Chapter 6: CNS infections

Question 1

pathogenesis of bacterial meningitis

Answer 1

1- infectious organisms gain entry to the subarachnoid space and CSF.
a) most commonly by bacteremia, gaining entry through the large venous channels.
B) by nasopharyngeal spread through a CSF leak caused by cribriform plate defect or basilar skull fracture.
c) direct spread from a brain abscess or air sinus infection.
2- rapid growth occurs in the CSF because the blood-brain barrier blocks entry of immunoglobulins and complement.
3- inflammation damages the blood brain barrier, increasing permeability, allowing entry of serum protein, and impairing glucose transport.
4- progressive cerebral edema, increased CSF pressure, and decreased cerebral blood glow lead to irreversible ischemic damage.

Question 2

clinical manifestations

Answer 2

1- upper respiratory or ear infection interrupted by the abrupt onset of meningeal symptoms:

a) generalized, sever headache
b) neck stiffness
c) vomiting
d) depression of mental status

2- physical findings

a) brudzinski (neck flexion) and kernig (straight leg raise) signs are insensitive; “head jolt” maneuver may have higher sensitivity.
b) abnormal ear exam (streptococcus pneumoniae or haemophilus influenzae), pharyngeal erythema (Neisseria meningitidis) or clear nasal discharge resulting from CSF leak (S.pneumoniae)
c) petechial or purpuric skin lesions most common with N. meningitides, also seen with rickettsial infection, echovirus 9, staphylococcus aureus, and asplenic sepsis.
d) neurologic examination should look for focal findings suggests space-occupuing lesion) and asses mental status (GCS is an important prognostic factor)

Question 3

diagnoses of bacterial meningitis

Answer 3

1- if meningitis is a consideration, lumbar puncture must be performed.

2- if focal neurologic deficits and papilledema are absent, a lumbar puncture can be performed before CT scan.

3- opening pressure of the CSF should be measured:; it is often elevated.

4- the CSF formula is very helpful in deciding whether a patient has bacterial meningitis. bacterial meningitis is suggested win the presence of

a) more than 90% polymorphonuclear leukocytes *except with listeria),
b) elevated CSF protein (usually 150-1000 mg/dl), and
c) low CSF glucose [ less than 2/3 of the serum value (less than 25mg/dl is prognosis of poor outcome)]

5- gram stain of CSF is positive in more than 75% of cases (except 25% in listeria)

6- blood and CSF allow for antibiotic sensitivity testing.

Question 4

treatment of bacterial meningitis

Answer 4

1. antibiotics should be given within 30 minutes if bacterial meningitis is suspected.
2. blood samples for culture should be drawn and antibiotics given before a CT scan is done
3. Maximal doses of antibiotics must be given because of limited passage through the blood brain barrier.
4. empiric therapy for
   a) community acquired disease, patient aged 3 months to 60 years is ceftriaxone or cefotaxime, if severely ill, add vancomycin. if more than 60 years or immunocompromised, use ceftriaxone or cefotaxime, plus ampicillin and vancomycin.
5. give dexamethasone 30 minutes before antibiotics in
   a) children (shown to be efficacious in hemophilus influenzae)
   b) adults (efficacious in streptococcus pneumonia with GCS score 8-11)
6. maintain ventilation, prevent increase in PaCO2, or decrease in PaO2
7. avoid hypotonic solutions, and consider mannitol or glycerol for increase CSF pressure.
8. antiseizure medications after first seizure.

Question 5

outcomes of bacterial meningitis

Answer 5

1. permanent sequelae are common:
   a) in children: mental retardation, hearing loss, seizure disorders, cerebral palsy.
   b) in adults: hydrocephalus, cerebellar dysfunction, paresis, seizure disorder, hearing loss.

Question 6

prevention (chemoprophylaxis)

Answer 6

a) H.Influenzae: rifampin within 6 days for household contacts with unvaccinated child under 2 years of age, and for children under 2 years of age exposed in a day care center.
b) N. Meningitidis: single dose ciprofloxacin within 5 days for household and daycare contacts, and for those exposed to oral secretion form the index case.

Question 7

viral meningitis caused by

Answer 7

a) enteroviruses, echovirus, and coxsackievirus
b) mumps in the nonimmune
C) herpes simplex type 2 (HSV-1)
d) Epstein-Barr virus and cytomegalovirus
e) lymphocytic choriomeningitis virus (excreted in rodent urine)
f) HIV

Question 8

primary clinical manifestations

Answer 8

a) headache and photophobia, stiff neck
b) no loss of consciousness, and
c) conjunctivitis, maculopapular rash, and occasionally with echovirus and petechial rash.
d) EBV AND CMV (rare)

Question 9

diagnoses of viral meningitis

Answer 9

1. CSF shows predominance of lymphocytes, early polymorphonuclear leukocytes(PMNs), normal glucose, and mild protein increase
2. PCR can make the diagnosis of HSV-1 OR -2and enterovirus, but diagnosis is often presumptive.

