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Dive into the research topics where Ronald L. Moolenaar is active.

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Featured researches published by Ronald L. Moolenaar.


The New England Journal of Medicine | 1994

Hantavirus Pulmonary Syndrome: A Clinical Description of 17 Patients with a Newly Recognized Disease

Jeffrey S. Duchin; Frederick Koster; Clarence J. Peters; Gary Simpson; Bruce Tempest; Sherif R. Zaki; Thomas G. Ksiazek; Pierre E. Rollin; Stuart T. Nichol; Edith Umland; Ronald L. Moolenaar; Susan E. Reef; Kurt B. Nolte; Margaret M. Gallaher; Jay C. Butler; Robert F. Breiman

Background In May 1993 an outbreak of severe respiratory illness occurred in the southwestern United States. A previously unknown hantavirus was identified as the cause. In Asia hantaviruses are associated with hemorrhagic fever and renal disease. They have not been known as a cause of human disease in North America. Methods We analyzed clinical, laboratory, and autopsy data on the first 17 persons with confirmed infection from this newly recognized strain of hantavirus. Results The mean age of the patients was 32.2 years (range, 13 to 64); 61 percent were women, 72 percent were Native American, 22 percent white, and 6 percent Hispanic. The most common prodromal symptoms were fever and myalgia (100 percent), cough or dyspnea (76 percent), gastrointestinal symptoms (76 percent), and headache (71 percent). The most common physical findings were tachypnea (100 percent), tachycardia (94 percent), and hypotension (50 percent). The laboratory findings included leukocytosis (median peak cell count, 26,000 per cu...


American Journal of Emergency Medicine | 2009

Acute health effects after exposure to chlorine gas released after a train derailment

David Van Sickle; Mary Anne Wenck; Amy Belflower; Dan Drociuk; Jill M. Ferdinands; Fernando Holguin; Erik Svendsen; Lena Bretous; Shirley Jankelevich; James J. Gibson; Paul Garbe; Ronald L. Moolenaar

In January 2005, a train derailment on the premises of a textile mill in South Carolina released 42 to 60 tons of chlorine gas in the middle of a small town. Medical records and autopsy reports were reviewed to describe the clinical presentation, hospital course, and pathology observed in persons hospitalized or deceased as a result of chlorine gas exposure. Eight persons died before reaching medical care; of the 71 persons hospitalized for acute health effects as a result of chlorine exposure, 1 died in the hospital. The mean age of the hospitalized persons was 40 years (range, 4 months-76 years); 87% were male. The median duration of hospitalization was 4 days (range, 1-29 days). Twenty-five (35%) persons were admitted to the intensive care unit; the median length of stay was 3 days. Many surviving victims developed significant pulmonary signs and severe airway inflammation; 41 (58%) hospitalized persons met PO2/FiO2 criteria for acute respiratory distress syndrome or acute lung injury. During their hospitalization, 40 (57%) developed abnormal x-ray findings, 74% of those within the first day. Hypoxia on room air and PO2/FiO2 ratio predicted severity of outcome as assessed by the duration of hospitalization and the need for intensive care support. This community release of chlorine gas caused widespread exposure and resulted in significant acute health effects and substantial health care requirements. Pulse oximetry and arterial blood gas analysis provided early indications of outcome severity.


Chest | 2009

Racial and ethnic disparities in asthma medication usage and health-care utilization: data from the National Asthma Survey.

Deidre Crocker; Clive Brown; Ronald L. Moolenaar; Jeanne E. Moorman; Cathy M. Bailey; David M. Mannino; Fernando Holguin

BACKGROUND Despite the availability of effective treatment, minority children continue to experience disproportionate morbidity from asthma. Our objective was to identify and characterize racial and ethnic disparities in health-care utilization and medication usage among US children with asthma in a large multistate asthma survey. METHODS We analyzed questions from the 2003-2004 four-state sample of the National Asthma Survey to assess symptom control, medication use, and health-care utilization among white, black, and Hispanic children < 18 years old with current asthma who were residing in Alabama, California, Illinois, or Texas. RESULTS Of the 1,485 children surveyed, 55% were white, 25% were Hispanic, and 20% were black. Twice as many black children had asthma-related ED visits (39% vs 18%, respectively; p < 0.001) and hospitalizations (12% vs 5%, respectively; p = 0.02) compared with white children. Significantly fewer black and Hispanic children reported using inhaled corticosteroids (ICSs) in the past 3 months (21% and 22%, respectively) compared to white children (33%; p = 0.001). Additionally, 26% of black children and 19% of Hispanic children reported receiving a daily dose of a short-acting beta-agonist compared with 12% of white children (p = 0.001). ED visits were positively correlated with short-acting beta-agonist use and were negatively correlated with ICS use when stratified by race/ethnicity. CONCLUSIONS Children with asthma in this large, multistate survey showed a dramatic underuse of ICSs. Black and Hispanic children compared with white children had more indicators of poorly controlled asthma, including increased emergency health-care utilization, more daily rescue medication use, and lower use of ICSs, regardless of symptom control.


