Lecture 15 The Gastrointestinal System PT2 - Microorganisms & Diseases

Question 1

Q: Compare bacterial, viral, and protist GI infections in terms of pathogenesis and symptoms.

Answer 1

A:

Bacterial infections (e.g., Salmonella, E. coli) cause inflammation through toxin production or invasion, leading to symptoms like diarrhea, vomiting, and fever.
Viral infections (e.g., rotavirus, norovirus) lead to rapid onset of diarrhea and vomiting, often self-limiting.
Protist infections (e.g., Entamoeba histolytica, Giardia intestinalis) cause dysentery or prolonged diarrhea by tissue invasion or nutrient malabsorption

Question 3

Q: What are the symptoms of polio, a non-diarrheal GI disease?

Answer 3

Symptoms:
– Majority of infections are asymptomatic
– May cause brief illness – fever, headache, sore throat
– Very rarely, may enter central nervous system and cause
paralysis (<1% cases)

Question 4

Q: What are the symptoms of polio, a non-diarrheal GI disease?

Answer 4

Symptoms:
– Majority of infections are asymptomatic
– May cause brief illness – fever, headache, sore throat
– Very rarely, may enter central nervous system and cause
paralysis (<1% cases)

Question 5

Q: What is polio, a non-diarrheal GI disease?

Answer 5

Poliomyelitis (Polio)
Poliovirus:
– Non-enveloped, positive-stranded RNA virus
– Family: Picornaviridae; genus: Human Enterovirus C

Question 6

Q: What are the transmission of polio, a non-diarrheal GI disease?

Answer 6

Transmission:
– infected faeces, person to person spread
– Virions are very stable, remain infectious in food and
water for extended periods (less frequent mode of
infection)

Question 7

Diarrhoeal disease and gastroenteritis symptpms

Answer 7

Symptoms: 12–60 hours:
* diarrhoea, vomiting, nausea, headache, fever, chills

Question 8

Diarrhoeal disease and gastroenteritis transmission

Answer 8

Transmission (faecal/oral):
* person to person
* via contaminated food/water
Incubation period 0-72hrs, cause dependent

Question 9

Diarrhoeal disease and gastroenteritis causes

Answer 9

arious causes
* Protists: Giardia lamblia, Entamoeba histolytica, Cryptosporidium
* Bacterial:
* infections: Salmonella gastroenteritis, Campylobacter, Vibrio cholerae
* intoxications: enterotoxogenic E. coli, Shigella
* Viral: rotavirus, norovirus, adenovirus

Question 10

Intestinal Protozoa : Amoebae

Answer 10

Catches food and moves above using pseudopodia
* Entamoeba histolytica: amoebic dysentery

Question 11

Intestinal Protozoa : Flagellated protists

Answer 11

• Protozoa that possess one to many flagella for movement
• Giardia intestinalis: Giardiasis

Question 12

Intestinal Protozoa : Sporozoans

Answer 12

Spore forming and/or complex life cycle
* Cryptosporidium: Sydney Water Scare 1998

Question 13

Q: What is the pathogenesis of amoebic dysentery caused by Entamoeba histolytica?

Answer 13

A: Ingested cysts excyst in the small intestine, releasing trophozoites that invade the large intestine, causing ulceration and bloody diarrhea.

Question 14

Entamoeba histolytica
Diagnosis

Answer 14

Diagnosis:
- Detection of cysts in stool (microscopy,
molecular (antigen/DNA)
- Serological testing

Question 15

Entamoeba histolytica
treatment

Answer 15

Treatment:
- Antimicrobials (metronidazole)
- All infections should be treated to avoid
spread and risk of extraintestinal invasion

Question 17

Giardia intestinalis: Giardiasis transmission + symptoms

Answer 17

Transmission: person to person; usually water-borne

symptoms:
– Carrier state, asymptomatic
– Symptoms within 7-10 days of ingestion: greasy or watery
diarrhoea, abdominal cramps, nausea, bloating, flatulence;
lasts 2-6 weeks
– Chronic infection leads to malnutrition, weight loss

Question 18

Entamoeba histolytica
Pathogenesis & Virulence

Answer 18

1. Infection occurs when cysts are ingested through contaminated food or water.
2. The cysts excyst in the small intestine and release trophozoites
3. after Entamoeba histolytica trophozoites are released in the intestines, they live in the large intestine, multiply via binary fission, and may invade the intestinal mucosa, causing ulcers and bloody dysentery.
   4.

