IUSM – Micro Review – Flashcards
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| Toxigenic bacteria |
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| Vibrio, clostridium, bacillus |
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| Extracellular bacteria |
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| strep, staph, haemophilus, neisseria, pseudomonas, enteric bacteria, pathogenic anaerobic bacteria |
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| Intracellular bacteria pathogens |
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| mycobacterium, listeria,legionella |
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| Atypical bacterial pathogens |
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| spirochetes, mycoplasma, chlamydia, rickettsia |
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| Non-fermentative gram negative rods |
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| pseudomonas, burkholderia, stenotrophomonas |
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| MacConkey agar, lactose (-), oxidase (+), green pigment, grow at 42 degrees, MDR, non-fermentative, G- rods, sweet odor, pyocyanin fluorescent pigments |
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| Pseudomonas aeroginosa |
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| Most serious ventilator associated pneumonia (VAP) |
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| P. aeruginosa |
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| Causes severe infections in immunocompromised, burn patients, patients w CF |
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| P. aeruginosa |
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| Produces pyocyanin fluorescent pigments |
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| P. aeruginosa |
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| Virulence factors of P. aeruginosa |
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| hemolysin, proteases, elastases, exoenzymes S/T, toxins, alginate, pyoverdin, pyocyanin, flagellum, pilus |
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| Major mechanism of resistance of pseudomona |
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| mutation of porin proteins |
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| Presentation of pseudomona in noncompromised hosts |
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| Folliculitis, otitis externa, eye infections, endocarditis <-- (drug abusers), nosocomial infections (UTI, pneumonia, IV line sepsis) |
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| Presentation of pseudomona in diabetics |
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| Malignant otitis externa |
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| Pseudomonas in severe neutropenic or burn victims |
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| Bacteremia |
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| Pseudomonas in pts w CF |
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| pneumonia, mortality rate is 70% |
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| Pseudomonas (another systematic infection) |
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| Ecythyma gangrenosum due to elastase production of pseudomonas, get hemorrhagic lesions |
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| Mechanism of pseudomonas infection in CF patients |
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| attach to cells using pili and flagella movement, lose "O" side chain, pili, and UPREGULATE ALGINATE to form biofilm |
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| Why pts w CF die |
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| Neutrophil recruitment, they release elastase, also get congestion of parenchyma |
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| Treatment of Pseudomonas |
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| combo treatment of pseudomonas-B lactam, and aminoglycosides |
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| Prevention of pseudomonas |
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| sterile equipment and avoiding inappropriate broad spectrum antibiotics |
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| Burkholderia cepacia |
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| Think nosocomial, 2nd most important IV catheter associated infection |
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| Stenotrophomonas maltophilia |
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| Opportunistic, like pseudomonas, nosocomial infections (pneumonia, bacteremia) |
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| Acinetobacter sp. |
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| Nosocomial, get soft tissue infections |
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| Enteric bacteria |
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| G-, rods, grow fast, oxidase (-) |
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| O antigen |
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| O polysacharide of LPS, Ag on enterics |
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| H antigens |
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| flagella antigens (shigella, kliebsiella, and yersinia have none --> nonmotile) |
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| K or Vi antigen |
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| found on capsules |
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| E. coli 0157: H7 |
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| identifies e. coli as having antigen O 157 and antigen H 7 |
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| Lipid A |
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| Endotoxin, part of LPS, activates complement and get leukocytosis and thrombocytopenia, shock/death |
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| Tons of e. coli where? |
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| GI tract |
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| Specialized virulence factors of e. coli |
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| Adhesins, exotoxins (shiga toxin, heat-stable or liable toxins, hemolysins) |
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| Leading G- cause of bacteremia and sepsis |
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| E. coli |
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| Leading cause of community acquired G- bacteremia |
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| E. coli. (P. aeruginosa is 2nd) |
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| Leading cause of G- bacteremia in ICU |
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| Enterobacter species (Klebsiella is 2nd, pseudomona = 3rd). |
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| Bacteremia and sepsis treatment |
