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Der Online-Shop des Christlichen Missions-Verlags (CMV) ist Edition Nehemia mit neuem Shop – Auch der kleine Verlag Edition Nehemia. Title: Verlagsvorschau CMV Herbst , Author: Christoph Merian Verlag, Name: Verlagsvorschau CMV Herbst , Length: 20 pages. Der Christoph Merian Verlag ist ein unabhängiger Schweizer Verlag, der Publikationen im Bereich Architektur und Kunst, Kultur und Gesellschaft sowie.

This article focus on adult infection. Presentation is variable, however generalized cognitive decline is most frequent. Focal neurological signs and cranial nerve palsies are uncommon to rare.

At autopsy active CMV infection is also seen systemically although clinical manifestations are variable:.

CMV infects the entire neuraxis brain, spinal cord, meninges, nerve roots, eye and therefore has variable presentation.

If ventriculitis is also present then enhancement of the ependymal surface and hydrocephalus may also be seen. Other white matter changes in HIV , especially :.

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J Comput Assist Tomogr. Pubmed citation 7. Cytomegalovirus pneumonia after bone marrow transplantation: high resolution CT findings. Br J Radiol.

Pubmed citation 8. Differences and similarities of cytomegalovirus and pneumocystis pneumonia in HIV-negative immunocompromised patients thin section CT morphology in the early phase of the disease.

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Transfus Med Hemother. Published online Dec Author information Article notes Copyright and License information Disclaimer.

Received Jun 11; Accepted Oct This article has been cited by other articles in PMC. Summary Traditionally, leukoreduction and selection of blood products from seronegative donors have been used as alternative strategies to reduce the risk of transfusion-transmitted cytomegalovirus infections TT-CMV in atrisk patients.

Introduction 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 ].

Incidence of Transfusion-Transmitted CMV Infections 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.

Open in a separate window. Identification of At-Risk Donors 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 ].

Several transfusion strategies have been proposed to reduce the risk of TT-CMV in addition to leukoreduction: i provision of seronegative blood products [ 7 ]; ii provision of CMV DNA-negative blood products NAT-negative products [ 32 ]; and iii provision of blood products from long-term seropositive donors [ 33 ].

Disclosure Statement None of the authors declares a conflict of interest. References 1. Klemola E, Kaariainen L.

Cytomegalovirus as a possible cause of a disease resembling infectious mononucleosis. Br Med J. Continuous cytomegalovirus seroconversion in a large group of healthy blood donors.

Vox Sang. The natural course of primary cytomegalovirus infection in blood donors. Rise of cytomegalovirus antibodies in an infectious-mononucleosis-like syndrome after transfusion.

Transfusion transmission of cytomegalovirus confirmed by restriction endonuclease analysis. J Pediatr.

Primary cytomegalovirus infection following open heart surgery. Acta Med Scand. Prevention of transfusion-acquired cytomegalovirus infections in newborn infants.

A comparison of filtered leukocyte-reduced and cytomegalovirus CMV seronegative blood products for the prevention of transfusion-associated CMV infection after marrow transplant.

Vamvakas EC. Is white blood cell reduction equivalent to antibody screening in preventing transmission of cytomegalovirus by transfusion?

A review of the literature and meta-analysis. Transfus Med Rev. Transmission of cytomegalovirus CMV infection by leukoreduced blood products not tested for CMV antibodies: a single-center prospective study in high-risk patients undergoing allogeneic hematopoietic stem cell transplantation CME Transfusion.

Safety of leukoreduced, cytomegalovirus CMV -untested components in CMV-negative allogeneic human progenitor cell transplant recipients.

Direct assessment of cytomegalovirus transfusion-transmitted risks after universal leukoreduction. Available at: www. Asymptomatic primary cytomegalovirus infection: Virologic and immunologic features.

J Infect Dis. High prevalence of cytomegalovirus DNA in plasma samples of blood donors in connection with seroconversion. Window period donations during primary cytomegalovirus infection and risk of transfusion-transmitted infections.

The impact of donor cytomegalovirus DNA on transfusion strategies for at-risk patients. Detection of cytomegalovirus infection during a vaccine clinical trial in healthy young women: Seroconversion and viral shedding.

J Clin Virol. Frequency and duration of plasma CMV viremia in seroconverting blood donors and recipients. The effect of leukocyte-reduction method on the amount of human cytomegalovirus in blood products: a comparison of apheresis and filtration methods.

Over half of adults have been infected with CMV by age 40, most with no signs or symptoms.

CMV is transmitted by direct contact with infectious body fluids, such as urine, saliva, blood, tears, semen, and breast milk.

CMV can be transmitted sexually and through transplanted organs and blood transfusions. Healthy infants and children who acquire CMV after birth generally have few, if any, symptoms or complications from the infection.

Although the virus is not highly contagious, it has been shown to spread among household members and young children in daycare centers.

No treatment is currently indicated for CMV infection in healthy people. Antiviral treatment is used for people with compromised immune systems who have either sight-related or life-threatening illnesses due to CMV infection.

Avoiding contact with saliva and urine from young children might reduce the risk of CMV infection. Healthcare providers should follow standard precautions.

Vaccines are still in the research and development stage. A woman who has a primary CMV infection during pregnancy is more likely to pass CMV to her fetus than a woman who has a subsequent infection during pregnancy.

