JAPANESE ENCEPHALITIS

- a mosquito-borne viral dse of humans as

well as horses, swine, and other domestic
animals
- Asia, northern Japan, Korea, China, Taiwan,
the Philippines, and the Indonesian
archipelago and from Indochina through the
Indian subcontinent
- Vector: Culez tritaeniorhynchus
summarosus
• A night-biting mosquito that feeds
preferentially on large domestic animals
and birds
• Infrequently on humans
- Summer outbreaks
- Pigs serve as an amplifying host
- Pigs maintain a high sustained viremia and
PATHOPHYSIOLOGY
may be hosts to thousands of mosquitoes in
- After virus is introduced by a mosquito bite,
a single night, thereby producing an
replication locally and within regional
abundant source of infected vectors that can
lymphatic tissue --> viremia and infection of
transmit the infection further
- The annual incidencein endemic areas various organs and the brain. Neuroinvasion
through cerebral capillaries --> infection
ranges from 1-10 per 10,000 population
- Children younger than 15 y/o are principally crosses from the vascular side of the
endothelial cells to the perivascular space
affected, w/ nearly universal exposure by
- Infiltrating T cells elicit a broad inflammatory
adulthood
response, with B and T cells and
macrophages found in perivascular cuffs
CLINICAL MANIFESTATIONS
- Lethargy, nausea or abdominal pain, and macrophages and T cells in the
parenchyma
headache, and feverishness
- In 2-3 days, lethargy increases and the child - The rapidity of the neutralizing antibody
response is the principal determinant of
may exhibit behavior and motor
outcome
abnormalities
- Sudden convulsion is frequently the initial - Fatal causes occurring within 5 days after
the onset of illness have no detectable CSF
symptom
- Unusual manifestations: acute psychosis antibody response while virus is recoverable
from the CSF
and Guillain-Barré syndrome
- Signs of meningeal irritation in 2/3 of cases
- Cranial nerve palsies, central facial paralysis DIAGNOSIS
- Muscle weakness, either flaccid or spastic - Lumbar puncture
- W/ hyperreflexia and ankle clonus • Opening pressures - normal or slightly
- Focal or generalized convulsions develop on elevated
50-75% of patients • CSF fluid - lymphocytic pleocytosis fewer
- Patients w/ fulminant infections often die than 10 cells to several thousand, with a
median of several hundred per cubic
during the first 5 days of illness
millimeter
• CSF glucose and protein levels are
generally normal
- Electroencephalograms - diffuse theta to
delta showing wave slowing
- CT - diffuse white matter edema and non-
enhancing low-density areas, mainly in the
thalamus, basal ganglia, and pons
• Thalamic lesions frequently are
associated with hemorrhage
- MRI - similar distribution of abnormalities
- Confirmed serologically by JE virus-specific
IgM antibody in serum or CSF by ELISA
- 4-fold titer between acute and convalescent-
phase serum
- Cross-reactions with dengue virus and other
flaviviruses are common
- Real-time PCR and 17 promoter-based
assays -- sensitive
- JE virus occasionally can be isolated from
the blood no later than 6-7 days after onset
TREATMENT
- No specific antiviral treatment
- A few patients have been treated with
interferon alpha -- efficacy has not been
evaluated in wider trials
- Supportive care and control of intracranial
pressure are critical
- Mannitol is used routinely
- Other supportive measures:
• Control of fever and convulsions
• Fluid balance
• Respiratory support
• Prevention and tx of secondary infections
PREVENTION
- Avoidance of vector mosquitoes
- Vaccine
• Inactivated
• Live-attenuated
ZIKA VIRUS
- Mosquito-borne flavivirus (Aedes
mosquitoes)
- First identified in Uganda in 1947 in
monkeys
- Identified in humans in 1952 in Uganda and
the United Republic of Tanzania
- Outbreaks of Zika virus dse have been
recorded in Africa, the America, Asia and the
Pacific
- 2015: Brazil reported an association of
Guillan-Barré syndrome and
microcephaly
- Can be transmitted through sexual
intercourse
- Concern due to an association between Zika
virus and adverse pregnancy and fetal
outcomes
SIGNS AND SYMPTOMS
- Incubation period is unclear
- Symptoms are similar to dengue
• Fever
• Skin rashes
• Conjunctivitis
• Muscle and joint pain
• Malaise and headache
• Mild and last for 2-7 days
DIAGNOSIS
- Clinical: travel hx and exposure
- Nucleic Acid Testing (NAT) - whole blood,
serum and/or urine collected from patients
presenting with onset of symptoms </=7
days
- Serology: IgM detection
TREATMENT
- No specific tx
PREVENTION
- Protection against mosquito bites is Key
measure to prevent
- Physical barriers such as window screens or
closing
CHIKUNGUNYA VIRUS
- Transmitted by Aedes species and
Anopheles sp.
