Source Of Cytomegalovirus Infection Research Articles

Primary cytomegalovirus infection as a common cause of wheezing in infants

RATIONALE: Respiratory tract infection in infants often manifests bronchial asthma-like symptoms such as wheezing and dyspnea. Although cytomegalovirus (CMV) is known to induce prolonged and intractable wheezing in infancy, the frequency of CMV infection-associated wheezing attacks in infancy has not been prospectively studied. METHODS: Forty admitted infants who presented with the first episode of wheezing and dyspnea between October 2002 and September 2003 were prospectively studied. For every patient, nasopharyngeal aspirates were tested for respiratory syncytial virus (RSV), and CMV antibody titer was measured using paired serum samples. The subjects were classified into the following three groups: infants with primary CMV infection (CMV group), those with RSV infection (RSV group), and those with no detectable CMV or RSV infection (RSV-/CMV- group). RESULTS: Twenty-one infants (53%) had RSV infection, and 7 (18%) had primary CMV infection. Splenomegaly was significantly more common in CMV group (86%) than in the other two groups. No statistically significant differences were observed between the CMV group and the other two groups in the duration of wheezing, febrile period, presence of X-ray shadow indicating pulmonary infiltration, breastfeeding, lymphocyte or atypical lymphocyte count during hospitalization. The role of breast milk as a source of CMV infection was not confirmed. CONCLUSIONS: Primary CMV infection is a common cause of wheezing in infants, particularly in those with splenomegaly.

Breast Milk: A Major Source of CMV Infection in Preemies

Cytomegalovirus (CMV) acquired postnatally can cause disease in low-birth-weight infants. CMV shedding in breast milk, documented during reactivation

Cytomegalovirus infections in heart and heart-lung transplant recipients

Of the first 250 heart and 41 heart-lung transplant recipients in the Papworth series, 244 who survived for longer than one month after transplantation were studied for evidence of cytomegalovirus (CMV) infection by serological methods. Overall, 43 (17.6%) patients acquired primary CMV infection and 76 (31.1%) had evidence of CMV reactivation or reinfection. The source of CMV infection was found to be important. CMV infection was more severe when acquired from the donor organ than from blood or blood products and all seven fatal primary CMV infections were associated with CMV antibody-positive donors. Thus, we now have a CMV matching policy in our unit; whenever possible organs from CMV antibody-positive donors are not given to CMV antibody-negative recipients. Those CMV antibody-positive recipients who received organs from CMV antibody-positive donors had more severe CMV reactivation or reinfection than those who received organs from CMV antibody-negative donors. The severity of CMV disease was found to be dependent on the degree of immunosuppression patients received and heart-lung transplant recipients had more serious CMV infections than heart transplant patients. The severity of CMV infections in heart-lung transplant recipients was modified in the later part of the series by the use of prophylactic anti-CMV hyperimmune globulin and treatment of CMV infection with ganciclovir. While 75% of heart-lung transplant recipients who did not receive this treatment died of primary donor-acquired CMV infection, all three comparable patients given CMV hyperimmune globulin and ganciclovir survived. The outcome of CMV infections in the Papworth heart and heart-lung transplant recipients is compared with that in other comparable transplant centres.

Cytomegalovirus infections in renal, heart, heart-lung and liver transplantation

Although infection with cytomegalovirus (CMV) continue to be recognized relatively frequently after organ transplantation, a decrease in their severity has been described with the use of newer immunosuppressive regimens. In particular whereas antithymocyte globulin was associated with an increase in morbidity and mortality, the use of cyclosporin A has resulted in a decrease in the frequency of symptomatic infections. Several sources of CMV infection in transplant recipients are: immunosuppression secondary to drug therapy can result in reactivation of the latent infection present before transplantation; blood transfusion, either pretransplant red blood cell transfusion or blood required at the time of surgery can also result in transmission of CMV and primary infection; the transplanted kidney or heart, particularly in situations in which seropositive organs are transmitted into seronegatives can serve as the vehicle for transmission. Recent data suggest that transmission of organ donor CMV can occur even in seropositive recipients. The clinical manifestations of CMV infection in transplant recipients range from asymptomatic or mild mononucleosis syndromes to severe infection. It is generally accepted that primary infections in patients who were seronegative before transplantation are more severe than reactivated infections. Involvement of multiple organ systems has been common, with retinitis, pneumonitis and gastrointestinal manifestations occurring most commonly. A specific CMV infection of the kidney has also been described but its manifestations are variable. The association of CMV infections with rejection remains controversial in human transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)

Young children as a probable source of maternal and congenital cytomegalovirus infection.

