Characteristics of C.jejuni?
• curved, rod-shaped, non-spore forming
Guillain-Barre syndrome ?
• an acute demylinating neuropathy
• associated with C.jejuni
Enteritis caused by C.jejuni?
• LOWER abdominal pain --> may mimic appendicitis
• diarrhea, fever, malaise, dysentery
• usually self-limiting --> respond to antibiotics too
DOC for C.jejuni infection?
• susceptible to --> macrolides, fluoroquinolones
C.jejuni - microaerophilic?
Yes, it's best with 5-10% O2
Energy for C.jejuni?
Don't breakdown carbohydrates --> use Amino acid and metabolic intermediates
Metabolism of C.jejuni?
• oxidase +ve
• catalse +ve
• reduce nitrate
Infective dose for C.jejuni?
Low infective dose
Colonisation of C.jejuni
it naturally colonise GIT of birds --> animal reservoirs
How human get infected with C.jejuni?
eat contaminated food --> undercooked poultry + unpasteurised milk
C.jejuni grows best at temperature?
42°C (normal avian temperature) --> on selective "CAMP" agar
What is "selective Skirrow's medium"?
blood agar infused with a cocktail of antibiotics (vancomycin, polymixin-B and trimethoprim) --> under microaerophilic conditions at 42°C
Characteristics of Vibrio cholerae?
• gram -ve, comma-shaped, polar flagellum
• higly motile, non-spore forming, oxidase +ve
• in seawater
2 major biotypes of V.cholerae ?
dentified by hemaggluttination testing:
• classical --> only in Bangladesh
• El Tor --> worldwide
Vibrio cholerae grows best in?
alkaline environment --> hate acids
Types of vibrioe?
• V.cholera --> extremely watery diarrhoea (rice water stool)
• V.parahaemolyticus --> in undercooked SEAFOOD
• V.vulnificus --> sepsis and wound infection + linked to RAW OYSTERS and IRON overload
Serotypes of V.cholerae that cause diarrhoea?
O1 and O139
Cholera toxin (CT) ?
• an AB-type ADP-ribosylating toxin --> released from V.cholerae
• a pentameric = 1 A subunit (enzymatic) + 5 B subunit (receptor binding) --> these 2 parts connected by a disulfide bond
What part (B) of cholera toxin does?
binds to "GM1 gangliosides" on surface of intestinal epithelium
What part (A) of cholera toxin does?
detaches upon binding --> get inside into intestinal cells (via "receptor-mediated endocytosis") --> cause diarrhoea
What happens to part (A) of cholera toxin once it's inside cell?
(A) permanently ribosylates "Gs α subunit" of G protein --> cAMP production --> secretion of H2O, Na+, K+, Cl-, and HCO3- into lumen of small intestine --> rapid dehydration and other factors associated with cholera
Incubation period for v.cholerae?
How does human get infected with V.cholerae?
because of untreated water supply
infective dose for V.cholerae?
it needs large doses to multiply and colonise (in small intestine)
K+ and HCO3- losses caused by V.cholerae?
will cause hypokalemia and acidosis
Rice water stools by V.cholerae?
• has mucous flecks
Diagnosis for V.cholerae?
stool culture --> use "selective media" (MacConkey or blood agar"
V.cholerae is best isolated on?
TCBS agar (thosulfate-citrate-bile salt-sucrose) --> green to yellow
Characteristics of Helicobacter pylori?
• Gram -ve, microaerophilic
• helix-shaped (curved rod, not spirochaete)
• polar flagella, slow grower (3-5 days)
• makes oxidase, catalase, and urease
Why H.pylori contains hydrogenase ?
to oxidise molecular hydrogen (H2) produced by intestinal bacteria --> for its energy
Survival factors for H.pylori?
capable of forming biofilms + can convert from spiral to a possibly viable but nonculturable coccoid form
5 outer membrane proteins (OMP) families of H.pylori?
• adhesins --> helps its adhesion to host cells
• porins --> act as a pore through which H.pylori can diffuse
• iron transporters
• flagellum-associated proteins
• some proteins of unknown function
outer membrane of H.pylori consists of?
• phsopholipids, LPS
• O antigen of LPS --> may be fucosylated and mimic Lewis blood group antigens found on gastric epithelium
• cholesterol glucosides (also found in few other bacteria)
Why H.pylori is highly motile?
has 4-6 lophotrichous flagella (sheathed) --> composed of 2 copolymerized flagellins, FlaA and FlaB
"cagA genes" of H.pylori?
ability to cause ulcers
"cag pathogenicity island (PAI)" of H.pylori?
has about 30 genes --> code for a complex "type IV secretion system" --> to inject peptidoglycan --> stimulates expression of cytokines --> promote inflammation
Habitat for H.pylori?
can inhabit various areas of stomach (esp. antrum)
How H.pylori colonises acidic stomach?
• burrow into mucus --> reach its niche (close to stomach's epithelial cell layer)
• use its flagella to move through stomach lumen --> drills into mucoid lining of stomach
Why H.pylori makes adhesins?
bind to membrane-associated lipids and carbohydrates --> help it adhere to epithelial cells.
"adhesin BabA" of H.pylori?
binds to Lewis b antigen displayed on surface of stomach epithelial cells
"Urease" of H.pylori?
• localised inside and outside of H.pylori
• to break down UREA (normally secreted into stomach) --> to CO2 + NH3 (ammonia)
• NH3 converted to NH+4 (ammonium) --> by taking H+ from water --> leaves hydroxyl ion, OH-
• OH- react with CO2 --> make bicarbonate --> neutralizes gastric acid
• survival of H. pylori in acidic stomach --> dependent on urease.
How H.pylori damages host cells?
• Urease, proteases
• vacuolating cytotoxin A (VacA) --> cause apoptosis in host cells
• certain phospholipases
Location of H.pylori in people producing too much acid?
It will colonise antrum (avoid the too much acid stomach body)
Location of H.pylori in people producing normal or reduce acid?
can also colonise the body of stomach
How H.pylori can cause cancer?
• enhanced production of free radicals near H. pylori + increased rate of host cell mutation
• enhancement of transformed host cell phenotype --> alterations in cell proteins
• induces inflammation and locally high levels of TNF-α and/or interleukin 6 (IL-6) --> alter gastric epithelial cell adhesion --> lead to migration of mutated epithelial cells
Diagnosis for H.pylori?
• checking for dyspeptic symptoms
• noninvasive test -->blood antibody test, stool antigen test, or carbon urea breath test ( patient drinks 14C- or 13C-labelled urea, which bacterium metabolizes, producing labelled CO2 that can be detected in breath)
• urine ELISA test = 96% sensitivity + 79% specificity.
Most reliable diagnosis for H.pylori?
biopsy check during endoscopy + a rapid urease test + histological examination + microbial culture
symptoms caused by H.pylori?
• UPPER abdominal pain (up to 2 weeks)
• years later --> gastritis + peptic ulcer
• perforation --> cause extensive bleeding + peritonitis (due to leakage of gastric contents into peritoneal cavity)
Treatment for H.pylori infection?
• Bismuth salts --> to coat stomach + antimicrobial
• metronidazole, tetracycline, clarithromycin, amoxcillin