TORCH

TORCH................................................................................................................................1
Rubella.................................................................................................................................1
Morphology / Characteristic............................................................................................1
Pathogenesis....................................................................................................................2
Laboratory Diagnosis.......................................................................................................2
Prevention........................................................................................................................2
Cytoegalovirus..................................................................................................................2
Morphology / Characteristic............................................................................................2
Pathogenesis....................................................................................................................!
Laboratory Diagnosis.......................................................................................................!
Prevention........................................................................................................................!
Rubella
Morphology / Characteristic
Rubella virus, Genus Rubivirus, Family Togavirus (Togaviridae)
The the causative agent in German measles.
This normally harmless childhood disease
Can cause severe embryopathies during the frst trimester of pregnancy.
Togaviruses possess an icosahedral capsid and a closeftting envelope.
The capsid measures !"#$ nm and the entire virion %$"%! nm.
The genome of the togaviruses is a single& stranded, polyadenylated, sense R'(.
Replication not only produces ne) #$* genomic R'(, but a subgenomic +%* R'( fragment as )ell,
)hich codes for the capsid proteins.
,iral progeny are released by -budding. at the cell surface.
Pathogenesis
-German measles. is a harmless e/anthemous infection in children and youths, caused by a rubivirus,
the rubella virus, and transmitted by direct contact.
The infections remain inapparent in nearly half the cases.
The virus at frst replicates in lymphoid organs at the portal of entry and in the nasopharyngeal space,
after )hich a viremia develops before the e/anthem manifests.
0n pregnant )omen, the virus ta1es this route through the placenta to the embryo, )here it can cause
congenital deformities or embryonic death, especially in the frst three months of pregnancy.
The organs in the developmental stage in this trimester are most seriously a2ected by the rubella
infection.
The most fre3uent congenital deformities are deafness, cataracts, cardiac defects, microcephaly, and
spina bifda.
0n intrauterine embryo deaths due to rubella infections the immediate cause of death is usually
myocardial damage.
( measles infection confrmed by 0g4 detection or a raised antibody count is therefore an indication
for a frst&trimester abortion.
Laboratory Diagnosis
*erodiagnosis is the method of choice in suspected alphavirus and rubivirus infections.
50( methods are also available for 0g4 detection.
Prevention
There are vaccines to protect against alphavirus infections and rubella.
The main aim of rubella prophyla/is is to prevent rubella&caused embryopathies.
*ince 6$"6!7 of young adults are still susceptible to rubella infections and a live vaccine )ith fe) side
e2ects that confers reliable immunity is available, serial vaccination of children (boys and girls8) is
done before puberty.
The vaccine is tolerated so )ell that prior immune status chec1s are not re3uired.
Cytomegalovirus
Morphology / Characteristic
Herpesviruses are large viruses.
Di""erent ebers o" the group share architectural #etails an# are in#istinguishable by electron
icroscopy.
$ll herpesviruses have a core o" #ouble% stran#e# D&$' in the "or o" a toroi#' surroun#e# by a
protein coat that e(hibits icosahe#ral syetry an# has 1)2 capsoeres.
The nucleocapsi# is surroun#e# by an envelope that is #erive# "ro the nuclear ebrane o" the
in"ecte# cell an# contains viral glycoprotein spi*es about + n long.
$n aorphous' soeties asyetrical structure bet,een the capsi# an# envelope is #esignate# the
teguent.
The envelope# "or easures 1-./2.. n0 the 1na*e#2 virion' 1.. n.
The #ouble%stran#e# D&$ genoe 312!/24- *bp5 is linear.
$ stri*ing "eature o" herpesvirus D&$s is their se6uence arrangeent
Herpesvirus genoes possess terinal an# internal repeate# se6uences.
7oe ebers' such as the herpes siple( viruses' un#ergo genoe rearrangeents' giving rise to
#i""erent genoe 1isoers.2
The base coposition o" herpesvirus D&$s varies "ro 418 to 9-8 3: ; C5.
There is little D&$ hoology aong #i""erent herpesviruses e(cept "or herpes siple( types 1 an# 2'
,hich sho, -.8 se6uence hoology' an# huan herpesviruses ) an# 9' ,hich #isplay liite# 34./
-.85 se6uence hoology.
Treatent ,ith restriction en#onucleases yiel#s characteristically #i""erent cleavage patterns "or
herpesviruses an# even "or #i""erent strains o" each type. This 1"ingerprinting2 o" strains allo,s
epi#eiologic tracing o" a given strain.
The herpesvirus genoe is large an# enco#es at least 1.. #i""erent proteins.
O" these' ore than 4- polypepti#es are involve# in the structure o" the virus particle0 soe are part o"
the viral envelope.
Herpesviruses enco#e an array o" virus% speci"ic en<yes involve# in nucleic aci# etabolis' D&$
synthesis' an# protein regulation 3D&$ polyerase' thyi#ine *inase' protein *inase5.
Cytoegalovirus has the largest genetic content o" the huan herpesviruses.
=ts D&$ genoe 32!. *bp5 is signi"icantly larger than that o" H7>.
Only a "e, o" the any proteins enco#e# by the virus 3over 2..5 have been characteri<e#.
