Zatrucie pokarmowe
Patofizjologia i mechanizm

Zatrucia pokarmowe dzielą się na infekcyjne, intoksykacyjne oraz toksykoinfekcyjne, różniące się mechanizmem patogenetycznym. Niezapalne zatrucia pokarmowe, wywołane przez enterotoksyny (np. Vibrio cholerae, enterotoksyczny E. coli, Clostridium perfringens, Bacillus cereus, Staphylococcus aureus), prowadzą do wodnistych biegunek bez krwi i ropy, często z głębokim odwodnieniem. Enterotoksyny działają poprzez stymulację cyklazy adenylowej i układu cAMP, hamowanie transportu glukozy oraz uszkodzenie nabłonka jelitowego. Z kolei zapalne zatrucia pokarmowe (np. Campylobacter jejuni, Salmonella spp., Shigella, EHEC) powodują inwazję i destrukcję błony śluzowej jelita, manifestując się biegunką krwistą z leukocytami, gorączką i objawami ogólnoustrojowymi. Szczególną uwagę zwraca botulizm, gdzie neurotoksyna botulinowa (typy A-G, masa cząsteczkowa 150 kDa) hamuje uwalnianie acetylocholiny, prowadząc do porażenia wiotkiego i potencjalnie śmierci z powodu niewydolności oddechowej.

Patogeneza zatrucia pokarmowego

Zatrucie pokarmowe to choroba wynikająca ze spożycia żywności lub wody zanieczyszczonej patogenami, ich toksynami lub szkodliwymi substancjami chemicznymi. Mechanizmy patogenetyczne leżące u podstaw zatruć pokarmowych są złożone i zależą od rodzaju czynnika wywołującego infekcję. Zrozumienie tych mechanizmów jest kluczowe dla właściwej diagnostyki i leczenia.12

Klasyfikacja patogenetyczna zatruć pokarmowych

Z punktu widzenia patogenezy, zatrucia pokarmowe można sklasyfikować jako:12

  • Zatrucia pokarmowe infekcyjne (foodborne infection) – spowodowane przez patogeny, które po spożyciu namnażają się w przewodzie pokarmowym i wywołują objawy12
  • Zatrucia pokarmowe intoksykacyjne (foodborne intoxication) – spowodowane przez toksyny wytworzone przez mikroorganizmy w żywności przed jej spożyciem12
  • Zatrucia pokarmowe toksykoinfekcyjne (foodborne toxicoinfection) – spowodowane przez bakterie, które po spożyciu kolonizują jelita i wytwarzają toksyny in vivo12

Niezapalne mechanizmy zatrucia pokarmowego

Niezapalne zatrucia pokarmowe są spowodowane działaniem enterotoksyn na mechanizmy wydzielnicze błony śluzowej jelita cienkiego, bez inwazji patogenów. Prowadzi to do obfitych, wodnistych stolców bez obecności krwi, ropy i bez silnego bólu brzucha. W niektórych przypadkach może wystąpić głębokie odwodnienie.1

Enterotoksyny i ich działanie

Enterotoksyny mogą być preformowane przed spożyciem lub wytwarzane w jelicie po spożyciu. Ich działanie polega na zaburzeniu funkcji błony śluzowej jelita:12

  • Stymulacja cyklazy adenylowej i układu cAMP w komórkach nabłonka jelitowego1
  • Hamowanie transportu glukozy w komórkach nabłonka jelitowego1
  • Uszkodzenie nabłonka jelitowego i utrata białek do światła jelita12

Do patogenów wywołujących niezapalne zatrucia pokarmowe należą: Vibrio cholerae, enterotoksyczny Escherichia coli, Clostridium perfringens, Bacillus cereus, Staphylococcus aureus, a także niektóre pasożyty jak Giardia lamblia, Cryptosporidium oraz wirusy takie jak rotawirus, norowirus i adenowirus.1

Szczególne mechanizmy działania toksyn

Staphylococcus aureus wytwarza termostabilne enterotoksyny (A-E, G-I), które są główną przyczyną zatruć pokarmowych. Toksyny te działają poprzez stymulację receptorów w przewodzie pokarmowym, które przekazują impulsy do ośrodków w rdzeniu przedłużonym, wywołując wymioty. Enterotoksyny stymulują również hipersekrecję w jelitach.123

Bacillus cereus produkuje dwa typy toksyn powodujących dwa odrębne zespoły chorobowe:123

  • Toksynę wymiotną (cereulid) – termostabilny dodekadepsypeptyd cykliczny działający jako drażniący żołądek, wiążący się z receptorami serotoninowymi w żołądku i jelicie cienkim oraz stymulujący nerw błędny123
  • Toksynę biegunkową – kompleks białkowy składający się z hemolizyny BL (Hbl), niehemorragicznej enterotoksyny (Nhe) i cytotoksyny K (CytK), które tworzą pory w błonach komórkowych i zaburzają połączenia międzykomórkowe12

Clostridium perfringens wytwarza enterotoksynę podczas sporulacji, która jest uwalniana wraz ze sporami podczas lizy komórki. Po uwolnieniu enterotoksyna wiąże się z komórkami nabłonka, powodując cytotoksyczne uszkodzenie błony komórkowej i późniejszą zmianę przepuszczalności, prowadzącą do biegunki i kurczów brzucha.12

Zapalne mechanizmy zatrucia pokarmowego

Zapalne zatrucia pokarmowe są spowodowane działaniem cytotoksyn na błonę śluzową, prowadzącym do inwazji i destrukcji. Zazwyczaj zajmują okrężnicę lub dystalną część jelita cienkiego. Biegunka jest zazwyczaj krwista, z obecnością śluzu i leukocytów. Pacjenci zwykle mają gorączkę i mogą wyglądać na zatrutych. Odwodnienie jest mniej prawdopodobne niż w przypadku niezapalnej biegunki z powodu mniejszej objętości stolca.1

Mechanizmy inwazji patogenów

W niektórych przypadkach organizmy przenikają przez błonę śluzową i namnażają się w lokalnej tkance limfatycznej, po czym następuje rozsiew ogólnoustrojowy. Do patogenów wywołujących zapalne zatrucia pokarmowe należą: Campylobacter jejuni, Vibrio parahaemolyticus, enterokrwotoczne i enteroinwazyjne E. coli, Yersinia enterocolitica, Clostridium difficile, Entamoeba histolytica oraz gatunki Salmonella i Shigella.1

Szczegółowe mechanizmy inwazji obejmują:123

  • Salmonella spp. – po spożyciu infekuje komórki nabłonkowe jelit i fagocyty, wykorzystując dynamiczne techniki do osłabienia i dezorientacji komórek układu odpornościowego. Potrafi indukować fagocytozę w określonych białych krwinkach oraz powodować wytwarzanie reaktywnych form tlenu (ROS) przez neutrofile, co sprzyja jej przetrwaniu dzięki posiadaniu arsenału peroksydaz i katalaz.12
  • E. coli O157:H7 (EHEC) – wydziela toksyny ułatwiające przyłączanie się do komórek nabłonkowych i ich niszczenie. Proces obejmuje wstrzyknięcie do komórki gospodarza cyklomoduliny, która zatrzymuje mitozę, spowalniając odnowę komórek nabłonkowych. Następnie bakteria wydziela toksyny Shiga, które dezaktywują podjednostkę 60S rybosomu.12
  • Campylobacter jejuni – kolonizuje okrężnicę i dystalną część jelita krętego, uwalniając termolabilną toksynę powodującą rozszerzenie komórek (CDT), która atakuje DNA komórek śródbłonka jelitowego, rekrutuje kinazy białkowe blokujące wejście komórek w mitozę i wywołuje lokalną reakcję zapalną, lizę komórek oraz wodnistą lub krwawą biegunkę z leukocytami w kale.12
  • Shigella – przemieszcza się do bazolateralnej powierzchni komórek nabłonkowych, gdzie komórki M transportują ją do makrofagów podnabłonkowych, które ją fagocytują. Następnie Shigella degraduje fagosom i wnika do komórek nabłonkowych jelita krętego i okrężnicy, gdzie może się namnażać wewnątrzkomórkowo.1

Neurotoksyczne zatrucia pokarmowe

W niektórych typach zatruć pokarmowych (np. spowodowanych przez Staphylococcus aureus, Bacillus cereus), wymioty są spowodowane toksyną działającą na ośrodkowy układ nerwowy. Szczególnym przykładem jest botulizm, gdzie neurotoksyna botuliny hamuje uwalnianie acetylocholiny w zakończeniach nerwowych.12

Mechanizm działania toksyny botulinowej

Clostridium botulinum wytwarza neurotoksynę, która jest najsilniejszą znaną trucizną. Istnieje siedem typów neurotoksyny botulinowej, od A do G, w zależności od specyficzności antygenowej toksyny wytwarzanej przez każdy szczep.12

Wszystkie typy toksyn są białkami o masie cząsteczkowej 150 000, które zapobiegają uwalnianiu acetylocholiny w połączeniu nerwowo-mięśniowym, powodując porażenie wiotkie. Objawy botulizmu obejmują początkowo nudności i wymioty, po których następują bardziej charakterystyczne objawy neurologiczne, w tym zaburzenia widzenia i ostre porażenie wiotkie, które zaczyna się od mięśni twarzy, głowy i gardła, zstępując do mięśni klatki piersiowej i kończyn, prowadząc do możliwej śmierci z powodu niewydolności oddechowej spowodowanej porażeniem górnych dróg oddechowych lub przepony.12

Toksyny morskie i zatrucia rybami

Zatrucia pokarmowe związane z konsumpcją ryb i owoców morza mają szczególne mechanizmy patogenetyczne:123

Zatrucie skombrotoksyczne (scombroid)

Zatrucie skombrotoksyczne jest chorobą pokarmową rozwijającą się po spożyciu świeżych ryb, które mają dobre cechy organoleptyczne, ale zawierają dużą ilość egzogennej histaminy. Patogeneza obejmuje złożony system interakcji między organizmem a czynnikami chemicznymi, takimi jak egzogenna histamina, inne aminy biogenne, kwas cis-urokanowy, salicylany i inne substancje uwalniające histaminę.12

