BACTERIA AFFECTING THE GI TRACT

what organs does the GI tract consist of (mainly)

• mouth

• oesophagus

• stomach

• small intestine

• large intestine

• rectum

• anus

what is gastroenteritis

gastroenteritis: syndrome characterised by GI symptoms including nausea, vomiting, diarrhoea and abdominal pain

what is diarrhoea

diarrhoea: abnormal faecal discharged characterised by frequent and/ or fluid stool

• associated with increased fluid and electrolyte loss - often disease of small intestine

what is dysentery

dysentery: abnormal inflammation of GI tract characterised by pain, fever, abdominal cramps

• often blood and pus in faces - often disease of large intestine

what is enterocolitis

enterocolitis: inflammation of the mucosa of the small and large intestine

what defences against pathogens are present in the mouth (4)

what defences against pathogens are present in the oesophagus (2)

what defences against pathogens are present in the stomach

what defences against pathogens are present in the small intestine (7)

what defences against pathogens are present in the large intestine (4)

what is food poisoning

strictly refers to the ingestion of toxins/ poisons in food e.g. bacterial toxins or heavy metals

• bacteria grow and multiple in food

• cooking kills bacteria but toxin can still be active » intoxication (TOXIN produced causes food poisoning not the actual bacteria)

which bacteria can cause food poisoning

• Staphylococcus aureus

• Clostridium botulinum

• Bacillus cereus

outline S.aureus as a cause of food poisoning

• grows in food after human contamination (mainly dairy)

  • cooked meats, pre-packed sandwiches

• 50% of strains produce heat-stable enterotoxins »

  • 3-6h of severe vomiting

  • self-limiting

how do the 50% of S.aureus strains cause food poisoning

they produce heat-stable enterotoxins that are resistant to stomach acid and digestive enzymes

what are the main routes of infection of S.aureus

• food preparation

• naso-pharyngeal carriage (commensal in nose and throat)

outline Clostridium botulinum

• neurotoxins produced by C.botulinum causes botulism

• heat-stable toxin ingested through food »

  • flaccid paralysis and death

• infant botulism most common

outline Bacillus cereus

• ‘fried rice syndrome’

• both self-limiting

is B.cereus Gram positive or negative

Gram positive

outline how the stomach protects the body against pathogens

• gastric acid provides effective barrier to most infections due to low pH (1-2)

• many bacteria transiently pass through the stomach before infecting the lower GI tract

  • but these must be able to resist the low pH during passage through the stomach

what does the bacteria Helicobacter pylori cause

gastric (stomach) ulcers

why is Helicobacter pylori special

• can resist and survive against the low pH in the stomach

• can therefore live in and infect the stomach » gastric ulcers

how does Helicobacter pylori survive in the low pH of the stomach

• produces urease (enzyme) which enables it to survive long enough to find a home in acidic environment

• ammonia neutralises acid in immediate area and creates a protective cloud around the bacteria

diagram showing infective cycle of H.pylori

if inflammatory process carries on for a long time (chronicity) it could lead to gastric cancer

what test can be done to detect H.pylori

ammonia basis of breath test

what are gastric ulcers treated with

proton-pump inhibitor PLUS metronidazole/ amoxicillin/ clarithromycin

what are food-associated infections

ingestion of contaminated food that contains an infectious dose of bacteria (>ID₅₀)

• faecal-oral spread

WASH HANDS!

outline the treatment for diarrhoea

• fluid and electrolyte replacement is essential

• antibiotic treatment often not successful and may worsen problem

  • because it wipes out competing organisms or stimulates toxin production (C.diff can cause these)

outline E.coli

• Gram-negative rod

• major cause of diarrhoeal disease and gastroenteritis worldwide

• some strains reside in normal commensal flora

• others infect urinary tract and cause meningitis

what is a complication of diarrhoeal disease caused by E.coli

haemolytic uremic syndrome (HUS)

• rare, serious medical condition that damages small blood vessels » blood clots

how does E.coli enter the body if it causes diarrhoea

ingested in food or via faecal-oral transmission

what does the genetic diversity of E.coli depend on (3)

genetic diversity dependent on:

• plasmid

• lysogenic phage

• transposon encoded ‘pathogenicity islands’

how is E.coli detected in a lab setting i.e. in culture

• MacConkey agar (contains lactose)

  • E.coli is one of the only gastropathogens that ferments lactose » pink/ red colonies

how would E.coli appear on Hektoen enteric agar

bright orange/ brown

if there was a serious E.coli outbreak, what tests would be used to detect E.coli and why

• PCR/ antigen tests for serotypes

  • to see if there are different strains are present

table showing pathogenic strains of E.coli

AMR = antimicrobial resistance

(remember diarrheagenic)

outline enteropathogenic E.coli (EPEC)

• bundle-forming pili important in attachment

• type III secretion system injects proteins into host to manipulate cytoskeleton

how does EPEC infect cells

via:

• Tir = translocated intimin receptor

• intimin - mediates intimate attachment to epithelial cells

how does EPEC » diarrhoea

• E.coli causes ‘attaching and effacing lesion ‘(specific type of damage to intestinal lining)

• leads to watery diarrhoea

outline enterotoxigenic E.coli (ETEC)

• attach via adhesive pili

• produce heat stable (ST) and labile (LT) enterotoxins that cause diarrhoea

  • enterotoxins are cholera-like

• common cause of travellers diarrhoea/ Delhi belly

  • no blood in diarrhoea

outline enterohemorrhagic E.coli (EHEC/ STEC)

• attachment similar to EPEC (bundle-forming pili)

