Pałeczka okrężnicy
Patofizjologia i mechanizm

Escherichia coli, będąca składnikiem fizjologicznej mikrobioty jelitowej, może nabywać geny wirulencji, przekształcając się w patogeny wywołujące szerokie spektrum chorób jelitowych i pozajelitowych. Zidentyfikowano dziewięć patotypów E. coli, m.in. EPEC, ETEC, EHEC, EIEC, EAEC, AIEC i UPEC, z których każdy charakteryzuje się specyficznymi mechanizmami patogenności, takimi jak adhezja za pomocą fimbrii, sekrecja białek efektorowych przez systemy T3SS i T6SS, produkcja toksyn (np. toksyna Shiga, enterotoksyny LT i ST, CNF-1) oraz zdolność do manipulacji cytoszkieletem komórek gospodarza. Patogeny te wywołują objawy od wodnistej biegunki (ETEC) po krwawą biegunkę i zespół hemolityczno-mocznicowy (EHEC O157:H7), a także zakażenia układu moczowego (UPEC) i choroby zapalne jelit (AIEC). Kluczowe czynniki wirulencji, takie jak locus LEE kodujący intiminę i system T3SS, umożliwiają ścisłe przyleganie i uszkodzenie nabłonka jelitowego, a zdolność do efektywnego pozyskiwania żelaza wspiera namnażanie patogenów w organizmie gospodarza.

Patogeneza E. coli (Pałeczka okrężnicy)

Escherichia coli to wszechstronne mikroorganizmy, będące ważnymi składnikami normalnej mikrobioty jelitowej ludzi i zwierząt. Te zazwyczaj nieszkodliwe komensale mogą nabywać mobilne elementy genetyczne zawierające geny kodujące czynniki wirulencji, przekształcając się w patogeny zdolne do wywoływania szerokiego spektrum chorób jelitowych i pozajelitowych. Zidentyfikowano dziewięć dobrze scharakteryzowanych patotypów E. coli, które mogą powodować schorzenia od różnych zaburzeń żołądkowo-jelitowych po zakażenia układu moczowego12.

Mechanizmy patogenności

Patogeneza to proces, w którym patogeny wywołują choroby poprzez ekspresję genów kodujących czynniki wirulencji. Każdy patotyp E. coli posiada charakterystyczne mechanizmy patogenności i specyficzny profil czynników wirulencji kodowanych przez określone klastry genów3. Geny związane z patogennością mogą kodować takie funkcje jak adhezja, inwazja, przyleganie, pobieranie żelaza, ruchliwość i aktywność toksynowa4.

Czynniki wirulencji są często kodowane na wyspach patogenności, plazmidach, bakteriofagach lub elementach transpozycyjnych. Patogenne szczepy E. coli wykorzystują te czynniki do kolonizacji, inwazji i uszkodzenia komórek gospodarza5. Większość patogennych szczepów E. coli posiada zdolność do przywierania do komórek nabłonkowych za pomocą fimbrii (pili), które umożliwiają kolonizację6.

Systemy sekrecji typu III i VI

Wiele patogennych szczepów E. coli wykorzystuje specjalistyczne systemy sekrecji typu III (T3SS) do wprowadzania białek efektorowych do komórek gospodarza. System ten działa jak „strzykawka”, umożliwiając bakteriom wprowadzanie swoich białek do komórek gospodarza, co zmusza je do współpracy w procesie zakażenia7. System T3SS jest kluczowy dla patogenezy szczepów EPEC (enteropatogenne E. coli) i EHEC (enterokrwotoczne E. coli), umożliwiając im przyleganie do komórek nabłonkowych jelita i wywoływanie charakterystycznych zmian w cytoszkielecie8.

Patogenne szczepy E. coli mogą również posiadać system sekrecji typu VI (T6SS), który służy zarówno do manipulowania funkcjami komórek gospodarza, jak i do konkurencji bakteryjnej9.

Patotypy E. coli i ich specyficzne mechanizmy wirulencji

Enteropatogenne E. coli (EPEC)

EPEC jest główną przyczyną biegunki u niemowląt na całym świecie. Charakterystyczną cechą zakażeń EPEC jest tworzenie zmian określanych jako „attaching and effacing” (A/E), które charakteryzują się przyleganiem bakterii do błony komórek nabłonkowych i zniszczeniem mikrokosmków1011.

Interakcja między EPEC a komórkami gospodarza jest opisywana jako proces czterostopniowy:

  1. Początkowe przyleganie bakterii do nabłonka jelitowego
  2. Formowanie mikrokolonii na powierzchni komórki poprzez Bfp i EspA, z charakterystycznym wzorem przylegania
  3. Wstrzykiwanie białek efektorowych (w tym Tir) do komórki gospodarza przez system T3SS
  4. Reorganizacja cytoszkieletu i tworzenie charakterystycznych struktur podobnych do piedestałów1213

EPEC zaburza transport elektrolitów w komórkach gospodarza i zakłóca funkcję bariery nabłonkowej, co prowadzi do szybkiego wystąpienia objawów biegunki, jeszcze przed pełnym rozwojem zmian A/E14. Białka efektorowe wprowadzane przez system T3SS manipulują komórkami gospodarza, ułatwiając kolonizację bakterii, ucieczkę przed układem odpornościowym i regulują odpowiedź zapalną15.

Enterotoksyczne E. coli (ETEC)

ETEC jest najczęstszą przyczyną biegunki podróżnych, z około 840 milionami przypadków rocznie na całym świecie16. Najważniejszym czynnikiem wirulencji ETEC jest wydzielanie enterotoksyn17.

ETEC produkuje dwa rodzaje enterotoksyn:

  • Toksyny wrażliwe na ciepło (LT-I, LT-II) – działają podobnie do toksyny cholery
  • Toksyny oporne na ciepło (STa i STb)18

Enterotoksyny ETEC stymulują nadmierną sekrecję płynów i elektrolitów przez komórki nabłonkowe jelita, powodując zmniejszenie absorpcji sodu i chlorków. Te zmiany prowadzą do wodnistej biegunki i stymulują wydzielanie prostaglandyn i cytokin prozapalnych, co skutkuje dalszą utratą wody1920.

Enterokrwotoczne E. coli (EHEC)

EHEC, szczególnie serotyp O157:H7, jest poważnym zagrożeniem dla zdrowia publicznego w Japonii, Europie i Ameryce Północnej21. Głównym czynnikiem wirulencji EHEC jest toksyna Shiga (SLT, zwana również werotoksyną), kodowana przez geny stx22.

Mechanizm działania toksyny Shiga obejmuje:

  1. Wiązanie podjednostki B toksyny do specyficznego glikolipidu (globotriasyloceramidu – Gb3) obecnego na komórkach nabłonkowych i śródbłonkowych
  2. Internalizację podjednostki A, która hamuje syntezę białek w komórkach gospodarza
  3. Uszkodzenie śródbłonka naczyń krwionośnych, prowadzące do krwawej biegunki i potencjalnie zespołu hemolityczno-mocznicowego (HUS)2324

EHEC kolonizuje jelito grube, tworząc charakterystyczne zmiany A/E podobne do EPEC, jednak obecność toksyny Shiga jest głównym czynnikiem odpowiedzialnym za ciężkie objawy kliniczne, w tym krwawą biegunkę i HUS25.

Enteroinwazyjne E. coli (EIEC)

EIEC różni się od innych patotypów E. coli, ponieważ jest obligatoryjnym patogenem wewnątrzkomórkowym, nieposiadającym czynników adhezji ani rzęsek26. Wirulencja tego patogenu wynika głównie z obecności plazmidu o wielkości 220 kb, kodującego kompleks T3SS, chaperony, regulatory transkrypcji, translokatory i ponad 25 białek efektorowych27.

Mechanizm patogenezy EIEC obejmuje:

  • Inwazję i zniszczenie nabłonka okrężnicy
  • Lizę fagocytarnych wakuoli i namnażanie się w cytoplazmie
  • Tworzenie „ogonów aktynowych”, które pomagają bakteriom przemieszczać się w cytoplazmie i pomiędzy sąsiednimi komórkami nabłonkowymi
  • Owrzodzenie okrężnicy w wyniku zniszczenia komórek nabłonkowych i stymulacji cytokin zapalnych28

EIEC powoduje zaburzenie funkcji absorpcyjnych i wydzielniczych jelit poprzez lizę komórek nabłonkowych, co prowadzi do biegunki29.

Enteroagregacyjne E. coli (EAEC)

EAEC wytwarza enteroagregacyjną toksynę oporną na ciepło i toksynę kodowaną przez plazmid, które indukują wydzielanie płynu30. Patogeneza EAEC charakteryzuje się agregacyjnym przyleganiem bakterii do komórek nabłonkowych, skróceniem mikrokosmków, naciekiem komórek jednojądrzastych i krwotokami, co prowadzi do zmniejszonej absorpcji płynów31.

Szczepy EAEC przywierają do komórek jelitowych, powodując podrażnienie lub zapalenie komórek jelitowych, co zakłóca absorpcję i wydzielanie w jelitach32.

Adherentno-inwazyjne E. coli (AIEC)

AIEC to patotyp jelitowy zdolny do przylegania i inwazji warstwy komórek nabłonkowych jelita oraz namnażania się wewnątrz makrofagów i komórek nabłonkowych33. Jest jednym z najważniejszych czynników etiologicznych idiopatycznych zaburzeń zapalnych, w tym choroby zapalnej jelit (IBD) i choroby Leśniowskiego-Crohna (CD)34.

AIEC wykorzystuje kilka czynników wirulencji, takich jak pęcherzyki błony zewnętrznej, białka błony zewnętrznej i długie fimbrie polarne, które są eksponowane po przyleganiu do komórek gospodarza i umożliwiają inwazję, zakażenie i replikację w makrofagach35.

Uropatogenne E. coli (UPEC)

UPEC jest odpowiedzialne za około 90% zakażeń układu moczowego (UTI) u osób z normalną anatomią36. UPEC wykorzystuje fimbrie P (pili związane z odmiedniczkowym zapaleniem nerek) do wiązania się z komórkami urotelium dróg moczowych i kolonizacji pęcherza37.

UPEC może unikać wrodzonej odpowiedzi immunologicznej organizmu (np. układu dopełniacza) poprzez inwazję powierzchniowych komórek umbrella i tworzenie wewnątrzkomórkowych społeczności bakteryjnych (IBC)38. Czynniki wirulencji UPEC można pogrupować jako adhezyny, toksyny, systemy pobierania żelaza i protektyny39.

UPEC produkuje również toksynę określaną jako cytotoksyczny czynnik nekrotyzujący typu 1 (CNF-1), który kataluzje deaminację glutaminy małych GTPaz RhoA, Rac i Cdc42, prowadząc do zakłócenia licznych funkcji komórkowych eukariotycznych, w tym tworzenia włókien stresu aktynowego i modulacji szlaków sygnalizacyjnych stanu zapalnego40.

Molekularne mechanizmy patogenezy

System Quorum Sensing

Aktywacja tworzenia biofilmu jest mediowana przez system quorum sensing kodowany przez gen supresora inhibitora podziału (SdiA)41. Quorum sensing umożliwia bakteriom komunikację międzykomórkową i regulację ekspresji genów w zależności od gęstości populacji bakteryjnej42.

Autoinduktor-2 (AI-2) jest cząsteczką sygnałową quorum sensing, wykorzystywaną do komunikacji wewnątrz- i międzygatunkowej. Chemotaksja w kierunku AI-2 przyczynia się do konkurencji o składniki odżywcze i wpływa na odporność kolonizacyjną nadawaną przez E. coli przeciwko patogenom jelitowym, takim jak Salmonella Typhimurium43.

Wyspa patogenności LEE

Locus of Enterocyte Effacement (LEE) to wyspa patogenności o wielkości około 35 kb, która zawiera geny kodujące intiminę, system sekrecji typu III, szereg wydzielanych białek (Esp) i translokowany receptor intiminy zwany Tir44.

Intimina, białko błony zewnętrznej o masie 94 kDa kodowane przez gen eae, jest odpowiedzialna za ścisłe przyleganie między bakteriami a błonami enterocytów45. Cząsteczki Esp (EspA, B i D) są zaangażowane w tworzenie translokonu, który dostarcza cząsteczki efektorowe do komórki gospodarza i zakłóca cytoszkielet, podporządkowując funkcje komórki gospodarza46.