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| Treat w urgent empiric, broad antibiotics, then beta lactam |
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| Uropathogenic e. coli |
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| specialized adhesins via P pili, more virulent cause of UTI than other e. coli |
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| Blueberies and cranberries |
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| release tannins that prevent adherence of e. coli to bladder and epithelium |
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| Treatment for UTI |
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| trimethoprim. This is a dihydrofolate reductase inhibitor |
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| Neonatal meningitis - top cause |
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| Group B strep = primary cause. (2nd is E. coli, 3rd is Listeria monocytogenes). |
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| EPEC |
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| Enteropathogenic e. coli |
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| ETEC |
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| enterotoxic e. coli |
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| EHEC |
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| enterohemorrhagic e. coli |
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| EIEC |
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| enteroinvasive e. coli |
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| EAEC |
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| enteroaggregative e. coli |
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| Major cause of infant diarrhea in developing countries |
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| EPEC (pathogenic) |
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| EPEC - how it looks clinically |
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| incubation of 2-6 days, acute onset of watery diarrhea that last 1-3 weeks! |
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| Pedestal formation |
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| think EPEC |
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| LEE pathogenicity island |
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| think EPEC. Intimin is an adhesin, binds Tir receptor protein. Get type3 secretion. End result is pedestal |
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| O157:H7 |
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| Most common EHEC serotype. |
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| Most common strain of e. coli in developed countries |
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| EHEC, O157:H7 |
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| Hamburger disease |
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| EHEC. feces-contaminated meat. Can also get EHEC from unpasteurized milk, fruit juice, and uncooked vegies/fruit |
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| STEC |
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| type of EHEC, produces shiga toxin. |
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| VTEC |
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| a type of EHEC. produces verotoxin |
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| How EHEC looks clinically |
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| Incubation 3-4 days. initially get watery diarrhea and abdominal pain/some vomitting. within 2 days, 50% of patients have bloody diarrhea w very bad pain (hemorrhagic colitis). Uncomplicated resolve in 1 week. |
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| Hemolytic uremic syndrome |
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| From EHEC. Shiga toxin enters blood. get renal failure, anemia, thrombocytopenia. Very serious neuro problems. |
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| Leading cause of acute renal failure in children |
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| Hemolytic uremic syndrome (HUS) --> from EHEC. |
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| What to test for when patient has bloody diarrhea |
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| O157:H7. This requires modified MacConkey agar with sorbitol. Do serology test for O157 antigen. Look for shiga toxin in stool sample under microscope |
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| Traveler's diarrhea |
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| think ETEC. |
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| ETEC symptoms |
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| 1-2 day incubation, diarrhea for 3-4 days. |
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| Incubation of 2-3 days, then watery diarrhea, then mucoid bloody stools/cramps/fever for 1-2 weeks |
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| EIEC. This is rare in US and uncommon in developing countries too. |
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| Causes PERSISTANT watery diarrhea and dehydration (if chronic get growth retardation). Mainly in developing countries. |
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| EAEC |
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| Forms a green sheen on EMB (eosin methylene blue) agar |
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| E. coli |
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| Shigella found in industrial countries |
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| Shigella sonnei |
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| Shigella found in developing countries |
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| Shigella flexneri |
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| Most severe form of shigella |
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| Shigella dysenteriae. Causes bacillary dysentery. |
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| Uncommon shigella |
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| Shigella boydii |
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| Oral fecal route, raw vegies/salads/milk/dairy/meat (fecal contamination of water and dirty food handlers), breakouts in daycares. Deadly!! |
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| Shigella |
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| Symptoms of shigellosis |
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| Incubation 1-7days, SMALL VOLUME diarrhea, varying severity of GI issues...can be horrible or just mild pain/diarrhea. 10-15% fatal. |
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| Treatment of shigella |
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| fluoroquinolones, guided by in vitro susceptibility test. |
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| Do not ferment lactose, produce H2S, motile |