- Similar to dengue
- Outbreaks occur
- Incubation period: 2-4 days
CLINICAL MANIFESTATIONS
- In infants --abrupt onset of fever, followed
by flushing of the ski
• Febrile convulsion in 1/3 of patients
• After 3-5 days of fever, a generalized
maculopapular rash and
lymphadenopathy
• Conjunctival injection, swelling of the
eyelids, pharyngitis, and symptoms and
signs of URT diseases are common
• No enanthem occurs; some infants have
a biphasic fever curve, and arthralgia may
be severe
- In older children
• Fever, headache, myalgia, and arthralgia
involving various joints
• Macular blush and a maculopapular rash
and marked lymphadenopathy precede
defervescence
• (+) tourniquet test -- rare
- Maculopapular rash, arthralgia or arthritis,
and conjunctival injection were more
common symptoms in chikungunya than in
dengue
- Shock and bleeding are rare
DIAGNOSIS
- Clinical
- IgM capture ELISA after 5 days of onset of
illness
- PCT
- Viral culture

TREATMENT
- Supportive
- Symptoms are refractory to aspirin or other
NSAIDs
- Chloroquine phosphate (250mg/day)
provides prompt relief from chronic
arthralgia in a high proportion of sufferers
- Analgesics or mild sedation to control pain
- Febrile convulsions: phenobarbital or
diazepam
- Fluids
Prodrome:
PREVENTION •3-5 days
- Vaccines - not yet available •Fever
- Avoidance of mosquito bites •Colds, cough,
- Control of mosquitoes conjunctivitis
- Epidemic measures •Kopliks spot --
- Health education pathognomonic
enanthem
MEASLES (Rubeola or Morbilli)
ETIOLOGY
- Family Paramyxovirus
- Genus morbillivirus
- Has an outer envelope composed pf M-
protein, H-protein, F-protein, and internal
core is RNA Rash
- 1st 24 hrs --> faint macules behind ears,
- Acute highly contagious along the hairline; become confluent
- Fever, URT catarrhial inflammation, koplik's maculopapular as it spreads to face, neck,
spots and maculopapular rash upper arms and chest
- 2nd 24 hrs --> spreads over back, abdomen,
EPIDEMIOLOGY entire arms/thighs
- Routes or administration - 3rd-4th days --> rash reaches legs and feet
• Airborne --> fading from head to feet --> fine branny
• Direct contact with infectious droplet desquamation and brownish discoloration
• Transplacentally acquired immunity is - Severity of disease is directly related to
protective for 4-6 mos; disappear at extent and confluence of rash
variable rates Fever
- Susceptibility of population - Temperature rises as rash appears
• 90% of susceptible contact acquire the - Fever and symptoms subside w/in 2 days
disease once rashes are on legs and feet
• Permanent immunity acquired after - If persistent after day 3-4 of exanthem, may
disease indicate complication
- Period of communicability
• 1-2 days before the onset of symptoms (3 Convalescent stage:
days before to 4-6 days after the onset of - Brown staining
rash) - Fine branny desquamation
• Incubation period: 8-12 days - Course: 10-14 days

Other manifestations:
• Anorexia
 • Lymphadenopathy
• Diarrhea and vomiting
• Abdominal pain
• Slight splenomegaly
DIAGNOSIS
- Clinical/epidemiological basis
- Definitive diagnosis:
• Measles IgM
• Increase in measles IgG in paired sera
• Viral isolation (urine, blood, NP
secretions)
COMPLICATIONS
- Otitis media - most common
- Laryngitis, tracheitis, bronchitis
- Interstitial pneumonia
- Bronchopneumonia
• Mc cause of death
• due to secondary bacterial infection
(pneumococcus, streptococcus,
staphylococcus, Hin)
- Exacerbation of an existing Tuberculous
process
