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micro unit 3 > bacterial infections of the CNS > Flashcards

bacterial infections of the CNS Flashcards

1
Q

N. meningitidis gram stain, growth pattern and capsule

A

it is gram (-), diploccocus, and does have a capsule

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2
Q

is N. meningitides human-restricted?

A

yes.

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3
Q

how many serotypes are there?

A

13

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4
Q

what are the other classifications for N. meningitidis (catalase, oxidase)?

A

it is catalase + and oxidase +

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5
Q

what does it eat/ferment?

A

it ferments glucose and maltose, but not sucrose or lactose.

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6
Q

will it grow on blood agar?

A

will not grow on blood agar, need to use chocolate or thayer-martin

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7
Q

how is meningitidis spread?

A

airborne droplets.

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8
Q

what virulence factors?

A

IgA protease (helps it to colonize the nasopharynx). polysaccharide capsule (primary factor that resists phago), LOS toxin for sepsis

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9
Q

how is the infection typically controlled by the body?

A

by IgG and complement fixation, neutrophils clear infection. there is usually lifelong immunity to controlled strain.

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10
Q

what factors contribute to spread throughout the body?

A

deficiency in complement c5-c9. the capsule of the bacteria can mainly help it escape immunity

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11
Q

where does the bacteria colonize outside of the nasopharynx

A

joints to give septic arthritis, meninges to give meningitis which is fatal if not treated.

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12
Q

what do you see on exam?

A

joint pain, and then age restricted symptoms of meningitis

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13
Q

adult meningitis

A

fever, HA, stiff neck.

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14
Q

pediatric meningitis 2/3 of cases.

A

irritability, convulsions, lassitude, fever, abdominal discomfort and vomiting

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15
Q

meningicoccemia symptoms

A

fever and hourly spreading rash (need to draw CSF and admit to ICU

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16
Q

waterhouse-friederichen syndrome

A

high fever, shock, widespread purpura, DIC, thrombocytopenia, destruction of adrenal glands, 50% fatal. classic things that we fear when think about meningitis

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17
Q

treatment for N. meningitidis

A

penicillin-G

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18
Q

alternative treatments for N. meningitidis

A

ceftriaxone, cefotaxime, cefuroxime, chlorophenicol

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19
Q

treatment for meninigococcemia

A

ICU support for circulation and renal function

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20
Q

prevention of meningitis

A

vaccine! prophylaxis for close contact.

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21
Q

group B strep organism, growth and gram stain

A

S. agalactiae, gram +, diplococcus

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22
Q

is GBS hemolytic?

A

beta.

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23
Q

does GBS have a capsule?

A

yes

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24
Q

what virulence factor?

A

polysaccharide toxin

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25
Q

is there is immunity against this?

A

yes these serotype specific antibody mediated immunity

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26
Q

Is GBS normal flora?

A

yes, vaginal (15-45%), also found in the GI, and upper respiratory.

27
Q

can this cause disease in healthy people

A

yes, but very rarely. causes UTI, cellulitis, bacteremia,

28
Q

what is the most common cause of neonatal sepsis/meningitis

A

GBS. this comes from a GBS mother 1-2%. cause early and late diseases.

29
Q

early GBS disease

A

pneumonia with bacteremia. presents in 1-7 days postpartum, this is the most common in US

30
Q

late GBS disease

A

bacteremia with meningitis. develops 1-12 weeks postpartum

31
Q

what serotype causes late GBS disease

A

most common type 3

32
Q

what are the risk factors for GBS disease of the newborn

A

prematurity, prolonged rupture of membranes for both early and late diseases.

33
Q

GBS in elderly? risk factors

A

does occur and becoming more prevalent due to older population, and immunosuppressed. risks are diabetes, malignancy, CHF.

34
Q

what are the two groups at highest risk for GBS and what are their illnesses?

A

neonate/mother.
mother gets UTI or uterine infection.
neonate gets early pneumonia or late meningitis

35
Q

what tests help to confirm?

A

CT/MRI for lesions in the brain, echocardiogram for heart vegetation (endocarditis), gram stain and culture for samples.

36
Q

treatment for GBS

A

amoxicillin or penicillin.

37
Q

alternative treatments for GBS if allergic.

A

vancomycin

38
Q

what surgical interventions might be needed for GBS

A

abscess drainage for cellulitis, heart valve replacement for endocarditis.

