neurology and related infectious disease by dr fitsum

1. CNS Infections
Fitsum Getahun, MD; Ass. Prof of
I.Medicine
Department of internal medicine
AMU, March 2018

2. CNS infections
• Meningitis-several forms
• Encephalitis
• Brain/intracranial Abscess

3. Definitions
Meningitis
􀂃 Inflammation of the leptomeninges
(the covering of the brain)
 Meningitis is the 9th deadliest disease in the
modern world
 The incidence of bacterial meningitis declined;
in part, due to the introduction of the conjugate
Haemophilus influenzae type b
and pneumococcal conjugate vaccines
Encephalitis
􀂃 Inflammation of the brain itself
􀂃 Caused by many types of organisms
but mainly viruses

4. Mortality and morbidity of
meningitis
 Depend on pathogen, patient's age and condition, and severity
of acute illness
 Pneumococcal meningitis causes the highest rates of mortality
(21%) and morbidity (15%).
 Mortality rate is 50-90%, if severe neurologic impairment is
evident at the time of presentation (or with extremely rapid
onset of illness), even with immediate medical treatment.
 Race, Age, Sex

5. Microorganisms
That Can Infect the Brain
Bacteria, Viruses, Fungi, Parasites,
Prions
 Aseptic meningitis (CSF pleocytosis and normal CSF glucose, negative
bacteria on Gram stain), is the most common CNS infection
 Most common microorganisms are
 enteroviruses (primarily cause infection in the summer and early fall,
account for up to 80% of all cases),
 human herpesvirus-2 (HHV-2), lymphocytic choriomeningitis virus
(LCM), VzV, EBV.
 HIV, and other viruses.
 Aseptic meningitis can also follow infection with Borrelia burgdorferi, the
causative agent of Lyme disease, and neurosyphilis etc plus drug-
induced (egNSAIDs, IVIG)

6. Bacterial Meningitis

7. Etiology
• Streptococcus pneumoniae (50%)
• Neisseria meningitis (25%)
• Group B Streptococci (15%)
• Listeria monocytogenes (10%)
• Haemophilus influenzae (<10%)
• M. tuberculosis,
• T. pallidum, B. burgdorferi,
• Leptospira (through exposure to animal fluids or
infected water)
• Brucella (through exposure to cattle or
unpasteurized milk)
• Nocardia asteroides (found in the soil; can
cause infection in immunocompromised

8. Risk and/or Predisposing Factor Bacterial Pathogen
Age 0-4 weeks S agalactiae (group B streptococci)
E coli K1
L monocytogenes
Age 4-12 weeks S agalactiae
E coli
H influenzae
S pneumoniae
N meningitidis
Age 3 months to 18 years N meningitidis S pneumoniae ; H influenzae
Age 18-50 years S pneumoniae ; N meningitidis ; H influenzae
Age older than 50 years S pneumoniae ; N meningitidis
L monocytogenes ; Aerobic gram-negative bacilli
Immunocompromised state S pneumoniae ; N meningitidis
L monocytogenes ;Aerobic gram-negative bacilli
Intracranial manipulation, including neurosurgery Staphylococcus aureus ;Coagulase-negative
staphylococci; Aerobic gram-negative bacilli, including
Pseudomonas aeruginosa
Basilar skull fracture S pneumoniae ;H influenzae ;Group A streptococci
CSF shunts Coagulase-negative staphylococci; S aureus
Aerobic gram-negative bacilli; Propionibacterium acnes

9. Slide 2. Neisseria meningitidis
meningitis
This cerebrospinal fluid contains a
high concentration of neutrophils
and many gram-negative diplococci
singly and in pairs. Although
Neisseria meningitidis is the most
likely organism, differentiation
from N. gonorrhoeae, which can
also cause meningitis, is not possible
with Gram stain.
But with the PCR
Slide 1. Streptococcus pneumoniae
meningitis
This cerebrospinal fluid from a child with
meningitis contains many neutrophils and
oval gram-positive cocci singly and in
pairs. Because the number of organisms in
infected cerebrospinal fluid is small, most
laboratories centrifuge the specimen to
increase the concentration and then use the
sediment for both stains and cultures. The
density of microbes per milliliter of fluid
cannot be estimated from a specimen that
has been centrifuged.