Routine screening for primary CMV infection during pregnancy is not recommended in the United States for several reasons:.

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. Correct and timely diagnosis of CMV infections is critical in the appropriate clinical management and the diagnosis should be based on appropriate clinical findings together with detection of the virus, viral antigens or DNA in blood, plasma or affected tissue [ ].

The latter two groups can exhibit the most severe CMV disease due to severely impaired cellular immunity. CMV infection in SOT remains one of the major causes of extended hospitalization resulting in a significant part of the overall cost of care provided to these patients.

Clinical manifestations of CMV infection in SOT recipients can be expressed as an acute systemic febrile illness with symptoms such as fever, malaise, arthralgia and rash.

Due to the immunomodulatory properties of CMV, infection can have indirect effects resulting in opportunistic infections with fungi or bacteria, or graft rejection [ , ].

Serologic methods are of limited usefulness for identification of CMV disease in immunocompromised individuals [ ].

However, these assays are used for pretransplant assessment of the solid organ transplant donor and recipient.

Serological testing is also useful to screen the donors of blood products to minimize the risk of CMV infection for seronegative recipients [ ].

In addition, pre-transplant serostatus in the recipient is determined to assess the potential for reactivation of latent virus in seropositive recipients when undergoing immunosupression.

It is important to monitor the levels of CMV viremia by either the pp65 antigenemia assay or by whole blood or plasma PCR in order to begin preemptive antiviral therapy promptly.

The use of plasma viral load measurement in risk assessment has limited value but may be helpful in specific cases [ ] The viral load level that triggers antiviral therapy varies from institution to institution [ ] and thresholds utilized in the assays may also vary according to the type of transplants and the individual PCR assays [ , ].

Although the detection of the virus in tissues might often be difficult, the demonstration of the virus by immunohistopathology or in-situ techniques in addition to histopathological changes compatible with CMV infection is required for the diagnosis of CMV end organ disease [ — ].

CMV disease usually presents as pneumonitis with interstitial pattern on radiographs with respiratory distress and hypoxemia or as gastrointestinal disease with mucosal inflammation or erosion anywhere in GI tract.

The indirect effects of CMV can be presented via its immunomodulatory properties potentially enhancing graft versus host disease GVHD and opportunistic infections.

It is important to screen blood products using serological techniques as well as nucleic acid amplification techniques before they are administered to HSCT patients.

This allows reduction of exposure of seronegative recipients to CMV containing products. Rapid detection techniques both antigen and nucleic acid detection are commonly and effectively used to monitor individuals at risk for CMV disease and for a timely start of preemptive antiviral therapy.

HSCT recipients are usually monitored on a weekly basis. Typically, pre-emptive antiviral therapy is initiated at this threshold [ ] but this can vary widely [ ].

However, pp65 antigenemia is prone to false negative results in this population due to neutropenia commonly observed following HSCT.

However, there are no uniform viral load threshold values because of the absence of a standardized PCR protocol across the different centers and laboratories [ ].

When compared to antigenemia and PCR, the shell vial assay is considered to be insufficiently sensitive to be routinely used after allogenic HSCT to monitor for CMV infections [ , ].

Other manifestations include peripheral neuropathy, polyradiculoneuritis, pneumonitis, gastritis or hepatitis and colitis.

An additional benefit of this novel assay is that it can be performed on frozen or lysed samples [ 47 ].

National Center for Biotechnology Information , U. Infect Disord Drug Targets. Author manuscript; available in PMC Aug 1.

Novak , S. Pati , and S. Author information Copyright and License information Disclaimer. Copyright notice. The publisher's final edited version of this article is available at Infect Disord Drug Targets.

See other articles in PMC that cite the published article. Abstract Cytomegalovirus CMV is recognized as the most common congenital viral infection in humans and an important cause of morbidity and mortality in immunocompromised hosts.

Keywords: cytomegalovirus, diagnosis, congenital infection, maternal infection, fetal infection, immunocompromised. Cell culture The traditional method for detecting CMV is through conventional cell culture.

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

Immunohistochemistry Immunohistochemistry is performed primarily on tissue or body fluid samples. Maternal infection 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.

Fetal infection Detection of CMV in the amniotic fluid has been the standard for diagnosis of infection of the fetus. 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.

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

Future Directions 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.

Solid organ transplantation SOT CMV infection in SOT remains one of the major causes of extended hospitalization resulting in a significant part of the overall cost of care provided to these patients.

Open in a separate window. Table 2 Laboratory diagnosis of cytomegalovirus infection by patient population.

Maternal Infection IgG seroconversion with two consecutive maternal blood samples most accurate IgM in addition to low IgG avidity Fetal Infection CMV PCR of amniotic fluid obtained after 21wga and 6 weeks past positive maternal serology Congenital Infection Detection of virus or viral antigens in saliva or urine using standard culture method and rapid culture methods.

PCR assays of saliva or urine are promising. End organ disease diagnosed by tissue immunohistopathology or in-situ techniques.

Footnotes Potential conflict of interest: None. Weller TH. Cytomegaloviruses: the difficult years. Demmler GJ. Summary of a workshop on surveillance for congenital cytomegalovirus disease.

Jacobson MA, Mills J.

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