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salmonella - diseases
typhoid fever
salmonella gastroenteritis
asymptomatic carrier
typhoid fever - causative agents
Salmonella typhi, Salmonella paratyphi
typhoid fever - infection location
terminal small intestine of human host
typhoid fever - pathogenesis
adhere to microvilli → transcytosis (transported across membrane in vesicle) → enter M cells (specialized epithelial cells in gut) → release into basolateral side → engulfed by macrophages but escape killling - no phagolysosome fusion → enter bloodstream → bacteremia — spread
typhoid fever - symptoms and complications
hepatosplenomegaly
rose spots
step-ladder fever
peyer’s patch ulceration → bowel perforation
cholecystitis (gall bladder inflam)
salmonella gastroenteritis - causative agents
Salmonella typhimurium, Salmonella enteritidis
salmonella gastroenteritis - host
animal - poultry, pig, rate, cattle, turtle
salmonella gastroenteritis - presentations
diarrhea
no hepatosplenomegaly
uncommon bacteremia and invasion (immunocompromised)
rare invasion: osteomyelitis (painful bone infection) → sickle cell anemia
salmonella asymptomatic carrier - risk factor
gallstones
Salmonella - agar and tests
XLD agar: H2S production (black colony)
produce gas from glucose
typhoid fever - test
punch biopsy
→ remove a cylindrical piece of skin using sharp instrument called punch → examination & diagnosis
Shigella - disease
shigellosis (bacillary dysentery)
shigellosis (bacillary dysentery) - symptoms
mucus bloody diarrhea
mucosal ulcerations
tenesmus (persistent painful sensation that you need poo or pee even tho empty bowel)
uncommon bacteremia
shigellosis (bacillary dysentery) - most severe causative agent
Shigella dysenteriae because also produce shiga toxin → HUS (hemolytic uremic syndrome) (like EHEC)
shigellosis (bacillary dysentery) - spread
spread by actin polymerization (like EIEC)
Shigella - virulence factor
survive low pH
Shigella - agar and tests
XLD agar: no H2S (not black)
produce acid (not gas) from glucose
WBC, RBC present in stool
lactose-fermenting aerobic gram-negative bacilli - common traits
all oxidase negative
pink on MacConkey agar
Escherichia coli - normal flora
GI
Escherichia coli - groups
commensal: detect feces contamination
extra-intestinal pathogenic (ExPEC)
intestinal pathogenic
extra-intestinal pathogenic E. coli - diseases
cystitis (inflam of urinary bladder), peritonitis (peritoneum infam)
cystitis
*urgency, frequent, dysuria
peritonitis
ascites (ท้องโต), esophageal varices (swollen enlarged veins in esophagus)
enterotoxigenic (ETEC) - diarrhea
watery secretory diarrhea
enterotoxigenic (ETEC) - disease
traveler’s diarrhea
enterotoxigenic (ETEC) - transmission
contaminated food and water
enterotoxigenic (ETEC) - toxins and effect
heat-labile (AB5): A subunit increases adenylate cyclase → increases cAMP
heat-stable toxin: small peptide increases guanylate cyclase → increases cGMP
both opens CFTR channels = chloride, sodium, water into lumen
→ water follows into lumen via osmosis → excess water in lumen → secretory diarrhea
enteropathogenic (EPEC) - diarrhea
watery osmotic diarrhea
enteropathogenic (EPEC) - symptoms
attaching and effacing lesions
enteropathogenic (EPEC) - pathogenesis
bundle-forming pilus (Type III secretion system) inject Tir (translocated intimin receptor) into host → binds to intimin → polymerize actin → decreases size of microvilli → attaching & effacing lesions (bacteria stick to the intestine and erase the tiny villi) → decreased absorption, increased lumen osmotic pressure = water is pulled into lumen → watery osmotic diarrhea
enteroinvasive (EIEC) - diarrhea
mucus bloody diarrhea
enteroinvasive (EIEC) - disease
dysentery (ปวดบิด)
enteroinvasive (EIEC) - pathogenesis
EIEC directly invades colon epithelium (host cell) → contained in phagosome & replicates itself → WBC try to kill → EIEC lyse and escape phagosome → move to adjacent cell → cell death → ulcer
enteroinvasive (EIEC) - symptoms