• Temporary loss of hypersensitivity
reaction to tuberculin for 4-6 wks
- Neurologic
• More common than in any other
exanthems
• Encephalitis: 1-2/1000 cases
• Sub-acute sclerosing panencephalitis
- Rare, degenerative CNS diseases
- Persistent measles virus infection
- Infections before 18 months increases
risk
- Boys > girls
• Subtle changes in behavior,
deterioration of school work -->
bizarre behavior --> frank dementia
• Massive, repetitive, symmetrical
myoclonic jerks
• True seizures --> progresses to
stupor and coma
• High measles antibody titers (HI&CF)
in sera and CSF
• Occur 10.8 years after original
infection
- Others: Guillain-Barré syndrome,
hemiplegia, cerebral thrombophlebitis,
retrobulbar neuritis
- Other complications
• Myocarditis
• Diarrhea w/ dehydration
• Idiopathic thrombocytopenia
• Hepatitis
• Appendicitis
MANAGEMENT
- Supportive (antipyretics, fluids and
electrolytes)
- Appropriate antibiotics for
bronchopneumonia and otitis media
- Oral Vitamin A
• 6 mos - 1y/o: 100,00 IU
• 1y/o and older: 200,00 IU
• Dose repeated the next day and at 4 wks
if w/ ophthalmic evidence of vitamin A
deficiency
PREVENTION
- Acute immunization
• Post-exposure immunization
- Measles vaccine if given w/in 72 hrs
after exposure may provide protection
in some cases
• Pre-exposure immunization
- 1st dose: at age 6 mos
- 2nd dose: 6-9 mos after 1st dose, as
monovalent vaccine or MMR
- 3rd dose: monovalent vaccine or MMR
at 4-6y/o or 11-12y/o
- Passive immunization
• Immune globulin can be given to prevent
or modify measles in a susceptible person
w/in 6 days of exposure
• Dose: 0.25mL/K IM
• Indications:
- Susceptible household contacts
especially <1 y/o
- Pregnant women
- Immunocompromised children
RUBELLA (German measles)
ETIOLOGY
- Rubella virus
- Togaviridae family
- German measles - first described by
German physicians, Friedrich Hoffman, in
the mid-eighteenth century
- Derived from the Latin, meaning little red
- "3-day measles"
• That starts initially on the face and neck
• Spreads centrifugally to the trunk and
extremities within 24 hours
• Begins to fade on the face on the second
day
- Congenital rubella syndrome (CRS)
described by Gregg in 1941
MODE OF TRANSMISSION
- Person to person via respiratory route
• Droplet from nose & throat
 • Droplet nuclei (aerosols)
• Maintain in human population by chain
transmission
- Acquired during pregnancy -- vertical
transmission
• Virus can enter via the placenta & infect
the fetus in utero (CRS)
- Period of communicability
• Few days before up to 5-7 days after the
rash
- Incubation period
• 14-21 days
PATHOGENESIS
CLINICAL MANIFESTATIONS
- Lymph nodes - suboccipital, postauricular,
and anterior cervical lymph nodes are most
prominent
- Rash - first manifestation
• Begins on the face and neck as small,
irregular pink macules that coalesce, and
it spreads centrifugally to involve the torso
and extremities, where it tends to occur
as discrete macules
- Forchheimer spots - time of onset of the
rash, examination of the oropharynx -- tiny
rose-colored lesions (Pathognomonic sign)
• Fleeting enanthema
• Pinpont or larger petechiae that usually
occur on the soft palate in 20% of patients
• Similar spots can be seen in measles and
scarlet fever
SIGNS AND SYMPTOMS
- RASH
• The primary symptom of the rubella virus
infection is the appearance of a rash
(exanthema) on the face which spreads to
the trunk and limbs and usually fades
after three days w/ no straining or peeling
of the skin.
