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312 Cards in this Set
- Front
- Back
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Type of ends?
5'----GAA TTC----3' 3'----CTT AAG----5' |
Blunt ends
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Type of ends?
5'----GAATT C----3' 3'----C TTAAG----5' |
5' overlapping ends
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Type of ends?
5'----G AATTC----3' 3'----CTTAA G----5' |
3' overlapping ends
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Restriction?
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host degrades DNA that looks foreign
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Modification?
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host alters own DNA to avoid cleavage, usually by methylating C and A
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Restriction endonucleases?
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degrades DNA
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Southern blot?
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detect DNA
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Northern blot?
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detect RNA
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Western blot?
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detect protein/antigen
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Normal flora?
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indigenous, normally found in healthy people
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Symbiotic relationship?
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flora benefits the host
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Commensal?
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flora is neutral to host
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Resident flora?
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present for extended periods of time
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Transcient flora?
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present for brief periods of time, compete with resident
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Carrier state?
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normal flora contains potential pathogens that can be transmitted
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Pathogen?
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any organism that can cause disease
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Infection?
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organism starts to multiply, alters normal tissue
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Disease?
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resposne to injury leading to pathology
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Infectious disease?
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pathology caused by organism
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Virulence?
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ability of agent to cause disease
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Strict pathogen?
(aka obligate, frank, primary) |
regularly causes infection in non-immune healthy person
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Opportunistic pathogen?
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causes disease when person's immune system is compromised
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Enterotoxins?
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extoxins only found in gut
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Endotoxins?
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found in LPS, cause immune response
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Exotoxins?
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inhibit function of cell
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Catalase Positive?
Coagulase Positive? Mannitol Positive? |
Staphylococcus aureus
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Catalase Positive?
Coagulase Negative? Mannitol Negative? |
Staphylococcus epidermidis
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Catalase Positive indicates?
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can reduce H2O2 to O2, will see bubbles
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Coagulase Positive indicates?
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can clot plasma, cause fibrin formation around the bacteria
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Mannitol Positve indicates?
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can make acid from mannitol, makes pH plate turn yellow
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Infective endocarditis?
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bacteria infection within endocardium
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Subacute endocarditis?
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presence of abnormal valve
low fever, lasts up to 2 yrs follows dental procedure or surgery |
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Acute endocarditis?
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normal valve
high fever lasts days to weeks |
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Oral cavity organisms?
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S. sanguis
S. salivarius S. mutans |
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IV drug users get?
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Staphylococcus aureus, candida
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Endogenous pathogen?
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part of normal flora
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Exogenous pathogen?
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outside sources: animals, soil, insects, humans, water, food
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Facultative intracellular pathogens?
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Grow both inside and outside host cells
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Obligate intracellular pathogens?
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can only replicate inside host cells
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Adhesin?
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protein on surface of bacteria, binds to host receptor
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Lectins?
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high affinity to carbohydrate
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Contiguous spread?
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infection spreads to nearby organs, cells, tissues
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Hematogenous spread?
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bacteremia or septicemia-- enters bloodsteam
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Endotoxins found in?
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Gram-negative bacteria
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Exotoxins found in?
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Gram-positive and gram-negative
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Genes for exotoxins are in?
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phage or plasmid
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Genes for endotoxins are in?
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bacterial chromosomes
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Are endotoxins antigenic?
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weakly antigenic
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Are exotoxins antigenic?
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highly antigenic
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Exotoxins can be neutralized by?
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antibody
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Exotoxins and heat?
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stable, withstands high temps
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Endotoxins and heat?
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inactivated at high temps
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Endotoxins released when?
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bacteria cells lyse
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Endotoxins found in?
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LPS of cell walls
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Affect of endotoxins?
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stimulate macrophages and endothelial cells to secrete cytokines
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TNF-α produced by?
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macrophages
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Endotoxins in the blood vessels?
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cause platelets to stick to sides (adherance to vascular endothelium)
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DIC is?
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disseminated intravascular coagulation- blood clots
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Increased TNF-α?
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Shock/anaphylaxis--> death
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Exotoxins activate what complement?
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C3 and alternative pathway
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Exotoxin B subunit?
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binding of toxins to host cell surface
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Exotoxin A subunit?
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causes host cell damage
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Cytotoxins or cytolysins?
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destroy host cell components that are important for structure
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hemolysins?