Question 10

treatment of viral meningitis

Answer 10

observation, antibiotics if CSF contains PMNs; self limiting disease, lasts 7-10 days.
HSV-2 will benefit from 10-14 days of acyclovir. those with recurrent disease do not benefit from prophylaxis

Question 11

tuberculous meningitis

Answer 11

a) basilar process involving the pons and optic chiasm
b) deficits of the third, fourth, and sixth cranial nerves
c) noncommunicating hydrocephalus a possibility
d) developmental of coma a bad prognostic sign

Question 12

diagnosis of tuberculous meningitis

Answer 12

CSF: culture should use large volumes of CSF; smear for acid-fast bacilli is positive in one-third of cases; PCR is sensitive test

Question 13

treatment of tuberculous meningitis

Answer 13

fatal if not treated within 5-8 weeks

isoniazid, rifampin and pyrazinamide, add corticosteroids for hydrocephalus.

Question 14

cryptococcal meningoencephalitis symptoms

Answer 14

a) headache is most common
b) personality change and confusion develop as disease progress
c) stiff neck is uncommon
d) deficits of the third, fourth fifth and eighth cranial nerves can occur

Question 15

diagnosis of cryptococcal meningoencephalitis

Answer 15

1. lumbar puncture required for diagnosis; increased CSF pressure often associated
   a) WBCs 20-200\ mm3 with mononuclear cells predominance
   b) mildly elevated protein and moderately depressed glucose.
   c) positive india ink preparation in 25-50% of cases, and positive cryptococcal antigen in approx 90%.
   d) culture usually positive in 5-7 days
2. CT or MRI scan with contrast may show hydrocephalus, cerebral edema, and ring enhancing lesions (cryptococcomas)

Question 16

treatment of cryptococcal meningoencephalitis

Answer 16

amphotericin B and flucytosine for 2 weeks, fluconazole for 3-6 months

mortality is 25-30%; prognosis is worse if CSF produce a positive India ink preparation, an antigen titer higher than 1:32, a WBC count below 20\mm3 or increase opening pressure

Question 17

three major categories of viral encephalitis

Answer 17

1. mosquito borne (arbovirus)
2. animal to human (rabies virus)
3. human to human [(HSV1), mumps, measles, varicella, human herpesvirus 6, less commonly, EBV, CMV, ENTEROVIRUSES]

Question 18

SYMPTOMS OF viral encephalitis

Answer 18

1. symptoms of cortical dysfunction:
   a) hallucinations, repetitive higher motor activity such as dressing and undressing.
   2) seizures
   c) sever headache
   d) ataxia
2. rabies causes distinct symptoms:
   a) hydrophobia
   b) rapid, short respirations
   c) hyperactivity and autonomic dysfunction
   d) less commonly (ascending paralysis)

Question 19

diagnosis of viral encephalitis

Answer 19

A)CSF shows a WBC count below 500\mm3, mild increase in protein, possibly red blood cells (incase of HSV-1)
B) PCR of CSF diagnoses HSV, culture is seldom positive
c) CT OR MRI scan may show temporal lobe abnormalities in HSV-1 infection.
d) an electroencephalogram may show localized temporal love abnormalities in HSV infection.
e) brain biopsy is likely necessary in the presence of temporal lobe abnormalities and no improvement on acyclovir

Question 20

what are anaerobic causes of brain abscess and whats their origin

Answer 20

from the mouth flora, pelvis, and GI
bacteroides
prevotella melaninogenica
propionibacterium, fusobacterium..

Question 21

causes of community acquired bacterial meningitis

Answer 21

a) streptococcus pneumoniae (most common). follows bacteremia from ear sinus, or lung infection. also associated with chronic leaks of CSF.
B) Neisseria meningitidis: begin with colonization of the nasopharynx. sporadic cases often associated with terminal complement defects. epidemics occur in crowded environment such as dormitories and military training camps.
c) listeria monocytogenes occur in neonates, pregnant woman, and immunocompromised patients. contracted by eating contaminated refrigerated foods.
d) haemophilus influenzae was the most common for in children.

Question 22

what’s the pathogenesis of brain abscess, causes and location of abscesses

Answer 22

brain abscess has to major causes

1) direct spread from middle ear, frontal sinus, or dental infection
2) hematogenous spread from chronic pulmonary, skin , pelvic, and intra abdominal infection, also endocarditis, bacteremia after esophageal dilation, cyanotic heart disease (multiple abscesses at the gray-white matter junction)

abscess location can be frontal or temporal, frontoparietal, parietal, cerebellar and occipital (anywhere)

cerebritis (acute inflammation and edema) progress to necrosis, followed by fibrotic capsule formation

Question 23

nosocomial meningitis causes

Answer 23

associated with neurosurgery or placement of ventriculostomy tube. caused by gram negative rods, staphylococcus aureus , enterococci, s. epidermidis.