Rola toksyn w patogenezie

E. coli wytwarza cztery rodzaje toksyn, które mają działanie cytotoksyczne na komórki gospodarza47:

Rodzaj toksyny Patotyp Mechanizm działania Efekt kliniczny
Toksyna Shiga (Stx1, Stx2) EHEC, STEC Hamowanie syntezy białek, uszkodzenie śródbłonka naczyń Krwawa biegunka, HUS, niewydolność nerek
Enterotoksyny ciepłochwiejne (LT) ETEC Aktywacja cyklazy adenylanowej, zwiększenie poziomów cAMP Wodnista biegunka
Enterotoksyny ciepłostałe (ST) ETEC Aktywacja cyklazy guanylanowej, zwiększenie poziomów cGMP Wodnista biegunka
Cytotoksyczny czynnik nekrotyzujący (CNF-1) UPEC Modyfikacja małych białek G (RhoA, Rac, Cdc42) Zaburzenia cytoszkieletu, modulacja stanu zapalnego
Kolibaktyna Szczepy zawierające wyspę pks Uszkodzenie DNA Starzenie komórkowe, potencjalnie nowotworzenie

Niektóre szczepy E. coli zawierają wyspę genomową syntazy poliketydowej (pks), która koduje multi-enzymatyczną maszynerię produkującą kolibaktynę, substancję uszkadzającą DNA. Kolibaktyna może powodować starzenie komórkowe lub nowotworzenie poprzez uszkodzenie DNA48.

Pobieranie żelaza

Patogenne szczepy E. coli mają zwiększoną liczbę receptorów sideroforów żelazowych i transporterów żelaza ABC, co ułatwia im pobieranie żelaza w środowisku gospodarza, gdzie dostępność żelaza jest ograniczona49. Obecność receptorów kompleksów żelazowych błony zewnętrznej i systemów pobierania żelaza ABC o wysokim powinowactwie koreluje ze sobą, sugerując koewolucję50.

Ta zdolność do efektywnego pozyskiwania żelaza w warunkach jego niedoboru jest kluczowym czynnikiem wirulencji, umożliwiającym patogennym szczepom E. coli namnażanie się w organizmie gospodarza51.

Interakcje z komórkami gospodarza

Przyleganie i inwazja

Patogenne bakterie zanieczyszczające środowisko są połykane przez podatne zwierzęta i dostają się do przewodu pokarmowego. Bakterie te posiadają fimbrialne adhezyny, które pośredniczą w przyleganiu do specyficznych receptorów na komórkach nabłonkowych jelit. Wynikająca z tego kolonizacja bakteryjna znajduje się głównie na błonie śluzowej jelita czczego i/lub krętego52.

Niektóre szczepy E. coli, jak EPEC i EHEC, wykorzystują specjalny system „wstrzykujący”, aby dostarczyć własne białka do komórki, którą inwadują. Bakterie używają tego systemu, działającego jak strzykawka, do wprowadzenia kilku białek bakteryjnych do komórki jelitowej, co zmusza ją do współpracy w procesie zakażenia53.

W przypadku EPEC, bakterie wytwarzają własny specyficzny receptor, który jest wstrzykiwany do komórki nabłonkowej gospodarza za pomocą aparatu bakteryjnego przypominającego strzykawkę. Bakteryjna adhezyna następnie pośredniczy w bardzo ścisłym przyleganiu bakterii do receptorów komórkowych, a sygnały bakteryjne stymulują zanik mikrokosmków, czyli rąbka szczoteczkowego, i reorganizację cytoszkieletu komórkowego54.

Manipulacja cytoszkieletem

Wiele patogennych szczepów E. coli wywiera swoje działanie poprzez manipulację cytoszkieletem komórek gospodarza. W przypadku EPEC i EHEC, po przyłączeniu się bakterii do komórki gospodarza, następuje reorganizacja cytoszkieletu, prowadząca do charakterystycznych zmian morfologicznych, w tym zaniku mikrokosmków i tworzenia struktur podobnych do piedestałów55.

Białka efektorowe wprowadzane przez system T3SS, takie jak EspG i EspG2, zakłócają sieci mikrotubul gospodarza, co wpływa na transport pęcherzykowy i lokalizację białek błonowych. Na przykład, infekcja EPEC hamuje aktywność wymiany Cl/OH w szczytowej błonie komórek nabłonkowych jelit poprzez zaangażowanie cząsteczek efektorowych EspG i EspG256.

Prawidłowa aktywność wymiany Cl/OH wymaga nienaruszonych mikrotubul. Infekcja EPEC w modelach in vitro i in vivo moduluje ekspresję białka DRA na szczytowej błonie komórkowej, prowadząc do redystrybucji białka DRA z powierzchni do przedziałów wewnątrzkomórkowych57.

Modulacja odpowiedzi immunologicznej

Patogenne szczepy E. coli posiadają mechanizmy umożliwiające im unikanie odpowiedzi immunologicznej gospodarza. UPEC ekspresjonuje białka błony zewnętrznej, takie jak traT i Iss, które mogą zwiększać oporność na surowicę poprzez unikanie działania układu dopełniacza58.

EIEC dostarcza integralność komórek gospodarza i przeżywalność we wczesnych stadiach zakażenia poprzez hamowanie odłączania komórek nabłonkowych jelit i ich obrotu, wykorzystując białka efektorowe OspE i IpaB59.

Interakcja między adhezynami Afa/Dr, rzęskami i receptorami DAF pośredniczy w wydzielaniu IL-8 i promuje transmigrację neutrofili wielojądrzastych (PMN)60. Ta manipulacja odpowiedzią zapalną może sprzyjać przetrwaniu i rozprzestrzenianiu się patogenu w organizmie gospodarza.

Czynniki środowiskowe i transmisja

Źródła zakażenia

Głównym rezerwuarem EHEC jest bydło, jednak inne zwierzęta, takie jak jelenie, są również znane jako nosiciele EHEC. Ponadto, ludzie służą jako rezerwuar61. Transmisja STEC i ETEC odbywa się drogą fekalno-oralną poprzez skażoną żywność, wodę pitną lub wodę rekreacyjną. Transmisja może również występować bezpośrednio od osoby do osoby i może obejmować pewne rodzaje kontaktów seksualnych62.

Dawka infekcyjna dla E. coli O157:H7 jest bardzo niska (około 100 organizmów). E. coli O157:H7 było związane ze spożyciem niedogotowanej skażonej wołowiny mielonej, niepasteryzowanego soku jabłkowego i cydru, niepasteryzowanego mleka i innych produktów mlecznych, surowych owoców i warzyw oraz salami63.

Bakterie E. coli są stale wydalane do bezpośredniego otoczenia zwierząt poprzez kał i zanieczyszczają boksy, ściółkę i podłogę zwierząt trzymanych w pomieszczeniach oraz glebę w przypadku zwierząt przebywających na zewnątrz. E. coli jest przenoszona na inne zwierzęta poprzez skażoną paszę, obsługujących i wodę pitną, a potencjalnie także z gospodarstwa na gospodarstwo przez pojazdy, takie jak ciężarówki transportowe64.

Rola warunków środowiskowych

Warunki środowiskowe mogą wpływać na ekspresję genów wirulencji w patogennych szczepach E. coli. Na przykład, ekspresja genów wirulencji ETEC jest regulowana przez różne sygnały żołądkowo-jelitowe65.

Badania wykazały, że większość genów wirulencji ETEC jest włączana w żołądku i wyłączana w wydzielinach jelita krętego i w późnym stadium po zakażeniu w okrężnicy wstępującej66. Toksyna LT może być produkowana zarówno w warunkach tlenowych, jak i beztlenowych67.

ETEC skutecznie penetruje warstwę śluzu poprzez białka degradujące mucynę, promując przyleganie ETEC do komórek nabłonkowych jelit. Takie przyleganie jest organizowane przez podstawowy zestaw fimbrii (np. CFA, FimH), adhezyn niefimbrialnych (np. Tia) i dodatkowych czynników kolonizacyjnych, takich jak EtpA68.

Odporność na antybiotyki

Patogenne szczepy E. coli mogą nabywać odporność na antybiotyki poprzez różne mechanizmy. Badania sekwencjonowania całego genomu wykazały, że szczepy E. coli o różnych poziomach oporności na ampicylinę zawierają różne mutacje69.

Mutacja promotora genu ampC może działać synergistycznie z innymi mutacjami i prowadzić do wyższej oporności70. Dane transkryptomiczne wykazują znaczące zmiany w ekspresji szeregu genów regulowanych przez marA i związanych z odpowiedzią na stres i opornością na antybiotyki71.

Geny oporności na antybiotyki mogą przenosić się z plazmidu bakteryjnego do chromosomu, gdzie są stabilnie integrowane. Jest to kluczowy krok w rozprzestrzenianiu się oporności na karbapenemy72.

Implikacje kliniczne

Spektrum objawów klinicznych

Zakażenie patogennymi E. coli może prezentować szerokie spektrum objawów klinicznych. Osoba może być bezobjawowa, mieć łagodną biegunkę bez krwi lub mieć jawną krwawą biegunkę. Większość zdiagnozowanych przypadków rozwija krwawą biegunkę w ciągu 6 do 48 godzin po wystąpieniu biegunki bezkrwistej73.

W ciężkich przypadkach pacjent może rozwinąć inne zespoły kliniczne, takie jak zespół hemolityczno-mocznicowy (HUS) lub zakrzepowa plamica małopłytkowa (TTP). Zespół hemolityczno-mocznicowy charakteryzuje się ostrym początkiem mikroangiopatycznej niedokrwistości hemolitycznej, uszkodzeniem nerek i niską liczbą płytek krwi. Zakrzepowa plamica małopłytkowa charakteryzuje się niedokrwistością i niską liczbą płytek krwi, ale może obejmować zajęcie ośrodkowego układu nerwowego (OUN) i gorączkę74.

Szczepy O157:H7 mogą powodować ciężką chorobę lub śmierć u osób starszych, bardzo młodych lub z obniżoną odpornością75. Niektóre szczepy E. coli, na przykład O157:H7, mogą wytwarzać toksynę Shiga. Toksyna Shiga powoduje odpowiedzi zapalne w komórkach docelowych jelita, pozostawiając zmiany, które skutkują krwawą biegunką będącą objawem zakażenia E. coli wytwarzającą toksynę Shiga (STEC)76.

Powikłania zakażeń

Większość zdrowych dorosłych wraca do zdrowia po chorobie wywołanej przez E. coli w ciągu tygodnia. Niektóre osoby, szczególnie małe dzieci i osoby starsze, mogą rozwinąć zagrażającą życiu formę niewydolności nerek zwaną zespołem hemolityczno-mocznicowym77.

Szczepy UPEC mogą inwazować komórki podściełające pęcherza moczowego i tworzyć uśpione rezerwuary, które są potencjalnie źródłem nawracających zakażeń78. E. coli wywołująca zapalenie opon mózgowych u noworodków wykazuje wysoką oporność na odpowiedź immunologiczną gospodarza i może przekraczać barierę krew-mózg, powodując chorobę79.

Zakażenia patogennymi E. coli mogą prowadzić do różnych chorób, w tym zapalenia żołądka i jelit, zakażeń układu moczowego, posocznicy/zapalenia opon mózgowych i zakażeń żołądkowo-jelitowych80.

Strategie terapeutyczne

Nie istnieje szczepionka ani lek, który chroniłby przed chorobą wywołaną przez E. coli, chociaż badacze badają potencjalne szczepionki81. Jedyną skuteczną metodą eliminacji STEC z żywności jest wprowadzenie zabiegu bakteriobójczego, takiego jak ogrzewanie (na przykład gotowanie lub pasteryzacja) lub napromieniowanie82.

STEC jest niszczone przez dokładne gotowanie żywności do momentu, gdy wszystkie części osiągną temperaturę 70°C lub wyższą83. Podstawowe dobre praktyki higieny żywności, zgodnie z opisem w Five keys to safer food WHO, mogą zapobiec przenoszeniu patogenów odpowiedzialnych za wiele chorób przenoszonych przez żywność, a także chronić przed chorobami przenoszonymi przez żywność wywołanymi przez STEC84.

Wiedza o mechanizmach patogennych patotypów E. coli doprowadziła do opracowania racjonalnych interwencji w leczeniu i zapobieganiu chorobom wywołanym przez E. coli85.

Kolejne rozdziały

Zapraszamy do dalszego czytania naszego leksykonu.

Wybierz kolejny rozdział z menu poniżej, aby otworzyć nową podstronę kompedium wiedzy i uzyskać szczegółowe informację o leku, substancji lub chorobie.

