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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 • Muscle and joint pain
IgM antibody in serum or CSF by ELISA • Malaise and headache
- 4-fold titer between acute and convalescent- • Mild and last for 2-7 days
phase serum
- Cross-reactions with dengue virus and other DIAGNOSIS
flaviviruses are common - Clinical: travel hx and exposure
- Real-time PCR and 17 promoter-based - Nucleic Acid Testing (NAT) - whole blood,
assays -- sensitive serum and/or urine collected from patients
- JE virus occasionally can be isolated from presenting with onset of symptoms </=7
the blood no later than 6-7 days after onset days
- Serology: IgM detection
TREATMENT
- No specific antiviral treatment TREATMENT
- A few patients have been treated with - No specific tx
interferon alpha -- efficacy has not been
evaluated in wider trials PREVENTION
- Supportive care and control of intracranial - Protection against mosquito bites is Key
pressure are critical measure to prevent
- Mannitol is used routinely - Physical barriers such as window screens or
- Other supportive measures: closing
• Control of fever and convulsions
• Fluid balance CHIKUNGUNYA VIRUS
• Respiratory support - Transmitted by Aedes species and
• Prevention and tx of secondary infections Anopheles sp.
- Similar to dengue
PREVENTION - Outbreaks occur
- Avoidance of vector mosquitoes - Incubation period: 2-4 days
- Vaccine
• Inactivated CLINICAL MANIFESTATIONS
• Live-attenuated - In infants --abrupt onset of fever, followed
by flushing of the ski
ZIKA VIRUS • Febrile convulsion in 1/3 of patients
- Mosquito-borne flavivirus (Aedes • After 3-5 days of fever, a generalized
mosquitoes) maculopapular rash and
- First identified in Uganda in 1947 in lymphadenopathy
monkeys • Conjunctival injection, swelling of the
- Identified in humans in 1952 in Uganda and eyelids, pharyngitis, and symptoms and
the United Republic of Tanzania signs of URT diseases are common
- Outbreaks of Zika virus dse have been • No enanthem occurs; some infants have
recorded in Africa, the America, Asia and the a biphasic fever curve, and arthralgia may
Pacific be severe
- 2015: Brazil reported an association of - In older children
Guillan-Barré syndrome and • Fever, headache, myalgia, and arthralgia
microcephaly involving various joints
- Can be transmitted through sexual • Macular blush and a maculopapular rash
intercourse and marked lymphadenopathy precede
- Concern due to an association between Zika defervescence
virus and adverse pregnancy and fetal • (+) tourniquet test -- rare
outcomes - Maculopapular rash, arthralgia or arthritis,
and conjunctival injection were more
SIGNS AND SYMPTOMS common symptoms in chikungunya than in
- Incubation period is unclear dengue
- Symptoms are similar to dengue - Shock and bleeding are rare
• Fever
• Skin rashes DIAGNOSIS
• Conjunctivitis - 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 MANAGEMENT
• Diarrhea and vomiting - Supportive (antipyretics, fluids and
• Abdominal pain electrolytes)
• Slight splenomegaly - Appropriate antibiotics for
bronchopneumonia and otitis media
DIAGNOSIS - Oral Vitamin A
- Clinical/epidemiological basis • 6 mos - 1y/o: 100,00 IU
- Definitive diagnosis: • 1y/o and older: 200,00 IU
• Measles IgM • Dose repeated the next day and at 4 wks
• Increase in measles IgG in paired sera if w/ ophthalmic evidence of vitamin A
• Viral isolation (urine, blood, NP deficiency
secretions)
PREVENTION
COMPLICATIONS - Acute immunization
- Otitis media - most common • Post-exposure immunization
- Laryngitis, tracheitis, bronchitis - Measles vaccine if given w/in 72 hrs
- Interstitial pneumonia after exposure may provide protection
- Bronchopneumonia in some cases
• Mc cause of death • Pre-exposure immunization