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| Salmonella |
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| Number of subtypes of salmonella |
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| 6. But, salmonella enterica is subdivided into 2200 serotypes. |
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| SPI 1 and SPI 2 |
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| Salmonella pathogenicity islands 1 and 2. SPI 1 = injected in M CELLS. SPI 2 live in MACROPHAGE |
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| 3rd most common food poisoning |
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| Salmonella enteritidis |
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| Enteritis |
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| Think birds/poultry, eggs, dairy, contact with pets. |
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| Replicate in macrophages, spread from GI to other organs, STEPWISE fever/bacteremia in wk 1, 2nd week = abdominal pain and rash, 3rd week get GI bleeding and enlarged spleen/liver, peritinitis. Deadly problem in developing countries. Bug persists in gallbladder. |
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| Typhoid fever. A type of salmonella found mostly and killing mostly developing countries. |
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| Treatment of typhoid fever |
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| Fluoroquinolones or chloramphenicol. 2 vaccines |
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| Mucoid appearance, nonmotile, ferment lactose, common in alcoholics w bad lungs. |
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| Klebsiella |
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| Expended spectrum betal lactamases |
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| Found in Enterobacter |
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| Serratia |
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| Causes nosocomial pneumonia |
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| Proteus |
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| Swarming motility and urease activity. Causes kidney stones and other UTI related nosocomial infections. |
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| Siderophilic, so you find this bacteria in hemochromatosis patients. |
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| Yersinia |
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| Blood transfusion related bacteremia |
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| think yersinia. |
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| Urban Plague or Black Death |
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| Yersinia pestis. carried in rats. Can cause major pandemic. Bioterrorism |
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| Sylvatic Plague |
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| Yersinia pestis. Found in squirrels, rabbits, rats |
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| Bubonic plague |
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| hallmark is swelling of lymph nodes (bubo). Yersinia pestis. |
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| Pneumonic plague |
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| Secondary to bacteremia of bubonic plague (Yersinia pestis). Causes necrotic pneumonia (90% fatal) |
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| Diagnosing yersinia pestis |
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| Rapid diagnostic test - F1 antigen. Bipolar staing. more like bi-winning. |
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| Treatment of yersinia pestis |
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| Streptomycin or tetracycline. isolation. |
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| Non-motile, non-spore forming, G+, aerobic, filimentous |
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| Mycobacteria |
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| Drug target for mycobacteria |
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| Mycolic acid |
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| Lipid content of mycobacteria |
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| 60%. makes it waxy and hydrophobic, and resistant to antibiotics. Membrane is LPS-like. Cannot be decolorized w acid! |
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| Pathogenic mycobacteria |
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| m. tuberculosis m. leprae m. avium-intracellulare |
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| Leading cause of morbidity and mortality worldwide |
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| Mycobacterium tuberculosis |
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| 4 outcomes of TB inhalation |
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| 1. immediate clearance 2. chronic/latent infection 3. rapid progression of disease (primary disease) 4. Active disease many years after infection --> most common worldwide |
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| TB virulence |
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| survive in macros. cord factor prevents fusion of phagosome w lysosomes. triggers Th1 response which is protective for infection. |
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| Trigger for TB infected macros to produce cytokines and chemokines |
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| LAM |
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| Lymphadenopathy |
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| Primary TB, when bacteria grow out of control and enter local draining lymph nodes |
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| Lesion resulting from the expansion of a tubercle into the lung and lymph node (in TB infection) |
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| Ghon complex |
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| Effective immune response against TB |
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| Cell mediated. If this response is weak, get caseation necrosis of lung. |
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| Caseation necrosis |
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| Think TB. When don't have a strong enough cell mediated immune response to beat TB. |
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| Millet seeds |
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| what disseminated miliary TB looks like. TB seeds spread to airways, liver and spleen |
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| Reactivation TB disease |
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| associated w AIDS and immunosuppressive problems. Persistant bacteria in host suddenly proliferate. |
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| Diagnosing TB |
