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Biomedical subjects

M Petric

Publications and source records attributed to M Petric.

At least 37 records · Page 2Linked to original sources
PubMed2001

Antibody response to Shiga toxins Stx2 and Stx1 in children with enteropathic hemolytic-uremic syndrome.

A Western blot (immunoblot) assay (WBA) for the detection of immunoglobulin G antibodies to Shiga toxins Stx2 and Stx1 in sera from 110 patients with enteropathic hemolytic-uremic syndrome (53 culture confirmed to have Shiga toxin-producing Escherichia coli [STEC] infection) and 110 age-matched controls was established by using a chemiluminescence detection system. Thirty-nine (74%) of the 53 culture-confirmed cases were infections with STEC serotype O157, and 14 (26%) were associated with infection by other STEC serotypes. The frequency of an anti-Stx2 response following infection by a Stx2-producing strain (34 of 48 cases; 71%) was higher than that of an anti-Stx1 response following Stx1-producing STEC infection (4 of 10). Furthermore, the frequency of an anti-Stx2 response in 110 control sera (10%) was significantly higher than the frequency of an anti-Stx1 response (1.8%) (P = 0.0325). For STEC O157 culture-confirmed cases WBA for toxin detection had a diagnostic sensitivity of 71% and a specificity of 90%. Because of its high specificity the assay might be a helpful tool for diagnosing suspected STEC infection when tests of stool samples or serological tests against various lipopolysaccharide antigens are negative. Furthermore, the prevalence of anti-Stx antibodies in healthy controls probably reflects the population immunity to systemic Stx-associated disease. It can thus serve as a basis for comparing immunity levels in different populations and for considering future Stx toxoid immunization strategies.

Adolescent↗
PubMed2000

The coxsackie-adenovirus receptor (CAR) is used by reference strains and clinical isolates representing all six serotypes of coxsackievirus group B and by swine vesicular disease virus.

Group B coxsackieviruses are etiologically linked to many human diseases, and cell surface receptors are postulated to play an important role in mediating their pathogenesis. The coxsackievirus adenovirus receptor (CAR) has been shown to function as a receptor for selected strains of coxsackievirus group B (CVB) serotypes 3, 4, and 5 and is postulated to serve as a receptor for all six serotypes. In this study, we demonstrate that CAR can serve as a receptor for laboratory reference strains and clinical isolates of all six CVB serotypes. Infection of CHO cells expressing human CAR results in a 1000-fold increase in CVB progeny virus titer compared to mock transfected cells. CAR was shown to be a functional receptor for swine vesicular disease virus (SVDV), as CHO-CAR cells but not CHO mock transfected controls were susceptible to SVDV infection, produced progeny SVDV, and developed cytopathic effects. Moreover, SVDV infection could be specifically blocked by monoclonal antibody to CAR (RmcB). SVDV infection of HeLa cells was also inhibited by an anti-CD55 MAb, suggesting that this virus, like some CVB, may interact with CD55 (decay accelerating factor) in addition to CAR. Finally, pretreatment of CVB or SVDV with soluble CAR effectively blocks virus infection of HeLa cell monolayers.

Animals↗
PubMed2000

Surveillance for outbreaks of respiratory tract infections in nursing homes.