Mechanizm działania polega na konwersji histydyny (występującej w wysokich stężeniach w tych rybach) do histaminy przez dekarboksylazę histydyny w bakteriach, które normalnie kolonizują ryby. Egzogenna histamina, oprócz efektu ogólnoustrojowego prowadzącego do głównych objawów zatrucia (zaczerwienienie, obrzęk, swędząca wysypka, hipotensja, ostry obrzęk płuc, skurcz oskrzeli), ma również wpływ na układ odpornościowy.12

Inne toksyny morskie

Inne mechanizmy zatruć związanych z owocami morza obejmują:1

  • Ciguatoksyna – otwiera kanały Na+, powodując depolaryzację
  • Tetrodotoksyna – neurotoksyna blokująca napięciowo-zależne kanały sodowe, co hamuje propagację potencjału czynnościowego

Głównym czynnikiem przyczyniającym się do zanieczyszczenia owoców morza patogenami pokarmowymi wydaje się być naturalnie występujące tworzenie biofilmu. Vibrio i Salmonella, Aeromonas hydrophila i Listeria monocytogenes to powszechne patogeny bakteryjne owoców morza, które tworzą biofilmy.1

Rola układu odpornościowego w patogenezie zatruć pokarmowych

Reakcja układu odpornościowego odgrywa kluczową rolę zarówno w ostrej fazie zatrucia pokarmowego, jak i w jego długoterminowych skutkach:123

Reakcja zapalna

Niektóre bakterie wywołują spustoszenie poprzez namnażanie się w organizmie przed uwolnieniem toksyn, które inicjują reakcję immunologiczną w jelicie. Bakterie lub enterotoksyny, które przetrwają trudne warunki żołądkowe, dostają się do jelit, gdzie rozpoczyna się proces chorobowy.1

Komórki odpornościowe uwalniają białka sygnalizacyjne zwane proza palnymi cytokinami, które inicjują serię kroków powodujących zapalenie i obrzęk jelit, prowadząc do dyskomfortu. Toksyny bakteryjne mogą powodować otwieranie porów w ścianie jelita, umożliwiając napływ wody i innych cząsteczek, co prowadzi do wodnistej biegunki, która pomaga wypłukać bakterie i ich toksyny, ale może powodować odwodnienie.12

Odporność nabyta i wrażliwość na zatrucia

Wcześniejsza ekspozycja na patogeny może znacznie zwiększyć tolerancję na kolejne ekspozycje. Miejscowa ludność w danym regionie może tolerować poziomy patogenów, które wywołałyby chorobę u podróżnych, dzięki pamięci immunologicznej rozwiniętej na skutek powtarzających się ekspozycji na niskie poziomy.1

Zatrucie pokarmowe często występuje jako biegunka podróżnych u osób, których mikrobiota jelitowa nie jest przyzwyczajona do organizmów endemicznych dla odwiedzanego regionu. Efekt tej mikrobiologicznej naiwności jest potęgowany przez wszelkie uchybienia w zakresie bezpieczeństwa żywności podczas przygotowywania posiłków.1

Zespół pokaźnnego jelita drażliwego (PI-IBS)

W przypadkach zatrucia pokarmowego, szczególnie biegunki podróżnych, objawy często wynikają z reakcji układu odpornościowego, a nie z bezpośredniego uszkodzenia przez patogen. Ta reakcja zapalna może prowadzić do pokaźnnego zespołu jelita drażliwego (PI-IBS), gdzie 3-20% dotkniętych osób rozwija przewlekłe objawy żołądkowo-jelitowe nawet po usunięciu patogenu. Sugeruje to, że reakcja immunologiczna organizmu, szczególnie zapalenie, odgrywa znaczącą rolę zarówno w ostrych objawach, jak i długoterminowych skutkach zatrucia pokarmowego.12

Czynniki wpływające na patogenezę zatruć pokarmowych

Kilka czynników wpływa na rozwój i nasilenie zatrucia pokarmowego:12

Dawka infekcyjna

Dawka infekcyjna to ilość czynnika, który musi zostać spożyty, aby wywołać objawy zatrucia pokarmowego, i różni się w zależności od czynnika i wieku oraz ogólnego stanu zdrowia konsumenta. Patogeny różnią się minimalną dawką infekcyjną; na przykład, Shigella sonnei ma niską szacowaną minimalną dawkę wynoszącą 500 jednostek tworzących kolonię (CFU), podczas gdy Staphylococcus aureus ma stosunkowo wysokie oszacowanie.1

Czynniki wzrostu bakterii

Bakterie powodujące zatrucia pokarmowe mogą namnażać się bardzo szybko, szczególnie w określonych warunkach. Czynniki wpływające na wzrost bakterii obejmują:1

  • Czas – w idealnych warunkach jedna bakteria może namnożyć się do ponad 2 milionów w ciągu 7 godzin
  • Temperatura – bakterie powodujące zatrucia pokarmowe najlepiej rozwijają się w zakresie temperatur między 5°C a 60°C, określanym jako strefa niebezpieczna temperatur
  • Składniki odżywcze – większość żywności zawiera wystarczającą ilość składników odżywczych dla wzrostu bakterii, szczególnie żywność potencjalnie wysokiego ryzyka, jak produkty mleczne i jajeczne, mięso, drób i owoce morza
  • Woda – bakterie potrzebują wody do wzrostu; bez wody wzrost może zwolnić lub zatrzymać się
  • pH – jest miarą kwasowości lub zasadowości i jest również ważny dla kontrolowania wzrostu bakterii; niskie pH (kwaśne warunki) generalnie zatrzymuje wzrost bakterii

Stan układu odpornościowego gospodarza

Układ odpornościowy odgrywa główną rolę w ochronie przed zatruciem pokarmowym; gdy układ odpornościowy jest osłabiony, człowiek staje się bardziej podatny. Zatrucie pokarmowe jest szczególnie groźne podczas ciąży, dla małych dzieci, osób starszych i osób z osłabionym układem odpornościowym. Te choroby mogą zagrażać życiu.12

Mechanizmy specyficzne dla patogenów

Różne patogeny wykazują unikalne mechanizmy patogenetyczne:123

Vibrio parahaemolyticus

Badania wykazały, że dwa białka wytwarzane przez Vibrio parahaemolyticus współpracują ze sobą w celu wykrywania i wychwytywania soli żółciowych w jelitach ludzi, którzy jedzą surowe lub niedogotowane owoce morza zawierające bakterie. Gdy ludzie spożywają surowe lub niedogotowane owoce morza zanieczyszczone Vibrio parahaemolyticus, bakterie wykorzystują te sole żółciowe jako sygnał do uwalniania toksyn.1

Odkryto, że nie jeden, ale dwa geny są wymagane, aby Vibrio otrzymało sygnał soli żółciowej. Te geny kodują dwa białka, które tworzą kompleks na powierzchni błony bakteryjnej, tworząc strukturę baryłkopodobną, która wiąże sole żółciowe i odbiera sygnał, aby powiedzieć komórce bakteryjnej, aby rozpoczęła produkcję toksyn.12

Niedawne badania wykazały, jak bakteria Vibrio parahaemolyticus tworzy struktury podobne do strzykawek, aby wstrzyknąć swoje toksyny do komórek jelitowych. Bakteria transkrybuje DNA w miejscu, gdzie potrzebny jest system sekrecji typu III (T3SS2), tłumaczy RNA na białko i montuje komponenty T3SS2 przez błonę w procesie znanym jako transertion. Te kroki były wcześniej uważane za zachodzące w bardziej rozproszonych lokalizacjach wokół komórki, ale zebranie maszynerii w jednym miejscu na błonie bakterii prawdopodobnie pomaga V. parahaemolyticus szybciej i wydajniej zbudować T3SS2 i zainfekować komórki.12

Clostridium perfringens

Clostridium perfringens wytwarza spory, które mają powłoki ochronne. Po zjedzeniu przez człowieka żywności zanieczyszczonej C. perfringens, bakterie mogą wytwarzać toksynę, która powoduje biegunkę. Najczęściej w ogniskach zatrucia pokarmowego C. perfringens biorą udział potrawy gotowane w dużych ilościach i przechowywane w niebezpiecznych temperaturach (między 40°F a 140°F).1

Zatrucie pokarmowe spowodowane przez C. perfringens występuje, gdy bakterie przetrwają proces gotowania i zaczną namnażać się, gdy żywność jest schładzana lub przechowywana w niewłaściwej temperaturze. Gdy spożywana jest żywność zawierająca dużą liczbę C. perfringens, bakterie wytwarzają toksynę w jelitach, która powoduje chorobę.1

Niedawno odkryto, że aminokwas seryna działa jako inhibitor sporulacji Clostridium perfringens. Obserwacje mikroskopowe wykazały, że seryna hamuje przebudowę ściany komórkowej bakterii, która jest niezbędna w procesie tworzenia spor.12

Bacillus cereus

Zatrucie pokarmowe wywołane przez B. cereus można postrzegać jako proces wieloczynnikowy, ponieważ przed wystąpieniem choroby należy uwzględnić szereg indywidualnych kroków, w tym występowanie i przeżycie B. cereus w różnych produktach spożywczych, przetrwanie przejścia przez żołądek, kiełkowanie spor, aktywny ruch w kierunku nabłonka jelitowego i przyleganie do niego, wytwarzanie enterotoksyn w warunkach jelitowych, a także wpływ spożywanej żywności i mikrobioty jelitowej na te procesy.1

Badania wykazały, że toksyna wydzielana przez B. cereus wiąże się bezpośrednio z komórkami w ludzkim ciele i przebija w nich dziury, aby je zabić, wywołując odpowiedź immunologiczną. Toksyna wymiotna, zwana cereulid, wiąże się z receptorami serotoninowymi w żołądku i jelicie cienkim oraz stymuluje nerw błędny, który kontroluje ruch mięśni w jelicie.12

Lektyny jako nowy mechanizm toksyczności

Lektyny obecne w niektórych nieprawidłowo gotowanych warzywach mogą powodować ostre zaburzenia żołądkowo-jelitowe, choć mechanizm toksyczności nie był znany. Badania wykazały, że toksyczność lektyn wynika z hamującego wpływu na naprawę błony komórkowej.1

