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Der Christoph Merian Verlag ist ein unabhängiger Schweizer Verlag, der Publikationen im Bereich Architektur und Kunst, Kultur und Gesellschaft sowie. Helen Balmer – Zeichen stellen in den Warenkorb legen. 20 von Artikeln. Weitere Artikel laden. © Christoph Merian Verlag Kontakt AGB Impressum. Der CMV (Christlicher Missions-Verlag) ist ein junger Verlag und wie der Betanien Verlag ebenfalls in Bielefeld ansässig. Gegründet wurde der CMV von​. Geschäftskunden-Portal des Christlichen Missions-Verlags (Bielefeld). War Augustin der erste Calvinist? Ab sofort lieferbar! Wir behalten uns vor, Lieferungen in die Schweiz durch unseren Partnerverlag CLKV vorzunehmen. 8,​50 €.

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Behance is the world's largest creative network for showcasing and discovering creative work. Der CMV (Christlicher Missions-Verlag) ist ein junger Verlag und wie der Betanien Verlag ebenfalls in Bielefeld ansässig. Gegründet wurde der CMV von​. Seit fast 20 Jahren steht der Christliche Medienvertrieb (CMV) für fundierte biblische Literatur und Medien. Unsere Webseite finden sie unter. Cmv Verlag The severity of CMV disease varies depending on the population, type of transplantation as well as visit web page the level of immunosupression and can range from a self-limiting febrile illness to multi-system disease. Application of article source kinetics to identify patients who develop cytomegalovirus disease after transplantation. Disease progression in babies who are infected in the womb, during birth or through breastfeeding may vary a great deal. CMV infects people of all ages. Fishman JA. The method is standardized but the mRNA extraction procedure is time consuming. URL of Article.

Even though there are conflicting data about the incidence of TT-CMV remaining after the introduction of leukodepletion, it has been clearly shown that both prevalence and concentration of CMV DNA in peripheral blood are highest in newly seropositive donors.

Therefore, avoidance of blood products from these donors is the most important goal of any transfusion strategy. This goal can be reached by: i selection of blood products from seronegative donors, ii provision of CMV DNA-negative blood products, or iii provision of blood from long-term seropositive donors.

Human cytomegalovirus CMV is a ubiquitous beta-herpesvirus transmitted by direct person-to-person contact and causing mostly asymptomatic or mild mononucleosis-like infections in immunocompetent subjects [ 1 ].

After development of suitable biochemical methods restriction endonuclease analysis , the molecular evidence for TT-CMV was provided by Tolpin and colleagues in [ 5 ].

In the s and s, the provision of blood products from seronegative donors and leukoreduction of blood products were introduced to reduce the incidence of TT-CMV in risk populations [ 7 , 8 ].

Currently, mainly seronegative patients undergoing hematopoietic stem cell transplantation HSCT , low-birth-weight infants, fetuses intrauterine transfusions , CMV-seronegative pregnant women and severely immunocompromised patients are considered as being at risk for TT-CMV [ 10 ].

After the universal introduction of leukodepletion for red blood cell and platelet concentrates, there is an ongoing controversy as to whether TT-CMV still exists in at-risk patients.

The patients received 1, leukoreduced, but CMV-untested, blood products from 3, donors median 55 units per patient, range units per patient.

CMV antibodies were tested in 22 patients. CMV nucleic acid testing NAT was performed twice weekly starting at the day after HSCT, and remained negative throughout the study period at least until day after transplantation.

Taken together, the data of Thiele et al. Contrarily to these data, Wu and colleagues [ 13 ] reported 3 cases of probable TT-CMV in 46 seronegative patients, who received 1, leukoreduced, but CMV-untested, cellular blood transfusions.

The study included patients who were 13 years of age or older, and were projected to receive multiple transfusions.

In the third patient, no CMV DNA was detected, but the interval between the last seronegative sample and the first seropositive sample was 2 months, so that a short period of systemic viremia might have been missed.

