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VIRAL INFECTIONS
A.
B.
C.
D.
E.
F.
Etiologic agent
Mode of Transmission
Clinical manifestations
Pathologic Features
Diagnosis
Treatment
NEUROLOGY
2. HERPES ZOSTER & POSTHERPETIC NEURALGIA
2.1. HERPES ZOSTER
A. Etiologic agent
Varicella virus (Human Herpes Virus-3)
B. Mode of Transmission
Mucosa of the upper respiratory tract or
conjunctiva
Direct contact with fluid from rash blisters
caused by blisters
C. Clinical manifestations
Malaise and fever followed by rash
Trunk > face> limbs > buccal & pharyngeal
mucosa
D. Pathologic Features
Inflammatory reaction in several adjacent
sensory ganglia of the spinal or cranial
nerves which may cause necrosis of all or
part of the ganglion with or without
hemorrhage.
Poliomyelitis (less common)
Mild leptomeningitis
E. Diagnosis
Prodromal sensory phenomena along 1 or
more skin dermatomes (lasting 1-10 days)
Patchy erythema with induration in the
dermatomal area of involvement
Regional lymphadenopathy
Grouped herpetiform vesicles on
erythematous base
Pain in dermatomal areas
Vesicular involution
Slow resolution of remaining erythematous
plaques, typically without visible sequelae
F. Treatment
Varicella in normal children = No treatment
Antivirals
2.2. POSTHERPETIC NEURALGIA
A. Etiologic agent
Varicella zoster
B. Mode of Transmission
Skin to skin contact= major source of spread
Oral sex= most common transmission
Chickenpox= airborne resp. droplets
C. Clinical manifestations
Pain: burning, sharp & jabbing, deep &
aching
Sensitivity: allodynia
Itching and numbness
Weakness or paralysis
D. Pathologic Features
Nerve damage by shingles disrupts the
proper functioning of the nerve
Port herpetic neuralgia= dorsal horn
atrophy; cell axon & myelin loss without
fibrosis in the sensory ganglion
E. Diagnosis
Pain is variable- mild to severe burning,
stabbing or gnawing
Symptoms
Areas of previous herpes zoster may
show evidence of cutaneous scarring
Altered sensorium
Muscle weakness, tremor, paralysis
Viral culture and immunoflourescence
Antibodies to HZV
MRI- lesions at brainstem & cervical
cord
F. Treatment
Control of pain
Anticonvulsants, TCA, analgesics
Topical treatment: pain relievers
Glucocorticoid therapy
3. MEASLES & SSPE
3.1. Measles
A. Etiologic agent
Measles virus
Paramyxovirus
o Genus Morbillivirus
NEUROLOGY
B. Mode of Transmission
Large resp. droplets
Airborne
Contagious
o 4days before and 4days after onset of
rash
C. Clinical manifestations
Fever
Rash
Runny nose, cough, red, watery eyes, small
white spots inside the cheeks
Complications
Most common in <5 y/o, >20 y/o
Miscarriage, preterm delivery
Most serious:
o Blindness
o Encephalitis
o Severe diarrhea
o Dehydration
o Ear infection
o Pneumonia
D. Pathologic Features
Oral cavity- mucosal lesions, necrosis, neutrophilic
exudates, neovascularization
Lymphoid organs follicular hyperplasia syncytial
giant cells (WARTHIN-FINKELDEY CELLS)
E. Diagnosis
Clinical
Serologic
Resp. secretions
Immunoflourescence staining
PCR or viral culture
EIA
F. Treatment
No specific treatment
Supportive
Hydration
Antipyretics
Antibiotics
Vitamin A
NEUROLOGY
4. CREUTZFELD JAKOB DISEASE (SUBACUTE
SPONGIFORM ENCEPHALOPATHY)
A. Etiologic agent
Prion protein (PrP)
PrP-c = normal
PrP-Res = resistance to proteolytic digestion
PrP-Sc = infectious form
B. Mode of Transmission
Sporadic CJD = no M.O.T.