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kill RBC, neutrophils, macrophages, platelets
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leukocidins?
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kill leukocytes
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2 neurotoxins?
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- botulinum toxin
- tetanus toxin |
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Enterotoxins cause?
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diarrhea (hypersecretion of water and electrolytes)
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Siderophores?
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steal iron from the host cell
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Hyaluronidase?
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hydrolyzes hyaluronic acid of connective tissue, helps to spread
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Post-streptococcal glomerulonephritis?
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Type III
immune complex deposition |
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Post-streptococcal rheumatic fever?
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Type II
autoimmune, molecular mimicry |
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infective phlebitis?
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bacterial/fungal infection of veins
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infective endarteritis?
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bacterial/fungal infection of arteries
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Subacute infective endocarditis?
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have abnormal heart valve
follows transcient bacteremia lasts up to 2 yrs |
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Acute infective endocarditis?
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infection of normal valve
lasts days to weeks |
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Agents of native abnormal/damaged valve endocarditis?
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viridans streptococci (found in oral cavity)
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Agents of native normal valve endocarditis?
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S. aureus, enterococci, Strep pneumoniae, Strep pyogenes
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Agents of prosthetic valve endocarditis?
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Staph epidermidis, candida
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Agents of IV drug use endocarditis?
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S. aureus, candida
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α-hemolytic?
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lyses some RBC, plate turns greenish
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β- hemolytic?
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lyses ALL RBC
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γ- hemolytic?
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non-hemolytic
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Staph aureus is ___ hemolytic?
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β- hemolytic
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Protein A?
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binds Fc part of IgG to activate complement and prevent opsonization
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Coagulase?
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activates thrombin, cause clotting (esp. in fingers)
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Lipase?
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breaks down lipids around hair follicles, body surface
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S. aureus contains enzymes?
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coagulase, hyaluronidase, staphlokinase, lipase
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Exfoliatin?
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breaks down stratus corneum in skin, causes SSSS (staph scalded skin syndrome)
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Toxic shock syndrome toxin (TSST-1)?
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binds to MHC II on macrophages--> massive T cell release--> increase TNF-α
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Impetigo?
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blisters in young children
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Folliculitis (boils), furuncles, sties?
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infection of hair follicles with pus
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Carbuncles?
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interconnected abscesses
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Food poisoning?
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ingestion of S. aureus endotoxin, recover within 2 days
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Toxic Shock Syndrome?
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S. aureus releases TSST-1 during infection of vagina...tampon case
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Osteomyelitis?
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abcess in bone, common under 12 yrs old
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bullous impetigo?
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large blisters that can rupture
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90% of Staph aureus are resistant to?
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penicillin (penicillinase)
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Coagulase + means?
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can clot blood
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Mannitol + means?
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can ferment mannitol,
turns agar yellow from acid |
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MRSA treated best with?
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vancomycin
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Prosthetic valve endocarditis caused mainly by?
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Staph epidermidis
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non-hemolytic, white colonies on blood agar indicative of?
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S. epidermidis cultures
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Enterococcus was formerly known as?
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Group D strep
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Group A strep includes?
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Strep pyogenes
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Group B strep includes?
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Strep agalactiae
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Catalase negative?
α- hemolytic? optochin resistant? |
Viridans streptococci
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S. sanguis causes?
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dental plaque
*most common* |
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S. mutans causes?
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cavities, tooth decay
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before dental procedures?
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should take pcn antibiotics to prevent heart valve damage
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pharyngitis mainly caused by?
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group A strep
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Epiglottitis mainly caused by?
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Hemophilus influenzae, type b
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otitis media mainly caused by?
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strep pneumoniae
hemophilus influenzae moraxella catarrhalis |
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Pharyngitis?
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inflamed throat, pain on swallowing, red swollen pharyngeal mucosa
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Otitis media?
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inflamed middle ear, fluid behind swollen red tympanic membrane, common in children
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M protein?
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attach to epithelial cells w/keratin
cross reactive with heart muscle |
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F protein?
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binds fibronectin in upper respiratory tract, upper female genital tract
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Necrotizing fasciitis?
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infection of fat and fascia
"flesh-eating bacteria" |
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Scarlet fever?
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rash on tongue or skin w/infection, caused by pyrogenic toxin
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Pyrogenic toxin?
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*superantigen*
toxic damage to skin, scarlet fever, delayed hypersensitivity response |
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Superantigen causes?
