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67 Cards in this Set
- Front
- Back
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What are the pathogenic factors for Clostridium perfringens?
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Collagenase
Hyaluronidase Necrotizing Toxin Lecithinase DNAase |
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Laboratory ID for Clostridium perfringens :
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-growth on blood agar in absence of O2
-gram stain -gas bubbles and clot formation in milk culture |
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Paragonimus Infection
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parasitic worm endemic to East Asia/Africa
-eggs hatch in the duodenum, burrow through intestinal wall and enter blood stream, travel though pleura then to lungs -can be transmitted by consuming freshwater crab/crayfish |
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Diseases associated with Staph aureus:
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(1) Cutaneous infection
(2) Soft tissue infections (3) Food poisoning (4) Bacteremia (5) Toxic shock syndrome (6) Pneumonia (7) Methicillin resistant staph aureus |
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Enzymes associated with Staph aureus :
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-Catalase - detoxifies hydrogen peroxide
-Coagulase - protein that clots plasma -Penicillinase - has a beta-lactamase ring (in 90%) |
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Toxins associated with Staph aureus :
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-Leukocidin - kills white blood cells
-Exfoliative Toxin - dissolves intracellular 'glue' on skin cells -Enterotoxins - food poisoning -Toxic Shock Syndrome Toxin (TSST-1) (is a superantigen) |
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what are some other pathogenic factors of S. aureus (besides toxins)?
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-Capsule - inhibits phagocytosis
-Protein A -ties up antibody and blocks opsonization (binds to the Fc region) |
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Laboratory identification of S. aureus :
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-Growth on blood agar - beta-hemolysis (lyses rbc around the colonies)
-Catalase positive - detoxifies H2O2 into H2O + O2 -Coagulase positive - creates fibrin clot |
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Treatment for S. aureus
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-Cephalosporin (has a beta lactam ring)
-Vancomycin (for MRSA, no beta lactam ring) |
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Genetic mechanisms for MRSA :
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SCC(mec) gene segment = staphylococcal cassette chromosome mobile genetic element (large, mobile gene segment that carries drug resistance horizontally between bacteria)
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Triclosan
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used in antibacterial soaps, causes antibiotic resistance
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Fimbria
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composed of M protein covered fimbria + lipoteichoic acid
-aids in attachment to human cells (binds to fibronectin) |
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streptococcal group A pathogenic factors:
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-M protein + lipoteichoic acid - attachment
-Toxins (pyrogenic exotoxins, streptolysins O and S - hemolysins) -Hyaluronidase -Streptokinase -Streptodornase |
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Streptococcus Pyogenes infections:
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•Localized - pharyngits, impetigo
•Invasive - -endocarditis -scarlet fever -Toxic Shock Syndrome -necrotizing fasciitis |
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Post-streptococcus infections (group A)
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-Glomerulonephritis (strep antigen-antibody complexes settle on kidney mambranes and damage glomeruli)
-Rheumatic fever (antibodies to cell membrane antigens in some strains cross-react with heart muscle and valves) |
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Lab identification of Group A Strep
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-gram positive cocci in chains
-beta-hemolysis on blood agar -rapid ID for streptococcus (quickVue test) |
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Treatment for Group A Strep
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Penicillin
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Streptococcus pneumoniae causes :
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-Bronchial pneumonia = infection of the bronchioles
-Lobar pneumonia = infection of alveoli |
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Lab ID of Strep pneumoniae:
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Quellung Test - coat bacteria capsule with antibody, becomes visible under microscope
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Streptococcus Mutans causes
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secretes dextran - becomes plaque, causing dental carries
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Identification of group B streptococcus:
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cAMP Test - augmented hemolysis
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Enterococcus faecalis -
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-most frequent cause of nosocomial infections
-primary infections: UTI, wounds, bacteremia, endocarditis -infants : meningitis, bacteremia |
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Pathogenic factors of enterococcus faecalis
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-colonization factors (adhesions) - facilitate plasmid exchange and adhere to cells
-Bacteriocins - virus-like bactericidal substances that inhibit growth of other gram + bacteria -beta-lactamase |
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Pathogenic factors of enterbacteriaceae:
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(1) Capsule (K antigen)
(2) Endotoxin (3) Exotoxin (eg travellers's diarrhea enterotoxin) (4) Pilus (5) Intracellular multiplication (protected from antibodies) (6) can be resistant to complement mediated killing |
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Traveller's Diarrhea Enterotoxin
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Enterotoxic E. coli
-toxin that acts on intestine -activates cAMP -cAMP causes ion excretion and water release by the cell |
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Enteroinvasive
Enteropathogenic Enterohemorrhagic |
(E. coli diarrhea diseases)
-diarrhea with bleeding -infant diarrhea -type of enteroinvasive, but very severe (O157:H7 - can cause hemolytic uremic syndrome - hemolysin of rbc and damage of kidneys) |
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Gastroenteritis / Colitis
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caused by Salmonella enteriditis and typhimurium
-nausea, vomiting, diarrhea (8-48 hrs) -ATR genes (acid tolerance response) - set of proteins that allow salmonella to survive pH of 2-3 in stomach acid by providing buffering effect |
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ATR genes
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Acid Tolerance Response genes
-in salmonella -set of proteins that allow bacteria to survive pH of 2-3 by providing buffering effect |
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Pathogenicity of Salmonella
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-bacteria attach to cell lining in intestinal tract
-bacteria invade/replicate in Microfold cells, then pass to macrophages, neutrophils, and lymphoid tissues -SPI-1 (salmonella pathogenicity island) - codes for 2 proteins that allow bacteria to enter cells lining intestinal tract |
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Salmonella typhi
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-colonization of gall bladder
-symptoms = fever, headache, malaise, anorexia, diarrhea |
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Superspreader
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(typhoid mary) person who spreads disease to many people, but does not show symptoms
