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Microbiology
| Question | Answer |
|---|---|
| Gram Stain | + are violet, - is red. stain adheres to peptidoglycan in cell wall. |
| Acid-fast bacteria | bacteria with outer waxy layer with high mycolic acid content retain stain upon acid treatment |
| vancomycin | inhibits linking of disaccharides in cell wall. changing linkers leads to resistance |
| penicillin | inhibits peptide crosslinks, penetrates through protective wall and activates autolysin. resistance comes from penicillinase. |
| bacitracin | inhibits regeneration of lipid carrier |
| sulfa drugs | inhibit folic acid synthesis (metabolism) by competition |
| aminoglycosides (neomycin, streptomycin) | bind 30S ribosome |
| macrolids (azithromycin) | bind 50s ribosome |
| tetracycline | inhibits tRNA |
| rifampin | inhibit RNA synthesis |
| fluoroquinolines | inhibit DNA synthesis |
| fastidious | unusual/complex needs-special media |
| non-fastidious | easier to grow, standard agar |
| differential media | distinguish between bacteria (color change) |
| selective media | inhibits/grows specific bacteria (high salt inhibits most) |
| blood agar plates | test for hemolytic bacteria |
| beta hemolytic | white on blood agar plates |
| alpha hemolytic | green on blood agar plates |
| gamma hemolytic | no hemolysis on blood agar plates |
| MIC | minimum inhibitory concentration |
| testing for antibiotic resistance | zones of clearing, E strips |
| type III secretion systems | interacting with the cell for secretion of toxins |
| exotoxins | proteins that are released and do damage. range of toxicity. usually produced by gram + bacteria. neurotoxins, cytotoxins, enterotoxins. |
| hemolysin | pore-forming cytotoxin. (exotoxin) |
| CNF | disrupts G proteins affecting signaling |
| Shiga toxin (Stx) | inhibits protein synthesis, causes capillary thrombosis and inflammation. produced by EHEC and leads to hemolytic uremic syndrome. |
| Labile toxin (LT) | increases cAMP, leads to loss of electrolytes and water--diarrhea. produced by ETEC. |
| Stable toxin (ST) | increases cAMP, leads to loss of electrolytes and water--diarrhea. produced ETEC |
| Symptoms of toxins | fever, diarrhea, nervous symptoms, shock, destruction of blood vessels |
| UPEC symptoms | cause cystis (urinary bladder infections), pyelonephritis (pelvis and kidney infection). dysuria |
| UPEC epidemiology | gram - rods, reservoir for infection is intestinal tract |
| UPEC treatment | resistant to ampicillin. susceptible to sulfa drugs, fluoroquinolines. |
| EHEC symptoms | bloody diarrhea, no pus. endotoxic effects if antibiotics given |
| EHEC pathogenesis | cause attachment and effacing lesions, produce Stx which leads to HUS. no tissue invasion |
| HUS | hemolytic uremic syndrome, caused by EHEC O157:H7. Renal failure, hemolytic anemia |
| EHEC epidemiology | gram - rods, low infecting dose. caused by consumption of contaminated animal products |
| EHEC treatment | don't treat with antibiotics due to endotoxic effects. supportive care. |
| ETEC epidemiology | gram - rods, high doses in uncooked food, virulence genes on plasmid. cause traveler's diarrhea. |
| ETEC pathogenesis | LT and ST cause watery diarrhea, no blood or pus. no tissue invasion. Destruction of mucus on small intestine as ETEC grows on brush border. immunity can be acquired. |
| EPEC epidemiology | hospital outbreaks, problems for infants |
| EPEC pathogenesis | attachment and effacing lesions-attach to gut epithelial cells and inject proteins into cells to modify cytoskeleton to form pedestal |
| Enteric bacteria | gram - rods. encounter: food, feces, fomites, fingers, flies, fluid, fornication. |
| enterobacteriaceae | most common cause of UTIs; cause diarrhea; endotoxic shock if spread to blood; facultative. serotypes: O-LPS, K-capsule, H-flagellar protein |
| vibrionaceae | single, polar flagellum, found in salt water |
| Vibro cholerae epidemiology | low acid tolerance, good alkaline tolerance. O1 and O139 serotypes cause cholera. can survive in environment associated with shellfish. incubation period of 2 days. endemic in India, Africa, Latin America. |
| Vibro cholera pathogenesis | have toxin co-regulated pilus (TCP) and cholera toxin (CT). No invasion of host cells. CT activates G protein, which increases cAMP leading to hypersecretion of ions and water. |
| Vibro cholera treatment | rehydration, antibiotics to prevent transmission but they won't shorten duration. infection gives immunity. |