10. • Neisseria meningitides and Streptococcus pneumoniae
account for 37% to 93% of acute bacterial meningitis

11. Slide 3. Haemophilus
influenzae meningitis
This cerebrospinal
fluid contains many
neutrophils and gram-
negative coccobacilli,
primarily in the
cytoplasm of the white
cells.
Slide 4. Listeria monocytogenes meningitis
This cerebrospinal fluid contains a few
neutrophils and two slender gram-positive
bacilli. Although Gram stains of cerebrospinal
fluid are positive in specimens from about
80% of all patients with bacterial meningitis,
organisms are detected in the cerebrospinal
fluid of only about 40% of patients with
Listeria meningitis. Even when specimens
reveal bacteria, only a small number may be
visible.

12. Common Signs & Symptoms of
Meningitis
 Fever > 90%
 Headache > 90%
 Neck Stiffness > 85%
 Altered mental status (irritability to somnolence,
delirium, and coma ) >=75%
 Vomiting 35%
 Seizures 30%
 Weakness 15%
 Photophobia
 Kerning's and Brudzinski’s Sign
 Signs of increased ICP eg.Papilledema
 Focal neurologic signs-Isolated cranial nerve
abnormalities (principally III, IV, VI, VII) in 10-20%
…worse outcome

13. Signs & Symptoms of Meningitis
 In partially treated meningitis (40%),
seizures may be the sole presenting
symptom
 Low-grade ventriculitis associated with VP
shunt: may have a less dramatic
presentation with headache, nausea,
minimal fever, and malaise
• Fungal meningitis: mild/fluctuating
headache, low-grade fever, and lethargy
are the primary symptoms
• Tuberculous meningitis: Fever, weight
loss, night sweats, and malaise, headache
and meningismus

14. Systemic findings
• Extracranial infection (eg, sinusitis, otitis
media, mastoiditis, pneumonia, urinary tract
infection) may be noted.
• Arthritis is seen with N meningitidis,
• Rash. Nonblanching petechiae and cutaneous
hemorrhages are seen classically with N
meningitidis; (can occur with other bacterial
and viral infections)
• Endotoxic shock with vascular collapse is
characteristic of severe N meningitidis
infection as is DIC and adrenal hemorrhage

16. Laboratory Studies
• CBC with differential
• Serum/urinary electrolytes and Renal/liver profile (dehydration or SIADH, to
assess organ functioning and adjust antibiotic dosing)
• Serum glucose as baseline for determining normal CSF glucose;
• Coagulation profile and platelets in patients with chronic alcohol use, liver
disease, or if DIC is suspected. (require platelets or FFP prior to LP.)
• Serum/CSF cryptococcal antigen/indian ink,
• Cultures (prior to antibiotics) : blood (80% positive in meningitis caused by H
influenzae, S pneumoniae, N meningitidis); nasopharynx, respiratory secretions,
urine, and skin lesions.
• Latex agglutination or counter immunoelectrophoresis (CIE) of blood, urine,
and CSF for specific bacterial antigens (partially treated meningitis)
• Serum/CSF- RPR/VDRL if neurosyphilis is in differential diagnosis. (CSF
VDRL may be negative)

17. Imaging Studies
• Head CT scan (contrast) or MRI (gadolinium)
• In patients with evidence of head trauma,
immunosuppression, altered mental status, or focal
findings.
• Presence of papilledema and inability to fully assess fundi
or neurologic status are indications for CT scan prior to
LP.
• Obtain blood cultures and initiate treatment before
imaging studies and LP in patients with suspected
bacterial meningitis.
• Results may be normal or demonstrate small ventricles,
effacement of sulci, and contrast enhancement over
convexities.
• Late findings include venous infarction and
communicating hydrocephalus.
• Rule out brain abscess, sinus or mastoid infection, skull
fracture, and congenital anomalies.
• Chest radiography- 50% of patients with pneumococcal
meningitis also have evidence of pneumonia
Non Contrast CT- mild ventriculomegaly
and sulcal effacement.
contrast-enhanced, axial T1-
weighted magnetic resonance
image shows leptomeningeal
enhancement