Archives of Environmental Health | 1994

Methyl Tertiary Butyl Ether in Human Blood after Exposure to Oxygenated Fuel in Fairbanks, Alaska

Ronald L. Moolenaar; Brockton J. Hefflin; David L. Ashley; John P. Middaugh; Ruth A. Etzel

Residents of Fairbanks, Alaska reported health complaints when 15%, by volume, methyl tertiary butyl ether (MTBE) was added to gasoline during an oxygenated fuel program. We conducted an exposure survey to investigate the effect of the program on human exposure to MTBE. We studied 18 workers in December 1992 during the program and 28 workers in February 1993 after the program was suspended. All workers were heavily exposed to motor vehicle exhaust or gasoline fumes. In December, the median post-shift blood concentration of MTBE in the workers was 1.8 micrograms/l (range, 0.2-37.0 micrograms/l), and in February the median post-shift blood concentration of MTBE in the 28 workers was 0.24 micrograms/l (range, 0.05-1.44 micrograms/l; p = .0001). Blood MTBE levels were measurably higher during the oxygenated fuel program in Fairbanks than after the program was suspended.


Annals of Internal Medicine | 2005

An Outbreak of Hepatitis C Virus Infections among Outpatients at a Hematology/Oncology Clinic

Alexandre Macedo de Oliveira; Kathryn L. White; Dennis P. Leschinsky; Brady D. Beecham; Tara M. Vogt; Ronald L. Moolenaar; Joseph F. Perz