Lektyny silnie hamują naprawę błony komórkowej i dlatego są toksyczne dla uszkodzonych komórek. Stanowi to nową formę toksyczności białkowej, która leży u podstaw zatrucia pokarmowego lektynami roślinnymi. Lektyny roślinne, które nie są skutecznie degradowane przez enzymy trawienne i mają powinowactwo do powierzchni komórek nabłonkowych jelita, takie jak te obecne w rodzinie Leguminosae, mogą być trujące.1

Wiązanie glikoprotein powierzchniowych komórek przez lektyny zakłóca zdarzenia egzocytotyczne związane z naprawą błony (wydzielanie śluzu) i silnie blokuje naprawę. Lektyny są toksyczne, gdy są obecne w przewodzie pokarmowym, na podstawie dwóch powiązanych ze sobą efektów:1

  • Brak uszczelnienia występuje w ogólnej populacji komórek przewodu pokarmowego normalnie narażonych na poziomy stresu mechanicznego uszkadzającego błonę, prowadząc do ich martwicy
  • Niepowodzenie egzocytozy w subpopulacji komórek przewodu pokarmowego, które normalnie wydzielają śluz, prowadzące do zmniejszenia wydzielania ochronnego, smarującego śluzu i związanego z tym wzrostu częstości zdarzeń uszkodzenia błony wywołanych mechanicznie

Te mechanizmy wyjaśniają, dlaczego spożycie niektórych nieprawidłowo przygotowanych roślin strączkowych może prowadzić do ostrych objawów zatrucia pokarmowego.1