• produces Shiga-toxin (STx)

• EHEC infections also cause hemorrhagic colitis and HUS

what is Shiga toxin

• a potent diarrhoeal toxin (causes diarrhoea)

• acts via damaging blood vessel (endothelial) cells directly

what is haemorrhagic colitis

• clinical syndrome characterised by bloody diarrhoea

• destruction of mucosa » bleeding » spread to kidneys

  • spread to kidneys can lead to haemolytic urinary syndrome (HUS)

what proportion of HUS leads to kidney failure

• 15% of HUS cases lead to kidney failure

what is Shigella and list some species

• bacteria that causes intestinal infection » diarrhoea

  • Shigella dysenteriae » bloody stools

  • Shigella sonnei (milder form)

  • Shigella flexneri (milder form)

how can Shigella sonnei and flexneri be differentiated in a lab

where is Shigella commonly found in and how is it spread

• more common in poorer countries with poor water quality

• spread faecal-orally often via water contamination

outline Salmonella

• historically most common food-associated pathogen in UK

  • former no.1 cause in UK

• spread from food (mainly chicken and dairy) but also person to person

• usually a severe but self-limiting diarrhoea and enterocolitis

how does Salmonella cause the characteristic symptoms of food poisoning

• invade M-cells then spread to surrounding epithelium

  • M-cells = specialised intestinal epithelial cells

Salmonella enterica causes…

causes uncomplicated diarrhoea

name other Salmonella spp.

• S.typhimurium

• S.enteritidis

what is the appearance of Salmonella on MacConkey agar

what is the appearance of Salmonella on Hektoen enteric agar

• blue-green colonies with a black centre/ completely black due to hydrogen sulfide production

which bacteria causes typhoid (enteric) fever

Salmonella typhi

outline how a typhoid fever infection starts and spreads

• infection initiates in the intestine

• spreads systemically - transported in macrophages around body

• seeds many organs before further spread

what symptoms does typhoid fever cause

• causes increasing fever over 14 days » GI symptoms

  • GI lesions and haemorrhage

  • toxicaemia (endocarditis)

  • meningitis

what is the mortality rate of typhoid fever and what proportion of people become carriers

• pre-antibiotics: 12-16% bacteria died

• estimated 11-20 million people get sick from typhoid

• 128,000-161,000 people die from it every year with increasing resistance

• 1-3% become carriers (gall-bladder » carriage » transmission)

how can typhoid fever be prevented

Vi antigen vaccine (recommended for travel)

what is the no.1 cause of food poisoning in the UK

Campylobacter spp.

• Campylobacter jejuni most common

what kind of bacterium is Campylobacter spp.

• Gram-negative

• micro-aerophile: requires environments containing lower levels of dioxygen than those present in the atmosphere

how is Campylobacter spp. acquired

• acquired by ingestion of contaminated food

• major reservoir in chickens (>75% of all we buy are colonised)

what are symptoms of a Campylobacter infection

• similar to shigellosis and samonellosis

  • ulceration of jejunum

  • diarrhoea (up to 10 movements a day)

what are complications of a Campylobacter infection

• Guillame-Barre syndrome

• reactive arthritis

what is unique about Campylobacter

longer lasting illness - up to 3 weeks

what is the most significant historical GI bug

Vibrio cholerae (causes cholera)

• cause of 8 recorded worldwide pandemics since 1817

outline Vibrio cholerae

• Gram-negative

• motile

• comma shaped bacterium

what areas are most affected by cholera

• mainly developing countries

  • estimated 1.3-4 million cholera cases per yr

  • 21,000-140,000 deaths due to cholera per yr

diagram showing how V.cholerae affects the body

why is there a possible marine invertebrate reservoir of V.cholerae

because V.cholerae can survive in fresh and sea water

is the infectious dose of V.cholerae small or large

large (>10⁸)

what are the effects of cholera caused bys

the cholera toxin

what is the most important cholera serotype

O1

what is the normal net flow of water

normal net flow of water is from lumen » tissue

how does the net flow of water change when the cholera toxin is present

what does the rapid fluid loss due to the cholera toxin result in

• loss of 1-2L of fluid per hr in full-blown cases

• rapid fluid and electrolyte replacement required or dehydration + death

what are signs and symptoms of cholera infection

• characteristic rice-water stool

• no tissue damage - all symptoms due to massive fluid loss

• extreme dehydration

how can cholera infection be prevented

• several vaccines now available but only temporary immunity was gained

  • WHO uses Shanchol^TM vaccines currently with 6m-2y of protection

• best prevention method: improvement of water system and sanitation

  • hard to get aid for this esp. in war-torn/ poor health coverage regions

what is one cause of community acquired C.diff infection (CDI)

• prescription of antibiotics leading to off-target consequences

what is another cause of GI infections

of the 3m infants that die from gastroenteritis 20% are viral sources (major problem in developing countries)

• children may have 60 days of diarrhoea per yr

  • major effect on growth and nutrition

• very hard to identify non-bacterial cases

how are viruses that cause GI infections spread

• mainly oral-faecal

which viruses cause GI infections

• rotaviruses

• winter vomiting virus (norovirus)

outline rotaviruses

• wheel-like viral particle

• diarrhoea caused by tissue damage in small intestine

  • main risk: dehydration

• very low infectious dose

• very contagious

• very resistant to cleaning products

outline winter vomiting virus

• norovirus

• common in hospital settings - hard to clean away

what are symptoms of norovirus

• chills

• headache

• fever

• nausea

• vomiting

after how long do you recover from norovirus

recovery in 24-48h