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| chest x-ray, sputem sample (acid fast bacilli stain), TB skin test. |
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| TB symptoms |
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| gradual onset weight loss fatigue, night sweats, productive cough, chest pain Possibly cough up blood |
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| >5 mm induration |
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| Positive for TB in immunosupressed, HIV, pts who've recently contacted TB cases |
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| >10 mm induration |
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| Positive for TB, with patients who recently arrived into country, children under 4, mycobacterium lab personnel, and prison/jail/nursing home facilities |
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| >15 mm induration |
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| Positive for TB in patients with no risk factors and the southeast regions of US |
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| Treating TB |
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| multiple drugs (isoniazid, ethambutol, rifampin, pyrazinamide |
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| Bacille Calmette-Guerin (BCG) vaccine |
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| an attenuated strain of m. bovis (vaccine for TB) |
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| Leprosy |
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| Think mycobacterium leprae. Most common in Asia, India, and Africa |
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| Armadillos |
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| got that there mycobacterium leprae |
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| Tuberculoid leprosy |
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| Elicit vigorous CMIR to mycobacterium leprae. aka paucibacillary Hansen's disease Hypopigmented skin macules, damage to nerves. |
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| Lepromatous leprosy |
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| Patients fail to elicit strong CMIR to mycobacterium leprae. aka multibacillary Hansen's disease Disfiguring skin lesions/nodules. Extensive tissue destruction |
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| Treat leprosy with: |
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| Paucibacillary: rifampin and dapsone for 6 months Multibacillary: rifampin + dapsone + clofazimine for 2 years |
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| MOTT |
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| Mycobacteria other than TB *M. avium or M. intracellulare *Thnk AIDS |
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| Most common mycobacterial disease in US |
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| MAC (M. avium complex) Think AIDS. Think soil, water, poultry. |
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| Treatment for MAC |
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| Clarithromycin and azithromycin |
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| G+, aerobic, filamentous, fragments, weakly acid fast, found in soil, acquired by inhalation or in cuts. |
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| Nocardia |
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| Primary site of nocardial infection |
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| Lungs |
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| Presentation of nocardiosis |
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| Present w brain, soft tissue damage, or cutaneous lesions w simultaneous or recent lung problems |
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| Treatment of nocardiosis |
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| sulfonamide |
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| G+, small rod, facultative anaerobe, motile. Found in poop, soil, birds, undercooked foods, and decaying vegies. Grows at 4-45 degrees. grows in high salt. |
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| Listeria monocytogenes |
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| Listeria grows in: |
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| macros and epithelial cells. it penetrates epithelium from enterocytes or M cells in peyer's. |
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| Listeria escapes phagolysosomes via: |
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| Exotoxin (listerolysin O) and phospholipace C |
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| Presentation of listeria - healthy adult |
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| flu-like w or without gastroenteritis |
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| Presentation of listeria - compromised pts or women |
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| Meningitis, primary bacteremia |
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| Presentation of listeria - Neonates |
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| early onset (hrs), from placenta - abscesses and granulomas in multiple organs, high mortality rate late onset (2 wks), from birth or environment - meningitis |
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| Treatment/prevention of listeria |
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| Ampicillin. Avoid processed meats if in high-risk group |
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| G-, aerobe, stains poorly, requires Fe and Cys. Lives in amoebaes in nature. Found in cooling towers, and water systems |
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| Legionella |
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| Bacteria that cannot be passed person to person, rare, affects only high risk. replicates in macrophage and prevents phagolysosome fusion. |
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| Legionella |
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| Pontiac fever |
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| Legionella. 95% of legionella cases |
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| Legionnaires disease |
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| low rate, severe, multiple organs (GI, liver, CNS, kidneys), respiratory failure kills |
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| Diagnosing and treating legionella |
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| grows on CHARCOAL YEAST EXTRACT agar, urinary antigen test, fluorescent probes in sputum. Treat w macrolides (clarithromycin and azithromycin) or treat w fluoroquinolones |
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| Small, obligate intracellular pathogen, G-, stain poorly due to low amts. of LPS and PEG, require direct contact or arthropod for transmission. |