• due to secondary bacterial infection - 1st dose: at age 6 mos
(pneumococcus, streptococcus, - 2nd dose: 6-9 mos after 1st dose, as
staphylococcus, Hin) monovalent vaccine or MMR
- Exacerbation of an existing Tuberculous - 3rd dose: monovalent vaccine or MMR
process at 4-6y/o or 11-12y/o
• Temporary loss of hypersensitivity - Passive immunization
reaction to tuberculin for 4-6 wks • Immune globulin can be given to prevent
- Neurologic or modify measles in a susceptible person
• More common than in any other w/in 6 days of exposure
exanthems • Dose: 0.25mL/K IM
• Encephalitis: 1-2/1000 cases • Indications:
• Sub-acute sclerosing panencephalitis - Susceptible household contacts
- Rare, degenerative CNS diseases especially <1 y/o
- Persistent measles virus infection - Pregnant women
- Infections before 18 months increases - Immunocompromised children
risk
- Boys > girls RUBELLA (German measles)
• Subtle changes in behavior,
deterioration of school work --> ETIOLOGY
bizarre behavior --> frank dementia - Rubella virus
• Massive, repetitive, symmetrical - Togaviridae family
myoclonic jerks - German measles - first described by
• True seizures --> progresses to German physicians, Friedrich Hoffman, in
stupor and coma the mid-eighteenth century
• High measles antibody titers (HI&CF) - Derived from the Latin, meaning little red
in sera and CSF - "3-day measles"
• Occur 10.8 years after original • That starts initially on the face and neck
infection • Spreads centrifugally to the trunk and
- Others: Guillain-Barré syndrome, extremities within 24 hours
hemiplegia, cerebral thrombophlebitis, • Begins to fade on the face on the second
retrobulbar neuritis day
- Other complications - Congenital rubella syndrome (CRS)
• Myocarditis described by Gregg in 1941
• Diarrhea w/ dehydration
• Idiopathic thrombocytopenia MODE OF TRANSMISSION
• Hepatitis - Person to person via respiratory route
• Appendicitis • Droplet from nose & throat
• Droplet nuclei (aerosols) - Forchheimer spots - time of onset of the
• Maintain in human population by chain rash, examination of the oropharynx -- tiny
transmission rose-colored lesions (Pathognomonic sign)
- Acquired during pregnancy -- vertical • Fleeting enanthema
transmission • Pinpont or larger petechiae that usually
• Virus can enter via the placenta & infect occur on the soft palate in 20% of patients
the fetus in utero (CRS) • Similar spots can be seen in measles and
- Period of communicability scarlet fever
• Few days before up to 5-7 days after the
rash SIGNS AND SYMPTOMS
- Incubation period - RASH
• 14-21 days • The primary symptom of the rubella virus
infection is the appearance of a rash
PATHOGENESIS (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
CLINICAL MANIFESTATIONS • General body aches
• Low-grade fever
• Chills
• Anorexia
• Nausea
• Arthritis
COMPLICATIONS
- May produce transient arthritis, particularly
in women
- Serious complications
• Thrombocytopenic purpura
• Encephalitis
IMMUNITY
- Lymph nodes - suboccipital, postauricular, - Antibodies appear in serum as rash fades
and anterior cervical lymph nodes are most
and antibody titer raise
prominent - Rapid raise in 1-3wks
- Rash - first manifestation - Rash in association with detection of IgM
• Begins on the face and neck as small, indicates recent infection
irregular pink macules that coalesce, and - IgG antibodies persist for life
it spreads centrifugally to involve the torso
and extremities, where it tends to occur
CONGENITAL RUBELLA SYNDROME
as discrete macules - Occurs during the 1st trimester of pregnancy
- Affects the development of the fetus
- May lead to several birth defects
- Infection may affect all organs ISOLATION AND IDENTIFICATION OF VIRUS
- May lead to fetal death or premature - Nasopharyngeal or throat swabs taken 6