• "Blueberry muffin lesions"
- LYMPH NODE
• tender lymphadenopathy (particularly post
auricular and suboccipital LN) persist up
to a week
- TEMPERATURE
• fever rarely rises above 38 C (100.4 F)
- OHER S/SX
• Eye pain on lateral and upward eye
movement (troublesome complaint)
• Conjunctivitis
• Sore throat
• Headache
• General body aches
• Low-grade fever
• Chills
• Anorexia
• Nausea
• Arthritis
COMPLICATIONS
- May produce transient arthritis, particularly
in women
- Serious complications
• Thrombocytopenic purpura
• Encephalitis
IMMUNITY
- Antibodies appear in serum as rash fades
and antibody titer raise
- Rapid raise in 1-3wks
- Rash in association with detection of IgM
indicates recent infection
- IgG antibodies persist for life
CONGENITAL RUBELLA SYNDROME
- Occurs during the 1st trimester of pregnancy
- Affects the development of the fetus
- May lead to several birth defects
- Infection may affect all organs
- May lead to fetal death or premature
delivery
- Severity of damage to fetus depends on
gestational age
- Infants: virus is isolated from urine and feces
MATERNAL RUBELLA INFECTION & RISK
OF CRS
- Before 11 wk of gestation - at 90%
- 11-12 wks - at 33%
- 13-14 wks - at 11%
- 15-16 wks - at 24%
- After 16 wks of gestation - uncommon
MANIFESTATIONS PF CONGENITAL
RUBELLA
- Sensorineural hearing loss - 58%
- Cataract, infantile glaucoma, micro-
ophthalmia, pigmentary retinopathy occur in
approximately 43%
- Congenital heart disease PDA and
pulmonary artery stenosis - 50%
- Bone lesions
- Psychiatric dso
- T1DM
- Hypogammaglobulinemia
- Generalized lymphadenopathy
- Intrauterine growth restriction
- Liver and spleen damage
• Hepatosplenomegaly, hepatitis, jaundice
• Thrombocytopenic purpura, with
petechiae and "blueberry muffin" lesions
- CNS
• Retardation, microcephaly
• Motor delay, behavioral dso, autism
• Intellectual disability - 13%
• A rare complication of panencephalitits
can occur in second decade with
congenital rubella syndrome may
progress to death
- CLASSIC TRIAD:
• Cataract
• Cardiac abnormalities
• Deafness
DIAGNOSIS
- Clinical diagnosis is unreliable
- Many viral infections mimic Rubella
- Specific diagnosis of infection with
1. Isolation of virus
2. Evidence of seroconversion
ISOLATION AND IDENTIFICATION OF VIRUS
- Nasopharyngeal or throat swabs taken 6
days prior or after appearance of rash is a
good source or Rubella virus
- Using cell cultured in shell vial antigens can
be detected by immunofluorescent methods
TREATMENT
- Post natal
• Mild illness
• Antipyretics and analgesics
• IVIg or corticosteroids can considered for
severe, non-remitting thrombocytopenia
- CRS
• Pediatric, cardiac, audiologic,
ophthalmologic, and neurologic evaluation
• Follow-up because many manifestations
may not be readily apparent initially or
may worsen with time
• Hearing screening
PREVENTION
- MMR: live and attenuated; confers lifelong
immunity
• Given to children 12-15 months and again
between 4-6 y/o
- Immunization of the young children and
teenage girls remain the best option to
prevent CRS
ROSEOLA INFANTUM (Exanthem subitu, or
Sixth disease)
- Mild febrile, exanthematous illness occurring
almost exclusively during infancy
- More than 95% of roseola cases occur in
children younger than 3 yrs w/ a peak of
6-15 mos of age
- Transplacental antibodies likely protect most
infants until 6 mos of age
- Infants w/ classic roseola exhibit a unique
constellation of findings displayed over a
short period of time
ETIOLOGY
- HHV-6: more common
- HHV-7
- Belong to the B-herpes virus subfamily of
herpes viruses
- CD4-T cells: principal target in vivo
- HHV 6 can also infect other cells
• CD8-T cells (suppressor), NK T-cells,
delta gamma cells, glial cells, epithelial
cells, monocytes, megakaryocytes, and
endothelial cells
CLINICAL MANIFESTATIONS
- Incubation period: averages 10 days (range
of 5-15 days)
- Prodromal period: usually asymptomatic
- Mild upper respiratory tract signs e.g.
