Bacterial Meningitis Flashcards
classic symptoms of meningitis
headache, fever, stiff neck, photophobia
pediactric meningitis symptoms
fever, refusing food, vomiting, fretful, pale blotchy skin, blank stare, drowsy, stiff neck, high pitched cry
neisseria meningitidis bacteriology
gram negative diplococci, facultative intracellular. encapsulated. oxidase positive, catalyse positive. ferments glucose and maltose. growth inhibited by fatty acids and metals, needs chocolate agar
N. meningitidis pathogenesis
transmitted by airborne droplets. colonise nasopharynx. infection often resolves without symptoms. IgG enhanced complement and neutrophils defend. many people immune by age 20
meningococcemia
if N. meningitidis enters bloodstream. colonizes joints, meninges. most common cause in age 2-18 range.
meningococci virulence factors
IgA protease: cleaves IgA, reduces defense of mucus membrane. Polysaccharide capsule resists phagocytosis. Endotoxin LOS causes fever and shock.
N. meningitidis exam
septic arthritis: joint pain, draw joint fluid. Meningitis: classic fever, headache, stiff neck. young kids show irritability, convulsions, lassitude, fever, vomiting. Draw CSF for both.
meningococcemia exam
fever and hourly-spreading petechial skin rash. draw blood and CSF. 5-15% develop waterhouse-friderichen syndrome: fever, shock, purpura, DIC, thrombocytopenia, destruction of adrenal glands
N. meningitidis lab
septic arthritis: gram stain and culture on chocolate agar of joint fluid. Meningitis: CSF: increased PMNs, gram stain and culture on choco agar. Gram (-) cocci in CSF smear suffice for diagnosis. Meningococcemia: gram stain and culture blood on choco agar.
how to differentiate meningitidis from gonnorrhoeae
only meningococci ferment maltose! can also use immunofluorescence
n. meningitidis treatment
penicillin G unless allergic. fulminant meningococcemia: admit to ICU, support circulation and renal function. prescribing glucocorticosteroids for the rash and arthritis is bad!!!!!!!
N. meningitidis prevention
close contacts of index case get prophylactic rifampin, ceftriaxone, or ciprofloxacin. vaccines recommended for travelers (mecca, college, etc).
group B strep bacteriology
group B strep = S. agalactiae. encapsulated Gram + cocci. beta hemo, polysaccharide toxin virulence factor. pilus like attachment virulence factor. serotype specific antibody mediated immunity. normal vaginal flora. may be normal flora in GI and UR tract
GBS pathogenesis in neonates
1-2% of neonates of GBS+ moms develop invasive disease. most common cause of neonatal sepsis. usually serotype 3. early disease: pneumonia w/ bacteremia, presents 1-7 days after birth. prevented by intrapartum IV antibiotics. late disease is bacteremia with meningitis. 1-2 weeks after birth
GBS pathogenesis in geriatric group
seen in old people with pre-existing major health conditions. diabetes, malignancy, congestive heart failure. rare infections are more common because of improved reporting and population becoming older and more immunosuppressed
GBS exam
pain, fever. meningitis: spinal tap for gram + cocci in pairs or short chains. Cellulitis, abscess: gram stain and culture of appropriate sample. CT/MRI for deep abscesses. echocardiogram for endocarditis
GBS lab
CAMP test: CAMP factor secreted by GBS enhances activity of beta hemolysin from staph aureus. Hippurase test: colorimetric test for hippurase, produced by GBS and other bugs
GBS treatment
IV penicillin or amoxicillin. if allergic, vancomycin. surgical intervention may be needed.
pneumococcus bacteriology
strep pneumoniae. gram +, catalase -, alpha hemo, facultative anaerobe. form diplococci in chains. most common cause of community acquired pneumonia, bacterial meningitis, bacteremia, and otitis media. major childhood pathogen
pneumococcus pathogenesis
easily colonizes upper respiratory tract using adhesion virulence factors. in healthy adults and older children, contained by innate immunity. major virulence factor is the capsule. also has IgA protease, and teichoic acid
direct extension pneumonia
starts in the throat and spreads without infecting the blood. mainly sticks to sinuses, eustachian tubes, and bronchi
hematogenous spread pneumonia
blood, joint fluid, peritoneum, CSF. capsule protects bacteria against phagocytosis and complement unless anti-capsule IgG is already present. pathogenic strains all produce pneumolysin, some also produce hemolysin, neuraminidase, hyaluronidase, but exact contribution of these exotoxins is unclear. infection raises a strong inflammatory response.
pneumococcus exam (direct extension)
sinusitis, otitis media, bronchitis, pneumonia. patient looks ill and anxious. predispositions: COPD, asthma, bronchitis, smoking. stethoscope hears rales in most patients, dullness to percussion in half. radiology findings shows lobar consolidation in adolescents and adults. infants and young children have scattered consolidation and bronchopneumonia
pneumococcus exam in hematogenous spread
meningitis, septic arthritis, pericarditis, endocarditis, osteomyelitis. bimodal distribution: patients younger than 5 or over 65. meningitis shows mental status changes, lethargy, delirium, brudzinski signs, cranial nerve palsies, focal neurologic defects