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release of IL-1, IL-2, IL-6, TNF-α
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pharyngitis and scarlet fever transmitted by?
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droplet infection from respiratory system
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gram positive?
catalase negative? α or γ hemolytic? |
Enterococcus
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Enterococci grow in?
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6.5% NaCl at 45C
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Catalase negative?
α hemolytic? optochin resistant? |
viridans streptococci
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chorea?
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uncontrolled involuntary movements
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gram positive?
catalase negative? β-hemolytic? |
strep pyogenes
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test for strep?
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ASO titer
anti-streptolysin O |
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catarrhal stage?
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1-2 weeks
lots of mucus from nose |
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paroxysmal coughing stage?
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2-4 weeks
coughing 40-50x/day elevated WBC |
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convalescent stage?
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3-4 weeks
gradual fade of symptoms |
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Toxic Shock Syndrome causes?
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TSST-1 penetrates vaginal mucosa, stimulates TNF-α and IL-1 release
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S. aureus gastroenteritis causes?
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N/V, diarrhea, abdominal pain for 12-24 hrs...basic food poisoning
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S. aureus gastroenteritis treated by?
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supportive care, caused by endotoxin so can't use antibiotics.
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Toxic Shock Syndrome symptoms?
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sudden onset of fever, N/V, watery diarrhea, rash, peeling of palms and soles of feet, organ damage
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Staph Scalded Skin Syndrome?
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caused by exfoliatin toxin, middle layer of skin sloughs off, usually in newborns with infected recently severed umbilical cord
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S. aureus-caused pneumonia?
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follows viral flu, quick onset fever, chills, lobar lung consolidation, pus in pleural space, cause holes in lung
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S. aureus-caused osteomyelitis?
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boys under 12, infection spreads to bone with fever and shakes
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S. aureus-caused endocarditis?
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sudden high fever, chills, usually mitral valve affected but normal to begin with
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S. aureus-caused septic arthritis?
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enters synovial fluid, have red swollen joint, fluid is yellow with high neutrophils
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S. epidermidis associated with?
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prosthetic heart valves, catheters
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S. saprophyticus associated with?
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UTI in sexually active young women in the community
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Gram positive, spore forming rods? (2)
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Bacillus and Clostridium
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Bacillus and oxygen?
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aerobic
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Clostridium and oxygen?
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anaerobic (air-tight CLOSet)
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Bacillus anthracis spores found in?
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soil, cows, sheep, goats
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Anthrax encoded on which plasmids?
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pX01 and pX02
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B. anthracis capsule?
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composed of protein (poly-D-glutamic acid)
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Anthrax spores germinate in the?
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macrophages located where the contact occurs
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anthrax exotoxin causes?
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localized tissue necrosis- black lesion with edema (malignant pustule)
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Woolsorter's disease?
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anthrax spores activated in lung macrophages, cause mediastinal widening, pleural effusions
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Gastrointestinal anthrax (rare)?
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ingested anthrax releases exotoxin, causes necrotic lesion in the intestine, vomiting, bloody diarrhea
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Edema factor (EF)?
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A subunit of exotoxin, increases cAMP which impairs neutrophil function, massive edema occurs
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Protective Antigen (PA)?
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like the B subunit, helps EF enter macrophages
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Lethal factor (LF)?
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inactivates protein kinase, stimulates macrophage to release TNF-α and IL-1--> shock
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People at risk for anthrax?
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petting or taking care of goats and sheep, military personnel, postal workers in 2001
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Treatment for anthrax?
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penicillin, doxycyclin, ciprofloxacin, levofloxacin
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Anthrax vaccine for humans contains?
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Protective antigen
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B. cereus causes?
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food poisoning ()
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B. cereus heat-labile toxin?
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like E. coli and cholera, cause N/V, diarrhea, abdominal pain for 12-24 hrs
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B. cereus heat-stable toxin?
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like S. aureus, short incubation with severe N/V and limited diarrhea
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Clostridium botulinum neurotoxin?
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blocks release of ACh from nerve terminals
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Botulism toxin causes?
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flaccid muscle paralysis
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Botulism toxin found in?
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smoked fish, canned vegetables, honey
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Botulism toxin treatment?
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anti-toxin through passive immunity to bind plasma toxins
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Infant botulism?
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floppy baby syndrome, baby eats honey with botulism spores
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Botulism symptoms in adults?