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

Materiały źródłowe

  • #1 Food Poisoning: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/175569-overview
    Food poisoning is defined as an illness caused by the consumption of food or water contaminated with bacteria and/or their toxins, or with parasites, viruses, or chemicals. The most common pathogens are Norovirus, Escherichia coli, Salmonella, Clostridium perfringens, Campylobacter, and Staphylococcus aureus. […] The pathogenesis of diarrhea in food poisoning is classified broadly into either noninflammatory or inflammatory types. Noninflammatory diarrhea is caused by the action of enterotoxins on the secretory mechanisms of the mucosa of the small intestine, without invasion. This leads to large volume watery stools in the absence of blood, pus, or severe abdominal pain. Occasionally, profound dehydration may result. The enterotoxins may be either preformed before ingestion or produced in the gut after ingestion. Examples include Vibrio cholerae, enterotoxic Escherichia coli, Clostridium perfringens, Bacillus cereus, Staphylococcus organisms, Giardia lamblia, Cryptosporidium, rotavirus, norovirus (genus Norovirus, previously called Norwalk virus), and adenovirus.
  • #1 Foodborne pathogens
    https://pmc.ncbi.nlm.nih.gov/articles/PMC6604998/
    Foodborne illness occurs when a pathogen is ingested with food and establishes itself (and usually multiplies) in the human host, or when a toxigenic pathogens establishes itself in a food product and produces a toxin, which is then ingested by the human host. Thus, foodborne illness is generally classified into: (a) foodborne infection and (b) foodborne intoxication. In foodborne infections, since an incubation period is usually involved, the time from ingestion until symptoms occur is much longer than that of foodborne intoxications. […] B. cereus produces two types of toxins, the emetic (vomiting) and the diarrhoeal one, causing two types of illness. The emetic syndrome is caused by emetic toxin produced by the bacteria during the growth phase in the food. The diarrhoeal syndrome is caused by diarrhoeal toxins produced during growth of the bacteria in the small intestine. The rapid onset of the emetic type is characterized by nausea and vomiting while the late onset of the diarrheal type is characterized by diarrhea and abdominal pain. Both syndromes (i.e., diarrheal and emetic) are a result of B. cereus endospores surviving the cooking process, after which germination and subsequent proliferation of vegetative cells occurs at some point during storage.
  • #1 Noninflammatory Gastroenteritis- Food Poisoning
    https://www.atsu.edu/faculty/chamberlain/website/tritzid/foodpoi.htm
    Food poisoning is a toxemia associated with the ingestion of preformed microbial toxins. It is NOT an infection. Since the toxins are ingested preformed and no microbial growth within the human is required, symptomology occurs rapidly, usually within 2-12 hours. These toxins either affect the intestine (enterotoxin of C. perfringens) or the central nervous system (neurotoxin of C. botulinum) or both (S. aureus and B. cereus). […] The enterotoxins stimulate the adenyl cyclase – cyclic AMP system in intestinal epithelial cells and cause fluid accumulation in the intestine. The neurotoxins cause vomiting through an unknown mechanism. […] A single heat-labile protein of 34000 molecular weight inhibits glucose transport in intestinal epithelial cells, damages the intestinal epithelium and causes protein loss into the intestinal lumen. This activity is maximal in the ileum and minimal in the duodenum.
  • #1 Food Poisoning Caused by Bacteria (Food Toxins) | IntechOpen
    https://www.intechopen.com/chapters/56521
    Among the microorganisms causing FBDs are bacteria that have different virulence factors that give them the ability to cause a disease; among these factors, we can find toxins that can be produced in food or once the pathogen has colonized the digestive tract. […] A bacterial toxin is a macromolecule mainly of protein origin, which can cause toxic damage in a specific organ of the host. […] Toxins can be divided in endotoxins and exotoxins: Endotoxins or lipopolysaccharides (LPS): These are the components of the outer membrane of the Gram-negative bacteria; they are considered the most important antigen of the bacteria; they are released into the medium after different processes such as lysis and cell division. […] Exotoxins of Gram-negative enteropathogenic bacteria play an important role in the pathogenesis of diarrheal disease, causing hypersecretion of liquids without the destruction and death of intestinal mucosal cells.
  • #1
    http://www.bccdc.ca/health-info/diseases-conditions/staphylocococcus-aureus
    Staphylococcal food poisoning is an acute intoxication that occurs when food contaminated with enterotoxin produced by this bacterium is consumed. […] The presence of staphylococcal enterotoxin in food is usually due to cross contamination of ready to eat food with either raw food or, most likely, contamination from a food handler that is carrying Staphylococcus aureus. […] For staphylococcal food poisoning to occur following the ingestion of a given food, two conditions are necessary. First, S. aureus has to be present in the food; second, foods stored at incorrect temperatures and time allow growth of this pathogen and the production of enterotoxin. […] Although S. aureus can be found in food-producing animals and raw foods, humans are considered the main reservoir for this pathogen.
  • #1 Bacterial Food Poisoning | California Poison Control System
    https://calpoison.org/content/bacterial-food-poisoning
    Some serotypes of B. cereus produce a mild emetic illness mediated by a dodecadepsipeptide gastric irritant called cereulide, while other serotypes produce a mild diarrheal illness mediated by Hemolysin BL, which punches pores or channels into intestinal cell membranes and disrupts tight junctions. […] Clostridium perfringens causes a toxin-mediated disease that closely resembles the diarrheal illness produced by B. cereus, and is the 3rd most commonly reported food-borne illness behind Salmonella and Campylobacter spp. Enteric toxins form pores or channels in host cell membranes and disrupt tight junctions. […] Staphylococcus aureus causes a toxin-mediated disease that closely resembles the emetic illness produced by B. cereus. S. aureus produces a number of enterotoxins that cause hyperemia and inflammation of the gastric mucosa, and stimulate gastric epithelial receptors to induce vomiting.
  • #1 Foodborne pathogens
    https://pmc.ncbi.nlm.nih.gov/articles/PMC6604998/
    The enterotoxin produced during sporulation is released with the spores during cell lysis. After release, the enterotoxin binds to epithelial cells, causing cytotoxic cell membrane damage and subsequent alteration of permeability, leading to diarrhea and abdominal cramping. […] Y. enterocolitica may pose a health hazard in contaminated refrigerated foods, although under refrigeration temperatures the pathogen is usually outgrown by other competing psychrotrophs. […] Y. enterocolitica toxin is heat stable, resists enzymatic degradation, remains stable during prolonged storage, and is of similar pH stability as the thermostable enterotoxin produced by ETEC. […] The genus Vibrio, belonging to the family Vibrionaceae, contains more than 35 species, of which nearly half have been described in the last 20 years and more than one-third are pathogenic to humans.
  • #1 Food Poisoning: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/175569-overview
    Inflammatory diarrhea is caused by the action of cytotoxins on the mucosa, leading to invasion and destruction. The colon or the distal small bowel commonly is involved. The diarrhea usually is bloody; mucoid and leukocytes are present. Patients are usually febrile and may appear toxic. Dehydration is less likely than with noninflammatory diarrhea because of smaller stool volumes. Fecal leukocytes or a positive stool lactoferrin test indicates an inflammatory process, and sheets of leukocytes indicate colitis. […] Sometimes, the organisms penetrate the mucosa and proliferate in the local lymphatic tissue, followed by systemic dissemination. Examples include Campylobacter jejuni, Vibrio parahaemolyticus, enterohemorrhagic and enteroinvasive E coli, Yersinia enterocolitica, Clostridium difficile, Entamoeba histolytica, and Salmonella and Shigella species.
  • #1 Foodborne Illness Part 3: How Does Salmonella Make Us Sick?
    https://asm.org/articles/2019/april/foodborne-illness-part-3-how-does-salmonella-make
    Salmonella are gram-negative bacteria and common causes of gastrointestinal illness. Infection typically manifests as severe stomach cramps, fever, and diarrhea that can last several days, though other disease presentations, such as sepsis, can also occur. […] Salmonella uses a variety of unique virulence mechanisms to invade our intestinal cells and confuse our immune cells, leading to many of the key symptoms associated with food poisoning. […] Lets assume you ate a questionable, undercooked omelette for breakfast and accidentally exposed yourself to a pathogenic, non-typhoidal S. enterica serovar typhimurium strainwhat happens next? Salmonella prefers to replicate and infect host cells intracellularly. Once Salmonella is ingested, it invades the epithelial cells of the intestine, as well as nearby phagocytic immune cells. Salmonella uses a variety of dynamic techniques to impair and confuse host immune cells, including its ability to induce phagocytosis in certain white blood cells, which allows the organism to gain entry into cells more effectively.
  • #1 Bacterial Food Poisoning | California Poison Control System
    https://calpoison.org/content/bacterial-food-poisoning
    E. coli O157:H7 (enterohemorrhagic E. coli, or EHEC) has emerged as the most notorious of these bacteria, based on the threat of E. coli to public health. […] Once colonized, EHEC elaborates toxins that mediate attachment to and effacement of GI villi cells. EHEC initially secretes a filamentous, needle-like chute that pierces the villous membrane, and then exports a second secretory protein down this chute, to form a pore. EHEC then sends a third protein to settle into this pore. This third protein becomes a new receptor, through which EHEC takes control of the villous epithelial cell. […] EHEC then injects cyclomodulin, halting mitosis, and slowing down epithelial cell turnover (an important defense mechanism of the GI epithelium against the colonization of foreign invaders). Finally, EHEC secretes Shiga-toxins, which deactivate the 60S ribosomal subunit.
  • #1 Bacterial Food Poisoning | California Poison Control System
    https://calpoison.org/content/bacterial-food-poisoning
    C. jejuni then colonizes in the colon and distal ileum, and releases a heat-labile, cytolethal-distending toxin (CDT), which: 1) attacks intestinal endothelial cell DNA, 2) recruits protein kinases to block cells from entering into mitosis, and 3) induces a local inflammatory reaction, cell lysis and watery or bloody diarrhea with fecal leukocytes. […] An important sequela to C. jejuni infection is Guillain-Barr syndrome. […] Shigella first travels to the basolateral surface of columnar epithelial cells, where lymphofollicular M cells transcytose Shigella to a subepithelial macrophage, which phagocytoses the organism. Shigella then degrades the phagosome, and invades columnar epithelial cells of the terminal ileum and colon, where they are free to multiply intracellularly. […] Salmonella excretes a heat-labile enterotoxin causing an inflammatory diarrhea by invading the mucosa.
  • #1 Food Poisoning: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/175569-overview
    In some types of food poisoning (eg, staphylococci, B cereus), vomiting is caused by a toxin acting on the central nervous system. The clinical syndrome of botulism results from the inhibition of acetylcholine release in nerve endings by the botulinum. […] A major contributor to seafood contamination with foodborne pathogens appears to be naturally occurring biofilm formation. Vibro and Salmonella species, Aeromonas hydrophila, and Listeria monocytogenes are common seafood bacterial pathogens that form biofilms.
  • #1 Foodborne pathogens
    https://pmc.ncbi.nlm.nih.gov/articles/PMC6604998/
    C. jejuni can colonize the intestines of both mammals and birds, and transmission to humans occurs via contaminated food products. This organism can invade the epithelial layer by first attaching to epithelial cells, then penetrating through them. Diarrhea results from damage to the epithelial cells. […] Cl. botulinum are motile by means of peritrichous flagella and produce botulinum neurotoxins, the most lethal poison known. There are seven types of botulinum neurotoxin, A through G, based on the antigenic specificity of the toxin produced by each strain. […] Cl. botulinum is present in soils, freshwater, marine sediments, and the intestinal tracts of animals. Food sources commonly sampled include primarily honey, which should not be fed to infants less than 1 year of age, as well as fish, meats, vegetables, and infant foods.
  • #1 Noninflammatory Gastroenteritis- Food Poisoning
    https://www.atsu.edu/faculty/chamberlain/website/tritzid/foodpoi.htm