delivery days prior or after appearance of rash is a
- Severity of damage to fetus depends on good source or Rubella virus
gestational age - Using cell cultured in shell vial antigens can
- Infants: virus is isolated from urine and feces be detected by immunofluorescent methods

MATERNAL RUBELLA INFECTION & RISK TREATMENT


OF CRS - Post natal
- Before 11 wk of gestation - at 90% • Mild illness
- 11-12 wks - at 33% • Antipyretics and analgesics
- 13-14 wks - at 11% • IVIg or corticosteroids can considered for
- 15-16 wks - at 24% severe, non-remitting thrombocytopenia
- After 16 wks of gestation - uncommon - CRS
• Pediatric, cardiac, audiologic,
MANIFESTATIONS PF CONGENITAL ophthalmologic, and neurologic evaluation
RUBELLA • Follow-up because many manifestations
- Sensorineural hearing loss - 58% may not be readily apparent initially or
- Cataract, infantile glaucoma, micro- may worsen with time
ophthalmia, pigmentary retinopathy occur in • Hearing screening
approximately 43%
- Congenital heart disease PDA and PREVENTION
pulmonary artery stenosis - 50% - MMR: live and attenuated; confers lifelong
- Bone lesions immunity
- Psychiatric dso • Given to children 12-15 months and again
- T1DM between 4-6 y/o
- Hypogammaglobulinemia - Immunization of the young children and
- Generalized lymphadenopathy teenage girls remain the best option to
- Intrauterine growth restriction prevent CRS
- Liver and spleen damage
• Hepatosplenomegaly, hepatitis, jaundice ROSEOLA INFANTUM (Exanthem subitu, or
• Thrombocytopenic purpura, with Sixth disease)
petechiae and "blueberry muffin" lesions - Mild febrile, exanthematous illness occurring
- CNS almost exclusively during infancy
• Retardation, microcephaly - More than 95% of roseola cases occur in
• Motor delay, behavioral dso, autism children younger than 3 yrs w/ a peak of
• Intellectual disability - 13% 6-15 mos of age
• A rare complication of panencephalitits - Transplacental antibodies likely protect most
can occur in second decade with infants until 6 mos of age
congenital rubella syndrome may - Infants w/ classic roseola exhibit a unique
progress to death constellation of findings displayed over a
- CLASSIC TRIAD: short period of time
• Cataract
• Cardiac abnormalities ETIOLOGY
• Deafness - HHV-6: more common
- HHV-7
DIAGNOSIS - Belong to the B-herpes virus subfamily of
- Clinical diagnosis is unreliable herpes viruses
- Many viral infections mimic Rubella - CD4-T cells: principal target in vivo
- Specific diagnosis of infection with - HHV 6 can also infect other cells
1. Isolation of virus • CD8-T cells (suppressor), NK T-cells,
2. Evidence of seroconversion delta gamma cells, glial cells, epithelial
cells, monocytes, megakaryocytes, and
endothelial cells
CLINICAL MANIFESTATIONS - Unusual or severe manifestations of
- Incubation period: averages 10 days (range primary or presumed reactivated HHv-6B
of 5-15 days) infections such as encephalitis/PALE,
- Prodromal period: usually asymptomatic especially in immunocompromised
- Mild upper respiratory tract signs e.g. patients, may benefit from treatment,
Minimal rhinorrhea, slight pharyngeal - Gancyclovir, foscarnet, and cidovodir
inflammation
- Mild conjunctival redness VARICELLA (Chicken pox)/ HERPES
- Fever - sudden onset, high grade ZOSTER (Shingles)
accompanied by fussiness w/o apparent ETIOLOGY
cause - Varicella - zoster virus
• Usually resolves acutely after 72 hrs - Herpes viridae family
- Rash coincident w/ the appearance of a faint - Herpes virus (DNA)
pink or rose-colored, non-pruritic, 2-3mm - Primsry infection results in varicella (chicken
morbilliform rash on the trunk usually lasts pox)
1-3 days but is often described as - Recurrent infection results in herpes zoster
evanescent and may be visible only for (shingles)
hours, spreading from the trunk to the face - Short survival in environment
