Fitzsimons Army Medical Center

BACKGROUND: Analyzing apoptosis has been an integral component of many biological studies. However, currently available methods for quantifying apoptosis have various limitations including multiple, sometimes cell-damaging steps, the inability to quantify live, necrotic and apoptotic cells at the same time, and non-specific detection (i.e. "false positive"). To overcome the shortcomings of current methods that quantify apoptosis in vitro and to take advantage of the 96-well plate format, we present here a modified ethidium bromide and acridine orange (EB/AO) staining assay, which may be performed entirely in a 96-well plate. Our method combines the advantages of the 96-well format and the conventional EB/AO method for apoptotic quantification. RESULTS: We compared our method and the conventional EB/AO method for quantifying apoptosis of suspension cells (Jurkat) and adherent cells (A375) under normal growth and apoptosis-inducing conditions. We found that our new EB/AO method achieved quantification results comparable to those produced using the conventional EB/AO method for both suspension and adherent cells. CONCLUSION: By eliminating the detaching and washing steps, our method drastically reduces the time needed to perform the test, minimizes damage to adherent cells, and decreases the possibility of losing floating cells. Overall, our method is an improvement over the currently available techniques especially for adherent cells.

The myofascial trigger point (MTrP) is the hallmark physical finding of the myofascial pain syndrome (MPS). The MTrP itself is characterized by distinctive physical features that include a tender point in a taut band of muscle, a local twitch response (LTR) to mechanical stimulation, a pain referral pattern characteristic of trigger points of specific areas in each muscle, and the reproduction of the patient's usual pain. No prior study has demonstrated that these physical features are reproducible among different examiners, thereby establishing the reliability of the physical examination in the diagnosis of the MPS. This paper reports an initial attempt to establish the interrater reliability of the trigger point examination that failed, and a second study by the same examiners that included a training period and that successfully established interrater reliability in the diagnosis of the MTrP. The study also showed that the interrater reliability of different features varies, the LTR being the most difficult, and that the interrater reliability of the identification of MTrP features among different muscles also varies.

While studying the αβ T cell receptor repertoire in rheumatoid arthritis (RA) patients, we found that the frequency of V β 14 + T cells was significantly higher in the synovial fluid of affected joints than in the peripheral blood. In fact, V β 14 + T cells were virtually undetectable in the peripheral blood of a majority of these RA patients. β-chain sequences indicated that one or a few clones dominated the V β 14 + population in the synovial fluid of individual RA patients, whereas oligoclonality was less marked for other Vβ's and for V β 14 in other types of inflammatory arthritis. These results implicate V β 14-bearing T cells in the pathology of RA. They also suggest that the etiology of RA may involve initial activation of V β 14 + T cells by a V β 14-specific superantigen with subsequent recruitment of a few activated autoreactive V β 14 + T cell clones to the joints while the majority of other V β 14 + T cells disappear.

Available data indicate that cardiovascular disease has become the leading cause of death in American Indians. However, limited information is available on cardiovascular disease incidence, prevalence, and risk factors in this population. Reported cardiovascular disease rates vary greatly among groups in different geographic areas. These rates have been obtained from studies of varying sizes and different methodologies. The Strong Heart Study, which uses standardized methodology, is designed to estimate cardiovascular disease mortality and morbidity rates and the prevalence of known and suspected cardiovascular disease risk factors in American Indians. The study population consists of 12 tribes in three geographic areas: an area near Phoenix, Arizona, the southwestern area of Oklahoma, and the Aberdeen area of North and South Dakota. The study includes three components. The first is a mortality survey to estimate cardiovascular disease mortality rates for 1984-1988 among tribal members aged 35-74 years, and the second is a morbidity survey to estimate incidence of both first and first or recurrent hospitalized myocardial infarction and stroke (cerebrovascular disease) among tribal members aged 45-74 years in 1984-1988, and the third is a clinical examination of 4,500 tribal members aged 45-74 years in order to estimate the prevalence of cardiovascular disease and its associations with risk factors. Family history, diet, alcohol and tobacco consumption, physical activity, degree of acculturation, and socioeconomic status are assessed in personal interviews. The physical examination includes measurements of body fat, body circumferences, and blood pressure, an examination of the heart and lungs, an evaluation of peripheral vascular disease, and a 12-lead electrocardiogram. Laboratory measurements include fasting and postload glucose, insulin, fasting lipids, apoproteins, fibrinogen, and glycated hemoglobin. Also measured are serum and urine creatinine and urinary albumin. DNA from lymphocytes is isolated and stored for future genetic studies.

