2.2_Microbio

A: G+ and Catalase - and B-hemolytic and Lancefield A.

A: G+ and Catalase - and B-hemolytic.

A: Strep B and Listeria monocytogenes and E Coli.

A: Oxygen labile enzyme, which is inactivated by oxygen, of Strep A that destroys RBCs and WBCs.

A: Oxygen stable enzyme of Strep A that destroys RBCs and WBCs.

A: Major virulence factor for Strep A.

A: caused by pyrogenic exotoxin from Strep A - Scarlet red rash. strawberry tongue. Pharyngitis.

A: Follows Strep pharyngitis - Antibody mediated. Fever. Myocarditis -valve damage years later-. Joint swelling. Chorea. Subcutaneous Nodules. Erythema marginatum (rash).

A: Inflammatory disease of the kidney following Strep pharyngitis or skin infection. Due to deposition of antigen-antibody complexes: Puffy face. Dark urine (hematuria and proteinuria)'. Hypervolumia which can cause high BP.

A: G+ and Catalase - and a-hemolytic -green-. Dental Infections -caries-. Endocarditis -subacute-. Abscesses.

A: Subgroup of Viridans Strep that causes abscesses.

A: G+ and catalase - and a-hemolytic. Normal bowel flora. Common in UTIs. Biliary infections. Subacute endocarditis. Not as virulent as Strep A. Opportunistic. Common cause of nosocomial infections. Resistant to many antibiotics, some even vancomycin.

A: G+ and catalase - and a-hemolytic -. Lancet-shaped Diplococci. Pneumonia. Meningitis in adults. Otitis media in kids.

A: high fever. Rigors. cp with respirations. sob. In lungs - pus and bacteria and exudates.

A: G+ and catalase + and B-hemolytic. gold pigment. In clusters. coagulase +. Scalded skin syndrome. Toxic shock syndrome. Gastroenteritis. Pneumonia. Meningitis and Brain abscess. Osteomyelitis. Acute endocarditis. Septic arthritis. Skin infections. Wound infections.

A: Protein A: Binds the Fc part of IgG. Coagulase leads to fibrin clot around bacteria, protecting it. Hemolysins destroy RBCs, neutrophils, macrophages, and platelets. Leukocidins destroy WBCs. Penicillinase inactivates penicillin.

A: Hyalurodinase: Breaks down proteoglycans in CT. Staphylokinase: Lyses fibrin clots. Lipase: Degrades fats.

A: Exfoliatin: Scalded skin syndrome. Enterotoxins: Food poisoning gastroenteritis. Toxic shock syndrome toxin (TSST-1).

A: Staph and Strep A. Shock. Renal failure. Rash. Respiratory Failure.

A: G+ and Catalase - and B-hemolytic. Can cause purulent infections like Strep A but no Rheumatic Fever or glomerulonephritis.

A: Strep D.

A: Group F Strep milleri and Viridans group Strep intermedias.

A: Staph Aureus and Listeria monocytogenes and Clostridium botulinum and Clostridium perfringens and Bacillus cereus.

A: G+ and Catalase + and B-hemolytic. Rods in pairs. Aerobic. Transmission from meat product. Bacterimia and meningitis in newborns. Likely to have obtained from birth canal. Common cause of food borne outbreaks and meat recalls.

A: Culture blood or CSF and B-hemolytic then not cornebacteria and Catalase + then not Strep B.

A: Also called diptheroids. G+ and rods forming Chinese character clusters. Large numbers on normal skin flora. Most often contaminants in culture. Assumed to be cause of the disease only if in 2 samples. Endocarditis in prosthetic heart valves.

A: opportunistic. Lymphadenitis. Abscesses. Meningitis. skin infections. bacterimia.

A: Pharyngitis with thick membrane and edema. May have cutaneous ulcers. When contains a bacteriophage produces exotoxin that effect myocardium and peripheral nervous system. Death by asphyxiation or myocarditis.

A: Listeria monocytogenes and Corynebacterium and Erysipelothrix rhusiopathiae and Bacillus and Lactobacillus.

A: G+ and rods that form long filaments and a-hemolytic. Produces hydrogen sulfide gas (unique among aerobic G+). Colonizes animals and causes infections in fisherman, butchers, and veterinarians. erysipeloid: ulcerating, erythematous skin infections.

A: G+ and large rods. Form spores (unique among aerobic G+). Bacterimia and endocarditis in drug abusers and immune compromised. B. anthracis and B. cereus.

