Enteric Pathogens II Flashcards
general properties of enterobacterials (enterobacteriaceae)
*gram NEG rods
*facultative anaerobes
*OXIDASE NEGATIVE
*CATALASE POSITIVE
oxidase status of enterobacteriaceae
oxidase NEGATIVE
catalase status of enterobacteriaceae
catalase POSITIVE
common virulence factors associated with enterobacteriaceae
-endotoxin (LPS/lipid A)
-capsule
-T3SS
-sequester iron
-resistance to serum killing
-antimicrobial resistance
-antigenic phase variation
what are the lactose POSITIVE enterobacteriaceae (ferment lactose)
-klebsiella
-enterobacter
-E. coli
what are the lactose NEGATIVE enterobacteriaceae (do NOT ferment lactose)
-salmonella
-shigella
E. coli - physiology, structure, virulence
*gram neg, facultative anaerobic rods
*oxidase NEG
*lactose fermenter (pink on Mac agar)
*LPS with outer O polysaccharide and lipid A
E. coli - epidemiology
*most common aerobic, gram negative rods in the GI tract
*most extra-intestinal infections (UTI, pneumonia) are ENDOgenous
*most strains causing gastroenteritis are EXOgenous
uropathogenic E. coli (UPEC)
*causes > 80% of UTIs
*adherence virulence factor:
-P fimbriae binds to Gal-Gal
-SFA on S fimbriae
-AFA
variety of diarrheagenic E. coli
-enterotoxigenic (ETEC)
-enteropathogenic (EPEC)
-enteroinvasive (EIEC)
-enteroaggregative (EAEC)
-enterohemorrhagic (EHEC) / shiga toxin producing (STEC)
enterotoxigenic E. coli (ETEC)
*most common cause of TRAVELER’S DIARRHEA worldwide
*s/s:
-profuse watery diarrhea
-abdominal cramps
-nausea
-low grade fever
-lasts 3-5 days
ETEC pathophysiology
*adhesins adhere to intestine (does not invade)
-colonization factor antigens (CFA/1, CFA/II, CFA/III)**
*toxins enhance intestinal secretion of chloride and decreased absorption
-heat labile toxin (LT-I and LT-II)**
-heat stable toxin (STa and STb)**
enteroaggregative E. coli (EAEC) pathophysiology
*adhesins: aggregative adherence fimbria (AAF/I, AAF/II, AAF/III)
toxins: SHET-1 (enteroaggregative heat stable toxin)
*forms biofilms on intestine
*“stack of bricks”
enteropathogenic E. coli (EPEC)
attaching and effacing:
-bundle forming pili (BFP) & intimin “ruffle” the cell wall causing leakage
enterohemorrhagic E. coli (EHEC) / shiga toxin producing (STEC)
*capable of producing Shiga toxin (a cytotoxic exotoxin)
*attaching and effacing
*BLOODY DIARRHEA
*NO fever
-associated with hemolytic uremic syndrome (HUS)
*serotype O157:H7
enteroinvasive E. coli
*closely related to Shigella
*causes diseases similar to shigellosis
*watery diarrhea; may or not progress to bloody diarrhea
*FEVER
salmonella infections
*gastroenteritis
*enteric fever
*bacteremia & endovascular infection
*sickle cell + osteomyelitis = salmonella
*ASYMPTOMATIC CHRONIC CARRIER STATE (typhoid Mary)
salmonella pathogenesis
*enters through GI tract
*attaches to mucosa and invades M cells in Peyer patches
*pathogenicity island I - T3SS & Ssps (salmonella-secreted invasion proteins)
*pathogenicity island II - block lysosome movement & another T3SS
salmonella exposure
*food/water: poultry, eggs, milk
*pets: turtles, snakes, lizard
salmonella - gastroenteritis
*watery diarrhea
*fever, abdominal cramps
*resolves over 3-10 dyas
*chronic carriers 4-5 weeks
salmonella - enteric fever
*typhoid fever (Salmonella typhi)
*systemic illness:
-fever
-headache
-ROSE SPOTS
-constipation > diarrhea
shigella - infectious dose
VERY LOW ID50 (don’t need a lot of organisms to cause infection)
shigella dysenteriae 1 (Sd1) - important features
*illness due to Sd1 is the most severe
*resistance to antimicrobials
*produce Shiga toxin!
shigella s/s
*biphasic illness (sick, better, sick again)
*cramps
*voluminous watery diarrhea, then dysentery
*treat ALL patients
shigella pathogenesis
*entry via M cells in Peyer patches
*T3SS secretes proteins and induce membrane ruffling
*escape to cytoplasm, following lysis of vacuole membrane
*multiplies in the cell
*uses actin for locomotion (push it from behind)
complications of shigella
*reactive arthritis
*“sausage digit” or monoarticular arthritis
*HLA-B27 genetic predisposition for more severe disease
yersinia - common characteristic
use T3SS to resist phagocytic killing
yersinia pestis - 2 forms of infection
*plague-causing
1) urban plague (rats = reservoir)
2) sylvatic plague (squirrels, rabbits, etc = reservoir)
yersinia pestis - bubonic plague presentation
*typical presentation
-high fever
-painful bubo (inflammatory swelling of lymph nodes)
-bacteriema
yersinia pestis - pneumonic plague
-high fever and malaise
*pulmonary signs develop quickly
*worse than bubonic
yersinia pestis - morphology
gram neg organism w/ SAFETY PIN appearance
klebsiella pneumoniae
*prominent capsule
*“Currant Jelly” sputum (necrotic destruction of alveolar spaces)
*also causes UTI’s or wound infections
klebsiella granulomatis
*cause of donovanosis (granuloma inguinale)
*ulceroglandular STI
KPC = Klebsiella pneumoniae carbapenamase
*most significant antimicrobial resistance mechanism in the US currently
*resistance to our most powerful, broad-spectrum antibiotics
proteus mirabilis
*produces a lot of UREASE
*urease raises pH and causes “staghorn calculi”
*mostly infects the urinary tract (causes STRUVITE stones)
listeria monocytogenes
*gram POSITIVE COCCOBACILLI
*contaminated food products (raw milk and cheese, processed meats
*CAN spread transplacentally from mother to neonate
*NOT enterobacterialis
listeria monocytogenes - virulence factors
*cell attachment factors = internalins
*hemolysins = listeriolysin O & 2 phospholipase C enzymes
*ActA (facilitates actin-directed motility)
listeria monocytogenes & at risk populations
*always draw blood cultures on a pregnant woman (3rd trimester) presenting with fever
*can cause meningitis in babies & older adults
listeria monocytogenes diagnosis
*lots of lymphocytes in CSF
listeria monocytogenes treatment
*penicillin/ampicillin
*TMP/SMX in penicillin allergies
