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81 terms

Infections of the GIT

STUDY
PLAY
Anatomic, Physiological & Biochemical barriers
to infection by normal flora and pathogen
An unbroken mucosal epithelium
Glycoxalyx - a glycoprotein and polysaccharide layer that
covers the surface of the epithelial cells

Mucous ␣ Acidity of the stomach
Bile

IgA
Lactoferrin ( in children)
WBC
Gut motility
Peyer's patch
Normal flora
Manifestation of Small intestine infection
watery diarrhoea and vomiting
Manifestation of large intestine infection
dysentery ( small faecal volume with mucus and many cases blood)
Types of Microbial Foodborne Diseases
1. Intoxication
2. Infection
3. Toxicoinfection
Infection
due to ingestion of microorganisms

Cells penetrate the through membranes multiply and produce toxins
Intoxication
due to ingestion of preformed toxins

KEY FEATURE: FAST ONSET

presence of organism in food is irrelevant to disease production

Staphylococcal intoxication - Staphylococcus aureus
Botulism ‐ Clostridium botulinum
Mycotoxicosis ‐ Moulds
Key difference between intoxication and infection
Time to onset
2 types of symptoms of infections
1. Enteric - local result of enteric infection and effect of toxin
eg. salmonella, shigella, EPEC, campylobacter jejuni, yersinia entercolotica

2. Non-enteric - when the pathogens or their toxins pass through the intestine and invade or affect other internal organs and tissues
eg. Listeria moncytogenes, Vibrio vulnificus, EHEC, Hepatitis A virus, etc
Toxicoinfection
1. Gram -negative bacteria

2. Sporeformers - need to ingest lots
Gastrointestinal Diseases Categorization
Intoxication
Gastroenteritis Non‐inflammatory Gastroenteritis - Food toxemia Inflammatory Gastroenteritis
Invasive Gastroentertis
Clinical syndromes GI disease
1. Enteric Fever - entire body, eg. typhoid fever

2. Gastritis

3. Gastroenteritis

4. Colitis - colon
Colitis
eg. dysentery, shigellosis, amoebiasis
damages the intestinal walls leading to bloody stools and mucus
Gastroenteritis
- diarrhoea, nausea, vomiting, crampy abd pain

stomach and intestine
eg. salmonellosis, rotavirus diarrhoea
Gastritis
sometimes bleeding, h. pylori, e. coli

stomach
3 clinical syndromes of diarrhoea
1. acute water diarrhoea
2. dysentery
3. persistent diarrhoea
Intoxications
S. aureus
C. botulinum
Mycotoxins
Toxicoinfections
Clostridium perfringens
Bacillus cereus
Vibrio cholerae
Enteropathogenic E. coli
Small intestine infections
1. Bacteria: E. coli (ETEC, EPEC), Clostridium perfringens, Cholera sp., Vibrio sp.


2. Viruses: Rotavirus, Norwalk virus, Adenovirus, Astrovirus, Calicivirus, Noroviruses ( Norwalk‐ like viruses)

3. Parasites: Giardia lamblia, Cryptosporidium parvum, Ascaris lumbricoides, Taenia solium, Taenia saginata, Cyclospora cayetanensis
Large intestine Infections
1. Bacteria: E. coli ( EHEC, EIEC, EAEC), Shigella sp., Salmonella sp., Campylobacter sp., Yersinia sp., Aeromonas sp., Pleisomonas sp., C. difficile


2. Parasites: Entamoeba histolytica, Trichuris trichiura
Short incubation
within 1 day usually < 16 h

Emetic syndrome (1‐ 6 h) or diarrhoeal syndrome (8 - 16 h)

S. aureus, B. cereus, C perfringens
Intermediate incubation
1 ‐3 days

Bacterial and viral agents

large bowel or small bowel enteritis
Long incubation
3 - 5 days

Haemorrhagic colitis with 5‐ 10% risk or progression to HUS
Very long incubation
1 - 4 weeks
Non - inflammatory Gastroenteritis
1. S aureus

2. Bacillus cereus

3. Clostridium botulinum
S. aureus enterotoxins
Type A most common
Water soluble
Low molecular weight proteins
Heat stable (resist boiling for 30 minutes)

High risk foods - custard, cream, tarts, processed foods
Symptoms of S. aureus enterotoxins
2 to 6 hrs after ingestion of food vomiting, stomach cramps (toxin binds to emetic reflex centre)
self limiting, 24 hr duration
Bacillus cereus
Produces spores in normal conditions

