Parvovirus Flashcards
Parvovirus -
meaning
enveloped or not
inactivated by
Small
non enveloped
resistant to most- except formalin, beta propionolactone, gamma irradiation, oxidizing agents
parvoviridae
subfamily
genera
species
parvovirinae (in vertebrates), densovirinae (in invertebrates)
5- TED BP
Tetraparvovirus (Parv4)
Erythroparvovirus (Parvo B19)
Dependovirus (Adnoassociated virus)
Bocaparvovirus (bocavirus)
Protoparvovirus (cuta, Bufa, Tusa)
Parv4
seroprevalence
clinical association
genotypes
0-25%
no clinical association
3 genotypes
Adnoassociated virus
why named so
how many tyoes
clinical association
use and why
require helper viruses (herpes or adeno) for replication
9
none
gene therapy vectors(no pathogenecity and can infect both replicating and non replicating cells)
bocavirus
seroprevalence (india)
types
causes what
how to diagnose
2-20% (2.5%)
1-4
1- URTI and LRTI in children
2-4 GI in children and adults
high titre viral load 10^4 in respiratory secretions/ dna in serum/ igm/ rising igg
Bufa virus- association
diarrhoea
Parvo B19- named so because
clinical causes
during evaluations of assays for hepatitis B surface antigen using panels of serum samples. Sample 19 in panel B (hence B19) gave an anomalous result
normal children, erythema infectiosum (EI),
normal adult, acute symmetrical polyarthropathy,
In persons with underlying hemolytic disorders or increased erythropoiesis, or both, transient aplastic crisis (TAC).
In the immunocompromised host, pure red cell aplasia (PRCA) and chronic anemia,
fetus <20 weeks, fetal death in utero, hydrops fetalis, or, rarely, the development of congenital anemia.
others: encephalitis, myocarditis, brachial neuropathy, glomerulonephritis
Parvovirus - genome products
Non structural proteins
NS
* DNA binding
* Adenosine triphosphatase activity
* Guanosine triphosphatase activity
* Inducer of apoptosis
* Critical for viral replication
11-KDa (Present in cytoplasm)- required for producing infectious virus
7.5-KDa (Function not known)
Structural proteins:
VP1 Minor (5% of capsid) – but larger in size: neutralising ab
VP1u (unique region):
* virion binding and internalization
* PLA2 activity
VP2 Major, self assembles into virus-like particles (VLPs)- first antibody to be produced
Parvovirus B19- genotypes and where; serotypes
3- 1 and 2 worldwide; 3 in ghana, brazil, europe and india
1 serotype- no reinfection
Parvovirus B19-
affects which cells
blood gorup P antigen - globoside
erythroid progenitor and erythroblasts
megakaryocytes
endothelial cells - vasculitits, transplacental
myocardial cells
NS expression causes apoptosis
co recptors for parvo b 19
alpha 5 beta 1 integrin (fibronectin)
Ku 80
seroprevalence in children by 15 yrs and older adults worldwide and india
50, 80
10, 50
transmission of parvo b19
routes of transmission
secondary attack rate
increased transmission in late winter, spring , summer
rates of infection increases every 3-4 years
respiratory secretions
close contact
blood transfusions (resist inactivation)
vertical
50%
erythema infectiosum- sympotms
natural course
IP 5-6 days :
symptoms: biphasic- 1st fever, malaise, mild gi illness, headache - peak at 8-9 days
coincides with viremia (>10^9 in peak- after this reduces to 10^5-6 persists for 4 months in serrum, but longer in tissues- liver, heart, synovium, bone marrow)
coicides with reticulocyte fall
Ig M in 10-12 days down in 2-3 months
IgG in 14 days and persists for life
As IgG increases second phase of symptoms - rash and arthropathy
Rash- slapped cheek- 1st stage
2nd: maculopapular on trunk and limbs, as it disappears - lacy appearance
3rd- persisting rash for weeks; maybe associated with pruritis, vesiculopustular rash, papulopetechial gloce and sock syndrome
arthropathy by parvo b19- symptoms and dd
symmetrical, small joints, lasts for 1-3 weeks, can persist
can also cause transient RF increase
TAC - predisposing, symptoms, other lineage differences
hemolytic stress- hemorrhage, iron def anemia, other types of anemia too
dyspnoea, lassitude and confusion, heart failure, severe bone marrow necrosis, CNS complications
neutropenia, thrombocytopenia, ITP HSP
coomunity azquired aplastic crisis mcc
parvo B19
Fetal infection by B19
Gestational Age Risk of adverse fetal outcome
(Weeks)
9-20 wks.
* Fetal loss - 9 %
* Hydrops fetalis- 3-11% (40-50% mortality without therapy)
(non-immune) > 20 wks. < 1 %
Gestational Age Risk of intrauterine (transplacental) infection
(Weeks)
< 4 wks. 0 %
5-16 wks. 15 %
> 16 wks. 25-70 %
(Increases with gestation)
B19 cause 10-15% o fall nonimmune hydrops fetalis
EI and polyarthropathy diagnosis, treatment and hic
IgM or IgG seroconversion
self limiting; NSAIDS
HIC- infective 2 weeks before
TAC - diagnosis, treatment and hic
DNA PCR in whole blood
IgM on day 3 of symptoms or IgG seroconversion
blood transfusion
7 days after
intrauterine infection - diagnosis, treatment
maternal- IgM/IgG seroconversion/ IgG avidity/ DNA levels
fetal- cord blood PCR, amniotic fluid PCR
may spontaneous resolve mostly; exchange transfusion if hydrops proven
PRCA - diagnosis, treatment and hic
DNA PCR in whole blood
reduction of immunosuppression
cidofovir
ivig 0.4g/kg/day for 5 days- followup by DNA, reticulocyte count and Hb level; if relapse in 6 months, maintenance ivig is once a month
till in hospital
Bone marrow finding
Reticulocyte reduction
Loss of erythroid progenitors and erythroblasts
Lantern cells- giant normoblasts - cytoplasmic vacuolations, immature chromatin, eosinophilic inclusion bodies in nucleus- shows apoptosis