All 3 patients received blood transfusions from seropositive donors prior to seroconversion. Therefore, both free CMV in plasma as well as residual leukocytes, despite pre-storage filtration with 3rd generation filters, might have caused these cases of TT-CMV, but even community-acquired CMV infections could not be ruled out by the authors.

For other risk groups, like low-birth-weight infants, to our knowledge no current data about the incidence of TT-CMV are available.

Until , only 2 suspected cases had been reported, which could not be confirmed by the Paul-Ehrlich Institute [ 15 ]. In contrast to the ongoing controversy about current rates of TT-CMV, the information gathered over the last few years has led a rather clear picture of the course of CMV infections in blood donors.

Primary CMV infections in blood donors occur in all age groups [ 2 ]. Mononucleosis-like symptoms due to primary CMV infections are rare.

In a recent study, for example, none of the 13 donors with primary CMV infection developed mononucleosis-like symptoms [ 3 ]. Unspecific symptoms of viral disease were common but not significantly increased compared to a matched control group [ 3 ].

In the study of Zanghellini et al. The closer the interval between the last seronegative and the first seropositive sample, the higher is the incidence of CMV DNA fig.

In donors with low interdonation intervals e. The figure is taken from Ziemann et al. Donors were categorized according to the interval between the last seronegative and the first seropositive sample.

Both prevalence and concentration of CMV DNA were shown to be higher in the first seropositive than in the last seronegative sample both for plasma and whole blood samples [ 18 , 19 ].

However, as the sampling interval ranged between several weeks to several months, even higher peak concentrations during primary CMV infection might have been missed.

The detection of peak CMV DNA concentrations after seroconversion is in accordance with the results of Zhang and colleagues [ 20 ], who screened young seronegative women for primary CMV infections in a placebo-controlled clinical trial of recombinant CMV glycoprotein B gB vaccine.

By regular screening with viral cultures, viable CMV in body fluids was detected between 0 and 12 weeks median 2 weeks after the first seropositive sample.

A delayed peak of CMV DNA and viable virus after development of antibodies has been explained by the hypothesis that primary CMV infections caused by direct person-to-person contact first lead to a localized lytic infection cycle, e.

After an interval of days to several weeks, this local infection is followed by viremia during which the virus spreads to other organs, like the kidneys.

At this stage, antibodies against glycoproteins of the viral envelope, e. The duration of viremia in immunocompetent subjects seems to be short in most subjects, but even cases with prolonged viremia up to several months have been reported [ 3 ].

In donors with remote CMV infection e. These data contradict the findings of Dumont and co-workers [ 22 ], who reported frequent reactivations of latent CMV infections in immunocompetent blood donors in temporal association to the pine tree pollen season.

This astonishing association could not be reproduced by others, and it is unclear whether the reactivation had been caused by, e.

Despite early assumptions that donations from only a small subgroup of donors can cause TT-CMV [ 23 , 24 , 25 ], traditionally all seropositive donors have been regarded as potentially infectious for at-risk patients [ 26 ].

To identify potentially infectious donors, testing the donors' urine for CMV has been suggested by Kane and colleagues [ 23 ] because CMV viruria is frequent in primarily infected donors, and urine usually contains a higher viral load than peripheral blood.

Presumably more feasible for daily practice are the suggestions of testing donors for rising antibody titers or IgM antibodies [ 24 ].

Primary infection is usually asymptomatic. As is the case with other herpes viruses, the virus remains dormant, and once a patient is severely immunocompromised reactivation occurs.

Mucosal damage is believed to be due to a vasculitis with focal regions of ulceration representing ischemic damage 1. The histological finding of large eosinophilic, intranucelear inclusion bodies with surrounding halo and cytomegalic cells of times the normal size is the gold standard for diagnosing CMV colitis 5.

Small well-circumscribed ulcers are present, with the mucosa between them appearing normal. Deep ulceration is uncommon 1. Typically there is involvement of the gastric antrum.

Fluoroscopy shows a nodular mucosal pattern with luminal narrowing 1. CT is particularly useful in CMV enterocolitis.