A: Large G+ rods. Rare in US but common elsewhere else. 3 forms: 1) cutaneous: painless ulcer with black eschar 2) inhalation: spore forming, severe SOB, appearance of extreme toxicity, and widened medistinum 3) GI form - deadly.

A: Commonly causes food poisoning. Associated with under cooked rice. Toxin mediated.

A: G+ and catalase - and a-hemolytic and small long slender rods. Major normal flora of GI tract and genital tract. Found in yogurt. Virtually always protective against infection.

A: Clostridium perfringes and Clostridium botulinum and Clostridium tetani and Clostridium difficiles and Propionibacterium and acnes.

A: G+ and large rods and spore forming. Gas gangrene. Necrotizing Fasciitis. Cellulitis. Puerperal sepsis. Food poisoning.

A: Clostidium perfringens. Rare. Rapidly progressing. Traumatic and surgical wounds. Destruction of muscle. Gas in tissue. Hemorrhagic bullae. Foul watery discharge. Liver and Renal failure. Shock and Death.

A: Clostridium perfringens. Strep A. Mixed aerobic and anaerobic. Doesn't involve muscle, more local, less lethal than gas gangrene.

A: G+ and large rods and spore forming. In soil, Common component of GI flora. Tetanospasmin toxin. Causes paralysis that is spastic. Fever. Difficulty swallowing.

A: G+ and large rods and spore forming. Common in soil. 8 toxins so no vaccine (bacteriophage required for production). Food poisoning. Wounds. Infections. Infant botulism.

A: generalized weakness, dry mouth, constipation, and urinary retention. Followed by descending paralysis, blurred vision, photophobia, dilated unreactive pupils.

A: Lesions appear 4 to 14 days after injury. similar clinical manifestations as food-bourn disease.

A: 3 to 20 week old infants. Constipation, weak suck, feeble cry, descending flaccidity, ptosis, absent gag reflex. seen in adults.

A: G+ and large rods and spore forming. GI flora, under antibiotic pressure makes toxins. psuedomembranous colitis. Fever. Diarrhea. ABD pain. Exudate and ulcer formation in large intestine. Failure to recognize and treat may lead to bowel perforation and peritonitis.

A: Prominent normal skin flora. Common contaminant. Infections in prosthetic devices (CNS shunts). Acne.

A: Gram - Large bacilli. aerobic or anaerobic. do NOT form spores. produce endotoxins. live in lower GI tract.

A: Cell wall lipopolysaccharide (heat stable). capsule polysacharide (heat labile). flagellar proteins.

A: 1) Gram - bacilli 2) ferment glucose 3) reduce nitrates to nitrites 4) oxidase.

A: 1) E. coli 2) Klebsiella 3) Enterobacter.

A: 1) Salmonella 2) Shigella 3) Yersinia.

A: 1) E. coli 2) Klebsiella 3) Enterobacter 4) Serratia 5) Citrobacter.

A: UTI. meningitis (most commonly in neonates). Nosocomial - wounds and bacterimia and pneumonia.

A: UTIs. Pneumonia. nosocomial infections.

A: nosocomial infections.

A: opportunistic. red pigment. blood of Christ dripping in church paintings.

A: neonatal meningitis and bacterimia. swarms.

A: swarms. UTI. wound infections. bacterimia.

A: nosocomial infections in pts with catheters.

A: Traveler’s diarrhea. Childhood diarrhea. Contaminated food and water.

A: Adhere to small intestinal wall. Enterotoxin - LT: heat labile toxin and ST: heat stable toxin.

A: Stools - copious and watery and no blood or RBCs. no fever.

A: Contaminated food - beef, unpasteurized milk, apple cider, fast food. Contaminated water. Person to person (daycares).

A: Adhere to large intestine wall. Shiga-like toxin 1 and 2. Damage endothelial cells in GI tract and renal glomeruli. Hemorrhagic colitis. Hemolytic uremic syndrome.

A: Stools - copious and bloody and no WBCs. No Fever.

A: No antibiotics, aggravate HUS. supportive care and dialysis. Prevention.

A: sporadic and uncommon.

A: Invades large intestine enterocytes. Necrosis. Ulceration. Inflammation.

A: Stools - scant and blood and WBCs and purulent. Fever.

A: infantile and childhood diarrhea.

A: Adhere to small intestine enterocytes. efface microvilli.