BACKGROUND: Outbreaks of respiratory tract infections are common in long-term care facilities for older people. The objective of our study was to determine both the frequency of such outbreaks and their clinical and epidemiological features. METHODS: Prospective surveillance for outbreaks of respiratory tract infections and a retrospective audit of surveillance records were conducted in 5 nursing homes in metropolitan Toronto over 3 years. The clinical manifestations of infected residents were identified and microbiological investigations for causal agents were conducted. RESULTS: Sixteen outbreaks, involving 480 of 1313 residents, were identified prospectively during 1 144 208 resident-days of surveillance, for an overall rate of 0.42 infections per 1000 resident-days. Another 30 outbreaks, involving 388 residents, were identified retrospectively. Outbreaks occurred year-round, with no seasonal pattern. Pathogens included influenza virus, parainfluenza virus, respiratory syncytial virus, Legionella sainthelensi and Chlamydia pneumoniae. Multiple pathogens were detected in 38% (6/16) of the prospectively identified outbreaks. Of the 480 residents in the prospectively identified outbreaks 398 (83%) had a cough, 194 (40%) had fever and 215 (45%) had coryza. Clinical findings were nonspecific and could not be used to distinguish between causal agents. Pneumonia developed in 72 (15%) of the 480 residents, and 58 (12%) required transfer to hospital. The case-fatality rate was 8% (37/480). INTERPRETATION: Our findings emphasize the importance of adequate surveillance for outbreaks of respiratory tract infections in nursing homes and of early diagnosis so that appropriate interventions can be promptly instituted.

Aged↗
PubMed2000

Hospitalization for community-acquired, rotavirus-associated diarrhea: a prospective, longitudinal, population-based study during the seasonal outbreak. The Greater Toronto Area/Peel Region PRESI Study Group. Pediatric Rotavirus Epidemiology Study for Immunization.

OBJECTIVES: To determine the age-specific hospitalization rate for rotavirus-associated diarrhea in Canadian children during the seasonal outbreak, and to characterize children and their households, for assessment of the need for a rotavirus vaccine. DESIGN: Prospective multisite cohort study. SETTINGS AND PARTICIPANTS: Children with an admission diagnosis of diarrhea admitted to 18 hospitals serving 132 study census tracts of a major urban region, from November 1, 1997, through June 30, 1998. Prospective centralized testing of stools was performed; research nurses administered a follow-up questionnaire to parents. MAIN OUTCOME MEASURE: Age-specific diarrhea and rotavirus-associated hospitalization rates. RESULTS: Of 224160 children younger than 5 years, the diarrhea hospitalization rate was 4.8 in 1000 (n = 1086) during the seasonal epidemic. Based on testing of 65% of the hospitalized children, the rotavirus-associated diarrhea hospitalization rate was 1.3 in 1000; the cumulative incidence to 5 years of age was 1 in 160. Rotavirus-associated diarrhea was reported in 37% of the 1001 hospitalized children undergoing testing inside and outside of the census tracts; in children aged 6 to 35 months, this rose to more than 70% during April and May. Ages of children with rotavirus-associated diarrhea were 0 to 2 months (2%), 3 to 5 months (5%), 6 to 23 months (60%), 24 to 35 months (15%), and 36 months or older (19%). Of children aged 0 to 5 and 6 to 11 months, 4 (19%) of 21 and 6 (10%) of 59, respectively, had been born prematurely; 20 (24%) of 83 younger than 1 year were breastfed at the time of illness. Of children younger than 36 months, 77% were cared for in their homes; 13%, in family day care homes; and 8%, in child care centers. The mean (+/- SD) duration of rotavirus hospitalization based on hospital records and parental questioning was 2.4 +/- 1.7 and 3.1 +/- 1.6 days, respectively; it was significantly longer (P < or = .001) in children with an underlying medical condition. One child required intensive care unit hospitalization. Diarrhea occurred concurrently in 74% of household contacts younger than 3 years; 38%, aged 3 to 18 years; and 29%, older than 18 years. Seventy-six percent of parents were married. Household incomes in Canadian dollars in the 81% reporting were less than $20000 in 20%, $20000 to $60000 in 44%, and greater than $60000 in 36%. Ethnicity was reported as 53% white, 15% black, 10% Asian, 12% East Indian, and 11% other. CONCLUSIONS: Based on testing of 65% of children with diarrhea, rotavirus resulted in hospitalization in a minimum of 1 in 160 children by 5 years of age during the seasonal outbreak. Had 100% of young children with diarrhea undergone testing, the extrapolated cumulative incidence of rotavirus-associated diarrhea by 5 years of age may have been 1 in 106.