The appearances are somewhat similar to that of inflammatory bowel disease , with mural thickening and surrounding stranding.

Unlike IBD, the thickening is often patchy and not circumferential 1,2. Ascites is seen in almost half of cases 2. Both diffuse and segmental patterns are described 1.

In some instances, the appearances are essentially normal and biopsy is therefore still required when clinical symptoms are suspicious.

Failing this, further treatment with foscarnet or cidofovir has been shown to improve symptoms 3. Patients who develop intestinal perforation and peritonitis or toxic megacolon require surgical intervention with resection.

In some cases of refractory CMV colitis, elective colectomy has also been advocated and performed 1. A person with a weakened immune system who develops CMV-related disease either primary infection or reactivation will often need lengthy treatment.

Improving the immune system is the best hope for combating any invading viruses. If you are pregnant and work in a day care center, reduce your risk of getting CMV by working with children who are older than 2 and a half years of age, especially if you have never been infected with CMV or are unsure if you have been exposed.

In some cases, people with AIDS or those who have had an organ or bone marrow transplant may need to take medication to prevent CMV reactivation.

If people with weakened immune systems need blood transfusions, they will probably receive blood that has had the white blood cells removed.

This lowers the risk of infection. This can help to avoid the loss of vision. The treatment of babies infected with CMV depends on the type and severity of symptoms.

Treatment should be provided by a specialist on a case-by-case basis. Although there is no cure for CMV, organ transplant recipients, people with AIDS and others with immune disorders may need treatment to suppress the latent infection.

Treatment for CMV may include trying to correct the underlying immune disorder. For example, experience in treating people with AIDS shows that when a person's immune system improves, CMV-related diseases can improve.

Side effects of ganciclovir and valganciclovir include the suppression of white blood cells needed to fight infection , red blood cells that carry oxygen and platelets that help the blood to clot.

Because cidofovir and foscarnet can cause kidney damage, kidney function needs to be monitored carefully. A doctor should see your baby if he or she has yellow skin jaundice , hearing problems, rash, fever, seizures or vomiting.

If you are a healthy adult, call your doctor if you have severe abdominal pain, vomiting or fevers that last longer than 48 hours or if you have significant fatigue, sweats, chills or are losing weight.

If you have a weakened immune system, see a doctor if you have visual changes, mental changes, difficulty or pain with swallowing, abdominal pain, vomiting or diarrhea, cough, fever or difficulty breathing.

In babies, consequences can last a lifetime or be fatal. In healthy people, CMV is almost always mild and goes away on its own.

People with weakened immune systems can lose their vision or have life-threatening and disabling illnesses that can require lifelong therapy to prevent these complications.

Always consult your healthcare provider to ensure the information displayed on this page applies to your personal circumstances.

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We comply with the HONcode standard for trustworthy health information - verify here. Skip to Content. Pneumonia caused by CMV can be life threatening.

CMV can affect any part of the gastrointestinal tract, including the esophagus, stomach, liver, gall bladder, pancreas and colon, causing ulcers, liver inflammation, intestinal obstruction and colitis.

Symptoms can include painful and difficult swallowing, nausea, vomiting, abdominal pain, yellow skin and watery or bloody diarrhea. CMV can infect the brain and other parts of the nervous system, causing symptoms like headache, confusion, and leg weakness.

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If the rectum is involved tenesmus may also be present. Transmural involvement does occur and signs and symptoms of peritonitis may develop, although it is important to note that due to the poor immune response in these patients, signs of peritonitis may be minimal or absent 1,2.

Primary infection is usually asymptomatic. As is the case with other herpes viruses, the virus remains dormant, and once a patient is severely immunocompromised reactivation occurs.

Mucosal damage is believed to be due to a vasculitis with focal regions of ulceration representing ischemic damage 1.

The histological finding of large eosinophilic, intranucelear inclusion bodies with surrounding halo and cytomegalic cells of times the normal size is the gold standard for diagnosing CMV colitis 5.

