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Biomedical subjects

J H Joncas

Publications and source records attributed to J H Joncas.

At least 19 recordsLinked to original sources
PubMed1990

Epstein-Barr virus polymorphic B-cell lymphoma associated with leukemia and with congenital immunodeficiencies.

Polymorphic B-cell lymphoma seen in four patients with congenital immunodeficiencies and in two patients with leukemia receiving chemotherapy was associated with the Epstein-Barr virus (EBV). The tumors had characteristic histologic features: they were polymorphic consisting of a mixture of lymphoblasts and differentiated cells including plasma cells, and areas of hemorrhagic necrosis were prominent. The tumors were either polyclonal, monoclonal, or multiclonal. Patients with congenital immunodeficiencies who developed these tumors died despite radiotherapy, corticosteroids plus acyclovir, or a combination of intravenous (IV) immunoglobulins and alpha 2 interferon. Patients with leukemia recovered when immunosuppressive drugs were discontinued and leukemia has not recurred over a period of 2 and 4 years, respectively, in the two patients.

Antineoplastic Agents↗
PubMed1989

DNA polymorphism among isolates from multiple sites of a patient with chronic herpes simplex virus, type 1 infection.

DNA polymorphisms among independent isolates of herpes simplex virus (HSV) type 1 were studied from a 7-year-old male patient with recurrent infections of the skin and internal organs. In the patient's serum, HSV antibodies could not be detected by complement fixation, enzyme-linked immunosorbent assay (ELISA), or neutralization tests. ELISA tests for the presence of antibodies to human immunodeficiency virus were also negative. One HSV isolate was obtained from mesenteric nodes biopsied in 1983; one from skin in 1984; and three (postmortem) from brain, lungs, and liver in 1985. Restriction enzymes Eco RI, Bgl II, Hind III, Kpn I, and Bam H1 digestion patterns of the five isolates were similar. However, Sal I digests of isolates from skin, mesenteric nodes, lungs, and liver showed variations that were distinct from that of the brain isolate. Although Sal I digests of skin, mesenteric nodes, lungs, and liver isolates share a common variation in lacking F and G, the liver isolate can be further differentiated because of the gain of a restriction site on the H fragment. Thus, the three distinct variants observed were the isolates from brain (variant 1); from skin, mesenteric nodes, and lungs (variant 2); and from liver (variant 3). The fragments involved in variations among these isolates (presence or absence of Sal, G and H) are from the unique short and long regions (invariable regions) of the genome and therefore do not show heterogeneity in size. The extent of variation among these isolates is less than that seen among epidemiologically unrelated strains, suggesting that they originated from a single infecting strain, probably the brain isolate.

Animals↗
PubMed1989

Comparison of two methods in the determination of the sensitivity of 84 herpes simplex virus (HSV) type 1 and 2 clinical isolates to acyclovir and alpha-interferon.

Two methods, the colorimetric method (neutral red dye uptake), and DNA hybridization using a HSV thymidine kinase gene probe (TK) have been used to examine the sensitivity of 84 herpes simplex virus (HSV) type 1 and 2 clinical isolates to two antiviral drugs, acyclovir (ACV) and alpha-interferon (alpha-IFN). Using the colorimetric method, HSV isolates had ED50s ranging from 0.03 +/- 0.02 micrograms/ml to 0.164 +/- 0.03 micrograms/ml for ACV and 6.3 +/- 5.2 IU/ml to 55.0 +/- 11.4 IU/ml for alpha-IFN. With the DNA hybridization method, ED50s ranged from 0.033 +/- 0.012 micrograms/ml to 0.190 +/- 0.031 micrograms/ml for ACV and 8.5 +/- 5.0 IU/ml to 43.5 +/- 6.0 IU/ml for alpha-IFN. Two strains of HSV-1 were found to be resistant to very high concentrations of ACV (greater than 50.0 micrograms/ml). The values obtained by the two methods showed good correlation (r = 0.724, P = 0.002). Furthermore, our results demonstrate that the two methods are reproducible, reliable and the dye uptake assay is suitable for use in a diagnostic virology laboratory.

