GIT infections Flashcards
How can GI pathogens cause damage?
Local inflammation
Ulceration/perforation of mucosal epithelium
Disruption of normal microbiota
Pharmacological action of bacterial toxins
Invasion to blood or lymphatics
What bacteria can cause diarrhoea and what are their incubation periods, durations and symptoms?
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
Vibrio cholerae
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
Consequences of cholera infection
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
Escherichia Coli
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)
What are the adherence strategies of E.coli and what are the mode of actions?
Pili/fimbriae
Pedestal formation
Mode of actions are:
LT - heat labile toxin
STa - heat stable toxin
Campylobacter jejuni
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
Salmonella spp
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
Typhoid fever and typhoid vaccines
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
Shigella spp
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
Listeria monocytogenes
Food-borne pathogen associated with pate, soft cheese etc, pregnant women/elderly/immunosuppressed at risk, usually presents as meningitis
Antibiotic associated diarrhoea
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
C.difficile infection
Produces spores for survival
Produces an enterotoxin and cytotoxin
Clostridium perfringens
Food-associated GI infection, spores survive cooking and germination takes place
Multiplication in LI, production of spores and enterotoxin, damage to int epithelium, diarrhoea
Rotavirus
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
Norovirus
Winter vomiting disease
Faceo-oral, contaminated water/shellfish, fomites
No vaccine yet
Giardia lambia
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
Cryptosporidium parvum
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
Entamoeba histolytica
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
Nematodes
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
Strongyloides stercoralis
Pinworm, disruption of SI mucosa, villous atrophy, marked loss of elasticity of intestinal wall
Clinically presents as dysentery, dehydration, malabsorption syndrome, association with appendicitis
Trichuris trichiura
Whipworm, 3 years in gut, ingesting eggs on vegetables
Ascaris lumbricoides
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
Enterobius vermicularis
Threadworm
Small cylindrical nematodes - intense itching, secondary bacterial infection, slight eosinophilia
Ancyclostoma duodenale
Hookworm
Often picked up walking barefoot in infected areas, attaches to SI, suck blood and protein, cause hypochromic anaemia
Taenia solium
Tapeworm
Acquired from ingesting worms or eggs in undercooked pork, reside in LI