    Types A, B and E cause almost all human botulism. All toxins are proteins of 150,000 molecular weight that prevent release of acetylcholine at the neuro-muscular junction causing a flaccid paralysis. […] Epithelial cell lysis is a microscopic pathologic effect of C. perfringens toxemia; rarely, with heavily contaminated foods, there is a diffuse, necrotizing enteritis of the jejunum, ileum and colon. The pathology associated with C. botulinum is minimum, inconsistent and non-diagnostic. […] The key features are the rapidity of onset of symptoms following ingestion of contaminated food or drink, the lack of fever and the absence of fecal leukocytes. All of the toxemias result in symptoms occurring within 12 hours of toxin ingestion as compared to an incubation period of 24-72 hours for infections.
  • #1 Molecular Mechanisms of Scombroid Food Poisoning – PubMed
    https://pubmed.ncbi.nlm.nih.gov/36614252/
    Scombroid food poisoning (SFP) is a foodborne disease that develops after consumption of fresh fish and, rarely, seafood that has fine organoleptic characteristics but contains a large amount of exogenous histamine. […] The pathogenesis of SFP includes a complex system of interactions between the body and chemical triggers such as exogenous histamine, other biogenic amines, cis-urocanic acid, salicylates, and other histamine liberators. […] Despite the vast and lengthy history of research on SFP mechanisms, there are still many blank spots in our understanding of this condition. […] The goals of this review are to differentiate various molecular mechanisms of SFP and describe methods of hygienic regulation of some biogenic amines that influence the concentration of histamine in the human body and play an important role in the mechanism of SFP.
  • #1 Food poisoning – Knowledge @ AMBOSS
    https://www.amboss.com/us/knowledge/food-poisoning/
    Pathophysiology: damage to the colonic mucosa blood in stool, fever. […] Pathogen: Staphylococcus aureus. […] Some strains produce heat-stable staphylococcal enterotoxins that cause food poisoning and, in severe cases, toxic shock syndrome. […] Pathogen: Clostridium perfringens serotype A. […] Transmission: ingestion of bacteria that produce enterotoxin in the GI tract. […] Bacillus cereus can produce two different enterotoxins which cause two distinct food poisoning syndromes. […] Mechanism of action: Histidine (found in high concentrations in these fish) is converted into histamine by histidine decarboxylase in the bacteria that normally colonize the fish. […] Mechanism of action: ingestion of ciguatoxin opening of Na+ channels depolarization. […] Mechanism of action: Tetrodotoxin is a neurotoxin that blocks voltage-gated sodium channels, which inhibits action potential propagation. […] Food and water precautions are the best means for preventing food poisoning.
  • #1 Foodborne illness – Wikipedia
    https://en.wikipedia.org/wiki/Foodborne_illness
    During the incubation period, microbes pass through the stomach into the intestine, attach to the cells lining the intestinal walls, and begin to multiply there. Some types of microbes stay in the intestine, some produce a toxin that is absorbed into the bloodstream, and some can directly invade the deeper body tissues. The symptoms produced depend on the type of microbe. […] In cases of foodborne illness, particularly traveler’s diarrhea, symptoms often result from the immune system’s response rather than direct pathogen damage. This inflammatory response can lead to post-infectious irritable bowel syndrome (PI-IBS), where 3-20% of affected individuals develop chronic gastrointestinal symptoms even after the pathogen is cleared. This suggests that the body’s immune reaction, particularly inflammation, plays a significant role in both acute symptoms and long-term effects of foodborne illness.
  • #1 What happens in my body when I get food poisoning? – BBC Science Focus Magazine
    https://www.sciencefocus.com/the-human-body/what-happens-in-my-body-when-i-get-food-poisoning
    Most of us are all too familiar with the unpleasant symptoms of food poisoning, from vomiting to diarrhoea and debilitating stomach cramps. […] Some bacteria wreak havoc by multiplying in the body before delivering their toxins, which spark an immune reaction in the gut. […] Some bacteria or enterotoxins (intestinal toxins) can survive harsh stomach conditions, making their way to the gut. There, the misery begins, sometimes up to 72 hours after eating the offending meal. […] Undetected by the bodys immune system, the bacteria quietly multiply, producing toxins. These invade and penetrate the gut lining, setting off a strong immune response. […] Immune cells release signalling proteins called pro-inflammatory cytokines, which set in motion a series of steps causing gut inflammation and swelling, leading to discomfort.
  • #1 Foodborne illness – Wikipedia
    https://en.wikipedia.org/wiki/Foodborne_illness
    The infectious dose is the amount of agent that must be consumed to give rise to symptoms of foodborne illness, and varies according to the agent and the consumer’s age and overall health. Pathogens vary in minimum infectious dose; for example, Shigella sonnei has a low estimated minimum dose of 500 colony-forming units (CFU) while Staphylococcus aureus has a relatively high estimate. […] Importantly, prior exposure to pathogens can significantly increase an individual’s tolerance to subsequent exposures. Locals in a region may tolerate pathogen levels that would cause illness in travelers due to immune memory developed from repeated low-level exposures. […] Foodborne illness often occurs as travelers’ diarrhea in persons whose gut microbiota is unaccustomed to organisms endemic to the visited region. This effect of microbiologic naiveté is compounded by any food safety lapses in the food’s preparation. […] Locals develop immunity to local food pathogens through repeated exposure, explaining why they often don’t get sick from food that affects travelers. This immune adaptation involves developing specific defenses against common local bacteria, viruses, and parasites.
  • #1 Food poisoning – prevention | Better Health Channel
    https://www.betterhealth.vic.gov.au/health/healthyliving/food-poisoning-prevention
    Food poisoning occurs when sufficient numbers of particular types of bacteria, or their toxins, are present in the food you eat. These bacteria are called pathogens. […] Pathogens such as Salmonella, Campylobacter and E. coli may be found in our food-producing animals. Care in processing, transport, storage, preparing and serving of food is necessary to reduce the risk of contamination. […] Food poisoning bacteria can multiply very quickly, particularly in certain conditions. The factors that affect bacterial growth include: Time – in ideal conditions, one bacterium can multiply to more than 2 million in 7 hours. Temperature – food poisoning bacteria grow best in the temperature range between 5 C and 60 C. This is referred to as the temperature danger zone. This means that we need to keep perishable food either very cold or very hot, in order to avoid food poisoning. Nutrients – most foods contain enough nutrients for bacteria to grow. This is especially the case with potentially high-risk foods such as dairy and egg products, meat, poultry and seafood. Water – bacteria need water for their growth. Without water, growth may slow down or stop. That is why dried foods do not spoil. pH – is the measure of acidity or alkalinity and is also important for controlling bacterial growth. Low pH (acid conditions) generally stops bacterial growth, but where the pH of food is neutral, as is the case for many foods, most bacteria grow quite well.
  • #1 Patient education: Foodborne illness (food poisoning) (Beyond the Basics) – UpToDate
    https://www.uptodate.com/contents/foodborne-illness-food-poisoning-beyond-the-basics
    Certain Escherichia coli (E. coli) bacteria can cause foodborne illness, particularly an illness known as „traveler’s diarrhea.” […] Hepatitis A virus is transmitted in foods contaminated by an infected human, such as a food handler, or from raw shellfish. […] Listeria is a bacterium that has traditionally been found in unpasteurized or contaminated milk, soft cheese, and other dairy products or in contaminated processed/deli meats, hot dogs, and smoked seafood. […] There are several factors that can increase your risk of developing foodborne illness. […] A weakened immune system – The immune system plays a major role in protecting against a foodborne illness; when your immune system is weakened, you become more vulnerable. […] Improper food storage or handling, leaving prepared food at room temperature for more than two hours, or improperly cooking or reheating food increase the risk of foodborne illness.
  • #1 Study finds sensing mechanism in food poisoning bug | ScienceDaily
    https://www.sciencedaily.com/releases/2016/07/160705085733.htm
    Researchers have uncovered a mechanism that a type of pathogenic bacteria found in shellfish use to sense when they are in the human gut, where they release toxins that cause food poisoning. […] The study found that two proteins made by Vibrio parahaemolyticus work together to detect and capture bile salts in the intestines of people who eat raw or undercooked seafood containing the bacteria. […] When humans eat raw or undercooked shellfish contaminated with Vibrio parahaemolyticus, the bacteria use those same bile salts as a signal to release toxins. […] We discovered that not one, but two genes are required for Vibrio to receive the bile salt signal. These genes encode two proteins that form a complex on the surface of the bacterial membrane. […] Using X-ray crystallography, we found that these proteins create a barrel-like structure that binds bile salts and receives the signal to tell the bacterial cell to start making toxins. […] Future experiments will aim to understand how binding of bile salt by this protein complex induces the release of toxins. […] Ultimately, we want to understand how other pathogenic bacteria sense environmental cues to produce toxins.
  • #1 UTSW researchers discover how food-poisoning bacteria infect the intestines: Newsroom – UT Southwestern, Dallas, Texas
    https://www.utsouthwestern.edu/newsroom/articles/year-2023/april-food-poisoning-bacteria.html
    DALLAS April 20, 2023 Researchers at UT Southwestern Medical Center have discovered how a bacterium that infects people after they eat raw or undercooked shellfish creates syringe-like structures to inject its toxins into intestinal cells. […] We have provided the first visual evidence of how a gut bacterial pathogen uses this assembly method to build a syringe to deliver a lethal injection to intestinal cells, said Kim Orth, Ph.D., Professor of Molecular Biology and Biochemistry, a Howard Hughes Medical Institute Investigator, and a W.W. Caruth, Jr. Scholar in Biomedical Research at UTSW. This work provides a new view of how enteric bacteria when exposed to bile acids efficiently respond and build a virulence system. […] Researchers knew that V. parahaemolyticus injects molecules into human cells using a structure called the type III secretion system 2 (T3SS2). However, these syringes, composed of 19 different proteins, are not produced or assembled until the bacteria are inside the intestines. Scientists were not sure exactly how this occurs.
  • #1 About C. perfringens food poisoning | C. perfringens | CDC
    https://www.cdc.gov/clostridium-perfringens/about/index.html
    C. perfringens makes spores, which have protective coatings. After a person eats food contaminated with the C. perfringens, the bacteria can make a toxin (poison) that causes diarrhea. […] Most often foods cooked in large batches and held at unsafe temperatures (between 40F and 140F) are involved in outbreaks of C. perfringens food poisoning. […] Outbreaks of C. perfringens food poisoning tend to happen in settings where large groups of people are served and keeping food at proper temperatures may be difficult.
  • #1 Bacterial Food Poisoning – Food Technology & Processing Food Technology & Processing
    https://aggie-horticulture.tamu.edu/food-technology/bacterial-food-poisoning/
    When food containing a large number of C. perfringens is consumed, the bacteria produce a toxin in the intestinal tract that causes illness. C. perfringens can exist as a heat-resistant spore, so it may survive cooking and grow to large numbers if the cooked food is held between 40 degrees F and 140 degrees F for an extensive time period. […] Botulism accounts for fewer than one of every 400 cases of food poisoning in the U.S., but two factors make it very important. First, it has caused death in approximately 30 percent of the cases; and secondly, it occurs mostly in home-canned foods. […] Food poisoning caused by this bacterium is a result of insufficient cooking and/or contamination of the cooked product by a raw product, followed by improper storage temperature. […] The key point is that refrigeration temperatures do not stop growth of Listeria. It is capable of doubling in numbers every 1.5 days at 39.5 degrees F. […] Control of enteropathogenic E. coli and other food-borne pathogens such as Salmonella and Staphylococcus aureus can be achieved. Precautions should include adequate cooking and avoidance of recontamination of cooked meat by contaminated equipment, water or infected food handlers.
  • #1 Azthena logo with the word Azthena
    https://www.news-medical.net/news/20241212/New-study-uncovers-role-of-amino-acid-serine-in-preventing-food-poisoning.aspx