Journal Article RESPIRATORY VIRUS IMMUNIZATION: A FIELD TRIAL OF TWO INACTIVATED RESPIRATORY VIRUS VACCINES; AN AQUEOUS TRIVALENT PARATNFLUENZA VIRUS VACCINE AND AN ALUM-PRECIPITATED RESPIRATORY SYNCYTIAL VIRUS VACCINE Get access V. A. FULGINITI, V. A. FULGINITI 2Department of Pediatrics, University of Colorado Medical Center. Currently, Department of Pediatrics, University of Arizons College of MedicineTucson, Arizona 85721 Search for other works by this author on: Oxford Academic PubMed Google Scholar J. J. ELLER, J. J. ELLER 3Department of Pediatrics, University of Colorado Medical Center. Currently, Virology Section, U. S. Army Medical Research and Nutrition Laboratory, Fitzsimons General HospitalDenver, Colorado Search for other works by this author on: Oxford Academic PubMed Google Scholar O. F. SIEBER, O. F. SIEBER 4Pediatric Service, Fitzsimons General Hospital Search for other works by this author on: Oxford Academic PubMed Google Scholar J. W. JOYNER, J. W. JOYNER 5Department of Pediatrics, University of Colorado Medical Center Search for other works by this author on: Oxford Academic PubMed Google Scholar M. MINAMITANI, M. MINAMITANI 6Department of Pediatrics, University of Colorado Medical Center. Currently, University of TokyoTokyo, Japan Search for other works by this author on: Oxford Academic PubMed Google Scholar G. MEIKLEJOHN G. MEIKLEJOHN 7Department of Medicine, University of Colorado Medical Center Search for other works by this author on: Oxford Academic PubMed Google Scholar American Journal of Epidemiology, Volume 89, Issue 4, April 1969, Pages 435–448, https://doi.org/10.1093/oxfordjournals.aje.a120956 Published: 01 April 1969 Article history Received: 23 August 1968 Published: 01 April 1969

Aronstam, Elmore M. MC, U.S.A.; Hewlett, Thomas H. MC, U.S.A.; Orbison, James A. MC, U.S.A.; Franklin, Robert B. MC, U.S.A.; Dixon, Leon M. MC, U.S.A. Author Information

(1973). Laboratory Tests for the Assessment of Nutritional Status. CRC Critical Reviews in Clinical Laboratory Sciences: Vol. 4, No. 3, pp. 215-340.

Glycogen synthase kinase-3β (GSK-3β) is a critical activator of neuronal apoptosis induced by a diverse array of neurotoxic insults. However, the downstream substrates of GSK-3β that ultimately induce neuronal death are unknown. Here, we show that GSK-3β phosphorylates and regulates the activity of Bax, a pro-apoptotic Bcl-2 family member that stimulates the intrinsic (mitochondrial) death pathway by eliciting cytochrome c release from mitochondria. In cerebellar granule neurons undergoing apoptosis, inhibition of GSK-3β suppressed both the mitochondrial translocation of an expressed green fluorescent protein (GFP)-Bax α fusion protein and the conformational activation of endogenous Bax. GSK-3β directly phosphorylated Bax α on Ser163, a residue found within a species-conserved, putative GSK-3β phosphorylation motif. Coexpression of GFP-Bax α with a constitutively active mutant of GSK-3β, GSK-3β(Ser9Ala), enhanced the in vivo phosphorylation of wild-type Bax α , but not a Ser163Ala mutant of Bax α , in transfected human embryonic kidney 293 (HEK293) cells. Moreover, cotransfection with constitutively active GSK-3β promoted the localization of Bax α to mitochondria and induced apoptosis in both transfected HEK293 cells and cerebellar granule neurons. In contrast, neither a Ser163Ala point mutant of Bax α nor a naturally occurring splice variant that lacks 13 amino acids encompassing Ser163 (Bax σ ) were driven to mitochondria in HEK293 cells coexpressing constitutively active GSK-3β. In a similar manner, either mutation or deletion of the identified GSK-3β phosphorylation motif prevented the localization of Bax to mitochondria in cerebellar granule neurons undergoing apoptosis. Our results indicate that GSK-3β exerts some of its pro-apoptotic effects in neurons by regulating the mitochondrial localization of Bax, a key component of the intrinsic apoptotic cascade.

Many recent studies have demonstrated recruitment of chromatin-modifying enzymes to double-strand breaks. Instead, we wanted to examine chromatin modifications during the repair of these double-strand breaks. We show that homologous recombination triggers the acetylation of N-terminal lysines on histones H3 and H4 flanking a double-strand break, followed by deacetylation of H3 and H4. Consistent with a requirement for acetylation and deacetylation during homologous recombination, Saccharomyces cerevisiae with substitutions of the acetylatable lysines of histone H4, deleted for the N-terminal tail of histone H3 or H4, deleted for the histone acetyltransferase GCN5 gene or the histone deacetylase RPD3 gene, shows inviability following induction of an HO lesion that is repaired primarily by homologous recombination. Furthermore, the histone acetyltransferases Gcn5 and Esa1 and the histone deacetylases Rpd3, Sir2, and Hst1 are recruited to the HO lesion during homologous recombinational repair. We have also observed a distinct pattern of histone deacetylation at the donor locus during homologous recombination. Our results demonstrate that dynamic changes in histone acetylation accompany homologous recombination and that the ability to modulate histone acetylation is essential for viability following homologous recombination.

Absolute ethanol was used to perform nine transcatheter embolizations and 21 direct percutaneous puncture embolizations in eight patients with unresectable vascular malformations. Six patients had arteriovenous malformations and two patients had hemangiomas. Four of these patients had undergone unsuccessful surgery, and the other four were not considered candidates for operation. All large complex symptomatic vascular malformations (SVMs) required multiple embolizations that were staged procedures. Ethanol embolotherapy, performed according to strict techniques, has proved efficacious in the management of SVMs.

Activation of the mesolimbic dopamine reward pathway by acute ethanol produces reinforcement and changes in gene expression that appear to be crucial to the molecular basis for adaptive behaviors and addiction. The inbred mouse strains DBA/2J and C57BL/6J exhibit contrasting acute behavioral responses to ethanol. We used oligonucleotide microarrays and bioinformatics methods to characterize patterns of gene expression in three brain regions of the mesolimbic reward pathway of these strains. Expression profiling included examination of both differences in gene expression 4 h after saline injection or acute ethanol (2 g/kg). Using a rigorous stepwise method for microarray analysis, we identified 788 genes differentially expressed in control DBA/2J versus C57BL/6J mice and 307 ethanol-regulated genes in the nucleus accumbens, prefrontal cortex, and ventral tegmental area. There were strikingly divergent patterns of ethanol-responsive gene expression in the two strains. Ethanol-responsive genes also showed clustering at discrete chromosomal regions, suggesting local chromatin effects in regulation. Ethanol-regulated genes were generally related to neuroplasticity, but regulation of discrete functional groups and pathways was brain region specific: glucocorticoid signaling, neurogenesis, and myelination in the prefrontal cortex; neuropeptide signaling and developmental genes, including factor Bdnf , in the nucleus accumbens; and retinoic acid signaling in the ventral tegmental area. Bioinformatics analysis identified several potential candidate genes for quantitative trait loci linked to ethanol behaviors, further supporting a role for expression profiling in identifying genes for complex traits. Brain region-specific changes in signaling and neuronal plasticity may be critical components in development of lasting ethanol behavioral phenotypes such as dependence, sensitization, and craving.

INTRODUCTION: Transforming growth factor (TGF)-beta suppresses breast cancer formation by preventing cell cycle progression in mammary epithelial cells (MECs). During the course of mammary tumorigenesis, genetic and epigenetic changes negate the cytostatic actions of TGF-beta, thus enabling TGF-beta to promote the acquisition and development of metastatic phenotypes. The molecular mechanisms underlying this conversion of TGF-beta function remain poorly understood but may involve signaling inputs from integrins. METHODS: beta3 Integrin expression or function in MECs was manipulated by retroviral transduction of active or inactive beta3 integrins, or by transient transfection of small interfering RNA (siRNA) against beta3 integrin. Altered proliferation, invasion, and epithelial-mesenchymal transition (EMT) stimulated by TGF-beta in control and beta3 integrin manipulated MECs was determined. Src involvement in beta3 integrin mediated alterations in TGF-beta signaling was assessed by performing Src protein kinase assays, and by interdicting Src function pharmacologically and genetically. RESULTS: TGF-beta stimulation induced alphavbeta3 integrin expression in a manner that coincided with EMT in MECs. Introduction of siRNA against beta3 integrin blocked its induction by TGF-beta and prevented TGF-beta stimulation of EMT in MECs. beta3 integrin interacted physically with the TGF-beta receptor (TbetaR) type II, thereby enhancing TGF-beta stimulation of mitogen-activated protein kinases (MAPKs), and of Smad2/3-mediated gene transcription in MECs. Formation of beta3 integrin:TbetaR-II complexes blocked TGF-beta mediated growth arrest and increased TGF-beta mediated invasion and EMT. Dual beta3 integrin:TbetaR-II activation induced tyrosine phosphorylation of TbetaR-II, a phosphotransferase reaction mediated by Src in vitro. Inhibiting Src activity in MECs prevented the ability of beta3 integrin to induce TbetaR-II tyrosine phosphorylation, MAPK activation, and EMT stimulated by TGF-beta. Lastly, wild-type and D119A beta3 integrin expression enhanced and abolished, respectively, TGF-beta stimulation of invasion in human breast cancer cells. CONCLUSION: We show that beta3 integrin alters TGF-beta signaling in MECs via Src-mediated TbetaR-II tyrosine phosphorylation, which significantly enhanced the ability of TGF-beta to induce EMT and invasion. Our findings suggest that beta3 integrin interdiction strategies may represent an innovative approach to re-establishing TGF-beta mediated tumor suppression in progressing human breast cancers.

Quantitation of the hepatitis C virus (HCV) provides a powerful epidemiologic and therapeutic method for the evaluation of infected patients. In this study semiquantitative reverse transcriptase polymerase chain reaction (PCR) is compared with a new branched DNA signal amplification methodology. Samples from HCV-infected patients as well as from human immunodeficiency virus-infected patients were evaluated. Reverse transcriptase PCR correlated well with the branched DNA assay (r = 0.7036, P < 0.05). HCV RNA was found to occur at significantly higher titers (P < 0.05) in patients coinfected with the human immunodeficiency virus compared with titers in those infected with HCV alone. Immune status as defined by the CD4+ count was not associated with the observed difference in viral titer.

Although coronary heart disease (CHD) is currently the leading cause of death among American Indians, information on the prevalence of CHD and its association with known cardiovascular risk factors is limited. The Strong Heart Study was initiated in 1988 to quantify cardiovascular disease and its risk factors among three geographically diverse groups of American Indians. Members of 13 Indian communities in Arizona, Oklahoma, and South and North Dakota between 45 and 74 years of age underwent a physical examination that included medical history; an electrocardiogram; anthropometric and blood pressure measurements; an oral glucose tolerance test; and measurements of fasting plasma lipoproteins, fibrinogen, insulin, hemoglobin A1c, and urinary albumin. Prevalence rates of definite myocardial infarction and definite CHD were higher in men than in women at all three centers (p < 0.0001) and higher in those with diabetes mellitus (p = 0.002 in men and p = 0.0003 in women). Diabetes was associated with relatively higher prevalence rates of myocardial infarction (diabetic:nondiabetic prevalence ratio = 3.8 vs. 1.9) and CHD (prevalence ratio = 4.6 vs. 1.8) in women than in men. Prevalence rates of heart disease were lowest in the communities in Arizona; prevalence rates were similar in Oklahoma and South Dakota/North Dakota and were two- to threefold higher than those in Arizona. By logistic regression, prevalent CHD among American Indians was significantly and independently related to age, diabetes, hypertension, albuminuria, percentage of body fat, smoking, high concentrations of plasma insulin, and low concentrations of high density lipoprotein cholesterol. In contrast to reports from other non-Indian populations, diabetes was the strongest risk factor. The lower prevalence of CHD among Indians in Arizona is distinctive in view of their higher rates of diabetes, obesity, hypertension, and albuminuria, but it may be partly related to their low frequency of smoking and their low concentrations of total and low density lipoprotein cholesterol. These findings from the initial Strong Heart Study examination emphasize the importance of diabetes and its associated variables as risk factors for CHD in Native American populations.

Clinical presentations, laboratory features, and responses to therapy of 102 patients treated at an army medical center for genitourinary tuberculosis between January 1961 and September 1972 are described. During that time, a total of 3109 patients had been treated for tuberculosis of all types. The study group included 72 men aged 18-59 with a mean age of 29, and 31 women aged 17-66, with a mean age of 31. There was often a latent period of 20 years or more between infection with the tubercle bacillus and the expression of genitourinary tuberculosis. The principal means of diagnosis was isolation of Mycobacterium tuberculosis from urine, obtained in 80%, or sputum, obtained in 38%. M. tuberculosis was not cultured in 13 patients. In patients with negative cultures, diagnosis was made by combinations of positive tuberculin skin test, caseating granulomata on biopsy, characteristic changes in the excretory urogram, characteristic bladder lesions on cystoscopy, and the presence of sterile pyuria or microscopic hematuria. A wide variety of signs and symptoms were encountered as was a high frequency of involvement of other organ systems. The most common laboratory abnormalities were pyuria, albuminuria, and hematuria. 75% of patients had an abnormal chest roentgenogram on admission. 88% of patients tested had positive skin tests and 63% tested had abnormal excretory urography. 16% showed renal calcification. Only 1 nephrectomy was done in the latter 5 years of the study, for hypertension. 2 women and 6 men had hypertension, but 1 woman and 2 men had nontuberculous renal disease which could have caused the hypertension. The evidence from the series is that infectivity of genitourinary tuberculosis is low. There was only 1 initial treatment failure, in a 47-year old man with active pulmonary and renal tuberculosis caused by an isoniazid-resistant organism. 2 men, only 1 of whom had had genitourinary disease originally, had recurrences of tuberculous disease after prematurely discontinuing medication.

STUDY DESIGN: Postoperative radiographs and computed tomography scans were used to evaluate 74 pedicle screws in 16 consecutive patients who underwent lumbar spine fusion with pedicle screw fixation. OBJECTIVE: To evaluate pedicle screw placement using plain radiographs versus computed tomographic scans. SUMMARY OF BACKGROUND DATA: Plain radiographs are the primary means of assessing pedicle screw placement. Comparison of plain radiographs and computed tomography has not been done. METHODS: Screws were graded as IN, OUT, or QUESTIONABLE; the direction of misplacement was noted. All evaluations were performed independently by three observers. RESULTS: Fewer screws were clearly within the pedicle on computed tomography when compared with plain radiographs. Computed tomography showed 10 times as many screws violating the medial cortex as did radiographs. Interobserver differences were not statistically significant. Intraobserver differences approached statistical significance when the two tests were compared. No recognized neurologic complications resulted from pedicle screw placement. CONCLUSIONS: Plain radiographs alone may not accurately reveal pedicle screw placement. Plain radiographs and thin section computed tomographic scans should be used to evaluate postoperative neurologic deficits in patients undergoing instrumented lumbar spine fusion with pedicle screws.

OBJECTIVE: To estimate prevalence rates of diabetes and impaired glucose tolerance (IGT) in three American Indian populations, using standardized diagnostic criteria, and to assess the association of diabetes with the following selected possible risk factors: age, obesity, family history of diabetes, and amount of Indian ancestry. RESEARCH DESIGN AND METHODS: This cross-sectional study involved enrolled members, men and women aged 45-74 years, of 13 American Indian tribes or communities in Arizona, Oklahoma, and South and North Dakota. Eligible participants were invited to the clinic for a personal interview and a physical examination. Diabetes and IGT status were defined by the World Health Organization criteria and were based on fasting plasma glucose and oral glucose tolerance test results. Data on age, family history of diabetes, and amount of Indian ancestry were obtained from the personal interview, and measures of obesity included body mass index, percentage body fat, and waist-to-hip ratio. RESULTS: A total of 4,549 eligible participants were examined, and diabetes status was determined for 4,304 (1,446 in Arizona, 1,449 in Oklahoma, and 1,409 in the Dakotas). In all three centers, diabetes was more prevalent in women than in men. Arizona had the highest age-adjusted rates of diabetes: 65% in men and 72% in women. Diabetes rates in Oklahoma (38% in men and 42% in women) and South and North Dakota (33% in men and 40% in women), although considerably lower than in Arizona, were several times higher than those reported for the U.S. population. Rates of IGT among the three populations (14-17%) were similar to those in the U.S. population. Diabetes rates were positively associated with age, level of obesity, amount of Indian ancestry, and parental diabetes status. CONCLUSIONS: Diabetes is found in epidemic proportions in Native American populations. Prevention programs and periodic screening should be implemented among American Indians. Standards of care and intervention have been developed by the Indian Health Service for individuals in whom diabetes is diagnosed. These programs should be expanded to include those with IGT to improve glycemic control or to reduce the risk of development of diabetes as well as to reduce the risk of diabetic complications.

In the course of studying the circulating TCR repertoire in humans, we noted several individuals with an increase in the percentage of CD8+ T cells expressing a particular V region. In some cases, these CD8 expansions were dramatic, occupying over 40% of the total CD8 repertoire. Using a panel of mAbs to different TCR V regions, we found that over 30% of healthy adults (> 35 years of age) harbor an expansion that alters the peripheral blood CD8 TCR repertoire. A wide range of V regions were expressed by these expansions. Considering that the mAbs used cover only a portion of the V beta repertoire, the data suggest that over 70% of adults are likely to harbor such expansions. Junctional region sequencing showed that the CD8 subset expansions were clonal, and serial studies as long as 4 years showed that they persisted indefinitely. Expansions were not identified in the CD4 population. Discordant expression of one large V beta 6.7+ clone was found in one identical twin set, suggesting the possibility that an environmental exposure is involved in their generation and/or expansion. In one large family, we found five family members with a large CD8 subset expansion. Remarkably similar usage of J beta regions was noted, and two individuals demonstrated V beta 3-expressing clones with homologous CDR3 regions, differing by only one major substitution. The repertoire data from this family suggest that the T cell clones have arisen in response to a common Ag. Studies of patients with rheumatoid arthritis found a significantly increased frequency of circulating CD8 subset expansions that expressed a different V region repertoire compared with the healthy individuals studied. Overall, our results emphasize a frequent alteration in the human CD8 TCR repertoire, most likely related to an environmental exposure, in both healthy individuals and patients with rheumatoid arthritis. The presence of these expansions will be important to consider in any study of human TCR repertoire, and their implication for health and disease will be important to understand.

BACKGROUND: Deposition of calcium in skin is currently categorized into a group of disorders referred to as calcinosis cutis. Divisions between types and subtypes within this confusing classification are predominantly based on morphologic differences in the calcification and serve to obscure pathogenesis. This is especially evident in a subtype of calcinosis cutis, known as tumoral calcinosis. Calcifications in cases of tumoral calcinosis share the following characteristics, but without evidence of a common pathogenesis: large size, juxtaarticular location, progressive enlargement over time, a tendency to recur after surgical removal, and an ability to encase adjacent normal structures. The goal of this study was to formulate a pathogenesis-based classification for cases of tumoral calcinosis. METHODS: In a literature review 121 cases of tumoral calcinosis were identified. These cases, along with a case evaluated in our clinic, were reviewed retrospectively, and their features compared. RESULTS: Analysis suggests three pathogenetically distinct subtypes of tumoral calcinosis: (1) Primary normophosphatemic tumoral calcinosis: patients have normal serum phosphate, normal serum calcium, and no evidence of disorders previously associated with soft tissue calcification; (2) primary hyperphosphatemic tumoral calcinosis: patents have elevated serum phosphate, normal serum calcium, and no evidence of disorders previously associated with soft tissue calcification; and (3) secondary tumoral calcinosis: patients have a concurrent disease capable of causing soft tissue calcification. Justification for this classification is based on the presence or absence of disorders known to promote soft tissue calcification and statistically significant differences in family history, mean calcification number, mean serum phosphate level, and calcification recurrence after excision. CONCLUSIONS: A classification for tumoral calcinosis is devised that outlines potential pathogenetic mechanisms and predicts response to therapy and prognosis. Analysis of other forms of calcinosis cutis may reveal definable pathogenetic differences that suggest a coherent classification for all cutaneous calcinoses.

Journal Article Efficacy of Infection Control Measures During a Nosocomial Outbreak of Disseminated Aspergillosis Associated with Hospital Construction Get access Steven M. Opal, Steven M. Opal Department ofMedicine and the Infection Control Service, Fitzsimons Army Medical Center, Aurora, Colorado Search for other works by this author on: Oxford Academic PubMed Google Scholar Arnold A. Asp, Arnold A. Asp Department ofMedicine and the Infection Control Service, Fitzsimons Army Medical Center, Aurora, Colorado Search for other works by this author on: Oxford Academic PubMed Google Scholar Preston B. Cannady, Preston B. Cannady Department ofMedicine and the Infection Control Service, Fitzsimons Army Medical Center, Aurora, Colorado Search for other works by this author on: Oxford Academic PubMed Google Scholar Pari L. Morse, Pari L. Morse Department ofMedicine and the Infection Control Service, Fitzsimons Army Medical Center, Aurora, Colorado Search for other works by this author on: Oxford Academic PubMed Google Scholar Linda J. Burton, Linda J. Burton Department ofMedicine and the Infection Control Service, Fitzsimons Army Medical Center, Aurora, Colorado Search for other works by this author on: Oxford Academic PubMed Google Scholar Phillip G. Hammer Phillip G. Hammer Department ofMedicine and the Infection Control Service, Fitzsimons Army Medical Center, Aurora, Colorado Search for other works by this author on: Oxford Academic PubMed Google Scholar The Journal of Infectious Diseases, Volume 153, Issue 3, March 1986, Pages 634–637, https://doi.org/10.1093/infdis/153.3.634 Published: 01 March 1986 Article history Received: 07 June 1985 Revision received: 26 September 1985 Published: 01 March 1986