L7 GIT Infections Flashcards
What is the normal human flora?
Microbiome on the human body where organisms naturally exist
Where is there an increased human microbiome?
Moist, protected areas of skin e.g. armpits, groin and between toes
Microbial cells: human cells
10:1
Commensal flora of gut (bacteria type)
More obligate anaerobic bacteria (e.g. bacteroides) than facultative anaerobic bacteria (e.g. E. coli) by 100:1
What are the beneficial effects of gut commensal flora?
Metabolism
Colonisation resistance
Antibody induction
Why does diet effect the composition of gut flora?
Bottle-fed babies develop adult microflora
Breast-fed babies develop ‘Bifidobacteria’ = probiotics that help to perform essential functions such as digestion
Most common gut commensal flora
Bacteroides
Prevotella
Obligate anaerobes
Clostrodia
Bifidobacteria
Facultative anaerobes
Enterobacteriacea
Enterococci
Bacterial gastroenteritis (enterotoxin production)
Vibrio cholerae E. Coli Shigella dysenteriae C. perfingens S. aureus B. cereus C. difficile
Bacterial gastroenteritis (adherence)
Shigella sonnei
E. coli
Campylobacter jejuni
Salmonella
Cholera cause
Vibrio Cholerae
Symptoms of cholera
Diarrhoea and vomiting
Transmission of cholera
Faecal-oral route (toxin mediated)
Management of cholera
Oral vaccine
Oral rehydration solution
What does salmonella enterica cause?
Food poisoning
Typhoid
Paratyphoid
Serovars of salmonella enterica
2500 serovars
Salmonella Newport is most common
Salmonella enterica cause
Contaminated foodstuff e.g. poultry
Mechanism of salmonella enterica
Type three secretion systems
Gastroentiritis treatment
Supportive management
Avoid antibiotics
May worsen E.coli HUS
Pathotypes of E.coli
8 pathotypes
E. coli O157
Cattle was a major source
Toxin causes premature destruction of RBC (clog kidneys) causing haemolytic-uremic syndrome (HUS)
E.coli mechanism
Toxin activates G protein
Increase cAMP
Activates ion channels (increase chloride excretion)
Water follows out of cell
Different toxins have different mechanisms
Common cause of C. difficile
From nosocomial infections
Symptoms of C. difficile
Diarrhoea
Toxic megacolon
Pseudomembranous colitis (inflammation of large intestine)
C. difficile mechanism
Toxin A: active component with toxic effects (increasing production of cAMP)
Toxin B: facilitate binding to certain receptor
Binary toxin
C. difficile: Overview of intracellular modification by TcdA and TcdB
Both act intracellularly as glycosyltransferases
Each toxin modifies small GTPases
Effects of modification = actin condensation/ transcriptional activation/ apoptosis
Exposure of TcdA = neutrophil infiltration, substance P production, chemokine production, reactive oxygen intermediate production, disruption of tight junctions and apoptosis
Exposure of TcdB leads to disruption of tight junctions and apoptosis
Combination of one or more of these activities leads to fluid accumulation in the host and inflammatory responses
Campylobacter complications
Reactive arthritis, Guillian-Barre syndrome, and BS
Campylobacter causes
Raw or undercooked meat
Unpasteurised milk
Untreated water
Outbreak of campylobacter
Clustering of cases due to common source e.g. recreational water/ food and water sources