    Food poisoning is a common, yet unpleasant, illness caused by eating contaminated items. It is sometimes caused by Clostridium perfringens, a pathogen widely found in soil and the intestinal tracts of animals. […] The pathogen multiplies in environments with little oxygen, for example, curry stored in a pot. After ingestion of the pathogen, they form spores in the small intestinal tracts. The toxins produced during spore formation cause diarrhea and abdominal pain, but the underlying mechanism of spore formation has not been fully understood. […] As a result, the team identified serine as an inhibitor of Clostridium perfringens spore formation. When observed under a microscope, it was found that serine inhibits the pathogen’s cell wall from remodeling, which is necessary in the process of becoming a spore.
  • #1 The Food Poisoning Toxins of Bacillus cereus
    https://www.mdpi.com/2072-6651/13/2/98
    Bacillus cereus is a ubiquitous soil bacterium responsible for two types of food-associated gastrointestinal diseases. […] Causative toxins are the cyclic dodecadepsipeptide cereulide, and the proteinaceous enterotoxins hemolysin BL (Hbl), nonhemolytic enterotoxin (Nhe) and cytotoxin K (CytK), respectively. […] The main focus of this review are the two tripartite enterotoxin complexes Hbl and Nhe, but the latest findings on cereulide and CytK are also presented, as well as methods for toxin detection, and the contribution of further putative virulence factors to the diarrheal disease. […] The second, diarrheal form of food poisoning is also associated with a variety of different foodstuffs. […] A food infection with enteropathogenic B. cereus can be seen as a multifactorial process, as a number of individual steps have to be considered before the onset of the disease, including prevalence and survival of B. cereus in different foodstuffs, survival of the stomach passage, germination of spores, active movement towards and adhesion to the intestinal epithelium, enterotoxin production under intestinal conditions, as well as the influence of consumed foods and the intestinal microbiota on these processes.
  • #1 What’s happening inside your body when you have food poisoning? A new study into Bacillus cereus has some clues – ABC News
    https://www.abc.net.au/news/health/2018-12-11/food-poisoning-bacillus-cereus-what-happens-inside-your-body/10601390
    Research published today has given us a slightly clearer idea, at least for one type of bacteria. […] A team from the Australian National University looked at the way the body responds to the bacteria Bacillus cereus, which can cause food poisoning and sometimes lead to serious infections elsewhere in the body, including sepsis, pneumonia and meningitis. […] They found a toxin secreted by the bacteria binds directly to cells in the human body and punches holes in the cells to kill them, triggering an immune response. […] Understanding the way toxins produced by this bacteria provoke inflammation in the body is a key to understanding how to treat it, said lead researcher Anukriti Mathur. […] Bacillus cereus produces more than 12 different toxins. One triggers vomiting and another diarrhea, Dr Ho explained.
  • #1 Lectin-Based Food Poisoning: A New Mechanism of Protein Toxicity | PLOS One
    https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0000687
    Ingestion of the lectins present in certain improperly cooked vegetables can result in acute GI tract distress, but the mechanism of toxicity is unknown. […] We therefore tested the novel hypothesis that lectin toxicity is due to an inhibitory effect on plasma membrane repair. […] Lectins potently inhibit plasma membrane repair, and hence are toxic to wounded cells. This represents a novel form of protein-based toxicity, one that, we propose, is the basis of plant lectin food poisoning. […] Plant lectins that are not efficiently degraded by digestive enzymes, and that have an affinity for the surface of gut epithelial cells, such as those present in the Leguminosae family, can be poisonous. […] Acute symptoms following ingestion include nausea, vomiting and diarrhea. […] Epithelial cells lining the GI tract in vivo, unlike cells in vitro, are constantly exposed to mechanical stress and, consequently, frequently suffer plasma membrane disruptions.
  • #1 Lectin-Based Food Poisoning: A New Mechanism of Protein Toxicity | PLOS One
    https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0000687
    However, cell death is not the only outcome of this type of injury: cells are capable of rapidly repairing and thereby surviving plasma membrane disruptions. […] Therefore, could the mechanism of lectin toxicity in vivo be due to an inhibitory effect on the exocytosis-based, constitutive membrane repair, and consequent death of wounded gut epithelial cells? […] We have shown here that binding of cell surface glycoproteins by lectins interferes with the exocytotic events associated with membrane repair (mucus secretion) and that lectins potently block repair. […] Lectins, we hypothesize, are toxic when present in the GI tract based on two, inter-related effects. First, resealing failure occurs within the general population of GI tract cells normally exposed to membrane disrupting levels of mechanical stress, leading to their necrosis. The second lectin-induced effect is exocytotic failure within the subpopulation of GI tract cells that normally secrete mucus, leading to a decrease in protective, lubricating mucus secretion and a consequent increase in the incidence of mechanically-induced membrane disruption events.
  • #2 Food poisoning – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/food-poisoning/symptoms-causes/syc-20356230
    Food poisoning, a type of foodborne illness, is a sickness people get from something they ate or drank. The causes are germs or other harmful things in the food or beverage. […] Many germs or harmful things, called contaminants, can cause foodborne illnesses. Food or drink that carries a contaminant is called „contaminated.” Food can be contaminated with any of the following: Bacteria. Viruses. Parasites that can live in the intestines. Poisons, also called toxins. Bacteria that carry or make toxins. Molds that make toxins. […] Food can be contaminated at any point from the farm or fishery to the table. The problem can begin during growing, harvesting or catching, processing, storing, shipping, or preparing. […] Food poisoning is especially serious during pregnancies and for young children, older adults and people with weakened immune systems. These illnesses may be life-threatening.
  • #2 Foodborne illness – Wikipedia
    https://en.wikipedia.org/wiki/Foodborne_illness
    Bacteria are a common cause of foodborne illness. […] Toxins from bacterial infections are delayed because the bacteria need time to multiply. As a result, symptoms associated with intoxication are usually not seen until 12-72 hours or more after eating contaminated food. However, in some cases, such as Staphylococcal food poisoning, the onset of illness can be as soon as 30 minutes after ingesting contaminated food. […] Enterotoxins are potent compounds produced by various microorganisms that specifically target and damage the intestines, causing many of the most rapid and severe forms of food poisoning. Unlike bacterial infections that require live organisms to multiply in the gut, enterotoxins (a type of exotoxin) can cause illness even when the bacteria that produced them have been killed through cooking or other preservation methods.
  • #2 General Mechanism of Pathogenesis for Foodborne Pathogens | SpringerLink
    https://link.springer.com/chapter/10.1007/978-0-387-74537-4_4
    The diseases caused by foodborne pathogens can be classified into three forms: foodborne infection, foodborne intoxication, and foodborne toxicoinfection and each are discussed below. The principal route of infection for foodborne pathogens is oral and the primary site of action is the intestine. Most foodborne microorganisms cause localized infection and tissue damage but some spread to deeper tissues to induce systemic infection. For successful enteric infection, several factors must work cooperatively in a host. First of all, pathogens must gain access to the host in sufficient numbers to initiate infection. The primary vehicle of transmission is food and water. However, they can be acquired from direct contact with an animal or a human, such as a food handler, from environments (soil, air) or from an arthropod vector. Once inside the host, the pathogens must survive in the changing environment, multiply and propagate. Pathogens must find a suitable niche for colonization, which is facilitated by adhesion factors, invasion factors, and chemotaxis. The microbial cell envelope also helps bacteria to survive in the hostile environment, as the capsule protects the bacteria from being engulfed by phagocytes. In addition, bacterial toxins and enzymes protect cells from elimination by the host immune system. Pathogens also damage the host tissues and cells by using exotoxins, endotoxins, or enzymes that cause cell death by apoptosis or necrosis and promote bacterial survival and multiplication.
  • #2 Food Poisoning: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/175569-overview
    Food poisoning is defined as an illness caused by the consumption of food or water contaminated with bacteria and/or their toxins, or with parasites, viruses, or chemicals. The most common pathogens are Norovirus, Escherichia coli, Salmonella, Clostridium perfringens, Campylobacter, and Staphylococcus aureus. […] The pathogenesis of diarrhea in food poisoning is classified broadly into either noninflammatory or inflammatory types. Noninflammatory diarrhea is caused by the action of enterotoxins on the secretory mechanisms of the mucosa of the small intestine, without invasion. This leads to large volume watery stools in the absence of blood, pus, or severe abdominal pain. Occasionally, profound dehydration may result. The enterotoxins may be either preformed before ingestion or produced in the gut after ingestion. Examples include Vibrio cholerae, enterotoxic Escherichia coli, Clostridium perfringens, Bacillus cereus, Staphylococcus organisms, Giardia lamblia, Cryptosporidium, rotavirus, norovirus (genus Norovirus, previously called Norwalk virus), and adenovirus.
  • #2 Food poisoning – Knowledge @ AMBOSS
    https://www.amboss.com/us/knowledge/food-poisoning/
    Food poisoning is a specific subset of foodborne illnesses and is caused by the ingestion of any substance that is contaminated with a preformed toxin. […] Most cases of food poisoning are self-limited and require only supportive care (e.g., oral and/or parenteral rehydration and antiemetics) to ensure adequate hydration. […] Clostridium botulinum is a rare and potentially fatal cause of food poisoning. […] Foodborne illness refers to any disease following ingestion of contaminated food. […] Pathophysiology: Vomiting is commonly due to delayed gastric emptying caused by changes to gastric motility. […] Pathophysiology: enterotoxin or bacterial invasion shifts water and electrolyte excretion/absorption in proximal small intestine watery diarrhea. […] Pathophysiology: penetration of mucosa and subsequent invasion of reticuloendothelial system in the distal small intestine enteric fever.
  • #2 Staphylococcus Aureus: A Major Pathogen of Food Poisoning | Auctores
    https://www.auctoresonline.org/article/staphylococcus-aureus-a-major-pathogen-of-food-poisoning
    Staphylococcus aureus is a major pathogen of food poisoning that can occur in sporadic and epidemic form. […] Enterotoxins produced by S. aureus play a vital role in the pathogenesis of staphylococcal food poisoning. […] The ingestion of food containing pre-formed Staphylococcus enterotoxins causes staphylococcal food poisoning. […] There are five serologically distinct enterotoxins (A, B, C, D, and E), with enterotoxin A being the most common cause of food poisoning outbreaks. […] Unsanitary food handling must be regarded as a major source of S. aureus contamination. […] Staphylococcal food poisoning symptoms onset quickly (30 minutes-8 hours) and include nausea, violent vomiting, abdominal cramping, with or without diarrhea. […] Although staphylococcal food poisoning is generally self-limiting and resolves within 24-48 hours of onset, it can cause life-threatening infections in children, the elderly, and immunocompromised people.
  • #2 Food poisoning – Knowledge @ AMBOSS
    https://www.amboss.com/us/knowledge/food-poisoning/
    Pathophysiology: damage to the colonic mucosa blood in stool, fever. […] Pathogen: Staphylococcus aureus. […] Some strains produce heat-stable staphylococcal enterotoxins that cause food poisoning and, in severe cases, toxic shock syndrome. […] Pathogen: Clostridium perfringens serotype A. […] Transmission: ingestion of bacteria that produce enterotoxin in the GI tract. […] Bacillus cereus can produce two different enterotoxins which cause two distinct food poisoning syndromes. […] Mechanism of action: Histidine (found in high concentrations in these fish) is converted into histamine by histidine decarboxylase in the bacteria that normally colonize the fish. […] Mechanism of action: ingestion of ciguatoxin opening of Na+ channels depolarization. […] Mechanism of action: Tetrodotoxin is a neurotoxin that blocks voltage-gated sodium channels, which inhibits action potential propagation. […] Food and water precautions are the best means for preventing food poisoning.