colonic ulceration, fever, tenesmus (feel like need to poo)
enterohemorrhagic (EHEC) - diarrhea
bloody diarrhea
enterohemorrhagic (EHEC) - spread from
undercooked beef, veggies (sprouts), unpasteurized milk
enterohemorrhagic (EHEC) - test
sorbital MacConkey agar (SMAC) - colourless
enterohemorrhagic (EHEC) - toxin
shiga toxin (Stx)
B subunit bind to Gb3 on endothelial, glomerulus → *hemorrhagic colitis
A subunit disrupt protein synthesis of endothelia → blood vessel broken → clotting → RBC squish → hemolysis
enterohemorrhagic (EHEC) - disease
hemolytic uremic syndrome (HUS) *thrombocytopenia → hemolytic anemia → AKI (acute kidney injury)
Enterobacterales - common characteristics
facultative anaerobes that ferment glucose except Campylobacter and Helicobacter
oxidase-negative - except Campylobacter, Helicobacter, Plesiomonas
catalase +
Enterobacterales - common virulence factors
somatic O polysaccharides
capsular K antigen
flagella H protein
Klebsiella pneumoniae - normal flora
intestine
Klebsiella pneumoniae - drugs
multidrug resistance
Klebsiella pneumoniae - diseases
pneumonia in alcoholic/diabetic, from aspiration *lobar consolidation
UTI
intraabdominal infections
liver abscess
Campylobacter jejuni & Helicobacter pylori - common characteristic
microaerophilic (thrives in low O2 environments)
Campylobacter jejuni - characteristics & morphology
curved spiral rod (seagull wing)
motile
oxidase +
Campylobacter jejuni - reservoir
environment
Campylobacter jejuni - diseases
gastroenteritis: *profuse watery diarrhea → dysentery (mucus bloody diarrhea)
guillain-barre syndrome: acute inflammatory demyelinating polyneuropathy (damage/disease of many peripheral nerves)
C. jejuni gastroenteritis - pathogenesis
release IL-18 to attract neutrophil
cytolethal distending toxin (CDT) → provides strong inflam response
C. jejuni Guillain-Barre syndrome - pathogenesis
cross-reacting lipooligosaccharide on C. jejuni with epitopes on myelin sheath
C. jejuni Guillain-Barre syndrome - symptoms
symmetrical muscle weakness starting from lower body
Helicobacter pylori - characteristics & morphology
spiral bacilli with polar flagella
most common bacteria
carcinogen
Helicobacter pylori - diseases
peptic ulcer, gastric adenocarcinoma
Helicobacter pylori - virulence factors
urease
mucinase
urease
urea → NH3 → increase pH → can survive in acidic stomach
Helicobacter pylori - diagnosis
stool antigen test
carbon urea breath test
biopsy → rapid urease test positive (red, pink)
gastric adenocarcinoma from Helicobacter pylori - pathogenesis
host cell mutate from free radical → progress from chronic atrophic gastritis
Vibrionaceae - common characteristics
curved rod/comma
polar flagella
oxidase +
non-lactose fermenting
halophile
TCBS agar
water-borne (seafood)
Vibrio cholerae - differentiating method
only vibrio that can grow without salt
TCBS agar: yellow
Vibrio cholerae - virulence factors
toxin-coregulated Pili A (TcpA)
cholera toxin (AB5)
toxin-coregulated Pili A (TcpA)
attach to enterocyte
cholera toxin (AB5)
increase adenylate cyclase → increase cAMP → increase CFTR
Vibrio cholerae - disease
cholera
cholera
watery secretory diarrhea (rice water)
dehydration
electrolyte imbalance
hypovolemic shock
cholera - treatment
rehydrate (oral rehydration salt), oral antibiotic
Vibrio parahaemolyticus - characteristics
halophile
TCBS agar: green
Vibrio parahaemolyticus - disease
watery diarrhea, mucus-bloody stool
Vibrio vulnificus - characteristics
TCBS agar: green
Vibrio vulnificus - infects what group
liver disease because decreased iron binding protein = increased free iron
Vibrio vulnificus - virulence factors
siderophore: acquire host iron
Vibrio vulnificus - diseases
skin, wound infection: hemorrhagic bleb
no diarrhea
difference between watery secretory & watery osmotic diarrhea
Secretory diarrhea = ion channel–mediated secretion → watery stool that continues during fasting (low osmotic gap).
Osmotic diarrhea = unabsorbed solutes → watery stool that stops with fasting (high osmotic gap).