  1. 10.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1 Virulence Factors of Enteric Pathogenic Escherichia coli: A Review
    https://pmc.ncbi.nlm.nih.gov/articles/PMC8468683/
    Escherichia coli are remarkably versatile microorganisms and important members of the normal intestinal microbiota of humans and animals. […] This harmless commensal organism can acquire a mixture of comprehensive mobile genetic elements that contain genes encoding virulence factors, becoming an emerging human pathogen capable of causing a broad spectrum of intestinal and extraintestinal diseases. […] Nine definite enteric E. coli pathotypes have been well characterized, causing diseases ranging from various gastrointestinal disorders to urinary tract infections. […] These pathotypes employ many virulence factors and effectors subverting the functions of host cells to mediate their virulence and pathogenesis. […] Pathogenesis is the process by which pathogens cause disease or disorder, often by expressing virulence-factor-encoding genes.
  • #2 Virulence Factors of Enteric Pathogenic Escherichia coli: A Review
    https://www.mdpi.com/1422-0067/22/18/9922
    Escherichia coli are remarkably versatile microorganisms and important members of the normal intestinal microbiota of humans and animals. This harmless commensal organism can acquire a mixture of comprehensive mobile genetic elements that contain genes encoding virulence factors, becoming an emerging human pathogen capable of causing a broad spectrum of intestinal and extraintestinal diseases. Nine definite enteric E. coli pathotypes have been well characterized, causing diseases ranging from various gastrointestinal disorders to urinary tract infections. […] Pathogenesis is the process by which pathogens cause disease or disorder, often by expressing virulence-factor-encoding genes. […] Each E. coli pathotype has its characteristic pathogenicity mechanisms and a specific profile of virulence factors encoded by specific gene clusters.
  • #3 Virulence Factors of Enteric Pathogenic Escherichia coli: A Review
    https://pmc.ncbi.nlm.nih.gov/articles/PMC8468683/
    Each E. coli pathotype has its characteristic pathogenicity mechanisms and a specific profile of virulence factors encoded by specific gene clusters. […] Genes associated with pathogenicity may encode activities such as adhesion, invasion, attachment, iron acquisition, motility, and toxin activity, among others. […] It is noteworthy that different enteric and extraintestinal pathotypes of E. coli isolates share the same virulence factors and strategies. […] Many virulence factors associated with enteric E. coli pathotypes implicated in intestinal and extraintestinal disorders have been identified in the last years. […] The investigation of these virulence factors and the associated encoding genes can provide explicit knowledge about the interaction between these factors in enteric E. coli pathotypes and host proteins at the molecular level, indicating how they lead to diseases and can implement preventive strategies against them.
  • #4 Virulence Factors of Enteric Pathogenic Escherichia coli: A Review
    https://pmc.ncbi.nlm.nih.gov/articles/PMC8468683/
    Each E. coli pathotype has its characteristic pathogenicity mechanisms and a specific profile of virulence factors encoded by specific gene clusters. […] Genes associated with pathogenicity may encode activities such as adhesion, invasion, attachment, iron acquisition, motility, and toxin activity, among others. […] It is noteworthy that different enteric and extraintestinal pathotypes of E. coli isolates share the same virulence factors and strategies. […] Many virulence factors associated with enteric E. coli pathotypes implicated in intestinal and extraintestinal disorders have been identified in the last years. […] The investigation of these virulence factors and the associated encoding genes can provide explicit knowledge about the interaction between these factors in enteric E. coli pathotypes and host proteins at the molecular level, indicating how they lead to diseases and can implement preventive strategies against them.
  • #5 Pathogenic Escherichia coli – Wikipedia
    https://en.wikipedia.org/wiki/Pathogenic_Escherichia_coli
    Strains of E. coli that can cause disease […] Most E. coli strains are harmless, but pathogenic varieties cause serious food poisoning, septic shock, meningitis, or urinary tract infections in humans. […] Unlike normal flora E. coli, the pathogenic varieties produce toxins and other virulence factors that enable them to reside in parts of the body normally not inhabited by E. coli, and to damage host cells. […] These pathogenic traits are encoded by virulence genes carried only by the pathogens. […] In humans and in domestic animals, virulent strains of E. coli can cause various diseases. […] Certain strains of E. coli, such as O157:H7, O104:H4, O121, O26, O103, O111, O145, and O104:H21, produce potentially lethal toxins. […] O157:H7 is also notorious for causing serious and even life-threatening complications such as hemolytic-uremic syndrome.
  • #6 Colibacillosis (E. coli diarrhea) | Iowa State University
    https://vetmed.iastate.edu/vdpam/about/focus-areas/swine/swine-disease-manual/index-diseases/colibacillosis
    Ingested pathogenic E. coli adhere to receptors on microvilli of enterocytes via pili. There they colonize, proliferate, and elaborate enterotoxins that cause excessive secretion of fluid and electrolytes by crypt epithelial cells which markedly exceeds absorptive capacity resulting in a net flow of tissue fluids into the lumen. […] The enterotoxins, endotoxin, and/or adhesins may damage the microvilli and enterocytes as well. This reduces the absorption of electrolytes, water and endogenous secretions from the lumen. The large intestine, sometimes also affected, is unable to absorb the excess fluid and diarrhea results. Damage to epithelial cells sometimes leads to septicemia. Diarrhea usually continues until death results from dehydration and metabolic acidosis or from terminal septicemia.
  • #7 E. coli Infection mechanism – DnaTube.com – Scientific Video and Animation Site
    https://www.dnatube.com/video/12233/E-coli-Infection-mechanism
    Watch this animation to see the molecular tricks that an infectious strain of Escherichia coli uses to infect your gut. […] An E. coli strain that’s capable of infecting the intestinal tract is called enteropathogenic E. coli. Infection by enteropathogenic E. coli can cause severe diarrhea and can even result in death. […] The tethered bacterium now uses a specialized injector system to deliver some of its own proteins into the cell that it is invading. […] The bacterium uses the injector system, much like a syringe, to introduce several bacterial proteins into the intestinal cell that force it to cooperate in its own infection. […] The bacterium is now firmly bound to the intestinal cell surface via the interaction between the Tir and intimin proteins. […] Once many enteropathogenic bacteria have adhered to the intestinal lining, symptoms of the infection (diarrhea) commence.
  • #8 New Molecular Mechanisms of Virulence and Pathogenesis in E. coli | SpringerLink
    https://link.springer.com/chapter/10.1007/978-3-031-29882-0_4
    The rapid progress in diverse approaches and technologies such as genome sequencing, gene mutation, site-directed mutagenesis, proteomics, crystallography, high-throughput screening and cryo-electron microscopy has provided unprecedented knowledge regarding novel functions during E. coli pathogenesis. […] In this chapter, we discuss six novel mechanisms of virulence and pathogenesis into the different E. coli pathotypes. These mechanisms include two nanomachines (T3SS and T6SS) used to colonize and hijack the host cell functions (T3SS, T6SS) or for bacterial competition (T6SS), as well as the mechanisms of T3SS protein-protein interaction, which has allowed the development of blocking compounds or peptides as preventing strategies; likewise, mechanisms of some pathogenic E. coli strains, which have developed sophisticated strategies to overcome the colonization barriers imposed by the microbiota; and finally, mechanisms to regulate the expression of factors related with the lifestyle of these bacterial pathogens as those forming bacterial communities or new mechanisms of remote interaction among bacteria and host cells, such as the delivery of vesicles containing cargo molecules.
  • #9 New Molecular Mechanisms of Virulence and Pathogenesis in E. coli | SpringerLink
    https://link.springer.com/chapter/10.1007/978-3-031-29882-0_4
    The rapid progress in diverse approaches and technologies such as genome sequencing, gene mutation, site-directed mutagenesis, proteomics, crystallography, high-throughput screening and cryo-electron microscopy has provided unprecedented knowledge regarding novel functions during E. coli pathogenesis. […] In this chapter, we discuss six novel mechanisms of virulence and pathogenesis into the different E. coli pathotypes. These mechanisms include two nanomachines (T3SS and T6SS) used to colonize and hijack the host cell functions (T3SS, T6SS) or for bacterial competition (T6SS), as well as the mechanisms of T3SS protein-protein interaction, which has allowed the development of blocking compounds or peptides as preventing strategies; likewise, mechanisms of some pathogenic E. coli strains, which have developed sophisticated strategies to overcome the colonization barriers imposed by the microbiota; and finally, mechanisms to regulate the expression of factors related with the lifestyle of these bacterial pathogens as those forming bacterial communities or new mechanisms of remote interaction among bacteria and host cells, such as the delivery of vesicles containing cargo molecules.
  • #10 Enteropathogenic Escherichia coli—A Summary of the Literature
    https://www.mdpi.com/2036-7422/12/1/4
    Attaching-and-effacing was described by Nataro and Kaper, in 1998, as the “hallmark” of the EPEC infections, a lesion that is characterized by the intimate attachment of the bacteria to the host epithelial cell membrane and the effacement of the microvilli. […] The interaction between EPEC and the host cells is described as a four-stage process. […] In the second step, EPEC strains adhere to the intestinal epithelium through Bfp and EspA, forming dense microcolonies on the cell’s surface, in a pattern described as localized adherence. The type-three-secretion-system creates a pore, enabling the bacteria to inject Tir and a large number (at least 25, up to 50) of effector molecules into the host cell. These effectors facilitate bacterial colonization, immune evasion, and regulate inflammatory response and host cell death.
  • #11 Typical and Atypical Enteropathogenic Escherichia coli – Volume 8, Number 5—May 2002 – Emerging Infectious Diseases journal – CDC
    https://wwwnc.cdc.gov/eid/article/8/5/01-0385_article
    Typical and atypical enteropathogenic Escherichia coli (EPEC) strains differ in several characteristics. […] The central mechanism of EPEC pathogenesis is a lesion called attaching and effacing (A/E), which is characterized by microvilli destruction, intimate adherence of bacteria to the intestinal epithelium, pedestal formation, and aggregation of polarized actin and other elements of the cytoskeleton at sites of bacterial attachment. […] The genetic determinants for the production of A/E lesions are located on the locus of enterocyte effacement (LEE), a pathogenicity island that contains the genes encoding intimin, a type III secretion system, a number of secreted (Esp) proteins, and the translocated intimin receptor named Tir. […] Intimin, a 94-kDa outer membrane protein encoded by the eae gene, is responsible for the intimate adherence between bacteria and enterocyte membranes.
  • #12 Enteropathogenic Escherichia coli—A Summary of the Literature
    https://www.mdpi.com/2036-7422/12/1/4
    Attaching-and-effacing was described by Nataro and Kaper, in 1998, as the “hallmark” of the EPEC infections, a lesion that is characterized by the intimate attachment of the bacteria to the host epithelial cell membrane and the effacement of the microvilli. […] The interaction between EPEC and the host cells is described as a four-stage process. […] In the second step, EPEC strains adhere to the intestinal epithelium through Bfp and EspA, forming dense microcolonies on the cell’s surface, in a pattern described as localized adherence. The type-three-secretion-system creates a pore, enabling the bacteria to inject Tir and a large number (at least 25, up to 50) of effector molecules into the host cell. These effectors facilitate bacterial colonization, immune evasion, and regulate inflammatory response and host cell death.
  • #13 Enteropathogenic Escherichia coli—A Summary of the Literature
    https://www.mdpi.com/2036-7422/12/1/4
    Enterocyte effacement and intimate bacterial attachment to the host cell characterizes the third step of EPEC infection. […] During the fourth step, the cytoskeletal elements, accumulated near the site of the attachment, leads to the formation of the pedestal structure, characteristic for EPEC. […] The clinical symptoms of EPEC diarrheal disease occurs before the complete establishment of the A/E lesions and the loss of the microvilli, so these mechanisms are most likely involved in the exacerbation of the diarrhea. […] EPEC can imbalance the host cells electrolyte transport, and by the dysregulation of these transport pathways, it is responsible for the rapid onset of the symptoms. […] EPEC is capable of disrupting the epithelial barrier function and structure. […] The inflammatory response is considered more likely to be involved in the severity and the duration of the disease than in the early stages of the infection.
  • #14 Enteropathogenic Escherichia coli—A Summary of the Literature
    https://www.mdpi.com/2036-7422/12/1/4
    Enterocyte effacement and intimate bacterial attachment to the host cell characterizes the third step of EPEC infection. […] During the fourth step, the cytoskeletal elements, accumulated near the site of the attachment, leads to the formation of the pedestal structure, characteristic for EPEC. […] The clinical symptoms of EPEC diarrheal disease occurs before the complete establishment of the A/E lesions and the loss of the microvilli, so these mechanisms are most likely involved in the exacerbation of the diarrhea. […] EPEC can imbalance the host cells electrolyte transport, and by the dysregulation of these transport pathways, it is responsible for the rapid onset of the symptoms. […] EPEC is capable of disrupting the epithelial barrier function and structure. […] The inflammatory response is considered more likely to be involved in the severity and the duration of the disease than in the early stages of the infection.