  • #2 What’s happening inside your body when you have food poisoning? A new study into Bacillus cereus has some clues – ABC News
    https://www.abc.net.au/news/health/2018-12-11/food-poisoning-bacillus-cereus-what-happens-inside-your-body/10601390
    The vomit-inducing toxin, called cereulide, binds to serotonin receptors in the stomach and small bowel and stimulates the vagus nerve, which controls muscle movement in the gut. […] The toxins are stimulating against receptors in the gut lining triggering a lot more movement of the muscle in the gut and the colon.
  • #2 The Food Poisoning Toxins of Bacillus cereus
    https://www.mdpi.com/2072-6651/13/2/98
    Nevertheless, production and action of the enterotoxins are of the upmost relevance for the course of the diarrheal disease. […] Three main, pore-forming protein enterotoxins are known, which are the tripartite hemolysin BL (Hbl) and non-hemolytic enterotoxin (Nhe), as well as the single protein cytotoxin K (CytK). […] Progress made in studies from the early 1990s until today on highly variable, strain-specific enterotoxin production (distribution, genetic organization, gene expression and toxin secretion), as well as on the mode of action and the effects on target cells of these pore-forming enterotoxins, is depicted in detail in the present review. […] The two three-component enterotoxin complexes Hbl and Nhe are the focus of attention. […] The enterotoxins Hbl and Nhe consist of three protein components each, which are encoded in operons on the chromosome.
  • #2 Bacterial Food Poisoning | California Poison Control System
    https://calpoison.org/content/bacterial-food-poisoning
    Some serotypes of B. cereus produce a mild emetic illness mediated by a dodecadepsipeptide gastric irritant called cereulide, while other serotypes produce a mild diarrheal illness mediated by Hemolysin BL, which punches pores or channels into intestinal cell membranes and disrupts tight junctions. […] Clostridium perfringens causes a toxin-mediated disease that closely resembles the diarrheal illness produced by B. cereus, and is the 3rd most commonly reported food-borne illness behind Salmonella and Campylobacter spp. Enteric toxins form pores or channels in host cell membranes and disrupt tight junctions. […] Staphylococcus aureus causes a toxin-mediated disease that closely resembles the emetic illness produced by B. cereus. S. aureus produces a number of enterotoxins that cause hyperemia and inflammation of the gastric mucosa, and stimulate gastric epithelial receptors to induce vomiting.
  • #2 Bacterial Food Poisoning | California Poison Control System
    https://calpoison.org/content/bacterial-food-poisoning
    E. coli O157:H7 (enterohemorrhagic E. coli, or EHEC) has emerged as the most notorious of these bacteria, based on the threat of E. coli to public health. […] Once colonized, EHEC elaborates toxins that mediate attachment to and effacement of GI villi cells. EHEC initially secretes a filamentous, needle-like chute that pierces the villous membrane, and then exports a second secretory protein down this chute, to form a pore. EHEC then sends a third protein to settle into this pore. This third protein becomes a new receptor, through which EHEC takes control of the villous epithelial cell. […] EHEC then injects cyclomodulin, halting mitosis, and slowing down epithelial cell turnover (an important defense mechanism of the GI epithelium against the colonization of foreign invaders). Finally, EHEC secretes Shiga-toxins, which deactivate the 60S ribosomal subunit.
  • #2 Foodborne Illness Part 3: How Does Salmonella Make Us Sick?
    https://asm.org/articles/2019/april/foodborne-illness-part-3-how-does-salmonella-make
    Salmonella undermines non-phagocytic immune cells too, by inducing reactive oxygen species (ROS) production from human neutrophils. This defense mechanism is intended to protect the host by damaging bacterial nucleic acids and proteins. However, Salmonella benefits from ROS production, because it has an arsenal of peroxidases and catalases to help it survive ROS exposure. […] Once inside the host cell, Salmonella divides rapidly, and can either enclose itself within membrane-bound vacuoles, or as was recently discovered, replicate within the cytosol of cells. Salmonellas preference to replicate in vacuoles versus in the cytosol possibly depends upon flagellar motility. […] Fortunately, the human immune system is equipped to fight Salmonellas invasive and evasive maneuvers. While innate immune cells, such as neutrophils and macrophages, can be fooled by Salmonellas immune evasive strategies, adaptive immune cells are vital for host defense. […] Other adaptive immune cells, including CD8+ T cells and B cells, also play important roles in fighting off Salmonella infections, with the strongest evidence pointing towards the protective role of CD8+ T cells during later stages of infection. CD8+ T cells are specialized cells that can target intracellular pathogens with the help of B cells, which can serve as antigen-presenting cells that help CD8+ T cells to recognize Salmonella-specific antigens and mount an inflammatory immune response to help clear infection. […] While the immune system is always hard at work, the best ways to prevent Salmonella infection are through careful handwashing, sanitary food preparation, and proper handling of pets and livestock. […]
  • #2 E. coli virotypes Food Poisoning, Infection and Illness
    https://microbenotes.com/e-coli-food-poisoning/
    EPEC do not produce toxins like ETEC but some strains of EPEC invades tissue cells and produce Shiga toxin. […] Pathogenesis of EPEC involves three stages: The first stage is an attachment of EPEC to the host cell with the help of fimbriae, the second stage includes signal transduction where the cell attaches and forms lesions destructing the microvilli and forms cup-like cytoskeletal protein. […] Then the attached EPEC alters the cytoskeleton of the host cell in the third stage that affects the mitochondrial function and increases membrane permeability resulting in loss of nutrients and ions from the body. […] Enterohemorrhagic E. coli causes bloody diarrhea and is the main pathogen responsible for causing hemorrhagic colitis outbreaks. […] EHEC also produces Shiga toxin that destroys Vero cells therefore, it is also known as verotoxin-producing E. coli (VTEC).
  • #2 Foodborne pathogens
    https://pmc.ncbi.nlm.nih.gov/articles/PMC6604998/
    C. jejuni can colonize the intestines of both mammals and birds, and transmission to humans occurs via contaminated food products. This organism can invade the epithelial layer by first attaching to epithelial cells, then penetrating through them. Diarrhea results from damage to the epithelial cells. […] Cl. botulinum are motile by means of peritrichous flagella and produce botulinum neurotoxins, the most lethal poison known. There are seven types of botulinum neurotoxin, A through G, based on the antigenic specificity of the toxin produced by each strain. […] Cl. botulinum is present in soils, freshwater, marine sediments, and the intestinal tracts of animals. Food sources commonly sampled include primarily honey, which should not be fed to infants less than 1 year of age, as well as fish, meats, vegetables, and infant foods.
  • #2 Staphylococcal Food Poisoning – Digestive Disorders – Merck Manual Consumer Version
    https://www.merckmanuals.com/home/digestive-disorders/gastroenteritis/staphylococcal-food-poisoning
    Staphylococcal food poisoning results from eating food contaminated with toxins produced by certain types of staphylococci, resulting in diarrhea and vomiting. […] This disorder can be caused by toxins produced by Staphylococcus aureus bacteria. […] The toxins are found in contaminated foods. […] Thus, staphylococcal food poisoning does not result from ingesting the bacteria but rather from ingesting the toxins in the food that were made by the bacteria. […] Staphylococcal food poisoning is a type of gastroenteritis (inflammation of the lining of the stomach and small and large intestines). […] Treatment of staphylococcal food poisoning usually consists of drinking an adequate amount of fluids. […] Careful food preparation can prevent staphylococcal food poisoning.
  • #2 Foodborne pathogens
    https://pmc.ncbi.nlm.nih.gov/articles/PMC6604998/
    Symptoms of botulinum neurotoxin ingestion appear 1236 h after consumption of contaminated food and initially may include nausea and vomiting. However, these symptoms are followed by the more characteristic neurological signs including visual impairment and acute flaccid paralysis that begins with the muscles of the face, head, and pharynx, descending to involve muscles of the thorax and extremities and leading to possible death from respiratory failure caused by upper airway or diaphragm paralysis. […] Cl. perfringens are estimated to be the second most common bacterial causes of foodborne illness in the US, causing one million illnesses each year. […] Foodborne illness almost always is a result of temperature abuse, and in many instances, the food vehicle has been improperly cooked meat or meat product that has been left to cook and/or cool too slowly or has undergone insufficient reheating, allowing surviving spores to germinate leading to vegetative cell proliferation.
  • #2 Molecular Mechanisms of Scombroid Food Poisoning – PubMed
    https://pubmed.ncbi.nlm.nih.gov/36614252/
    Scombroid food poisoning (SFP) is a foodborne disease that develops after consumption of fresh fish and, rarely, seafood that has fine organoleptic characteristics but contains a large amount of exogenous histamine. […] The pathogenesis of SFP includes a complex system of interactions between the body and chemical triggers such as exogenous histamine, other biogenic amines, cis-urocanic acid, salicylates, and other histamine liberators. […] Despite the vast and lengthy history of research on SFP mechanisms, there are still many blank spots in our understanding of this condition. […] The goals of this review are to differentiate various molecular mechanisms of SFP and describe methods of hygienic regulation of some biogenic amines that influence the concentration of histamine in the human body and play an important role in the mechanism of SFP.
  • #2 Molecular Mechanisms of Scombroid Food Poisoning
    https://www.mdpi.com/1422-0067/24/1/809
    Scombroid food poisoning (SFP) is a foodborne disease that develops after consumption of fresh fish and, rarely, seafood that has fine organoleptic characteristics but contains a large amount of exogenous histamine. […] The pathogenesis of SFP includes a complex system of interactions between the body and chemical triggers such as exogenous histamine, other biogenic amines, cis-urocanic acid, salicylates, and other histamine liberators. […] The SFP mechanism can be influenced by a combination of three external contributing factors (fish species, saprophytic microorganism species that convert histidine to histamine, and environmental conditions), as well as internal individual factors such as exogenous histamine consumed, inactivation speed, and individual sensitivity. […] There are no antigen-specific immune complexes in the SFP molecular mechanism, but there is histamine release, complement activation, atypical eicosanoids synthesis, and inhibition of bradykinin decomposition.
  • #2 Molecular Mechanisms of Scombroid Food Poisoning
    https://www.mdpi.com/1422-0067/24/1/809
    The leading role in the pathogenesis of SFP belongs to exogenous histamine. Histamine, in addition to its systemic effect, which leads to the development of the main symptoms of SPF (flushing, swelling, itchy rash, hypotension, acute pulmonary edema, bronchoconstriction) has an effect on the immune system. […] The molecular mechanism by which mast cell activation occurs under the action of exogenous histamine is shown in Figure 7. The mast cell membrane contains FcεRI receptors, which consist of one α, one β and two γ subunits. […] The complement system participates in natural immune response, but it may also be involved in SFP pathogenesis and damage the cells with anaphylatoxins: C3a, C5, and the membrane attack complex (C5b-C9). […] The molecular mechanisms of SFP include a complex system of interactions between the body and chemical triggers such as exogenous histamine, other biogenic amines, and cis-urocanic acid.
  • #2 What happens in my body when I get food poisoning? – BBC Science Focus Magazine
    https://www.sciencefocus.com/the-human-body/what-happens-in-my-body-when-i-get-food-poisoning
    Most of us are all too familiar with the unpleasant symptoms of food poisoning, from vomiting to diarrhoea and debilitating stomach cramps. […] Some bacteria wreak havoc by multiplying in the body before delivering their toxins, which spark an immune reaction in the gut. […] Some bacteria or enterotoxins (intestinal toxins) can survive harsh stomach conditions, making their way to the gut. There, the misery begins, sometimes up to 72 hours after eating the offending meal. […] Undetected by the bodys immune system, the bacteria quietly multiply, producing toxins. These invade and penetrate the gut lining, setting off a strong immune response. […] Immune cells release signalling proteins called pro-inflammatory cytokines, which set in motion a series of steps causing gut inflammation and swelling, leading to discomfort.
  • #2 What happens in my body when I get food poisoning? – BBC Science Focus Magazine