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muscle weakness, respiratory paralysis
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Clostridium tetani found?
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soil, animal feces
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Tetanus toxin causes?
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inhibition of GABA and glycine causing sustained contraction
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Risus sardonicus?
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"sardonic grin", facial muscle spasm
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patient with wound who was immunized but no tetanus booster in 10 years?
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need booster only
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Tetanus booster?
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given every 10 years, regenerates cirulating antibodies
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Trismus?
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lockjaw, causes risus sardonicus
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patient with wound with no tetanus immunity?
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need booster and passive antibody immunity
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Treatment for patient with tetanus (5)?
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passive immunity, booster, antibiotics, muscle relaxants, wound cleansing
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Clostridium perfringens found exogenously in?
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spores found in soil, water, sewage
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C. perfringens causes?
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gas gangrene and food poisoning
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C. perfringens found endogenously in?
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GI tract, female genital tract
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C. perfringens infections secondary to?
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abdominal surgery, trauma, amputations
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Gas gangrene/myonecrosis?
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fever, hemolysis, extensive necrosis, jaundice, gas, foul smell, shock, death
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C. perfringens cellulitis/wound infection?
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necrotic skin exposed to bacteria, bacteria grows into normal tissues
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Crepitus?
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moist, spongy, crackling consistency of skin from gas
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Lecithinase?
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hydrolyzes lecithin and sphingomyelin, disrupts cell and mitochondrial membranes
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C. perfringens contains enzymes (4)?
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collagenase, hyaluronidase, DNAse, lecithinase
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clostridial myonecrosis?
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trauma, C. perfringens enters muscle, releases exotoxins that destroy surrounding muscle, black fluid comes out of skin
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Treatment of C. perfringens?
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hyperbaric oxygen, removal of necrotic tissue, pcn
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C. difficile causes?
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pseudomembranous colitis (diarrhea)
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C. difficile common after?
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use of ampicillin, clindamycin, cephalosporins
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B. cereus spores found on?
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steamed or rapidly fried rice
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C. difficile toxin A?
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caues diarrhea
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C. difficile toxin B?
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kills colonic cells
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C. difficile treatment?
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discontinue initial antibiotic treatment, treat with METROnidazole or VANcomycin
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Why treat C. difficile with metronidazole and vancomycin?
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not absorbed into bloodstream, cruise into GI tract
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Gram positive, non-spore forming rods (2)?
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Cornyebacterium diptheria, Listeria monocytogenes
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Gram positive cocci(2)?
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staph and strep
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Cornyebacterium diptheriae effects mainly?
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children
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All effects of C. diptheriae due to?
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potent exotoxin
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C. diptheriae grows on?
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Tinsdale agar, contains potassium tellurite agar
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anaerobic, non-spore forming rod?
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Bacillius fragilis
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B. fragilis found?
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normal flora in GI tract
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B. fragilis responsible for most?
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infections below the diaphragm
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B. fragilis fatty acids?
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decrease phagocytosis, decrease Reactive Oxygen Species like H2O2
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B. fragilis treated with what drugs (5)?
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aminoglycosides, clindamycin, cefoxitin, chloramphenicol, cephalosporins (A4C)
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B. fragilis and penicillin?
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50% are resistant
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B. fragilis treatment?
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wound management and drainage
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Many GI tract infections caused by what family?
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Enterobacteriacea
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Gram negative?
Catalase positive? Oxidase negative? facultative anaerobes? |
Enterobacteriacea family
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Genus with type III secretion systems (4)?
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Escherichia, Salmonella, Yersinia, Shigella
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Foodborne GI pathogens (main 4)?
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Salmonella, Campylobacter, C. perfringens, Vibrio parahemolyticus
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Waterborne GI pathogen?
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Vibrio cholera
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Gastroenteritis?
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diarrhea, nausea/vomiting, abdominal discomfort
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diarrhea?
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frequent and/or fluid stool
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dysentery?
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blood and pus in feces
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enterocolitis?
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inflammation of large and small intestine
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Vaccines developed for?
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Salmonella typhi, Vibro cholera
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Bacillus cereus emetic toxin?
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usually in rice (chinese food), N/V, 4 hr incubation, heat stable
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Bacillus cereus diarrhea toxin?
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usually in meats/sauces, profuse diarrhea, 24 hr incubation, heat labile
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B. cereus diarrhea toxin resembles?