Small well-circumscribed ulcers are present, with the mucosa between them appearing normal. Deep ulceration is uncommon 1. Typically there is involvement of the gastric antrum.

Fluoroscopy shows a nodular mucosal pattern with luminal narrowing 1. CT is particularly useful in CMV enterocolitis. The appearances are somewhat similar to that of inflammatory bowel disease , with mural thickening and surrounding stranding.

Unlike IBD, the thickening is often patchy and not circumferential 1,2. Ascites is seen in almost half of cases 2.

Both diffuse and segmental patterns are described 1. In some instances, the appearances are essentially normal and biopsy is therefore still required when clinical symptoms are suspicious.

Failing this, further treatment with foscarnet or cidofovir has been shown to improve symptoms 3. Other possible problems include a small brain microcephaly or other nervous system disorders that can cause seizures, deafness, mental retardation or death.

This infection can cause the liver and spleen to become larger than normal, yellowing of the skin and eyes from liver disease , and blood disorders.

Newborns with CMV can have a rash that consists of small bruises called petechiae and larger bruises known as purpura.

A baby born to a mother who was already infected with CMV before she became pregnant is less likely to be born with CMV.

Only 0. When symptoms occur, they are similar to the symptoms of mononucleosis:. The virus usually becomes inactive latent or dormant in healthy people without specific treatment.

CMV is never completely cleared from the body, however, and can reactivate in situations such as immune suppression. Typically, latent virus from a previous infection the original CMV infection may have occurred many years earlier becomes active again because the person's immune system is weakened.

People with weakened immune systems are at greater risk of becoming very ill if they never had CMV in the past and acquire a new infection.

Doctors may order blood tests for babies with low birth weight, jaundice, small brains or other problems that can be associated with congenital CMV, but can also be caused by other things.

The diagnosis needs to be confirmed by testing blood or tissue from the infant within three weeks of birth.

Young, healthy adults usually do not need to be tested because they do not need to be treated specifically for CMV.

They usually recover over a period of weeks. In some instances, blood tests may be done to confirm the cause of the illness, since similar symptoms can be caused by Epstein-Barr virus EBV and even human immunodeficiency virus HIV.

Tests may also be needed to monitor blood levels and liver inflammation. Occasionally, ultrasound testing is needed to monitor the liver or spleen.

Depending on the symptoms, urine and stool samples may be tested. Sometimes, a biopsy of the affected organ, such as the lung or colon, is needed to confirm the diagnosis.

Disease progression in babies who are infected in the womb, during birth or through breastfeeding may vary a great deal. Some babies may die from the infection and some may have no long-lasting effects at all.

Prognosis depends on many factors and these babies should be seen by a specialist. Adults with a healthy immune system who are already infected with CMV can expect the virus to remain inactive.

No further symptoms related to CMV are expected to develop. A person with a weakened immune system who develops CMV-related disease either primary infection or reactivation will often need lengthy treatment.

Improving the immune system is the best hope for combating any invading viruses. If you are pregnant and work in a day care center, reduce your risk of getting CMV by working with children who are older than 2 and a half years of age, especially if you have never been infected with CMV or are unsure if you have been exposed.

In some cases, people with AIDS or those who have had an organ or bone marrow transplant may need to take medication to prevent CMV reactivation.

If people with weakened immune systems need blood transfusions, they will probably receive blood that has had the white blood cells removed.

This lowers the risk of infection. This can help to avoid the loss of vision. Because of the limitations of the IgM assays, IgG avidity assays are utilized in some populations to help distinguish primary from non-primary CMV infection.

These assays are based on the observation that IgG antibodies of low avidity are present during the first few months after the onset of infection and avidity increases over time reflecting maturation of the immune response.

Avidity levels are reported as the avidity index which is the percentage of IgG bound to the antigen following treatment with denaturing agents [ 7 ].

The traditional method for detecting CMV is through conventional cell culture. This approach utilizes clinical specimens which are inoculated onto human fibroblast cells and incubated and observed for a period of time ranging from 2 to 21 days.

