GIT infections

Question 1

How can GI pathogens cause damage?

Answer 1

Local inflammation
Ulceration/perforation of mucosal epithelium
Disruption of normal microbiota
Pharmacological action of bacterial toxins
Invasion to blood or lymphatics

Question 2

What bacteria can cause diarrhoea and what are their incubation periods, durations and symptoms?

Answer 2

Variable incubation period
Campylobacter - 2-11 days
Shigella - 1-4 days

Variable duration
Campylobacter - up to 3w
Shigella - 2-3 days

Variable symptoms
Campylobacter and Shigella - bloody stools
EPEC and cholera - watery stools

Question 3

Vibrio cholerae

Answer 3

Gram -ve, characterised by epidemics and pandemics, flourishes where no clean drinking water/sewage disposal

Based on O-antigens (O1 associated with early pandemics, non-o1 associated with recent outbreaks
Vaccines - parenteral has low protective efficiency, oral vaccine suitable for travellers

Only infective in large doses, many organisms killed in stomach, colonisation of SI involving flagellar motion, mucinase, attachment to specific receptors, loss of fluid and electrolytes without damage to enterocytes

Question 4

Consequences of cholera infection

Answer 4

Fluid loss of up to 1l/hr
Electrolyte imbalance leading to dehydration, metabolic acidosis and hypokalemia
Hypovolaemic shock
40-60% mortality but <1% if ORT given

Question 5

Escherichia Coli

Answer 5

Gram -ve, normal GI microbiota, some strains cause virulence factors enabling them to cause disease

Examples are
EPEC (enteropathogenic) - sporadic cases and outbreaks of infection in <5y/o
ETEC (enterotoxigenic) - traveller’s diarrhoea
VTEC/STEC - sporadic cases and outbreaks of gastroenteritis
EIEC (enteroinvasive) - food-borne infection in areas of poor hygiene (often persistent diarrhoea)

Question 6

What are the adherence strategies of E.coli and what are the mode of actions?

Answer 6

Pili/fimbriae
Pedestal formation

Mode of actions are:
LT - heat labile toxin
STa - heat stable toxin

Question 7

Campylobacter jejuni

Answer 7

Gram -ve, causes food-associated diarrhoea, large animal reservoir, transmission through consumption of raw meat and contaminated milk, mucosal inflammation and fluid secretion

Inflammation involves entire mucosa, villous atrophy, necrotic debris in crypts, thickening of basement membrane

Question 8

Salmonella spp

Answer 8

Gram -ve, food-associated diarrhoea through raw/uncooked meat, secondary spread can be human-human

Important species are S. typhi, S. paratyphi and S, enteritidis

Absorption to epithelial cells in terminal SI, penetration of cells and migration to lamina propria, infamm response mediates response of prostaglandins, CAMP stimulation, release of fluid and electrolytes causing diarrhoea

S. typhi and S. paratyphi causes enteric fevers, systemic infections initiated in GIT, multiply within and transported around body in macrophages

Question 9

Typhoid fever and typhoid vaccines

Answer 9

Patient can excrete S. typhi in faeces for several weeks after recovery, 1-3% become chronic carriers so it is a notifiable disease

vaccines are either oral live attenuated (booster after 5y) or parenteral (booster after 2y), recommended for travellers to endemic areas

Question 10

Shigella spp

Answer 10

Causes shigellosis (bacillary dysentery), human only pathogen
4 species - S. dysenteriae, S. flexneri, S.boydii, S. sonnei

Attaches to mucosal epithelium of distal ileum and colon, inflammation and ulceration, rarely invasive, diarrhoea watery initially but later can contain blood and mucus, usually self-limiting

Question 11

Listeria monocytogenes

Answer 11

Food-borne pathogen associated with pate, soft cheese etc, pregnant women/elderly/immunosuppressed at risk, usually presents as meningitis

