://www.health.harvard.edu/a_to_z/antibiotic-associated-diarrhea-a-to-z
    In healthy people, many different species of bacteria live inside the bowel. Many are harmless or even helpful to the body, but a few have the potential to be aggressive troublemakers. Under normal circumstances, the „bad” bacteria are far outnumbered. So, the bowel’s natural ecological balance keeps them under control. […] This can change dramatically when a person begins treatment with an antibiotic. This is because antibiotics can kill large numbers of the bowel’s normal bacteria, altering the delicate balance among the various species. […] One type of bacteria in particular, a species called Clostridium difficile (C. difficile), can overgrow inside the bowel, producing irritating chemicals that damage the bowel wall and trigger bowel inflammation, called colitis. This can cause abdominal pain, cramps, diarrhea, and fever. In some cases, high-volume, diarrhea is so frequent that the person develops dehydration (very low levels of body water).
  • #6 Antibiotic-Associated Diarrhea and Colitis | Musculoskeletal Key
    https://musculoskeletalkey.com/antibiotic-associated-diarrhea-and-colitis/1000
    Antibiotic-Associated Diarrhea and Colitis W. Daniel Jackson Richard J. Grand A spectrum of gastrointestinal disturbances ranging from transient diarrhea to frank pseudomembranous colitis has been associated with antibiotic treatment in adults and children. […] Studies have identified cytopathic toxins elaborated by Clostridium difficile as the cause of most cases of antibiotic-associated pseudomembranous colitis and most nosocomial cases of antibiotic-associated diarrhea. […] The ability of the indigenous flora to limit proliferation or exclude colonization of pathogenic bacteria is called colonization resistance and is important in protecting the host at the gut interface with the environment. […] Oral or intravenous antibiotic agents that produce fecal levels sufficient to alter the bowel flora, particularly antibiotics active against the indigenous anaerobic population, reduce the colonization resistance of the intestinal lumen to C. difficile.
  • #7 Antibiotic-Associated Diarrhea – Gastrointestinal Infections – Intestinal Diseases – Gastrointestinal Diseases – Gastroenterology – Diseases – McMaster Textbook of Internal Medicine
    https://empendium.com/mcmtextbook/chapter/B31.II.4.24.1.7.
    Antibiotic-associated diarrhea develops in the course of antimicrobial treatment or within 2 months of its discontinuation. […] Antibiotic treatment has a direct influence on the gastrointestinal tract and induces quantitative and qualitative changes in the intestinal flora, which lead to impaired digestion and metabolism of some nutrients (this is nonspecific antibiotic-associated diarrhea, accounting for 70%-80% of cases). […] The disease may also be caused by selection of antibiotic-resistant bacterial strains, predominantly Clostridioides difficile strains producing toxin B (15%-25% of cases, associated with the most severe disease) or rarely other bacteria (~3% of cases: Klebsiella oxytoca, enterotoxic strains of Staphylococcus aureus, Clostridium perfringens type A).
  • #8 Metronidazole in the prevention of antibiotic-associated diarrhoea and Clostridium difficile infection in high-risk hospitalised patients | Gastroenterología y Hepatología (English Edition)
    https://www.elsevier.es/pt-revista-gastroenterologia-hepatologia-english-edition–382-articulo-metronidazole-in-prevention-antibiotic-associated-diarrhoea-S2444382418301111
    Antibiotic-associated diarrhoea (AAD) is a common disease in hospitalised patients. Its main mechanism is disruption of the intestinal flora with subsequent changes in carbohydrate metabolism, short-chain fatty acids and bile acids. […] The primary finding of the study was that 16.4% of patients in the observation group and 4.9% in the intervention group had AAD with a P of 0.109 and an OR of 0.26 (0.051.29). The study was unable to establish a relationship between the administration of metronidazole and a lower number of patients with AAD. […] This constitutes the first prospective study that evaluated the effectiveness of these drugs, normally used in the treatment of CDI, as a preventive measure in selected patients. It found that receiving metronidazole does not significantly prevent the onset of AAD.
  • #9
    https://pmc.ncbi.nlm.nih.gov/articles/PMC6334067/
    Antibiotic-associated diarrhoea is among the most common adverse events related to antibiotic use. […] Recent developments in our understanding of the biology of the gut microbiota have provided new insights into the pathogenesis of these conditions, and have revealed a role for manipulation of the gut microbiota as a novel therapeutic approach. […] One key mechanism of AAD appears to be changes in the gut microbiota that cause decreased short-chain fatty acid absorption, resulting in osmotic diarrhoea. […] Antibiotic use is the major risk factor for CDI, causing antibiotic-related loss of gut microbial communities that protect against gut infection, thereby facilitating the germination and vegetative growth of the organism when it enters the gut of vulnerable people. […] Given that all forms of AAD represent a perturbation of the gut microbiota, restoration of the usual commensal microbiota is an appealing means of treating the condition.
  • #10 Mechanisms of Preventing Antibiotic-Associated Diarrhea and the Role for Probiotics
    https://ctv.veeva.com/study/mechanisms-of-preventing-antibiotic-associated-diarrhea-and-the-role-for-probiotics
    The focus of the study is to better understand the mechanisms causing antibiotic-associated diarrhea (AAD) and how probiotics may prevent some of the iatrogenic effects of antibiotic medications. […] Data from several studies suggest that antibiotic-induced disruption of commensal bacteria in the colon results in a significant (up to 50%) reduction in short chain fatty acid (SCFA) production and a concomitant reduction in Na-dependent fluid absorption resulting in AAD. […] Data from several studies are consistent with the notion that antibiotic-induced disruption of commensal bacteria in the colon results in a significant reduction of short chain fatty acid (SCFA) production and a concomitant reduction in Na-dependent fluid absorption resulting in AAD. […] The primary hypothesis is that antibiotics will result in a reduction in fecal SCFA, but BB-12 supplementation will protect against antibiotic-induced SCFA reduction and/or be associated with a more rapid return to baseline SCFA levels as compared to controls.
  • #11 Diarrhea Caused by Primarily Non-Gastrointestinal Infections – Page 7
    https://www.medscape.com/viewarticle/505473_7
    In patients with primarily non-gastrointestinal infections, diarrhea occurs in 5-25% of those receiving antibiotic treatment. The major mechanisms of antibiotic-associated diarrhea (AAD) involve disturbances of the gut microflora and the direct effects of antibiotics on the mucous membranes. The anerobic gut microflora metabolizes high-molecular-weight carbohydrates to absorbable short-chain fatty acids. When the gut microflora is altered by antibiotics, high-molecular-weight carbohydrates accumulate in the colon and cause osmotic diarrhea. Bile acids, which escape absorption in the small bowel, are usually deconjugated and dehydroxylated by bacteria. When the bacterial flora is disturbed, unmetabolized dihydroxy bile acids, which are potent secretory agents, lead to development of secretory diarrhea in the colon.
  • #12 Mechanisms of Preventing Antibiotic-Associated Diarrhea and the Role for Probiotics
    https://ctv.veeva.com/study/mechanisms-of-preventing-antibiotic-associated-diarrhea-and-the-role-for-probiotics
    The focus of the study is to better understand the mechanisms causing antibiotic-associated diarrhea (AAD) and how probiotics may prevent some of the iatrogenic effects of antibiotic medications. […] Data from several studies suggest that antibiotic-induced disruption of commensal bacteria in the colon results in a significant (up to 50%) reduction in short chain fatty acid (SCFA) production and a concomitant reduction in Na-dependent fluid absorption resulting in AAD. […] Data from several studies are consistent with the notion that antibiotic-induced disruption of commensal bacteria in the colon results in a significant reduction of short chain fatty acid (SCFA) production and a concomitant reduction in Na-dependent fluid absorption resulting in AAD. […] The primary hypothesis is that antibiotics will result in a reduction in fecal SCFA, but BB-12 supplementation will protect against antibiotic-induced SCFA reduction and/or be associated with a more rapid return to baseline SCFA levels as compared to controls.
  • #13 Diarrhea Caused by Primarily Non-Gastrointestinal Infections – Page 7
    https://www.medscape.com/viewarticle/505473_7
    In patients with primarily non-gastrointestinal infections, diarrhea occurs in 5-25% of those receiving antibiotic treatment. The major mechanisms of antibiotic-associated diarrhea (AAD) involve disturbances of the gut microflora and the direct effects of antibiotics on the mucous membranes. The anerobic gut microflora metabolizes high-molecular-weight carbohydrates to absorbable short-chain fatty acids. When the gut microflora is altered by antibiotics, high-molecular-weight carbohydrates accumulate in the colon and cause osmotic diarrhea. Bile acids, which escape absorption in the small bowel, are usually deconjugated and dehydroxylated by bacteria. When the bacterial flora is disturbed, unmetabolized dihydroxy bile acids, which are potent secretory agents, lead to development of secretory diarrhea in the colon.
  • #14 Antibiotic associated diarrhea | PPT
    https://www.slideshare.net/slideshow/antibiotic-associated-diarrhea1/12980136
    Antibiotic-Associated Diarrhea (AAD) 5 25% depending on causative antibiotic Motilin receptor agonist Erythromycin Stimulate bowel motility Clavulanate Intestinal flora alteration Decreased carbohydrate metab SCFA Osmotic diarrhea Decreased PBA metabolism PBA Secretory diarrhea Overgrowth of pathogenic micro-organisms SCFA: Short Chain Fatty Acid PBA: Primary Biliary Acid Gorkiewicz G. Int J Antimicrobial Agents 2009 ; 33 : S37 S41. […] Major infectious agent in AAD Causative agent unknown in most cases Candida overgrowth Controversial Clostridium Perfringens Food poisoning Necrotizing entero-colitis Staphylococcus Aureus Food poisoning Diarrhea (majority MRSA*) Klebsiella Oxytoca Antibiotic-associated hemorrhagic colitis Clostridium Difficile 30% of AAD in hospitals * MRSA: Methicillin-Resistant Staphylococcus Aureus Gorkiewicz G. Int J Antimicrobial Agents 2009 ; 33 : S37 S41.
