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Enterobacteriaceae and Gut Diseases
Description
Microbiology Mind Map on Enterobacteriaceae and Gut Diseases, created by maisie_oj on 15/04/2013.
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microbiology
microbiology
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Resource summary
Enterobacteriaceae and Gut Diseases
Enterobacteriaceae
Small, Gram -ve rods (2-5 by 0.5 um)
Inner membrane - phospholipid bilayer
Solid membrane - murein layer, muopeptide, peptidoglycan
Outer membrane - lipopolysaccharide, lipoprotein (and O antigen repeat side chains)
LPS is involved in shock, fever, hypoglycaemia, DIC, thrombosis, vascular permeability, hypotension and decreased iron levels
Mostly motile with peritrichious flagella (except Shigella and Klebsiella)
Oxidase negative facultative anaerobes
Reduce nitrate and ferment glucose (and other carbohydrates)
Some strains are opportunistic pathogens, some are true pathogens (Salmonella, Yersinia, some E. coli, Shigella)
Many genera: Escherichia, Salmonella, Shigella, Yersinia, Klebsiella, Proteus, Enterobacter etc.
Sites of infection
CNS - Escherichia
Bloodstream - Escherichia, Enterobacter, Klebsiella
Lower respiratory tract - Klebsiella, Enterobacter, Eshcerichia
Gastrointestinal - Salmonella, Escherichia, Shigella, Yersinia
Urinary tract - Proteus, Escherichia, Klebsiella, Providencia
Different genera have different antigens on their capsule
E. coli - K antigen, S. typhi - Vi antigen, K. pneumonia - serotype antigen
Exotoxins vs Endotoxins
Exotoxins
Released from the cell before or after lysis
Are proteins
Heat-labile
Antigenic and immunogenic
Toxoids can be produced
Specific effect on host
Profuced by Gram -ve and +ve bacteria
Endotoxins
Integral part of cell wall
Are LPS - lipid A is the toxic component (hydrophobic fatty acids)
Heat-stable
Antigenic
Toxoids cannot be produced
Many effects on host
Produced by Gram -ve organisms only
Bacillary Dysentry (Shigellosis)
Acute infectious disease of the intestines caused by dysentery bacilli
Symptoms
Fever
Abdominal pain
Diarrhoea
Tensmus (constant feeling of needing to defacate)
Stool mixed with mucus, blood and pus
Shock and toxic encepalopothy
Etiology
Gram -ve, short rod, non-motile
Shigella
4 groups, 47 serotypes
S. dysenteriae is the most severe
S. flexneri causes epidemics and can become chronic
S. boydii found in tropical areas
S. sonnei is the most mild
Pathogenicity
Endotoxins and interotoxins (exotoxins)
Invasiveness
Attach-penetrate-multiply
Resistance - strong
Can survive 1-2 weeks on fruit/vegetables/soil
Destroyed by heating for 30 mins at 60 'C
Transmitted via faecal-oral route
Immunity is short and unsteady - no cross-immunity
Treated with Quinolones
Features
Diffuse fibrous exudative inflammation and lesions in sigmoid and rectum with superficial ulceration
Hyperemia, oedema, leukocyte infiltration and necrosis
Shigella Infection
Bacteria enters intestine
Normal bacterial flora and sIgA prevent attachment
Bacteria penetrate mucus and multiply in epithelial cells and propria lamina
Inflammation and vessel contraction
Superficial mucosal necrosis and ulcer
Diarrhoea mixed with blood, pus and mucus with abdominal pain
Endotoxin
Endogenous pyrogen
Fever
Allergy to endotoxin
Increased dimethyl-adrenaline
Micro-circulatory failure
Shock, Disseminated Intravascular Coagulation (DIC)
Cerebral oedema/hernia
Invade neighbouring cells to form abcess and evade immune system - rarely enter blood stream
Typhoid Fever vs Salmonellosis
Salmonella
Caused by Salmonella enterica
Treatment involves oral rehydration
Causes nausea and diarrhoea
Infection
Bacteria enters intestinal epithelial cell
Multiplies within vesicle of cell
Multiplication in mucosal cells results in inflammatory response
Diarrhoea
Bacteria can cross epithelial membrane to enter lymphatics and blood stream
Typhoid fever
Caused by Salmonella typhi
Bacteria spread throughout body in phagocytes
1-3% of patients become chronic carriers
Treated with Quinolones and Cephalosporins
Causes high fever and high mortality
Both involve infection and endotoxins
Both diagnosed by isolation and serotyping
Vibrios
Cholera
Vibrio cholera serotypes that produce cholera toxin (O:1 and O:139)
Toxins cause cells to release Cl-, HCO- and water
Exotoxins
Causes diarrhoea and severe water loss
Treated with doxycycline and rehydration
Non-cholera Vibrios
Usually come from contaminated crustaceans or mollusks
Include V. cholera subtypes (not including O:1 or O:139), V. parahaemolyticus and V. vulnificus
Causes cholera-like diarrhoea but milder (V. parahaemolyticus) and rapidly spreading tissue destruction (V. vulnificus)
Caused by infection, enterotoxin (V. parahaemolyticus)/siderophores (V. vulnificus)
Treated with antibiotics (and rehydration for V. parahaemolyticus)
Campylobacter
Campylobacter jejuni
Causes fever, abdominal pain and diarrhoea
Caused by infection
Found in chicken and cows' milk
Helicobacter
Helicobacter pylori
Ammonia from bacterial activity neutralises stomach HCl
Causes more HCl production
Leads to peptic ulcers
Diagnosis by urea test and and bacterial culture
Caused by infection
Treatment with antibacterials
Yersinia
Y. enterolytica/ Y. pseudotuberculosis
Symptoms
Diarrhoea
Abdominal pain (usually mild)
May be confused with appendicitis
Caused by infection and endotoxins
Found in meat and milk
Diagnosed with bacterial culture and serotyping
Clostridium vs Bascillus
B. cereus
Causes nausea, vomiting and diarrhoea
Caused by intoxication
Diagnosed by bacterial isolation
Found in reheated rice
C. difficile/C. perfringens
Caused by infection and exotoxin
Cause diarrhoea (to colitis for C. difficile)
Diagnosed by bacterial isolation/cytotoxin assay (for C. difficile)
C. perfringens found in meat
C. difficile caused by elimination of normal flora
C. difficile treated with metronidazole
Escherichia coli
Bacteria attach to intestinal cells via fimbrae
Produces toxins
Cells may aggregate
Entertoxigenic, Enteroinvasive, Enteraggregative
Cause Traveller's Diarrhoea
Shiga-toxin producing (STEC)
Causes Shigella'like dysentery, hemorrhagic colitis and haemolyitic uremic syndrom
Detected by bacterial isolation
STEC treated with Quinolones and Cephalosporins (other treated with rehydration)
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