and extremities
- Associated signs & symptoms EPIDEMIOLOGY
• Bulging fontanels - 26-30% - Mode of transmission
• Seizures - 5-35% • Direct inoculation w/ skin lesions (varicella
• Occipital or cervical lymphadenopathy - or herpes zoster)
30-35% • Airborne spread (varicella)
• Respiratory signs & symptoms - 55-70% • Highly contagious; 80-90% household
• Edematous eyelids - 0-30% transmission rate
• Mild diarrhea - 55-70% - Period of communicability
- in asian countries, ulcers at the • 1-2 days before the rash start until 5-7
uvulopalatoglossal junction (Nagayama days after the rash and the lesions have
spots) are common in infants w/ roseola crusted
- Exanthems associated with roseola - Incubation period:
• The roseola rash begins as discrete, • 10-21 days
small (2-5mm), slightly raised pink • 1-16 days in infant born to mother w/
lesions on the trunk and usually spreads active varicella
to the neck, face, and proximal
extremities PATHOGENESIS
Respiratory transmission of virus
DIAGNOSIS ⬇
- Clinically recognized based on fever, Replication in nasopharynx and regional lymph
defervescence and exanthem pattern nodes
- CBC show leukopenia w/ lymphocytosis
- Definitive diagnosis (research labs) ⬇
• Viral isolation (peripheral lymphocytes) Repeated episodes of viremia
• 4-fold rise in Ab titer (new infection or ⬇ Varicella
reactivation) Multiple tissues, including sensory ganglia,
• Detection of HHV-6 Ag by PCR infected during viremia

DIFFERENTIAL DIAGNOSIS
- Rubella Virus is transported in a retrograde manner
- Measles through sensory axons to the dorsal root
- Roseola-like illness i.e. Enteroviruses ganglia throughout the spinal cord (latency)
- Scarlet fever ⬇ virus reach the ganglia by the hematogenous
- Drug hypersensitivity route
Subsequent reactivation of latent virus
TREATMENT ⬇
- Supportive care - antipyretic hydration Herpes zoster
- Localized, unilateral vesicular lesions in 1-3
VARICELLA CLINICAL FEATURES dermatomes
- Incubation period 14-16 days (range 10-21 - Infrequently associated with localized pain,
days) hyperesthesia, pruritus and low grade fever
- Mild prodrome for 1-2 days - Complete resolution in 1-2 wks
• 24-48hrs before rash - Postherpetic neuralgia (pain >1 month)
- Fever, malaise, anorexia, headache unusual in children
and mild abdominal pain - Disseminated cutaneous disease and/or
- RASH visceral dissemination in
• Generally appear first on the head; most immunocompromised patients
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

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
PROGRESSIVE SEVERE VARICELLA syndrome, hemolytic-uremic syndrome,
- Continuing eruption of lesions (large, myocarditis/pericarditis, pancreatitis,
umbilicated and hemorrhagic) w/ high fever orchitis
unto 2nd week of illness - Bacterial superinfection
- Primary varicella pneumonia, hepatitis, • Skin
encephalitis - S.pyogenes or S.aureus
- Seen in healthy adolescent and adults, - Range from superficial impetigo to
newborn infants and immunocompromised cellulitis, lymphadenitis and
patients subcutaneous abscesses
- Suspected if with erythema of the base
HERPES ZOSTER of new vesicle or recrudescence of
- Reactivation of varicella zoster virus fever 3-4 days after initial rash
- Associated with • More invasive infections:
• Aging immunosuppression - Sepsis
• Intrauterine exposure - Pneumonia
• Varicella at <18 month of age - Arthritis
- Osteomyelitis C. Long term salicylate therapy
- Varicella gangrenosa D. Short, intermittent or
- Necrotizing fasciitis aerosolized courses of
- Toxic shock syndrome corticosteroid
- Dose:
CONGENITAL VARICELLA SYNDROME • Immunocompetent hosts
- Results from maternal infection during - Oral: 80mg/k/day in 4 divided doss
pregnancy x 5 days (max 3200mg/day)