18. Diagnosis
 CT Head (SOL/Increased ICP)
 LP
 Blood Cultures
 CSF
o ↑ Opening Pressure (>180mm H2O)
o ↑ WBC (PMN),
o ↓ Glucose (<2.2mmol/L), ↓ CSF/Serum Glucose
(<0.4),
o ↑ Protein (>0.45g/L),
o CSF culture and gram stain
o Latex agglutination test-detects bacterial antigens
o PCR-Can detect small numbers of bacteria
o CIE-(Counter Immunoelectropheresis)
 Able to detect small amounts of antigen
 Early detection (~24h)

19. .

20. • Open P. AIDS patients with crypto meningitis
have increased risk of blindness, death unless
opening pressure maintained at <30 cm In
Bact mening-Lymphocytosis with normal
CSF chemistries seen in 15-25%, especially
when cell counts <1000 or if partially treated.
• In Viral mening Up to 48 hours, significant
PMN pleocytosis may be indistinguishable
from early bacterial meningitis.

21. • After 8-12 hours, reexamine the CSF. If
initial granulocytosis changes to mononuclear
predominance, CSF glucose remains normal,
and patient continues to look well, the infection
is most likely nonbacterial.
• Nontraumatic RBCs in 80% of HSV
meningoencephalitis, although 10% have
normal CSF results.

22. • ~90% of patients with VP shunts have CSF
WBC count >100 cells/mm3 are infected; CSF
glucose usually normal, and organisms are less
pathogenic (Staph epi, Propionibacterium
acnes, and diphtheroids) and S aureus,
coliforms.
• India ink 80-90% effective for fungi; AFB
stain 40% effective for TB.
• Prior antibiotics may cause gram-positive
organisms to appear gram negative and
decrease culture yield on average 20%.

23. • lowest levels of CSF glucose are seen in TB,
primary amebic meningoencephalitis,
neurocysticercosis.
• An aseptic profile - bacterial (eg,
Mycoplasma, Listeria, Leptospira species,
Borrelia burgdorferi [Lyme], spirochetes),
partially treated bacterial , HSV and
arboviruses.
• TB meningitis and parasites resemble the
fungal profile more closely.

24. • In acutely ill patients, perform an LP (if appropriate) and administer first
dose(s) of antibiotics +/- steroids within 30 minutes of presentation to ED.
• Initiate empiric therapy if LP cannot be performed within 30 minutes.
• Begin empiric therapy prior to head CT scan if a focal neurologic deficit
is present. If no mass effect is present, perform LP
• Treat systemic complications : hypotension and/or shock, hypoxemia,
hyponatremia (SIADH), DIC,cardiac arrhythmias and ischemia, seizure and
CVA
• Seizure precautions in ED: Aggressively control seizures if present, since
seizure activity increases ICP (ie, lorazepam 0.1 mg/kg IV and IV load with
phenytoin 15 mg/kg or phenobarbital 5-10 mg/kg).
• Dexamethasone may be beneficial in bacterial meningitis if given 15-20
mins before or with the first dose of antibacterial therapy, especially for
H.Inf, N.meng, S.pneumoniae or TB meningitis, raised ICP

25. Treatment of complications
• Look for signs of hydrocephalus and increasing ICP.
• Manage fever and pain, control straining and coughing, avoid seizures, and
avoid systemic hypotension.
• In stable patients, elevating head and monitoring neurologic status.
• Diuresis (ie, mannitol 1 g/kg IV), provided circulatory volume is protected.
• Hyperventilation in intubated patients, with a goal of PaCO2 25-30 mm
Hg, may briefly lower ICP; hyperventilation with PaCO2 <25 mm Hg may
decrease CBF disproportionately and lead to CNS ischemia.
• Consider placing an ICP monitor in comatose patients or in those with
signs of increased ICP.
• With elevated ICP, remove CSF until pressure decreases by 50% and
maintain at less than 300 mm water.
• Meningococal meningitis/ H. flu needs droplet isolation