  • #15 Diarrhea Caused by Primarily Non-Gastrointestinal Infections – Page 7
    https://www.medscape.com/viewarticle/505473_7
    In patients with primarily non-gastrointestinal infections, diarrhea occurs in 5-25% of those receiving antibiotic treatment. The major mechanisms of antibiotic-associated diarrhea (AAD) involve disturbances of the gut microflora and the direct effects of antibiotics on the mucous membranes. The anerobic gut microflora metabolizes high-molecular-weight carbohydrates to absorbable short-chain fatty acids. When the gut microflora is altered by antibiotics, high-molecular-weight carbohydrates accumulate in the colon and cause osmotic diarrhea. Bile acids, which escape absorption in the small bowel, are usually deconjugated and dehydroxylated by bacteria. When the bacterial flora is disturbed, unmetabolized dihydroxy bile acids, which are potent secretory agents, lead to development of secretory diarrhea in the colon.
  • #16 PATHOGENESIS OF ANTIBIOTIC-INDUCED DIARRHEA NOT DUE TO CLOSTRIDIUM DIFFICILE (CD) | Pediatric Research
    https://www.nature.com/articles/pr1986165
    We wished to identify, in the in vitro rabbit intestine, the pathogenesis of post-antibiotic non CD-mediated diarrhea. […] In conclusion: 1) both CD+ and CD-animals show secretory changes in the small and large intestine, more pronounced in CD-; 2) jejunal influx of nutrients is hampered only in CD+ animals. Thus, the pathogenesis of post-antibiotic CD-mediated diarrhea appears essentially invasive, while that not due to CD appears essentially secretory.
  • #17 Antibiotic associated diarrhea | PPT
    https://www.slideshare.net/slideshow/antibiotic-associated-diarrhea1/12980136
    Antibiotic-Associated Diarrhea (AAD) 5 25% depending on causative antibiotic Motilin receptor agonist Erythromycin Stimulate bowel motility Clavulanate Intestinal flora alteration Decreased carbohydrate metab SCFA Osmotic diarrhea Decreased PBA metabolism PBA Secretory diarrhea Overgrowth of pathogenic micro-organisms SCFA: Short Chain Fatty Acid PBA: Primary Biliary Acid Gorkiewicz G. Int J Antimicrobial Agents 2009 ; 33 : S37 S41. […] Major infectious agent in AAD Causative agent unknown in most cases Candida overgrowth Controversial Clostridium Perfringens Food poisoning Necrotizing entero-colitis Staphylococcus Aureus Food poisoning Diarrhea (majority MRSA*) Klebsiella Oxytoca Antibiotic-associated hemorrhagic colitis Clostridium Difficile 30% of AAD in hospitals * MRSA: Methicillin-Resistant Staphylococcus Aureus Gorkiewicz G. Int J Antimicrobial Agents 2009 ; 33 : S37 S41.
  • #18 Diarrhea: antimicrobial associated in Horses (Equis) | Vetlexicon
    https://www.vetlexicon.com/equis/gastrohepatology/articles/diarrhea-antimicrobial-associated/
    Certain antibiotics have been associated with diarrhea during or shortly after their administration orally or systemically. […] Most commonly disruption of normal GI tract flora allowing overgrowth of pathogenic bacteria; direct toxicity can cause irritation, increased secretion and disrupted motility patterns. […] Tetracyclines and macrolides are associated with enterocolitis syndrome that can be induced experimentally. […] Other antibiotics can include ampicillin, penicillin and potentiated sulfonamides. […] Most commonly disrupt GI tract microflora overgrowth of pathogenic bacteria or conversion of common commensal organisms into pathogens. […] Direct toxicity irritation, increased secretion and disrupted motility patterns. […] Most common mechanism is disruption of GI tract flora, ie depletion of population of normal large intestinal flora especially anaerobes, streptococci and Lactobacillus, which protect the host from colonization by pathogenic bacteria (colonization resistance).
  • #19 Mechanisms and management of antibiotic-associated diarrhea – PubMed
    https://pubmed.ncbi.nlm.nih.gov/9798020/
    Only 10%-20% of all cases of antibiotic-associated diarrhea (AAD) are caused by infection with Clostridium difficile. Other infectious organisms causing AAD include Clostridium perfringens, Staphylococcus aureus, Klebsiella oxytoca, Candida species, and Salmonella species. […] Most of the clinically mild AAD cases are due to functional disturbances of intestinal carbohydrate or bile acid metabolism, to allergic and toxic effects of antibiotics on intestinal mucosa, or to pharmacological effects on motility. […] Mild cases of AAD that may or may not be caused by C. difficile can be resolved by discontinuation of antibiotic therapy and by dietary carbohydrate reduction. Only severe AAD caused by C. difficile requires specific antibiotic treatment.
  • #20 Mechanisms and management of antibiotic-associated diarrhea – PubMed
    https://pubmed.ncbi.nlm.nih.gov/9798020/
    Only 10%-20% of all cases of antibiotic-associated diarrhea (AAD) are caused by infection with Clostridium difficile. Other infectious organisms causing AAD include Clostridium perfringens, Staphylococcus aureus, Klebsiella oxytoca, Candida species, and Salmonella species. […] Most of the clinically mild AAD cases are due to functional disturbances of intestinal carbohydrate or bile acid metabolism, to allergic and toxic effects of antibiotics on intestinal mucosa, or to pharmacological effects on motility. […] Mild cases of AAD that may or may not be caused by C. difficile can be resolved by discontinuation of antibiotic therapy and by dietary carbohydrate reduction. Only severe AAD caused by C. difficile requires specific antibiotic treatment.
  • #21 Antibiotic-Associated Diarrhea – Gastrointestinal Infections – Intestinal Diseases – Gastrointestinal Diseases – Gastroenterology – Diseases – McMaster Textbook of Internal Medicine
    https://empendium.com/mcmtextbook/chapter/B31.II.4.24.1.7.
    Antibiotic-associated diarrhea develops in the course of antimicrobial treatment or within 2 months of its discontinuation. […] Antibiotic treatment has a direct influence on the gastrointestinal tract and induces quantitative and qualitative changes in the intestinal flora, which lead to impaired digestion and metabolism of some nutrients (this is nonspecific antibiotic-associated diarrhea, accounting for 70%-80% of cases). […] The disease may also be caused by selection of antibiotic-resistant bacterial strains, predominantly Clostridioides difficile strains producing toxin B (15%-25% of cases, associated with the most severe disease) or rarely other bacteria (~3% of cases: Klebsiella oxytoca, enterotoxic strains of Staphylococcus aureus, Clostridium perfringens type A).
  • #22 Antibiotic-Associated Diarrhea Beyond C. Difficile: A Scoping Review | Published in Journal of Brown Hospital Medicine
    https://bhm.scholasticahq.com/article/39745-antibiotic-associated-diarrhea-beyond-c-difficile-a-scoping-review
    The two main toxins of C. difficile, toxins A and B play a critical role in the pathophysiology of CDI. Both are enterotoxic and cytotoxic; however, traditionally toxin A is named enterotoxin A and toxin B is named cytotoxin B. […] Although C. difficile is implicated in most AAD cases, other causes of Non-C. difficile Pathogen-specific AAD should also be considered. […] The role of Candida spp. in AAD has been debated since the 1950s and continues to be controversial. […] Only 40% of AAD can be accounted for by the above causes leaving a majority of AAD cases without an etiology.
  • #23 Clostridioides difficile infection – Wikipedia
    https://en.wikipedia.org/wiki/Clostridioides_difficile_infection
    Pathogenic C. difficile strains produce multiple toxins. The most well-characterized are enterotoxin (Clostridium difficile toxin A) and cytotoxin (Clostridium difficile toxin B), both of which may produce diarrhea and inflammation in infected people, although their relative contributions have been debated. Toxins A and B are glucosyltransferases that target and inactivate the Rho family of GTPases. Toxin B (cytotoxin) induces actin depolymerization by a mechanism correlated with a decrease in the ADP-ribosylation of the low molecular mass GTP-binding Rho proteins.
  • #24 Antibiotic-Associated Diarrhea and Colitis | Musculoskeletal Key
    https://musculoskeletalkey.com/antibiotic-associated-diarrhea-and-colitis/1000
    The mechanism of toxin A-mediated inflammation begins with receptor binding and internalization by colonocytes, followed promptly by localization in mitochondria causing cessation of production of adenosine 5-triphosphate (ATP) and generation of reactive oxygen species. […] These processes account for the intense secretory response, inflammation, and necrosis of colonic epithelium exposed to C. difficile toxins. […] Most cases of antibiotic-associated enterocolitis occur in patients without underlying gastrointestinal disorders who are treated with antibiotics for other conditions (e.g., respiratory illness, often with questionable indication) or receive short-term preoperative antibiotics.
  • #25 Clostridioides (Clostridium) Difficile Colitis: Background, Etiology, Pathophysiology
    https://emedicine.medscape.com/article/186458-overview
    Clostridioides difficile (formerly Clostridium difficile) is a gram-positive, anaerobic, spore-forming bacillus that is responsible for the development of antibiotic-associated diarrhea and colitis. C difficile colitis results from a disturbance of the normal bacterial flora of the colon, colonization by C difficile, and the release of toxins that cause mucosal inflammation and damage. […] C difficile colitis results from a disruption of the normal bacterial flora of the colon, colonization with C difficile, and release of toxins that cause mucosal inflammation, mucosal damage, and diarrhea. […] The use of antibiotics, which alter and suppress the normal flora, allows proliferation of C difficile, toxin production, and diarrhea. […] Pathogenic strains of C difficile produce two distinct toxins. Toxin A is an enterotoxin, and toxin B is a cytotoxin; both are high molecular weight proteins capable of binding to specific receptors on the intestinal mucosal cells. Receptor-bound toxins gain intracellular entry by catalyzing a specific alteration of Rho proteins small glutamyl transpeptidase (GTP) binding proteins that assist in actin polymerization, cytoskeletal architecture, and cell movement. Both toxin A and toxin B appear to play a role in the pathogenesis of C difficile colitis in humans.