Acyclovir↗
PubMed1988

Standardization and kinetics of in vitro bovine blood lymphocyte stimulation with bovine rotavirus.

Two groups of 3-month old calves were immunized intramuscularly with attenuated bovine rotavirus and boosted 21 and 42 days later. The first group of three calves were vaccinated with live virus emulsified with incomplete Freund's adjuvant (IFA) and the second group was immunized with live virus suspended in phosphate buffered saline (PBS). Three other calves, serving as controls, were inoculated with PBS emulsified with IFA. The specific cell-mediated and antibody responses of the animals were studied. Preliminary analysis of in vitro peripheral blood lymphocyte transformation to bovine rotavirus determined optimal conditions as: 96 h culture period, 5 X 10(5) cells per culture in RPMI 1640 medium containing 10% heat-inactivated bovine fetal serum and the use of inactivated virus in the cell culture at a concentration of 5 X 10(6) median tissue culture infective dose before inactivation. Specific blastic stimulation was observed on calves immunized with the rotavirus emulsified with IFA after the second and third vaccine inoculation with stimulation index values varying from 2.00 to 5.73. Serum neutralizing antibody titers of 1/25,600 were also induced in the same calves. Calves immunized with rotavirus-PBS suspension developed a mean antibody titer of 1/1,600, but showed no specific lymphocyte stimulation. No increase in specific immune responses was detected in the control animals.

Animals↗
PubMed1988

Immune response of pregnant heifers and cows to bovine rotavirus inoculation and passive protection to rotavirus infection in newborn calves fed colostral antibodies or colostral lymphocytes.

The efficacy of an adjuvanted bovine rotavirus vaccine in pregnant cattle (15 heifers and 2 cows) was studied. Each of 4 animals was inoculated IM at 8, 5, and 2 weeks before parturition with a water-in-oil emulsion containing live purified bovine rotavirus, mineral oil, and a mannide oleate compound. Four other animals were treated identically, except that muramyl dipeptide was added to the virus preparation. Five additional animals were inoculated orally at the same time intervals with adjuvant-free viral suspension, and 4 other pregnant animals inoculated only with buffer served as uninoculated controls. Kinetic studies of the specific immune responses were determined by quantification of the rotavirus-neutralizing antibodies and by a rotavirus lymphocyte stimulation test in vitro. Results showed that only the emulsions induced marked enhancement of rotavirus antibody titers in the serum, colostrum, and milk of inoculated cows. Colostral and milk lymphocytes isolated from these cows had a positive in vitro proliferative response to rotavirus stimulation, which lasted at least 21 days after parturition. The values of the stimulation index obtained with the colostral/milk lymphocytes were higher than those of the blood lymphocytes, reflecting increased lymphocyte activity in the colostrum/milk. However, addition of muramyl dipeptide to the emulsion preparation did not exert any potentiating effect on the immune response to rotavirus. Calves fed for the first 5 days after birth with a rotavirus-immune cell-free colostrum supplement were protected from a rotavirus challenge exposure on the third day after birth. Virus was not detectable in their feces.(ABSTRACT TRUNCATED AT 250 WORDS)

Adjuvants, Immunologic↗
PubMed1987

Biomolecular analysis of a defective nontransforming Epstein-Barr virus (EBV) from a patient with chronic active EBV infection.

A virus recovered from the saliva of a child with chronic active Epstein-Barr virus (EBV) infection for 8 years was shown to induce EBV early antigen (EBV-EA) in Raji cells and to be expressed into EBV-EA in fresh EBV-negative peripheral blood leukocytes. However, it did not replicate its DNA. Oropharyngeal epithelial cells scraped from recurrent mouth lesions were similarly positive for EBV-EA. DNA extracted from these cells and digested with BamHI contained a 6-kilobase-pair fragment homologous to BamHI fragment V and B1 EBV DNA probes. Furthermore, Southern blots of the BamHI and EcoRI digests of the DNA extracted from the cell lines of the patient (transformed with EBV strain B95-8) and of her mother (spontaneous) revealed, in addition to the expected BamHI G, H, H2, and B1 fragments used as probes, additional shorter ones of a presumably endogenous defective virus.