Context Hepatitis C virus (HCV) may be transmitted through health careassociated exposure involving poor aseptic technique. Contribution In an outpatient hematology/oncology clinic, 99 patients who did not have previously known HCV infection acquired the virus, apparently because a health care worker reused contaminated syringes and saline bags. Cautions Researchers may have missed some cases because the investigation occurred more than a year after the outbreak. Implications We need active, effective infection-control programs for outpatient care settings. The Editors Hepatitis C virus (HCV) infection is a leading cause of chronic liver disease in the United States (1). It is transmitted primarily through percutaneous exposure to contaminated blood (2). Health careassociated HCV transmission has been attributed to breaches in aseptic technique (3-5). In September 2002, a gastroenterologist notified the Office of Epidemiology at the Nebraska Health and Human Services System in Lincoln, Nebraska, of a cluster of 4 HCV genotype 3a infections in patients who received care at a single outpatient clinic in eastern Nebraska. Because these patients reported no typical risk factors for HCV infection and genotype 3a accounts for less than 8% of HCV infections in the United States, we suspected health careassociated transmission (1). The implicated facility was an independently owned and operated hematology/oncology clinic located inside a hospital complex. The clinic opened in January 1998, and approximately 500 patient visits occurred per month. The staff comprised an oncologist, a registered nurse, a certified nurse assistant, and a secretary. In October 2002, 1 month after the gastroenterologists report, the clinic voluntarily closed. We compared clinic patient lists with Nebraskas HCV, HIV, and hepatitis B virus (HBV) registries and identified a patient with preexisting chronic HCV genotype 3a infection who enrolled at the clinic in March 2000. We found no evidence of HIV or HBV transmission. Preliminary interviews with clinic staff revealed that the nurse who had worked at the clinic since its opening was dismissed in July 2001 because of breaches in infection- control practices. We initiated an investigation to confirm the hypothesis of health careassociated transmission and to determine the extent of the outbreak and its mechanism of transmission. Methods Case Finding and Laboratory Testing Using clinic records, we identified all patients who visited the clinic from March 2000 through December 2001. We contacted all living patients and offered them free HCV testing. Structured in-person interviews were conducted in a private setting with participating patients to assess their medical history, including previous hepatitis diagnosis and risk factors for HCV infection. All specimens were tested for HCV antibodies by using enzyme immunoassay (EIA) (Abbott HCV EIA 2.0, Abbott Laboratories, Abbott Park, Illinois). Positive results on EIA were confirmed by using recombinant immunoblot assay (RIBA) (Chiron RIBA HCV 3.0 SIA, Chiron Corp., Emeryville, California) or HCV qualitative polymerase chain reaction (PCR) (Cobas Amplicor HCV Test v2.0, Roche Molecular Diagnostic Systems, Branchburg, New Jersey) (6). Because of concerns that immunosuppressed patients could have impaired antibody response, we also tested specimens from patients seen before July 2001 by using a transcription-mediated amplification (TMA) assay (Gen-Probe Inc., San Diego, California). A positive HCV test result was defined as a positive finding on TMA or a confirmed positive finding on EIA. Samples that were positive on PCR or TMA were genotyped by using gene sequencing of the 5 untranslated region (PE Applied Biosystems, Foster City, California). Epidemiologic Investigation We reviewed and abstracted the medical records and medication sheets of the tested patients using structured forms to identify clinic-associated risk factors for HCV transmission, such as number of clinic visits, presence of a central venous catheter, and percutaneous exposures. A case was defined as a positive HCV test result in a clinic patient treated from March 2000 through December 2001 who did not have evidence of preexisting HCV infection (that is, abnormal alanine aminotransferase [ALT] levels or positive HCV test results) before enrollment at the clinic. We considered the date of HCV infection onset to be the date when an ALT level greater than 3 times the upper limit of normal was first recorded (7). We conducted a cohort analysis to evaluate the association between exposures at the clinic and HCV infection. To further evaluate the variables associated with HCV infection in the cohort analysis and to investigate potential confounding among these variables, we performed an analysis that focused on risk factor exposure during the period of probable transmission (Appendix). Review of Infection-Control Practices The physician and nurse who worked at the clinic during the outbreak period were unavailable or unwilling to submit to interviews and HCV testing. We interviewed other health care workers and patients to corroborate staff adherence to infection-control standards. Statistical Analysis We made comparisons by using the t-test, the Fisher exact test, or the chi-square test, as appropriate (Epi Info, version 3.01, 2003, Centers for Disease Control and Prevention, Atlanta, Georgia). P values less than 0.05 were considered statistically significant. Results Case Finding and Laboratory Testing A total of 842 patients attended the clinic from March 2000 through December 2001. We contacted the 613 (73%) living patients; 494 of these (81%) agreed to testing. Twenty-one tested patients whose medical charts could not be located were excluded from analysis. No cases were seen among the 103 tested patients who began treatment after the nurses dismissal in July 2001. Therefore, we defined our study period as March 2000 to July 2001 and considered only exposures that occurred during this period. Among the 370 eligible patients, 101 tested positive for HCV: 80 were EIA positive and PCR positive; 18 were EIA negative but TMA positive; and 3 were EIA positive, PCR negative, and RIBA positive. One patient with inconclusive HCV test results (positive EIA, negative PCR and TMA, and indeterminate RIBA results) was excluded from analysis. We also excluded 2 persons with evidence of preexisting HCV infection. One visited the clinic only once, in March 2001, and had elevated ALT levels before that visit. The other person was the presumed outbreak source-patient identified during our preliminary investigation. This patient enrolled at the clinic in March 2000 with preexisting chronic HCV genotype 3a infection (viral load > 200000 copies/mL); a central venous catheter was implanted at that time. The resulting cohort of 367 patients seen at the clinic from March 2000 to July 2001 consisted of 99 HCV-positive patients who lacked evidence of preexisting HCV infection and met the case definition and 268 HCV-negative patients. The overall attack rate was 27% (99 of 367 patients). Genotype 3a was identified in 95 (96%) cases; in 4 cases, low levels or absence of HCV RNA precluded genotype determination. Epidemiologic Investigation Descriptive Epidemiology Most infected patients were female (60%), and the median age was 66 years (range, 21 to 95 years). Ninety-five of the 99 patients (96%) had cancer as an underlying disease, and the median number of clinic visits was 21 (range, 3 to 78 visits). Signs and symptoms of acute HCV infection were uncommon: Four (4%) patients had clinical jaundice, and 16 (16%) reported nausea. We estimated an onset date of infection for 56 (57%) case-patients (Figure). Only 2 (2%) case-patients exhibited spontaneous viral clearance (that is, undetectable HCV RNA) at the time of the investigation. Figure. Number of cases of hepatitis C virus infection, by estimated onset date ( n = 56) (Nebraska, March 2000July 2001). Eighty-three (84%) infected patients had a central venous catheter in place while receiving care at the clinic. Twenty-six (26%) infected patients did not receive any intravenous drug at the clinic during the outbreak period, but did have catheters flushed with saline solution. All 99 patients who developed HCV infection visited the clinic the same day as a previously HCV-infected patient and had saline flushes on those days. Analytic Epidemiology Among the 367 patients in the cohort analysis, 140 (38%) received 1 or more saline flushes during the study period (Table 1). Of those, 99 (71%) became infected, compared with no infection among the 227 patients who did not receive a saline flush during that time (relative risk, undefined; P< 0.001). Bivariate analysis also indicated an association between HCV infection and 5 other variables: sex, underlying diagnosis, presence of central venous catheter, exposure to subcutaneous injections, and number of clinic visits. Table 1. Attack Rates of Hepatitis C Virus Infection, by Demographic and Selected Clinical Characteristics, among 367 Tested Patients at the Hematology/Oncology Clinic, March 2000July 2001 In the multivariable analysis using the case-patients with estimated date of onset, only the number of saline flushes remained significantly associated with HCV infection in our model (adjusted odds ratio, 2.1 [95% CI, 1.3 to 3.2]) (Table 2; methods described in Appendix). Of note, the 10 case-patients with the earliest onset dates all received a saline flush on a day when the source-patient visited the clinic (Appendix Figure). Appendix Figure. Timeline of clinic visits for the 10 case-patients with the earliest dates of onset and for the source-patient (Nebraska, March 2000July 2001). Table 2. Unconditional Multivariable Analysis of Risk Factors for Hepatitis C Virus Infection Using the 56 Case-Patients with Estimated Dates of Onset and 56 Controls, March 2000July 2001 Review of Infection-Control Practices Our i