Minimal rhinorrhea, slight pharyngeal
inflammation
- Mild conjunctival redness
- Fever - sudden onset, high grade
accompanied by fussiness w/o apparent
cause
• Usually resolves acutely after 72 hrs
- Rash coincident w/ the appearance of a faint
pink or rose-colored, non-pruritic, 2-3mm
morbilliform rash on the trunk usually lasts
1-3 days but is often described as
evanescent and may be visible only for
hours, spreading from the trunk to the face
and extremities
- Associated signs & symptoms
• Bulging fontanels - 26-30%
• Seizures - 5-35%
• Occipital or cervical lymphadenopathy -
30-35%
• Respiratory signs & symptoms - 55-70%
• Edematous eyelids - 0-30%
• Mild diarrhea - 55-70%
- in asian countries, ulcers at the
uvulopalatoglossal junction (Nagayama
spots) are common in infants w/ roseola
- Exanthems associated with roseola
• The roseola rash begins as discrete,
small (2-5mm), slightly raised pink
lesions on the trunk and usually spreads
to the neck, face, and proximal
extremities
DIAGNOSIS
- Clinically recognized based on fever,
defervescence and exanthem pattern
- CBC show leukopenia w/ lymphocytosis
- Definitive diagnosis (research labs)
• Viral isolation (peripheral lymphocytes)
• 4-fold rise in Ab titer (new infection or
reactivation)
• Detection of HHV-6 Ag by PCR
DIFFERENTIAL DIAGNOSIS
- Rubella
- Measles
- Roseola-like illness i.e. Enteroviruses
- Scarlet fever
- Drug hypersensitivity
TREATMENT
- Supportive care - antipyretic hydration
- Unusual or severe manifestations of
primary or presumed reactivated HHv-6B
infections such as encephalitis/PALE,
especially in immunocompromised
patients, may benefit from treatment,
- Gancyclovir, foscarnet, and cidovodir
VARICELLA (Chicken pox)/ HERPES
ZOSTER (Shingles)
ETIOLOGY
- Varicella - zoster virus
- Herpes viridae family
- Herpes virus (DNA)
- Primsry infection results in varicella (chicken
pox)
- Recurrent infection results in herpes zoster
(shingles)
- Short survival in environment
EPIDEMIOLOGY
- Mode of transmission
• Direct inoculation w/ skin lesions (varicella
or herpes zoster)
• Airborne spread (varicella)
• Highly contagious; 80-90% household
transmission rate
- Period of communicability
• 1-2 days before the rash start until 5-7
days after the rash and the lesions have
crusted
- Incubation period:
• 10-21 days
• 1-16 days in infant born to mother w/
active varicella
PATHOGENESIS
Respiratory transmission of virus
⬇
Replication in nasopharynx and regional lymph
nodes
⬇
Repeated episodes of viremia
⬇ Varicella
Multiple tissues, including sensory ganglia,
infected during viremia
⬇
Virus is transported in a retrograde manner
through sensory axons to the dorsal root
ganglia throughout the spinal cord (latency)
⬇ virus reach the ganglia by the hematogenous
route
Subsequent reactivation of latent virus
⬇
Herpes zoster

VARICELLA CLINICAL FEATURES
- Incubation period 14-16 days (range 10-21
days)
- Mild prodrome for 1-2 days
• 24-48hrs before rash
- Fever, malaise, anorexia, headache
and mild abdominal pain
- RASH
• Generally appear first on the head; most
concentrated on trunk
• Appear as very pruritic macules on scalp,
face or trunk
- Macules rapidly progress to vesicular --
> pustular --> crusting stages
- New crops of lesions daily x 3-7 days
