Meningitis Flashcards

1
Q

What are the 3 most common organisms that cause acute bacterial meningitis?

somepeople BS nomeningitis

A

Streptococcus pneumoniae (SP)
 Primary agent in adults and young children
 In US, leading causing of bacterial meningitis post Hib
 ~60% decline in rates of meningitis due to S. pneumo since introduction of Prevnar vaccine in children(NM)

Neisseria meningitidis
 Most common in children/adolescents/ young adults

Group B beta-hemolytic Streptococcus
 Most common cause in neonates

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2
Q

What all all common causes of Bacterial meningitis

some people bs no meningits have generic sad and bad lies

A

S. pneumo

Group B strep

Neisseria meningitis

Haemophilus influenzae type b (Hib)
 Less common secondary to vaccine

Gram-negative enterics
 E. coli
and others are important pathogens in neonates
 Uncommon in adults and children

Listeria monocytogenes
 Elderly, neonates, immunocompromised

Staphylococcus aureus
 Uncommon meningeal pathogen

Bacillus anthracis

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3
Q

What is the mechanism for NM infection?

A

Transiently colonizing bacteria of upper respiratory tract are common etiologic agents
 Nasopharyngeal mucosal epithelium provides local immunity; also is attachment site for bacteria
pili
 ie, N. meningitidis

 Organism breeches host defenses
 N. meningitidis produce IgA protease and escape
phagocytosis by capsular polysaccharide
 Encapsulated organisms inhibit neutrophil phagocytosis and complement-mediated killing

Seeding of meninges by blood-borne
organisms via choroid plexus
 Penetration of blood-brain barrier
 Development of inflammatory response
 Brain edema and increased intracranial pressure
 Brain ischemia
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4
Q

What are the 3 edemas ,

vasogenic
cytotoxic
interstitial

A

Vasogenic edema
 Disruption of BBB and leakage of capillary vessels

Cytotoxic edema
 Increased intracellular fluid 2° cell injury, endothelial cells themselves are swollen

Interstitial edema
-edema between cells,
 Purulent exudate in arachnoid space interferes with
reabsorption of CSF and obstruction of flow
 Movement of fluid from ventricular system to
parenchyma

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5
Q

What are the clinical characteristics of meningitis

A

Bacterial Meningitis
 Increased intracranial pressure

 Infants: bulging fontanelle
 Adults: headache

Cerebral edema and ischemia, thrombosis of cerebral vessels, cortical necrosis
> Coma, ataxia, seizures, focal neurological signs, cranial nerve palsies (deafness, ocular muscle weakness)

 Papilledema is unusual

Special features/clues
 NM meningitis associated with petechiae (1mm non-blanching, red, flat skin lesions) and/or purpura

 SP meningitis may be associated with respiratory infections (ear or sinus infection)

 Neonates
Non-specific findings:
 Poor feeding, increased sleeping, decreased
urine output, irritability, vomiting and
diarrhea
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6
Q

What are CSF findings in bacterial meningitis

normal
# cells: 0-5/mm^3
Protein: 15-45 mg/dL
Glucose: 50-75 mg/dL

A

> 1000 cells
opening pressure HIGH

*polymorphonuclear cells

high protein >150
Low glucose 20-40

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7
Q

What are CSF findings for tuberculosis and fungal

normal
# cells: 0-5/mm^3
Protein: 15-45 mg/dL
Glucose: 50-75 mg/dL

A

<5000 cells
opening pressure HIGH

  • lymphocytes ** distinguishes from bacterial
  • increased protein >150
  • low glucose (20-40)
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8
Q

What are the findings for viral meningitis in CSF?

normal
# cells: 0-5/mm^3
Protein: 15-45 mg/dL
Glucose: 50-75 mg/dL

A

<1000 cells

  • normal or high opening pressure
  • increased lymphocytes
  • normal or high protein
  • *glucose NORMAL
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9
Q

What are aseptic causes of meningitis

Enter hermes abode less have meningitis

A

Enterovirus* (echovirus, coxsackie b)
 Leading cause of aseptic cases
 Seasonal presentation: most cases in summer, early fall

Herpes viruses (HSV2*>HSV1, Varicella zoster, Cytomegalovirus, Epstein-Barr virus)

Arbovirus (eastern, western equine, St. Louis)- Insect vector

Mumps -unimmunized
HIV
LCV - rare cause

*Mycobacterium tuberculosis is also aseptic because it doesn’t grow on regular medium