Acute Disease↗
PubMed2000

Rotavirus-associated diarrhea in outpatient settings and child care centers. The Greater Toronto Area/Peel Region PRESI Study Group. Pediatric Rotavirus Epidemiology Study for Immunization.

OBJECTIVES: To determine the prevalence of rotavirus infection in outpatient and child care center (CCC) settings during the seasonal rotavirus outbreak and to describe associated health care utilization. DESIGN: Prospective, multisite cohort study in various ambulatory settings. SETTINGS AND PARTICIPANTS: Participants were children with diarrhea (1) presenting to hospital emergency departments (EDs) and receiving intravenous (IV; n = 8) or oral (n = 1) hydration, (2) seen in pediatric practices (n=4), or (3) attending CCCs (n = 19) between November 1, 1997, and June 30, 1998. Prospective centralized testing of stool samples for rotavirus was performed using enzyme-linked immunosorbent assay and electron microscopy. Study nurses administered follow-up parent questionnaires for rotavirus-positive children. MAIN OUTCOME MEASURE: Prevalence of rotavirus-associated diarrhea. RESULTS: During the 8-month study, rotavirus was identified in 92 children with diarrhea: ED-IV, 20 (44%) of 45; ED-oral, 9 (47%) of 19; pediatric practices, 30 (20%) of 147; and CCCs, 33 (18%) of 186. Of 226 children with diarrhea in pediatric practices, all 5 who progressed to ED-IV hydration or hospitalization were tested, and 3 (60%) were rotavirus positive. Of 211 children in CCCs with diarrhea, 84% who required no health care visits were tested, and of these 10% were positive; of 56 who went on to require a health care visit and 8 who required ED-IV hydration or hospitalization, all were tested, and 27% and 75%, respectively, were rotavirus positive. Among 16 children with rotavirus followed up with ED-IV hydration, 4 (25%) returned and were hospitalized. Maximal health care intervention among 29 children with rotavirus enrolled in pediatric practices included 22 (76%) seeing the pediatrician only, 5 (17%) seeking further care in the ED, 1 (3%) receiving further ED-IV hydration, and 1 (3%) being hospitalized briefly. Maximal health care intervention for 33 children with rotavirus enrolled in CCCs included 13 (39%) who did not visit a physician, 11 (33%) who did, 3 (9%) who sought care in the ED, 1 (3%) who received ED-IV hydration, and 5 (15%) who were hospitalized. In CCCs, rates of diarrhea per 100 child-months of observation were as follows: ages 0 to 23 months, 6.6 episodes; ages 24 to 35 months, 1.9 episodes; and 3 years and older, 0.07 episodes; rates of rotavirus-associated diarrhea were as follows: ages 0 to 23 months, 1.1 episodes (28 of 2547); ages 24 to 35 months, 0.23 episodes (5 of 2185); and 3 years and older, 0 episodes (0 of 4124). CONCLUSION: Across a variety of outpatient and CCC settings, rotavirus is an important cause of diarrhea and a major cause of health care utilization.

Child↗
PubMed2000

Etiology of community-acquired pediatric viral diarrhea: a prospective longitudinal study in hospitals, emergency departments, pediatric practices and child care centers during the winter rotavirus outbreak, 1997 to 1998. The Pediatric Rotavirus Epidemiology Study for Immunization Study Group.