Question 24

treatment of brain abscess

Answer 24

antibiotic therapy must be prolonged (6-8wks) and must use high doses of intravenous:

a) penicillin
b) metronidazole
c) ceftriaxone or cefotaxime
d) nafcillin or oxacillin ( for abscess following head trauma, neurosurgery, or staphylococcus aureus bacteremia.) use vancomycin if MRSA.

Question 25

how to take culture in brain abscess

Answer 25

neurosurgery usually required for culture and drainage. always consult a neurosurgeon.

a) needle aspiration is usually preferred (less collateral damage)
b) open resection is recommended after head trauma and with fungal abscess
c) use observation in cases of early cerebritis, with frequent follow up imaging (CT OR MRI)

Question 26

what are possible fungal abscess causing strains

Answer 26

Toxoplasmosis
nocardia
aspergillus

Question 27

poor prognosis associated with

Answer 27

1. rapid progression in hospital
2. coma or admission
   3, rupture into the ventricle

Question 28

how do you diagnose brain abscess

Answer 28

signs and symptoms lead to possibility of a space occupying lesion, lumbar puncture is CONTRAINDICATED
after blood culture and empiric antibiotics, perform CT or MRI those detect cerebritis and smaller lesions early
four stages are detectable on imaging:
1)early cerebritis (edema, no ring enhancement)
2)later cerebritis(enhancement rings with edema)
3)late cerebritis (necrosis, ring without contrast, nonuniform contrast enhancing ring)
4)healed abscess (no longer ring enhancing, lesion becomes isodense (not different in density throughout

lumbar puncture is CONTRAINDICATED

Question 29

what are the symptoms and signs of brain abscess

Answer 29

symptoms are initially nonspecific and a delay in diagnosis is common(2 weeks)
severe headache localized to the sides of the abscess
neck stiffness in occipital brain abscess after rupture into a ventricle
alteration in mental status, inattentiveness, lethargy, coma may be seen

physical findings are minimal
fever in 50%
focal neurological findings appear late
papilledema is a late manifestation
deficits in the 6th and 3rd cranial Neves duo to increased CSF pressure
seizures most common in association with frontal abscess

Question 30

how do you diagnose brain abscess

Answer 30

signs and symptoms lead to posisibitly of a space occupying lesion, lumbar puncture is CONTRAINDICATED
after blood culture and empiric antibiotics, perform CT or MRI those detect cerebritis and smaller lesions early
four stages are detectable on imaging:
1)early cerebritis (edema, no ring enhancement)
2)later cerebritis(enhancement rings with edema)
3)late cerebritis (necrosis, ring without contrast, nonuniform contrast enhancing ring)
4)healed abscess (no longer ring enhancing, lesion becomes isodense (not different in density throughout

lumbar puncture is CONTRAINDICATED

Question 31

how to take culture in brain abscess

Answer 31

neurosurgery usually required for culture and drainage. always consult a neurosurgeon.

a) needle aspiration is usually preferred (less collateral damage)
b) open resection is recommended after head trauma and with fungal abscess
c) use observation in cases of early cerebritis, with frequent follow up imaging (CT OR MRI)

Question 32

WHY IS dexamethasone preferably avoided and when is it not avoided

Answer 32

its avoided cause,

a) reduces contrast enhancement during imaging;
b) slows capsule formation and increases the risk of ventricular rupture
c) reduces antibiotic penetration into the abscess

used in the presence of mass effect and depressed mental status

Question 33

source of infection that leads to epidural absecess

Answer 33

spread from osteomyelitis or disk space infection
spinal surgery or epidural catheter placement
hematogenous spread from skin or UTI or IV drug abuse

Question 34

symptoms and signs of epidural abscess

Answer 34

lower back pain and fever
radicular pain (pain that radiates from your back and hip into your legs)
LMN deficit
signs of cord compression in later stages (Babinski, hyperreflexia..) [IRREVIRSIBLE PARAPLEGIA MAY OCCUR ]
localized spinous process tenderness in posterior epidural abscesses

in the patient with back pain and fever, always consider spinal epidural abscess

Question 35

diagnosis of epidural abscess

Answer 35

MRI with contrast

Question 36

treatment of epidural abscess

Answer 36

prolonged antibiotic therapy (4-6 weeks)

with nafcillin or oxacillin, metronidazole and ceftriaxone.