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10
Q

What are the pathophysiology of brain abscesses

A

-Contigous (middle ear, mastoid, sinuses): you get a head and neck infection usually in middle ear, extension of infection up into skull, thru the brain, this is the most common cause of brain abscesses

 Hematogenous dissemination - lung abscess, empyema, congenital heart disease, bronchiectasis, infective endocarditis

 Trauma (cranial fracture, neurosurgery, foreign
body injury

 Cryptogenic

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11
Q

Most common locations of brain abscesses

A

Sinusitis
Frontal lobe most common, temporal lobe or sella turcica in sphenoid sinusitis
 Otitis media>temporal lobe or cerebellum
 Dental infections>usually frontal lobe
 Multiple locations implies hematogenous seeding

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12
Q

What are differences between brain abscesses and meningitis

A
  1. Nuccal rigidity is uncommon
  2. Systemic features (fever) are usually absent
  3. Lumbar puncture is contraindicated, you have increased pressure, you are at risk of herniation.
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13
Q

Toxoplasmosis and brain abscesses

A

Toxoplasma gondii most common protozoal cause of brain abscess.
 Transmission mainly by ingestion of tissue cysts in contaminated meat or food or oocysts in food/water
contaminated from cat feces.
 Various clinical presentations but most common is
intracerebral mass lesions or encephalitis in immuncompromised hosts (HIV, transplant, malignancy)
 Can have focal or nonfocal neurological symptoms
(weakness, HA, altered mental status, lethargy) initially with
most developing focal symptoms, some rapidly fatal
encephalitis
 Prediliction for basal ganglia and brainstem

MRI brain is test of choice. CT can also be used.
 Rounded isodense or hypodense lesions with ring
enhancment-usually multiple lesions
 Can have mass effect and edema.
 Serology (serum IgG titers)
 CSF PCR
 AIDS pts-consistent CT or MRI findings with positive
serology empiric treatment with repeat imaging in 10-14
days (should show imprvement)

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14
Q

Cranial Subdural Empyema

microbio is same as brain abscesses, staphylococci, streptococci.

A

Neurologic emergency: progress rapidly and spread to different areas

Most common predisposing condition is ear and sinus infections

 Polymicrobial infections common.
 Signs and symptoms secondary to increased intracranial pressure,
meningeal irritation, or focal cortical inflammation
 Fever is present in most cases
 Headache predominant complaint, Vomiting is common as ICP
increases.
 Altered mental status
 Focal neurologic signs (hemiparesis, hemiplegia, ocular palsies, dilated pupils, \ hemaniopsia, cerebellar signs

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15
Q

Spinal Subdural Empyema

A

Rare condition usually occurs secondary to metastatic infection from another site.
 Most frequently caused by Staphylococcus aureus *** also in FA
 Coagulase negative Staph, gram negatives, and strep less
frequent.
 Clinical presentation: radicular pain and symptoms of
cord compression (can occur at multiple levels)
 Can be difficult to distinguish from epidural abscess and
can occur simultaneously.
 MRI is diagnostic procedure of choice.
 Empiric antibiotics until culture results and surgical
decompression.

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16
Q

Cranial Epidural abscess

A

More indolent course (as opposed to subdural abscess)
 Initial focus usually sinuses, ear, mastoid infections but can occur after
trauma or surgical procedures.
 Signs and symptoms include headache, fever, seizures, focal
neurologic signs, altered mental status but may be overshadowed by
symptoms/signs from primary source of infection.
 Fever and headache
are most common complaint and patient may
feel well until progresses to subdural empyema, meningitis, or brain
abscess.
 MRI diagnostic procedure of choice-can cross midline unlike subdural
 Combined medical and surgical treatment.

17
Q

Spinal Epidural Abscess

A

May develop within hours to days (after hematogenous seeding) or
may be more chronic (weeks to months, usually with vertebral osteo or contigous focus), TB also more gradual
 Pain most consistent symptom
 Fever in 60-70% patients
 Neurologic signs depend on level affected
 Neurologic manifestations can be reversible before complete
paralysis occurs so need to do imaging and intervention emergently
if considering diagnosis.

Usually occurs secondary to hematogenous spread
 IV drug users, infective endocarditis

Blood cultures frequently positive-bacteremia
Contigous foci (1/3 of cases)
 Often occurs with vertebral osteomyelitis
 Unidentified source (20-40% cases)
 Diabetes present in up to 50% patients.