  • #15
    https://www.jci.org/articles/view/JCI29625v1
    Enteropathogenic E. coli (EPEC) is a major cause of infantile diarrhea, but the pathophysiology underlying associated diarrhea is poorly understood. […] We examined the role of the luminal membrane Cl/OH exchange process in EPEC pathogenesis using in vitro and in vivo models. […] EPEC infection (60 minutes-3 hours) inhibited apical Cl/OH exchange activity in human intestinal Caco-2 and T84 cells. […] This effect was dependent upon the bacterial type III secretory system (TTSS) and involved secreted effector molecules EspG and EspG2, known to disrupt the host microtubular network. […] Our data demonstrate that EspG and EspG2 play an important role in contributing to EPEC infection-associated inhibition of luminal membrane chloride transport via modulation of surface DRA expression. […] We demonstrated that EPEC infection of intestinal epithelial cells inhibited Cl/OH exchange activity via the involvement of the effector molecules EspG and EspG2.
  • #16 Escherichia coli – Wikipedia
    https://en.wikipedia.org/wiki/Escherichia_coli
    Uropathogenic E. coli (UPEC) is one of the main causes of urinary tract infections. […] Enterotoxigenic E. coli (ETEC) is the most common cause of traveler’s diarrhea, with as many as 840 million cases worldwide in developing countries each year. […] Certain strains of E. coli are a major cause of foodborne illness.
  • #17 Virulence Factors of Enteric Pathogenic Escherichia coli: A Review
    https://www.mdpi.com/1422-0067/22/18/9922
    EHEC serotypes are a subgroup of STEC strains containing adhesin and attachment virulence factors encoded by the LEE pathogenicity island. […] The first step of EHEC adherence to intestinal epithelial cells is initial attachment. […] The most prominent and effective virulence factor of ETEC is the secretion of enterotoxins. […] The activation of biofilm formation is mediated by Quorum-sensing encoded by the suppressor of the division inhibitor (SdiA) gene. […] The virulence of this pathogen is primarily due to 220-kb plasmid-encoding virulence factors including the T3SS complex, chaperones, transcriptional regulators, translocators, and more than 25 effector proteins. […] EIEC provides host cell integrity and survival in the early stages of infection by inhibiting intestinal epithelial cell detachment and turnover utilizing protein effectors OspE and IpaB, respectively.
  • #18 E.coli-Epidemiology, Pathogenesis and Treatment – Microbiology Notes
    https://microbiologynotes.org/e-coli-epidemiology-pathogenesis-and-treatment/
    E.coli strains produce four types of toxins that have a cytotoxic effect on the host cells. […] Two types of Enterotoxin are produced by ETEC: Heat-labile Toxins (LT-I, LT-II) and Heat Stable Toxins (STa and STb). […] Because of interaction, cyclic adenosine monophosphate (cAMP) levels increase, which causes more secretion of chloride, and absorption of sodium and chloride is decreased. […] These modified alterations lead to watery diarrhea and also triggers the secretion of prostaglandin produce inflammatory cytokines, which results in further water loss. […] Initially, bacteria get attached to small intestine epithelial surface cells along with the disruption of the microvillus (known as effacement), which gives a lesion on the microvillus known as Attachment/ Effacement [A/E] histopathology.
  • #19 E.coli-Epidemiology, Pathogenesis and Treatment – Microbiology Notes
    https://microbiologynotes.org/e-coli-epidemiology-pathogenesis-and-treatment/
    E.coli strains produce four types of toxins that have a cytotoxic effect on the host cells. […] Two types of Enterotoxin are produced by ETEC: Heat-labile Toxins (LT-I, LT-II) and Heat Stable Toxins (STa and STb). […] Because of interaction, cyclic adenosine monophosphate (cAMP) levels increase, which causes more secretion of chloride, and absorption of sodium and chloride is decreased. […] These modified alterations lead to watery diarrhea and also triggers the secretion of prostaglandin produce inflammatory cytokines, which results in further water loss. […] Initially, bacteria get attached to small intestine epithelial surface cells along with the disruption of the microvillus (known as effacement), which gives a lesion on the microvillus known as Attachment/ Effacement [A/E] histopathology.
  • #20 Enterovirulent E. coli (EEC) Mechanism of Action & Antibiotics
    https://www.medicinenet.com/enterovirulent_e_coli_eec/article.htm
    EPEC group organisms also can produce a toxin closely related to Shigella toxin that has many of the same properties as Shiga toxin although the serotypes cause the disease (sometimes milder) mainly in children. […] The ETEC group does not produce Shiga toxins or their closely related toxins, but ETEC does produce two other exotoxins that stimulate the intestines to secrete fluid and mucus. […] EIEC organisms, these bacteria can penetrate the epithelial cells that line areas of the human intestines. EIEC organisms then cause many of the cells to lyse thus disrupting the fluid adsorption and secretion capacity of the intestines. […] Both EAEC and EAggEC groups of bacteria, by attaching to intestinal cells, cause irritation or inflammation of the intestinal cells. This physiologic and immunologic response also disrupts adsorption and secretion in the intestines.
  • #21 Virulence Factors of Enteric Pathogenic Escherichia coli: A Review
    https://www.mdpi.com/1422-0067/22/18/9922
    Many virulence factors associated with enteric E. coli pathotypes implicated in intestinal and extraintestinal disorders have been identified in the last years. […] The investigation of these virulence factors and the associated encoding genes can provide explicit knowledge about the interaction between these factors in enteric E. coli pathotypes and host proteins at the molecular level, indicating how they lead to diseases and can implement preventive strategies against them. […] The next step in EPEC pathogenesis is the translocation of LEE and Nle effectors and proteins into the host cell through the T3SS. […] The most important serotype playing a role in EHEC outbreaks is O157: H7, which is still considered a serious health concern in Japan, Europe, and North America. […] The shiga-like toxin (SLT), also termed verotoxin and encoded by stx genes, is the main virulence factor in EHEC serotypes which belongs to the shiga-toxin producing E. coli group and is responsible for pathological manifestations leading to specific disease symptoms caused during EHEC infections, such as HUS and renal failure.
  • #22 Virulence Factors of Enteric Pathogenic Escherichia coli: A Review
    https://pmc.ncbi.nlm.nih.gov/articles/PMC8468683/
    The next step in EPEC pathogenesis is the translocation of LEE and Nle effectors and proteins into the host cell through the T3SS. […] The activation of biofilm formation is mediated by Quorum-sensing encoded by the suppressor of the division inhibitor (SdiA) gene. […] The shiga-like toxin (SLT), also termed verotoxin and encoded by stx genes, is the main virulence factor in EHEC serotypes which belongs to the shiga-toxin producing E. coli group and is responsible for pathological manifestations leading to specific disease symptoms caused during EHEC infections, such as HUS and renal failure. […] EIEC differs from other pathovars of E. coli because it is an obligate intracellular pathogen with neither adherence nor flagella factors. […] The virulence of this pathogen is primarily due to 220-kb plasmid-encoding virulence factors including the T3SS complex, chaperones, transcriptional regulators, translocators, and more than 25 effector proteins.
  • #23 E.coli-Epidemiology, Pathogenesis and Treatment – Microbiology Notes
    https://microbiologynotes.org/e-coli-epidemiology-pathogenesis-and-treatment/
    The binding of Tir receptors and intimin results in actin polymerization and cytoskeletal elements accumulation, under the attached bacteria, which cause cell death. […] EAEC produces enteroaggregative heat-stable toxic and plasmid-encoded toxin which induces secretion of the fluid. […] EHEC produces Shiga toxins (Stx-1 and Stx-2), both are AB-type toxins, where B subunits bind to the specific glycolipid such as globotriasylceramide[Gb3] present on the host renal endothelial cell and intestinal villi. […] A subunit is internalized, and cleave into two molecules, one part binds to 28S rRNA and ceases protein synthesis. […] Bacteria invade and cause destruction in the colonic epithelium. […] Bacterial invasion is mediated by pInv genes. […] Bacteria cause lysis of phagocytic vacuoles and multiply in the cytoplasm. […] The formation of actin tails helps bacteria to move within the cytoplasm and across the neighboring epithelial cells. […] Colonic ulceration occurs because of epithelial cell destruction with inflammatory cytokines stimulated by bacteria.
  • #24 E. coli – Pathogenic | Health & Human Services
    https://hhs.iowa.gov/center-acute-disease-epidemiology/epi-manual/reportable-diseases/e-coli-pathogenic
    In severe cases, the patient may progress to develop other clinical syndromes such as hemolytic uremic syndrome (HUS) or thrombotic thrombocytopenic purpura (TTP). Hemolytic uremic syndrome (HUS) is characterized by the acute onset of microangiopathic hemolytic anemia, renal injury, and low platelet count. Thrombotic thrombocytopenic purpura (TTP) is characterized by anemia and low platelet counts but can include central nervous system (CNS) involvement and fever. […] EHEC: Cattle appear to be a reservoir of significant public health importance; however, other animals, such as deer, are also known to carry EHEC. In addition, humans serve as a reservoir. […] STEC and ETEC transmission occurs fecal-orally via contaminated food, drinking water or recreational water. Transmission may also occur directly from person-to-person; and can include certain types of sexual contact.
  • #25 Virulence Factors of Enteric Pathogenic Escherichia coli: A Review
    https://www.mdpi.com/1422-0067/22/18/9922
    Many virulence factors associated with enteric E. coli pathotypes implicated in intestinal and extraintestinal disorders have been identified in the last years. […] The investigation of these virulence factors and the associated encoding genes can provide explicit knowledge about the interaction between these factors in enteric E. coli pathotypes and host proteins at the molecular level, indicating how they lead to diseases and can implement preventive strategies against them. […] The next step in EPEC pathogenesis is the translocation of LEE and Nle effectors and proteins into the host cell through the T3SS. […] The most important serotype playing a role in EHEC outbreaks is O157: H7, which is still considered a serious health concern in Japan, Europe, and North America. […] The shiga-like toxin (SLT), also termed verotoxin and encoded by stx genes, is the main virulence factor in EHEC serotypes which belongs to the shiga-toxin producing E. coli group and is responsible for pathological manifestations leading to specific disease symptoms caused during EHEC infections, such as HUS and renal failure.
  • #26 Virulence Factors of Enteric Pathogenic Escherichia coli: A Review
    https://pmc.ncbi.nlm.nih.gov/articles/PMC8468683/
    The next step in EPEC pathogenesis is the translocation of LEE and Nle effectors and proteins into the host cell through the T3SS. […] The activation of biofilm formation is mediated by Quorum-sensing encoded by the suppressor of the division inhibitor (SdiA) gene. […] The shiga-like toxin (SLT), also termed verotoxin and encoded by stx genes, is the main virulence factor in EHEC serotypes which belongs to the shiga-toxin producing E. coli group and is responsible for pathological manifestations leading to specific disease symptoms caused during EHEC infections, such as HUS and renal failure. […] EIEC differs from other pathovars of E. coli because it is an obligate intracellular pathogen with neither adherence nor flagella factors. […] The virulence of this pathogen is primarily due to 220-kb plasmid-encoding virulence factors including the T3SS complex, chaperones, transcriptional regulators, translocators, and more than 25 effector proteins.
  • #27 Virulence Factors of Enteric Pathogenic Escherichia coli: A Review
    https://pmc.ncbi.nlm.nih.gov/articles/PMC8468683/
    The next step in EPEC pathogenesis is the translocation of LEE and Nle effectors and proteins into the host cell through the T3SS. […] The activation of biofilm formation is mediated by Quorum-sensing encoded by the suppressor of the division inhibitor (SdiA) gene. […] The shiga-like toxin (SLT), also termed verotoxin and encoded by stx genes, is the main virulence factor in EHEC serotypes which belongs to the shiga-toxin producing E. coli group and is responsible for pathological manifestations leading to specific disease symptoms caused during EHEC infections, such as HUS and renal failure. […] EIEC differs from other pathovars of E. coli because it is an obligate intracellular pathogen with neither adherence nor flagella factors. […] The virulence of this pathogen is primarily due to 220-kb plasmid-encoding virulence factors including the T3SS complex, chaperones, transcriptional regulators, translocators, and more than 25 effector proteins.
  • #28 E.coli-Epidemiology, Pathogenesis and Treatment – Microbiology Notes
    https://microbiologynotes.org/e-coli-epidemiology-pathogenesis-and-treatment/
    The binding of Tir receptors and intimin results in actin polymerization and cytoskeletal elements accumulation, under the attached bacteria, which cause cell death. […] EAEC produces enteroaggregative heat-stable toxic and plasmid-encoded toxin which induces secretion of the fluid. […] EHEC produces Shiga toxins (Stx-1 and Stx-2), both are AB-type toxins, where B subunits bind to the specific glycolipid such as globotriasylceramide[Gb3] present on the host renal endothelial cell and intestinal villi. […] A subunit is internalized, and cleave into two molecules, one part binds to 28S rRNA and ceases protein synthesis. […] Bacteria invade and cause destruction in the colonic epithelium. […] Bacterial invasion is mediated by pInv genes. […] Bacteria cause lysis of phagocytic vacuoles and multiply in the cytoplasm. […] The formation of actin tails helps bacteria to move within the cytoplasm and across the neighboring epithelial cells. […] Colonic ulceration occurs because of epithelial cell destruction with inflammatory cytokines stimulated by bacteria.