However, this method is slow and requires 2—3 weeks until a result can be reported as negative. Shell vial assay is a modified viral culture by a centrifugation-amplification technique designed to decrease the length of time needed for rapid virus detection.

It utilizes fibroblast cell cultures propagated on cover slips contained in flat bottom plates. Centrifugation of specimen onto the cell monolayer greatly assists adsorption of virus, effectively increasing infectivity of the viral inoculum [ 12 ].

Viral antigens might be detected by monoclonal antibody directed at the CMV immediate-early IE viral antigen by indirect immuno-fluorescence after 16 hours of incubation [ 13 ].

This method was adapted to be performed in well microtiter plates [ 14 ] allowing for the screening of larger numbers of samples.

The antigenemia assay has been commonly used for more than a decade for CMV virus quantification in blood specimens.

This assay depends on the use of monoclonal antibodies that detect the viral pp65 antigen, a structural late protein expressed in blood leukocytes during the early phase of the CMV replication cycle.

This test is limited to detection of the virus in leukocytes; the demonstration of positive-staining signals in the nuclei of leukocytes indicates a positive result.

The test not only gives a qualitative result but is also quantitative, correlating closely with viremia and clinical disease severity in immunosupressed populations [ 20 — 22 ].

The disadvantages of the antigenemia assay are that it is labor intensive with low throughput and not amenable to automation. It is also affected by subjective bias demanding skilled persons for accurate test performance and interpretation of results.

Particularly in neutropenic patients, false-negative results may occur, since the antigenemia test depends on the presence of a sufficient number of polymorphonuclear leukocytes [ 24 ].

Polymerase chain reaction PCR is a widely available rapid and sensitive method of CMV detection based on amplification of nucleic acids.

The techniques usually target major immediate early and late antigen genes in their well conserved regions [ 25 — 27 ], but a number of other genes have been used as targets for detection of CMV DNA.

Specimen deterioration with time after sample collection is not as problematic with PCR assays as other tests for CMV [ 34 ].

The threshold of the qualitative method needs to be carefully calibrated for preventing over-detection.

The quantitative PCR Real-Time PCR allows for continuous monitoring of immunocompromised individuals to identify patients at risk for CMV disease for preemptive therapy and to determine response to treatment [ 35 — 37 ].

This method is generally more expensive compared to the antigenemia assay, but it is rapid and can be automated. Immunohistochemistry is performed primarily on tissue or body fluid samples.

Slides are made from frozen sections of biopsy tissue samples liver, lung or by centrifuging cells onto a slide. Then monoclonal or polyclonal antibodies against early CMV antigens are applied and visualized by fluorescently labeled antibodies or enzyme labeled secondary antibodies which are visualized by the change of color of the substrate.

The stained slides are then examined by fluorescent or light microscopy. This technique is more sensitive and very specific compared to plain histological microscopy but it is very labor intensive and requires experienced personnel to read the slides [ 43 ].

False negative results can also occur due to focal distribution of the virus [ 44 ]. The assay allows the specific nucleic assay sequence-based amplification of unspliced viral mRNAs late pp67 mRNA expression in a background of DNA using a specific isothermal technique of amplification.

Whole blood samples can be stored prior to testing, and the test can be completed in a day. The method is standardized but the mRNA extraction procedure is time consuming.

Because it detects DNA without amplification its sensitivity is questionable [ 48 ]. The natural history of CMV infection during pregnancy is complex and not fully understood.

However, unlike toxoplasmosis and rubella, preconceptional immunity to CMV is incomplete and intrauterine transmission and damaging fetal infection can occur in women who CMV seroimmune prior to pregnancy [ 52 — 56 ].

No reliable tests can define transmission of infection to the fetus. The diagnosis of primary CMV infection is accomplished by documenting seroconversion through the de novo appearance of virus specific IgG antibodies in the serum of a pregnant woman known previously to be seronegative.