Almost all source is Staphylococci and Streptococci

MRI is diagnostic procedure of choice.
 Empiric antibiotics should include coverage for S. aureus
and gram negative bacilli
 Surgical therapy is imperative if signs of neurologic
dysfunction (paralysis less than 24-36 hours)
 Nonsurgical therapy if no neurologic deficits or too high risk
but requires frequent monitoring.

18
Q

What are the stages of spinal epidural abscess 4 stages

A

back pain and tenderness at level of infection

radicular pain and paresthesias

impaired spinal cord function; motor paresis and sensory deficits

complete paralysis

19
Q

Encephalitis

A

Inflammatory process involving brain parenchyma with
clinical or laboratory evidence of neurologic dysfunction.

 Viruses, bacteria, and auotimmune form majority of known
cases.
Differs from meningitis:
 there is a Region of inflammation
 Altered mental status (hallmark of encephalitis)
 CSF exam similar in both
-viruses are also the more common cause

20
Q

HSV-1

A

Herpes Simplex Encephalitis
 Among most severe of all human viral infections of brain
 >70% mortality with no or ineffective therapy
 Accounts for10-20% of encephalitis viral infections
 Occurs throughout the year and in patients of all ages
 Majority caused by HSV-1
 Clinical features: Fever, **personality change, dysphasia, autonomic dysfunction: altered mental status
 Requires high index of clinical suspicion

Cerebrospinal fluid (CSF) findings
 Lymphocytic meningitis (mean of 100 cells/mm3)
 Presence of red blood cells
 Elevated protein
 Normal in 5-10% of patients on first evaluation
 CSF Polymerase Chain Reaction
 Sensitivity 98%
 Specificity 94%
 Positive predictive value 95%
 Negative predictive value 98%
 If negative, may need new CSF sample in 3-7 days

21
Q

Treatment of HSV-1 and 2

A

Acyclovir

22
Q

West Nile Virus

A

Most people:
No clinical illness or symptoms (~80%)

Some develop West Nile Fever (~20%)

Severe WNV Disease (1 in 150)
 Meningitis
 Encephalitis/Meningoencephalitis
 Poliomyelitis-like flaccid paralysis

Diagnosis
 Serum IgM antibody (8-14 days of illness onset)
 CSF reveals lymphocytic pleocytosis and elevated
protein; glucose is normal
 CSF IgM (positive in >90%)
 CSF PCR (<60% sensitivity)
 Neuroimaging
 Treatment is usually supportive
23
Q

St Louis encephalitis virus

Japanese encephalitis virus

EEE virus

A

St. Louis encephalitis virus
 Mosquito vector; bird reservoir
 Endemic in western US; periodic outbreaks in eastern US
 Urinary symptoms early; SIADH (one-third of cases)
 Serology; CSF IgM

Japanese encephalitis virus
 Most common cause of mosquito-borne encephalitis worldwide
 Mainly children; rice fields where vectors breed
 Seizures and parkinsonian features; poliomyelitis-like flaccid paralysis
 Serology; CSF IgM

Eastern equine encephalitis
Mosquito vector; bird reservoir in North America
 Primarily Atlantic and Gulf coast states
 Abrupt onset with fulminant course; seizures common
 High case-fatality rate (50-70%)
 Serologic testing
 High CSF WBC count (>1000 cells/mm3)

24
Q

Powassan virus

A

Powassan virus
 Tick vector (Ixodes scapularis in NE); rodent reservoir
 Prevalence among animal hosts and vectors increasing
 New England states
 Serology; CSF IgM

25
Q

Rhabdovirus

A
Encephalitic (furious) form (80%)
 Agitation alternating with lucidity
  Hypersalivation
 Hydrophobia
  Bizarre behavior
 Disorientation, stupor, coma, death

Paralytic (dumb) form
 Ascending paralysis; early muscle weakness
 Later cerebral involvement

Diagnosis
 Culture and RT-PCR of saliva
 Immunofluorescent detection of viral antigens and RT-PCR in nuchal
biopsy
 CSF antibodies and RT-PCR
 Brain biopsy (antigen detection/Negri bodies)

Therapy
 Supportive
 Post-exposure prophylaxis (rabies immune globulin at bite site and vaccine)