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Results for “CYTOMEGALIC INCLUSION DISEASE”

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At least 37 records · Page 2Linked to original sources
PubMed1992

Cytomegalic inclusion disease presenting acute intrahepatic cholestasis.

An 83-year-old man suffering from pulmonary emphysema was admitted to our hospital because of jaundice. He was diagnosed as acute intrahepatic cholestasis but the etiology could not be determined during the treatment period. In spite of treatment, the jaundice worsened progressively without any elevation in serum transaminase, and he died of respiratory failure 58 days later. An autopsy revealed a generalized cytomegalic inclusion disease, predominantly in the biliary tracts, liver and lungs. This is a rare case of cytomegalic inclusion disease presenting acute intrahepatic cholestasis without any elevation of transaminase during the clinical course.

Acute Disease↗
PubMed1993

Temporal bone histopathology 14 years after cytomegalic inclusion disease: a case study.

Temporal bones were examined from a 14-year-old male who died of sequelae of congenital cytomegalic inclusion disease (CID). Cytomegalovirus (CMV) was not isolated from inner ear fluid or multiple systemic tissues at the time of death. Examination of temporal bones revealed chronic pathology of both cochlear and vestibular sensory and nonsensory tissues. Endolymphatic hydrops was observed in the basal turn of the cochlear duct, while Reissner's membrane was collapsed in the more apical turns. Strial atrophy and a loss of cochlear hair cells were observed along the entire length of the basilar membrane. Vestibular neuroepithelial regions were degenerated and fibrosis was seen within the vestibular perilymphatic tissue spaces, suggesting prior labyrinthitis within the perilymph compartment in addition to the more typical pattern of endolabyrinthitis associated with human CMV infection. Distention of the saccular membrane was evident. In both cochlear and vestibular tissues, there were isolated regions of calcifications that appeared characteristic to that reported in other organ systems of individuals with CID. Collectively, these chronic, pathological findings in this case of CID demonstrate more extensive injury than has been identified in the previously reported acute temporal bone pathology of CID.

Cochlea↗
PubMed1983

Two-dimensional ultrasonography of the brain: its diagnostic usefullness in herpes simplex encephalitis and cytomegalic inclusion disease.

We have used brain ultrasonography in diagnosing and following up two infants, one with herpes simplex encephalitis and the other with cytomegalic inclusion disease. It was found that this technique was very useful to observe the changes of the brain parenchyma such as cystic degeneration and periventricular calcification. Also because it is non-invasive and an easy procedure, ultrasonography can be applied even for infants in critical condition when needed.

Calcinosis↗
PubMedDate not supplied

Cytomegalic inclusion disease: intrauterine sonographic diagnosis using findings involving the brain.

Two second-trimester cases and one third-trimester case of intrauterine cytomegalic inclusion disease (CID) are presented, each having a different intracranial sonographic presentation. The findings are correlated with radiographic studies and the known pathophysiology. Sonographic evidence of intrauterine cerebral necrosis or calcification should alert one to the possibility of CID, particularly if other signs of in utero infection are present. A pattern of bilateral periventricular calcifications, which may be preceded by hypoechoic periventricular ringlike zones, seems to be specific for intrauterine CID. However, CID also may result in widespread cerebral destruction. If the sonographic study produces an uncertain diagnosis, sonography can still aid in the prenatal diagnosis of CID by guiding percutaneous umbilical cord blood sampling for serology or by directing amniocentesis for cytomegalovirus culture. The ability of sonography to demonstrate specific characteristics of CID in utero enables prenatal diagnosis of this disease.

Adult↗
PubMed1992

[Congenital cytomegalic inclusion disease--clinico-anatomical characteristics].

Analysis of labor histories, case histories, and autopsy records over a decade, 1980-1990, has revealed 32 cases of cytomegalic inclusion disease in children. Eleven placentas of seropositive mothers were histologically examined. The findings evidence that cytomegaloviral infection was mostly combined with other bacterial and viral diseases. The central nervous system, kidneys, and lungs were the most sensitive to the virus effects. The DIC syndrome was present in all the cases.