  • #29 Enterovirulent E. coli (EEC) Mechanism of Action & Antibiotics
    https://www.medicinenet.com/enterovirulent_e_coli_eec/article.htm
    EPEC group organisms also can produce a toxin closely related to Shigella toxin that has many of the same properties as Shiga toxin although the serotypes cause the disease (sometimes milder) mainly in children. […] The ETEC group does not produce Shiga toxins or their closely related toxins, but ETEC does produce two other exotoxins that stimulate the intestines to secrete fluid and mucus. […] EIEC organisms, these bacteria can penetrate the epithelial cells that line areas of the human intestines. EIEC organisms then cause many of the cells to lyse thus disrupting the fluid adsorption and secretion capacity of the intestines. […] Both EAEC and EAggEC groups of bacteria, by attaching to intestinal cells, cause irritation or inflammation of the intestinal cells. This physiologic and immunologic response also disrupts adsorption and secretion in the intestines.
  • #30 E.coli-Epidemiology, Pathogenesis and Treatment – Microbiology Notes
    https://microbiologynotes.org/e-coli-epidemiology-pathogenesis-and-treatment/
    The binding of Tir receptors and intimin results in actin polymerization and cytoskeletal elements accumulation, under the attached bacteria, which cause cell death. […] EAEC produces enteroaggregative heat-stable toxic and plasmid-encoded toxin which induces secretion of the fluid. […] EHEC produces Shiga toxins (Stx-1 and Stx-2), both are AB-type toxins, where B subunits bind to the specific glycolipid such as globotriasylceramide[Gb3] present on the host renal endothelial cell and intestinal villi. […] A subunit is internalized, and cleave into two molecules, one part binds to 28S rRNA and ceases protein synthesis. […] Bacteria invade and cause destruction in the colonic epithelium. […] Bacterial invasion is mediated by pInv genes. […] Bacteria cause lysis of phagocytic vacuoles and multiply in the cytoplasm. […] The formation of actin tails helps bacteria to move within the cytoplasm and across the neighboring epithelial cells. […] Colonic ulceration occurs because of epithelial cell destruction with inflammatory cytokines stimulated by bacteria.
  • #31 E. coli (Escherichia coli)- An Overview – Microbe Notes
    https://microbenotes.com/escherichia-coli-e-coli/
    EAEC causes infant diarrhea in developing and probably developed countries along with travelers diarrhea. Pathogenesis involves plasmid-mediated aggregative adherence of rods (stacked bricks) with shortening of microvilli, mononuclear infiltration, and hemorrhage; decreased fluid absorption. […] STEC causes hemorrhagic colitis. STEC evolved from EPEC; A/E lesions with the destruction of intestinal microvilli, resulting in decreased absorption; pathology mediated by cytotoxic Shiga toxins (Stx1, Stx2), which disrupt protein synthesis. […] EIEC causes disease which is rare in developing and developed countries. Pathogenesis involves plasmid-mediated invasion and destruction of epithelial cells lining the colon. […] Most gram-negative rods that produce UTIs originate in the colon, contaminate the urethra, ascend into the bladder, and may migrate to the kidney or prostate.
  • #32 Molecular mechanisms of Escherichia coli pathogenicity | Nature Reviews Microbiology
    https://www.nature.com/articles/nrmicro2265
    Other pathovars, such as enterotoxigenic E. coli, elaborate toxins that cause disease, whereas the attachment of enteroaggregative and diffusely adherent E. coli stimulates cellular signalling events that stimulate inflammation. […] The extraintestinal isolates have remarkable lifestyles. Uropathogenic E. coli can invade the underlying bladder cells and form quiescent reservoirs, which are possibly the source of recurrent infections. Neonatal meningitis E. coli has been shown to be highly resistant to host immune responses and can cross the bloodbrain barrier to cause disease. […] In this Review, we focus on the recent advances in our understanding of the different pathogenic mechanisms that are used by various E. coli pathovars and how they cause disease in humans.
  • #33 Virulence Factors of Enteric Pathogenic Escherichia coli: A Review
    https://pmc.ncbi.nlm.nih.gov/articles/PMC8468683/
    The AIEC pathotype is an enteric pathogen able to adhere to and invade the intestinal epithelial cell layer and multiply within macrophages and epithelial cells. […] Several virulence factors and associated encoding genes have been identified to play a role in the pathogenic interaction with the intestinal mucosa.
  • #34 Virulence Factors of Enteric Pathogenic Escherichia coli: A Review
    https://www.mdpi.com/1422-0067/22/18/9922
    The interaction between Afa/Dr adhesins, flagella, and DAF receptors mediates IL-8 secretion and promotes the transmigration of polymorphonuclear neutrophils (PMNs). […] AIEC is one of the most important causative agents of idiopathic inflammatory disorders, including IBD and CD, and primarily affect the human small bowel. […] Several virulence factors, such as outer membrane vesicles, outer membrane proteins, and long polar fimbriae, are expressed and utilized by AIEC strain after the adhesion to the epithelial host cells to mediate invasion, infect, and replicate within the macrophages.
  • #35 Virulence Factors of Enteric Pathogenic Escherichia coli: A Review
    https://www.mdpi.com/1422-0067/22/18/9922
    The interaction between Afa/Dr adhesins, flagella, and DAF receptors mediates IL-8 secretion and promotes the transmigration of polymorphonuclear neutrophils (PMNs). […] AIEC is one of the most important causative agents of idiopathic inflammatory disorders, including IBD and CD, and primarily affect the human small bowel. […] Several virulence factors, such as outer membrane vesicles, outer membrane proteins, and long polar fimbriae, are expressed and utilized by AIEC strain after the adhesion to the epithelial host cells to mediate invasion, infect, and replicate within the macrophages.
  • #36 Pathogenic Escherichia coli – Wikipedia
    https://en.wikipedia.org/wiki/Pathogenic_Escherichia_coli
    The O104:H4 strain is equally virulent. […] Uropathogenic E. coli (UPEC) is responsible for approximately 90% of urinary tract infections (UTI) seen in individuals with ordinary anatomy. […] Uropathogenic E. coli use P fimbriae (pyelonephritis-associated pili) to bind urinary tract urothelial cells and colonize the bladder. […] UPEC can evade the body’s innate immune defences (e.g. the complement system) by invading superficial umbrella cells to form intracellular bacterial communities (IBCs). […] Some E. coli strains contain a polyketide synthase genomic island (pks), which encodes a multi-enzymatic machinery that produces colibactin, a substance that damages DNA. […] Colibactin can cause cellular senescence or cancer by damaging DNA. […] In animals, virulent strains of E. coli are responsible of a variety of diseases, among others sepsis and diarrhea in newborn calves, acute mastitis in dairy cows, colibacillosis also associated with chronic respiratory disease with Mycoplasma where it causes perihepatitis, pericarditis, septicaemic lungs, peritonitis etc. in poultry, and Alabama rot in dogs.
  • #37 Pathogenic Escherichia coli – Wikipedia
    https://en.wikipedia.org/wiki/Pathogenic_Escherichia_coli
    The O104:H4 strain is equally virulent. […] Uropathogenic E. coli (UPEC) is responsible for approximately 90% of urinary tract infections (UTI) seen in individuals with ordinary anatomy. […] Uropathogenic E. coli use P fimbriae (pyelonephritis-associated pili) to bind urinary tract urothelial cells and colonize the bladder. […] UPEC can evade the body’s innate immune defences (e.g. the complement system) by invading superficial umbrella cells to form intracellular bacterial communities (IBCs). […] Some E. coli strains contain a polyketide synthase genomic island (pks), which encodes a multi-enzymatic machinery that produces colibactin, a substance that damages DNA. […] Colibactin can cause cellular senescence or cancer by damaging DNA. […] In animals, virulent strains of E. coli are responsible of a variety of diseases, among others sepsis and diarrhea in newborn calves, acute mastitis in dairy cows, colibacillosis also associated with chronic respiratory disease with Mycoplasma where it causes perihepatitis, pericarditis, septicaemic lungs, peritonitis etc. in poultry, and Alabama rot in dogs.
  • #38 Pathogenic Escherichia coli – Wikipedia
    https://en.wikipedia.org/wiki/Pathogenic_Escherichia_coli
    The O104:H4 strain is equally virulent. […] Uropathogenic E. coli (UPEC) is responsible for approximately 90% of urinary tract infections (UTI) seen in individuals with ordinary anatomy. […] Uropathogenic E. coli use P fimbriae (pyelonephritis-associated pili) to bind urinary tract urothelial cells and colonize the bladder. […] UPEC can evade the body’s innate immune defences (e.g. the complement system) by invading superficial umbrella cells to form intracellular bacterial communities (IBCs). […] Some E. coli strains contain a polyketide synthase genomic island (pks), which encodes a multi-enzymatic machinery that produces colibactin, a substance that damages DNA. […] Colibactin can cause cellular senescence or cancer by damaging DNA. […] In animals, virulent strains of E. coli are responsible of a variety of diseases, among others sepsis and diarrhea in newborn calves, acute mastitis in dairy cows, colibacillosis also associated with chronic respiratory disease with Mycoplasma where it causes perihepatitis, pericarditis, septicaemic lungs, peritonitis etc. in poultry, and Alabama rot in dogs.
  • #39 The Pathogenesis of Escherichia coli Urinary Tract Infection | IntechOpen
    https://www.intechopen.com/chapters/56154
    UPEC VFs are grouped by functional categories as adhesins, toxins, iron acquisition systems, and protectins. […] Adhesins, which appear as hair-like fibers called fimbriae (or pili), facilitate the colonization with E. coli in the urinary tract by attaching to host epithelial cells. […] UPEC also produce a toxin referred to as cytotoxic necrotising factor type 1 (CNF-1). CNF-1 is a chromosomally encoded UPEC toxin that catalyzes the glutamine deamination of the small GTPases RhoA, Rac, and Cdc 42, leading to the disturbance of numerous eukaryotic cellular functions including formation of actin stress fibers, lamellipodia, filopodia, and modulation of inflammatory signaling pathways. […] UPEC also express outer membrane proteins, such as traT and Iss, which may enhance serum resistance through avoidance of complement killing. […] Biofilm production by E. coli is an important VF which may also protect bacteria from antibiotic action and so contribute to resistance.
  • #40 The Pathogenesis of Escherichia coli Urinary Tract Infection | IntechOpen
    https://www.intechopen.com/chapters/56154
    UPEC VFs are grouped by functional categories as adhesins, toxins, iron acquisition systems, and protectins. […] Adhesins, which appear as hair-like fibers called fimbriae (or pili), facilitate the colonization with E. coli in the urinary tract by attaching to host epithelial cells. […] UPEC also produce a toxin referred to as cytotoxic necrotising factor type 1 (CNF-1). CNF-1 is a chromosomally encoded UPEC toxin that catalyzes the glutamine deamination of the small GTPases RhoA, Rac, and Cdc 42, leading to the disturbance of numerous eukaryotic cellular functions including formation of actin stress fibers, lamellipodia, filopodia, and modulation of inflammatory signaling pathways. […] UPEC also express outer membrane proteins, such as traT and Iss, which may enhance serum resistance through avoidance of complement killing. […] Biofilm production by E. coli is an important VF which may also protect bacteria from antibiotic action and so contribute to resistance.
  • #41 Virulence Factors of Enteric Pathogenic Escherichia coli: A Review
    https://pmc.ncbi.nlm.nih.gov/articles/PMC8468683/
    The next step in EPEC pathogenesis is the translocation of LEE and Nle effectors and proteins into the host cell through the T3SS. […] The activation of biofilm formation is mediated by Quorum-sensing encoded by the suppressor of the division inhibitor (SdiA) gene. […] The shiga-like toxin (SLT), also termed verotoxin and encoded by stx genes, is the main virulence factor in EHEC serotypes which belongs to the shiga-toxin producing E. coli group and is responsible for pathological manifestations leading to specific disease symptoms caused during EHEC infections, such as HUS and renal failure. […] EIEC differs from other pathovars of E. coli because it is an obligate intracellular pathogen with neither adherence nor flagella factors. […] The virulence of this pathogen is primarily due to 220-kb plasmid-encoding virulence factors including the T3SS complex, chaperones, transcriptional regulators, translocators, and more than 25 effector proteins.
  • #42 Interplay between chemotaxis, quorum sensing, and metabolism regulates Escherichia coli-Salmonella Typhimurium interactions in vivo | PLOS Pathogens
    https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1013156
    Motile bacteria use chemotaxis to navigate complex environments like the mammalian gut. […] One such cue molecule is the intra- and interspecies quorum sensing signaling molecule, autoinducer-2 (AI-2). […] However, the impact of AI-2-dependent niche occupation by E. coli on interspecies interactions in vivo is not fully understood. […] Using the C57BL/6J mouse infection model, we show that chemotaxis towards AI-2 contributes to nutrient competition and thereby affects colonization resistance conferred by E. coli against the enteric pathogen Salmonella enterica serovar Typhimurium (S. Tm). […] The role of quorum sensing and chemotaxis in metabolic competition among bacteria remains largely unexplored. […] Here, we provide initial evidence that AI-2-dependent nutrient competition occurs between S. Tm and E. coli at specific time points during infection.
