Lecture 8 Flashcards
What are the normal microbiota of the digestive system?
Small numbers of microorganisms in stomach and small intestine (Due to acidic/low pH environments)
Large intestine: Bacteroides, lactobacillus, E.Choli, Enterobacter, Klebsiella, Proteus
Diarrhea?
Watery stool
Dysentery?
severe diarrhea with blood and mucus in stool
pain on defecation
Diarrhea and dysentery accompanied by:
Abdominal cramps, nausea, vomiting.
Why are diarrhea and vomiting useful?
Defense mechanism to rid the body of harmful material
What is gastroenteritis?
Inflammation of stomach and intestinal mucosa
What is foodborne intoxication?
Ingestion of food containing Toxin
What is the major difference between food intoxication and food infection
The origin of the illness-causing toxins. While food intoxication/poisoning is caused by toxins released by microorganisms after they are ingested, food infections are caused by the presence of toxins in food before consumption.
What are the causes of foodborne intoxication?
- Production of toxin due to growth of microbes in food
- Ingestion of microbes themselves maybe be harmless however they’re toxins can make you sick
- Toxins are created by microorganisms while growing outside of the food, and these toxins get concentrated in the food.
- Chemical contamination of food
Time of Appearance of symptoms of foodborne intoxication?
1-48hrs after uptake
What is a foodborne infection?
Ingestion of microbes in food
What is a foodborne infection illness caused by:
Entering and proliferation of pathogen in gastrointestinal tract causing harm to the gut OR Toxin production in the gastrointestinal tract (Toxin mediated infection.
Foodborne illness symptoms appearance time:
12hr to 2 weeks after ingestion
Penetration of mucosa and spread to other organs
What bacteria causes foodborne intoxication as cause of diarrhea?
Staphylococcus Aureus
Bacillus Cereus
Clostridium Botulinum
Food Intoxication due to Staphylococcus Aureus?
Common inhabitants of humans –>25% adults carriers
Contaminates food during processing
Amino Acids and vitamin B needed
High osmotic pressure foods
Heat stable toxin (superantigen) produced during S. Aureus in food.
Multiplication of bacteria in food to produce enough toxin to cause illness.
Nausea, vomiting, cramping, diarrhea
Bacillus Cereus–> Gastroenteritis
Cooking food kills vegetative cells but the endospores of B. Cereus survive.
Spores germinate and proliferate in food(fried or boiled rice) under aerobic conditions.
Different strains produce different heat stable toxins.
Depending on toxin two different syndromes can develop:
Emetic Syndrome: Nausea and Vomiting
Diarrheal Syndrome: Watery diarrhea
Clostridium Botulinum- Botulism
Cooking kills vegetative cells but endospores of C.Botulinum survive.
Spores can germinate and proliferate in food under anaerobic conditions.
Frequently spoilage of canned food
Toxin denatured at 80C for 10 minutes or boiling for 2-3 minutes.
Symptoms of Botulism caused by Clostridium Botulinum
Flaccid paralysis–> Double vision, difficult eye movement, swallowing, speech.
Fatality rate–> 5-10%
Mode of Food poisoning for S. Aureus
- Contamination of food by worker with staphylococci on hands
- Holding of food at room temperature. Proliferation of bacteria in food. Formation and release of toxin.
- Reheating of food will kill Staphylococci but not toxin
- Intoxication
Mode of food poisoning for Bacillus Cereus/Clostridium Botulinum
- Germination of spores in food.
- Reheating of food will destroy Botulinum toxin but not B. Cereus toxin
Bacteria involved in Toxin Mediated infections as the cause of Diarrhea
Clostridium Perfringens
Vibrio Cholerae
Campylobacter sp
Clostridium Perfringens–> Perfringens Diarrhea
Cattle, sheep, goat generally infected by bacteria.
Meats and Meat stews contaminated with
intestinal content of animals during
slaughtering
* Foods meet nutritional requirements of
the bacteria for amino acids
* Cooking of food kills vegetative cells,
endospores of C. perfringens survive
* Spores germinate and proliferate in food
as cooking generates partially anaerobic
conditions
* Chili in a large pot inadequate
cooling in fridge
Doubling time and growth of Clostridium perfringens
Doubling time is less than 20 minutes, grows well in the small interstine and produces exotoxins (alpha exotoxin=phopholipase) and a lot of gas.