Question 19

Q: How does Entamoeba histolytica survive outside the host?

Answer 19

Cysts are a protective, dormant form that some protozoa =>a tough outer wall that protects the organism,
Once inside the host, the cysts undergo excystation, releasing active trophozoites.

trophoizites = active, feeding form, use pesudopodia to move and ivade LI, causint tissue damage and symptomgs e.g. ulceration and diarrhea

trophozoites can convert back to cysts before leaving the body. This process is called encystation and occurs in the colon.
=> Cysts are expelled in stool and survive in the environment, ready to infect a new host.

Question 20

Q: What are the main virulence mechanisms of Entamoeba histolytica?

Answer 20

A:

Trophozoites invade host tissues, graze on epithelial cells, and can consume red blood cells, causing tissue destruction and bleeding.
This invasion leads to bloody diarrhea.

Question 21

Q: What are the complications of Entamoeba histolytica infection?

Answer 21

A: Complications include secondary amoebiasis, where trophozoites spread via the bloodstream to other organs (liver, brain, spleen, lungs), forming abscesses.

Question 22

Q: Why can asymptomatic carriers of Entamoeba histolytica still spread the infection?

Answer 22

A: Even in asymptomatic infections, individuals can still pass cysts in their stool, which can infect others.

Question 23

Giardia intestinalis diagnosis

Answer 23

Diagnosis:
* Identification of trophozoites or cysts in stool
* Immunoassay for antigen in stool specimens

Question 24

Giardia intestinalis treatment

Answer 24

Treatment:
* Antimicrobials (metronidazole) for severe or persistent infections

Question 25

Giardia intestinalis control

Answer 25

Control:
* water sanitation; quite resistant to chlorine, slow sand filtration can be used
* prevent faecal contamination of food
* hand washing

Question 26

Salmonella gastroenteritis

Answer 26

Reservoir: intestines of birds and other animals
* Generally acquired via ingestion of contaminated food/water
* Typically associated with raw meat, poultry, eggs, fruit, vegetables,
chocolate!

Symptoms:
* Asymptomatic or symptoms within 12-72hrs of ingestion
* Nausea, vomiting, diarrhoea, abdominal pain, fever
* Dose dependent; Resolves after 4-10 days

Question 27

Salmonella Gastroenteritis Pathogenesis & Virulence

Answer 27

Entry: Ingestion of contaminated food or water.
Attachment: Uses fimbriae to adhere to the intestinal mucosa.
Invasion: Penetrates epithelial cells via type III secretion systems (T3SS), injecting effector proteins that induce endocytosis.
Pathogenicity Islands: Contains genes (e.g., SPI-1) for invasion and SPI-2 for survival within host cells.
Inflammatory Response: Triggers release of cytokines, leading to diarrhea and gastrointestinal inflammation.
Symptoms: Include fever, abdominal cramps, and non-bloody diarrhea.

Question 28

Giardia intestinalis pathogensis amnd virulence

Answer 28

1. when cysts are ingested, and stomach acid triggers excystation in the duodenum (upper small intestine).
2. trophozoites attach to the epithelial layer of the small intestine using a large sucking disc, competing for nutrients and damaging the epithelial cells.
3. to avoid being flushed out of the small intestine, it anchors to the epithelial cells with its sucking disc, helping it resist being washed away by the rapid flow of the small intestine

Question 29

Giardia intestinalis effects

Answer 29

A: The infection decreases the absorption of nutrients, leading to malabsorption of fats and fluids.

