Block III Gram (-) Bacteria part II

ptheodore's version from 2015-11-12 13:48


Question Answer
Which virulent factor of GNB contribute to pathogenesis in most infectionsLPS
Which virulent factor causes pathogen to adhere to epithelial cell in urogenital tract leading to UTI Pili
Which virulent factor allows pathogen to cross the BBB & penetrate into the brainCapsule
The Lipid A of LPS binds toTLR4/CD14
Macrophages produce pro-inflammatory cytokine which induces feverIL-6
Macrophages produce pro-inflammatory cytokine which induces inflammationIl-1 & TNF-alpha
Macrophages produce pro-inflammatory cytokine which induces septic shockExcess TNF-alpha
LipoPolySaccharide aka LPS is anendotoxin
Capsulated bacteria are strongly associated withSystemic & meningial infections
Prevents binding to C3bR (CR1), thus bacteria cannot be phagocytosedPolysaccharide capsule
E.coli O157(H7)EHEC
E.coli K1NMEC
Which E.Coli can penetrate into the brainE.coli K1
Which type of mechanism do E.coli K1 use to penetrate into the brain?Capsule
is a critical virulence factor for Gram Negative to navigate water/food intermediate and to penetrate mucus layerFlagella
Needle mechanism to directly inject effector molecules* into host cellType 3 secretion system T3SS
Gram Negative Bacilli, Lactose Fermenter, Encapsulated K-1Neonatal Meningitis E. Coli (NMEC)
Gram stain of CSF CSF --> Cloudy, PMNs, low glucose, high protein is a diagnosis forNeonatal Meningitis E. Coli (NMEC)
Drug to treat Neonatal Meningitis E. Coli (NMEC)Cefotaxime
High fever, vomiting, irritability lethargy, bulging fontanelle are clinical presentation forNeonatal Meningitis E. Coli (NMEC)
How does the baby becomes affected with Neonatal Meningitis E. Coli (NMEC)vaginal birth
A Gram Negative Bacilli, Lactose Fermenter, Reduce Nitrate to NitriteUroPathogenic E.coli UPEC
Mode of transmission of UroPathogenic E.coli UPECNormal colon flora gain access to urethra, catheters or bad hygienes
attaches to uro-epithelial cells and biofilm is formedFimbriae & Pili
Pyogenic symptoms are mediated by......... and immune response to....Hemolysin & LPS
UTI/Cystitis (90% of cases), Low grade fever, dysuria, Pyelonephritis, high fever, dysuria, low flank pain are clinical presentation ofUroPathogenic E.coli UPEC
Urinalysis (counts/nitrite) is the diagnosis test forUroPathogenic E.coli UPEC
Treatment for UroPathogenic E.coli UPECTMP-SMX/Fluoquinolones
A Gram Negative Bacilli, Lactose Non-Fermenter, Urease (+), Swarming MotilityProteus
UTI & Struvite Kidney stones are clinical presentation forProteus
Treatment for ProteusTMP-SMX/Fluoroquinolones
Urease reduces urea->ammonia, leading to alkalization->precipitation of magnesium ammonium phosphate (struvite) and calcium-> kidney stonesProteus Struvite Kidney Stones
A Gram Negative Bacilli, Lactose Fermenter, Purple Mucoid, Encapsulated Klebsiella pneumoniae
UTI/Cystitis , Pneumonia esp. D-VAP*, Meningitis are clinical presentation forKlebsiella pneumoniae
Alcoholics prone to pneumoniaKlebsiella pneumoniae
Treatment for Klebsiella pneumoniaCarbepenem-Resistance (CRKP)
What is the major virulence factor for Klebsiella pneumonia?Capsule
Purple-pink mucoid-colonies on MacConkey due to sugar glycocalyxKlebsiella pneumoniae
Alcoholics and homeless patients, Usually aspiration-associated, “Current grape jelly” purple viscous sputum are clinical presentation forKlebsiella pneumonia
Nosocomial Ventilator-Associated Pneumonia VAP, Delayed* presentation (~5-7 days after ventilator) are clinical presentation forKlebsiella pneumonia
What virulence for do all GNB have in common & can lead to septic shock?LPS
A Gram Negative Bacilli, Lactose Fermenter, Red prodigiosin-pigmentSerratia marcescens
UTI, Pneumonia, Sepsis->Meningitis, Osteomyelitis esp. Chronic Granulomatous Disease in infancy are clinical presentation for Serratia marcescens
Treatment for Serratia marcescensCiproflaxin
Neonatal meningitis , LPS, K1 capsuleE.Coli K1 (NMEC)
UTI, systemic, LPS, Pili and hemolysinUropathogenic E.Coli (UPEC)
UTI, kidney stones, LPS, urease & flagellaProteus
UTI, pneumonia, systemic, LPS, capsuleKlebsiella pneumonia
LPS, UTI, systemic, osteomyelitisSerratia marcescens
UTI, pneumonia, LPS, systemicEnterobacter/Cittrobacter