What are the symptoms of perfringens Diarrhea caused by Clostridium Perfringens?
Watery diarrhea with severe gas
Nausea and cramping but no vomiting
Rarely fatal
Common but unrecognized form of food poisoning
Bacteria also responsible for gas gangrene
Clostridioides difficile – Associated Diarrhea
- Until 2016 called Clostridium difficile
- Found in the stool of many healthy
individuals; asymptomatic carriers - Extended use of antibiotics, esp.
quinolones, kills microflora in intestine
that usually competes with C. difficile - Unrestricted growth of C. difficile results
in massive exotoxin production (ABtoxins; glucosyltransferases)
Symptoms of Clostridiodes difficile
Range from mild diarrhea to pseudomembranous colitis which is the inflammation of the inner membrane of the large interstines.
Responsible for a high number of deaths.
Vibrio cholerae - Cholera
gram -ve
facultative aerobic
curved rods
Often found in brackish water and estuaries
Transmission by contaminated water
Penetration of mucous layer and adherence to microvilli
Production of Cholera Toxin
Abrupt onset of watery diarrhea
* Muscle cramps as water and
electrolytes are lost from tissue
Which types of vibrio cholerae for virulence and what does the toxin do?
Among appr. 150 serotypes of Vibrio cholerae, just the
serotypes O1 and O139 virulent
* Serotypes O1 and O139 possess genes for type IV pilin
(adhesin) and cholera toxin
* Toxin causes host cells to secrete Cl–, HCO–, and water
Campylobacter sp.
- Campylobacter: Gram-negative,
spiral-shaped bacteria - C. jejuni and C. coli most common
Campylobacter species responsible
for enteritis (inflammation of small interstine) - As C. jejuni and C. coli are very
similar, both are often referred to as
C. jejuni
Where is the Campylobacter sp found?
Commonly found in the intestinal tract of poultry
What causes human infection by campylobacter?
Ingestion of contaminated food or water
Infectious does of 500-800 bacteria.
How do the campylobacter colononize the small and large interstine?
- Penetration of human mucus by high motility and spiral shape.
- Adherence to epithelial cellls
- Secretion of cytolethal distending toxin (CDT)
- CdtB is translocated to nucleus of host cell; induces cell
cycle arrest in G2 phase (nuclease activity); increase in cell size before cell death
* Clinical manifestations are fever, abdominal cramps,
diarrhea or even dysentery
What are the bacterial infections as the cause of Diarrhea?
Listeria monocytogenes
* Enterobacteriaceae
* Salmonella
* Shigella
* Yersinia
* Gastropathogenic E. coli strains
Listeria Monocytogenes
Gram-positive, rod-shaped, sometimes forming
short chains, non-spore forming
* On blood agar medium: beta-hemolytic
* Found in soil, stream water, sewage, plants,
and food
* at least 42 mammalian and 17 avian species
used as hosts, also lower animals
* found in the intestinal tract of 5-10% of the
human population without any symptoms
* Causes listeriolosis in humans and animals
* food-borne disease, 25% mortality
L. monocytogenes: Pathogenesis
- Clinical manifestations: from mild influenza-like
symptoms to meningitis, meningoencephalitis
and sepsis - Disease most likely in pregnant women,
neonates, the elderly and immunocompromised
individuals - frequently newborn infections
- Infection of fetus by penetration of endothelial
layer of the placenta
Growth at temperatures between 4°C and 37°C - flagella formation at temperatures below 37°C
How does listeria monocytogenes infect a person?
Ingestion with raw, contaminated food
* Penetration of host epithelial cells by bacterial
invasin
* In immunocompetent persons,
elimination of infection before
spread of infection
* In immunocompromised,
development of systemic disease
* Unrestricted multiplication in
macrophages and parenchymal
cells
* Hijacking of host´s actin
cytoskeleton:
* induction of actin polymerization
* intracellular spread from cell to cell
Enterobacteriaceae as the cause of diarrhea. What are the features?
Gram negative
Facultative anaerobic rods
Oxidase negative
Many species flagellated
Natural inhabitants of interstinal tracts of humans and animals
Enterobacteriaceae that don’t ferment lactose?
Salmonella
Shigella
Yersinia
Enterobacteriaceae that do ferment lactose?