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| Rickettsia and related genera |
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| Grow within endothelial cells |
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| Rickettsiae |
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| Bacteria that is sometimes called virus |
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| Rickettsia. They have unique method of transmission. lay eggs. passsed on from arthropod vector. |
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| Greatly increased vascular permeability, thrombogenesis, peripheral vascular collapse, and non-cardiogenic shock. |
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| Indicate rickettsia may be possibility. |
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| Infection cycle: attachment, enter, phagocytosed, hemolysis of phagosome by PLA, released, multiply, accumulate along cell membrane, PLA digests cell membrane, lysis of cell |
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| Infection of cell by rickettsia |
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| Most severe tick-borne rickettsial illness |
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| Rocky Mountain Spotted Fever |
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| Rocky Mtn. Spotted Fever most prevalent in this region of US: |
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| Southeastern states (NC, SC, AK, OK, Mizzou) |
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| Rocky Mtn. Spotted Fever presentation |
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| Non-specific: 2-12 days. Fever, severe headache, malaise, myalgia, nausea. Specific: Rash. maculopapular. STARTS ON ANKLES, WRISTS, and FOREHEAD. May have neuro, coughing, or bleeding symptoms too. |
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| Weil-Felix Test |
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| Old test for Rocky Mtn. Spotted Fever |
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| Microimmunofluorescence (MIF) |
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| Test for Rocky Mtn. Spotted Fever |
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| Treat RMSF with: |
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| Tetracycline or chloramphenicol |
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| Spread of rickettsia akari due to: |
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| Mite bites. Usually in urban areas. Looks very similar to chickenpox. |
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| Epidemic typhus |
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| Rickettsia prowazekii |
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| Endemic typhus |
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| Rickettsia typhi |
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| Spread through feces of human body lice. |
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| Epidemic typhus (Rickettsia prowazekii) |
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| Rash starts on shoulders and upper back, then spreads to periphery. Macular initially, then maculopapular. Possibly becomes petechial or hemmorhagic. |
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| Epidemic typhus |
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| Systemic signs of endemic typhus |
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| Moist rales, cough, diarrhea, generalize edema, peripheral necrosis, renal failure, mental disorders. |
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| Main causes of death in typhus? |
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| Tissue anoxia results in peripheral vascular collapse. Results in heart attack, ischemia, stroke, or intractable shock. |
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| Rickettsia typhus most common in this area of US: |
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| Southwest. Due to rat flea or rat lice. |
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| Is there vaccine for typhus? |
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| Yes. Given to high risk populations. Also, treatment for pts with typhus is tetracycline |
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| Obligate intracellular bacteria. G- rods, stain poorly. Live in host cell vacuoles. |
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| Ehrlichiae |
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| Similarity of eherlichiae to rickettsia. Difference of the two? |
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| Vector born. Ehrlichia remains in phagocytic vacuole after entry. |
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| Ehrlichia chaffeensis. |
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| Causes Human Monocytic Ehrlichiosis (HME) |
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| Caused by lone star tick. Infects monocytes and one-nucleus phagocytes. |
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| HME. Human monocytic ehrlichiosis |
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| Diagnosis and treatment of HME |
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| Sometimes diagnosed as "rashless" RMSF. Antibodies to ehrlichia. Inclusions in macros. Treat w doxycycline. |
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| Human Anaplasmosis |
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| Human Granulocytic Ehrlichiosis (HGE) |
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| Deer tick causes. Often co-infected w Borrelia burgdorferi. Infects neutrophils. 10% get rash. |
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| Human Granulocytic Ehrlichiosis (HGE) |
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| Name this bacteria. Diagnosed by showing PMN's have inclusions. Detect antigen using IFA. Treat w doxycycline. |
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| HGE. HME would be right, if they were mononucleated phagocytes instead of PMN's. |
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| Causes Q Fever |
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| Coxiella burnetii |
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| Farm animals are primary reservoir. Infections from tick bites, inhalation of airborne particles, or ingesting unpaseurized milk. |
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| Coxiella burnetii |
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| 2 variants of Coxiella burnetii |
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| 1) Small cell - infectious, survive months 2) Large cell - multiple bacteria found in phagolysosome/monocytes/macros. |
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| Varient of Coxiella burnetii that replicates in respiration system |