27. Prophylaxis For Close Contacts
• Close contact with patient with suspected N meningitidis for at least
4 hours during the week before onset (eg, house mates, daycare
center, cell mates) or were exposed to patient's nasopharyngeal
secretions (eg, kissing, mouth-to-mouth resuscitation, intubation,
nasotracheal suctioning).,
• Rifampin (pediatric dose: children <1 mo - 5 mg/kg q12h; children
>1 mo - 10 mg/kg q12h; adult dose: 600 mg PO bid) for 4 doses
• Alternative - Ciprofloxacin (adults) 500 mg PO single dose or
ceftriaxone (<15 y: 125 mg; >15 y: 250 mg) IM single dose
• Meningococcal vaccine only in established epidemics or in
travelers to epidemic countries
• Prophylaxis for H influenzae type b is controversial. Most
authorities treat contacts to protect unvaccinated children, younger
than 4 years.

28. Trauma/ Surgery
• Basilar skull
Fracture
S.
pneumoniae,
H. influenzae &
group A beta
hemolytic
streptococci
• Treatment-
Vancomycin
and
Ceftriaxone
• Penetrating
Trauma and
neurosurgery/VPS
S. aureus,
S.
epidermidis,
Pseudomonas
• Treatment-
Vancomycin
& Cefepime,
or
ceftazidime
or
meropenem

29. Tuberculous Meningitis-TBM
• Most common cause of subacute to chronic meningitis is
Mycobacterium tuberculosis (40%-60%)
• Mycobacterium tuberculosis may infect CNS by crossing the
BBB or rupture of a Rich focus.
• Following active primary pulm TB but may be absent
• Travel Hx, HIV- Immunosuppressants, alcoholics,
• Presentation is nonspecific, (headache, fever, malaise, lethargy,
and confusion-over 1 to 2 weeks, )
• Diagnosis- CSF-AFB smear (higher-grade infection, xpert
assay, PCR (expensive) & AFB cultures (weeks)
• CSF findings include increased opening pressure, lymphocytosis,
increased protein levels, decreased glucose levels

30. Tuberculous Meningitis-TBM
• Treatment: longer than that for pulmonary TB (6m) extended to 1
to 2 years in neurologically compromised or immunosuppressed.
• Tx: rifampin 10 mg/kg/day orally, isoniazid 5 mg/kg/day orally
(with pyridoxine), pyrazinamide 15 to 30 mg/kg/day orally, and
ethambutol 15 to 20 mg/kg/day orally followed by 10 months of
rifampin and isoniazid.
• Most common side effects peripheral neuropathy (isoniazid), flulike
illness, urine discoloration (rifampin),
nausea/vomiting/malaise/hyperurecemia (pyrazinamide), and optic
neuropathy-eye (ethambutol). All of the agents may cause rash and
hepatotoxicity.
• Steroids for the first 12 weeks.
• Household contacts should be tested and treated for latent TB

31. Syphilitic meningitis (Neurosyphilis)
• Due to Treponema pallidum in the primary or secondary stage
of infection
• both immunocompetent and immunocompromised (especially
HIV/AIDS) individuals
• evolves within months of inoculation, but frequently is
asymptomatic.
• Fever often is absent, but headache and confusion may be
evident.
• Typical CSF findings include (Aseptic profile) lymphocytosis,
increased protein levels, normal glucose levels, and positive
serologic tests for syphilis. (CSF) VDRL & FTA-Abs
• Treatment- Penicillin G, Aggressive dosing (24 million
units/day IV) x 14 days
• allergy to penicillin, desensitization
• With initiation of penicillin G, a release of endotoxin may occur,
resulting in skin rash and an inflammatory response(JHR)

32. Lyme Meningitis (neuroborreliosis )
• Due to Borrelia burgdorferi in stage 2
• exposure to an ixodid tick
• presents after the characteristic Lyme disease rash
disappears
• main symptoms are peripheral and cranial neuropathies
(71%)
• CSF findings include (Aseptic profile) lymphocytosis,
increased protein levels, normal glucose levels, and
positive serologic tests for B burgdorferi.
• treatment is ceftriaxone 2 g/day IV or penicillin G 20
million units/day IV for 10 to 14 days.
• Doxycycline 100 mg/day IV may be used in patients
who are allergic to penicillins or cephalosporins
• Symptoms usually resolve slowly over weeks to months

