CNS Infections Flashcards

1
Q

types of aseptic meningitis (neg bacterial cultures)

A

viral meningitis, fungal infections, bacterial infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

clinical signs and symptoms - meningitis

A

petechiae rash first 3 days; purpuric lesions; severe headache, fever, pos Brudzinski’s sign (cervical rigidity), hamstring spasm, pos blood culture may be seen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

describe Brudzinski’s sign and Kernig’s sign

A

Brudzinski’s: cervical rigidity causing knees to pop up; Kernig’s sign: unable to straighten leg in 90 degree angle without pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

signs and symptoms of bacteremia

A

upper RTI, pos blood culture but not much replication, transient with fever, resolves in 1-2 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

signs and symptoms of meningococcemia

A

pos blood culture, replication in the blood, malaise, rash, may resolve or proceed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

*signs and symptoms of meningitis

A

sudden onset fever, nausea, vomiting, headache, decreased ability to concentrate, myalgias; may have disseminated intravascular coagulation, shock; will have pos Brudzinski’s and Kernig’s signs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what causes disseminated intravascular coagulation?

A

activation of extrinsic and intrinsic clotting cascade by macrophage production of procoagulant tissue factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the symptoms and signs of DIC?

A

widespread ischemic changes and bleeding due to using up of clotting factors; septic shock; increased vascular permeability, fluid loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is Waterhouse-Friderichsen syndrome?

A

adrenal infarction leading to acute adrenal insufficiency (associated with DIC, not meningitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

highest incidence of meningitis in this age group

A

children 6-12 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

morphology of Neisseria meningitidis

A

gram-neg, diplococcic, lipooligosaccharide to form effective capsule, has serogroups

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

metabolism of Neisseria meningitidis

A

aerobic but can grow anaerobic, cyt c oxidase positive, ideally grown in increased CO2, grows on blood agar, choc agar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Neisseria meningitides pathogenesis- function of capsule, pili, and LOS

A

capsule resistance to phagocytosis, pili for adherence, LOS production of cytokines esp. TNF (may result in septic shock)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

major cause of N. meningitides pathology

A

LOS (TNF, inflammation)- activates macrophages through the Toll pathway, which leads to production of procoagulant TF, subsequent bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

physical findings on path slides for N. meningitidis

A

PMN’s, gram neg diplococcic on gram stain of CSF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

diagnosis procedures for N. meningitidis

A

culture of CSF on blood and choc agars (gold standard), blood cultures when meningococcemia suspected.

17
Q

treatment of suspected meningitis needs to cover..// what ABs should be used?

A

meningococcus, pneumococcus, hemophilus (cefotaxime, vancomycin); rif and ciprofloxacin for contacts

18
Q

methods of immunity to meningitis

A

antibodies directed against the CAPSULE, vaccines available

19
Q

life cycle of toxoplasma gondii

A

oocyst in cat feces, ingested, sporozoites hatch into tachyzoites in the gut of the animal, goes through asexual repro, infects primarily macrophages (liver, lungs)

20
Q

the definitive host (cat) houses which stages of the organism?

A

sexual and asexual stages (psuedocysts form containing bradyzoites)

21
Q

toxo is asymptomatic in what percentage of cases?

A

80-90%

22
Q

picture of toxo resembles..

A

infectious mono or CMV infection

23
Q

how severe toxo manigefests

A

CNS disease: encephalopathy, meningoencephalitis

24
Q

describe infection of congenital toxo

A

newly acquired in mother during pregnancy; systemic spread to the fetus

25
Q

what is the outcome of toxo infection during 1st trimester?

A

spontaneous abortion, stillbirth, severe disease

26
Q

what is the outcome/signs of toxo infection in 2nd/3rd trimester?

A

chorioretinitis (25% of cases), epilepsy, encephalitis, hydrocephaly, retardation

27
Q

diagnosis of toxo

A

serology: determination of 4-fold increase in titer essential to diagnosis of acute infection (1/3 of pop. is seropositive); brain imaging

28
Q

treatment for HIV-associated toxo

A

sulfadiazine and pyrimethamine; maintain to prevent recurrence

29
Q

bugs that cause primary amoebic meningoencephalitis

A

Naegleria fowleri, Acanthamoeba sp.

30
Q

where Naegleria fowleri is found

A

amoeba-flagellate in soil, water; found in 50% of fresh (WARM) water

31
Q

how is Naegleria fowleri acquired by humans?

A

getting water in nose; amoeba penetrates the cribriform plate

32
Q

signs of meningoencephalitis caused by Naegleria fowleri

A

headache, stiff neck, fever, lethargy, rapid progression to confusion, convulsions, coma

33
Q

naegleria fowleri infection is fatal in how much time?

A

6-`7 days (mean=10)

34
Q

blood work picture for diagnosis of meningitis

A

high protein, low glucose, a few WBC’s; gram stain is NEGATIVE (why?)

35
Q

describe the detection methods of amoeba in purulent CSF

A

wet mount; gram stain is difficult to recognize, use Wright stain because its distinctive

36
Q

treatment of meningitis caused by naegleria fowleri

A

all: amphotericin (IV and intrathecally), fluconazole, azithromycin, rifampin, miltefosine, dexamethasone

37
Q

Acanthamoeba is acquired by

A

water in nose, penetration of cribriform plate

38
Q

infections associated with Acanthamoeba

A

CNS infection (longer, chronic granulomatoud encephalitis); ocular infection (bruised eye contaminated with dirt, contaminated contacts, results in keratitis)