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| Large cell. They are found in monocytes/macros/phagolysosomes. |
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| Found in patients w underlying valvular heart problems or immunosupression. Causes subacute endocarditis. 65% untreated mortality rate. |
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| Chronic Q fever. |
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| Treatment for acute Q fever |
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| doxycycline, respiratory isolation |
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| Treatment for chronic Q fever |
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| Doxycycline and fluoroquinolones for extended length. |
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| No cell wall. Cholesterol in cell membrane of bacteria. Tiny (0.2 um), and grows slowly. |
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| Mycoplasmas. |
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| Walking pneumonia |
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| Another term for atypical pneumonia. Mild (except for Legionaire's and SARS). CANNOT BE TREATED W COMMON ANTIBIOTICS |
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| Leading cause of atypical pneumonia |
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| Mycoplasma pneumoniae. Followed by chlamydophila pneumoniae (#2), and Legionella (#3). |
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| How m. pneumonia spreads |
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| Respiratory droplets. Common in summer/fall. Common in school-aged, military, and college students. |
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| Terminal protein attachmt factor (P1) |
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| Found in m. pneumonia |
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| Pathogenesis of m. pneumonia |
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| *Attach to resp. epithelia via P1. *H2O2 damages resp. cilia *Many features of pathogenesis may be immune-mediated |
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| Treating atypical pneumonia empirically: |
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| Azithromycin, clarithromycin or erythromycin |
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| This pneumonia bacteria is slow to grow. Also, PCR on throat swabs results in poor specificity. |
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| Mycoplasma |
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| Treating mycoplasma specifically |
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| Doxycycline, erythromycin, or fluoroquinolones |
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| Nongonococcal urethritis |
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| Can be caused by mycoplasma urethritis or ureaplasma urealyticum. |
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| Mycoplasma hominis causes what: |
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| vaginits, cervicitis, pyelonephritis, PID, and postpartem fever |
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| Chlamydiae. Intra or extracellular? |
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| Obligate intracellular |
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| 2 forms of chlamydiae |
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| *Elementary form = nonmultiplying but infective *Reticulate bodies = intracellular, multiplying, not infectious |
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| Leading bacterial infection worldwide |
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| Chlamydia trachomatis |
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| #1 cause of bacterial STDs |
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| Chlamydia trachomatis |
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| Syndromes of chlamydia |
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| Trachoma, urethritis, inclusion conjunctivitis, neonatal pneumonia, lymphogranuloma venereum (LGV) |
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| Trachoma, urethritis, inclusion conjunctivitis, neonatal pneumonia, lymphogranuloma venereum (LGV) |
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| Syndromes associated w chlamydia |
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| Serotype variants causing chlamydia trachomatis |
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| D-K. |
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| Causes NGU, often co-infected w N. gonorrhea, incubation time is 3-4 weeks |
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| Chlamydia trachomatis |
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| Men infected w c. trachomatis |
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| epididymitis, groin pain, burning during urination |
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| women infected w c. trachomatis |
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| vaginal discharge, lower abdomen pain, many asymptomatic, PID...which has many associated problems w pregnancy/birth/pain/death |
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| Inclusion conjunctivitis |
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| aka chlamydial conjunctivitis |
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| Mucopurulent discharge in eyes 2-25 days after birth. Inflammed and swollen. Associated w pneumonia |
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| Chlamydial conjunctivitis |
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| Lymphogranuloma venereum |
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| Think Chlamydia trachomatis. Serotypes L1-L3. |
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| When you get granulomas in lymph nodes near pubic region, think: |
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| LGV due to serotypes L1-L3 of Chlamydia trachomatis. |
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| What continents would you most likely find lymphogranuloma venereum? |
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| Africa, Asia, South America |
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| Trachoma |
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| Blindness. Acquired through genital to eye transmission, or via flies/gnat feet. Think poor regions of world. |
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| Growth of lashes into eye |
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| Trichiasis (from trachoma infection) |
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| Diagnosing and treating chlamydia trachomatis |
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| Diagnose via scrapes in mucosa. Treat w doxy or erythromycin |
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| 2nd leading cause of atypical pneumonia |