Wide temperature range (normal body and refrigerated temps)

survive pasteurisation and heating, cooking, soil and vegetation, germinate upon cooling
Pathogenicity of B. cereus
1. Non gastrointestinal disease:
- four hemolysins
- three different types of phospholipase C (Tissue damage)

2. Gastrointestinal diseases
-emetic toxin
- two enterotoxin complexes
Enterotoxins
TYPE 1 - emetic - high carbohydrate foods
TYPE 2 - diarrhoeal - high protein
Botulism
Canned food and commercial sterility
A, B, E & F - human diseases
Mode of action of Botulinum toxin
1. B portion - protects the toxin from being inactivated by stomach acid ␣ Gets the A portion inside the nerve cells

2. A portion - metalloproteinase
Blocks neurotransmission of cholinergic synapses by preventing the release of acetylcholine at the neuromuscular junction

FLACCID PARALYSIS
Clinical features of botulism
weakness, dizziness, dryness of mouth, nausea, vomiting, no fever
-neurological symptoms
-blurred vision, dysphagia, speech difficulties
-descending flaccid paralysis
-death from respiratory/cardiac failure

Death from respiratory problems
infant botulism
Endospores

constipation, listlessness, general weakness, and poor appetite; death may result from respiratory failure
Clostridium difficile
␣ excessive antibiotic use - amoxicillin, ampicillin, clindamycin, cephalosporins
Antibiotic‐Associated Colitis (Pseudomembranous Colitis)
Clostridium difficile (C. difficile associated diarrhea - CDAD)
1. uncomplicated diarrhea

2. pseudomembranous colitis
viscous collection of inflammatory cells, dead cells, necrotic tissue, and fibrin that obstructs the intestine

3. toxic megacolon inflammation resulting in intestinal tissue death
C. difficile Virulence Factors
toxin A (enterotoxin causing diarrhea)
toxin B (cytotoxin kills cells)
C. difficile symptoms
inflammation, diarrhea, fever, nausea, cramping

most common cause of diarrhea in hospitalized patients
C. difficile treatment
stop the antibiotic regime and replace the intestinal flora and if need be treat with vancomycin or metronidazole
Cholera :
Infection of small intestine
Cholera mechanism of action
1. colonisation, toxin production
2. upregulate cyclic AMP
3. Na+ blocked. Lots of Cl into lumen
4. Lots of water into lumen
Vibrio cholerae
acid sensitive
Attach to the microvilli of the glycocalyx of epithelial cells of the jejunum and ileum

Multiply and liberate:
1. cholera enterotoxin
2. Mucinase
3. Endotoxin
Clinical Symptoms - Cholera
Abrupt, watery diarrhoea
Vomiting may ensure after diarrhoea
Patient is cyanotic and has sunken eyes and cheeks A scaphoid abdomen Poor skin turgor and thready or absent peripheral pulses

Vital signs include, tachycardia and low or unobtainable pressure
Escherichia coli Gastroenteritis
traveler's diarrhea
enterotoxigenic E. coli (ETEC)
heat stability
enteropathogenic E. coli (EPEC)
causes effacing lesions
caused by destruction of brush border microvilli on intestinal epithelial cells
Enterohaemorrhagic E. coli (EHEC)
O157:H7

(O antigen on LPS layer of gram negative; H antigen on flagella)

lesions, leading to hemorrhagic colitis
Campylobacter jejuni
animals - poultry or milk

Severe diarrhoea with fever, ulceration and bleeding
Campylobacter jejuni - Two types of infection
1. Enterotoxin mediated diarrhoea
2. Inflammatory invasive diarrhoea
Clinical Syndromes of Salmonella
1. Enteritis (acute gastroenteritis)

2. Enteric fever (prototype is typhoid fever and less severe paratyphoid fever)

3. Septicemia (particularly S. Choleraesuis, S. Typhi,
and S. Paratyphi)

4. Asymptomatic carriage (Salmonella Typhi)
Salmonella enteritis
Nausea, vomiting, nonbloody diarrhea, fever, cramps,
myalgia and headache common

6-48hr incubation, highly infectious dose,
Difference of clinical progression of salmonella enteritis vs enteric fever
Enteric fever - INTRALUMINAL MULTIPLICATION intracellular multiplication happens in reticuloendothelial system - liver, spleen, bone marrow

causing necrosis, haemorrhage, perforation of intestinal wall

ENTERITIS - LAMINA PROPRIA
Enteric fevers
Initially signs of sepsis/bacteremia with sustained fever (delirium) for > one week before abd painand gastrointestinal symptoms
S. Typhi - reservoir
ONLY: Gallbladder
Are antibiotics recommended for
1. Enteritis
2. Enteric Fever
1. NO - may prolong duration, preparation of poultry and eggs