| Vibro cholera clinical aspects | rice water stool with flecks of mucus but no blood, massive fluid loss. rapid onset. prevention by water sanitation. |
| Vibro cholera chemotaxis | Flagella seems to be important for flagella and vibro follow a chemotactic gradient to lower small intestine. Without following chemotactic gradient, they can infect upper small intestine as well, making them more virulent. |
| Shigella epidemiology | strictly human disease. low infecting dose, non-motile. gram - rods |
| Shigella pathogenesis | acid-resistant. target M cells in small intestine, rearrange host cell actin to move. can break down membranes to leave pinocytic vessel. infect macrophages. cause ulcers by destroying eptithelial cells, dysentary (diarrhea, pus, blood), fever |
| Shigella clinical aspects | dysentary, fever, tenesmus (straining to pass stool), resolves in a week. antibiotics limit spread and duration. short-lived immunity from infection |
| Salmonella epidemiology | gram - rods. leading cause of food-borne intestinal infections. higher infecting dose than Shigella. human carriers. pili and flagella |
| Salmonella pathogenesis | motile, invade small intestine but don't break down pinocytic vacuole. infect macrophages and escape phagosome. |
| Typhoid fever | caused by salmonella. strictly human disease. infected macrophages spread throughout body, infect gallbladder, liver, kidney. treat with antibiotics to reduce mortality |
| Salmonella clinical aspects | typhoid fever: infected organs, treat with antibiotics. septicemia: blood infection, rapid fever enterocolitis: intestinal infection. low fever, bloody, watery, copius diarrhea, sometimes pus. treating with antibiotics may increase carrier state. |
| Staphlococci aureus epidemiology | gram + cocci, grape-clusters, non-motile, pyogenic (pus forming). Beta hemolytic (white/gold), colonize nose, can survive drying. |
| S. aureus toxins | alpha toxin: cytotoxin that forms pores in membranes exfoliative toxins: splits intraepidermal junctions and causes SSSS superantigen toxins: aggregate MHC II, only produced aerobically and cause TSS enterotoxin: heat stable, food poisoning |
| S. aureus pathogenesis | coagulase causes fibrin clot, kill leukocytes, lyse red blood cells, protein A on it's surface binds the Fc region of Ig |
| S. aureus clinical aspects | boils, skin abscesses from localized infection SSSS: staph scaled skin syndrome in babies due to exfoliative toxin TSS (TSST-1): toxic shock syndrome from superantigen toxin |
| S. aureus treatment | penicillin resistant MRSA-methicillin resistant s. aureus important to eliminate environmental carrier state by washing bedding |
| Streptococci Group A epidemiology | gram + cocci, grow in chains, non-motile, cause extensive tissue damage. pili |
| Strep group A toxins | streptolysins: cause Beta hemolysis superantigen toxins: cause scarlet fever and toxic shock C5a peptidase |
| Strep group A pathogenesis | pili and M proteins important in acute infections; escape phagocytosis by diminishing complement. |
| Strep group A clinical aspects | STSS-strep toxic shock syndrome, see site of infection, muscle pain, chills, nausea, organ failure pharyngitis scarlet fever-sandpaper rash, strawberry tongue skin infection rheumatic fever-carditis due to molecular mimicry immune system attack, arthr |
| Strep group B epidemiology | large colonies, non-distinct Beta hemolysis |
| Strep pneumoniae | diplococci, group b strep, alpha-hemolytic, secret pnuemonlysin which disrupts cilia of respiratory tract, capsulated to protect from phagocytosis. pneumonia begins abruptly, lasts 5-10 days. mostly affect young and old. |
| Strep group B pathogenesis | leading cause of bacterial meningitis, cause neonatal sepsis, pneumonia. treat with penicillin. |
| Clostridium | gram - rods, cause disease by exotoxins. anaerobic and fastidious growth requirements. spores can live in environment, easily spread in hospitals |
| C. perfringens | cause gagne green, food poisoning-rapid onset, mild |
| C. botulinum | potent neuro toxin blocks release of excitatory neuro-transmitters. flaccid paralysis, respiratory distress |
| C. tenani | toxin blocks release of inhibitory neuro-transmitters. binding is irreversible-must wait for new synapses to form. cause rigid paralysis. vaccine. |