OBJECTIVE: To determine the viral etiology of community-acquired diarrhea in children admitted to hospitals and presenting in emergency departments, pediatric practices and child care centers from November 1, 1997, to June 30, 1998. STUDY DESIGN: Children with diarrhea were identified in a prospective multisite cohort study and analyzed according to age, gender and duration of hospitalization. Stools were tested for rotavirus by enzyme immunoassay and for all other enteric viruses by electron microscopy. RESULTS: Of the 2524 children identified with diarrhea, stools of 1386 (55%) were tested by enzyme immunoassay for rotavirus, and of these 1365 (54%) were screened by electron microscopy for all identifiable enteric viruses. Rotavirus was found in 32% (n = 437), adenovirus in 4% (n = 55), torovirus in 3% (n = 44), Norwalk-like viruses in 2% (n = 25) and astrovirus (n = 14) and calicivirus (n = 7) in fewer than 1% of the specimens tested. The proportion of rotavirus was significantly higher in children 12 to 23 months of age (43% of tested stools, n = 159) and 24 to 35 months of age (38% of tested stools, n = 64) (P < 0.001) than in any other age group. Toroviruses were found to approximately the same extent in children > or =36 months of age (6% of tested stools, n = 19) as those <36 months of age. Rotavirus (36% of tested stools, n = 375, P < 0.0005) and torovirus (4% of tested stools, n = 43, P < 0.004) were most often found in hospitalized patients. In contrast Norwalk-like viruses (P < 0.001) and astroviruses (P < 0.01) were more commonly detected in specimens from patients who presented to physicians' offices and who were symptomatic for gastroenteritis in child care centers. CONCLUSION: This study demonstrates that although all known gastroenteritis viruses were diagnosed in symptomatic children, rotavirus was the etiologic agent in most cases of diarrhea managed in the community and in the hospital.

Child Day Care Centers↗
PubMed2000

Comprehensive PCR-based assay for detection and species identification of human herpesviruses.

The description and evaluation of a PCR-based assay for the detection and species identification of the eight known human herpesviruses are presented. Two primer pairs targeting well-conserved regions of the genome allowed the amplification of the DNAs of all known human herpesviruses at a high level of sensitivity (10 to 100 genome copies for most viruses). Identification of the virus species was achieved through restriction enzyme digestion with BamHI and BstUI, which yielded fragment sizes that were characteristic for each herpesvirus. Furthermore, it was demonstrated that this restriction enzyme panel allowed the discrimination between human herpesvirus 6 variant A and variant B. This assay format was validated over the course of 1 year in a clinical virology laboratory setting, where it was shown that it readily detected human herpesviruses, including occasional multiple infections, in a variety of clinical samples. The PCR assay was compared to isolation and electron microscopy for the detection of herpes simplex (HSV) and varicella-zoster virus (VZV) in clinical samples. All specimens positive by conventional methods were also positive by PCR. However, in a number of clinical specimens in which HSV or VZV could not be detected by conventional methods, PCR was able to demonstrate the presence of the virus.

Blood↗
PubMed1999

The complete consensus sequence of coxsackievirus B6 and generation of infectious clones by long RT-PCR.

The full length sequence for the human pathogen coxsackievirus B6 (CVB6, Schmitt strain) has been determined. We used long RT-PCR to generate full length DNA amplicon of CVB6, and then directly sequenced the amplicons. One-step cloning of the full length amplicon enabled us to obtain an infectious clone of CVB6. RNA generated from CVB6 amplicon DNA or CVB6 clones, by transcription with T7 RNA polymerase, was demonstrated to be infectious upon transfection into HeLa cells in vitro. The CVB6 genome is characteristic of enteroviruses, with a 5'-non-translated region (743 nucleotides) followed by an open reading frame (encoding a 2184 amino acid polyprotein) and a 3'-non-translated region (100 nucleotides) and polyadenylated tail. The predicted amino acid sequence of CVB6 clustered with the other CVB serotypes and swine vesicular disease virus (SVDV).

3' Untranslated Regions↗
PubMed1999

The novel hemagglutinin-esterase genes of human torovirus and Breda virus.