A: Giardia secretes cysteine proteases, which can damage host tissues and play a role in immune modulation by degrading chemokines.

Question 30

Salmonella gastroenteritis: Diagnosis, treatment and control

Answer 30

• Diagnosis: stool culture; culture independent
• Treatment: rehydration, self-limiting
• Control: avoid faecal contamination of food, hand washing

Question 31

ETEC virulence

Answer 31

Enterotoxic E. coli (toxins)
Virulence: Produces toxins (heat-labile and heat-stable enterotoxins).
Effect: Causes watery diarrhea by stimulating excessive secretion in the intestines.
Transmission: Contaminated water or food.

Question 32

EIEC virulence

Answer 32

Enteroinvasive E. coli (invade cells)
Virulence: Invades intestinal epithelial cells, similar to Shigella.
Effect: Causes dysentery-like symptoms with fever, cramps, and bloody diarrhea due to cell invasion and destruction.
Mechanism: Penetrates and multiplies within cells, leading to inflammation.

Question 33

EPEC virulence

Answer 33

Enteropathogenic E. coli (destroy brush border)
Virulence: Destroys the brush border of the small intestine using a type III secretion system.
Effect: Causes watery diarrhea, especially in infants.
Mechanism: Leads to a characteristic attaching and effacing lesion that disrupts absorption.

Question 34

EAEC

Answer 34

– Enteroaggregative E. coli (adherent/toxins)
Virulence: Forms a biofilm on the intestinal surface and produces toxins.
Effect: Causes persistent watery diarrhea, often with mucus, particularly in children.
Mechanism: Adheres in a “stacked-brick” pattern.

Question 35

EHEC/STEC

Answer 35

Enterohemorrhagic/Shiga toxin
producing E. coli (Shiga toxin)
Virulence: Produces Shiga toxin, which can damage blood vessels in the intestines and kidneys.
Effect: Causes bloody diarrhea and can lead to hemolytic uremic syndrome (HUS), a serious complication affecting the kidneys.
Common Strain: E. coli O157

Question 36

Intoxication: Enterotoxigenic E. coli (ETEC) symptoms and treatment

Answer 36

Symptoms
* Watery diarrhoea
* Most common cause of travellers’ diarrhoea
* In acute cases salts and fluid loss > dehydration, death

Treatment
* Rehydration therapy very effective: isotonic salt solutions readily taken up in stomach

Question 37

Q: How does Salmonella survive the stomach environment?

Answer 37

A: Salmonella can survive the low pH of the stomach, allowing it to reach the intestines and initiate infection.

Question 38

salmonella pathogenesis + virulence

Answer 38

The Type 3 secretion system helps Salmonella inject effector proteins into host epithelial cells, aiding in invasion and evasion of the immune response.

Salmonella invades intestinal lining : attaches to specific receptors on the epithelial lining of the ileum and colon, invades the cells, and multiplies within the phagosome without escaping it.

A: The invasion triggers an acute inflammatory response, which increases secretion and leads to the symptoms of gastroenteritis.

Question 39

Is Salmonella infection confined to a specific area of the body?

Answer 39

A: Yes, Salmonella infection is typically confined to the intestines.

Question 40

Enterotoxigenic E. coli (ETEC) toxins

Answer 40

ETEC produces two toxins:
1. Heat-stable enterotoxin (ST).
2/ Heat-labile enterotoxin (LT), which disrupts ion and water flow across the intestinal membrane, leading to massive secretion of water and salts, causing watery diarrhea
==>A: The toxins produced by ETEC disrupt ion and water transport across the intestinal membrane, leading to excessive water and salt secretion into the intestinal lumen, causing watery diarrhea.