  • #26 Clostridioides (Clostridium) Difficile Colitis: Background, Etiology, Pathophysiology
    https://emedicine.medscape.com/article/186458-overview
    More recently, rat studies suggest that C difficile toxin B induces senescence in enteric glial cells (EGCs); investigators hypothesize that EGCs that survive toxin B and acquire senescence potentially cause the development of irritable bowel syndrome and inflammatory bowel disease via persistent inflammation, transfer of senescence status, and stimulation of preneoplastic cells. […] The NAP1 hypervirulent strain of C difficile is associated with the most serious sequelae of CDI, causing severe and fulminant colitis that is characterized by leukocytosis, renal failure, and toxic megacolon. […] Ultimately, many of the genetic influences on CDI and the clinical course of C difficile colitis likely remain unknown. At this point, it is understood that subtle differences in the immune system may significantly influence the natural history of C difficile disease.
  • #27 Clostridium difficile and Antibiotic-associated Diarrhea
    https://ijccm.org/abstractArticleContentBrowse/IJCCM/21585/JPJ/fullText
    The new variant of C. difficile (BI/NAP1/027) strain is a hypervirulent strain.12,13 This strain changes the severity dramatically with more incidence of septic shock toxic megacolon, gut perforation, and death. This type of strains can secrete much higher amounts of toxins A and B and are more resistant to standard antibiotic therapy.
  • #28 Diarrhea Caused by Primarily Non-Gastrointestinal Infections – Page 7
    https://www.medscape.com/viewarticle/505473_7
    Disturbances of the gut microflora also promote the overgrowth of distinct pathogenic bacteria. About 16-20% of AAD cases are caused by Clostridium difficile and 2-8% by Clostridium perfringens. Rare cases of diarrhea due to Klebsiella oxytoca (also known as penicillin-associated colitis) and Salmonella spp. have been reported after antibiotic treatment. Candida overgrowth has long been postulated to cause AAD, but recent studies clearly indicate that elevated Candida counts in the stool are a result of antibiotic treatment or diarrhea per se rather than a cause of AAD.
  • #29 A worldwide systematic review and meta-analysis of bacteria related to antibiotic-associated diarrhea in hospitalized patients | PLOS One
    https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0260667
    Antibiotic-associated diarrhea (AAD) is a major hospital problem and a common adverse effect of antibiotic treatment. The aim of this study was to investigate the prevalence of the most important bacteria that cause AAD in hospitalized patients. […] The results of this study emphasize the need for a surveillance program, as well as timely public and hospital health measures in order to control and treat AAD infections. […] Approximately 25% of AAD cases are caused by C. difficile, but it is difficult to estimate the prevalence in developing countries where knowledge, diagnostic resources and monitoring protocols are limited. […] C. perfringens enterotoxin (CPE)-positive toxinotype A (currently called C. perfringens type F strain) is considered as the most important causative agent of AAD.
  • #30 Antibiotic-Associated Diarrhea Beyond C. Difficile: A Scoping Review | Published in Journal of Brown Hospital Medicine
    https://bhm.scholasticahq.com/article/39745
    C. difficile is the most identified cause of AAD. […] The two main toxins of C. difficile, toxins A and B play a critical role in the pathophysiology of CDI. […] Although C. difficile is implicated in most AAD cases, other causes of Non-C. difficile Pathogen-specific AAD should also be considered. […] S. aureus induced AAD was identified early in the antibiotic era as a cause of AAD in hospitalized patients. […] K. oxytoca, a gram-negative facultative aerobic enterobacterium, has been shown to be the causative agent of antibiotic associated hemorrhagic colitis (AAHC). […] The role of Candida spp. in AAD has been debated since the 1950s and continues to be controversial. […] Only 40% of AAD can be accounted for by the above causes leaving a majority of AAD cases without an etiology. […] Non-microbial-causes of AAD tend to occur within 48-72 hours of starting antibiotics, tend to be less severe and usually are self-limiting.
  • #31 A worldwide systematic review and meta-analysis of bacteria related to antibiotic-associated diarrhea in hospitalized patients | PLOS One
    https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0260667
    The particular form of AAHC induced by K. oxytoca performed by Kochs postulates has received much more attention. […] Staphylococcus aureus is also a less-known agent for AAD, often referred to as large-scale enterocolitis of watery diarrhea. […] The highest resistance of C. difficile was estimated to ciprofloxacin and the lowest resistances were reported to chloramphenicol, vancomycin, and metronidazole. […] The prevalence of all four bacteria was higher in Europe compared to other continents.
  • #32 Antibiotic-Associated Diarrhea Beyond C. Difficile: A Scoping Review | Published in Journal of Brown Hospital Medicine
    https://bhm.scholasticahq.com/article/39745
    C. difficile is the most identified cause of AAD. […] The two main toxins of C. difficile, toxins A and B play a critical role in the pathophysiology of CDI. […] Although C. difficile is implicated in most AAD cases, other causes of Non-C. difficile Pathogen-specific AAD should also be considered. […] S. aureus induced AAD was identified early in the antibiotic era as a cause of AAD in hospitalized patients. […] K. oxytoca, a gram-negative facultative aerobic enterobacterium, has been shown to be the causative agent of antibiotic associated hemorrhagic colitis (AAHC). […] The role of Candida spp. in AAD has been debated since the 1950s and continues to be controversial. […] Only 40% of AAD can be accounted for by the above causes leaving a majority of AAD cases without an etiology. […] Non-microbial-causes of AAD tend to occur within 48-72 hours of starting antibiotics, tend to be less severe and usually are self-limiting.
  • #33 A worldwide systematic review and meta-analysis of bacteria related to antibiotic-associated diarrhea in hospitalized patients | PLOS One
    https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0260667
    The particular form of AAHC induced by K. oxytoca performed by Kochs postulates has received much more attention. […] Staphylococcus aureus is also a less-known agent for AAD, often referred to as large-scale enterocolitis of watery diarrhea. […] The highest resistance of C. difficile was estimated to ciprofloxacin and the lowest resistances were reported to chloramphenicol, vancomycin, and metronidazole. […] The prevalence of all four bacteria was higher in Europe compared to other continents.
  • #34 Antibiotic-Associated Diarrhea Beyond C. Difficile: A Scoping Review | Published in Journal of Brown Hospital Medicine
    https://bhm.scholasticahq.com/article/39745
    C. difficile is the most identified cause of AAD. […] The two main toxins of C. difficile, toxins A and B play a critical role in the pathophysiology of CDI. […] Although C. difficile is implicated in most AAD cases, other causes of Non-C. difficile Pathogen-specific AAD should also be considered. […] S. aureus induced AAD was identified early in the antibiotic era as a cause of AAD in hospitalized patients. […] K. oxytoca, a gram-negative facultative aerobic enterobacterium, has been shown to be the causative agent of antibiotic associated hemorrhagic colitis (AAHC). […] The role of Candida spp. in AAD has been debated since the 1950s and continues to be controversial. […] Only 40% of AAD can be accounted for by the above causes leaving a majority of AAD cases without an etiology. […] Non-microbial-causes of AAD tend to occur within 48-72 hours of starting antibiotics, tend to be less severe and usually are self-limiting.
  • #35 Diarrhea Caused by Primarily Non-Gastrointestinal Infections – Page 7
    https://www.medscape.com/viewarticle/505473_7
    Disturbances of the gut microflora also promote the overgrowth of distinct pathogenic bacteria. About 16-20% of AAD cases are caused by Clostridium difficile and 2-8% by Clostridium perfringens. Rare cases of diarrhea due to Klebsiella oxytoca (also known as penicillin-associated colitis) and Salmonella spp. have been reported after antibiotic treatment. Candida overgrowth has long been postulated to cause AAD, but recent studies clearly indicate that elevated Candida counts in the stool are a result of antibiotic treatment or diarrhea per se rather than a cause of AAD.
  • #36 Mechanisms and management of antibiotic-associated diarrhea – PubMed
    https://pubmed.ncbi.nlm.nih.gov/9798020/
    Only 10%-20% of all cases of antibiotic-associated diarrhea (AAD) are caused by infection with Clostridium difficile. Other infectious organisms causing AAD include Clostridium perfringens, Staphylococcus aureus, Klebsiella oxytoca, Candida species, and Salmonella species. […] Most of the clinically mild AAD cases are due to functional disturbances of intestinal carbohydrate or bile acid metabolism, to allergic and toxic effects of antibiotics on intestinal mucosa, or to pharmacological effects on motility. […] Mild cases of AAD that may or may not be caused by C. difficile can be resolved by discontinuation of antibiotic therapy and by dietary carbohydrate reduction. Only severe AAD caused by C. difficile requires specific antibiotic treatment.
  • #37 Diarrhea Caused by Primarily Non-Gastrointestinal Infections – Page 7
    https://www.medscape.com/viewarticle/505473_7
    Disturbances of the gut microflora also promote the overgrowth of distinct pathogenic bacteria. About 16-20% of AAD cases are caused by Clostridium difficile and 2-8% by Clostridium perfringens. Rare cases of diarrhea due to Klebsiella oxytoca (also known as penicillin-associated colitis) and Salmonella spp. have been reported after antibiotic treatment. Candida overgrowth has long been postulated to cause AAD, but recent studies clearly indicate that elevated Candida counts in the stool are a result of antibiotic treatment or diarrhea per se rather than a cause of AAD.
  • #38 Antibiotic-Associated Diarrhea Beyond C. Difficile: A Scoping Review | Published in Journal of Brown Hospital Medicine
    https://bhm.scholasticahq.com/article/39745
    C. difficile is the most identified cause of AAD. […] The two main toxins of C. difficile, toxins A and B play a critical role in the pathophysiology of CDI. […] Although C. difficile is implicated in most AAD cases, other causes of Non-C. difficile Pathogen-specific AAD should also be considered. […] S. aureus induced AAD was identified early in the antibiotic era as a cause of AAD in hospitalized patients. […] K. oxytoca, a gram-negative facultative aerobic enterobacterium, has been shown to be the causative agent of antibiotic associated hemorrhagic colitis (AAHC). […] The role of Candida spp. in AAD has been debated since the 1950s and continues to be controversial. […] Only 40% of AAD can be accounted for by the above causes leaving a majority of AAD cases without an etiology. […] Non-microbial-causes of AAD tend to occur within 48-72 hours of starting antibiotics, tend to be less severe and usually are self-limiting.