A: Stool - copious and watery and no blood and few WBCs. Fever.

A: Adhere to enterocytes.

A: Stools - watery and no blood and no WBCs. Fever occasionally.

A: Strictly human disease. Needs very low inoculum. Fecal-oral transmission. Contaminated food or water.

A: Invades colonic mucosa - but no further. Makes Shiga toxin. causes HUS. - S. dysentery and S. sonnei.

A: Abd cramps. Tenesmus - painful straining to poo. Fever. Stools - bloody and mucoid and large # of fecal leucocytes.

A: fever. systemic symptoms. watery diarrhea.

A: none, it will go away on its own. Antibiotics prevent transmission and shorten clinical course.

A: improper food handling. poultry (eggs) most common. exotic pet turtles. Affects mostly the very old and the young.

A: Adhere to brush border of intestinal cells. Ruffles in intestinal wall. Invade enterocytes.

A: onset 24-48 hrs. duration 3-4 days. Nausea. Vomiting. Cramping. Diarrhea. Fever (50 percent). Bacterimia (old and young).

A: Resolves spontaneously. fluids and electrolytes. Antibiotics only for those at risk for bacterimia (very old and young).

A: Salmonella typhi. Enter and kill M cells. Invade macrophages and multiply. Bacterimia. rose spots.

A: Fever. Headache. Constipation more than diarrhea. may have intestinal perforations.

A: Antimicrobics. Vaccine.

A: asymptomatic. Salmonella in stools or urine for years. reservoir for epidemics.

A: Invade M cells of peyer's patches. Proliferation in lymph nodes. Small intestinal inflammations and ulceration.

A: Fever. Diarrhea. Abd PN (like appendicitis).

A: Comma shaped Gram - rod.

A: Unsanitary water systems leading to Traveler's diarrhea. Imported seafood (raw oysters). Requires huge inoculation.

A: non-invasive. Attach to intestinal wall and produce toxin. Inhibits cAMP and water reabsorbtion. 15 L absorbed by gut a day is lost.

A: Incubation is from hours to 5 days. Onset is sudden. Stools - rice water stools and no tenesmus and vomiting common and volume shock.

A: Fluids (water, electrolytes, glucose). Self limited. Tetracyclin or other antibiotics reduce duration of illness. Prevention includes vaccine and sanitation.

A: acute gastroenteritis after eating seafood. self limited. Iron loving - grow more and more virulent and dangerous to people with liver disease.

A: Wound infections (unique among vibrios). Fishermen. iron loving. dangerous to people with liver disease.

A: Gram - comma shaped or spiral rods. requires special conditions for isolation.

A: Most common cause of bacterial gastroenteritis in US. 5-12 percent of diarrheal stool samples. Food and water contamination. Animal reservoirs - Fowl, cattle, swine, pets. Fecal oral spread.

A: Invades intestinal mucosa.

A: Incubation 1-7 days. Rapid onset. Fever. Abd PN. Stools - copious and watery and mucoid and bile stained and WBCs and blood. May relapse.

A: Spontaneous clearance. IgG and IgM produced. Often antibiotics not used but can decrease chance of bacterimia. Treat early with quinolones.

A: 60 percent of adults exposed by age 50.

A: Limited to stomach mucosa. High urease activity - cleaves urea to ammonia and protects from stomach acid.

A: Gastritis - Gastric ulcer (50-70 percent of them) and Duodenal ulcer (90 percent of them) and Possible role in gastric carcinoma.

A: Staph aureus and Bacillus cereus and Clostridium perfringes and Clostridium botulinum.

A: upper level disease. Nauseaandvomiting. Abd PN. onset within hours.

A: Vibrios and V. cholera and V. parahemolyticus and E. coli and ETEC and EHEC and EPEC and EAEC.

A: Block water reabsorbtion. Copious, watery stools. Vomiting. little PN or toxicity. generally self limiting. 2-3 day onset.

A: Salmonella and Shigella (low inoculum) and Yersinia and Campylobacter (most common) and Helicobacter pylori and EIEC and Listeria monocytogenes.

A: Toxic, Fever, Abd PN, Stools - small volume and blood and WBCs and purulent. 2-5 day onset.

A: Gram - cocci. usually kidney bean shaped and diplococci like a donut. N. meningitides and N. gonorrhea.

A: 1) Capsule 2) Endotoxin (LPS): causes blood vessel destruction and petechiae 3) IgA protease.

A: Yes.