Cytomegalovirus↗
PubMed1986

Glomerulonephritis in congenital cytomegalic inclusion disease.

Except for renal transplant recipients, glomerulonephritis has only very rarely been associated with renal cytomegalovirus (CMV) infection. The kidneys of five infants with congenital cytomegalic inclusion disease, including renal infection, were examined at autopsy. Two of the infants had glomerulonephritis. The younger, a 4-month-old female, had diffuse proliferative and necrotizing glomerulonephritis; virus was present in nuclei and cytoplasm of glomerular endothelial cells and, possibly, in leukocytes as well. There were no electron-dense deposits. The other infant, a 5-month-old male, had diffuse mesangial and focal segmental proliferative and sclerosing glomerulonephritis; electron-dense mesangial deposits were seen ultrastructurally. Three additional infants (a newborn male, a 2-day-old male, a 6-week-old female), all with CMV in tubules and one with a single glomerular inclusion, had only rare glomerular abnormalities, i.e., mesangial proliferation in less than 10 per cent of glomeruli (one infant) and segmental sclerosis in less than 1 per cent of glomeruli (all three infants). Thus, congenital renal CMV infection was associated with proliferative glomerulonephritis in the two infants who survived the longest. The three with shorter survival times had only minor glomerular alterations.

Cytomegalovirus Infections↗
PubMed2000

Severe fetal cytomegalic inclusion disease after documented maternal reactivation of cytomegalovirus infection during pregnancy.

Recurrent cytomegalovirus infection during pregnancy is considered less dangerous for the fetus than primary infection. We present a case of severe fetal cytomegalic inclusion disease after maternal reactivation of cytomegalovirus during the first trimester of pregnancy. The possibility of such fetal injury is an argument for prenatal diagnosis in seropositive pregnant women when ultrasonographic findings suggest cytomegalovirus infection.

Adult↗
PubMedDate not supplied

[Cytomegalic inclusion disease. Report of a case in a newborn].

A clinical case of this disease in a newborn is reported. The clinical signs and laboratory results were typical and were confirmed by pathological studies. The modern literature stresses the high frequency of this disease, specially in the U.S.A. and England, where reports reach 4% in pregnant women and 1% of newborns with cytomegalic inclusion disease. We do not know its frequency in Mexico.

Autopsy↗
PubMed1988

Spontaneous disseminated cytomegalic inclusion disease in an ageing laboratory mouse.

An untreated C57BL/6NCrlBR male mouse in a life-long longevity study, killed in extremis at 761 days of age, had mild focal necrotic hepatitis and extensive focal necrotic adrenalitis. Characteristic cytomegalic cells bearing intranuclear and cytoplasmic inclusions and cytoplasmic vacuoles were seen in necrotic areas. Scattered intranuclear inclusions were also seen in the reticulum cells of the spleen and acinar epithelium of the submaxillary glands. We believe this to be the first report of spontaneous disseminated cytomegalic inclusion disease in aged mice.

Adrenal Glands↗
PubMed1971

Incidence of cytomegaloviremia in blood-bank donors and in infants with congenital cytomegalic inclusion disease.

During a 15-month period, cytomegalovirus (CMV) isolations were attempted from leukocytes derived from 290 healthy blood-bank donors. The major proportion of the specimens were tested 2 to 5 hr after donation. However, CMV was not recovered from any of the specimens examined. At the time of donation, 75% of donors had CMV complement-fixing antibodies demonstrable in titers of 10 to >/=320. The age of the study group ranged from 17 to 57 years. During the same time period and with the use of identical isolation techniques, postnatal cytomegaloviremia was demonstrated in four infants with cytomegalic inclusion disease. Failure to detect cytomegaloviremia in 290 normal blood donors questions its occurrence outside pathological conditions. These results do not support the concept that CMV infection, concurrent with post-transfusion mononucleosis syndrome, is transmitted through the blood donor's leukocytes.

Journal Article↗