Infection Control and Hospital Epidemiology | 2004

A large nosocomial outbreak of hepatitis C and hepatitis B among patients receiving pain remediation treatments.

R. Dawn Comstock; Sue Mallonee; Jan L. Fox; Ronald L. Moolenaar; Tara M. Vogt; Joseph F. Perz; Beth P. Bell; James M. Crutcher

BACKGROUND AND OBJECTIVE In August 2002, the Oklahoma State Department of Health received a report of six patients with unexplained hepatitis C virus (HCV) infection treated in the same pain remediation clinic. We investigated the outbreaks extent and etiology. DESIGN, SETTING, AND PARTICIPANTS We conducted a retrospective cohort study of clinic patients, including a serologic survey, interviews of infected patients, and reviews of medical records and staff infection control practices. Patients received outpatient pain remediation treatments one afternoon a week in a clinic within a hospital. Cases were defined as HCV or hepatitis B virus (HBV) infections among patients who reported no prior diagnosis or risk factors for disease or reported previous risk factors but had evidence of acute infection. RESULTS Of 908 patients, 795 (87.6%) were tested, and 71 HCV-infected patients (8.9%) and 31 HBV-infected patients (3.9%) met the case definition. Multiple HCV genotypes were identified. Significantly higher HCV infection rates were found among individuals treated after an HCV-infected patient during the same visit (adjusted odds ratio [AOR], 6.2; 95% confidence interval [CI95], 2.4-15.8); a similar association was observed for HBV (AOR, 2.9; CI95, 1.3-6.5). Review of staff practices revealed the nurse anesthetist had been using the same syringe-needle to sequentially administer sedation medications to every treated patient each clinic day. CONCLUSIONS Reuse of needles-syringes was the mechanism for patient-to-patient transmission of HCV and HBV in this large nosocomial outbreak. Further education and stricter oversight of infection control practices may prevent future outbreaks.


Journal of Food Protection | 2004

A multistate outbreak of Salmonella enterica serotype typhimurium infection linked to raw milk consumption--Ohio, 2003.

Jacek M. Mazurek; Ellen Salehi; Dennis Propes; Jo Holt; Tammy Bannerman; Lisa Nicholson; Mark Bundesen; Rosemary E. Duffy; Ronald L. Moolenaar

In December 2002, the Ohio Department of Health was notified of two children with Salmonella infection. Both had a history of drinking raw milk from a combination dairy-restaurant-petting zoo (dairy). The dairy was the only establishment in Ohio licensed to sell raw milk and reported 1.35 million visitors annually. We investigated to determine the extent of the outbreak and identify illness risk factors. A case patient was any person with pulsed-field gel electrophoresis-matched Salmonella enterica serotype Typhimurium from 30 November 2002 to 18 February 2003. Sixty-two met the confirmed case definition. Forty dairy case patient patrons were included in a case-control study; 56 controls were their well meal companions. Consumption of raw milk was found to be associated with illness (odds ratio, 45.1; 95% confidence interval, 8.8 to 311.9). The dairy discontinued selling raw milk. Because 27 other states still allow the sale of raw milk, awareness of the hazards of its consumption should be raised and relevant regulations carefully reviewed.