39
Q

prevention of GBS disease

A

test preterm mothers by swab and culture, if positive then treat with pen or amox.

40
Q

what if pregnant mothers are allergic to amox/pen

A

treat with clindomycin or erythromycin

41
Q

pneumococcus organism, gram, growth pattern

A

staph, pneumoniae. gram +, diplococcus. note this is a facultative anaerobe.

42
Q

catalase for pneumonia?

A

negative.

43
Q

virulence for pneumonia

A

pathogenic strains are encapsulated. adhesive virulence factors allow for colonization. exotoxins, such as hyaluronidase, neuramidase, hemolysin.

44
Q

what diseases is this organism responsible for?

A

most common cause of community acquired pneumonia, bacterial meningitis, bacteremia, and otitis media. also causes sinusitis, septic arthritis, osteomyelitis, peritonitis, endocarditis.

45
Q

where does pneumoniae usually colonize? what causes spread?

A

easily coloizes the upper respiratory tract, but is contained by innate immunity. spread caused by pre-existing asthma, COPD, bronchitis, smoking and by direct extension (sinuses, eustacian tube, bronchi) or by hematogenous (blood, peritoneum, CSF, joint)

46
Q

what role does the capsule play in immunity for pneumonia?

A

protects it from immunity and phagocytosis, unless IgG already exists.

47
Q

what causes the clinical disease symptoms for pneumoniae?

A

the inflammatory response to the bacteria.

48
Q

when does the disease peak?

A

fall and winter, or when people are closer together.

49
Q

non-invasive or direct extension disease for pneumonia examples?

A

sinusitis, otitis media, bronchitis, pneumonia.

50
Q

what does pneumonia look like on exam?

A

significant mortality morbidity (10-20%). patient will look ill and anxious. hear rales in most. dullness to percussion as well. there will be lobar consolidation on chest X.

51
Q

how is pneumonia different for infants and children?

A

harder to diagnose, they have scattered parenchymal consolidation and bronchopneumonia.

52
Q

other considerations for non-invasive pneumonia

A

there is tachypnea in elderly, there may be pleural effusions, and it gets worse with influenza.

53
Q

hematogenous pneumoniae (invasive) who is at risk? what kind of spread is this called?

A

bimodal distribution: younger the 5, older than 65. anyone who is immunosuppressed.

54
Q

what ethnicities get pneumonia more frequently

A

alaskans, native americans, african americans.

55
Q

pneumonia meningitis development and symptoms

A

develops over hours or days, neurologic signs prevalent: mental status changes, lethargy, delirium, brudzinski +, cranial nerve palsy, focal neurologic deficits.

56
Q

brudzinski sign for meningitis

A

when you force flexion of the neck, the person has reflex of hip extension or knee extension.

57
Q

diagnosing invasive staph pneumonia

A

blood cultures gram staining, urine antigen testing, spinal tap.

58
Q

spinal tap findings typical of bacterial meningitis

A

elevated opening pressure, elevated WBC (neutrophils), elevated protein, decreased glucose, highly elevated lactic acid, gram stain.

59
Q

treatment for staph pneumoniae noninvasive

A

antibiotics, amox/cephalosporin for everyone. fluoroquinolones or doxycycline for adults only outpatient.
for severe, admit and vancomycin

60
Q

treatment of invasive staph pneumoniare

A

admit, start antibiotics then start cultures. need to perform susceptibility. antibiotics are vancomycin and ceftriaxone or cefotaxime.

61
Q

treatment for invasive staph pneumonia that is resistant

A

add rifampin, meropenem, or chloramphenicol to the vancomycin and ceftriaxone.

62
Q

antibiotic resistance in s pneumonia

A

the resistance can be overcome by higher doses due to the mutations being in the cell wall structures that the antibiotics bind, just making the binding less efficient. but the resistance is on a transposon that includes resistance to multiple, so if resistant to one, then probably many.

63
Q

prevention of pneumonia

A

prevar7 vaccine, raises protective IgG. childhood vaccinations have decreased the invasive disease by 90%. rates of carriage of the serotypes decreased dramatically as herd immunity was developed. rates of other serotypes increased. prevar13 vaccine covers the previous 7 plus 6 new ones. this can be given to children or as booster.

micro unit 3 (2 decks)

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