  • #43 Interplay between chemotaxis, quorum sensing, and metabolism regulates Escherichia coli-Salmonella Typhimurium interactions in vivo | PLOS Pathogens
    https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1013156
    Motile bacteria use chemotaxis to navigate complex environments like the mammalian gut. […] One such cue molecule is the intra- and interspecies quorum sensing signaling molecule, autoinducer-2 (AI-2). […] However, the impact of AI-2-dependent niche occupation by E. coli on interspecies interactions in vivo is not fully understood. […] Using the C57BL/6J mouse infection model, we show that chemotaxis towards AI-2 contributes to nutrient competition and thereby affects colonization resistance conferred by E. coli against the enteric pathogen Salmonella enterica serovar Typhimurium (S. Tm). […] The role of quorum sensing and chemotaxis in metabolic competition among bacteria remains largely unexplored. […] Here, we provide initial evidence that AI-2-dependent nutrient competition occurs between S. Tm and E. coli at specific time points during infection.
  • #44 Typical and Atypical Enteropathogenic Escherichia coli – Volume 8, Number 5—May 2002 – Emerging Infectious Diseases journal – CDC
    https://wwwnc.cdc.gov/eid/article/8/5/01-0385_article
    Typical and atypical enteropathogenic Escherichia coli (EPEC) strains differ in several characteristics. […] The central mechanism of EPEC pathogenesis is a lesion called attaching and effacing (A/E), which is characterized by microvilli destruction, intimate adherence of bacteria to the intestinal epithelium, pedestal formation, and aggregation of polarized actin and other elements of the cytoskeleton at sites of bacterial attachment. […] The genetic determinants for the production of A/E lesions are located on the locus of enterocyte effacement (LEE), a pathogenicity island that contains the genes encoding intimin, a type III secretion system, a number of secreted (Esp) proteins, and the translocated intimin receptor named Tir. […] Intimin, a 94-kDa outer membrane protein encoded by the eae gene, is responsible for the intimate adherence between bacteria and enterocyte membranes.
  • #45 Typical and Atypical Enteropathogenic Escherichia coli – Volume 8, Number 5—May 2002 – Emerging Infectious Diseases journal – CDC
    https://wwwnc.cdc.gov/eid/article/8/5/01-0385_article
    Typical and atypical enteropathogenic Escherichia coli (EPEC) strains differ in several characteristics. […] The central mechanism of EPEC pathogenesis is a lesion called attaching and effacing (A/E), which is characterized by microvilli destruction, intimate adherence of bacteria to the intestinal epithelium, pedestal formation, and aggregation of polarized actin and other elements of the cytoskeleton at sites of bacterial attachment. […] The genetic determinants for the production of A/E lesions are located on the locus of enterocyte effacement (LEE), a pathogenicity island that contains the genes encoding intimin, a type III secretion system, a number of secreted (Esp) proteins, and the translocated intimin receptor named Tir. […] Intimin, a 94-kDa outer membrane protein encoded by the eae gene, is responsible for the intimate adherence between bacteria and enterocyte membranes.
  • #46 Typical and Atypical Enteropathogenic Escherichia coli – Volume 8, Number 5—May 2002 – Emerging Infectious Diseases journal – CDC
    https://wwwnc.cdc.gov/eid/article/8/5/01-0385_article
    The Esp molecules (EspA, B, and D) are involved in the formation of a translocon that delivers effector molecules to the host cell and disrupts the cytoskeleton, subverting the host cell functions. […] The EAF plasmid is not essential for the formation of A/E lesions, although its presence enhances their efficiency, probably through the influence of a cluster of plasmid-borne regulatory genes that increase expression of the chromosomal LEE genes. […] The pathogenicity of most typical EPEC serotypes has been confirmed by volunteer studies. […] The atypical EPEC strains may be less virulent than the typical ones. […] Typical EPEC serotypes are strongly associated with diarrhea in children 1 year of age. […] Typical EPEC serotypes have not been found in animals, suggesting that humans are the only living reservoir for these organisms. In contrast, most atypical EPEC serotypes have been isolated from different animal species. […] Typical and atypical EPEC seem to constitute two groups of distinct organisms that have in common the LEE pathogenicity island. Atypical EPEC are closer to STEC in genetic characteristics, serotypes, production of toxins, reservoir, and other epidemiologic aspects.
  • #47 E.coli-Epidemiology, Pathogenesis and Treatment – Microbiology Notes
    https://microbiologynotes.org/e-coli-epidemiology-pathogenesis-and-treatment/
    E.coli strains produce four types of toxins that have a cytotoxic effect on the host cells. […] Two types of Enterotoxin are produced by ETEC: Heat-labile Toxins (LT-I, LT-II) and Heat Stable Toxins (STa and STb). […] Because of interaction, cyclic adenosine monophosphate (cAMP) levels increase, which causes more secretion of chloride, and absorption of sodium and chloride is decreased. […] These modified alterations lead to watery diarrhea and also triggers the secretion of prostaglandin produce inflammatory cytokines, which results in further water loss. […] Initially, bacteria get attached to small intestine epithelial surface cells along with the disruption of the microvillus (known as effacement), which gives a lesion on the microvillus known as Attachment/ Effacement [A/E] histopathology.
  • #48 Pathogenic Escherichia coli – Wikipedia
    https://en.wikipedia.org/wiki/Pathogenic_Escherichia_coli
    The O104:H4 strain is equally virulent. […] Uropathogenic E. coli (UPEC) is responsible for approximately 90% of urinary tract infections (UTI) seen in individuals with ordinary anatomy. […] Uropathogenic E. coli use P fimbriae (pyelonephritis-associated pili) to bind urinary tract urothelial cells and colonize the bladder. […] UPEC can evade the body’s innate immune defences (e.g. the complement system) by invading superficial umbrella cells to form intracellular bacterial communities (IBCs). […] Some E. coli strains contain a polyketide synthase genomic island (pks), which encodes a multi-enzymatic machinery that produces colibactin, a substance that damages DNA. […] Colibactin can cause cellular senescence or cancer by damaging DNA. […] In animals, virulent strains of E. coli are responsible of a variety of diseases, among others sepsis and diarrhea in newborn calves, acute mastitis in dairy cows, colibacillosis also associated with chronic respiratory disease with Mycoplasma where it causes perihepatitis, pericarditis, septicaemic lungs, peritonitis etc. in poultry, and Alabama rot in dogs.
  • #49 Transport proteins promoting E. coli pathogenesis /
    https://escholarship.org/uc/item/05d6c0bq
    Escherichia coli is a genetically diverse species infecting hundreds of millions of people worldwide annually. […] We examined seven well-characterized E. coli pathogens causing urinary tract infections, gastroenteritis, pyelonephritis and haemorrhagic colitis. Their transport proteins were identified and compared with each other and a non-pathogenic E. coli K12 strain to identify transport proteins related to pathogenesis. Each pathogen possesses a unique set of protein secretion systems for export to the cell surface or for injecting effector proteins into host cells. […] Pathogens have increased numbers of iron siderophore receptors and ABC iron uptake transporters, but the numbers and types of low-affinity secondary iron carriers were uniform in all strains. The presence of outer membrane iron complex receptors and high-affinity ABC iron uptake systems correlated, suggesting co-evolution.
  • #50 Transport proteins promoting E. coli pathogenesis /
    https://escholarship.org/uc/item/05d6c0bq
    Escherichia coli is a genetically diverse species infecting hundreds of millions of people worldwide annually. […] We examined seven well-characterized E. coli pathogens causing urinary tract infections, gastroenteritis, pyelonephritis and haemorrhagic colitis. Their transport proteins were identified and compared with each other and a non-pathogenic E. coli K12 strain to identify transport proteins related to pathogenesis. Each pathogen possesses a unique set of protein secretion systems for export to the cell surface or for injecting effector proteins into host cells. […] Pathogens have increased numbers of iron siderophore receptors and ABC iron uptake transporters, but the numbers and types of low-affinity secondary iron carriers were uniform in all strains. The presence of outer membrane iron complex receptors and high-affinity ABC iron uptake systems correlated, suggesting co-evolution.
  • #51 Transport proteins promoting Escherichia coli pathogenesis
    https://escholarship.org/uc/item/8954221k
    Escherichia coli is a genetically diverse species infecting hundreds of millions of people worldwide annually. […] We examined seven well-characterized E. coli pathogens causing urinary tract infections, gastroenteritis, pyelonephritis and haemorrhagic colitis. Their transport proteins were identified and compared with each other and a non-pathogenic E. coli K12 strain to identify transport proteins related to pathogenesis. Each pathogen possesses a unique set of protein secretion systems for export to the cell surface or for injecting effector proteins into host cells. Pathogens have increased numbers of iron siderophore receptors and ABC iron uptake transporters, but the numbers and types of low-affinity secondary iron carriers were uniform in all strains. The presence of outer membrane iron complex receptors and high-affinity ABC iron uptake systems correlated, suggesting co-evolution. Each pathovar encodes a different set of pore-forming toxins and virulence-related outer membrane proteins lacking in K12. Intracellular pathogens proved to have a characteristically distinctive set of nutrient uptake porters, different from those of extracellular pathogens. The results presented in this report provide information about transport systems relevant to various types of E. coli pathogenesis that can be exploited in future basic and applied studies.
  • #52 Pathogenesis – EcL (The Escherichia coli Laboratory)
    http://www.ecl-lab.ca/en/ecoli/pathogenesis.asp
    The pathogenic E. coli within each pathotype may be further classified as virotypes, based on the virulence genes that they possess. A virotype is a particular combination of virulence genes. Important virulence factors encoded by these genes include fimbrial adhesins, enterotoxins, cytotoxins, capsule, and lipopolysaccharide, or LPS. […] Pathogenic bacteria contaminating the environment are ingested by susceptible animals and enter the intestinal tract. These bacteria possess fimbrial adhesins which mediate adherence to specific receptors on the intestinal epithelial cells. Resulting bacterial colonization is found mostly on the jejunal and or ileal mucosa. The adherent bacteria produce enterotoxins which stimulate water and electrolyte loss into the intestinal lumen, leading to dehydration and possibly death, and a decreased weight gain in surviving animals.
  • #53 E. coli Infection mechanism – DnaTube.com – Scientific Video and Animation Site
    https://www.dnatube.com/video/12233/E-coli-Infection-mechanism
    Watch this animation to see the molecular tricks that an infectious strain of Escherichia coli uses to infect your gut. […] An E. coli strain that’s capable of infecting the intestinal tract is called enteropathogenic E. coli. Infection by enteropathogenic E. coli can cause severe diarrhea and can even result in death. […] The tethered bacterium now uses a specialized injector system to deliver some of its own proteins into the cell that it is invading. […] The bacterium uses the injector system, much like a syringe, to introduce several bacterial proteins into the intestinal cell that force it to cooperate in its own infection. […] The bacterium is now firmly bound to the intestinal cell surface via the interaction between the Tir and intimin proteins. […] Once many enteropathogenic bacteria have adhered to the intestinal lining, symptoms of the infection (diarrhea) commence.
  • #54 Pathogenesis – EcL (The Escherichia coli Laboratory)
    http://www.ecl-lab.ca/en/ecoli/pathogenesis.asp
    The adherent bacteria produce a toxin which is transported across the epithelial cells to the circulation. This toxin acts on the endothelial cells of blood vessels, resulting in edema in different tissues, leading to the manifestation of such symptoms as ataxia and death. […] Bacteria produce their own specific receptor which is injected into the host epithelial cell via a syringe-like bacterial apparatus. A bacterial adhesin then mediates a very intimate attachment of the bacteria to the cell receptors and bacterial signals stimulate effacement of the microvilli, or brush border, and reorganization of the cell cytoskeleton. The adherent bacteria also stimulate epithelial cell degeneration, and infiltration of PMN’s in lamina propria. These cell changes may lead to the appearance of diarrhea.
  • #55 Enteropathogenic Escherichia coli (EPEC)
    https://microbenotes.com/enteropathogenic-escherichia-coli-epec/
    The initial aggregation of typical EPEC leading to the formation of microcolonies on the epithelial cell surface is mediated by plasmid-encoded bundle-forming pili (BFP); however, this plasmid is not present in atypical EPEC. […] The subsequent stages of attachment are regulated by genes encoded on the LEE pathogenicity island. This island of more than 40 genes is responsible for attachment and destruction of the host cell surface. […] Following the loose attachment, active secretion of bacterial proteins into the host epithelial cell occurs by the bacterial type III secretion system. […] One protein, translocated intimin receptor (Tir), is inserted into the epithelial cell membrane and functions as a receptor for an outer membrane bacterial adhesin, intimin. […] Binding of intimin to Tir results in polymerization of actin, accumulation of cytoskeletal elements beneath the attached bacteria, loss of cell surface integrity, and eventual cell death. […] Formation of A/E lesions (attaching and effacing lesions): These are typical lesions produced on the intestinal epithelium which leads to disruption of brush border epithelium causing increased secretion and watery diarrhea.