However, maternal reinfection with a different strain of CMV can occur and such reinfections have been associated with intrauterine transmission, damaging fetal infection, and long-term sequelae [ 52 , 53 , 59 ].

IgM assays have been assessed in pregnant women as an indicator of acute or recent infection. Recently, assays utilizing protein microarray technology have been developed to detect CMV antibodies in sera but are in the early stages of development and testing [ 61 ].

With most IgM assays, detection of IgM in the serum of a pregnant woman can indicate a primary infection.

However, IgM can be produced in pregnant women with nonprimary CMV infections [ 62 ] and false positive results are common [ 63 , 64 ] and can occur in patients with other viral infections.

Because of the limitations of the IgM assays, IgG avidity assays are utilized to help distinguish primary from non-primary CMV infection.

Studies from investigators in Italy examined the sensitivity of IgG avidity and IgM by immunoblot in serum samples obtained at 6—18 weeks gestation and at 20—23 weeks gestation in pregnant women.

They found that in early gestation, IgG avidity was able to detect all women who had an infected fetus or newborn. Other researchers have utilized microneutralization testing in combination to avidity testing for diagnosing recent primary CMV infection in the second trimester of pregnancy [ 67 ].

Based on these data, some investigators propose screening pregnant women with serum IgG and IgM. If IgM is positive, then serum IgG avidity should be performed to help determine recent or past infection.

Using this algorithm, some argue the sensitivity is similar to documenting de novo seroconversion [ 65 , 68 , 69 ]. Lazzarotto et al examined a cohort of pregnant women referred to their center because of a positive screening CMV IgM.

Several studies have examined the utility of maternal virological tests in diagnosing recent primary infection and determining risk of transmission to offspring.

Detection of CMV in the amniotic fluid has been the standard for diagnosis of infection of the fetus. This allows adequate time for maternal transmission of the virus to the fetus and diuresis by the fetal kidney which is the primary site of viral shedding [ 77 — 79 , 82 ].

However, even when PCR on amniotic fluid is performed at the optimal time, false negative results may occur. In a recent study, investigators in Italy showed that among women who underwent prenatal diagnosis of congenital CMV infection, 8 mothers with negative amniotic fluid culture results for CMV delivered infants who were confirmed to be CMV infected [ 70 ].

Recently, CMV DNA quantification in amniotic fluid samples has been proposed as a means to evaluate the risk that a fetus can develop infection or disease.

However, other studies have failed to confirm a correlation between CMV DNA levels and the clinical status at birth [ 85 , 86 ]. Rather, CMV viral load in the amniotic fluid correlated with the time during the pregnancy when the amniocentesis was performed, with higher CMV viral loads observed later in gestation [ 84 , 85 ].

In addition to CMV viral load, some investigators have examined the prognostic value of determining the CMV genotype in infected fetuses.

Studies examining the two polymorphic CMV genes, gB and UL, have failed to correlate a particular viral genotype with severity of fetal infection [ 87 , 88 ].

Fetal blood sampling has been evaluated to determine the prognostic value of virologic assays in the diagnosis of congenital infection as well as nonspecific tests in determining severity of disease from CMV infection.

Although these assays were highly specific, the sensitivity was shown to be poor However, investigators from Belgium documented fetal loss after funipuncture in an uninfected child.

Thus, it is important to balance the value of cordocentesis against that known risk of miscarriage [ 78 , 90 ]. The more common abnormalities on ultrasound include ascites, fetal growth retardation, microcephaly, and structural abnormalities of the brain [ 79 ].

However, the majority of infected fetuses will not have abnormalities on ultrasound examination [ 58 ]. In a recent retrospective study of mothers with primary CMV infection by Guerra et al.

Furthermore, when the fetal infection status was unknown, ultrasound abnormalities predicted symptomatic congenital infection in only a third of infected infants [ 91 ].

Fetal MRI has been evaluated in a few small retrospective studies to assess its utility in detecting fetal abnormalities in utero.

However, more studies are needed to determine the true diagnostic and prognostic value of MRI in CMV infected fetuses.