  • #39 Antibiotic associated diarrhea | PPT
    https://www.slideshare.net/slideshow/antibiotic-associated-diarrhea1/12980136
    CDI epidemiology Incidence of CDI appears to be increasing in the US 348,950 138,954 Healthcare Cost and Utilization Project (HCUP). http://hcupnet.ahrq.gov. […] Risk factors for C. difficile infection Exposure to antimicrobial agents Most important Advanced age 65 years Duration of hospitalization Cancer chemotherapy Effect of neutropenia Human immunodeficiency virus Manipulation of GIT Surgery Tube feeding Gastric acid suppression PPIs H2RA Clinical practice guidelines for Clostridium difficile infection in adults. Infect Control Hosp Epidemiol 2010 ; 31 : 431 455. […] Antimicrobial agents predisposing to CDI Classification particularly useful High risk Moderate risk Low risk Cephalosporins Ampicillins Parenteral aminoglycosides Clindamycin Macrolides Vancomycin Tetracyclines Metronidazole Fluoroquinolones Rifampin Co-trimoxazole Rifaximin Any antibiotic, at any dose, for any length of time, potentially allowing C difficile to proliferate cause disease Shannon-Lowe J et al. BMJ 2010 ; 340 : 641 646.
  • #40 Clostridioides (formerly Clostridium) difficile–Induced Diarrhea – Infectious Diseases – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/infectious-diseases/anaerobic-bacteria/clostridioides-formerly-clostridium-difficile-induced-diarrhea
    Toxins produced by Clostridioides difficile strains in the gastrointestinal tract cause pseudomembranous colitis, typically after antibiotic use. […] Antibiotic-induced changes in gastrointestinal flora are the dominant predisposing factors. […] Although most antibiotics have been implicated, the following pose the highest risk: Cephalosporins (particularly 3rd-generation), Penicillins (particularly ampicillin and amoxicillin), Clindamycin, Fluoroquinolones. […] The organism secretes both an enterotoxin and a cytotoxin, typically referred to as toxins A and B. […] The main effect of the toxin is on the colon, which secretes fluid and develops characteristic pseudomembranes discrete yellow-white plaques that are easily dislodged. […] Toxic megacolon, which rarely develops, is somewhat more likely after use of antimotility medications.
  • #41 Antibiotic associated diarrhea | PPT
    https://www.slideshare.net/slideshow/antibiotic-associated-diarrhea1/12980136
    CDI epidemiology Incidence of CDI appears to be increasing in the US 348,950 138,954 Healthcare Cost and Utilization Project (HCUP). http://hcupnet.ahrq.gov. […] Risk factors for C. difficile infection Exposure to antimicrobial agents Most important Advanced age 65 years Duration of hospitalization Cancer chemotherapy Effect of neutropenia Human immunodeficiency virus Manipulation of GIT Surgery Tube feeding Gastric acid suppression PPIs H2RA Clinical practice guidelines for Clostridium difficile infection in adults. Infect Control Hosp Epidemiol 2010 ; 31 : 431 455. […] Antimicrobial agents predisposing to CDI Classification particularly useful High risk Moderate risk Low risk Cephalosporins Ampicillins Parenteral aminoglycosides Clindamycin Macrolides Vancomycin Tetracyclines Metronidazole Fluoroquinolones Rifampin Co-trimoxazole Rifaximin Any antibiotic, at any dose, for any length of time, potentially allowing C difficile to proliferate cause disease Shannon-Lowe J et al. BMJ 2010 ; 340 : 641 646.
  • #42 Antibiotic associated diarrhea | PPT
    https://www.slideshare.net/slideshow/antibiotic-associated-diarrhea1/12980136
    CDI epidemiology Incidence of CDI appears to be increasing in the US 348,950 138,954 Healthcare Cost and Utilization Project (HCUP). http://hcupnet.ahrq.gov. […] Risk factors for C. difficile infection Exposure to antimicrobial agents Most important Advanced age 65 years Duration of hospitalization Cancer chemotherapy Effect of neutropenia Human immunodeficiency virus Manipulation of GIT Surgery Tube feeding Gastric acid suppression PPIs H2RA Clinical practice guidelines for Clostridium difficile infection in adults. Infect Control Hosp Epidemiol 2010 ; 31 : 431 455. […] Antimicrobial agents predisposing to CDI Classification particularly useful High risk Moderate risk Low risk Cephalosporins Ampicillins Parenteral aminoglycosides Clindamycin Macrolides Vancomycin Tetracyclines Metronidazole Fluoroquinolones Rifampin Co-trimoxazole Rifaximin Any antibiotic, at any dose, for any length of time, potentially allowing C difficile to proliferate cause disease Shannon-Lowe J et al. BMJ 2010 ; 340 : 641 646.
  • #43
    https://journals.lww.com/infectdis/fulltext/2002/02000/antibiotic_associated_diarrhea.24.aspx
    This is a review of antibiotic associated diarrhea with the following points: Antibiotics: The highest rates of AAD are with amoxicillin, amoxicillin-clavulanate (Augmentin) and cefixime; lower rates of 25% are seen with most other antibiotics including oral cephalosporins, fluoroquinolones, macrolides and tetracycline. […] Major other causes of antibiotic-associated diarrhea are: other enteric pathogens (C. perfringens type A, S. aureus and salmonella), direct effect on the gut by antibiotics (erythromycin, clavulanate) and, probably most important, the results of reducing fecal anaerobes (decreased metabolism of carbohydrates with osmotic diarrhea and reduced breakdown of primary bile acids which are potent colonic secretory agents). […] The major problem with antibiotic treatment of the antibiotic-associated complication is relapses noted in 20-25%; these occur with equal frequency with metronidazole or vancomycin and they are easily diagnosed by the patients history showing they now have the identical symptoms back. […] The recent data showing relapses occur in patients who do not mount an IgG anti-toxin A response supports the potential value of IVIG, but experience is nil and cost is high.
  • #44 Clostridium difficile–Associated Diarrhea | AAFP
    https://www.aafp.org/pubs/afp/issues/2005/0301/p921.html?___
    Clostridium difficile infection is responsible for approximately 3 million cases of diarrhea and colitis annually in the United States. Major predisposing factors for symptomatic C. difficile colitis include antibiotic therapy; advanced age; multiple, severe underlying diseases; and a faulty immune response to C. difficile toxins. The precipitating event for C. difficile colitis is disruption of the normal colonic microflora. This disruption usually is caused by broad-spectrum antibiotics, with clindamycin and broad-spectrum penicillins and cephalosporins most commonly implicated. The risk of developing antibiotic-associated diarrhea more than doubles with longer than three days of antibiotic therapy. After disruption of the colonic microflora, colonization of C. difficile generally occurs through the ingestion of heat-resistant spores, which convert to vegetative forms in the colon. Depending on host factors, an asymptomatic carrier state or clinical manifestations of C. difficile colitis develop. C. difficile associated diarrhea can occur up to eight weeks after the discontinuation of antibiotics. Most cases of C. difficile infection occur on days 4 through 9 of antibiotic therapy. The major host factors predisposing patients to the development of symptomatic C. difficile associated diarrhea include antibiotic therapy, advanced age, number and severity of underlying diseases, and faulty immune response to C. difficile toxins. C. difficile causes toxin-mediated colitis. Pathogenic strains of C. difficile produce two protein exotoxins: toxin A and toxin B. Toxin A activates macrophages and mast cells. Activation of these cells causes the production of inflammatory mediators, which leads to fluid secretion and increased mucosal permeability. Toxin B has little enterotoxic activity but is extremely cytotoxic in vitro. C. difficile toxins also cause leukocyte chemotaxis and the upregulation of cytokines and other inflammatory mediators. Consequently, there is a profound colonic inflammatory response, which is evidenced clinically by a high WBC count. As colitis worsens, focal ulcerations occur, and the accumulation of purulent and necrotic debris forms the typical pseudomembrane.
  • #45 Antibiotics and antibiotic-associated diarrhea: a real-world disproportionality study of the FDA adverse event reporting system from 2004 to 2022 | BMC Pharmacology and Toxicology | Full Text
    https://bmcpharmacoltoxicol.biomedcentral.com/articles/10.1186/s40360-023-00710-w
    While almost all antibiotics can lead to CDI, broad-spectrum penicillins and cephalosporins, clindamycin, and fluoroquinolones have a higher risk of inducing CDI. […] The excessive and inappropriate use of antibiotics and the emergence of novel antibiotics in recent years has resulted in an increase in the global incidence rate and severity of AAD. […] Our findings showed that patients aged 65 years or older had a higher ROR value, indicating that their probability of developing AAD was higher. […] Our study found that nearly all antibiotics were strongly associated with AAD events, consistent with a clinical retrospective study. […] The results were consistent with previous research indicating that broad-spectrum antibiotics such as lincomycin, cephalosporin, and penicillin were more likely to result in AAD.