33. Meningitis:
Complications
• Predictors of poor
outcome in meningitis
(1) decreased level of consciousness on
admission,
(2) onset of seizures within 24 h of
admission, (3) signs of increased ICP, (
(4) young age (infancy) and age >50,
(5) the presence of comorbid conditions
including shock and/or the need for
mechanical ventilation, and
(6) delay in the initiation of treatment.
(7) decreased CSF glucose concentration
(<2.2 mmol/L [<40 mg/dL]) and markedly
increased CSF protein concentration (>3
g/L [> 300 mg/dL])
 Death
 Hearing loss
 Seizure disorder
 Intellectual (Learning
and memory)
 Gait abnormality
 Dizziness

34. Brain Abscess
• The most common organisms are streptocooci, staphylococci
and anaerobes
• May develop from:
• Spread from a cranial infection
• Sinusitis
• Dental infection- anaerobes, frontal lobe
• Otitis media, (temporal lobe and cerebellum-Strep,
pseudomonas, haemophilus)
• Head trauma
• Neurosurgery
• Hematogenous spread- MCA
Posterior frontal and parietal lobes- multiple abscess that
are poorly encapsulated and located at the gray-white junction

35. Evolution of Brain abscess
• Influenced by the nature of the infecting organism and by the
immunocompetence of the host.
 The early cerebritis stage (days 1–3)
 perivascular infiltration of inflammatory cells, which surround a central
core of coagulative necrosis.
 Marked edema.
 Late cerebritis stage (days 4–9)
 pus formation with enlargement of the necrotic center with thin capsule
 Early capsule formation (days 10–13),
 capsule better developed on the cortical than on the ventricular side of
the lesion.
 a ring-enhancing capsule on neuroimaging
 Late capsule formation (day 14 and beyond),
 well-formed necrotic center surrounded by a dense collagenous
capsule

36. Brain Abscess
• Symptoms
• Headache, fever, focal/general neuro
deficits
• Mass effect, Cerebral edema
• Frontal lobe-hemiparesis
• Temporal lobe-dysphasia
• Cerebellum-ataxia
• Diagnosis
• MRI, CT
• Gram stain and culture by needle aspiration
• NO LP!

37. Brain Abscess
• Treatment-
• Parenteral antibiotics-6-8wks
• Ceftriaxone and Metronidazole
• Trauma-Use cefepime or
ceftazidime for pseudomonas and
vancomycin for staphylococci
• Neurosurgical Drainage-standard

38. Subdural Empyema & Epidural Abscess
both are rare ..SDE more common
• Diagnosis
• Sinusitis in SDE, Trauma/surgery in EA
• MRI, CT
• NO LP!
• Treatment
• Emergency surgical evacuation of
empyema
• 3rd generation cephalosporin, vancomycin
& metronidazole (Parenteral)
• Fluid gram stain and culture

39. Fungal Meningitis
• Most common fungal cause of chronic meningitis is Cryptococcus
neoformans (an encapsulated yeast), most often in patients with HIV/AIDS
• Others are Coccidioides immitis, Histoplasma capsulatum, Blastomyces
dermatitidis, Aspergillus fumigatus, Candida albicans, and Sporothrix
schenckii.
• Immunocompromised individuals, and presentation depends on the fungus
involved.
• Cryptococcal meningitis usually presents as headache, fever, and lethargy.
Other symptoms are visual impairment, cranial neuropathies, ataxia, seizures,
and altered cognition.