Congenital CMV infection has been recognized as a leading cause of congenital infection and brain disease in children in the U. About 20, to 40, infants are born each year in the U.

Many children with CMV-associated SNHL do have normal hearing at birth and the deficit can continue to deteriorate during early childhood [ 95 — 97 ].

Therefore, most infants with congenital CMV infection will not have detectable clinical abnormalities and the newborn hearing screening will not identify a significant proportion of children with CMV-associated SNHL.

Early identification of congenitally infected infants at increased risk for SNHL is essential to provide appropriate monitoring and intervention measures during critical stages of speech and language development [ 98 ].

The diagnosis of congenital CMV infection is typically made by the demonstration of the virus or viral antigens in newborn samples, urine or saliva.

The detection of virus in urine and samples obtained from infants within the first two weeks of age is considered the gold standard method for the diagnosis of congenital CMV infection.

In contrast to the symptomatic infants, most infants with asymptomatic congenital CMV infection are not identified because of the absence of clinical findings.

Furthermore, identification of the virus or viral antigens in samples obtained from infants after the first two to three weeks of age may represent natal or postnatal acquisition of CMV and therefore, it is not possible to confirm congenital CMV infection in infants older than three weeks.

Serological methods are unreliable for the diagnosis of congenital infection. In addition, currently available tests for the detection of CMV-IgM antibody do not have the high level of sensitivity and specificity as viral isolation methods [ 99 , ].

Detection of CMV in the saliva and urine of infants is easily accomplished because newborns with congenital CMV infection shed large amounts of virus.

Traditional tissue culture techniques and recent modification of the tube culture method, centrifugation-enhanced rapid culture methods shell vial assay using monoclonal antibodies to stain for immediate early protein, pp72 of CMV are considered the standard methods for the diagnosis of congenital CMV infection [ 6 , — ].

The rapid culture methods have been shown to have comparable sensitivity and specificity to the standard cell culture assays and the results are available within 24 to 36 hours.

A rapid method a well microtiter plate and a monoclonal antibody to the CMV immediate early antigen and was shown to be This microtiter plate assay has been adapted for use with saliva specimens with comparable sensitivity and specificity [ ].

These rapid culture techniques are presently the standard for the diagnosis of congenital CMV infection.

The CMV antigenemia assay, which detects the pp65 protein in polymorphonuclear leucocytes, is used widely to diagnose CMV infections and monitor treatment in immunocompromised patients [ ].

However, the utility of this assay in the diagnosis of congenital CMV infection has not been evaluated. The PCR assay is used routinely for the diagnosis of CMV infection in allograft recipients at increased risk for invasive CMV disease and in other immunocompromised hosts.

Quantitative PCR has also been proven to be useful in the monitoring of these patient groups for their response to antiviral therapy [ — ].

However, the usefulness of PCR or other nucleic acid amplification assays in the diagnosis of congenital CMV infection has not been defined.

An early study by Demmler et al. In a study by Warren et al. Nelson and colleagues were able to detect CMV DNA in the serum samples of all 18 children with symptomatic congenital infection tested, in 1 of 2 children with asymptomatic infection and in 0 of 32 controls [ ].

DNA hybridization assay has excellent sensitivity and specificity for the rapid diagnosis of CMV infections [ ]. However, the requirement for virus concentration using high speed centrifugation and the need for hybridization using radio labeled probes renders this method cumbersome and impractical for the routine diagnosis of congenital CMV infection.

Since dried blood spots DBS are collected from all infants born in the U. Most of the reports have studied selected infant populations and a prospective comparison of DBS PCR results to a standard i.

Early studies have examined the utility of DBS PCR on preserved blood spots that were obtained from infants in the nursery to diagnose congenital CMV infection retrospectively at the time of the detection of hearing loss.

A study by Johansson et al. These results have major public health implications because they indicate that such methods as currently performed will not be suitable for the mass screening of newborns for congenital CMV infection.