One' a cell sur"ace glycoprotein' acts as an ?c receptor that can nonspeci"ically bin# the ?c portion o"
iunoglobulins.
This ay help in"ecte# cells eva#e iune eliination by provi#ing a protective coating o" irrelevant
host iunoglobulins.
The a@or ie#iate early prooter% enhancer o" cytoegalovirus is one o" the strongest *no,n
enhancers' #ue to the concentration o" bin#ing sites "or cellular transcription "actors.
=t is use# e(perientally to support high%level e(pression o" "oreign genes.
Many genetically #i""erent strains o" cytoegalovirus are circulating in the huan population.
The strains are su""iciently relate# antigenically' ho,ever' so that strain #i""erences are probably not
iportant #eterinants in huan #isease.
Cytoegaloviruses are very species% speci"ic an# cell type%speci"ic.
$ll attepts to in"ect anials ,ith huan cytoegalovirus have "aile#.
$ nuber o" anial cytoegaloviruses e(ist' all o" the species%speci"ic.
Huan cytoegalovirus replicates in vitro only in huan "ibroblasts' although the virus is o"ten
isolate# "ro epithelial cells o" the host.
Cytoegalovirus replicates very slo,ly in culture# cells' ,ith gro,th procee#ing ore slo,ly than
that o" H7> or varicella%<oster virus.
>ery little virus becoes cell%"ree0 in"ection is sprea# priarily cell%to%cell.
=t ay ta*e several ,ee*s "or an entire onolayer to becoe involve#.
Cytoegalovirus pro#uces a characteristic cytopathic e""ect
Perinuclear cytoplasic inclusions "or in a##ition to the intranuclear inclusions typical o"
herpesviruses.
Multinucleate# cells are seen.
Many a""ecte# cells becoe greatly enlarge#.
=nclusion%bearing cytoegalic cells can be "oun# in saples "ro in"ecte# in#ivi#uals
Pathogenesis
C4, is characteri9ed by a narro) spectrum of hosts, slo) replication, fre3uently involving formation of
giant cells and late, slo) development of cytopathology.
(n initial infection )ith cytomegaly is inapparent in most persons, even in very early:perinatal or
postnatal:infections.
The virus apparently persists in the latent state in mononuclear cells.
Reactivation can also run an asymptomatic course, but symptoms may also develop that are generally
relatively mild, such a mononucleosisli1e clinical pictures, mild forms of hepatitis or other febrile
illnesses.
;roplet infection is the most fre3uent route of transmission, but smear infections and nursing
infections are also possible.
Generali9ed contamination )ith this pathogen (over <$7 of the adult population is infected), fre3uent
reactivation )ith, in some cases, months of continued e/cretion of viruses in saliva and urine and the
)ide variety of potential clinical pictures are all factors that often ma1e it di=cult to implicate C4, as
the etiological cause of an observed illness.
The virus infection can manifest as a se3uel instead of a cause, for instance of a >uli1e illness.
To labor the point some)hat, it could be said that the patient is not primarily ill due to a C4, infection,
but rather has a >orid C4, infection because he or she is ill.
The situation is di2erent in (0;*, transplantation or malignancy patients, in )hom a fresh C4,
infection or reactivation:similarly to ?*, and ,@,:can result in severe generali9ed infections )ith
lethal outcome.
The liver and lungs are the main organs involved.
Retinitis is also fre3uent in (0;* patients.
0n 1idney transplant patients, a C4, infection of the mesangial cells can result in reAection of the
transplant.
(nother feared C4,&caused condition is an intrauterine fetal infection, )hich almost al)ays results
from a primary infection in the motherB in 6$7 of cases the infection results in severe deformities
Laboratory Diagnosis
(mplifcation cultures from saliva, urine, bu2y coat, tissue, or C(D (bronchoalveolar lavage) are a
suitable method of confrming a >orid C4, infection.
0n transplantation patients, the ris1 of a C4, manifestation can be estimated by immunocytochemical
monitoring of the C4,positive cell count in the peripheral blood (-antigenemia test.), since this count
normally rises several days before clinical manifestations appear.
Cased on such an early)arning, antiviral therapy can be started in time (ganciclovir, foscarnet).
ECR results must be interpreted )ith a clear idea of ho) sensitive the method used can be, since the
numbers of viruses found may be clinically insignifcant.
?asty conclusions can result in -overdiagnosis,. above all in C4,&positive transplant recipients.
*erological results are hardly useful in clarifying a >orid infection due to the high level of generali9ed
contamination.
(dded to this is the fact that the immunoincompetent patients in )hom diagnosis of this infection
)ould be particularly important are serologically problematical any)ay.
*erology does contribute to clearing up the C4, status of transplant recipients and donors.
Prevention
C4, is transmitted by contact or smear infection, usually in childhood or adolescence.
0mmunosuppressed patients can be treated )ith hyperimmunoglobulin to provide passive immunity
against infection or recidivation.
Ganciclovir and foscarnet are therapeutically useful in transplantation, and particularly in (0;*
patients, to combat C4,&induced pneumonia, encephalitis, and retinitis.