Human torovirus (HTV) and Breda virus (BRV), members of the genus torovirus in the family Coronaviridae, are established infectious agents of humans and cattle, respectively. The hemagglutinin-esterase (HE) gene of Breda virus serotype 2 (BRV-2) has been identified and the nucleotide sequence for BRV serotype 1 (BRV-1) genome which contains the open reading frames for the viral structural proteins has been reported revealing the presence of a 1. 25 kb gene whose nucleotide sequence is identical to that of the BRV-2 HE gene. In this study, we amplified the 1.2kb HE gene from the HTV genome using long RT-PCR and sequenced the amplicon directly. At the nucleotide level, the HTV HE gene manifests 85% sequence identity to the HE genes of BRV-1 and BRV-2 and 89% identity with the X pseudogene sequence of BEV. The 1.25 kb amplicons which contained the HE genes of BRV-1 and HTV were cloned and expressed in a baculovirus system and the proteins purified by sodium dodecyl sulphate-polyacrylamide gel electrophoresis. Hyperimmune sera prepared in guinea pigs against these proteins were reactive with both bovine torovirus (BTV) and human torovirus (HTV) antigens. By immunoblot, they reacted specifically with a 65 kDa protein corresponding in size to the torovirus HE protein. Furthermore, the hyperimmune sera but not the preimmune sera reacted with a series of BTV-positive and HTV-positive fecal specimens by immunoblot and dot blot analysis. By immunoelectron microscopy (IEM) torovirus particles from BTV-positive specimens from calves with diarrhea and HTV-positive specimens from patients were aggregated by the hyperimmune sera. Human convalescent sera and gnotobiotic calf post-infection sera reacted by immunoblot with the expressed 65 kDa protein. The expressed HE protein of HTV has important diagnostic potential.

Acetylesterase↗
PubMed1999

Effects of thyroid-stimulating hormone on the replicative cycle of vesicular stomatitis virus in primary cultured sheep thyroid cells.

Sheep thyroid cells in primary culture are highly sensitive to thyroid stimulating hormone (TSH). We infected thyroid cells with vesicular stomatitis virus (VSV) in the course of studies on cell polarity, and we found that TSH augmented the speed of the replicative cycle of VSV but did not affect the final yield of the virus. Three hours post-infection, at a multiplicity of infection of 10, the virus was detected in the cell layer of the cultures incubated with TSH but not in those without TSH. Five hours post-infection, there was a 100-fold increase in the medium in the yield of VSV and a 60-fold increase in the cell-associated virus in the TSH-treated cells compared with the cells without TSH. We found that the early stages of infection were accelerated by TSH. This effect appears to be due, at least in part, to increased processing in the lysosomes, thus allowing deposition of the transcriptionally-active nucleocapsid into the cytoplasm. These studies show that TSH is critically involved in the infectivity of VSV and that by manipulating cell culture conditions, an increased rate of virus production can be achieved.

Animals↗
PubMed1999

Measles inclusion-body encephalitis caused by the vaccine strain of measles virus.

We report a case of measles inclusion-body encephalitis (MIBE) occurring in an apparently healthy 21-month-old boy 8.5 months after measles-mumps-rubella vaccination. He had no prior evidence of immune deficiency and no history of measles exposure or clinical disease. During hospitalization, a primary immunodeficiency characterized by a profoundly depressed CD8 cell count and dysgammaglobulinemia was demonstrated. A brain biopsy revealed histopathologic features consistent with MIBE, and measles antigens were detected by immunohistochemical staining. Electron microscopy revealed inclusions characteristic of paramyxovirus nucleocapsids within neurons, oligodendroglia, and astrocytes. The presence of measles virus in the brain tissue was confirmed by reverse transcription polymerase chain reaction. The nucleotide sequence in the nucleoprotein and fusion gene regions was identical to that of the Moraten and Schwarz vaccine strains; the fusion gene differed from known genotype A wild-type viruses.

Encephalitis, Viral↗
PubMed1999

Evaluation of a microplate latex agglutination method (Verotox-F assay) for detecting and characterizing verotoxins (Shiga toxins) in Escherichia coli.