PCR testing of peripheral blood has been widely used as a standard diagnostic method to detect invasive CMV infections in immunocompromised individuals including allograft recipients and patients with AIDS [ , ].

However, it is likely that the pathogenesis of congenital CMV infection is different from that in immunocompromised hosts since such patients usually experience acute CMV infection or symptomatic reactivation shortly before testing, whereas congenitally infected infants may have acquired CMV infection months before birth and thus are no longer viremic when tested as newborns.

Therefore, based on the results of our large multi-center newborn CMV screening study, it appears that DBS are probably not appropriate samples for newborn CMV screening.

These findings underscore the need for further evaluation of high throughput methods performed on saliva or other samples that can be adapted to large-scale newborn CMV screening.

Several previous studies that included smaller number of subjects examined the utility of testing saliva samples with PCR-based methods demonstrated the feasibility and high sensitivity of these methods [ 54 , , ].

However, none of these studies have included screening of unselected newborns as well as a direct comparison of saliva PCR assay with the standard rapid culture method of saliva or urine.

Although a more recent study from Brazil in which more than 8, newborns were screened for congenital CMV infection demonstrated the utility of saliva PCR assay to screen newborns for CMV, the PCR assay was not directly compared to the standard culture based assay [ 55 ].

As part of an ongoing multicenter newborn screening study, the utility of real-time PCR of saliva samples in identifying infants with congenital CMV infection is being evaluated.

A major advantage of the saliva real-PCR assay used in that study was that there was no need for processing of saliva samples for DNA extraction.

This elimination of the DNA extraction step will make it easier to adapt this assay for screening large number of newborns in a high throughput fashion.

These findings demonstrate that saliva PCR could become a useful approach to screen newborns for congenital CMV infection.

Continual advances are being made in our understanding of the natural history and pathogenesis of congenital CMV infection and the role of antiviral therapy for congenitally infected children.

It is hoped that the ongoing work in developing and standardizing molecular diagnostic methods will result in the availability of reliable, rapid, and simple methods for routine clinical use in the future.

In addition, there is also growing interest in examining the feasibility of a newborn CMV screening program in conjunction with universal newborn hearing screening.

It is somewhat disappointing that DBS PCR assays have not been shown to have sufficient sensitivity for the identification of most infants with congenital CMV infection.

Nevertheless, the development of saliva PCR assays could have the potential to adapt these methods in a high throughput fashion to screen large number of newborns for congenital CMV infection.

In addition, the ability to measure virus burden in saliva specimens from infants with asymptomatic congenital CMV infection using saliva PCR assays could provide the means to identify at-risk infants early in life thus, ensuring judicious use of resources by targeting at-risk children for follow-up and monitoring.

Perinatal infections can be acquired by three routes, 1 contact with virus in maternal genital tract secretions during delivery, 2 ingestion of breast milk containing virus or 3 through transfusions of CMV seropositive blood.

Transmission via breast milk and through blood transfusion can result in severe symptoms in premature, very low birth weight VLBW infants [ , ].

For definitive diagnosis of perinatal CMV infection, it is important to demonstrate an absence of viral shedding for first two weeks of life.

There is no standard method for diagnosis of perinatal CMV infections. However, similar to blood PCR assays to diagnose congenital infection, not all infants who shed virus in their urine or saliva as a result of perinatal infection have detectable CMV DNA in their blood [ ].

In perinatal CMV infection, serological assays have the same limitations described above for infants with congenital CMV infection.

CMV is one of the most common and difficult opportunistic pathogens which complicates care of immunocompromised patients.

Advances in diagnostic and therapeutic modalities have reduced the frequency of life-threatening CMV complications and improved overall survival.

CMV disease in immunocompromised hosts can result from primary infection, reinfection with a new virus strain or reactivation of the latent virus.

The severity of CMV disease varies depending on the population, type of transplantation as well as on the level of immunosupression and can range from a self-limiting febrile illness to multi-system disease.

CMV also has a number of indirect effects that contribute to increased morbidity and poorer outcome after transplantation.

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