  • #46 Antibiotic-associated diarrhea – sboulardii – CNCM i-745
    https://www.saccharomycesboulardii.com/therapeutic-area/antibiotic-associated-diarrhea/
    Up to 35% of adults receiving antibiotics experience antibiotic-associated diarrhea (AAD).4 However, AAD occurs in a wide variety of populations including outpatients and residents of long-term care facilities4, with risk-associated factors such as a history of AAD, young or elderly age4 and co-morbidities.4 […] Probiotics are living microorganisms that when administered in adequate amounts confer a health benefit.6 The single-strain yeast probiotic Saccharomyces boulardii CNCM I-745 is proven to help reduce the occurrence of antibiotic-associated diarrhea.6 For example, it has been demonstrated that the occurrence of diarrhea is reduced by 53% in adults when Saccharomyces boulardii CNCM I-745 is taken at the same time as antibiotics.6 In addition the yeast reduces the impact of antibiotics on the microbiota during treatment.7 […] Unlike bacterial probiotics, S. boulardii CNCM I-745 is naturally resistant to antibiotics which means that it can be taken at the same time as antibiotics to act on the immediate effect of the antibiotics on the microbiota and reduce the risk of antibiotic-associated diarrhea.8
  • #47 Antibiotic-associated diarrhea – sboulardii – CNCM i-745
    https://www.saccharomycesboulardii.com/therapeutic-area/antibiotic-associated-diarrhea/
    Up to 35% of adults receiving antibiotics experience antibiotic-associated diarrhea (AAD).4 However, AAD occurs in a wide variety of populations including outpatients and residents of long-term care facilities4, with risk-associated factors such as a history of AAD, young or elderly age4 and co-morbidities.4 […] Probiotics are living microorganisms that when administered in adequate amounts confer a health benefit.6 The single-strain yeast probiotic Saccharomyces boulardii CNCM I-745 is proven to help reduce the occurrence of antibiotic-associated diarrhea.6 For example, it has been demonstrated that the occurrence of diarrhea is reduced by 53% in adults when Saccharomyces boulardii CNCM I-745 is taken at the same time as antibiotics.6 In addition the yeast reduces the impact of antibiotics on the microbiota during treatment.7 […] Unlike bacterial probiotics, S. boulardii CNCM I-745 is naturally resistant to antibiotics which means that it can be taken at the same time as antibiotics to act on the immediate effect of the antibiotics on the microbiota and reduce the risk of antibiotic-associated diarrhea.8
  • #48 Clostridium difficile–Associated Diarrhea | AAFP
    https://www.aafp.org/pubs/afp/issues/2005/0301/p921.html?___
    Clostridium difficile infection is responsible for approximately 3 million cases of diarrhea and colitis annually in the United States. Major predisposing factors for symptomatic C. difficile colitis include antibiotic therapy; advanced age; multiple, severe underlying diseases; and a faulty immune response to C. difficile toxins. The precipitating event for C. difficile colitis is disruption of the normal colonic microflora. This disruption usually is caused by broad-spectrum antibiotics, with clindamycin and broad-spectrum penicillins and cephalosporins most commonly implicated. The risk of developing antibiotic-associated diarrhea more than doubles with longer than three days of antibiotic therapy. After disruption of the colonic microflora, colonization of C. difficile generally occurs through the ingestion of heat-resistant spores, which convert to vegetative forms in the colon. Depending on host factors, an asymptomatic carrier state or clinical manifestations of C. difficile colitis develop. C. difficile associated diarrhea can occur up to eight weeks after the discontinuation of antibiotics. Most cases of C. difficile infection occur on days 4 through 9 of antibiotic therapy. The major host factors predisposing patients to the development of symptomatic C. difficile associated diarrhea include antibiotic therapy, advanced age, number and severity of underlying diseases, and faulty immune response to C. difficile toxins. C. difficile causes toxin-mediated colitis. Pathogenic strains of C. difficile produce two protein exotoxins: toxin A and toxin B. Toxin A activates macrophages and mast cells. Activation of these cells causes the production of inflammatory mediators, which leads to fluid secretion and increased mucosal permeability. Toxin B has little enterotoxic activity but is extremely cytotoxic in vitro. C. difficile toxins also cause leukocyte chemotaxis and the upregulation of cytokines and other inflammatory mediators. Consequently, there is a profound colonic inflammatory response, which is evidenced clinically by a high WBC count. As colitis worsens, focal ulcerations occur, and the accumulation of purulent and necrotic debris forms the typical pseudomembrane.
  • #49 Antibiotic associated diarrhea | PPT
    https://www.slideshare.net/slideshow/antibiotic-associated-diarrhea1/12980136
    CDI epidemiology Incidence of CDI appears to be increasing in the US 348,950 138,954 Healthcare Cost and Utilization Project (HCUP). http://hcupnet.ahrq.gov. […] Risk factors for C. difficile infection Exposure to antimicrobial agents Most important Advanced age 65 years Duration of hospitalization Cancer chemotherapy Effect of neutropenia Human immunodeficiency virus Manipulation of GIT Surgery Tube feeding Gastric acid suppression PPIs H2RA Clinical practice guidelines for Clostridium difficile infection in adults. Infect Control Hosp Epidemiol 2010 ; 31 : 431 455. […] Antimicrobial agents predisposing to CDI Classification particularly useful High risk Moderate risk Low risk Cephalosporins Ampicillins Parenteral aminoglycosides Clindamycin Macrolides Vancomycin Tetracyclines Metronidazole Fluoroquinolones Rifampin Co-trimoxazole Rifaximin Any antibiotic, at any dose, for any length of time, potentially allowing C difficile to proliferate cause disease Shannon-Lowe J et al. BMJ 2010 ; 340 : 641 646.
  • #50 Fighting antibiotic-associated diarrhoea and antibiotic resistance – Hospital Pharmacy EuropeHospital Pharmacy Europe
    https://hospitalpharmacyeurope.com/clinical-zones/gastroenterology/fighting-antibiotic-associated-diarrhoea-and-antibiotic-resistance/
    Another demonstration of the important connection between gut microbial imbalance and C. difficile infection is that the use of gastric acid suppressing drugs, like proton pump inhibitors, known to remarkably alter the composition of the gut microbiota, also significantly increases the incidence of CDAD. […] A substantial number of randomised clinical trials have now addressed the prevention of the development of AAD and CDAD using probiotic bacterial cultures. […] The results of these rigorous systematic reviews and meta-analyses are helping more scientists and clinicians to realise that there is sufficient evidence to conclude that administration of high-quality probiotic bacteria, as an adjunct to antibiotic treatment, is associated with a reduced risk of developing these debilitating and potentially life-threatening conditions.
  • #51 Antibiotic-Associated Clostridium difficile Diarrhoea in Tertiary Care Hospital – A Study from Western India – Journal of Pure and Applied Microbiology
    https://microbiologyjournal.org/antibiotic-associated-clostridium-difficile-diarrhoea-in-tertiary-care-hospital-a-study-from-western-india/
    Risk factors associated with CDI include old age, chronic kidney disease, recent hospitalization, use of proton pump inhibitors, chemotherapy and tube feeding. […] Disruption of the normal gastrointestinal flora occurs as a result of prolonged antibiotic use resulting in decreased defences of body against C. difficile, which can easily produce toxins. […] Among the antibiotics that have increased risk of causing CDI, cephalosporins rank among the highest. […] Colonization and infection with CD can also be stimulated by acid suppression due to usage of PPI. […] Significant presence of CDI in this hospital population is demonstrated by this study. Cephalosporins, piperacillin-tazobactam and carbapenems were found to be the most common agents responsible for AAD caused by CD. Occurence of CDI may be reduced by choosing the antibiotic which has lower risk of producing AAD, from the susceptibility panel as well as avoiding the usage of -lactam and -lactamase inhibitors (BL-BLIs) as empirical therapy.
  • #52 Antibiotic associated diarrhea | PPT
    https://www.slideshare.net/slideshow/antibiotic-associated-diarrhea1/12980136
    CDI epidemiology Incidence of CDI appears to be increasing in the US 348,950 138,954 Healthcare Cost and Utilization Project (HCUP). http://hcupnet.ahrq.gov. […] Risk factors for C. difficile infection Exposure to antimicrobial agents Most important Advanced age 65 years Duration of hospitalization Cancer chemotherapy Effect of neutropenia Human immunodeficiency virus Manipulation of GIT Surgery Tube feeding Gastric acid suppression PPIs H2RA Clinical practice guidelines for Clostridium difficile infection in adults. Infect Control Hosp Epidemiol 2010 ; 31 : 431 455. […] Antimicrobial agents predisposing to CDI Classification particularly useful High risk Moderate risk Low risk Cephalosporins Ampicillins Parenteral aminoglycosides Clindamycin Macrolides Vancomycin Tetracyclines Metronidazole Fluoroquinolones Rifampin Co-trimoxazole Rifaximin Any antibiotic, at any dose, for any length of time, potentially allowing C difficile to proliferate cause disease Shannon-Lowe J et al. BMJ 2010 ; 340 : 641 646.
  • #53 Antibiotic associated diarrhea | PPT
    https://www.slideshare.net/slideshow/antibiotic-associated-diarrhea1/12980136
    CDI epidemiology Incidence of CDI appears to be increasing in the US 348,950 138,954 Healthcare Cost and Utilization Project (HCUP). http://hcupnet.ahrq.gov. […] Risk factors for C. difficile infection Exposure to antimicrobial agents Most important Advanced age 65 years Duration of hospitalization Cancer chemotherapy Effect of neutropenia Human immunodeficiency virus Manipulation of GIT Surgery Tube feeding Gastric acid suppression PPIs H2RA Clinical practice guidelines for Clostridium difficile infection in adults. Infect Control Hosp Epidemiol 2010 ; 31 : 431 455. […] Antimicrobial agents predisposing to CDI Classification particularly useful High risk Moderate risk Low risk Cephalosporins Ampicillins Parenteral aminoglycosides Clindamycin Macrolides Vancomycin Tetracyclines Metronidazole Fluoroquinolones Rifampin Co-trimoxazole Rifaximin Any antibiotic, at any dose, for any length of time, potentially allowing C difficile to proliferate cause disease Shannon-Lowe J et al. BMJ 2010 ; 340 : 641 646.
  • #54 Antibiotic-Associated Clostridium difficile Diarrhoea in Tertiary Care Hospital – A Study from Western India – Journal of Pure and Applied Microbiology
    https://microbiologyjournal.org/antibiotic-associated-clostridium-difficile-diarrhoea-in-tertiary-care-hospital-a-study-from-western-india/
    Risk factors associated with CDI include old age, chronic kidney disease, recent hospitalization, use of proton pump inhibitors, chemotherapy and tube feeding. […] Disruption of the normal gastrointestinal flora occurs as a result of prolonged antibiotic use resulting in decreased defences of body against C. difficile, which can easily produce toxins. […] Among the antibiotics that have increased risk of causing CDI, cephalosporins rank among the highest. […] Colonization and infection with CD can also be stimulated by acid suppression due to usage of PPI. […] Significant presence of CDI in this hospital population is demonstrated by this study. Cephalosporins, piperacillin-tazobactam and carbapenems were found to be the most common agents responsible for AAD caused by CD. Occurence of CDI may be reduced by choosing the antibiotic which has lower risk of producing AAD, from the susceptibility panel as well as avoiding the usage of -lactam and -lactamase inhibitors (BL-BLIs) as empirical therapy.