Environmental Research | 2008

Resident cleanup activities, characteristics of flood-damaged homes and airborne microbial concentrations in New Orleans, Louisiana, October 2005

Margaret A. Riggs; Carol Y. Rao; Clive Brown; David Van Sickle; Kristin J. Cummings; Kevin H. Dunn; James A. Deddens; Jill M. Ferdinands; David Callahan; Ronald L. Moolenaar; Lynne E. Pinkerton

BACKGROUND Flooding in the greater New Orleans (GNO) area after the hurricanes caused extensive mold growth in homes resulting in public health concerns. OBJECTIVES We conducted an environmental assessment of homes to determine the extent and type of microbial growth. METHODS We randomly selected 112 homes, stratified by water damage, and then visually assessed mold growth. Air samples from a subset of 20 homes were analyzed for culturable fungi, fungal spores, and markers of mold ((1-->3, 1-->6)-beta-D-glucans) and bacteria (endotoxin). RESULTS Visible mold growth occurred in 49 (44%) homes; 18 (16%) homes had >50% mold coverage. Flood levels were >6 ft at 20 (19%), 3-6 ft at 20 (19%), and <3 ft at 28 (26%) homes out of 107; no flooding at 39 (36%) homes. The residents spent an average of 18 h (range: 1-84) doing heavy cleaning and of those, 22 (38%) reported using an N-95 or other respirator. Visible mold growth was significantly associated with flood height 3 ft and the predominant fungi indoors were Aspergillus and Penicillium species, which were in higher concentrations in homes with a flood level 3 ft. Geometric mean (GM) levels of endotoxin were as high as 40.2 EU/m(3), while GM glucan levels were as high as 3.5 microg/m(3) even when flooding was 3 ft. CONCLUSIONS Based on our observations of visible mold, we estimated that elevated mold growth was present in 194,000 (44%) homes in the GNO area and 70,000 (16%) homes had heavy mold growth. Concentrations of endotoxin and glucans exceeded those previously associated with health effects. With such high levels of microbial growth following flooding, potentially harmful inhalation exposures can be present for persons entering or cleaning affected homes. Persons exposed to water-damaged homes should follow the CDC recommendations developed following the 2005 hurricanes for appropriate respiratory precautions.


Seminars in Pediatric Infectious Diseases | 1997

Hantavirus pulmonary syndrome

Ralph T. Bryan; Timothy J. Doyle; Ronald L. Moolenaar; Anne K. Pflieger; Ali S. Khan; Thomas G. Ksiazek; Clarence J. Peters

Hantavirus Pulmonary Syndrome (HPS)1 is an acute zoonotic viral disease often characterized by fever, myalgia, and gastrointestinal complaints followed by the abrupt onset of respiratory distress and hypotension. The illness can progress rapidly to severe respiratory failure and shock. The reservoir for the virus in New Mexico is rodents of the genus Peromyscus, mainly the deer mouse Peromyscus maniculatus, which excretes the virus in its urine, feces, and saliva. Humans acquire infection primarily when they breathe in air contaminated with aerosolized virus particles from rodent urine, droppings, or saliva, and rarely through direct contact with infected rodents, rodent droppings, or nests.


Cancer | 2004

Investigation of Healthcare-Associated Transmission of Mycobacterium tuberculosis among Patients with Malignancies at Three Hospitals and at a Residential Facility

Joseph L. Malone; Kashef Ijaz; Lauren A. Lambert; Louie Rosencrans; Lynelle Phillips; Victor Tomlinson; Michael Arbise; Ronald L. Moolenaar; Mark S. Dworkin; Eduardo J. Simoes

Immunocompromised patients have an increased risk of experiencing progression of latent Mycobacterium tuberculosis infection (LTBI) to active tuberculosis (TB) disease. In January 2002, 2 patients with leukemia (Patients 1 and 2) developed pulmonary TB after recent exposure at 3 hospitals (Hospital A, Hospital B, and Hospital C) and at a residential facility for patients with cancer. Neither was known to have LTBI. Within 1 year, 3 other patients with malignancy and TB disease had been identified at these facilities, prompting an investigation of healthcare facility–associated transmission of M. tuberculosis.

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Clarence J. Peters

Centers for Disease Control and Prevention

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David L. Ashley

Centers for Disease Control and Prevention

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David Van Sickle

Centers for Disease Control and Prevention

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Jill M. Ferdinands

Centers for Disease Control and Prevention

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John P. Middaugh

Alaska Department of Health and Social Services

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Ruth A. Etzel

George Washington University

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Stephen B. Thacker

Centers for Disease Control and Prevention

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Thomas G. Ksiazek

University of Texas Medical Branch

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Brockton J. Hefflin

Centers for Disease Control and Prevention

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Clive Brown

Centers for Disease Control and Prevention

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