Antigens, Viral↗
PubMed1986

Pathogens in children with severe combined immune deficiency disease or AIDS.

We evaluated the frequency and severity of illnesses caused by various microbial pathogens in 15 children with severe combined immune deficiency disease (SCID) and 8 with acquired immune deficiency syndrome (AIDS). There were 35 viral, 23 bacterial, 19 mycotic and 13 parasitic infections. Nineteen of the 23 patients died of infection; Pneumocystis carinii pneumonia, giant-cell pneumonia due to paramyxoviruses and various disseminated viral infections were responsible for most deaths in both groups. The emerging role of paramyxoviruses was illustrated by the fact that they were responsible for giant-cell pneumonia in seven patients. Viral enteric infections were frequent in both groups. The variety of infectious microorganisms and the severity of resulting illnesses in the patients with AIDS were similar to those in the patients with SCID.

Acquired Immunodeficiency Syndrome↗
PubMed1986

In vitro comparison of ampicillin-chloramphenicol and ampicillin-cefotaxime against 284 Haemophilus isolates.

Since November 1982 at the Sainte-Justine Hospital in Montreal, ampicillin and cefotaxime were used in association as initial treatment (greater than or equal to 48 h) for childhood bacterial meningitis. In this report is described the in vitro interaction of the new regimen in comparison with that of the previous ampicillin-chloramphenicol combination against 284 Haemophilus isolates. Among the 156 ampicillin-susceptible, beta-lactamase-negative isolates, synergy was detected in 13 with ampicillin-cefotaxime, and antagonism was detected in only 1; in contrast, synergy was found in only 2 strains with ampicillin-chloramphenicol, and antagonism was found in 15. These differences were statistically significant (P less than 0.01). Such significant differences were not observed among the 128 ampicillin-resistant, beta-lactamase-positive Haemophilus isolates. The synergy of ampicillin-cefotaxime did not contribute to a decrease of the MIC of cefotaxime for 90% of isolates tested, whereas the antagonism of ampicillin-chloramphenicol did not contribute to increase the MIC of ampicillin for 90% of isolates tested.

Ampicillin↗
PubMed1984

Lytic, nontransforming Epstein-Barr virus (EBV) from a patient with chronic active EBV infection.

A new wild-type isolate of Epstein-Barr virus (EBV) was identified in follow-up studies of a case of chronic active EBV infection in an 8-year-old girl who had high titres of antibody to viral capsid antigen and early antigen (EA) (greater than 20 480 and 2560 respectively), persistent splenomegaly and abnormal immunologic features. More than 10 throat washings from this patient failed to transform cord blood lymphocytes (CBL), but at least 7 were able to induce EA in Raji cells. Supernatants from cultures of the lymphoblastoid cell line obtained by in-vitro infection of this patient's leukocytes with the B95-8 strain of EBV revealed a herpesvirus particle when examined by electron microscopy. The same supernatants were unable to transform CBL but could induce EA in Raji cells upon superinfection. In 30 or more trials the patient's lymphocytes never transformed spontaneously but did become positive for EBV nuclear antigen and EA in the first week of culture at least twice. Parallel studies performed on the father of the patient yielded similar results. This, then, is the first report documenting lytic activity associated with a wild-type EBV isolate.

Antigens, Viral↗
PubMed1984

A familial syndrome of susceptibility to chronic active Epstein-Barr virus infection.