  • #55 Antibiotic-associated diarrhea – sboulardii – CNCM i-745
    https://www.saccharomycesboulardii.com/therapeutic-area/antibiotic-associated-diarrhea/
    The major consequence of antibiotic-induced changes to gut microbiota diversity is antibiotic-associated diarrhea (AAD).1 Diarrhea is the signal that there is an imbalance in the diversity of the microbiota in the gut.1 AAD generally occurs during antibiotic treatment, however diarrhea can occur 2 to 8 weeks after treatment has finished.4 […] How quickly AAD occurs can be influenced by the type of antibiotic and the type of harmful bacteria that increases in the gut following antibiotics can influence the severity/rate at which AAD develops.4 For example, 1/3 of AAD cases are caused by the bacteria Clostridium difficile4, and is often recurrent.4 […] The harmful bacteria compete with the normal microbiota for nutrients and can produce substances that destroy the beneficial bacteria, as well as create toxins that affect the normal gut function.4
  • #56 Clostridioides (formerly Clostridium) difficile–Induced Diarrhea – Infectious Diseases – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/infectious-diseases/anaerobic-bacteria/clostridioides-formerly-clostridium-difficile-induced-diarrhea
    Symptoms of C. difficile induced diarrhea typically begin 5 to 10 days after starting antibiotics but may occur on the first day or up to 2 months later. […] C. difficile induced diarrhea should be suspected in any patient who develops diarrhea within 2 months of antibiotic use or 72 hours of hospital admission. […] Antibiotic therapy can cause intestinal overgrowth of toxin-secreting C. difficile, resulting in a pseudomembranous colitis that can be severe and difficult to cure. […] Recurrence is common; re-treat with antibiotics, and consider fecal transplantation or bezlotoxumab for refractory recurrences.
  • #57 Clostridioides (formerly Clostridium) difficile–Induced Diarrhea – Infectious Diseases – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/infectious-diseases/anaerobic-bacteria/clostridioides-formerly-clostridium-difficile-induced-diarrhea
    Symptoms of C. difficile induced diarrhea typically begin 5 to 10 days after starting antibiotics but may occur on the first day or up to 2 months later. […] C. difficile induced diarrhea should be suspected in any patient who develops diarrhea within 2 months of antibiotic use or 72 hours of hospital admission. […] Antibiotic therapy can cause intestinal overgrowth of toxin-secreting C. difficile, resulting in a pseudomembranous colitis that can be severe and difficult to cure. […] Recurrence is common; re-treat with antibiotics, and consider fecal transplantation or bezlotoxumab for refractory recurrences.
  • #58 Clostridium difficile–Associated Diarrhea | AAFP
    https://www.aafp.org/pubs/afp/issues/2005/0301/p921.html?___
    Clostridium difficile infection is responsible for approximately 3 million cases of diarrhea and colitis annually in the United States. Major predisposing factors for symptomatic C. difficile colitis include antibiotic therapy; advanced age; multiple, severe underlying diseases; and a faulty immune response to C. difficile toxins. The precipitating event for C. difficile colitis is disruption of the normal colonic microflora. This disruption usually is caused by broad-spectrum antibiotics, with clindamycin and broad-spectrum penicillins and cephalosporins most commonly implicated. The risk of developing antibiotic-associated diarrhea more than doubles with longer than three days of antibiotic therapy. After disruption of the colonic microflora, colonization of C. difficile generally occurs through the ingestion of heat-resistant spores, which convert to vegetative forms in the colon. Depending on host factors, an asymptomatic carrier state or clinical manifestations of C. difficile colitis develop. C. difficile associated diarrhea can occur up to eight weeks after the discontinuation of antibiotics. Most cases of C. difficile infection occur on days 4 through 9 of antibiotic therapy. The major host factors predisposing patients to the development of symptomatic C. difficile associated diarrhea include antibiotic therapy, advanced age, number and severity of underlying diseases, and faulty immune response to C. difficile toxins. C. difficile causes toxin-mediated colitis. Pathogenic strains of C. difficile produce two protein exotoxins: toxin A and toxin B. Toxin A activates macrophages and mast cells. Activation of these cells causes the production of inflammatory mediators, which leads to fluid secretion and increased mucosal permeability. Toxin B has little enterotoxic activity but is extremely cytotoxic in vitro. C. difficile toxins also cause leukocyte chemotaxis and the upregulation of cytokines and other inflammatory mediators. Consequently, there is a profound colonic inflammatory response, which is evidenced clinically by a high WBC count. As colitis worsens, focal ulcerations occur, and the accumulation of purulent and necrotic debris forms the typical pseudomembrane.
  • #59 Antibiotic-Associated Diarrhea Beyond C. Difficile: A Scoping Review | Published in Journal of Brown Hospital Medicine
    https://bhm.scholasticahq.com/article/39745
    C. difficile is the most identified cause of AAD. […] The two main toxins of C. difficile, toxins A and B play a critical role in the pathophysiology of CDI. […] Although C. difficile is implicated in most AAD cases, other causes of Non-C. difficile Pathogen-specific AAD should also be considered. […] S. aureus induced AAD was identified early in the antibiotic era as a cause of AAD in hospitalized patients. […] K. oxytoca, a gram-negative facultative aerobic enterobacterium, has been shown to be the causative agent of antibiotic associated hemorrhagic colitis (AAHC). […] The role of Candida spp. in AAD has been debated since the 1950s and continues to be controversial. […] Only 40% of AAD can be accounted for by the above causes leaving a majority of AAD cases without an etiology. […] Non-microbial-causes of AAD tend to occur within 48-72 hours of starting antibiotics, tend to be less severe and usually are self-limiting.
  • #60 Clostridioides (Clostridium) Difficile Colitis: Background, Etiology, Pathophysiology
    https://emedicine.medscape.com/article/186458-overview
    Clostridioides difficile (formerly Clostridium difficile) is a gram-positive, anaerobic, spore-forming bacillus that is responsible for the development of antibiotic-associated diarrhea and colitis. C difficile colitis results from a disturbance of the normal bacterial flora of the colon, colonization by C difficile, and the release of toxins that cause mucosal inflammation and damage. […] C difficile colitis results from a disruption of the normal bacterial flora of the colon, colonization with C difficile, and release of toxins that cause mucosal inflammation, mucosal damage, and diarrhea. […] The use of antibiotics, which alter and suppress the normal flora, allows proliferation of C difficile, toxin production, and diarrhea. […] Pathogenic strains of C difficile produce two distinct toxins. Toxin A is an enterotoxin, and toxin B is a cytotoxin; both are high molecular weight proteins capable of binding to specific receptors on the intestinal mucosal cells. Receptor-bound toxins gain intracellular entry by catalyzing a specific alteration of Rho proteins small glutamyl transpeptidase (GTP) binding proteins that assist in actin polymerization, cytoskeletal architecture, and cell movement. Both toxin A and toxin B appear to play a role in the pathogenesis of C difficile colitis in humans.
  • #61 Clostridium difficile–Associated Diarrhea | AAFP
    https://www.aafp.org/pubs/afp/issues/2005/0301/p921.html?___
    Clostridium difficile infection is responsible for approximately 3 million cases of diarrhea and colitis annually in the United States. Major predisposing factors for symptomatic C. difficile colitis include antibiotic therapy; advanced age; multiple, severe underlying diseases; and a faulty immune response to C. difficile toxins. The precipitating event for C. difficile colitis is disruption of the normal colonic microflora. This disruption usually is caused by broad-spectrum antibiotics, with clindamycin and broad-spectrum penicillins and cephalosporins most commonly implicated. The risk of developing antibiotic-associated diarrhea more than doubles with longer than three days of antibiotic therapy. After disruption of the colonic microflora, colonization of C. difficile generally occurs through the ingestion of heat-resistant spores, which convert to vegetative forms in the colon. Depending on host factors, an asymptomatic carrier state or clinical manifestations of C. difficile colitis develop. C. difficile associated diarrhea can occur up to eight weeks after the discontinuation of antibiotics. Most cases of C. difficile infection occur on days 4 through 9 of antibiotic therapy. The major host factors predisposing patients to the development of symptomatic C. difficile associated diarrhea include antibiotic therapy, advanced age, number and severity of underlying diseases, and faulty immune response to C. difficile toxins. C. difficile causes toxin-mediated colitis. Pathogenic strains of C. difficile produce two protein exotoxins: toxin A and toxin B. Toxin A activates macrophages and mast cells. Activation of these cells causes the production of inflammatory mediators, which leads to fluid secretion and increased mucosal permeability. Toxin B has little enterotoxic activity but is extremely cytotoxic in vitro. C. difficile toxins also cause leukocyte chemotaxis and the upregulation of cytokines and other inflammatory mediators. Consequently, there is a profound colonic inflammatory response, which is evidenced clinically by a high WBC count. As colitis worsens, focal ulcerations occur, and the accumulation of purulent and necrotic debris forms the typical pseudomembrane.
  • #62 Antibiotic associated diarrhea | PPT
    https://www.slideshare.net/slideshow/antibiotic-associated-diarrhea1/12980136
    Enterotoxin-producing C. perfringens Major cause of food poisoning worldwide Can cause necrotising enterocolitis in infants adults Can cause AAD sporadic diarrhea 15% of AAD tested positive for C. perfringens or its toxin Mere colonization due to growth after antibiotic treatment Not generally accepted as causative agent of AAD Testing considered in severe AAD negative for C. difficile * MRSA: Methicillin-Resistant Staphylococcus Aureus Gorkiewicz G. Int J Antimicrobial Agents 2009 ; 33 : S37 S41. […] Clostridium difficile pathogenicity locus Five genes (TcdA E) TcdA Gene encoding toxin A TcdB Gene encoding toxin B TcdD Gene encoding positive regulator of toxin transcription TcdC Gene encoding negative regulator of toxin production TcdE Gene encoding toxin disrupting bacterial membrane […] Pathogenesis of CD-associated diarrhea colitis Kyne L et al. Gastroenterol Clin North Am 2001; 30 : 753.
  • #63 Antibiotic-Associated Diarrhea and Colitis | Musculoskeletal Key
    https://musculoskeletalkey.com/antibiotic-associated-diarrhea-and-colitis/1000
    The mechanism of toxin A-mediated inflammation begins with receptor binding and internalization by colonocytes, followed promptly by localization in mitochondria causing cessation of production of adenosine 5-triphosphate (ATP) and generation of reactive oxygen species. […] These processes account for the intense secretory response, inflammation, and necrosis of colonic epithelium exposed to C. difficile toxins. […] Most cases of antibiotic-associated enterocolitis occur in patients without underlying gastrointestinal disorders who are treated with antibiotics for other conditions (e.g., respiratory illness, often with questionable indication) or receive short-term preoperative antibiotics.
