Infections of the GIT

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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

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