In two members of a family (daughter and father) active Epstein-Barr virus (EBV) infections persisted over periods of 4 and 3 years respectively (possibly 10 years in the father). Both had persistent splenomegaly and occasional bouts of unexplained fever but lived otherwise normal lives. The other members of the family (mother and son) were healthy. The titres of antibody to the EBV viral capsid antigen (VCA) and early antigen (EA) were extremely high in the daughter's blood, whereas the titres of antibody to the Epstein-Barr nuclear antigen were low in the daughter's blood and undetectable in the father's. Target cells of the EBV infection that were obtained from the daughter's blood were established in culture with great difficulty and showed increased expression of VCA and EA. Other immunologic investigations in the two patients revealed that the ratio of helper to suppressor T lymphocytes was inverted, natural killer-cell activity was abnormally low, lymphocyte responses to certain mitogens were depressed and there was a serum factor blocking mitogen-induced transformation. The possibility that the patients' unusual susceptibility to EBV infection represented an inherited syndrome (perhaps X-linked) is discussed.

Antibodies, Viral↗
PubMed1984

A comparison of ampicillin-cefotaxime and ampicillin-chloramphenicol in childhood bacterial meningitis: an experience in 55 patients.

Ampicillin-cefotaxime was tested as initial therapy of presumptive bacterial meningitis in 55 children greater than or equal to 2 months of age at our hospital. During the first year of this ongoing trial, 11 patients, 10 whose CSF yielded ampicillin-resistant Haemophilus influenzae type b (MIC greater than 16 mg/l, beta-lactamase +) and one, indole-negative proteus (MIC 4 mg/l), were begun on ampicillin-cefotaxime and then continued on cefotaxime alone. All did well clinically except one who convulsed briefly but recovered without sequelae. The cefotaxime MICs/MBCs of the beta-lactamase-positive H. influenzae isolates (less than or equal to 0.007 to 0.03/less than or equal to 0.007 to 0.12) and the proteus isolate (0.03/0.12) were significantly lower than chloramphenicol MICs/MBCs (0.25 to 1.0/0.5 to 1.0 and 8/greater than 16). We followed 44 other children with meningitis due to ampicillin-sensitive organisms who were treated with ampicillin or penicillin after 1 or 2 days of ampicillin-cefotaxime. Aetiological agents included ampicillin-sensitive H. influenzae (25), pneumococci (9), meningococci (8), Strept. MG (1) and Listeria monocytogenes (1). 40/44 recovered uneventfully. There were 4 neurological complications: the streptococcal meningitis sustained a brain abscess and the three others were motor incoordination (sensitive haemophilus), hearing loss and subdural effusion (2 pneumococci). There were no deaths. 18/48 children managed initially with ampicillin-chloramphenicol during the same 12-month period one year earlier had significant neurological complications and/or sequelae and there was one death; aetiological agents included sensitive H. influenzae (30), pneumococci (9), ampicillin-resistant haemophilus (5), meningococci (3) and pneumococci plus strept. MG (1). The two groups were comparable except for the number of resistant haemophilus and meningococcal strains and underlying disease more frequent in the ampicillin-cefotaxime group. A significant reduction of neurological morbidity (5/55 or 9.1% vs. 18/48 or 37.5%:P less than 0.001) was therefore associated with the ampicillin-cefotaxime schedule in the initial treatment of proven bacterial meningitis. A prolonged hospitalization (greater than 15 days) was less frequent (P less than 0.01) in the ampicillin-cefotaxime group (3/55 or 5.5% vs. 13/48 or 27.1%). The results of the trial to date are considered to be very promising.

Adolescent↗
PubMed1984

Giant cell pneumonia due to respiratory syncytial virus. Occurrence in severe combined immunodeficiency syndrome.

A 6-month-old male infant with a severe combined immunodeficiency syndrome was hospitalized for progressive respiratory distress. Examination during hospitalization disclosed widespread pulmonary infiltrates that did not respond to intensive therapy. The patient died eight days after admission. Autopsy disclosed Pneumocystis carinii pneumonia and widespread giant cell pneumonia. Respiratory syncytial virus (RSV) was grown from a lung specimen obtained at autopsy. Specific immunofluorescent staining of the cytoplasm of alveolar lining cells with RSV antiserum was demonstrated. The electron microscopic appearance of giant cells was compatible with RSV infection. The RSV should be added to the list of viruses causing giant cell pneumonia.

Humans↗