40. Cryptococcus neoformans & HIV
Cryptococcal meningitis is the most common
opportunistic infection of the CNS, affecting 5-7% of
patients with AIDS. The second most common type of
meningitis is aseptic meningitis, which may be caused by
HIV-1 itself.
HIV-associated meningitis develops within days to weeks
after HIV infection. It appears as a mononucleosis-like
illness and is rarely associated with encephalitis. Tx with
HAART

41. Fungal Meningitis
• Diagnosis-CSF (Aseptic profile) lymphocytosis, decreased
glucose levels, increased protein levels, positive culture tests,
and a greatly elevated opening pressure upon lumbar
puncture
• Cultures and serology.C. neoformans-India ink stain/Crypto
antigen (may be neg in capsule-deficient C neoformans)
• Amphotericin B AMB deoxycholate (AMBD) 0.7 to 1
mg/kg/day with flucytosine 100 mg/kg/day for 2 weeks,
followed by fluconazole 400 mg/day orally for at least 10
weeks. Long-term fluconazole (usually 400 mg/day orally)
may be used for secondary prophylaxis

42. Parasitic Meningitis
􀂃 Chronic meningitis include Taenia solium (pork tapeworm-
Neurocycticercosis, the most common parasitic infection
of the CNS in immunocompetent), Angiostrongylus
cantonensis (Rat lungworm), Toxoplasma gondii, and
Acanthamoeba species. Echinococcus granulosus (Hydatid
Disease)

43. Neurocycticercosis
• most common in Latin America, Asia, Africa, and parts of
Europe
• can affect subcutaneous, muscle, or CNS ( ~ 50% meningitis)
• can be asymptomatic, but sometimes symptoms such as severe
headache, seizures, vision changes, and ischemic cerebrovascular
disease
• CSF findings usually include elevated protein levels, normal
glucose levels, and eosinophilia.
• albendazole 400 mg twice daily orally for 15 days, then 400
mg/day orally for 15 days and prednisone 60 mg/day orally for 3
days

44. TOXOPLASMOSIS--- Sxs like brain abscess
•eating undercooked
meat of animals
harboring tissue
cysts .
•consuming food or
water contaminated with
cat feces or by
contaminated
environmental samples
(such as fecal-
contaminated soil or
changing the litter box of
a pet cat) .
•blood transfusion or
organ
transplantation .
•transplacentally from
mother to fetus
Laboratory Studies
Serology
Anti-Toxoplasma
immunoglobulin detection
Rising serum (IgG) titers
(IgM) antibody response in
newly acquired toxoplasmosis or
Toxoplasma encephalitis.
may be unreliable in immunodeficient
individuals especially in AIDS
PCR
may facilitate the diagnosis and
follow-up of patients with AIDS
(sensitivity of 83.3% and
specificity of 95.7%.)
Toxoplasma gondii
abscesses

45. TOXOPLASMOSIS
CT scan or MRI
Single or multiple hypodense or hypointense lesions in
white matter and basal ganglia with mass effects may be
observed.
Lesions may enhance in a homogeneous or ring pattern
with contrast.
Imaging studies may be normal in diffuse toxoplasmosis.
•MRI is more sensitive than CT scan in detecting multiple
lesions.
• Single lesions favor the diagnosis of lymphoma over
that of toxoplasmosis.
•Thallium Th 201 brain single-photon emission computed
tomography (SPECT) may be useful in distinguishing
between lymphoma(increased uptake) and toxoplasmosis.
•Procedures
•Indications for brain biopsy include the following:
• Single mass lesion and negative serologic results
• No response to 14 days of empiric therapy
tissue cyst and tachyzoites in the
brain parenchyma
Ring-enhanced lesions in
the right basal ganglia and
the left frontal lobe with a
large mass effect and
peripheral oedema.
ring-enhanced parieto-
occipital lesion with a
large mass effect and
peripheral oedema.

46. • ring-enhanced parieto-occipital
lesion with a large mass effect and
peripheral oedema.