Question Answer
Watery diarrhea is a result of bacterial attachment
Profuse watery diarrhea is a result of Exotoxin
A non-invasive GI infection, no fever but with Profuse watery diarrhea is a result of exotoxinVibrio Cholera Toxin
A non-invasive GI infection, no fever but with Profuse bloody diarrhea is a result of exotoxinShigella
infection of colon, tenesmus, significant pus/RBC/WBC and low volume diarrheaDysentery
inflammation, as defined by the presence of neutrophils, of small intestine/colon, high volume watery diarrhea with possible presence of RBC and WBCGastroenteritis/Colitis
profuse blood due to damage to blood vessels from exo-toxinHemorrhagic
Bacterial colonization of spleen and liverTyphoid
Viable bacteria in bloodBacteremia
Bacteremia with sepsis (High TNF-a)Septicemia
There was a fourth of July picnic in Washington D.C where individuals consumed a lot hamburgers & beef. Next day all individuals from the picnic developed profuse bloody diarrhea. What is the pathogen? Entero-Pathogenic E. coli (EHEC)
Culture on MacConkey (pink colonies), Culture on S-Mac* for EHEC (white) are diagnosis forEPEC
Self-resolving Profuse Watery Secretory Diarrhea without fever(ETEC) Entero-Toxigenic E. coli
Traveler’s diarrhea, very common in developing countries aka Montezuma’s Revenge, tow enterotoxins LT, ST cause symptomsETEC
A/B toxin similar to Cholera toxin, GPCR is activated via Gαs thus activating adenylyl cyclase. Activates guanylate cyclase, increasing cGMP. Net result is altered cAMP levels and anion effluxLT (Heat-Labile toxin)
MCC of traveler diarrheaETEC
Profuse watery diarrheaETEC
Able to gain access to lamina propria and triggers inflammation and high fever, via LPS->TLR4->NFkB->IL1, IL8, TNFα, Attaches to colon IEC via fimbriae EIEC
Attaches to small intestinal cells via T3SS system actin pedestal formation calledAttaching and Effacing A/E Lesions
Self-resolving Secretory Watery Diarrhea without fever, **Comparable to Vibrio parahemolyticusEPEC
leads to disruption of absorption and causes symptom of EIECEffacement (loss of microvilli)
What is the virulence factor for the EPEC?Type 3 secretion system
Effectors are injected into host byT3SS
serves as the binding receptor for EPECTir
Colonization leads to destruction of microvilli, thus pedestals are calledAttaching and Effacing A/E Lesions (virulence factor of EPEC)
Watery Diarrhea followed by Profuse Bloody Diarrhea* without fever or WBCsEHEC
Destroys endothelial cells which causes bloody diarrhea symptoms of EHECShiga-toxin
Form A/E lesions similar to EPEC which cause initial watery diarrhea symptomsEHEC
Can lead to HUS Hemolytic Uremic SyndromeEHEC
The hemorrhaging is because the toxin invading endothelial cell, not because of bacteria invasionEHEC
Type 3 secretion system plus attachment & formation of actin pedastralEHEC
MC food reservoir for EHECCow
Attaches to IEC of Large Intestine, Injects effectors via T3SS, Form actin-pedestals and A/E lesions, like EPEC, Bacteria remain in lumen, Secretes soluble Shiga-toxin, StxEHEC
Is NOT technically invasive, so fever is most often absent with transient colitisEHEC
Was obtained via transduction of Shigella bactertiophageShiga-toxin Stx
is an A/B toxin that attaches to receptors on intestinal villi and renal endothelial cells Shiga-Toxin Stx
Cleaves host 28s RNA ribosomeShiga-toxin Stx
Destruction of endothelial cells results in hemorrhagingShiga-Toxin Stx
More common in <5 yrs old, esp. if antibiotics (TMP/SMX) are administeredHemolytic Uremic Syndrome
Fever, Acute renal failure (fever, hypertension, dry skin, rash), Thrombocytopenia, Microangiopathic hemolytic anemia (Hb decreased), Neurological manifestations are clinical presentation forHemolytic Uremic Syndrome
colonies on Sorbitol-MacConkey agar (S-Mac), does not ferment sorbitolEHEC
Supportive rehydration only is mode of treatment forEHEC
Fimbriae, ST/LT enterotoxinETEC
Cell-to-cell rocketing, hemolysinEIEC
A/E LesionsEPEC
A/E Lesions, Shiga-toxinEHEC
Gram Negative Bacilli, Non-Motile, Non-fermenter, No H2S productionShigella
A bacteria that destroys cells but it is not intracellular and it can cause watery diarrhea with blood pus: Shigella Dysenteriae (Group A)
Question Answer
Which bacterial toxin targets 28s rRNA, ceasing translation in endothelial cellsShiga-toxin
Non-motile, Oxidase (-), Non-lactose fermenting, No H2S production are biological features forShigella
Which organism can only penetrate the colon via M-cell?Shigella
Which pathogen can lyse open macrophages via T3SS after phagocytosis, triggering inflammation? Shigella
Which pathogen cannot survive long inside intracellular cells, has no capsuleShigella
“Rocket” from IEC cell-to-cell via T3SS, causing shallow ulcerations resulting in bloody diarrhea & pusShigella
Which pathogen directly destroys cells & induces PMNs to trigger cell damage?Shigella
Cleaves 28S rRNA ceasing translation resulting in cellular apoptosis & is a soluble A/B toxin that binds to Gb3 receptor on colon epithelial cells, endothelial cells, esp. renal epithelial cellsStx
Very high fever (up to 106°F), Small volume bloody diarrhea containing WBC and mucus, Profuse blood-liquid diarrhea if Stx-strainShigella Dysenteriae
Septic Arthritis, Reactive Arthritis in HLA-B27 Patients, HUS* –Hemolytic Uremic SyndromeShigella complications
Culture of White colonies in Hektoen (HE) AgarShigella
Culture of black colonies in Hektoen (HE) AgarSalmonella
Non-motile only grow on stab lineShigella
Soft agar allows motile strains to grow away from the inoculated stab lineSalmonella