- Various stages of evolution
- Ulcerative lesions in oropharynx,
conjunctivae and genital mucus
membranes
PROGRESSIVE SEVERE VARICELLA
- Continuing eruption of lesions (large,
umbilicated and hemorrhagic) w/ high fever
unto 2nd week of illness
- Primary varicella pneumonia, hepatitis,
encephalitis
- Seen in healthy adolescent and adults,
newborn infants and immunocompromised
patients
HERPES ZOSTER
- Reactivation of varicella zoster virus
- Associated with
• Aging immunosuppression
• Intrauterine exposure
• Varicella at <18 month of age
- Localized, unilateral vesicular lesions in 1-3
dermatomes
- Infrequently associated with localized pain,
hyperesthesia, pruritus and low grade fever
- Complete resolution in 1-2 wks
- Postherpetic neuralgia (pain >1 month)
unusual in children
- Disseminated cutaneous disease and/or
visceral dissemination in
immunocompromised patients
Groups at increased risk of complications of
varicella:
- Normal adults
- Immunocompromised persons
- Newborns with maternal rash onset w/in 5
days before to 48 hrs after delivery
COMPLICATIONS
- Pneumonia
• Most common complication in adults
- Hepatitis
• Relatively common; usually subclinical
- Encephalitis and Cerebellar ataxia
- Others
• Thrombocytopenia, nephritis/nephrotic
syndrome, hemolytic-uremic syndrome,
myocarditis/pericarditis, pancreatitis,
orchitis
- Bacterial superinfection
• Skin
- S.pyogenes or S.aureus
- Range from superficial impetigo to
cellulitis, lymphadenitis and
subcutaneous abscesses
- Suspected if with erythema of the base
of new vesicle or recrudescence of
fever 3-4 days after initial rash
• More invasive infections:
- Sepsis
- Pneumonia
- Arthritis
 - Osteomyelitis
- Varicella gangrenosa
- Necrotizing fasciitis
- Toxic shock syndrome
CONGENITAL VARICELLA SYNDROME
- Results from maternal infection during
pregnancy
- Period of risk may extend through first 20
wks of pregnancy
- Atrophy of extermity with skin scarring
(Cicatrix), low birth weight, eye and
neurologic abnormalities
- Risk appears to be small (<2%)
Stigmata of Varicella-Zoster Virus Fetopathy
- Damage to sensory nerves:
• Cicatricial skin lesions
• Hypopigmentation
- Damage to optic stalk and lens vesicle
• Microphthalmia
• Chorioretinitis
• Cataracts
• Optic atrophy
- Damage to brain/Encephalitis:
• Microcephaly/ hydrocephaly
• Calcifications/aplasia of brain
- Damage to cervical or lumbar cord
• Hypoplasia of extremity
• Motor/sensory deficits
• Absent DTRs
• Anisocoria/Horner syndrome
• Anal/vesical sphincter dysfunction
DIAGNOSIS
- Clinical
- Definitive diagnosis:
• Tissue culture - distinguishes VZV from
HSV
• Direct fluorescent antigen - more rapid/
sensitive than culture
• Tzanck smear - not specific for VZV
• PCT - distinguish wild type strains from
vaccine virus
• Varicella IgG - retrospective diagnosis
TREATMENT
- Acyclovir - DOC for varicella/herpes zoster
when indicated
• For Varicella:
- Not routine in healthy children
- Considered in patients at increased risk
of moderate to severe varicella
A. >12 y/o
B. Chronic cutaneous or
pulmonary disorders
C. Long term salicylate therapy
D. Short, intermittent or
aerosolized courses of
corticosteroid
- Dose:
• Immunocompetent hosts
- Oral: 80mg/k/day in 4 divided doss