    https://www.sciencefocus.com/the-human-body/what-happens-in-my-body-when-i-get-food-poisoning
    Bacterial toxins can cause pores to open in the wall, allowing water and other molecules to flood in. […] The excess fluid and electrolytes in the gut lead to watery diarrhoea, which has a beneficial role of flushing out the bacteria and their toxins. It can, however, cause dehydration. […] Some bacteria dont cause vomiting, but Staphylococcus aureus enterotoxins do. Research suggests that they may stimulate the vagus nerve which transmits a signal to the brains vomiting centre.
  • #2 The Pathology of Food Poisoning | Food Poisoning News
    https://www.foodpoisoningnews.com/the-pathology-of-food-poisoning/
    Food poisoning symptoms include nausea, vomiting, diarrhea, abdominal cramps, and fever, as the body attempts to expel the pathogen or toxin. Bacterial infections like those from Salmonella and Campylobacter cause inflammation in the gut, resulting in diarrhea and fever. Severe infections, like those from certain strains of E. coli, can cause HUS, a potentially life-threatening complication marked by kidney failure. […] Although most cases of food poisoning resolve within a few days, certain infections can have long-term effects. Salmonella and Campylobacter can lead to post-infectious irritable bowel syndrome (IBS), which involves chronic abdominal pain, bloating, and altered bowel habits. These bacteria may also trigger reactive arthritis, an autoimmune condition that can persist for months or years.
  • #2 Food poisoning – prevention | Better Health Channel
    https://www.betterhealth.vic.gov.au/health/healthyliving/food-poisoning-prevention
    Food poisoning occurs when sufficient numbers of particular types of bacteria, or their toxins, are present in the food you eat. These bacteria are called pathogens. […] Pathogens such as Salmonella, Campylobacter and E. coli may be found in our food-producing animals. Care in processing, transport, storage, preparing and serving of food is necessary to reduce the risk of contamination. […] Food poisoning bacteria can multiply very quickly, particularly in certain conditions. The factors that affect bacterial growth include: Time – in ideal conditions, one bacterium can multiply to more than 2 million in 7 hours. Temperature – food poisoning bacteria grow best in the temperature range between 5 C and 60 C. This is referred to as the temperature danger zone. This means that we need to keep perishable food either very cold or very hot, in order to avoid food poisoning. Nutrients – most foods contain enough nutrients for bacteria to grow. This is especially the case with potentially high-risk foods such as dairy and egg products, meat, poultry and seafood. Water – bacteria need water for their growth. Without water, growth may slow down or stop. That is why dried foods do not spoil. pH – is the measure of acidity or alkalinity and is also important for controlling bacterial growth. Low pH (acid conditions) generally stops bacterial growth, but where the pH of food is neutral, as is the case for many foods, most bacteria grow quite well.
  • #2 Bacterial Food Poisoning | California Poison Control System
    https://calpoison.org/content/bacterial-food-poisoning
    C. jejuni then colonizes in the colon and distal ileum, and releases a heat-labile, cytolethal-distending toxin (CDT), which: 1) attacks intestinal endothelial cell DNA, 2) recruits protein kinases to block cells from entering into mitosis, and 3) induces a local inflammatory reaction, cell lysis and watery or bloody diarrhea with fecal leukocytes. […] An important sequela to C. jejuni infection is Guillain-Barr syndrome. […] Shigella first travels to the basolateral surface of columnar epithelial cells, where lymphofollicular M cells transcytose Shigella to a subepithelial macrophage, which phagocytoses the organism. Shigella then degrades the phagosome, and invades columnar epithelial cells of the terminal ileum and colon, where they are free to multiply intracellularly. […] Salmonella excretes a heat-labile enterotoxin causing an inflammatory diarrhea by invading the mucosa.
  • #2 A Sensing Mechanism in a Food Poisoning Bug | Advanced Photon Source
    https://www.aps.anl.gov/APS-Science-Highlight/2016-07-06/a-sensing-mechanism-in-a-food-poisoning-bug
    Researchers from Howard Hughes Medical Institute (HHMI) at the University of Texas (UT) Southwestern Medical Center have uncovered a mechanism that a type of pathogenic bacteria found in shellfish use to sense when they are in the human gut, where they release toxins that cause food poisoning. […] The study found that two proteins made by Vibrio parahaemolyticus form an obligate heterodimer and work together to detect and capture bile salts in the intestines of people who eat raw or undercooked seafood containing the bacteria. […] „When humans eat raw or undercooked shellfish contaminated with Vibrio parahaemolyticus, the bacteria use those same bile salts as a signal to release toxins,” said Orth. […] „We discovered that not one, but two genes are required for Vibrio to receive the bile salt signal. These genes encode two proteins that form a complex on the surface of the bacterial membrane.
  • #2 UTSW researchers discover how food-poisoning bacteria infect the intestines: Newsroom – UT Southwestern, Dallas, Texas
    https://www.utsouthwestern.edu/newsroom/articles/year-2023/april-food-poisoning-bacteria.html
    The latest findings build on the work of a previous study by the Orth lab. […] Then, at the exact site where the T3SS2 is needed, V. parahaemolyticus transcribes that DNA into RNA, translates the RNA into protein, and assembles the components of the T3SS2 through the membrane in a process known as transertion. […] These steps were previously thought to occur in more disparate locations around a cell, but pulling the machinery together into one place on the bacteriums membrane likely helps V. parahaemolyticus more quickly and efficiently build the T3SS2 and infect cells. […] Our findings imply that other gastrointestinal pathogens may also use this mechanism to mediate efficient assembly of complex molecular machines in response to environmental cues, said UTSW research specialist Karan Kaval, Ph.D., first author of the paper. […] More work is needed to know which bacteria use transertion to build their T3SS structures and whether drugs could be developed that block transertion to treat V. parahaemolyticus infections.
  • #2 Azthena logo with the word Azthena
    https://www.news-medical.net/news/20241212/New-study-uncovers-role-of-amino-acid-serine-in-preventing-food-poisoning.aspx
    This is the first reported case where a single amino acid inhibits spore-forming anaerobic bacteria. In the future, we hope to understand serine inhibition, the pathogenic mechanisms of Clostridium perfringens food poisoning, and the survival strategies of pathogenic microorganisms in the human body.
  • #3 Food Poisoning Clinical Presentation: History, Physical, Causes
    https://emedicine.medscape.com/article/175569-clinical
    The presence of a common source, types of specific food, travel history, and use of antibiotics always should be investigated. […] The presenting complaints, typical features and pathogenesis of various causative agents, and diagnosis and treatment information can be found in Table 1 in the Causes section. […] Enterotoxin acts on receptors in the gut that transmit impulses to the medullary centers. […] Enterotoxin produced in the gut, and food causes hypersecretion in the small intestine. […] Toxin absorbed from the gut blocks the release of acetylcholine in the neuromuscular junction. […] Enterotoxin causes hypersecretion in small and large intestine via guanylate cyclase activation. […] Cytotoxin results in endothelial damage and leads to platelet aggregation and microvascular fibrin thrombi. […] Enterotoxin produces secretion. […] Shigalike toxin facilitates invasion. […] Direct invasion and enterotoxin.
  • #3 The Food Poisoning Toxins of Bacillus cereus
    https://www.mdpi.com/2072-6651/13/2/98
    Bacillus cereus is a ubiquitous soil bacterium responsible for two types of food-associated gastrointestinal diseases. […] Causative toxins are the cyclic dodecadepsipeptide cereulide, and the proteinaceous enterotoxins hemolysin BL (Hbl), nonhemolytic enterotoxin (Nhe) and cytotoxin K (CytK), respectively. […] The main focus of this review are the two tripartite enterotoxin complexes Hbl and Nhe, but the latest findings on cereulide and CytK are also presented, as well as methods for toxin detection, and the contribution of further putative virulence factors to the diarrheal disease. […] The second, diarrheal form of food poisoning is also associated with a variety of different foodstuffs. […] A food infection with enteropathogenic B. cereus can be seen as a multifactorial process, as a number of individual steps have to be considered before the onset of the disease, including prevalence and survival of B. cereus in different foodstuffs, survival of the stomach passage, germination of spores, active movement towards and adhesion to the intestinal epithelium, enterotoxin production under intestinal conditions, as well as the influence of consumed foods and the intestinal microbiota on these processes.
  • #3 Bacterial Food Poisoning | California Poison Control System
    https://calpoison.org/content/bacterial-food-poisoning
    C. jejuni then colonizes in the colon and distal ileum, and releases a heat-labile, cytolethal-distending toxin (CDT), which: 1) attacks intestinal endothelial cell DNA, 2) recruits protein kinases to block cells from entering into mitosis, and 3) induces a local inflammatory reaction, cell lysis and watery or bloody diarrhea with fecal leukocytes. […] An important sequela to C. jejuni infection is Guillain-Barr syndrome. […] Shigella first travels to the basolateral surface of columnar epithelial cells, where lymphofollicular M cells transcytose Shigella to a subepithelial macrophage, which phagocytoses the organism. Shigella then degrades the phagosome, and invades columnar epithelial cells of the terminal ileum and colon, where they are free to multiply intracellularly. […] Salmonella excretes a heat-labile enterotoxin causing an inflammatory diarrhea by invading the mucosa.
  • #3 Molecular Mechanisms of Scombroid Food Poisoning
    https://www.mdpi.com/1422-0067/24/1/809
    Scombroid food poisoning (SFP) is a foodborne disease that develops after consumption of fresh fish and, rarely, seafood that has fine organoleptic characteristics but contains a large amount of exogenous histamine. […] The pathogenesis of SFP includes a complex system of interactions between the body and chemical triggers such as exogenous histamine, other biogenic amines, cis-urocanic acid, salicylates, and other histamine liberators. […] The SFP mechanism can be influenced by a combination of three external contributing factors (fish species, saprophytic microorganism species that convert histidine to histamine, and environmental conditions), as well as internal individual factors such as exogenous histamine consumed, inactivation speed, and individual sensitivity. […] There are no antigen-specific immune complexes in the SFP molecular mechanism, but there is histamine release, complement activation, atypical eicosanoids synthesis, and inhibition of bradykinin decomposition.
  • #3 The Pathology of Food Poisoning | Food Poisoning News
    https://www.foodpoisoningnews.com/the-pathology-of-food-poisoning/
    Food poisoning symptoms include nausea, vomiting, diarrhea, abdominal cramps, and fever, as the body attempts to expel the pathogen or toxin. Bacterial infections like those from Salmonella and Campylobacter cause inflammation in the gut, resulting in diarrhea and fever. Severe infections, like those from certain strains of E. coli, can cause HUS, a potentially life-threatening complication marked by kidney failure. […] Although most cases of food poisoning resolve within a few days, certain infections can have long-term effects. Salmonella and Campylobacter can lead to post-infectious irritable bowel syndrome (IBS), which involves chronic abdominal pain, bloating, and altered bowel habits. These bacteria may also trigger reactive arthritis, an autoimmune condition that can persist for months or years.
  • #3 Foodborne Illness Part 3: How Does Salmonella Make Us Sick?
    https://asm.org/articles/2019/april/foodborne-illness-part-3-how-does-salmonella-make
    Salmonella are gram-negative bacteria and common causes of gastrointestinal illness. Infection typically manifests as severe stomach cramps, fever, and diarrhea that can last several days, though other disease presentations, such as sepsis, can also occur. […] Salmonella uses a variety of unique virulence mechanisms to invade our intestinal cells and confuse our immune cells, leading to many of the key symptoms associated with food poisoning. […] Lets assume you ate a questionable, undercooked omelette for breakfast and accidentally exposed yourself to a pathogenic, non-typhoidal S. enterica serovar typhimurium strainwhat happens next? Salmonella prefers to replicate and infect host cells intracellularly. Once Salmonella is ingested, it invades the epithelial cells of the intestine, as well as nearby phagocytic immune cells. Salmonella uses a variety of dynamic techniques to impair and confuse host immune cells, including its ability to induce phagocytosis in certain white blood cells, which allows the organism to gain entry into cells more effectively.