2. YES
- avoids carrier state
- vaccination
- carriers of S. typhi and s. paratyphi
Confirmation of Salmonella
• Stool cultures ‐ gastroenteritis
• Typhoid fever - Stools, Urine and blood cultures +
Widal agglutination test with specific antisera
• Enrichment broth
• Media
• Biochemical tests
• Microbact
• PCR
H. pylori treatment
amoxycillin + clarithromycin + antacid
Dysentery syndrome
Infection of colon with blood and mucus in stools

1. bacillary - shigella, EIEC
2. Amoebic - entamoeba histolytica
Shigellosis
Dysentery (bloody diarrhea)
Only need to ingest small inoculum

faecal-oral spread, contaminated foods
Shiga Toxin Effects in Shigellosis
Enterotoxic Effect:
1. Adheres to small intestine receptors
2. Produces diarrhoea
3. Can cause Meningismus and coma
4. Ulceration of intestine
5. Blocks absorption (uptake) of electrolytes, glucose, and amino acids from the intestinal lumen - mucous secretion
NAD glycohydrolase Effect
1. Destroys all the NAD in the human cell 2. Virtually shuts down the cellular metabolism
3. Results in cell death
Listeriosis
can cross the placental barrier
Listeria monocytogenes infections
almost an y organ
most common = meningitis

Gastroenteritis = resulting fever, nausea, vomiting, and diarrhoea as well as bacteraemia.

respiratorydistress, poorfeeding, lethargy and erythematous rash.
4 classical symptoms of meningitis
headache, fever, neck stiffness and altered mental status.
Listeria monocytogenes and Pregnancy
Listeriosis in pregnancy usually occurs during the third trimester, as the result of the major decline in cell mediated immunity.

Abortion, foetal distress, premature birth, foetal or neonatal death as well as listerial infection of the neonate.
Viral Gastroenteritis
Low grade fever and destroys mature epithelial cells in the middle and upper
villus

Decreased absorption of Na and water from the bowel lumen
Hep A - clinical manifestations
anorexia, general malaise, nausea, diarrhea, fever,
and chills
␣ occasionally viremia occurs leading to liver infection
jaundice
Hep E
~15%-25% fatality rates in pregnant women

water
Protozoal Infections - history
Travel to underdeveloped areas

Outbreak of associated illness (Giardia, Trichinella)

Daycare exposure (Giardia)

Homosexual behavior (Giardia, Entamoebia)

Animal Exposure

Diet: uncooked foods

Immunocompromised
Protozoa and worms - examples
diagram
Amoebiasis (Amoebic Dysentery) - clinical manifestations
asymptomatic to fulminating dysentery, exhaustive diarrhea, appendicitis, and abscesses of liver, lungs, and brain

Asymptomatic to diarrhea
Abdominal Cramps
Flatus, fever, hepatitis
Shoulder pain due to hepatitis
Amoebiasis - signs
Bloody diarrhea
Perianal ulcers
RUQ tenderness
Pulmonary (pneumonia‐ emphysema)
Giardia (Giardiasis)
Test: Microscopic exam of stool for cysts (also the ELISA antigen test)

It is an upper GI parasite and stool examination can be negative
Giardia (Giardiasis) - Treatment
Metronidazole
Giardia (Giardiasis) - Symptoms
1. Diarrhea
2. Abdominal pain&cramps
3. Flatus
4. Fatty, greasy, foul smelling stool (steatorrhea)
Cryptosporidiosis
Crpytosporidium parvum

water contaminant, animals, fish, mammals, reptiles

oocysts resistant to chlorination, but conventional cooking can kill it

immunocompromised pts = persistent chrnoic diarrhoea (>50 stools a day_
Ascariasis
Most common intestinal helminth
Ascaris lumbricoides (the large
intestine round worm)

1. Pulmonary Phase - loffler's syndrome

2. Intestinal phase - eggs in stool
Ascariasis - MoA
Penetrate the intestine & invade liver, lung, heart
Treatment - Ascariasis
Albendazole and Pyrantel pamoate
Tapeworms
Cestodes (segmented worms)
Adults live in GI tract, larvae can be found in almost any organ (neuro, muscle, eye) (cysticercosis)
Notifiable foodborne illnesses in Australia
(Oznet)
Campylobacter infections
non‐typhoidal Salmonella infections
Listeria infections
Shigella infections
Salmonella Typhi
Hepatitis A
Botulism
Shiga Toxin‐producing Escherichia coli (STEC)
Haemolytic Uraemic Syndrome (HUS)
Bacteria on your hands
daigram