x 5 days (max 3200mg/day)
• Immunocompromised hosts
- IV
• <1 y/o - 30mg/k/day in 3 divided
doses x 7-10 days
• >1 y/o - 1500mg/m2/day in 3
divided doses x 7-10 days
• For Zoster:
- Immunocompetent host
• IV: all ages - 30mg/k/day x 7-10 days
• Oral: >/= 12y/o - 4000mg/day in 5
divided doses x 5-7 days
- Immunocompromised host
• IV
- <12y/o: 60mg/k/day q8 x7-10 days
- >12 y/o: 30mg/k/day q8 x 7 days
Varicella vaccine:
- Live attenuated wild Oka strain
- Dose: 0.5mL SQ
- 2 doses:
• <13 y/o - at 12 mos and after 3 mos or at
4-6 y/o
• 13 y/o and older - 2 dose, 1 month apart
- Efficacy:
• 85-95% effective for prevention of
varicella in Children during outbreaks
• 100% effective for prevention of moderate
or severe disease
PREVENTION
- Passive immunization
• Varicella zoster immunoglobulin
- Candidates for VZIg after significant
exposure:
1. Immunocompromised patients w/o
previous infection
2. Susceptible pregnant women
3. New born whose mother had chicken
pox 5 days before or within 48 hrs after
delivery
4. Hospitalized premature (>28wks AOG)
whose mother w/o varicella or negative
serostatus
5. Hospitalized premature (<28wks AOG)
regardless pf maternal hx of varicella or
serostatus
PARVOVIRUS B 19
- Small, DNA-containing virus
EPIDEMIOLOGY
- Humans are the only known hosts
- Transmitted primarily by respiratory
secretion
- Transmissible in blood/ blood products
- Most adults have been infected
• Most infections are subclinical
• IgG is detectable in most healthy people
- Sporadic outbreaks, usually among children,
occur each year
- Transmission from patient to health care
staff is not uncommon
• Role in nosocomial transmission to other
patients
Parvovirus infections
- Diseases
• Fifth disease (cutaneous rash)
• Transient aplastic crisis (Severe acute
anemia)
• Pure red cell aplasia (chronic anemia)
• Hydrops fetalis (fatal fetal anemia)
FIFTH DISEASE
- Target is RBC progenitors
- Pain in joints
- Results in lysis of cells, thus depleting
source of mature red cells
- Anemia ensues
- Rarely fatal and w/o complications
COMPLICATIONS
- Persistent arthritis after EI
- Thrombocytopenic purpura
- Aseptic meningitis
- Virus - associated hemophagocytic
syndrome
DIAGNOSIS
- Laboratory tests not routinely available
- Not isolated by culture
- Based on observation of Typical Rash and
exclusion of other conditions
- (+) IgM anti-B19 - best marker of recent or
acute infection
- IgG anti-B19 - past infection or immunity
TREATMENT
- No specific antiviral treatment
- IVIg for immunodeficient patients w/ chronic
anemia
- Transfusion a d supportive care for patients
w/ aplastic crisis
- Intra-uterine blood transfusion in some
cases of B-19 infected hydrops fetalis
--end

TRANSIENT APLASTIC CRISIS

- B 19 infection of those with other hemolytic
anemias
• Sickle cell disease
• Thalassemias
- Can complicate crises
- Sometimes fatal

Other clinical manifestations:

- Arthritis/ arthralgia
- Fetal infections
• Occur with primary infection in mother
• 2nd trimester = most sensitive time
• Mom-immune hydrops and/or fetal death
• Lytic infection of erythrocyte precursors --
> red cell aplasia --> profound anemia -->
high output failure --> Hydrops
• Infected infants in utero born normally at
term ecen with evidence of hydrops by
UTZ