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Septicemia
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most invasive salmonella infection
-most likely to occur with S. typhi |
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Treatment of Salmonella infections:
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-gastroenteritis usually doesn't require treatment
-replacement of fluids and electolytes -ampicillin or cephalosporin (for invasive infections) |
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Types of Shigella :
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-Shigella sonnei
-Shigella flexneri -Shigella dysenteriae |
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Shigella sonnei and Shigella flexneri
-cause - -pathogenic factors - |
•Gastroenteritis
•Pathogenic factors - -pilus (adhere to lining of intestine) -endotoxin (inflammation of intestinal wall) -infection of manifold cells |
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Shigella dysenteriae
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-profuse, watery diarrhea
-severe cramps, pus, and blood -invasion of intestinal mucosa -exotoxin (shigella dysenteriae exotoxin) -produces apoptosis in phagocytic cells -causes Hemolytic Uremic Syndrome -treatment - cyprofloxacin |
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shigella dysenteriae exotoxin
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-A subunit - enters intestinal, cuts ribosomal RNA and disrupts cellular protein synthesis, causes Hemolyic Uremic Syndrome if enough toxin enters blood stream
-B subunit - binds to host cell glycolipid |
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Pathogenic factors for Helicobacter pylori
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-flagella - helps to burrow in mucus membrane
-Acid Inhibitory Protein - buffering effect in bacteria -Proteases, Hemolysins (enzymes) -Adhesins -Urease -Mucinase-disrupts gastric mucus -Superoxide dismutase -Catalase -breaks down peroxides |
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Lab ID for Helicobacter pylori
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-Skirrows media - chocolate agar + antibiotics - makes a selective media for H. pylori
-Urease Test - put sample on slide, add urea - CO2 bubbles and becomes red (from yellow) |
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Treatment for Helicobacter pylori
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Triple treatment -
-Metronidazole -Tetracycline -Pepsid AC |
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Cag A gene of H. pylori
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-Chronic Astrophic Gastritis
-proteins promoted by the gene activate kinases associated with cancer |
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Campylobacter Gastroenteritis
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(caused by jejuni and coli)
-diarrhea, 5-8 days, fever, headache -sometimes causes septicemia -lipopolysacchardie endotoxin -cytopathic toxins |
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Lab ID of campylobacter
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-Skirrow's media - chocolate agar + antoibiotics
-requires low O2 and high CO2 for growth |
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Human prion diseases
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-Kuru (fore tribe in new guinea)
-Creutzfold-Jakob Disease (CJD) -Gerstmann-straussler-scheinker syndrome -Alper's Syndrome (infants) |
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Animal prion diseases
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-Scrapie (sheep and goats)
-transmissible mink encephalopathy -chronic wasting disease (mule, deer, elk) -Bovine spongiform encephalopathy (Mad Cow) |
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bacteria that causes gonorrhea :
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Neisseria gonorrhoeae
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bacteria that causes meningitis
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Neisseria meningitidis
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bacteria that causes syphilis :
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Treponema pallidum
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Membrane proteins for Neisseria
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-Por -creates pores through outer membrane
-Opa - adhesion molecule -Rmp - helps Por form pores |
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Acquired syphilis
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-primary syphilis - chancre, lymphadenopathy
-secondary syphilis - fever, rash over whole body -tertiary syphilis - destructuring of multiple tissues |
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treatment for gonorrhea
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Ceftriaxone - synthetic penicillin derivative with penicillinase-resistant lactam ring
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Gummas
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granulomas in skin, bones, liver
(types of tertiary syphilis) |
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Congenital Syphilis
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latent infection
-multirogan malformation -death of fetus or newborns |
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diagnosis of primary syphilis:
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-use darkfield microscope to see rods
-fluorescent antibody staining -serological tests -indirect immunofluorescece |
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Types of tuberculosis lesions:
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(1) Exudative - acute inflammatory reaction
-alveoli filled with fluid -phagocytic cells surround bacteria (2) Productive -granuloma formation -tubercle formation |
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granuloma
tubercle |
•develops into tubercle
-center = giant cells containing bacteria -outer = lymphocytes and fibroblasts •Tubercle - center becomes necrotic and caseous -fibrous capsule develops and califies |
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Dormant infection of TB
Latent infection of TB |
-does not develop productive or exudative
-also quiet, occurs after exudative and productive, occurs when no treatment |
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Stages of TB
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-Primary infection (exudative and productive lesions develop)
-Latency -Reactivation |
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testing for TB
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tuberculin skin test:
-testing atnigen -positive test - red area develops in 24 -48 hours |
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False positive for TB
False negative for TB can be cause by ... |
•nontuberculosis mycobacterium, BCG vaccination
•recent TB infection, very young age, live-virus vaccine |
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Diagnosis of TB
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-sputum smear is stained with Ziehl-Neelson stain
-fluorescence antibody stain -sample is cultured in selective media -positive cultures identified with PCR |
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Treatment for TB
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Isoniazid + rifampin for 9 months
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stages of HIV
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-acute HIV infection
-clinical latency -persistent generalized lymphadenopathy -AIDS |
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Lab diagnosis of HIV
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Serological tests:
-screening assays - EIAs -confirmatory assays - western blot |
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HIV treatment
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-Combination therapy
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HAART
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highly active anti-retroviral therapy
-2 nucleoside reverse transcriptase inhibitors and protease inhibitors |
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types of anti-retroviral susceptibility testing :
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(1) Phenotypic - difficult and expensive, more accurate
(2) Genotypic - the RT and Protease genes are sequenced |