  • #56
    https://www.jci.org/articles/view/JCI29625v1
    Enteropathogenic E. coli (EPEC) is a major cause of infantile diarrhea, but the pathophysiology underlying associated diarrhea is poorly understood. […] We examined the role of the luminal membrane Cl/OH exchange process in EPEC pathogenesis using in vitro and in vivo models. […] EPEC infection (60 minutes-3 hours) inhibited apical Cl/OH exchange activity in human intestinal Caco-2 and T84 cells. […] This effect was dependent upon the bacterial type III secretory system (TTSS) and involved secreted effector molecules EspG and EspG2, known to disrupt the host microtubular network. […] Our data demonstrate that EspG and EspG2 play an important role in contributing to EPEC infection-associated inhibition of luminal membrane chloride transport via modulation of surface DRA expression. […] We demonstrated that EPEC infection of intestinal epithelial cells inhibited Cl/OH exchange activity via the involvement of the effector molecules EspG and EspG2.
  • #57
    https://www.jci.org/articles/view/JCI29625v1
    Our results also reveal that optimal Cl/OH exchange activity requires an intact tubulin network. […] EPEC infection in in vitro and in vivo models was shown to modulate DRA protein expression on the apical plasma membrane. […] These biochemical studies were complemented with qualitative immunofluorescence studies that also showed redistribution of DRA protein from surface to intracellular compartments. […] The current studies were aimed at examining in detail the role of the luminal Cl/OH(HCO3) exchange process in the pathophysiology of EPEC-induced diarrhea. […] The effects of EPEC on apical Cl/OH exchange activity were found to be dependent upon an intact TTSS, as mutation of the putative ATPase (escN) ablated the alteration in Cl/OH exchange activity. […] EspG and EspG2 have been shown to play an important role in the disruption of host microtubular network.
  • #58 The Pathogenesis of Escherichia coli Urinary Tract Infection | IntechOpen
    https://www.intechopen.com/chapters/56154
    UPEC VFs are grouped by functional categories as adhesins, toxins, iron acquisition systems, and protectins. […] Adhesins, which appear as hair-like fibers called fimbriae (or pili), facilitate the colonization with E. coli in the urinary tract by attaching to host epithelial cells. […] UPEC also produce a toxin referred to as cytotoxic necrotising factor type 1 (CNF-1). CNF-1 is a chromosomally encoded UPEC toxin that catalyzes the glutamine deamination of the small GTPases RhoA, Rac, and Cdc 42, leading to the disturbance of numerous eukaryotic cellular functions including formation of actin stress fibers, lamellipodia, filopodia, and modulation of inflammatory signaling pathways. […] UPEC also express outer membrane proteins, such as traT and Iss, which may enhance serum resistance through avoidance of complement killing. […] Biofilm production by E. coli is an important VF which may also protect bacteria from antibiotic action and so contribute to resistance.
  • #59 Virulence Factors of Enteric Pathogenic Escherichia coli: A Review
    https://www.mdpi.com/1422-0067/22/18/9922
    EHEC serotypes are a subgroup of STEC strains containing adhesin and attachment virulence factors encoded by the LEE pathogenicity island. […] The first step of EHEC adherence to intestinal epithelial cells is initial attachment. […] The most prominent and effective virulence factor of ETEC is the secretion of enterotoxins. […] The activation of biofilm formation is mediated by Quorum-sensing encoded by the suppressor of the division inhibitor (SdiA) gene. […] The virulence of this pathogen is primarily due to 220-kb plasmid-encoding virulence factors including the T3SS complex, chaperones, transcriptional regulators, translocators, and more than 25 effector proteins. […] EIEC provides host cell integrity and survival in the early stages of infection by inhibiting intestinal epithelial cell detachment and turnover utilizing protein effectors OspE and IpaB, respectively.
  • #60 Virulence Factors of Enteric Pathogenic Escherichia coli: A Review
    https://www.mdpi.com/1422-0067/22/18/9922
    The interaction between Afa/Dr adhesins, flagella, and DAF receptors mediates IL-8 secretion and promotes the transmigration of polymorphonuclear neutrophils (PMNs). […] AIEC is one of the most important causative agents of idiopathic inflammatory disorders, including IBD and CD, and primarily affect the human small bowel. […] Several virulence factors, such as outer membrane vesicles, outer membrane proteins, and long polar fimbriae, are expressed and utilized by AIEC strain after the adhesion to the epithelial host cells to mediate invasion, infect, and replicate within the macrophages.
  • #61 E. coli – Pathogenic | Health & Human Services
    https://hhs.iowa.gov/center-acute-disease-epidemiology/epi-manual/reportable-diseases/e-coli-pathogenic
    In severe cases, the patient may progress to develop other clinical syndromes such as hemolytic uremic syndrome (HUS) or thrombotic thrombocytopenic purpura (TTP). Hemolytic uremic syndrome (HUS) is characterized by the acute onset of microangiopathic hemolytic anemia, renal injury, and low platelet count. Thrombotic thrombocytopenic purpura (TTP) is characterized by anemia and low platelet counts but can include central nervous system (CNS) involvement and fever. […] EHEC: Cattle appear to be a reservoir of significant public health importance; however, other animals, such as deer, are also known to carry EHEC. In addition, humans serve as a reservoir. […] STEC and ETEC transmission occurs fecal-orally via contaminated food, drinking water or recreational water. Transmission may also occur directly from person-to-person; and can include certain types of sexual contact.
  • #62 E. coli – Pathogenic | Health & Human Services
    https://hhs.iowa.gov/center-acute-disease-epidemiology/epi-manual/reportable-diseases/e-coli-pathogenic
    In severe cases, the patient may progress to develop other clinical syndromes such as hemolytic uremic syndrome (HUS) or thrombotic thrombocytopenic purpura (TTP). Hemolytic uremic syndrome (HUS) is characterized by the acute onset of microangiopathic hemolytic anemia, renal injury, and low platelet count. Thrombotic thrombocytopenic purpura (TTP) is characterized by anemia and low platelet counts but can include central nervous system (CNS) involvement and fever. […] EHEC: Cattle appear to be a reservoir of significant public health importance; however, other animals, such as deer, are also known to carry EHEC. In addition, humans serve as a reservoir. […] STEC and ETEC transmission occurs fecal-orally via contaminated food, drinking water or recreational water. Transmission may also occur directly from person-to-person; and can include certain types of sexual contact.
  • #63 E. coli – Pathogenic | Health & Human Services
    https://hhs.iowa.gov/center-acute-disease-epidemiology/epi-manual/reportable-diseases/e-coli-pathogenic
    The infectious dose for E. coli O157:H7 is very low (about 100 organisms). E. coli O157:H7 has been associated with the consumption of undercooked contaminated ground beef, unpasteurized apple juice and cider, unpasteurized milk and other dairy products, raw fruits and vegetables, and salami. […] Category B Agent: E. coli has been identified as a potential category B bioterrorism agent as a food safety threat.
  • #64 Pathogenic E. coli – EcL (The Escherichia coli Laboratory)
    http://www.ecl-lab.ca/en/ecoli/index.asp
    E. coli is classified into 150 to 200 serotypes or serogroups based on somatic (O), capsular (K), fimbrial (F) and flagellar (H) antigens. […] Only a small proportion of strains are pathogenic, producing virulence factors permitting them to cause disease. […] Pathogenic E. coli are classified into categories or pathotypes based on the production of broad classes of virulence factors and on the mechanisms by which they cause disease. […] Strains of a particular pathotype belong to a restricted number of serotypes or clones. […] E. coli bacteria are constantly being shed into the immediate environment of the animals via the faeces, and contaminate the pens, litter, and floor of animals being housed indoors and the soil for outdoor animals. […] E. coli is transmitted to other animals via contaminated feed, handlers, and drinking water, and possibly farm to farm by vehicles such as transport trucks.
  • #65 Spatial and temporal modulation of enterotoxigenic E. coli H10407 pathogenesis and interplay with microbiota in human gut models | BMC Biology | Full Text
    https://bmcbiol.biomedcentral.com/articles/10.1186/s12915-020-00860-x
    ETEC effectively penetrates the mucus layer through mucin-degrading proteins, promoting ETEC attachment to the intestinal epithelial cells. […] Such adhesion is orchestrated by a primary set of fimbrial (e.g., CFA, FimH), non-fimbrial (e.g., Tia) adhesins, and accessory colonization factors like EtpA. […] The adhesion will facilitate the production and delivery of heat-labile (LT) and/or heat-stable (ST) enterotoxins, the hallmark of ETEC pathogenesis. […] Upon release and binding in the small intestine, LT and/or ST enzymatic activity results in the opening of cystic fibrosis transmembrane regulator which creates an osmotic movement of water into the intestinal lumen, leading to profuse watery diarrhea. […] The potency of ETEC to infect its host depends on virulence gene expression which is in turn determined by many gastrointestinal cues.
  • #66 Spatial and temporal modulation of enterotoxigenic E. coli H10407 pathogenesis and interplay with microbiota in human gut models | BMC Biology | Full Text
    https://bmcbiol.biomedcentral.com/articles/10.1186/s12915-020-00860-x
    We profiled not less than seven virulence genes encoding for enterotoxins (eltB and estP), enterotoxin release (leoA and tolC), adhesins (cfa/Ib, tia, fimH), stress response (rpoS) genes, and the actual enterotoxin LT production. […] We found most of the virulence genes to be switched on in the stomach and switched off in the TIM-1 ileal effluents, at late post-infectious stage in the M-SHIME ileum and in the ascending colon. […] The LT toxin can be associated with the lipopolysaccharide of the outer membrane of ETEC cells. […] Our results also demonstrated that the LT toxin can be produced both under aerobic or anaerobic conditions, as previously shown in static cultures. […] In comparison with eltB, we found that estP encoding for ST toxin does not follow the same expression profiles in both TIM-1 and M-SHIME.
  • #67 Spatial and temporal modulation of enterotoxigenic E. coli H10407 pathogenesis and interplay with microbiota in human gut models | BMC Biology | Full Text
    https://bmcbiol.biomedcentral.com/articles/10.1186/s12915-020-00860-x
    We profiled not less than seven virulence genes encoding for enterotoxins (eltB and estP), enterotoxin release (leoA and tolC), adhesins (cfa/Ib, tia, fimH), stress response (rpoS) genes, and the actual enterotoxin LT production. […] We found most of the virulence genes to be switched on in the stomach and switched off in the TIM-1 ileal effluents, at late post-infectious stage in the M-SHIME ileum and in the ascending colon. […] The LT toxin can be associated with the lipopolysaccharide of the outer membrane of ETEC cells. […] Our results also demonstrated that the LT toxin can be produced both under aerobic or anaerobic conditions, as previously shown in static cultures. […] In comparison with eltB, we found that estP encoding for ST toxin does not follow the same expression profiles in both TIM-1 and M-SHIME.
  • #68 Spatial and temporal modulation of enterotoxigenic E. coli H10407 pathogenesis and interplay with microbiota in human gut models | BMC Biology | Full Text
    https://bmcbiol.biomedcentral.com/articles/10.1186/s12915-020-00860-x
    ETEC effectively penetrates the mucus layer through mucin-degrading proteins, promoting ETEC attachment to the intestinal epithelial cells. […] Such adhesion is orchestrated by a primary set of fimbrial (e.g., CFA, FimH), non-fimbrial (e.g., Tia) adhesins, and accessory colonization factors like EtpA. […] The adhesion will facilitate the production and delivery of heat-labile (LT) and/or heat-stable (ST) enterotoxins, the hallmark of ETEC pathogenesis. […] Upon release and binding in the small intestine, LT and/or ST enzymatic activity results in the opening of cystic fibrosis transmembrane regulator which creates an osmotic movement of water into the intestinal lumen, leading to profuse watery diarrhea. […] The potency of ETEC to infect its host depends on virulence gene expression which is in turn determined by many gastrointestinal cues.
  • #69
    https://link.springer.com/article/10.1007/s00253-023-12929-y
    Antibiotic resistance is an important problem that threatens medical treatment. […] Therefore, the molecular reasons underlying the differences in the level of antibiotic resistance need to be clarified. […] Whole-genome sequencing of strains with different levels of resistance detected five mutations in strains with 10-fold resistance and two additional mutations in strains with 95-fold resistance. […] While it was thought that 10-fold resistance was achieved by the effect of mutations in the ftsI, marAR, and rpoC genes, it was found that 95-fold resistance was achieved by the synergistic effect of five mutations and the ampC mutation. […] This study will improve our view of resistance mechanisms in bacteria with different levels of resistance and provide the basis for our understanding of the molecular mechanism of antibiotic resistance in ampicillin-resistant E. coli strains.
  • #70
    https://link.springer.com/article/10.1007/s00253-023-12929-y
    The mutation of the ampC promoter may act synergistically with other mutations and lead to higher resistance. […] Similar transcriptomic responses to ampicillin are induced in strains with different levels of resistance. […] Low antibiotic concentrations are the steps that allow rapid achievement of high antibiotic resistance. […] It is very important to understand the molecular mechanisms involved in the emergence of antibiotic resistance and to identify the causes of different levels of resistance in order to prolong the life of antibiotics. […] Whole-genome sequencing revealed that E. coli W3110-10 contained five mutations, whereas two additional mutations were detected in E. coli W3110-95. […] The cumulative effect of these mutations resulted in a 10-fold increase in bacterial resistance.