Pathogenic E.Choli
ETEC: Enterotoxigenic E.Choli
EIEC: Enteroinvasive E.Choli
EPEC: Enteropathogenic E.Choli
EHEC: Enterohemorrhagic E.Choli
Salmonella Infections
All pathogenic Salmonella belong to single species: S. enterica
* More than 2400 serovars of S. enterica
* S. enterica serovar typhimurium = S. typhimurium
* Gastroenteritis = Salmonellosis
* S. enterica serovar typhi = S. typhi
* Typhoid fever
Salmonella Gastroenteritis-Salmonellosis
Bacteria inhabit intestinal tract of
humans and animals
* Contamination of water/meat
products by intestinal content
* Infection of eggs before they are
laid; can survive in egg white
despite lysozyme and lactoferrin
* Ingestion of food/water
contaminated with Salmonella
* Invasion of intestinal epithelilum
and multiplication there
* abdominal discomfort, diarrhea;
nausea and vomiting at times,
headache, low grade fever
Shigella basic features
Four pathogenic species:
S. dysenteriae,S. flexneri,
S. boydii,S. sonnei
* Humans and apes only hosts
* Contamination of food/water with human
feces
* Bacteria invade epithelial cells in large
intestine; lysis of phagosome; migration
and spread by actin polymerization
* Production of Shiga toxin by S.
dysenteriae kills host cells (toxinmediated infection)
* Tissue destruction results in dysentery
* Diarrhea with blood and mucus, fever,
abdominal cramps
Shigellosis
Adherence of Shigella to epithelial cells
lining intestinal tract
Entry of Shigella into epithelial cell
Multiplication of bacteria within epithelial cell
Invasion of neighboring epithelial cells by Shigella,
thereby avoiding immune system
Killing of epithelial cells results in abscess formation;
Rare spread of the bacteria in the bloodstream
Yersinia Gastroenteritis - Yersiniosis
- Caused by Yersinia enterocolitica and
Y. pseudotuberculosis - Intestinal inhabitants of many domestic
animals - Contamination of water/food by fecal
contents - Bacteria can reproduce at 4°C
- Diarrhea, fever, headache, severe
abdominal pain - Often misdiagnosed as appendicitis
- Y. pseudotuberculosis is progenitor of
Y. pestis, happened appr. 10,000 years
ago
- Five classes of pathogenic E. coli :
EHEC: enterohemorrhagic E. coli
EPEC: enteropathogenic E. coli
ETEC: enterotoxigenic E. coli
EIEC: enteroinvasive E. coli
EAggEC: enteroaggregative E. coli
Escherichia coli Gastroenteritis
Occurs as traveler’s diarrhea and epidemic diarrhea in
nurseries
* 2-3% of feedlot cattle may have enterohemorrhagic
strains in their intestines
* Enterohemorrhagic strains such as E. coli O157:H7
produce Shiga toxin (toxin-mediated infection)
* O = cell wall antigen
* H = flagellar antigen
What is similar between EHEC and EPEC?
- Pedestal formation
- Identical mode of cell adherence and
pedestal formation
What does EPEC do?
severe diarrhea in children
>1 Mio deaths
What does EHEC do?
cattle (1-3%) as reservoir;
no symptoms in cattle
- ground beef frequently
contaminated
- low infectious dosis (<100)
- hemorrhagic colitis
- hemolytic uremic syndrome
(kidney failure)
- toxin-mediated infection
What does EIEC do?
invasion of intestinal epithelial
cells identical to that of Shigella
- no production of toxins
- inflammation of mucosa, fever,
sometimes dysentery
What does ETEC do?
common source of travellers
diarrhea
- formation of two toxins
- heat-labile toxin: activates
host adenylate cyclase
- heat-stable toxin: activates
host guanylate cyclase
- no inflammation, no fever
- toxin-mediated infection
What are the Treatment of Diseases of the Digestive System?
Oral rehydration of patients
* severely dehydrated patients are
given intravenous fluids
* Optional antibiotic treatment
Helicobacter Peptic ulcer disease
H. pylori is Gram-negative, spiral shaped
and microaerophilic
* Human gastrointestinal tracts are the only
reservoirs for H. pylori
* H. pylori has a great ability to resist
destruction by stomach acid by producing
a very efficient urease
* Flagella enable movement into and within
the protective mucus layer of the stomach
* Protecting mucus vanishes due to
inflammation, leaving epithelium
susceptible to hydrochloric acid
* formation of gastric/ duodenal ulcers and
occasionally stomach cancer