The performance of a commercial microplate latex agglutination assay, the Verotox-F assay, was compared with that of the Vero cell assay for the detection and characterization of Escherichia coli verocytotoxins (VTs). Culture filtrates of 68 VT-positive E. coli strains (65 human isolates [33 of serotype O157:H7/H-, 32 of non-O157 serotypes] and 3 reference strains) and 104 VT-negative strains (100 human isolates and 4 reference strains) were investigated. The toxin phenotypes and genotypes of the 68 VT-positive isolates were VT1 only (18 strains), VT2 and/or VT2c (33 strains), and VT1 plus VT2 (17 strains). The Verotox-F assay involved incubation of serial dilutions of culture filtrates with equal volumes of latex particles sensitized with anti-VT1 antibody or anti-VT2 antibody in 96-well microtiter plates with appropriate controls and examination for latex agglutination after 20 to 24 h. Compared to the results of the Vero cell assay, the Verotox-F assay was 100% sensitive and 100% specific for the detection of VTs in culture filtrates and correctly identified the toxin types of all 68 VT producers. By checkerboard titration with purified toxins, the sensitivity of the Verotox-F assay was found to be 14 pg (0.7 ng/ml) for VT1, 12 pg (0.6 ng/ml) for VT2, and 350 pg (17.5 ng/ml) for VT2c; this sensitivity is comparable to that of the bioassay. The anti-VT2 latex reagent detected both VT2 and VT2c and did not cross-react with VT1. The anti-VT1 reagent showed a low-level cross-reaction with VT2c only at levels (>/=4.5 microg/ml) that were about 1,000-fold higher than those found in culture filtrates. We conclude that the Verotox-F assay is highly sensitive and specific for the detection and characterization of VTs in culture filtrates of human E. coli isolates. The test is rapid, reliable, and easy to perform; its results are easy to interpret; and it should allow testing for VT to become more widely performed.

Animals↗
PubMed1998

Cardiovirulent coxsackieviruses and the decay-accelerating factor (CD55) receptor.

Group B coxsackieviruses are etiologically linked with many human diseases including acute myocarditis and associated chronic dilated cardiomyopathy. Well-established CVB3 cardiovirulent strains (CVB3c(s)) with known phenotypic difference have been used to study the pathogenesis of virus-induced heart disease. The receptor-binding characteristics of cardiovirulent CVB3 are not known, but may represent one mechanism accounting for differences in disease virulence. In this study, interactions between CVB3c(s) and the decay-accelerating factor (DAF or CD55) cell surface receptor were examined. Anti-DAF monoclonal antibodies (MAbs) blocked virus binding and infection of susceptible HeLa cells. Virus binding was significantly reduced by treatment of these cells with phosphatidylinositol phospholipase C enzyme, which rendered them DAF-deficient CVB3c(s) exhibited a differential propensity for the DAF receptor, as several cardiovirulent strains interacted more strongly than others. However, virus binding and infection was always most effectively blocked by MAbs directed against the SCR 2 and 3 domains of DAF, suggesting that binding occurs at a similar site(s) on the molecule for all strains. Virus binding and internalization were associated with DAF down-regulation at the cell surface, as monitored by flow cytometry analysis. Cardiovirulent CVB3 did not interact with molecules functionally and/or structurally related to DAF, including CD35, CD46, Factor H, or C4-binding protein. Adenovirus type 2 (Ad2) does not use the DAF receptor. However, competitive binding assays between Ad2 and CVB1-6, CVB3c(s), anti-DAF MAbs, or DAF-reduced cells indicated that DAF is associated with Ad2 receptors on the HeLa cell membrane. In summary, this study indicates that DAF is an attachment receptor for cardiovirulent CVB3 and that DAF interaction may be important in the pathogenesis of CVB-mediated heart disease.

Adenoviridae↗
PubMed1998

Bovine torovirus: sequencing of the structural genes and expression of the nucleocapsid protein of Breda virus.