47. TOXOPLASMOSIS
Prevention & Treatment
• Most healthy people recover from
toxoplasmosis without treatment.
• Persons who are ill can be treated with a
combination of drugs such as
pyrimethamine and sulfadiazine, plus
folinic acid.
• Cotrimoxazole =drug of choice in our
setup
• Steroids if significant surrounding edema

48. Viral Meningitis
• Enteroviruses
(Poliovirus/Echovirus/
Coxsackievirus A/B)=most
common
• Paramyxovirus (Mumps/Measles
virus)
• Herpesvirus (HSV-1 and HSV
2/Varicella-zoster
virus/EBV/CMV/HHV*-6 HHV-
7
• Rabies virus
• HIV
• LCM virus (Lymphocytic
choriomeningitis)
Morbilliform
rash with
pharyngitis and
adenopathy
may suggest a
viral etiology
(eg, Epstein-Barr
virus [EBV],
cytomegalovirus
[CMV],
adenovirus,
HIV).
Varicella zoster virus (VZV), or HHV-3, and
CMV are causes of meningitis in
immunocompromised hosts, especially
patients with AIDS and transplant recipients.
HIV encephalitis.
Plain CT scan. Bilateral and
symmetric diffuse
hypodensity in the
periventricular white matter
without any mass effect

49. Viral Meningitis
C/F
• Present with sudden onset of fever; headache; nuchal
rigidity;
• Constitutional signs, including vomiting, anorexia, diarrhea,
cough, pharyngitis, and myalgias.
• The physical examination should include a careful search
for stigmata of enterovirus infection, including exanthems,
hand-foot-mouth disease, herpangina, pleurodynia,
myopericarditis, and hemorrhagic conjunctivitis.

50. Viral Meningitis
DIFFERENTIAL DIAGNOSIS
 Untreated or partially treated bacterial meningitis;
 Early stages of meningitis caused by fungi, mycobacteria, or
Treponema pallidum (neurosyphilis),;
 Meningitis due to Mycoplasma, Listeria spp., Brucella spp., Coxiella
spp., Leptospira spp., and Rickettsia spp.;
 Parameningeal infections;
 Neoplastic meningitis;
 Meningitis secondary to noninfectious inflammatory diseases, including
autoimmune and hypersensitivity meningitis,SLE and other
rheumatologic diseases, sarcoidosis, Behcet’s syndrome, and the
uveomeningitic syndromes.

51. Viral Meningitis
Dx… Clinical ,CSF analysis
Rx…analgesics, antipyretics, and
antiemetics.

52. Viral Encephalitidis
Arboviruses are the most
common causes of
episodic encephalitis
with
(1) St Louis
encephalitis,
(2) equine encephalitis
(EE)

53. CMV Encephlitis
• Cytomegaloviral (CMV) infection usually
presents as an encephaloventriculitis with
possible meningeal involvement.
Proton density-
weighted (SE,
2700/30) axial
and coronal
images disclose
hyperintensity
surrounding the
frontal horns and
trigones of the
lateral ventricles
and also
involving the
splenium of the
corpus callosum
(arrows).

54. Herpes simplex encephalitis (HSE)
• HSV-1: most often seen in persons under age 20 or
over age 40,
• single most important cause of fatal sporadic
encephalitis in the U.S.
• Type 2 virus (genital herpes) is most often transmitted
through sexual contact.
• more related with Meningitis; mainly in recurrent
one

55. Herpes simplex encephalitis
• Typical symptoms
include the
following:
• Fever (90%)
• Headache (81%)
• Psychiatric
symptoms (71%)
• Seizures (67%)
• Vomiting (46%)
• Focal weakness
(33%)
• Memory loss
(24%)
Typical findings on presentation
include the following:
Alteration of consciousness (97%)
Fever (92%)
Dysphasia (76%)
Ataxia (40%)
Seizures (38%)
Focal (28%)
Generalized (10%)
Hemiparesis (38%)
Cranial nerve defects (32%)
Visual field loss (14%)
Papilledema (14%)

56. Herpes simplex encephalitis
Laboratory Studies
Serologic evaluation of blood or CSF may be useful for retrospective
diagnosis,
CSF=mononuclear pleocytosis of 10-500 WBCs/µL (average, 100 WBCs/µL), RBC
count may be elevated (10-500 RBCs/µL), Protein levels are elevated to the range 60-
700 mg/dL (average, 100 mg/dL);Glucose values may be normal or mildly decreased
(30-40 mg/dL).
Viral cultures of CSF are rarely positive and should not be relied on to confirm the
diagnosis.
PCR analysis of CSF for the detection of HSV DNA has virtually replaced brain biopsy
as the criterion standard for diagnosis.
PCR is highly sensitive (94-98%) and specific (98-100%).
Become positive within 24 hours of the onset of symptoms and remain positive
for at least 5-7 days after the start of antiviral therapy.
False-negative findings may occur early in the course of the disease when viral
DNA levels are low (within 72 h of the onset of symptoms) or when blood is
present in the CSF, as hemoglobin may interfere with.