  • #71
    https://link.springer.com/article/10.1007/s00253-023-12929-y
    The resulting transcriptome data show significant changes in the expression of a number of genes regulated by marA and associated with stress response and antibiotic resistance. […] The increase in expression in both strains compared with E. coli W3110, which does not contain the mutation, indicates that the upstream mutation affects marA expression. […] According to the RNA-seq data, a 52.98-fold increase in ampC gene expression was observed in E. coli W3110-95 containing the mutation, whereas no change was detected in E. coli W3110-10 without the mutation. […] These results show that gene expression increases significantly with insertion in the promoter region of the ampC gene. […] This shows that mutation of the ampC promoter has a significant effect on increasing antibiotic resistance from 10-fold to 95-fold.
  • #72 Escherichia coli bacteria establish antibiotic resistance via a defense mechanism | Institut Pasteur
    https://www.pasteur.fr/en/research-journal/news/escherichia-coli-bacteria-establish-antibiotic-resistance-defense-mechanism?language=fr
    A defense system has been discovered in Escherichia coli bacteria by Institut Pasteur scientists. […] In defending themselves, the bacteria establish antibiotic resistance. […] The spread of plasmids, especially in E. coli bacteria, is therefore a major threat for public health. […] But unfortunately the resistance genes can move from the bacterial plasmid to the chromosome, where they are integrated in a stable way. […] We were previously unaware of how antibiotic resistance genes were able to move from plasmids to establish themselves in the chromosome, despite the fact that this is a key step in the spread of carbapenem resistance. […] This is a defense system that destabilizes the plasmid. […] This protein system also promotes the integration of resistance genes in the chromosome. […] This discovery can help us understand the mechanism by which antibiotic resistance genes become established in bacterial chromosomes.
  • #73 E. coli – Pathogenic | Health & Human Services
    https://hhs.iowa.gov/center-acute-disease-epidemiology/epi-manual/reportable-diseases/e-coli-pathogenic
    Escherichia coli includes over a hundred different serotypes belonging to the group of gram-negative bacteria. Most serotypes are harmless and live in the intestines of healthy humans and animals. […] Six major categories of Escherichia coli strains cause diarrhea: Shiga-toxin producing E. coli, (STEC) including Enterohemorrhagic E. coli (EHEC), Enterotoxigenic (individual cases are not reportable), Enteroinvasive (individual cases are not reportable), Enteropathogenic (individual cases are not reportable), Intestinal E. coli infection-Other enteroaggregative E. coli and diffuse-adherent E. coli (individual cases are not reportable). […] Shiga toxin-producing E. coli (STEC) include O157:H7, O26, O111, O103, O45, and O121. EHEC produce potent cytotoxins called Shiga toxin 1 and 2. […] Infection with pathogenic E. coli may present with a wide spectrum of clinical manifestations. An individual may be asymptomatic, have mild non-bloody diarrhea, or have grossly bloody diarrhea. Most diagnosed cases develop bloody diarrhea 6 to 48 hours after the onset of non-bloody diarrhea.
  • #74 E. coli – Pathogenic | Health & Human Services
    https://hhs.iowa.gov/center-acute-disease-epidemiology/epi-manual/reportable-diseases/e-coli-pathogenic
    In severe cases, the patient may progress to develop other clinical syndromes such as hemolytic uremic syndrome (HUS) or thrombotic thrombocytopenic purpura (TTP). Hemolytic uremic syndrome (HUS) is characterized by the acute onset of microangiopathic hemolytic anemia, renal injury, and low platelet count. Thrombotic thrombocytopenic purpura (TTP) is characterized by anemia and low platelet counts but can include central nervous system (CNS) involvement and fever. […] EHEC: Cattle appear to be a reservoir of significant public health importance; however, other animals, such as deer, are also known to carry EHEC. In addition, humans serve as a reservoir. […] STEC and ETEC transmission occurs fecal-orally via contaminated food, drinking water or recreational water. Transmission may also occur directly from person-to-person; and can include certain types of sexual contact.
  • #75 Escherichia coli – Wikipedia
    https://en.wikipedia.org/wiki/Escherichia_coli
    Some serotypes, such as EPEC and ETEC, are pathogenic, causing serious food poisoning in their hosts. […] Fecal-oral transmission is the major route through which pathogenic strains of the bacterium cause disease. […] A growing body of research, though, has examined environmentally persistent E. coli which can survive for many days and grow outside a host. […] Some strains develop traits that can be harmful to a host animal. These virulent strains typically cause a bout of diarrhea that is often self-limiting in healthy adults but is frequently lethal to children in the developing world. […] More virulent strains, such as O157:H7, cause serious illness or death in the elderly, the very young, or the immunocompromised. […] Some strains of E. coli, for example O157:H7, can produce Shiga toxin. The Shiga toxin causes inflammatory responses in target cells of the gut, leaving behind lesions which result in the bloody diarrhea that is a symptom of a Shiga toxin-producing E. coli (STEC) infection.
  • #76 Escherichia coli – Wikipedia
    https://en.wikipedia.org/wiki/Escherichia_coli
    Some serotypes, such as EPEC and ETEC, are pathogenic, causing serious food poisoning in their hosts. […] Fecal-oral transmission is the major route through which pathogenic strains of the bacterium cause disease. […] A growing body of research, though, has examined environmentally persistent E. coli which can survive for many days and grow outside a host. […] Some strains develop traits that can be harmful to a host animal. These virulent strains typically cause a bout of diarrhea that is often self-limiting in healthy adults but is frequently lethal to children in the developing world. […] More virulent strains, such as O157:H7, cause serious illness or death in the elderly, the very young, or the immunocompromised. […] Some strains of E. coli, for example O157:H7, can produce Shiga toxin. The Shiga toxin causes inflammatory responses in target cells of the gut, leaving behind lesions which result in the bloody diarrhea that is a symptom of a Shiga toxin-producing E. coli (STEC) infection.
  • #77 E. coli – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/e-coli/symptoms-causes/syc-20372058
    Escherichia coli (E. coli) bacteria normally live in the intestines of healthy people and animals. […] But a few strains, such as E. coli O157:H7, can cause severe stomach cramps, bloody diarrhea and vomiting. […] The E. coli O157:H7 strain belongs to a group of E. coli that produces a powerful toxin that damages the lining of the small intestine. This can cause bloody diarrhea. […] Unlike many other disease-causing bacteria, E. coli can cause an infection even if you ingest only small amounts. […] E. coli bacteria can easily travel from person to person, especially when infected adults and children don’t wash their hands properly. […] Most healthy adults recover from E. coli illness within a week. Some people particularly young children and older adults may develop a life-threatening form of kidney failure called hemolytic uremic syndrome.
  • #78 Molecular mechanisms of Escherichia coli pathogenicity | Nature Reviews Microbiology
    https://www.nature.com/articles/nrmicro2265
    Other pathovars, such as enterotoxigenic E. coli, elaborate toxins that cause disease, whereas the attachment of enteroaggregative and diffusely adherent E. coli stimulates cellular signalling events that stimulate inflammation. […] The extraintestinal isolates have remarkable lifestyles. Uropathogenic E. coli can invade the underlying bladder cells and form quiescent reservoirs, which are possibly the source of recurrent infections. Neonatal meningitis E. coli has been shown to be highly resistant to host immune responses and can cross the bloodbrain barrier to cause disease. […] In this Review, we focus on the recent advances in our understanding of the different pathogenic mechanisms that are used by various E. coli pathovars and how they cause disease in humans.
  • #79 Molecular mechanisms of Escherichia coli pathogenicity | Nature Reviews Microbiology
    https://www.nature.com/articles/nrmicro2265
    Other pathovars, such as enterotoxigenic E. coli, elaborate toxins that cause disease, whereas the attachment of enteroaggregative and diffusely adherent E. coli stimulates cellular signalling events that stimulate inflammation. […] The extraintestinal isolates have remarkable lifestyles. Uropathogenic E. coli can invade the underlying bladder cells and form quiescent reservoirs, which are possibly the source of recurrent infections. Neonatal meningitis E. coli has been shown to be highly resistant to host immune responses and can cross the bloodbrain barrier to cause disease. […] In this Review, we focus on the recent advances in our understanding of the different pathogenic mechanisms that are used by various E. coli pathovars and how they cause disease in humans.
  • #80 SciELO Brazil – The versatile strategies of Escherichia coli pathotypes: a mini review The versatile strategies of Escherichia coli pathotypes: a mini review
    https://www.scielo.br/j/jvatitd/a/LnS9mzjsKZ8J5kFkmNqrBYM/
    The widespread species Escherichia coli includes a broad variety of different types, ranging from highly pathogenic strains to avirulent isolates. […] Pathogenic strains remain a leading cause of severe and persistent infant diarrhea in developing countries. […] They may be limited to colonization of a mucosal surface or can disseminate throughout the body and have been implicated in urinary tract infection, sepsis/meningitis and gastrointestinal infection. […] The human gastrointestinal tract is susceptible to diarrheagenic E. coli infections. […] Escherichia coli have effectively managed to subvert the host cytoskeleton for their own purposes causing substantial diarrheal disease, a major public health problem worldwide. […] This review deals with the different strategies regarding E. coli as a pathogen and the virulence traits of its pathotypes highlighting the species as a commensal, opportunistic and specialized pathogen.
  • #81 E. coli – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/e-coli/symptoms-causes/syc-20372058
    No vaccine or medication can protect you from E. coli-based illness, though researchers are investigating potential vaccines. […] E. coli bacteria can create some stomach-turning symptoms, like abdominal pain and nausea. […] There’s a specific type of E. coli. It’s called O157:H7, which can cause bloody diarrhea and has been associated with a condition that can cause kidney damage, especially in young children.
  • #82
    https://www.who.int/news-room/fact-sheets/detail/e-coli
    The only effective method of eliminating STEC from foods is to introduce a bactericidal treatment, such as heating (for example, cooking or pasteurization) or irradiation. […] Basic good food hygiene practices, as described in the WHO Five keys to safer food, can prevent the transmission of pathogens responsible for many foodborne diseases, and also protect against foodborne diseases caused by STEC.
  • #83
    https://www.who.int/news-room/fact-sheets/detail/e-coli
    Escherichia coli (E. coli) is a bacterium that is commonly found in the gut of humans and warm-blooded animals. Some strains however, such as Shiga toxin-producing E. coli (STEC), can cause severe foodborne disease. […] STEC produces toxins, known as Shiga-toxins because of their similarity to the toxins produced by Shigella dysenteriae. […] STEC is destroyed by thorough cooking of foods until all parts reach a temperature of 70 C or higher. […] Most available information on STEC relates to serotype O157:H7, since it is easily differentiated biochemically from other E. coli strains. […] E. coli O157:H7 is transmitted to humans primarily through consumption of contaminated foods, such as raw or undercooked ground meat products and raw milk. […] An asymptomatic carrier state has been reported, where individuals show no clinical signs of disease but are capable of infecting others.
  • #84
    https://www.who.int/news-room/fact-sheets/detail/e-coli
    The only effective method of eliminating STEC from foods is to introduce a bactericidal treatment, such as heating (for example, cooking or pasteurization) or irradiation. […] Basic good food hygiene practices, as described in the WHO Five keys to safer food, can prevent the transmission of pathogens responsible for many foodborne diseases, and also protect against foodborne diseases caused by STEC.
  • #85 SciELO Brazil – The versatile strategies of Escherichia coli pathotypes: a mini review The versatile strategies of Escherichia coli pathotypes: a mini review
    https://www.scielo.br/j/jvatitd/a/LnS9mzjsKZ8J5kFkmNqrBYM/
    Although most E. coli are harmless commensals of the human and animal intestine, certain specific, highly-adapted E. coli strains are capable of causing a variety of different diseases. […] Several different E. coli strains cause diverse intestinal and extraintestinal diseases by means of virulence factors that affect a wide range of cellular processes. […] Infections due to pathogenic E. coli may be limited to colonization of a mucosal surface or can disseminate throughout the body and have been implicated in urinary tract infection, sepsis/meningitis and gastrointestinal infection. […] The toxins synthesized by ExPEC strains, mainly represented by hemolysin and cytotoxic necrotizing factor, contribute to destruction of eukaryotic cells. […] Co-expression of virulence factors contributes to the host’s defense system defeat and onset of infection. […] Knowledge of the pathogenic mechanisms of E. coli pathotypes has led to the development of rational interventions for the treatment and prevention of E. coli-induced diseases.