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V. cholera and ETEC, raises cAMP levels
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6 types of E. coli?
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ETEC, EPEC, EHEC, EIEC, EAEC, DAEC
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ETEC produces what toxins?
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LT and ST
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EHEC serotype?
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0157:H7
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EHEC triad?
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nephropathy, thrombocytopenia, hemolytic anemia
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EHEC toxins?
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VT1 and/or VT2..similar to Shigella
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EHEC toxins do what?
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bind to 23S ribosomal subunit, inhibit protein synthesis
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EHEC in children?
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hemolytic uremic syndrome (kidney damage), can be fatal
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EHEC in adults?
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bloody diarrhea, colitis
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EIEC symptom?
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dysentery, perforates large intestine wall
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EAEC and stool?
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mucus but NO BLOOD
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EAEC appearance?
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stacked brick
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DAEC infects?
|
young children 1-5 yrs
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DAEC stool?
|
watery, high risk for dehydration
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E. coli leading cause of?
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UTI and neonatal meningitis
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DAEC in intestine?
|
elongates microvilli and adheres so can't absorb
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EPEC stool?
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watery, profuse diarrhea
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EPEC causes what?
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infantile gastroenteritis and Traveler's diarrhea
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EPEC adheres to?
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epithelium
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Treat E. coli with?
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TMP-SMX: trimethoprim and sulfamethoxazole
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Vibrio cholera found where?
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Southeast Asia, Northern Africa, Peru, Brazil, coastal Texas and Louisiana
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V. cholera mucinase toxin?
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stimulates IL-8 to cause inflammation, loss of tight junctions
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v. cholera on TCBS media?
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turns yellow
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V. cholera is a ______ fermentor?
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lactose fermentor
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V. cholera symptoms?
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rice water stool, frequent, non-bloody diarrhea causing acute dehydration
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V. cholera source?
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crustaceans or surface water
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Treat V. cholera with?
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hydration, electrolytes, tetracycline, doxycycline
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comma shaped rod?
gram negative? oxidase positive? |
V. cholera
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Vibrio parahemolyticus on TCBS media?
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turns blue-green
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TCBS media contains?
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bile salt and sucrose
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V. parahemolyticus enterotoxin?
|
increases Ca+2 secretion
|
|
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V. parahemolyticus found where?
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cruise ships, 25% of diarrheas in Japan, coastal USA
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V. parahemolyticus symptoms?
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explosive watery diarrhea, occasionally bloody, N/V, cramps and fever
|
|
|
V. parahemolyticus causes increase in serum ____?
|
serum iron
|
|
|
Hemochromatosis?
|
hyperglycemia, hyperbilirubinemia, increased serum iron
|
|
|
Vibrio vulnificus causes?
|
septicemia, hemochromatosis, skin infection
|
|
|
V. vulnificus on TCBS turns?
|
blue-green
|
|
|
V. vulnificus found in?
|
shellfish in Mexico and Gulf Coast
|
|
|
Clostridium difficile caused by?
|
prolonged antibiotic treatment
|
|
|
C. difficile structure?
|
gram positive anaerobic rod
|
|
|
C. difficile Toxin A?
|
fluid secretion, hemorrhagic necrosis
|
|
|
C. difficile Toxin B?
|
depolymerizes actin, destroys cytoskeleton
|
|
|
Chocolate agar?
|
blood argar heated to 80-90 degs to partially lyse RBC
|
|
|
Modified Thayer Martin Medium?
|
chocolate agar that selects for Neisseria by adding antibiotics
|
|
|
Colistin?
|
inhibits most gram negative bacteria EXCEPT Neisseria
|
|
|
Vancomycin?
|
inhibits most gram positive bacteria
|
|
|
Nystatin?
|
inhibits yeast
|
|
|
Trimethoprim lactate?
|
prevents swarming growth of species
|
|
|
Unlike most bacteria, Neisseria ferment in?
|
oxidative pathway
|
|
|
Phenol indicator in acid turns from ____ to _____?
|
red to yellow
|
|
|
N. Gonorrheae ferments?
|
Glucose
|
|
|
N. MeninGitidis ferments?
|
Glucse and Maltose
|
|
|
N. meningitidis killed by?
|
naturally within 24 hrs, antiseptics, soaps
|
|
|
N. gonorrheae killed by?
|
drying, heating, dies naturally outside of host within 1-2 hrs
|
|
|
N. meningitidis smooth?
|
encapsulated, resistant to phagocytosis, virulent
|
|
|
N. meningitidis rough?
|
no capsule, avirulent
|
|
|
Most common N. mengitidis capsule serotypes worldwide?
