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49 Cards in this Set
- Front
- Back
properties of Ecoli(5)
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gram negative rods
Enterobacteriaceae Ferments Lactose Oxidase negative Facultative anaerobe |
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URINARY TRACT INFECTIONS
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Ecoli
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Main pathogenicity factor or Ecoli causing UTI
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pili associated with pyelonephritis
Mobility enables E. coli to ascend urethra into bladder & ureter into kidney. |
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UTI limited to bladder
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cystitis or uretritis characterized by pain & frequency of urination
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UTI limited to kidneys
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pyelonephritis – characterized by fever, chills, & flank pain, means infection is systemic and is ascended pyelonephritis
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Patient presents with fever, shaking chills, dysuria (burning urination), increased in frequency of urination, risk factors: indwelling catheter, disurea, burning urination, or increased frequency of urination. Lab shows gram negative rod, lactose fermenter, or facultative
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E. coli
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Patient with a bladder indwelling catheter starts to develop a fever, hypotension, and going into multi-organ failure.
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Patient is going into septic shock.
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what is the mechanism of action of E. coli causing septic shock?
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Endotoxin in the outer lipopolysaccharide memberane, blood culture will grow a gram negative organism
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Enterotoxigenic E. coli (ETEC)
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- “Travellers’ diarrhea” - Watery, non-bloody diarrhoea.
- Disease is of short duration (1 to 3 days) & self-limiting. |
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History if travel to South America or another developing country, person drank tap water or juice with ice, patient comes down with watery diarrhea
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traveler’s diarrhea. bacteria produces a toxin (comparable to Cholera toxin – but cholera causes MASSIVE diarrhea) that ADP-ribosylates a Gs protein, increasing cAMP, causing water retention & watery diarrhea
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Enterohemorrhagic E. coli
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EHEC or VTEC - O157:H7 is most common)
Causes bloody diarrhea but NO INFLAMMATION, NO NEUTROPHILS in stools (no PMNs) Fecal oral route of spread |
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VEROTOXIN
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shiga-like toxin
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• Associated with outbreaks of diarrhea following ingestion of undercooked hamburgers
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VEROTOXIN – “shiga-like toxin”
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HEMOLYTIC-UREMIC SYNDROME
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Life-threatening complication of O157:H7 (risk may be increased by treatment of infection with antibiotics)
o Non-immune hemolytic anemia, thrombocytopenia, & acute renal failure |
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O157:H7
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HEMOLYTIC-UREMIC SYNDROME
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Patient comes in with bloody diarrhea, increased BUN & serum creatinine, symptoms indicated hemolysis & renal failure
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hemolytic-uremic syndrome
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Patient comes in with bloody diarrhea, increased BUN & serum creatinine, symptoms indicated hemolysis & renal failure. How does the child contract this disease?
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Most common sources of enterohemorrhagic E. coli infection is undercooked beef burgers. Toxin is SHIGELLA-LIKE toxin
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SHIGELLA-LIKE toxin MOA
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nicks the 60s subunit and interferes with protein synthesis.
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HISTORY OF BLOODY DIARRHEA WITH INGESTION OF UNDERCOOKED BEEF
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ENTEROHEMORRHAGIC E. coli, but if HEMOLYTIC-UREMIC SYNDROME (ELEVATED BUN & SERUM CREATININE) = O157:H7 strain
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how do you distinguish O157:H7 from other strains of E. coli
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O157:H7 does not ferment sorbital
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xteristics Salmonella enteric
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MOTILE Gram negative
Oxidase negative Urease negative (distinguishes Salmonella from Proteus on TSI) Produces H2S (shigella does not), does NOT ferment LACTOSE (different with E. coli) |
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How do you dintinguish salmonella from proteus on TSI
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Salmonella is Urease negative
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how do u disntiguish Salmonella from E coli
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E coli ferments lactose
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Vi (virulence) antigens
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Salmonella
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Enterocolitis
Enteric fever (ex. typhoid fever) Septicemia with metastatic infections |
Salmonella
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Which category of salmonella have only human reservoirs with no animal reservior
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S. typhi
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o Inadequately cooked meat, dogs, & less common pets (turtles, snakes, lizards, & iguanas)
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Salmonella
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Typhoid fever
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S. typhi
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Enteric fever
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S. Paratyphi
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Infection starts in ileocecal region of small intestine with few GI symptoms, organisms multiply & enter mononuclear phagocytes of Peyer’s patches, then spread to phagocytes of liver, gallbladder – can result in carrier state, & spleen (characteristic feature: multiplication in phagosomes & invasion of gallbladder) leading to bacteremia causing fever & other symptoms resulting from endotoxin. Patient can get ulcers.