To identify possible sources of cytomegalovirus infection in pregnant women, we studied seven families with a recent case of congenital or maternal cytomegalovirus infection and a history of maternal contact with a young child shedding the virus. We used restriction-endonuclease techniques to compare the DNA of viral isolates collected from family members. Five families contained an infant who had congenital or perinatal infection, a mother who had had evidence of primary infection during her most recent pregnancy, and a child less than three years of age who was excreting cytomegalovirus. All five of the young children attended day-care centers at least part-time. In each of these five families, strains from family members were identical, and it is most likely that the toddler-aged child was the source of the virus for both the mother and the fetus or infant. In two other families, acquisition of cytomegalovirus by children in a day-care center was followed by seroconversion in the mother along with excretion of a strain of the virus identical to that in her child, as demonstrated by restriction-endonuclease analysis. Five of the seven fathers were tested for antibody to cytomegalovirus; four were seronegative, ruling them out as a source of infection in the mothers. These results not only strengthen evidence for the transmission of cytomegalovirus from child to mother but also indicate that infections acquired by a mother from a child can be transmitted to her fetus.

Transfusion of Cytomegalovirus: A Review of the Problem

It is clearly recognized that cytomegalovirus (CMV) is a cause of postperfusion syndrome. Whether some of these infections are due to reactivation of latent virus or to primary infection is not clear. Thus, there is still some debate on whether blood transfusion is the exogenous source of CMV infection in certain cases, or whether it is the stimulus for reactivation of endogenous virus. Various methods of avoiding transfusion-associated CMV infection have been proposed. This review examines the rationale behind these methods in order to provide a realistic approach to the problem.

Cytomegalovirus Infection in Guinea Pigs. I. Viremia during Acute Primary and Chronic Persistent Infection

Studies on the pathogenesis of cytomegalovirus (CMV) infection in guinea pigs have revealed two distinct phases of infection, without any signs of clinical disease. During acute primary infection, viremia was easily demonstrated and infectious virus was recovered from various tissues, including lung, spleen, and kidney, of the infected animal two to 10 days after inoculation. Chronic persistent infection was readily established thereafter. In animals with chronic persistent infection with high levels of circulating antibody, infectious virus was consistently isolated from the salivary gland and pancreas. Evidence of CMV in the blood of the persistently infected animals was detected only occasionally and only when a highly sensitive method and/or a large inoculum was used. However, the anticoagulant heparin was found to inactivate CMV significantly during collection of blood. These data suggest that CMV was indeed circulating in the blood of apparently health but persistently infected animals for prolonged periods. Such infected blood could conceivably be the source of CMV infection when large quantities of blood are given to susceptible recipients.

The Transplanted Kidney as a Source of Cytomegalovirus Infection

The Transplanted Kidney as a Source of Cytomegalovirus Infection

The Transplanted Kidney as a Source of Cytomegalovirus Infection

To determine the incidence of cytomegalovirus infection in renal-transplant recipients we followed 32 prospectively for six months after operation. As judged by serologic change and virus isolation the infection rate for the entire group was 66 per cent (21 of 32 patients) - 59 per cent (13 of 22) for seronegative patients and 80 per cent (eight of 10) for seropositive patients. Of 10 seronegative patients who received kidneys from seronegative donors, only three became infected. However, of 12 seronegative patients who received kidneys from seropositive donors, 10 became infected. Thus, there was a significant correlation between development of infection and seropositivity of the donor (P = 0.03), particularly when the recipient was seronegative (P = 0.02). Five possible and four definite recognizable clinical illnesses were associated with cytomegalovirus infection; all except two were in initially seronegative subjects who received kidneys from seropositive donors. Primary infection and disease in nonimmune recipients may be caused by cytomegalovirus transmitted by the kidneys of latently infected seropositive donors.