  • #64 Clostridioides difficile infection – Wikipedia
    https://en.wikipedia.org/wiki/Clostridioides_difficile_infection
    Pathogenic C. difficile strains produce multiple toxins. The most well-characterized are enterotoxin (Clostridium difficile toxin A) and cytotoxin (Clostridium difficile toxin B), both of which may produce diarrhea and inflammation in infected people, although their relative contributions have been debated. Toxins A and B are glucosyltransferases that target and inactivate the Rho family of GTPases. Toxin B (cytotoxin) induces actin depolymerization by a mechanism correlated with a decrease in the ADP-ribosylation of the low molecular mass GTP-binding Rho proteins.
  • #65 Clostridium difficile–Associated Diarrhea | AAFP
    https://www.aafp.org/pubs/afp/issues/2005/0301/p921.html
    Clostridium difficile infection is responsible for approximately 3 million cases of diarrhea and colitis annually in the United States. Major predisposing factors for symptomatic C. difficile colitis include antibiotic therapy; advanced age; multiple, severe underlying diseases; and a faulty immune response to C. difficile toxins. The precipitating event for C. difficile colitis is disruption of the normal colonic microflora. This disruption usually is caused by broad-spectrum antibiotics, with clindamycin and broad-spectrum penicillins and cephalosporins most commonly implicated. The risk of developing antibiotic-associated diarrhea more than doubles with longer than three days of antibiotic therapy. After disruption of the colonic microflora, colonization of C. difficile generally occurs through the ingestion of heat-resistant spores, which convert to vegetative forms in the colon. Depending on host factors, an asymptomatic carrier state or clinical manifestations of C. difficile colitis develop. C. difficile associated diarrhea can occur up to eight weeks after the discontinuation of antibiotics. Most cases of C. difficile infection occur on days 4 through 9 of antibiotic therapy. The major host factors predisposing patients to the development of symptomatic C. difficile associated diarrhea include antibiotic therapy, advanced age, number and severity of underlying diseases, and faulty immune response to C. difficile toxins. C. difficile causes toxin-mediated colitis. Pathogenic strains of C. difficile produce two protein exotoxins: toxin A and toxin B. Toxin A activates macrophages and mast cells. Activation of these cells causes the production of inflammatory mediators, which leads to fluid secretion and increased mucosal permeability. Toxin B has little enterotoxic activity but is extremely cytotoxic in vitro. C. difficile toxins also cause leukocyte chemotaxis and the upregulation of cytokines and other inflammatory mediators. Consequently, there is a profound colonic inflammatory response, which is evidenced clinically by a high WBC count. As colitis worsens, focal ulcerations occur, and the accumulation of purulent and necrotic debris forms the typical pseudomembrane.
  • #66 Clostridioides (formerly Clostridium) difficile–Induced Diarrhea – Infectious Diseases – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/infectious-diseases/anaerobic-bacteria/clostridioides-formerly-clostridium-difficile-induced-diarrhea
    Toxins produced by Clostridioides difficile strains in the gastrointestinal tract cause pseudomembranous colitis, typically after antibiotic use. […] Antibiotic-induced changes in gastrointestinal flora are the dominant predisposing factors. […] Although most antibiotics have been implicated, the following pose the highest risk: Cephalosporins (particularly 3rd-generation), Penicillins (particularly ampicillin and amoxicillin), Clindamycin, Fluoroquinolones. […] The organism secretes both an enterotoxin and a cytotoxin, typically referred to as toxins A and B. […] The main effect of the toxin is on the colon, which secretes fluid and develops characteristic pseudomembranes discrete yellow-white plaques that are easily dislodged. […] Toxic megacolon, which rarely develops, is somewhat more likely after use of antimotility medications.
  • #67 Clostridium difficile–Associated Diarrhea | AAFP
    https://www.aafp.org/pubs/afp/issues/2005/0301/p921.html?___
    Clostridium difficile infection is responsible for approximately 3 million cases of diarrhea and colitis annually in the United States. Major predisposing factors for symptomatic C. difficile colitis include antibiotic therapy; advanced age; multiple, severe underlying diseases; and a faulty immune response to C. difficile toxins. The precipitating event for C. difficile colitis is disruption of the normal colonic microflora. This disruption usually is caused by broad-spectrum antibiotics, with clindamycin and broad-spectrum penicillins and cephalosporins most commonly implicated. The risk of developing antibiotic-associated diarrhea more than doubles with longer than three days of antibiotic therapy. After disruption of the colonic microflora, colonization of C. difficile generally occurs through the ingestion of heat-resistant spores, which convert to vegetative forms in the colon. Depending on host factors, an asymptomatic carrier state or clinical manifestations of C. difficile colitis develop. C. difficile associated diarrhea can occur up to eight weeks after the discontinuation of antibiotics. Most cases of C. difficile infection occur on days 4 through 9 of antibiotic therapy. The major host factors predisposing patients to the development of symptomatic C. difficile associated diarrhea include antibiotic therapy, advanced age, number and severity of underlying diseases, and faulty immune response to C. difficile toxins. C. difficile causes toxin-mediated colitis. Pathogenic strains of C. difficile produce two protein exotoxins: toxin A and toxin B. Toxin A activates macrophages and mast cells. Activation of these cells causes the production of inflammatory mediators, which leads to fluid secretion and increased mucosal permeability. Toxin B has little enterotoxic activity but is extremely cytotoxic in vitro. C. difficile toxins also cause leukocyte chemotaxis and the upregulation of cytokines and other inflammatory mediators. Consequently, there is a profound colonic inflammatory response, which is evidenced clinically by a high WBC count. As colitis worsens, focal ulcerations occur, and the accumulation of purulent and necrotic debris forms the typical pseudomembrane.
  • #68 Antibiotic associated diarrhea | PPT
    https://www.slideshare.net/slideshow/antibiotic-associated-diarrhea1/12980136
    Enterotoxin-producing C. perfringens Major cause of food poisoning worldwide Can cause necrotising enterocolitis in infants adults Can cause AAD sporadic diarrhea 15% of AAD tested positive for C. perfringens or its toxin Mere colonization due to growth after antibiotic treatment Not generally accepted as causative agent of AAD Testing considered in severe AAD negative for C. difficile * MRSA: Methicillin-Resistant Staphylococcus Aureus Gorkiewicz G. Int J Antimicrobial Agents 2009 ; 33 : S37 S41. […] Clostridium difficile pathogenicity locus Five genes (TcdA E) TcdA Gene encoding toxin A TcdB Gene encoding toxin B TcdD Gene encoding positive regulator of toxin transcription TcdC Gene encoding negative regulator of toxin production TcdE Gene encoding toxin disrupting bacterial membrane […] Pathogenesis of CD-associated diarrhea colitis Kyne L et al. Gastroenterol Clin North Am 2001; 30 : 753.
  • #69 Clostridioides difficile infection in adults: Epidemiology, microbiology, and pathophysiology – UpToDate
    https://www.uptodate.com/contents/clostridioides-difficile-infection-in-adults-epidemiology-microbiology-and-pathophysiology
    Clostridioides difficile is the causative organism of antibiotic-associated colitis. Colonization of the intestinal tract occurs via the fecal-oral route and is facilitated by disruption of normal intestinal flora (often due to antimicrobial therapy). […] Antibiotic-associated diarrhea and colitis were well established soon after widespread use of antibiotics. In 1978, C. difficile was identified as the causative pathogen in the majority of cases of antibiotic-associated colitis; many early cases were attributed to clindamycin. […] This strain appears to be more virulent than other strains, which may be attributable to increased toxin production compared with previous strains. Fluoroquinolone use has strongly correlated with the emergence of this strain, and development of fluoroquinolone resistance by outbreak strains appears to have been associated with the increasing frequency of CDI outbreaks. […] Since 2005, CDI due to ribotype 078 has emerged in the Netherlands; the severity is similar to CDI caused by ribotype 027.
  • #70 Study sheds light on antibiotics-associated diarrhea | MIT News | Massachusetts Institute of Technology
    https://news.mit.edu/2022/study-sheds-light-antibiotics-associated-diarrhea-0228
    A joint study by the Singapore General Hospital (SGH) and Singapore-MIT Alliance for Research and Technology (SMART), MITs research enterprise in Singapore, may have found the reason some patients experience diarrhea after taking the antibiotic amoxicillin-clavulanate, commonly known as Augmentin. […] The team of researchers found that the level of gut Ruminococcaceae, a family of bacteria that plays an important role in maintaining an individuals gut health, strongly impacts diarrheal outcomes following antibiotic treatment. […] Results showed that Ruminococcaceae levels in the stools of study volunteers who developed diarrhea were significantly lower when compared to those who did not, both before and during treatment with amoxicillin-clavulanate. This suggests that individuals may, depending on their gut composition, be predisposed to antibiotic-associated diarrhea. […] Our findings provide evidence that an individuals gut microbial composition can influence the risk of developing antibiotics-associated diarrhea.
  • #71 EXPLORATORY PILOT STUDIES TO DEMONSTRATE MECHANISMS OF PREVENTING ANTIBIOTIC-ASSOCIATED DIARRHEA AND THE ROLE FOR PROBIOTICS | National Agricultural Library
    https://www.nal.usda.gov/research-tools/food-safety-research-projects/exploratory-pilot-studies-demonstrate-mechanisms
    Probiotics are live microorganisms that, when administered in adequate amounts, confer a health benefit on the host. One of the most common indications for probiotic treatment is the prevention of antibiotic-associated diarrhea (AAD). […] Data from several studies suggest antibiotic-induced disruption of commensal colonic bacteria results in a significant reduction in short chain fatty acid (SCFA) production and a concomitant reduction in Na-dependent fluid absorption, ultimately resulting in AAD. […] The primary aim of the R61 phase (N=60) is to determine if BB-12 can mitigate antibiotic-induced reduction in SCFA concentration, as reflected in fecal acetate levels. […] Antibiotic administration also lowers total microbial counts and diversity in the gut microbiota, disrupting the homeostasis of the gut ecosystem and allowing colonization by pathogens.
