Bacterial and Viral Infections of the GI Tract Flashcards
How does our GI tract help prevent infection?
Barriers:
- strong stomach acid that kills bacteria
- peristaltic mechanisms to stop bacteria from sitting in one part of the GI tract for a long period of time
- gut flora which has a symbiotic relationship with us and fights off pathogenic mechanisms by out-competing them
What is intoxication?
ingestion of food containing biologically active toxins which cause disease
What is infection
ingestion of live microbes:
- can multiply readily on food prior to consumption
- use food only as a vector
What are some methods of transmission of infection?
- faecal-oral
- food
- fluids
- fingers
- person-person
What are some personal and public health measures to prevent GI infection?
Personal:
- hand hygiene
- cook foods properly
- avoid cross contamination
- wash it, peel it, cook it or forget it
Public health:
- pasteurisation of milk and dairy products
- proper sewage disposal
- provision of safe, clean drinking water
- vaccination
What are some viruses that cause GI infection?
- norovirus
- adenovirus
- rotavirus
(causes most infections)
What is the clinical presentation of norovirus and the population affected?
- projectile vomiting
- diarrhoea
- abdominal cramps
- headache
- muscle ache
(infectious period from onset till 48hrs after symptoms stop) - can affect anyone (young-adults, sick-healthy)
What is the clinical presentation of rotavirus and the population affected?
- watery diarrhoea
- vomiting
- abdominal cramps
- fever
- mainly affects young children, elderly and immunocompromised
- there is access to live attenuated vaccine
What is the clinical presentation of adenovirus and the population affected?
- mild prolonged diarrhoea
* affects mainly young children, elderly and immunocompromised
What is the level of immunity after GI infection caused by these viruses?
- norovirus immunity only lasts a year after infection
- adenovirus and rotavirus have lifelong immunity after infection
What are the gram-negative bacteria that can cause infection in the GI tract?
- campylobacter
- vibrio cholerae
- salmonella
- shigella
- E.coli
- yersinia enterocolitica
How is campylobacter spread, its pathogenesis and clinical presentation?
Transmission:
- animals
- contaminated food
Pathogenesis:
- invasion of bowel leading to inflammation and ulceration
Presentation:
- bloody diarrhoea
- abdominal pain
- fever
What is the transmission, pathogenesis and clinical presentation of vibrio cholerae?
Transmission:
- contaminated food or water
Pathogenesis:
- polar flagella with mucinase facilitate penetration of intestinal mucus
- disease caused by exotoxin
Symptoms:
- severe, profuse watery diarrhoea
- profound fluid and electrolyte loss
- hypovolaemic shock
- cardiac failure
What is the pathogenesis and clinical presentation of salmonella?
Pathogenesis:
- invasion and inflammation of the bowel
- absorbed at terminal ileum and multiplies in Peyer’s patches
- inflammatory response mediates release of prostaglandins that stimulate cyclic AMP
Symptoms:
- watery diarrhoea
- vomiting
- fever
Give detail on the pathogenesis of the salmonella infection
- ingestion of large number of bacteria
- absorption into the terminal ileum
- bacteria multiply in Peyer’s patches
- inflammatory response mediates release of prostaglandins
- stimulates cyclic AMP
- release of fluid and electrolytes causing watery diarrhoea
What are the other forms of salmonella and its presentation?
- enteric fevers: typhoid and paratyphoid
- systemic infections in the GI tract
- malaise
- headache
- cough
- rose spot rash (significant)
- fever
- bradycardia (significant)
lethargy - constipation etc
What is the pathogenesis and clinical presentation of shigella?
Pathogenesis:
- production of shiga toxin which damages intestinal epithelium
- toxin can cause haemolytic uremic syndrome
Symptoms:
- watery followed by bloody diarrhoea
- crampy abdo pain
- fever
Why would you not want to give antibiotics to a shigella infection?
- causes a burst of the bacteria which causes a big release of the shiga toxin
- increases risk of haemolytic uremic syndrome
What is the pathogenesis and clinical presentation of ETEC?
Pathogenesis:
- heat-labile (structural and functional analogue of cholera toxin)
- heat-stable (produced in addition to or instead of LT)
Presentation:
- watery diarrhoea
- abdominal pain
- vomiting
- no associated fever
Describe the mode of action of the ETEC enterotoxins
- heat-labile toxin works in same way as cholera toxin by activating adenylate cyclase
- heat-stable toxin activates guanylase cyclase increases which acts as an on switch for secretory mechanisms
What is the pathogenesis and clinical presentation of EHEC?
Pathogenesis:
- production of shiga like toxins which target the glomerular endothelium causing haemolytic uremic syndrome
Presentation:
- bloody diarrhoea
- abdo pain
- vomiting
What is the pathogenesis and clinical presentation of yersinia enterocolitica?
Pathogenesis:
- invasion of terminal ileum with inflammation of mesenteric lymph nodes
Presentation:
- bloody diarrhoea
- abdo pain
- fever
What are the gram-positive bacteria that can cause infection in the GI tract?
- staphylococcus aureus
- clostridium botulinum
- clostridium difficile
- listeria monocytogenes
What is the pathogenesis and clinical presentation of S. aureus?
Pathogenesis:
- heat stable and acid-resistant protein toxins resulting in emetic disease
Presentation:
- profuse comiting
- abdo cramps
- no diarrhoea or fever
What is a unique feature of the adenovirus?
- only first infection symptomatic (except in the vulnerable)
- asymptomatic infection common
Describe how the cholera toxin works
- subunit B binds to receptor on surface of cells
- subunit A refolds and becomes active to promote activity of adenylate cyclase
- activates cAMP which pushes chloride ions out of the cell
- positive Na follows and water follows due to osmosis
What is haemolytic uremic syndrome?
- group of blood disorders characterised by low RBC, acute kidney failure, and low platelets
What is the pathogenesis and clinical presentation of C. botulinium?
Pathogenesis:
- produces heat powerful heat-labile protein neurotoxin
- absorbed toxins spread by bloodstream and enter peripheral nerves where they cause neuromuscular block
Symptoms:
- flaccid paralysis
- progressive muscle weakness ( can cause resp failure)
What is the pathogenesis and clinical presentation of C. difficile?
Pathogenesis:
- disruption of normal protective gut flora due to antibiotics, chemo or antacids
- release of toxins A and B
Presentation:
- mild to severe diarrhoea
- pseudomembranous colitis
- toxic colon dilation or perforation
What is the pathogenesis and clinical presentation of listeria monocytes?
Pathogenesis:
- invasive infection
Presention:
- initial flu-like illness with or without diarrhoea
- can cause severe systemic infection
- IV antibiotics needed
What is the pathogenesis and clinical presentation of helicobacter pylori?
Pathogenesis:
- cytotoxin production and range or factors to promote adhesion and colonisation
- produces urease to generate ammonia from urea and elevates pH
Presentation:
- asymptomatic unless ulceration develops