- Period of risk may extend through first 20 • Immunocompromised hosts
wks of pregnancy - IV
- Atrophy of extermity with skin scarring • <1 y/o - 30mg/k/day in 3 divided
(Cicatrix), low birth weight, eye and doses x 7-10 days
neurologic abnormalities • >1 y/o - 1500mg/m2/day in 3
- Risk appears to be small (<2%) divided doses x 7-10 days
• For Zoster:
Stigmata of Varicella-Zoster Virus Fetopathy - Immunocompetent host
- Damage to sensory nerves: • IV: all ages - 30mg/k/day x 7-10 days
• Cicatricial skin lesions • Oral: >/= 12y/o - 4000mg/day in 5
• Hypopigmentation divided doses x 5-7 days
- Damage to optic stalk and lens vesicle - Immunocompromised host
• Microphthalmia • IV
• Chorioretinitis - <12y/o: 60mg/k/day q8 x7-10 days
• Cataracts - >12 y/o: 30mg/k/day q8 x 7 days
• Optic atrophy
- Damage to brain/Encephalitis: Varicella vaccine:
• Microcephaly/ hydrocephaly - Live attenuated wild Oka strain
• Calcifications/aplasia of brain - Dose: 0.5mL SQ
- Damage to cervical or lumbar cord - 2 doses:
• Hypoplasia of extremity • <13 y/o - at 12 mos and after 3 mos or at
• Motor/sensory deficits 4-6 y/o
• Absent DTRs • 13 y/o and older - 2 dose, 1 month apart
• Anisocoria/Horner syndrome - Efficacy:
• Anal/vesical sphincter dysfunction • 85-95% effective for prevention of
varicella in Children during outbreaks
DIAGNOSIS • 100% effective for prevention of moderate
- Clinical or severe disease
- Definitive diagnosis:
• Tissue culture - distinguishes VZV from PREVENTION
HSV - Passive immunization
• Direct fluorescent antigen - more rapid/ • Varicella zoster immunoglobulin
sensitive than culture - Candidates for VZIg after significant
• Tzanck smear - not specific for VZV exposure:
• PCT - distinguish wild type strains from 1. Immunocompromised patients w/o
vaccine virus previous infection
• Varicella IgG - retrospective diagnosis 2. Susceptible pregnant women
3. New born whose mother had chicken
TREATMENT pox 5 days before or within 48 hrs after
- Acyclovir - DOC for varicella/herpes zoster delivery
when indicated 4. Hospitalized premature (>28wks AOG)
• For Varicella: whose mother w/o varicella or negative
- Not routine in healthy children serostatus
- Considered in patients at increased risk 5. Hospitalized premature (<28wks AOG)
of moderate to severe varicella regardless pf maternal hx of varicella or
A. >12 y/o serostatus
B. Chronic cutaneous or
pulmonary disorders
PARVOVIRUS B 19 COMPLICATIONS
- Small, DNA-containing virus - Persistent arthritis after EI
- Thrombocytopenic purpura
EPIDEMIOLOGY - Aseptic meningitis
- Humans are the only known hosts - Virus - associated hemophagocytic
- Transmitted primarily by respiratory syndrome
secretion
- Transmissible in blood/ blood products DIAGNOSIS
- Most adults have been infected - Laboratory tests not routinely available
• Most infections are subclinical - Not isolated by culture
• IgG is detectable in most healthy people - Based on observation of Typical Rash and
- Sporadic outbreaks, usually among children, exclusion of other conditions
occur each year - (+) IgM anti-B19 - best marker of recent or
- Transmission from patient to health care acute infection
staff is not uncommon - IgG anti-B19 - past infection or immunity
• Role in nosocomial transmission to other
patients TREATMENT
- No specific antiviral treatment
Parvovirus infections - IVIg for immunodeficient patients w/ chronic
- Diseases anemia
• Fifth disease (cutaneous rash) - Transfusion a d supportive care for patients
• Transient aplastic crisis (Severe acute w/ aplastic crisis
anemia) - Intra-uterine blood transfusion in some
• Pure red cell aplasia (chronic anemia) cases of B-19 infected hydrops fetalis
• Hydrops fetalis (fatal fetal anemia)
--end
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

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