Question 41

ETEC fimbriae

Answer 41

ETEC attaches to SI using fimbriae, thread-like structures, to attach to the epithelial wall of the small intestine. Adhesin proteins at the tip of the fimbriae allow it to bind to specific molecules on the intestinal cells
==> A: Fimbriae help ETEC avoid being washed away by the rapid flow of food in the small intestine, allowing it to remain attached and produce toxins.

Question 42

Q: How is ETEC similar to cholera in terms of pathogenesis?

Answer 42

A: The heat-labile enterotoxin (LT) produced by ETEC is structurally and functionally similar to cholera toxin, both causing disruption of ion transport in the intestines.

Question 43

viral gastroenterities transmission +symptoms

Answer 43

Acquisition:
* Faecal-oral
* highly contagious, shedding

Symptoms:
* acute diarrhea, vomiting, abdominal cramps, headache,
nausea, low-grade fever
* begin 24-48hrs after ingestion: lasts 24-48hrs, self-limiting

Question 44

viral gastroenterities treatment + control

Answer 44

Treatment: Self-limiting, rehydration
– Infection results in short-term immunity ~12 weeks

– Control:
* hand washing
* cleaning, disinfection
* careful monitoring of water purification

Question 45

Norovirus Gastroenteritis what it is and how its trasnmitted

Answer 45

Non-enveloped, single strand RNA virus, Caliciviridae

Transmission:
* person to person, exposure to aerosols of norovirus from vomiting
persons
* direct or indirect faecal contamination found on fomites
* ingest faecally-contaminated food or water

Question 46

Rotavirus Gastroenteritis what it is and how its trasnmitted

Answer 46

Non-enveloped, double-stranded RNA (dsRNA),
segmented genome, Reoviridae

Transmission:
* Virus shed in large quantities
* Faecal-oral and fomite transmission
* Low infectious dose

Question 47

rotavirus treatment

Answer 47

Live attenuated vaccine, oral
* In Australia, infants < 6 months old receive vaccine
* Reduces severity and hospitalisation in children

Question 48

Q: Why is Norovirus considered a highly effective pathogen? Explain key terms.

Answer 48

A:

Lacks durable immunity: Immunity after infection is short-lived, typically only lasting for a few weeks, meaning people can get reinfected easily.
Very low infectious dose: It takes only 10-100 viral particles (virions) to cause an infection, which is extremely small compared to many other pathogens. This means it spreads very easily.
Short incubation period: Symptoms develop quickly, usually within 24-48 hours after being exposed to the virus.
Persistent: Infected individuals can continue to shed the virus in their feces for up to 60 days, even after symptoms resolve, meaning they can spread the virus for a long time.
Environmental persistence: Norovirus can survive on surfaces for extended periods, making it very difficult to eliminate in communal settings (e.g., cruise ships, schools).

Question 49

Q: Describe the pathogenesis of Norovirus.

Answer 49

A:

Ingestion: Norovirus is ingested through contaminated food, water, or surfaces.
Binding: The virus binds to Histo-Blood Group Antigens (HBGA) on the surface of intestinal mucosal cells.
Infection: It invades enterocytes (intestinal cells) and immune cells like macrophages and dendritic cells, causing damage.
Blunt villi and microvilli: This leads to inflammation and edema (swelling), impairing the intestine’s ability to absorb water and nutrients, which causes diarrhea.
Short-term damage: The infection causes transient (temporary) lesions in the intestinal mucosa that usually resolve in a few weeks.

Question 50

Q: How does Rotavirus cause symptoms, and why is it non-inflammatory?

Answer 50

A:

Infects enterocytes: Rotavirus infects the cells lining the small intestine, called enterocytes.
NSP4 toxin: Unlike many infections that cause inflammation, Rotavirus symptoms are caused by the NSP4 toxin.
How NSP4 works:
It disrupts chloride channels in the intestinal cells, causing water to be released into the intestine (leading to diarrhea).
It also increases intestinal motility (movement) by stimulating neurons in the gut, contributing to faster passage of food and water (further worsening diarrhea).