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Cedar City, GA, United States

Foote E.M.,University of Washington | Singleton R.J.,Centers for Disease Control and Prevention | Holman R.C.,Centers for Disease Control and Prevention | Seeman S.M.,NCEZID | And 2 more authors.
International Journal of Circumpolar Health | Year: 2015

Background. The lower respiratory tract infection (LRTI)-associated hospitalization rate in American Indian and Alaska Native (AI/AN) children aged <5 years declined during 1998–2008, yet remained 1.6 times higher than the general US child population in 2006–2008. Purpose. