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T V Murphy

Publications and source records attributed to T V Murphy.

At least 19 recordsLinked to original sources

Intussusception among infants given an oral rotavirus vaccine.

BACKGROUND: Intussusception is a form of intestinal obstruction in which a segment of the bowel prolapses into a more distal segment. Our investigation began on May 27, 1999, after nine cases of infants who had intussusception after receiving the tetravalent rhesus-human reassortant rotavirus vaccine (RRV-TV) were reported to the Vaccine Adverse Event Reporting System. METHODS: In 19 states, we assessed the potential association between RRV-TV and intussusception among infants at least 1 but less than 12 months old. Infants hospitalized between November 1, 1998, and June 30, 1999, were identified by systematic reviews of medical and radiologic records. Each infant with intussusception was matched according to age with four healthy control infants who had been born at the same hospital as the infant with intussusception. Information on vaccinations was verified by the provider. RESULTS: Data were analyzed for 429 infants with intussusception and 1763 matched controls in a case-control analysis as well as for 432 infants with intussusception in a case-series analysis. Seventy-four of the 429 infants with intussusception (17.2 percent) and 226 of the 1763 controls (12.8 percent) had received RRV-TV (P=0.02). An increased risk of intussusception 3 to 14 days after the first dose of RRV-TV was found in the case-control analysis (adjusted odds ratio, 21.7; 95 percent confidence interval, 9.6 to 48.9). In the case-series analysis, the incidence-rate ratio was 29.4 (95 percent confidence interval, 16.1 to 53.6) for days 3 through 14 after a first dose. There was also an increase in the risk of intussusception after the second dose of the vaccine, but it was smaller than the increase in risk after the first dose. Assuming full implementation of a national program of vaccination with RRV-TV, we estimated that 1 case of intussusception attributable to the vaccine would occur for every 4670 to 9474 infants vaccinated. CONCLUSIONS: The strong association between vaccination with RRV-TV and intussusception among otherwise healthy infants supports the existence of a causal relation. Rotavirus vaccines with an improved safety profile are urgently needed.

Case-Control Studies↗

Tyrosine phosphorylation following alterations in arteriolar intraluminal pressure and wall tension.

Arterioles respond to increased transmural pressure with myogenic constriction. The present study investigated the role of tyrosine phosphorylation in myogenic activity. Cannulated segments of a rat cremaster arteriole were fixed under pressure, followed by incubation with fluorescein isothiocyanate (FITC)-conjugated anti-phosphotyrosine. Smooth muscle cell fluorescence intensity was measured with the use of confocal laser-scanning microscopy. Anti-phosphotyrosine fluorescence intensity in muscle cells of arterioles maintained at 100 mmHg was reduced by the tyrosine kinase inhibitor tyrphostin A47 (30 microM) and increased by the tyrosine phosphatase inhibitor pervanadate (100 microM). In time-course experiments, anti-phosphotyrosine fluorescence increased slowly (over 5 min) after an acute increase in intraluminal pressure, and was dissociated from myogenic contraction (within 1 min). In contrast, angiotensin II (0.1 microM) caused rapid constriction and increased tyrosine phosphorylation. Anti-phosphotyrosine fluorescence was also pressure dependent (10-100 mmHg). Abolition of myogenic activity, either through removal of extracellular Ca2+, or exposure to verapamil (5 microM) or forskolin (0.1 microM) caused a further increase in anti-phosphotyrosine fluorescence. We conclude that transmural pressure and/or wall tension in arterioles causes increased tyrosine phosphorylation; however, this is not involved in the acute phase of myogenic constriction but may be involved in later responses, such as sustained myogenic tone or mechanisms possibly related to growth.

Angiotensin II↗

Poliomyelitis prevention in the United States. Updated recommendations of the Advisory Committee on Immunization Practices (ACIP).

These recommendations of the Advisory Committee on Immunization Practices (ACIP) for poliomyelitis prevention replace those issued in 1997. As of January 1, 2000, ACIP recommends exclusive use of inactivated poliovirus vaccine (IPV) for routine childhood polio vaccination in the United States. All children should receive four doses of IPV at ages 2, 4, and 6-18 months and 4-6 years. Oral poliovirus vaccine (OPV) should be used only in certain circumstances, which are detailed in these recommendations. Since 1979, the only indigenous cases of polio reported in the United States have been associated with the use of the live OPV. Until recently, the benefits of OPV use (i.e., intestinal immunity, secondary spread) outweighed the risk for vaccine-associated paralytic poliomyelitis (VAPP) (i.e., one case among 2.4 million vaccine doses distributed). In 1997, to decrease the risk for VAPP but maintain the benefits of OPV, ACIP recommended replacing the all-OPV schedule with a sequential schedule of IPV followed by OPV. Since 1997, the global polio eradication initiative has progressed rapidly, and the likelihood of poliovirus importation into the United States has decreased substantially. In addition, the sequential schedule has been well accepted. No declines in childhood immunization coverage were observed, despite the need for additional injections. On the basis of these data, ACIP recommended on June 17, 1999, an all-IPV schedule for routine childhood polio vaccination in the United States to eliminate the risk for VAPP. ACIP reaffirms its support for the global polio eradication initiative and the use of OPV as the only vaccine recommended to eradicate polio from the remaining countries where polio is endemic.

Child↗

Effects of mibefradil and nifedipine on arteriolar myogenic responsiveness and intracellular Ca(2+).

1. Ca(2+) entry mechanisms underlying spontaneous arteriolar tone and acute myogenic reactivity remain uncertain. These studies aimed to compare the effects of nifedipine and the putative T-channel blocker, mibefradil, on arteriolar myogenic responsiveness and intracellular Ca(2+) (Ca(2+)(i)). 2. First order cremaster muscle arterioles (1A) were isolated from rats, cannulated, pressurized to 70 mmHg in the absence of intraluminal flow, and mechanical responses studied by video microscopy. The Ca(2+)(i) was measured using fluorescence imaging of Fura 2 loaded arterioles. 3. Both nifedipine and mibefradil showed dose-dependent inhibition of spontaneous myogenic tone (at 70 mmHg; pEC(50) 7.04+/-0.17 vs 6.65+/-0.20 respectively, n=6 for both, n.s.) and KCl-induced vasoconstriction (at 70 mmHg; pEC(50) 6.93+/-0. 38 vs 6.45+/-0.27 respectively, n=6 for both, n.s.). 4. In arterioles maintained at 50 mmHg, nifedipine (10(-7) and 10(-5) M) caused a concentration dependent reduction in Ca(2+)(i), however, mibefradil (10(-7) and 10(-5) M) had no effect. Furthermore nifedipine significantly attenuated the increase in Ca(2+)(i) associated with an acute pressure step (50 - 120 mmHg) whereas mibefradil was considerably less effective. 5. Mibefradil (10(-7) M) significantly attenuated contractile responses to 60 mM KCl without altering the KCl-induced increase in Ca(2+)(i), in contrast to nifedipine (10(-7) M) which reduced both Ca(2+)(i) and contraction. 6. Membrane potential of arterioles with spontaneous myogenic tone (70 mmHg) was -41.5+/-1. 0 mV. Nifedipine (10(-7) or 10(-5) M) had no effect on membrane potential, however mibefradil (10(-5) M) caused significant depolarization. 7. In summary, both mibefradil and nifedipine inhibit arteriolar spontaneous tone and acute myogenic reactivity. While there may be overlap in the mechanisms by which these agents inhibit tone, differences in effects on membrane potential and intracellular Ca(2+) levels suggest mibefradil exhibits actions other than blockade of Ca(2+) entry in skeletal muscle arterioles.

Animals↗

Meningococcal disease in Dallas County, Texas: results of a six-year population-based study.

OBJECTIVE: Neisseria meningitidis is an important cause of serious bacterial infection in children and adults in the US. From 1992 to 1997 invasive disease caused by N. meningitidis was studied among 1.9 million residents of Dallas County, TX METHODS: The demographic characteristics and diagnoses of 151 patients were identified through active, population-based surveillance and review of medical records. Serogroups were determined for strains infecting 129 (85%) patients. RESULTS: The average annualized incidence rate was 1.3 cases per 100,000 person years and was highest for children <1 year (13 cases/100,000 person years). Older patients (50+ years old) were more likely to present with pneumonia and less likely to present with meningitis than younger patients. Neither the fatality rate nor the duration of hospitalization for surviving patients was associated with age. Among patients with a known serogroup, serogroup C disease was found in 35% of cases <1 year old, 64% of those 1 to 49 years old and 44% of those 50+ years old. Serogroup B strains were isolated from 26% of patients <1 year, 17% of patients 1 to 49 years old and none of the patients 50+ years old. Serogroup Y disease increased from 22% to 35% of cases between 1992 and 1997 (P = 0.03). This serogroup was identified in 26% of patients <1 year old, 17% of patients 1 to 49 years old and in 50% of patients 50+ years old. Serogroup C and Y accounted for 61% of cases in children <1 year old and for 79% of cases in all age groups. CONCLUSION: The results underscore the importance of conjugate vaccines for serogroups C and Y.

Adolescent↗

Tyrosine phosphorylation modulates arteriolar tone but is not fundamental to myogenic response.

The present study investigated the role of protein tyrosine phosphorylation in myogenic responsiveness of rat skeletal muscle arterioles. Arteriolar segments were cannulated and pressurized without intraluminal flow. All vessels studied developed spontaneous tone and demonstrated significant myogenic constriction to step changes in pressure with a resultant increase in myogenic tone over an intraluminal pressure range of 50-150 mmHg. Step increases in intraluminal pressure from 50 to 120 mmHg caused a rapid and sustained elevation in intracellular [Ca(2+)], as measured using fura 2. Vessels with myogenic tone dilated in response to tyrosine kinase inhibitors genistein (10 or 30 microM) and tyrphostin A47 (10 or 30 microM) and constricted to the tyrosine phosphatase inhibitor pervanadate (1 or 10 microM). Despite the dilator effect, myogenic reactivity was not blocked by the inhibitors. Daidzein (10 microM), a compound structurally similar to genistein but without tyrosine kinase-inhibiting activity, did not alter vessel tone or myogenic responses. Preincubation of arterioles with genistein or tyrphostin A47 did not significantly alter baseline arteriolar [Ca(2+)], and neither drug reduced the increase in [Ca(2+)] following an acute increase in intraluminal pressure. Constriction induced by pervanadate (10 microM) was not accompanied by a significant increase in intracellular [Ca(2+)], even though removal of extracellular Ca(2+) reversed the constriction. Examination of smooth muscle tyrosine phosphorylation, using a fluorescent phosphotyrosine antibody and confocal microscopy, showed that increased intraluminal pressure resulted in an increase in anti-phosphotyrosine fluorescence. Because manipulation of tyrosine kinase activity was found to alter vessel diameter, these data support a role for tyrosine phosphorylation in modulation of arteriolar tone. However, the results indicate that acute arteriolar myogenic constriction does not require tyrosine phosphorylation.

Animals↗

Structural determinants of phorbol ester binding in synaptosomes: pharmacokinetics and pharmacodynamics.

The present study used structurally distinct phorbol esters to investigate the relationship between their pharmacokinetics of binding to protein kinase C (PKC) in rat brain cortex synaptosomes, their affinity for PKC in synaptosomes and ability to enhance noradrenaline release from rat brain cortex. Affinity binding studies using [3deoxyphorbol 13-tetradecanoate (dPT)=PDB&z. Gt;12-deoxyphorbol 13-acetate (dPA)=phorbol 12,13-diacetate (PDA). In intact synaptosomes PDB, dPA and PDA rapidly displaced bound [3H]PDB whereas PMA and dPT were comparatively slow. However, the displacement rates for all the phorbol esters were equally rapid in synaptosomal membranes or synaptosomes permeabilised with Staphylococcus alpha-toxin. These results suggest that the lipophilic phorbol esters (dPT and PMA) are slower to displace [3H]PDB binding because they are hindered by the plasma membrane. In brain cortex slices it was found that the rate of displacement of [3H]PDB binding was closely correlated with the degree of elevation of transmitter noradrenaline release. Thus kinetic characteristics may determine biological responses and this may be particularly evident in events which occur rapidly or where there is fast counter-regulation.

Animals↗

Invasive pneumococcal disease in Dallas County, Texas: results from population-based surveillance in 1995.

We studied the epidemiology of invasive disease caused by Streptococcus pneumoniae in 1995 among 1.9 million residents of Dallas County, Texas. The sociodemographic characteristics and chronic medical conditions of 432 patients were identified through active, population-based surveillance and review of medical records. The incidence of disease was 22 cases per 100,000 person-years and was highest for children < 2 years of age (136 cases per 100,000 person-years) and for adults > or = 65 years of age (80 cases per 100,000 person-years). Twenty percent of isolates were nonsusceptible to penicillin; the highest rates of resistance were among the youngest and oldest age groups (28% and 22% of isolates, respectively). An increased incidence of disease was associated with low income (42 cases per 100,000 person-years) and black race (39 cases per 100,000 person-years). The frequency of most chronic medical conditions increased with age; smoking, heavy alcohol use, and infection due to human immunodeficiency virus were most common between 30 and 64 years of age. Of otherwise healthy patients 30-64 years of age, 47% were current smokers, an association requiring further investigation. Characterizing groups at risk for invasive pneumococcal disease could aid in the development of prevention programs and increase the benefits from wide use of effective vaccines.

Adolescent↗

Methicillin-resistant Staphylococcus aureus in two child care centers.

Methicillin-resistant Staphylococcus aureus (MRSA) has not been studied in child care centers. The prevalence of MRSA colonization was determined at two centers with an index patient. Two (3%) of 61 children at center X had MRSA; strains from both children and the index illness were pulsed-field gel electrophoresis type B. Nine (24%) of 40 children at center Y had MRSA; strains from 5 children and the index illness were type B, and strains from 4 children were type A. Ten of 11 colonized children were in classes with 2- and 3-year-old children. Colonization with MRSA was not associated with health care contact by subjects or by members of their households. MRSA in child day care centers indicates accelerated spread of MRSA in the community.

Child↗

17Beta-oestradiol enhances nitric oxide synthase activity in endothelium-denuded rat aorta.

1. It has been suggested that oestrogen-produced vasodilatation is due to induction of endothelial nitric oxide synthase (NOS), but there are many reports of direct effects on vascular smooth muscle. In the present study, these processes were investigated in rat aorta isolated from ovariectomized rats. 2. Short-term treatment (10 min) with 17beta-oestradiol (10 micromol/L) produced a small attenuation of the phenylephrine (PE)-induced constriction, which was unaffected by the nitric oxide synthase inhibitor L-N5(-1-iminoethyl)ornithine (NIO; 100 micromol/L). Long-term treatment (6 h) with 17beta-oestradiol (10 micromol/L) did not affect acetylcholine-mediated vasorelaxation in endothelium-intact aortic rings, but did attenuate PE-induced constriction. This attenuation was also observed in endothelium-denuded preparations after 17beta-oestradiol (10 micromol/L for 6 h) and was far greater than the acute effect of 17beta-oestradiol (10 micromol/L). 3. The attenuation produced by 17beta-oestradiol (10 micromol/L for 6 h) was significantly inhibited by concomitant treatment with cycloheximide (1 micromol/L), suggesting that protein synthesis was involved. NIO (100 micromol/L) also attenuated the effect, which suggests that the anti-constrictor effect of 17beta-oestradiol occurs through the increased production of nitric oxide (NO). 17Beta-oestradiol increased NO production, as assessed by the conversion of [3H]-arginine to [3H]-citrulline in rat aorta. These effects were prevented by cycloheximide and NIO. The anti-constrictor effect of oestrogen was blocked by the oestrogen receptor antagonist ICI 182 780 (100 nmol/L). 4. Western blotting using an antibody specific for inducible nitric oxide synthase (NOS) revealed that 17beta-oestradiol (10 micromol/L for 24 h) treatment induced the formation of inducible NOS protein in the aorta, an effect blocked by cycloheximide. The results indicate that 17beta-oestradiol can attenuate the vasoconstrictor effect of PE by a specific receptor-mediated process that involves induction of inducible NOS.

Acetylcholine↗

Noradrenaline release and the effect of endogenous activation of the phospholipase C/protein kinase C signalling pathway in rat atria.

1. It has been proposed that protein kinase C (PKC) in sympathetic nerves is activated during action-potential evoked release of noradrenaline and helps maintain transmitter output. We studied this phenomenon further in rat atria radiolabelled with [3H]-noradrenaline. 2. Noradrenaline release was elevated by continuous electrical stimulation of the atria for 10 min at either 5 or 10 Hz. Two inhibitors of PKC, polymyxin B (21 microM) and Ro 318220 (3 microM), markedly inhibited the release of noradrenaline but only at the higher stimulation frequency. 3. Further experiments were conducted with 10 Hz stimulation but for shorter train durations. In this case polymyxin B inhibited noradrenaline release during a 10 or 15 s train of impulses but not during a 5 s train. This suggests that PKC effects are induced during the stimulation train by some process. 4. The diacylglycerol kinase inhibitor R59949 (10 microM), which prevents the breakdown of diacylglycerol, enhanced noradrenaline release elicited by stimulation at 10 Hz for 10 or 15 s. This effect was not seen if polymyxin B was present and suggests that diacylglycerol is the endogenous activator of PKC. 5. The source of the diacylglycerol may be through phospholipase C pathways, since the phospholipase C inhibitor U73122 (3 microM) inhibited noradrenaline release at 10 Hz for 10 s and the effect was not seen if polymyxin B was also present. 6. It is unlikely that phospholipase D is the source of diacylglycerol. Although the phospholipase D inhibitor wortmannin (1 microM) inhibited noradrenaline release, this effect was still observed in the presence of polymyxin B. Furthermore ethanol, which inhibits diacylglycerol formation by phospholipase D, had no effect on noradrenaline release. 7. We therefore suggest that during a train of high frequency pulses phospholipase C is activated and this results in the production of diacylglycerol which in turn activates PKC. This enables the neurones to maintain transmitter release at a high level.

Androstadienes↗

Factors associated with unnecessary immunization given to children.

OBJECTIVE: To determine the factors associated with unnecessary immunization during the pre-school years. METHODS: Children were selected from birth certificates and their parents were interviewed to identify all immunizations to 72 months of age. The immunizations were verified. RESULTS: Of 187 children studied 34 (18%) received unnecessary immunization. Unnecessary immunization was strongly associated with ever receiving immunization in a large system of public clinics (designated "Public A") (33%) compared with other providers (5%) (P < 0.00001). Among children immunized in Public A, unnecessary immunization was associated with the parent having an incomplete or no copy of the child's immunization record (P = 0.007) and with not being up to date for immunizations at 24 months of age (P = 0.04). Complete documentation of immunizations either in the Public. A record or in the parent's copy of the record was associated with a 4% rate of unnecessary immunization; incomplete or no documentation in both the Public A and the parent's record was associated with a 45% rate of unnecessary immunization (P = 0.001). CONCLUSIONS: Access to a complete immunization record, be it the provider's, the parent's or ideally both, decreases substantially a child's risk of unnecessary immunization.

Analysis of Variance↗

Protein kinase C and transmitter release.

1. Protein kinase C (PKC) is an important second messenger-activated enzyme. In noradrenergic nerves it appears to be tonically activated by diacylglycerol (DAG) to facilitate transmitter release and the steps in this involve activation of phospholipase C, generation of DAG and activation of PKC. It is suggested that the subsequent facilitation of transmitter release is due to the phosphorylation of proteins involved in the release process distal to Ca2+ entry, presumably those involved in vesicle dynamics. 2. There are differences between central noradrenergic neurons and sympathetic nerves. In central neurons PKC appears to be tonically active and its inhibition results in a decrease in noradrenaline release under most, if not all, conditions. 3. In sympathetic nerves PKC inhibitors only decrease transmitter release during high-frequency stimulation and not during low-frequency stimulation. At high frequency there is a gradual increase in the effect of PKC inhibitors on transmitter release during the first 15 s of a stimulation train. It is suggested that this is due to a progressive rise in intracellular Ca2+ and a consequent activation of PKC. 4. Activation of PKC by phorbol esters produces a large enhancement in action potential-evoked noradrenaline release in both the central nervous system and in peripheral tissues. The structural requirements of the phorbol esters for maximal effect suggest that the phorbol esters must access the interior of the nerve terminal to activate PKC and the neural membrane acts as a barrier for highly lipophilic phorbol esters, thereby reducing their activity. Activation of PKC represents one of the most powerful ways to enhance transmitter release and may have therapeutic potential.

Animals↗

Specific accumulation of inositol 1,4,5-trisphosphate in rabbit basilar artery in response to noradrenaline but not 5-hydroxytryptamine.

This study examined the ability of 5-hydroxytryptamine and noradrenaline to stimulate inositol 1,4,5-trisphosphate (IP3) mass accumulation in segments of the rabbit basilar artery. 5-Hydroxytryptamine (5-HT, 100 microM) failed to stimulate any significant accumulation of IP3 during the 5 min period following its application. In the presence of prazosin, 5-HT (300 microM) caused a rapid, transient decrease in IP3 accumulation which was significant after 5 s but had increased to pre-stimulation levels within 15 s. In contrast, noradrenaline (10 microM) stimulated a rapid, transient accumulation of IP3 which was significant after 5 s but had declined to basal levels after 60 s. In basilar artery segments bathed in Krebs solution containing 25.7 mM K+ (normal concentration 5.7 mM), the basal IP3 concentration was significantly elevated. The IP3 accumulation stimulated by either 5-HT or raised K+ was not reduced by the presence of the alpha 1-adrenoceptor antagonist, prazosin (0.1 microM). In the presence of raised K+, 5-hydroxytryptamine caused a rapid, transient inhibition of the K(+)-induced IP3 accumulation, which was maximal after 5 s but had increased to pre-stimulation levels within 30 s in the continued presence of 5-hydroxytryptamine. Noradrenaline did not affect the IP3 accumulation induced by raised extracellular [K+]. These results provide further evidence that IP3 is not involved in 5-hydroxytryptamine-induced smooth muscle contraction in the rabbit basilar artery, but support a role for this second messenger in the contraction induced in response to noradrenaline.

Animals↗

Characterisation of inositol 1,4,5-trisphosphate binding sites in rabbit aortic smooth muscle.

The present study investigated the characteristics of D-myo-inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) binding sites in crude membrane preparations of rabbit aortic smooth muscle. A particular aim was to demonstrate if increases in cytoplasmic cyclic guanosine 3':5' monophosphate (cGMP), which mediates the effect of nitrovasodilators, may cause smooth muscle relaxation in part by the displacement of Ins(1,4,5)P3 binding. Negligible Ins(1,4,5)P3 binding was observed at pH < 7, while maximum binding occurred over the pH range 8-9. Saturation analysis of isotopic dilution binding data revealed an apparently homogenous population of Ins(1,4,5)P3 binding sites with a KD of 4.02 +/- 0.53 nM and a Bmax of 27.7 +/- 4.6 fmol/mg protein. Heparin, an Ins(1,4,5)P3 receptor antagonist, inhibited binding with an IC50 of 11.43 +/- 2.81 micrograms/ml. The ability of other polyphosphate compounds to inhibit Ins(1,4,5)P3 binding in this preparation was also examined. D-myo-Inositol 1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P4), adenosine 5'-triphosphate (ATP) and guanosine 5'-triphosphate (GTP) inhibited Ins(1,4,5)P3 binding, although each was significantly less potent that Ins(1,4,5)P3. In contrast, cyclic guanosine 3':5' monophosphate (cGMP) did not significantly alter Ins(1,4,5)P3 binding in rabbit aortic smooth muscle. This observation suggests that competitive inhibition of Ins(1,4,5)P3 receptor binding is not an important consideration in cGMP-mediated vascular smooth muscle cell relaxation.

Adenine Nucleotides↗

Pediatric clinical clerkships are associated with an excess risk of acute infection.

OBJECTIVE: To determine the incidence of acute respiratory and gastrointestinal tract illness and associated absence by third-year medical students during pediatric and nonpediatric (control) clinical clerkships. DESIGN: A self-administered questionnaire was completed by students after the first 4 weeks of two pediatric clerkships (inpatient and outpatient) and two non-pediatric clerkships (obstetrics-gynecology and psychiatry). Information was obtained on the symptoms of acute respiratory and gastrointestinal tract illness and related absences. ANALYSIS: Results from each student's pediatric clerkship were compared with the results from the same student's control clerkship by means of matched-pair analysis. SUBJECTS: Students who made up the junior class at the University of Texas Southwestern Medical School at Dallas, July 1, 1990, to June 30, 1991. RESULTS: Of 177 students (77%) who completed questionnaires after one pediatric and one control clerkship, 108 students (61%) had had an acute illness while on pediatric clerkships in contrast to 69 students (39%) on control clerkships (odds ratio, 3.3; 95% confidence interval, 2.0 to 5.4; P < .001). More students were absent for illness during pediatric than control clerkships (23 [13%] vs nine [5%], respectively; odds ratio, 2.7; 95% confidence interval, 1.2 to 6.2; P = .02). The higher risk of illness during pediatric clerkships was not related to the order of the pediatric or control clerkship, the order of inpatient and outpatient pediatrics, or the season of the year. CONCLUSION: Pediatric clinical clerkships in the third year of medical school were associated with excess morbidity from acute infectious illness. Studies are needed to determine whether emphasizing infection control practices decrease this morbidity and any resulting nosocomial spread to patients.

Absenteeism↗

Estimating immunization coverage from school-based childhood immunization records.

To determine the accuracy of school-based childhood immunization records and to describe the effects of their use on estimates of community-wide immunization coverage, we verified the immunizations to 72 months of age for children born in 1986 to residents in Dallas County, TX, and in Minnesota. Verified immunizations were compared with those documented in the school record. Major transcription errors accounted for fewer than 1% of discrepancies between school and provider records. For 99 subjects with 987 verified immunizations in Minnesota, age-appropriate immunization coverage estimated from the school records was within two percent of actual coverage. For 86 subjects with 981 verified immunizations in Dallas County, age-appropriate immunization coverage from the school records underestimated actual coverage by as much as 21%. The primary factor explaining the underestimate in Dallas was incomplete school immunization records for 33 (38%) subjects and 126 (13%) immunizations. Selective recording of immunizations related to the minimum state requirements in Texas contributed to incomplete school records in Dallas County. Verification of the completeness of records selected to estimate immunization coverage is essential if the estimates are used to monitor trends or to make public policy decisions.

Child↗