57. Herpes simplex encephalitis)
Imaging Studies
 MRI of the brain is the preferred.
 Abnormal in 90% of patients with HSE;
 may be normal early in the course of illness.
 Findings of localized temporal abnormalities are highly
suggestive
 confirmation of the diagnosis depends on the identification
of HSV by means of PCR or brain biopsy.
Head CT is less sensitive than MRI.
Approximately one third of patients with HSE have normal CT
findings on presentation.
Electroencephalography
Electroencephalography (EEG) shows focal abnormalities, such as
spike and slow- or periodic sharp-wave patterns over the
involved temporal lobes.
EEG is 84% sensitive to abnormal patterns in HSE but lacks
specificity (32%)
Axial gadolinium-enhanced T1-
weighted image reveals
enhancement of the right anterior
temporal lobe and parahippocampal
gyrus. At the right anterior temporal
tip is a hypointense, crescentic
region surrounded by enhancement
consistent with a small epidural
abscess.

58. Herpes simplex encephalitis (HSE)
• The diagnosis of HSE should be considered in any patient with a
rapidly progressively deteriorating level of consciousness, fever,
abnormal CSF findings, and focal neurological abnormalities in
the absence of any other causes.
• Rapid initiation of acyclovir therapy is crucial to reduce mortality
and morbidity risks.
• Since most relapses occur within 3 months of completing an
initial course of intravenous acyclovir, a prolonged course of an
oral antiviral agent (eg, valacyclovir) has been suggested
following initial treatment.
• Steroids have been used to reduce cerebral edema in patients
with severe HSE.

59. RABIES
Patients with
rabies could
present
atypically with
aseptic
meningitis,
and rabies
should be
suspected in a
patient with a
history of
animal bite
(eg, skunk,
raccoon, dog,
fox, bat).

60. RABIES -
IF A PERSON IS BITTEN...
• 1. Wash with soap and water
• 2. Rabies immunoglobulin (RIG)
• 􀂄 Given immediately into the wound
• 3. Rabies vaccination
• 􀂄 Given at day 0, 3, 7, 14, and 28

61. Progressive Multifocal
Leukoencephalopathy (PML)
• Due to JC virus
• Most patients are immunocompromised
• multifocal areas of demyelination of varying size distributed throughout the
brain
• CF- Visual deficits (45%), typically a homonymous hemianopia; mental
impairment (38%) (dementia, confusion, personality change);
weakness(hemi- or monoparesis); ataxia, Seizures (~20%)
• Diagnosis
• MRI-Periventricular white matter lesions
• CSF typically normal
• PCR for JCV DNA
• Treatment-No effective treatment except HAART for HIV

62. Prions
i. Kuru Variant
ii. Creutzfield-Jacob
Disease(Mad Cow Disease)
iii. Chronic Wasting Disease
(CWD) in deer

63. Noninfectious Causes
• Leukemia
• Neurosarcoidosis-
• noncaseating granulomas in the lungs, skin, joints, eyes, and—rarely acute
aseptic meningitis or chronic meningitis, meningeal mass lesions.
• Rx=oral corticosteroids. Methotrexate may be added to shorten the time
• SLE
• Medications eg..NSAIDs, azathioprine
• WG (GPA)
• severe, necrotizing, granulomatous systemic vasculitis associated with the
ANCA antibody.
• mostly involves the respiratory tract and kidneys, but may also affect the
eyes and CNS.
• Chronic meningitis, a rare complication of WG, is treated with high-dose
corticosteroids and cyclophosphamide
• Behcet’s disease
• Chemical exposure