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Salmonella
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Patient comes in with a history of constipation then person starts to develop a fever, goes to liver, then spleen, has an enlarged abdomen, hepatosplenomegaly, characteristically they will tell you there is a presence of ROSE SPOTS on the abdomen
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Salmonella
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what causes enterocolitis
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S. Enteritidis & S. typhimurium
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incubation period of enterocolitis
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24 to 48 hours
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symptoms enterocolitis
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nausea, vomiting, progressing to abdominal pain, mild to severe diarrhea (with or without blood – usually mild and self resolving
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child playing with turtles at home and didn’t wash hands, ate food and came in with a diarrhea type of illness; diarrhea can be watery but can also become bloody
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- ENTEROCOLITIS
Caused by S. Enteritidis & S. typhimurium |
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SEPTICEMIA
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S. cholerasius
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A patient with sickle cell anemia has a hemolytic crisis or vaso occlusive crisis, they present with excruciating bone pain. X-ray of bone is taken, a diagnosis is made, and you treat the patient with antibiotics. What is the causative agent causing the pain in the patient
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Salmonella is the #1 cause of OSTEOMYELITIS in children with sickle cell anemia
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Shigella xteristics
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- NON-MOTILE Gram (-)
- Does NOT ferment LACTOSE or H2S - Species: S. Dysenteriae, S. Flexneri, S. Boydii, & S. Sonnei o S. sonnei – 75% of cases in US – most common cause o S. dysenteriae – causes most serious disease o Some strains produce SHIGA TOXIN (exotoxin) nicks 60s subunit and interferes with protein synthesis. |
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Bacilliary (bacterial) dysentery
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Shigella - bloody diarrhea occasionally may get septicemia
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pathogenesis of shigella
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Invades mucosal cells of ileum & colon resulting in bloody diarrhea
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: Patient presents with fever, abdominal cramps, watery diarrhea which later turns bloody with mucous (may say blood with pus or bloody stool that produces dysentery),
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this is an INVASIVE DIARRHEA. Toxin responsible for all clinical effects is SHIGA TOXIN – causes BLOOD DIARRHEA or BACILLIARY DYSENTARY
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Vibrio xteristics
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Gram negative - Curved, comma-shaped
Oxidase positive Polar Flagella (at the end - key point to distinguish from Enterobacteriaceae, goes under genus: Vibrioaceae) Grows in alkaline media or TCBS (thiosulfate citrate bile salt sucrose medium) |
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transmission of vibrio
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FECAL ORAL, water contamination, or by ingestion of inadequately cooked shellfish, can get outbreaks
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watery diarrhea
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Vibrio cholera
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vibrio cholera MOA AB exotoxin
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- AB exotoxin: ADP-ribosylates Gs, leading to overproduction of cAMP & efflux of Cl- & water, but the key is that the person is losing a lot of potassium & bicarbonate, massive diarrhea (massive fluid loss of > 16-19L/day), leads to decreased CO – heart failure, decreased GFR – renal shut down, stool has hardly any fecal matter, a few shed epithelial cells, and specks of mucus – called rice water stool. There is no RBCs & WBCs, or PMNs in the stool
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Vibrio cholera diarrhoea contains which of the ff
1 RBCs & neutrophils 2 Only neutrophils 3 Just mucus & shed epithelial cells |
• Just mucus & shed epithelial cells****correct answer
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Pt. produces a traumatic type of illness where you have a profound water loss, pt. is hypokalemic, and has cardiac failure
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think about losing volume, GFR is low, reduced urinary output, & renal shut down - vibrio cholera
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pt. presents with a diarrheal illness, develops cardiac toxicity or renal failure, and dies
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vibrio cholera
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pt. presents with a diarrheal illness, develops cardiac toxicity or renal failure,
Pt. is taking antacids like Omiprazole -effect |
cholera cause decreased acid ph -antacids will increase ph and kill organism
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