Question 12

Antibiotic associated diarrhoea

Answer 12

Disruption of gut microbiota
Tetracycline - allows colonisation by S.aureus and candida sp
CLindamycin allows C.difficile to multiply
C.difficile infection now associated with vanc resistance

Question 13

C.difficile infection

Answer 13

Produces spores for survival

Produces an enterotoxin and cytotoxin

Question 14

Clostridium perfringens

Answer 14

Food-associated GI infection, spores survive cooking and germination takes place
Multiplication in LI, production of spores and enterotoxin, damage to int epithelium, diarrhoea

Question 15

Rotavirus

Answer 15

Commonest in children <2, commonest in winter, transmission faeco-oral but may also be faeco-respiratory

Intubation period 1-2 days, replication of virus in SI epithelal cells at tips of villi, damage caused to infected cells leaving immature cells with reduced absorptive capacity for sugar, water and electrolytes
Onset of vomiting lasting 4-7 days

Oral vaccine

Question 16

Norovirus

Answer 16

Winter vomiting disease
Faceo-oral, contaminated water/shellfish, fomites

No vaccine yet

Question 17

Giardia lambia

Answer 17

Drinking and recreational water, can be passed person-person, diagnosis by stool samples microscopy

Two stages - trophozoite (lives in upper SI, adheres to brush border of epithelial cells), cyst (formed when trophozoite forms resistant wall, passes out in stools, can survive for several weeks)

Present in duodenum, jejunum and upper ileum, causes damage to mucosa and villous atrophy, leads to food malabsorption, may swim up bile duct to gallbladder

Mild infections asymptomatic, diarrhoea usually self-limiting (7-10days), chronic diarrhoea presents in immuno-compromised patients

Question 18

Cryptosporidium parvum

Answer 18

Transmission through faecally contaminated drinking water
Asexual and sexual development within host, ingestion of resistant oocysts, invasion of microvilus border of int epithelium, after sexual phase oocysts released

Mod-severe diarrhoea, usually self-limiting, prolonged and may become irreversible and life-threatening

Question 19

Entamoeba histolytica

Answer 19

Ingestion of contaminated food, anal sexual activity
Cysts pass through stomach into SI, adhere to epithelial cells and cause damage. After mucosal invasion, cysts invade RBCs giving rise to amoebic colitis. Trophozoite stages live in LI and pass out as resistant infective cysts

Resists immune defence, produces hydrolytic enzymes and proteinases, produces protein which lyses neutrophils, contents of which toxic to host

Clinically presents as small superficial ulcers leading to mild diarrhoea, entire colonic mucosa may become deeply ulcerated leading to severe amoebic dysentery. Complications include int perforation, may spread to liver and other organs

Question 20

Nematodes

Answer 20

Roundworms, bisexual, cylindrical

Most clinically important intestinal worms, often soil-transmitted
Infection occurs by either swallowing infective eggs or active skin penetration by larvae and systemic migration through lung to intestine

Question 21

Strongyloides stercoralis

Answer 21

Pinworm, disruption of SI mucosa, villous atrophy, marked loss of elasticity of intestinal wall

Clinically presents as dysentery, dehydration, malabsorption syndrome, association with appendicitis

Question 22

Trichuris trichiura

Answer 22

Whipworm, 3 years in gut, ingesting eggs on vegetables

Question 23

Ascaris lumbricoides

Answer 23

Giant roundworm, large thick white worm, adults live in gut for 2 yrs

Allergic reaction in sensitised people, digestive upsets, protein/energy malnutrition, intestinal blockages, worm may invade mouth/nose etc

Question 24

Enterobius vermicularis

Answer 24

Threadworm

Small cylindrical nematodes - intense itching, secondary bacterial infection, slight eosinophilia

Question 25

Ancyclostoma duodenale

Answer 25

Hookworm

Often picked up walking barefoot in infected areas, attaches to SI, suck blood and protein, cause hypochromic anaemia

Question 26

Taenia solium

Answer 26

Tapeworm

Acquired from ingesting worms or eggs in undercooked pork, reside in LI