  • #72
    https://link.springer.com/article/10.1007/s12602-023-10150-x
    Probiotics can increase mucin secretion, upregulate ZO-1 and occludin protein synthesis, thus repairing intestinal permeability caused by AAD. […] Probiotic supplementation can significantly increase SCFAs, contributing to the improvement of intestinal health. […] This work demonstrated that L. plantarum ELF051 can attenuate antibiotic-induced intestinal inflammation in a mouse AAD model by suppressing the pro-inflammatory response and modulating the gut microbiota. […] The present study showed that administration of L. plantarum ELF051 increased the levels of SCFAs in the intestine. […] The results of this study indicated that in AAD mice, there was an increase in the expression of PI3K and AKT proteins, activating NF-B, leading to an increase in the levels of phosphorylated IB and p65, thereby promoting the secretion of cytokines IL-1, IL-6, and TNF-. […] The findings suggest that treatment with L. plantarum ELF051 may potentially improve gut microbiota dysbiosis in AAD mice.
  • #73
    https://link.springer.com/article/10.1007/s12602-023-10150-x
    Probiotics are widely recognized for their ability to prevent and therapy antibiotic-associated diarrhea (AAD). […] Antibiotic therapy may induce AAD by disrupting the gut microbiota, altering the intestinal short-chain fatty acids (SCFAs) content, and changing the intestinal structure and barrier function. […] AAD is often accompanied by systemic inflammation, characterized by an increase in pro-inflammatory cytokines and a decrease in anti-inflammatory cytokines, indicating that anti-inflammatory may be a potential mechanism for probiotics to alleviate AAD. […] The specific molecular mechanisms underlying the treatment and prevention of AAD by probiotics primarily involve the following aspects: (i) Modulating the gut microbiome. […] The administration of probiotics has been proved to regulate the disorder of gut microbiota.
  • #74
    https://link.springer.com/article/10.1007/s12602-023-10150-x
    Probiotics can increase mucin secretion, upregulate ZO-1 and occludin protein synthesis, thus repairing intestinal permeability caused by AAD. […] Probiotic supplementation can significantly increase SCFAs, contributing to the improvement of intestinal health. […] This work demonstrated that L. plantarum ELF051 can attenuate antibiotic-induced intestinal inflammation in a mouse AAD model by suppressing the pro-inflammatory response and modulating the gut microbiota. […] The present study showed that administration of L. plantarum ELF051 increased the levels of SCFAs in the intestine. […] The results of this study indicated that in AAD mice, there was an increase in the expression of PI3K and AKT proteins, activating NF-B, leading to an increase in the levels of phosphorylated IB and p65, thereby promoting the secretion of cytokines IL-1, IL-6, and TNF-. […] The findings suggest that treatment with L. plantarum ELF051 may potentially improve gut microbiota dysbiosis in AAD mice.
  • #75 Probiotics for the Prevention of Antibiotic-Associated Diarrhea
    https://www.mdpi.com/2227-9032/10/8/1450
    There are different mechanisms and factors by which antibiotics can not only cause but also increase diarrhea, as follows: (i) Altering the diversity of gut bacteria, (ii) Age of patient, (iii) Spectrum of antibiotics, (iv) Metabolic disturbances, (v) Loss of colonization resistance. […] AAD occurs in patients from the start of the treatment and can last up to two months after the end of the treatment. […] Recently, probiotics have become a more common option for patients suffering from AAD as a safe way to reduce the adverse side effects of antibiotics on gastrointestinal function. […] The hypothesis behind using probiotics to mitigate the symptoms and pathophysiology of gastrointestinal disorders is that they can help normalize an unbalanced flora. […] Probiotics have been tested for a number of clinical uses. The most common clinical use of probiotics is the prevention of antibiotic-associated diarrhea.
  • #76 Probiotics for the Prevention of Antibiotic-Associated Diarrhea
    https://www.mdpi.com/2227-9032/10/8/1450
    There are different mechanisms and factors by which antibiotics can not only cause but also increase diarrhea, as follows: (i) Altering the diversity of gut bacteria, (ii) Age of patient, (iii) Spectrum of antibiotics, (iv) Metabolic disturbances, (v) Loss of colonization resistance. […] AAD occurs in patients from the start of the treatment and can last up to two months after the end of the treatment. […] Recently, probiotics have become a more common option for patients suffering from AAD as a safe way to reduce the adverse side effects of antibiotics on gastrointestinal function. […] The hypothesis behind using probiotics to mitigate the symptoms and pathophysiology of gastrointestinal disorders is that they can help normalize an unbalanced flora. […] Probiotics have been tested for a number of clinical uses. The most common clinical use of probiotics is the prevention of antibiotic-associated diarrhea.
  • #77 Probiotics for the Prevention of Antibiotic-Associated Diarrhea
    https://www.mdpi.com/2227-9032/10/8/1450
    There are different mechanisms and factors by which antibiotics can not only cause but also increase diarrhea, as follows: (i) Altering the diversity of gut bacteria, (ii) Age of patient, (iii) Spectrum of antibiotics, (iv) Metabolic disturbances, (v) Loss of colonization resistance. […] AAD occurs in patients from the start of the treatment and can last up to two months after the end of the treatment. […] Recently, probiotics have become a more common option for patients suffering from AAD as a safe way to reduce the adverse side effects of antibiotics on gastrointestinal function. […] The hypothesis behind using probiotics to mitigate the symptoms and pathophysiology of gastrointestinal disorders is that they can help normalize an unbalanced flora. […] Probiotics have been tested for a number of clinical uses. The most common clinical use of probiotics is the prevention of antibiotic-associated diarrhea.
  • #78 Preventing pediatric antibiotic-associated diarrhea and Clostridium difficile infections with probiotics: A meta-analysis
    https://www.wjgnet.com/2308-3840/full/v1/i3/102.htm
    A meta-analysis was conducted (1985-2013) for clinical trials testing probiotics for the prevention of pediatric antibiotic-associated diarrhea (AAD) or Clostridium difficile infections (CDI). Overall, probiotics significantly reduced the incidence of pediatric AAD (pooled from 22 trials RR = 0.42, 95%CI: 0.33-0.53) and significantly reduced pediatric CDI (pooled from five trials RR = 0.35, 95%CI: 0.13-0.92). […] Because the efficacy to prevent AAD and CDI has been determined to be specific by probiotic strain, it is imperative that data are analyzed by separate strains.
  • #79
    https://pmc.ncbi.nlm.nih.gov/articles/PMC6334067/
    Antibiotic-associated diarrhoea is among the most common adverse events related to antibiotic use. […] Recent developments in our understanding of the biology of the gut microbiota have provided new insights into the pathogenesis of these conditions, and have revealed a role for manipulation of the gut microbiota as a novel therapeutic approach. […] One key mechanism of AAD appears to be changes in the gut microbiota that cause decreased short-chain fatty acid absorption, resulting in osmotic diarrhoea. […] Antibiotic use is the major risk factor for CDI, causing antibiotic-related loss of gut microbial communities that protect against gut infection, thereby facilitating the germination and vegetative growth of the organism when it enters the gut of vulnerable people. […] Given that all forms of AAD represent a perturbation of the gut microbiota, restoration of the usual commensal microbiota is an appealing means of treating the condition.
  • #80 Antibiotic associated diarrhea & Clostridium difficile infection | PPT
    https://www.slideshare.net/slideshow/antibiotic-associated-diarrhea-clostridium-difficile-infection/93186857
    Treatment-IDSA guideline update 2018 […] Fecal Microbiota Transplantation Cure rates greater than 85% and many greater than 90%. […] Infection Control and Prevention Antibiotic stewardship Contact precautions Isolation Hand hygiene and barrier precautions, Single-use disposable equipment should be used Disinfection of environmental surfaces […] C Difficile Vaccine Which contains inactivated toxoid A and B. Immunogenic and in a small case series, vaccination was associated with resolution of recurrent C. difficile diarrhea
  • #81
    https://pmc.ncbi.nlm.nih.gov/articles/PMC6334067/
    A number of novel approaches for the treatment of CDI are at various stages of development. […] Developments in our understanding of the importance of the gut microbiota, and the marked efficacy of FMT in clinical trials, have raised the profile of CDI research and the search for more refined, targeted therapies.
  • #82 Antibiotic-Associated Diarrhea Beyond C. Difficile: A Scoping Review | Published in Journal of Brown Hospital Medicine
    https://bhm.scholasticahq.com/article/39745-antibiotic-associated-diarrhea-beyond-c-difficile-a-scoping-review
    A common complication of antibiotic use is the development of diarrheal illness. The pathogenesis of antibiotic associated diarrhea (AAD) may be mediated through alteration of intestinal microbiota, overgrowth of opportunistic pathogens, and direct drug toxicity on the gut. […] The likely pathogenesis of AAD includes alteration of intestinal microbiota, direct drug toxicity on the gut and development of a superinfection by a pathogenic microbe. […] Although the role of C. difficile in the pathogenesis of AAD has been well studied, there are considerable gaps in our understanding of the pathogenesis of non-CDI AAD due to putative microbial etiologies including C. perfringens, S. aureus, K. oxytoca, and Candida species. Identifying the etiology and understanding the pathogenesis of AAD will help in improving healthcare and in reducing the economic burden.
  • #83 Pathogenesis of antibiotic-associated diarrhea (AAD)—a systematic review
    https://digitalcommons.library.tmc.edu/dissertations/AAI1515607/
    A common complication of antibiotic use is the development of diarrheal illness. The pathogenesis of antibiotic associated diarrhea (AAD) may be mediated through alteration of intestinal microbiota, overgrowth of opportunistic pathogens, and direct drug toxicity on the gut. Alterations in the intestinal microbiota result in metabolic imbalances, loss of colonization resistance and in turn allow proliferation of opportunistic pathogens. Currently less than 33% of AAD cases can be attributable to Clostridium difficile leaving a large number of cases undiagnosed and poorly treated. Although the pathogenesis of Clostridium difficile infection (CDI) has been well documented, the role of other putative microbial etiologies (Clostridium perfringens, Staphylococcus aureus, Klebsiella oxytoca, Candida species) and their pathogenic mechanisms in AAD has been unclear. […] This review provides a comprehensive and systematic approach to the existing data on AAD and includes concise descriptions of the pathogenesis of CDI and non-CDI AAD in the form of figures.