|
A and B
|
|
|
Most common N. mengitidis capsule serotypes in US?
|
B, C, W135, Y
|
|
|
IgA1 protease?
|
cleaves Fc region from IgA, decreases attachment of bacteria to epithelial cells, activates alternative complement pathway
|
|
|
Lipo-oligosaccharide (LOS) causes?
|
rash, septic shock from IL-1 and TNF-α
|
|
|
Lipo-oligosaccharide (LOS) contains?
|
Lipid A + core oligosaccharide
|
|
|
Lipo-oligosaccharide (LOS) binds?
|
Toll-like receptors on phagocytic cells
|
|
|
N. meningitidis infection starts as?
|
mild nasopharyngitis
|
|
|
N. meningitis infection can be stopped in the nasopharynx if?
|
antibodies and complement are present to limit colonization
|
|
|
N. meningitis in adults?
|
fever, N/V, photophobia, petechiae or purpura
|
|
|
N. meningitis in babies?
|
vomiting, hypothermia, apnea, seizures, coma, poor motor tone
|
|
|
Petechiae?
|
tiny hemmoragic spots in the skin
|
|
|
Purpura?
|
large hemorrhages into the skin
|
|
|
Meningitis causes?
|
intense inflammatory response inside subarachnoid space
|
|
|
Other symptoms of meningitis?
|
nuchal rigidity, irritability, confusion
|
|
|
nuchal rigidity?
|
stiff neck
|
|
|
Meningiococcemia causes?
|
small vessel thrombosis, skin lesions leading to petechial rash and purpura, destroys adrenal glands
|
|
|
Meningiococcemia caused by?
|
endotoxin released from live and dead bacteria
|
|
|
Fulminant meningiococcemia symptoms?
|
sudden high fever, chills, N/V, headache, muscle pain, confusion
|
|
|
Fulminant mengingiococcemia mortality?
|
many die within 24 hrs despite hospitalization
|
|
|
Waterhouse-Friderichsen syndrome
|
fulminating meningitis and bacteremia, death from adrenal insufficiency
|
|
|
N. meningitidis establishes systemic infections in?
|
people without serum antibodies against cell wall antigens
|
|
|
N. meningitidis highest in?
|
infants 3 mos to 1 yr, young adults, children 5-6
|
|
|
Spinal tap shows?
|
high WBC, low glucose, high protein
|
|
|
Treatment of meningitis?
|
penicillin, cefotaxime
|
|
|
Prevention of meningitis for playmates and siblings?
|
rifampin or minocycline
|
|
|
Vaccines for meningitis?
|
contains protein from groups A, C, Y, W135
|
|
|
Strep pneumoniae causes meningitis how?
|
spread to CNS after bacteremia, ear or sinus infections, head trauma
|
|
|
Strep pneumoniae in population?
|
highest in community-acquired meningitis in adults
|
|
|
Strep pneumoniae risk groups?
|
alcoholics, sickle cell disease, multiple myeloma
|
|
|
strep pneumoniae mortality?
|
up to 40%
|
|
|
Treatment of strep pneumoniae?
|
penicillin, cefotaxime, ceftriazone, vancomycin
|
|
|
Age group at risk for E. coli meningitis?
|
neonates
|
|
|
Age group at risk for Group B strep meningitis?
|
neonates up to 3 months
|
|
|
Age group at risk for Listeria monocytogenes meningitis?
|
neonates up to 3 mos and elderly
|
|
|
Age group at risk for Hemophilus influencae meningitis?
|
6 mos to 5 yrs, occasionally found in all
|
|
|
Age group at risk for Neisseria meningitis?
|
6 mos to 5 yrs, young adults, up to 60 yrs old
|
|
|
Age group at risk for Streptococcus pneumoniae meningitis?
|
all age groups especially elderly
|
|
|
Acute/purulent meningitis?
|
headache, fever, nuchal rigidity, nausea, lethargy, seizures, reduced consciousness
|
|
|
Chronic meningitis?
|
progression over weeks, caused by M. tuberculosis, fungi, parasites
|
|
|
Lumbar puncture most sensitive in?
|
S. pneumoniae, H. influenzae, N. meningitidis
|