Familial CJD = autosomal dominant
Iatrogenic CJD
corneal transplant
dural grafts
EEG electrodes
Variant CJD
Consuming meat from infected cow
o Bovine spongiform encephalitis
o Mad cow disease
C. Clinical manifestations
Prodrome
Cerebellar ataxia
Visual disturbance
Headache
Vertigo
Sensory
D. Pathologic Features
Accumulation of PrP-Sc in neural tissues
E. Diagnosis
Western blot
No single diagnostic test for CJD
brain biopsy = confirmatory
F. Treatment
No specific treatment
Workers exposed to infected materials should
wash thoroughly with soap and water
5. VIRAL MENINGITIS
A. Etiologic agent
Enterovirus- most common
Most common cause of aseptic
meningitis in neonates older than 7
days
Arbovirus
Herpes virus
Acute HIV infection
Mumps
Measles
Japanese B encephalitis virus
Most common in epidemic viral
meningitis worldwide
B. Mode of Transmission
Person to person
Respiratory secretions
C. Clinical manifestations
Fever
Headache
Meningeal irritation
Predominant lymphocytic
Pleocytosis with Normal CSF glucose
Photophobia
Pain on eye movement
Paresthesias
Isolated strabismus
D. Pathologic Features
E. Diagnosis
Naso-oropharyngeal swabs
Rectal swabs
Stool, CSF and blood
F. Treatment
No specific treatment
Resolves spontaneously
NEUROLOGY
6. PROGRESSIVE MULTIFOCAL
LEUKOENCEPHALOPATHY (PML)
A. Etiologic agent
JC virus
Papova virus
B. Mode of Transmission
Respiratory route
C. Clinical manifestations
Behavioral
Speech
Cognitive
Motor
Visual
Rapid progression
Associated with AIDS
D. Pathologic Features
Mild cortical atrophy
Multiple demyelinative foci
Perivascular inflammatory infiltrates
Necrotic and cystic lesions
Nuclear inclusions
Cellular atypia
E. Diagnosis
CT/MRI
Single confluent lesions without mass
effect
PML lesions are hyperintense
F. Treatment
Antiretroviral therapy
7. HIV ENCEPHALITIS
A. Etiologic agent
HIV-1
Most common cause of HIV
2 families:
1. Lentivirus
2. Oncornavirus
B. Mode of Transmission
Sexual transmission
C.
D.
E.
F.
Blood
Occupational
Maternal-fetal/ infant transmission
Other body fluids
Clinical manifestations
AIDS dementia complex
HIV-associated progressive encephalopathy
Symptoms:
Cognitive
Motor
Behavioral
Pathologic Features
Diagnosis
Standardized neuropsychological testing
(ADC stage)
ELISA
Western blot
Blood test
CSF exam
CT/MRI
Proton MR spectroscopy (MRS)
Brain biopsy
Treatment
Highly Active Antiretroviral Therapy
(HAART)
8. RABIES ENCEPHALITIS
A. Etiologic agent
Rabies virus
Family Rhabdoviridae
Genus Lyssavirus
B. Mode of Transmission
Animal bite
Open wound, saliva, scratches
Human to human
C. Clinical manifestations
Asymptomatic (incubation period: 20-90
days)
Prodromal
Malaise
NEUROLOGY
Anorexia
Headache
Fever/chills
Pharyngitis
Nausea/vomiting
Diarrhea
Anxiety
Agitation
Insomnia
Depression
Neurologic period
Fasciculation
Priapism
Convulsion
coma
D. Pathologic Features
NEGRI BODIES
BABES NODULES
E. Diagnosis
CSF, saliva, skin, brain biopsy
Rabies-specific antibodies
RT-PCR amplification
Direct fluorescent antibody test
F. Treatment
No established treatment
Antiviral
Ketamine
Therapeutic coma measures
Post-exposure prophylaxis
Local wound care
Human rabies Immunoglobulin
9. DENGUE ENCEPHALITIS
A. Etiologic agent
Dengue virus
Family Flaviviridae
Vector
Aedes aegypti
B. Mode of Transmission
Mosquito bite from female Aedes aegypti
C. Clinical manifestations
Non-specific
Headache
Dizziness
Delirium
Drowsiness
Sleeplessness
Severe symptoms
Depressed sensorium
Lethargy
Confusion
Seizures
Meningismus
Paresis
Coma
Delayed symptoms
Paralysis of upper/ lower ext.
Seizures
Tremors
Amnesia
Loss of sensation
Manic psychosis
Depression
Dementia
GBS
D. Pathologic Features
Inflammation
Inclusion bodies
Necrosis
Microglial formation
Demyelination
E. Diagnosis
CSF
Cells = lymphocytes
Protein = increased
Glucose = normal
Serology
Serum IgM/IgG (+)
CSF IgM/IgG (+)
NEUROLOGY
Chronic
Papule
Plaque
Tumor
erythroderma
E. Diagnosis
Diagnostic Criteria
1. Antibody detection against HTLV-1 in
peripheral blood
2. Hypercalcemia
3. (+) tumor
4. Biopsy of suspicious lesions
F. Treatment
Arsenic trioxide
Zidovudine
-interferon
chemotherapy, antiviral therapy, allogenic
hematopoietic stem cell transplantation