Breda virus (BRV), a member of the genus torovirus, is an established etiological agent of diarrhea of cattle, which is found as two separate serotypes, BRV-1 and BRV-2. In this study, a 7.5 kb fragment of the BRV-1 genome that bracketed the genes for the structural proteins of BRV was amplified by long RT-PCR and the amplicon purified and sequenced directly. Sequence analysis revealed the presence of four open reading frames (ORF) corresponding to the peplomer (S), envelope (M), and nucleocapsid (N) genes, and an ORF for a novel 1.2 kb gene located between the M and N genes. This new gene was identical in nucleotide sequence to the hemagglutinin-esterase (HE) gene of BRV-2. With the exception of this new ORF, BRV-1 manifests 80% nucleotide sequence identity with the torovirus prototype, Berne virus (BEV) in the 7.5 kb region from the 3' end of the genome that contains the genes for the structural proteins. A 504 base segment containing the ORF for the BRV-1 N gene was amplified by RT-PCR, and cloned into an Escherichia coli expression system. The resulting protein was purified by SDS-PAGE and used to immunize guinea pigs. Hyperimmune serum was reactive with bovine torovirus (BTV) and human torovirus (HTV) antigens. By immunoelectron microscopy, it was shown to aggregate broken but not intact torovirus particles from BTV-positive fecal specimens. By immunoblot, the hyperimmune serum reacted specifically with the 20 kD N proteins of both BTV and HTV, as well as with the expressed N protein. BRV-1 and BRV-2 immune sera from gnotobiotic calves, but not human convalescent sera from HTV-infected patients, reacted with the expressed N protein by immunoblot. These findings were applied to the design of a dot blot assay that could specifically detect BTV and HTV from fecal specimens.

Amino Acid Sequence↗
PubMed1998

Human torovirus: a new nosocomial gastrointestinal pathogen.

Studies were undertaken to determine if human torovirus is associated with gastroenteritis and to examine the clinical features of torovirus illness in children. The fecal excretion of torovirus in patients with gastroenteritis was compared with that in matched asymptomatic controls in a case-control study. Toroviruses were identified in 72 (35.0%) of 206 gastroenteritis cases compared with 30 (14.5%) of 206 controls (P<.001). Clinical features of torovirus gastroenteritis in 172 patients positive for torovirus were compared with those of 115 patients infected with rotavirus or astrovirus. Persons infected with torovirus were more frequently immunocompromised (43.0% vs. 15.7%) and nosocomially infected (57.6% vs. 31.3%). They also experienced less vomiting (46.4% vs. 66.7%) but had more bloody diarrhea (11.2% vs. 1.8%). An antibody response to torovirus developed mainly in older, nonimmunocompromised children (P<.01). These studies demonstrate an association between torovirus excretion and gastroenteritis in the pediatric population among immunocompromised hospitalized patients and in previously healthy patients.

Adolescent↗
PubMed1998

Etiology of acute childhood encephalitis at The Hospital for Sick Children, Toronto, 1994-1995.

Of 145 patients admitted to our hospital because of encephalitis-like illness, 50 patients hospitalized for > or =72 hours underwent standardized microbiological investigations. A confirmed or probable etiologic agent was identified in 20 cases (40%), including Mycoplasma pneumoniae (9 cases). M. pneumoniae and enterovirus (2), herpes simplex virus (4), Epstein-Barr virus (1), human herpes-virus 6 (HHV-6) (1), HHV-6 and influenza virus type A (1), influenza virus type A (1), and Powassan virus (1). In 13 cases (26%), a possible pathogen was identified, including M. pneumoniae in nine cases. Presenting features included fever (80% of patients), seizures (78%), focal neurological findings (78%), and decreased consciousness (47%). The frequency of findings at the time of admission vs. later in hospitalization was as follows: pleocytosis, 59% vs. 63%; electroencephalogram abnormalities, 87% vs. 96%; and neuroimaging abnormalities, 37% vs. 69%, respectively. The outcomes at the time of discharge were as follows: normal results of physical examination, 32% (16) of the patients; death, 2% (1); motor difficulties, 26% (13); global neurological deficits, 16% (severe, 6; mild, 2); mental status changes, 14% (7); visual defects, 8% (4); and hearing impairment, 2% (1).

Acute Disease↗