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| chlamydophila pneumoniae |
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| Chlamydophila pneumonia affects what age group |
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| elderly |
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| Mycoplasma pneumoniae affects what age groups? |
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| Younger. Not elderly too much! |
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| This airborne disease causes bronchitis, sinusitis, pharyngitis, and atypical pneumonia...and diagnosis is difficult |
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| C. pneumoniae |
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| This pneumonia may be associated w atherosclerosis |
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| C. pneumoniae |
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| Treating C. pneumoniae |
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| Tetracycline or macrolides |
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| Parrot fever |
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| Caused by Chlamydophila psittaci |
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| Psittacosis, ornithosis, and parrot fever caused by |
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| Chlamydophila psittaci |
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| Breathing contaminated bird feces causes: |
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| Chlamydophila psittaci |
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| Treating chlamydophila psittaci |
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| Respiratory isolation, tetracycline or macrolides |
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| Presentation of chlamydophila psittaci |
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| fever, chills, headache, pneumonitis. Cna progress to high fever, confusion, INTERSTITIAL pneumonitis, vomiting, cyanosis, encaphalitis, coma |
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| Psittacine birds |
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| Parrots, toucan and other brightly colored exotic birds |
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| Helical, G- like, duale membrane, labile, contain endoflagella |
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| Spirochetes |
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| Spirochete pattern of disease |
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| 1) Invasive 2) Latent 3) Secondary and then tertiary disease 4) Immune-mediated tertiary disease |
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| Key pathogen in treponema |
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| T. pallidum. Makes hyaluronidase that helps w perivascular penetration. Induces destructive immune response. |
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| 3rd most common STD in US |
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| Syphilis |
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| How syphilis is transmitted |
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| transplacentally or via sex |
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| Phases of syphilis |
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| Primary - localized lesion Secondary - Disseminated w lesions Tertiary - cardiac, connective tissue, or CNS disease (after period of latency) |
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| Primary syphilis |
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| Treponemes enter mucus membranes, multiply, then spread through lymph/blood. *10-120 days for intense inflammation. *Get hard, painless, shallow ulcer. *Also get satellite buboes. |
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| When secondary syphilis sets in |
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| 6-8 weeks after primary chancre/ulcer |
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| Secondary syphilis symptoms |
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| Flu-like, then disseminated skin rash in skin/mucous lining. Rash/other symptoms disappear in 2-6 weeks |
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| Late latent syphilis |
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| Women can spread disease in utero during this stage |
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| Early latent syphilis |
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| First year after resolution of primary or secondary syphilis |
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| Treponemes present during latent syphilis? |
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| Yes. Grow on endothelium and induce inflammatory response. This pushes patient towards the tertiary stage of syphilis. |
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| Infectious during tertiary syphilis? |
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| No |
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| Gumma |
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| granulomatous lesions 1-10 years after primary syphilis. Called late benign syphilis. |
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| Neurosyphilis |
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| A form of tertiary syphilis. Associated w HIV. 8% of patients develop between 5-35 years after primary syphilis |
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| Cardiovascular syphilis |
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| A tertiary syphilis |
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| Risk of transplacental transfer of primary syphilis to baby |
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| 100% |
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| Transplacental transfer of syphilis during secondary syphilis |
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| 90% |
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| Risk of transplacental transfer of syphilis during tertiary syphilis |
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| 30% |
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| Congenital syphilis |
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| Patients will become sero-positive and will have multi-organ problems. *Deafness, blindness, cardio problems |
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| Hutchison's incisors |
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| Think congenital syphilis |
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| Saddle nose |
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| Think congenital syphilis |
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| 2 types of tests for syphilis |
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| Nontreponemal and treponemal. *Nontreponemal is a screening test. *Treponemal is a confirmation and highly specific test. |