| Pseudomonas aeruginosa | gram - rod, single polar flagellum. inhabits soil and water. flexible nutrient requirements and prevalent opportunistic pathogen. cause skin lesions, outer ear infections, problems if have cystic fibrosis. high antibiotic resistance. nocosomal infections |
| Neissera | gram - diplococcus. obligate human pathogens, there are asymptomatic carriers. pili and ligooligosaccharides (LOS) aid in attachment. phase variation: surface structures (pili, LOS, OMPs) change by recombination. |
| Neissera meningitidis epidemiology | rapidly progressive, spread person to person, 10% of people are carriers in nasopharynx. peaks in young (>2) and around 18 years old. serotype A causes epidemics |
| Neissera meningitidis pathogenesis | passes through mucuosa into bloodstream, capsule protects against complement, crosses blood-brain barrier. Treat with penicillin for active infection, rifampin for prophaylaxis. MCV4 vaccine. |
| Neissera gonorrhea epidemiology | difficult to grow-chocolate agar and CO2. difficult to detect carriers. no capsule |
| Neissera gonorrhea pathogenesis | localized genital infection, pus and dysuria, vaginal discharge, increase urination frequency, PID, disseminate gonococcal infection (DGI). transmission to infants result in blindness. single dose treatments of cephalosporins, quinolones, azithromycin. |
| Helicobacter pylori epidemiology | gram - bacillus, infects 1/3 of people but only a few clinically. associated with cancer. |
| Helicobacter pylori pathogenesis | infection fecal-oral, infect mucus layer in gastric mucosa, cause inflammation, can lead to ulcers, adenocarcinomas, epigastric pain. diagnose via endoscopy, culture. treat with antibiotics and acid-reducers. proteins: urease, vacuolating cytotoxin |
| Mycobacterium | acid-fast bacillus, strict aerobes, grow slowly, resistant to drying and disinfectants but not heat, biochemical tests to distinguish strains |
| Mycobacterium tuberculosis epidemiology | 1/3 of people infected; TB/HIV co-infection increases disease risk from 10% over lifetime to 10% annually; drug resistance; spread through air-respiratory droplets |
| Mycobacterium tuberculosis pathogenesis | droplets deposited in lungs, bacteria go to lymph nodes. 4 fates: killed; multiply and cause primary infection in 2-8 weeks (5%); remain dormant; reactivate after dormant phase (5%). skin test. treat with combination of antibiotics for long periods. |
| Mycobacterium leprae epidemiology | endemic in India, Africa, Brazil |
| Mycobacterium leprae pathogenesis | tuberculoid: isolated lesions lepromatous: lots of lesions |
| Treponema pallidum epidemiology | spirochete, strict human pathogen, causes syphilis, grows slowly in culture, gram - but without LPS, very sensitive to deviation from physiological conditions, spread by sexual contact. very sensitive to penicillin. |
| Treponema pallidum pathogensis | primary: 3 week incubation, painless chancre secondary: 2-8 weeks after chancre, rash, fever, skin lesions, warty erosions latent: no symptoms after secondary tertiary: 1/3 of people, 5-10 years after infection, neurosyphilis and cardiovascular syphill |
| Borrelia burgdorferi epidemiology | long spirochetes with multiple flagella and differentially expressed surface proteins (Osps). ticks infect mice (reservoir) and deer, which reinfect ticks, which infect humans. cause lyme disease. |
| Borrelia burgdorferi pathogensis | OspA (ticks) and OspC (humans) involved, lacks LPS but peptidoglycan causes inflammation. down-regulates immune response leading to a chronic state. |
| Borrelia burgdorferi clinical aspects | bulls-eye rash (erythema migrans) within a month of tick bite and febrile aches late disease: arthritis; nervous system-numbness, pain, paralysis, meningitis; cardiac-irregular heart rhythms; fatigue, headache treat with oral/IV antibiotics. |
| Rickettsia epidemiology | small, gram - cocci, poorly stained, obligate intracellular parasites (need cofactors and ATP); arthropod borne disease, humans accidental hosts. |
| Rickettsia pathogenesis | entry into cells by induced phagocytosis, escape from phagosome, exit via host actin propulsion, necrosis of cells. |
| Rickettsia clinical aspects | initial symptoms: fever, nausea, vomiting, no appetite, pain, headache later symptoms: rash, abdominal pain, joint pain, diarrhea classic triad: fever, rash, tick bite-only 3% treat with tetracylcine or doxycycline |
Created by:
clcazer
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