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Biomedical subjects

L D Frenkel

Publications and source records attributed to L D Frenkel.

36 records · Page 2Linked to original sources
PubMed1985

Avian antigen.

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Adult↗
PubMed1982

Postoperative infection caused by an unusual serotype of Streptococcus pneumoniae associated with multiple drug resistance.

A 15-month-old child developed an infectious pulmonary complication of open heart surgery. Cultures of the respiratory secretions showed growth of a 9L serotype of Streptococcus pneumoniae which was resistant to penicillin, tetracycline, and chloramphenicol. There was no evidence that the organism was spread among the family of the patient or hospital personnel.

Chloramphenicol↗
PubMed1980

Clinical anophthalmia associated with congenital cytomegalovirus infection.

Three cases of congenital clinical anophthalmia associated with congenital cytomegalovirus infection were diagnosed by positive viral cultures and immunologic studies. Ultrasonography in one infant with clinically detected anophthalmia showed the presence of severe microphthalmia with cyst. These findings suggest that maternal infection occurred within the first trimester of gestation.

Anophthalmos↗
PubMed1980

Unusual eye abnormalities associated with congenital cytomegalovirus infection.

Seven children with congenital cytomegalovirus infection demonstrated a higher than expected incidence of "rare" ophthalmological abnormalities, including anophthalmia and Peters' anomaly. These data suggest that appropriate investigation for evidence of cytomegalovirus infection should be instituted in any child with congenital ocular defects.

Anophthalmos↗
PubMed1977

Characteristic early electroencephalographic changes in herpes simplex encephalitis.

We review electroencephalograms taken from 17 patients with severe meningoencephalitis within seven days of onset of CNS symptoms and prior to cortical brain biopsies. All patients had CNS disease clinically compatible with the diagnosis of herpes simplex encephalitis (HSE). The diagnosis was demonstrated by the isolation of virus from the brain in five patients (group 1) but considered highly unlikely in the other 12 patients (group 2) by negative immunofluorescent studies and failure of viral isolation from the brain tissue. Abnormal but nonspecific EEGs with diffuse or focal slowing were found in all patients. Distinctive high-voltage, 1-cycle-per-2-to-3 seconds periodic sharp waves from unilateral temporal lobes were seen only in three of the five patients with virologically proved HSE but in none of the 12 patients without viral isolation. This EEG pattern is strikingly similar in all three patients, regardless of their age, and may be specific for the early diagnosis of HSE prior to brain biopsy. The EEGs of the other two patients with proved HSE did not contain such abnormalities. Athough periodic EEGs with some resemblance to those previously described may occur in other CNS disorders, their presence strongly suggests the diagnosis of HSE when recorded from patients with viral meningoencephalitis. Moreover, EEGs may help locate the best site for cerebral biopsy since maximal yield of the virus in this study was from unilateral temperoal lobes corresponding with the site of local EEG changes.

Adolescent↗
PubMed1977

Specific impairment of cell-mediated immunity in mothers of infants with congenital infection due to cytomegalovirus.

Specific lymphocyte-mediated cytotoxicity to cytomegalovirus (CMV) in eight infants (six to 27 months old) with congenital CMV infection and in the mothers of six of these infants was evaluated with use of a 51chromium (51Cr)-release microassay. The control population consisted of 25 normal newborns, children, and adults. The titers of indirect hemagglutinating (IHA) antibody to CMV in the infected infants ranged from 1:16 to 1:1,024. All of these infants had detectable specific immune release of 51Cr that ranged from 3.3% to 48.9% (mean +/-SE, 21.0%+/-5.6%). The mothers of these infants demonstrated significantly elevated titers of IHA antibody to CMV (geometric mean titer, 1:410) as compared with a mean titer of 1:22 in controls (t = 5.71; P less than 0.001) but showed significantly depressed specific immune release (9.2% +/- 3.2%) compared with that of normal seropositive controls (24.8% +/- 2.8%; t = 3.31; P less than 0.001). In addition, two adult nulliparous women with persistent CMV viruria were also found to have depressed specific immune release to CMV (10.8% and 16.2%). These data suggest that a specific impairment in cell-mediated immunity to CMV occurs in mothers of infants with congenital CMV infection and in some persons who persistently excrete CMV.

Adult↗
PubMed1975

Ascorbic acid for the common cold. A prophylactic and therapeutic trial.

Three hundred eleven employees of the National Institutes of Health volunteered to take 1 gm of ascorbic acid or lactose placebo in capsules three times a day for nine months. At the onset of a cold, the volunteers were given an additional 3 gm daily of either a placebo or ascorbic acid. One hundred ninety volunteers completed the study. Dropouts were defined as those who missed at least one month of drug ingestion. They represented 44% of the placebo group and 34% of those taking ascorbic acid. Analysis of these data showed that ascorbic acid had at best only a minor influence on the duration and severity of colds, and that the effects demonstrated might be explained equally well by a break in the double blind.

Adult↗
PubMed1975

Antiviral chemotherapy and neonatal herpes simplex virus infecition: a pilot study--experience with adenine arabinoside (ARA-A).

Among 13 neonates with herpes simplex virus (HSV) infection, eight had disseminated disease, one localized CNS disease, and in four the infection was confined to the skin and eyes. Ara-A, a purine nucleoside with anti-viral activity against DNA-VIRUSES, WAS GIVEN (10 TO 20 MG/MG/DAY) BY A CONTINUOUS 12-HOUR INTRAVENOUS DRIP FOR 10 TO 15 DAYS. In all, ara-A administration was begun within three to eight days after the appearance of skin vesicles which represented the hallmark of the disease. Both diagnosis and ara-A treatment were much delayed in one infant without skin vesicles and four infants whose skin vesicles appeared late, long after the occurrence of CNS damage. In this group of infants with disseminated disease, four died and one infant was left with severe neurological deficits. Eight infants (four with disseminated and four with localized skin disease) with skin vesicles as the earliest sign of infection received ara-A early, within three days after the onset of neurologic signs. All survived with no neurologic deficit at 6 months to 1 year of age. There was no apparent toxicity of ara-A to the bonemarrow, liver, or kidney.

Adolescent↗
PubMedDate not supplied

Cytomegalovirus infection in children with AIDS.

Data for 38 children perinatally exposed to human immunodeficiency virus (HIV) were evaluated to determine the impact of cytomegalovirus (CMV) infection on the course of perinatally acquired HIV infection. Thirteen children belonged to the P0 (indeterminate) group, one to the P1 (asymptomatic) group, and 24 to the P2 (symptomatic) group, per the classification of the Centers for Disease Control. Of the 24 children in the P2 group, 10 died. The mean follow-up time was 22.8 months for the 10 children who died and 16.3 months for the 13 children in the P0 group. Serial cultures of urine were performed for all 38 patients. CMV was isolated from seven of 10 children who died and from four of 14 children who survived (P less than .05). Only one of the 13 P0 children was culture-positive for CMV, as compared with 11 of 24 P2 children (P less than .05). All CMV-infected children continued to demonstrate CMV viruria in serial cultures. The mean age at the time of the first culture positive for CMV was 13 months. Microcephaly was present in 15 (65%) of 23 P2 children but in none of the P0 and P1 children (P less than .05). Eight of 11 CMV-infected children were microcephalic; seven of 12 children not infected with CMV were microcephalic (P greater than .05). These data suggest that the prevalence of active CMV infection is significantly higher in P2 children than in P0 and P1 children. In addition, there is a significant association between CMV infection and mortality among P2 children.

Acquired Immunodeficiency Syndrome↗