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| FTA-ABS |
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| Treponemal test, confirming less specific syphilis tests |
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| Treating syphilis |
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| Penicillin G. If allergic to this, use Tetracycline or Doxy |
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| Vaccine for syphilis? |
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| No |
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| Borrelia burgdorferi |
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| Lyme disease |
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| Borelia recurrentis |
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| louse-borne relapsing fever |
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| Borrelia hermsii |
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| tick-borne relapsing fever |
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| Most reported arthopod-borne disease in US |
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| Lyme disease |
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| Ixodes scapularis --> Humans. What disease? |
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| Lyme disease. Ixodes scapularis is deer tick. |
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| Most lyme disease in what 2 regions of US? |
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| Northeast, and Minnesota/Wisconsin region |
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| Can be cultured in vitro, lacks LPS toxin, and genome encodes 135 lipoproteins |
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| Borrelia burgdorferi |
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| OspA |
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| Virulence factor of Borrelia burgdorferi. Expressed in unfed ticks. OspA is required for tick colonization. |
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| OspC |
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| Virulence factor of Borrelia burgdorferi. Expressed during tick feeding and the early phase of mammal host infection. This is required for infection of humans. |
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| Stage 1 of lyme disease |
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| 3-30 days after tick bite. Last 1 month. Papule spreads to become erythema migrans. Flu-like (headache, fatigue, low fever) and lymphadenopathy. |
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| Percentage of patients w stage 1 lyme disease that progress to stage 2 |
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| 73% |
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| Stage 2 of lyme disease |
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| Disseminated disease for 1-9 months. Neuro (facial palsy), cardiac, migratory pain, chronic fatigue. |
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| Stage 3 lyme disease |
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| Acute or chronic arthritis due to lipoproteins in joints, causing immune complexes. |
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| Southern tick-associated rash illness (STARI) |
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| forms skin lesion similar to erythema migrans in lyme disease |
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| Are serological tests for lyme disease definitive? |
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| No. Many false positives and negatives. Lyme disease should not be diagnosed solely on basis of sero tests. |
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| Treatment of lyme disease |
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| Oral doxycycline or amoxicillin |
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| Vaccine available for lyme disease? |
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| No. Withdrew from market in 2001. |
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| Hard ticks |
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| Deer ticks are hard ticks and slow feeders. |
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| Tick-borne relapsing fever occurs when/where: |
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| Summer, Western US. Think rustic cabins = tick-borne RUSTIC fever. SOFT TICKS! |
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| Louse-borne relapsing fever occurs where: |
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| Africa. Mortality high (30-70%) |
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| Symptoms of relapsing fevers |
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| 2-15 days after infection you get: FEVER, chills, headache, lethargy, muscle/joint pain, weakness. Possible photophobia or rash. Relapses for 5-10 days. Recurring attacks (up to 9) that get less severe. |
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| Treating relapsing fever |
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| Tetracycline or erythromycin |
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| Hook shaped on one or both ends |
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| Leptospira interrogans |
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| Bacteria colonize in renal tubules of rodents. They are aerobic spirochetes with LPS. Acquired via contact w infected animal urine/contaminated water. |
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| Leptospira interrogans |
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| Rice-field fever |
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| Aka Leptospirosis. Other names = hemorrhagic jaundice and yellow fever. |
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| Appear 2-20 days after infection. Disseminate to all tissues. Damage endothelial cells of small blood vessels and induce immune response/damage. |
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| Leptospirosis |
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| 2 phases of leptospirosis |
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| First phase - dissemination. flue like. Second phase - headache, chills, ab pain, CONJUNCTIVAL SUFFUSION, ICTERIC DISEASE (Weil's disease), meningitis, and liver/kidney failure! |
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| Diagnosis of leptospira |
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| Antibodies to leptospira. Can take 8 weeks. |
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| Treatment of leptospira |
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| Penicillin G or tetracycline and macrolides |
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| Vaccine for leptospira |
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| No |
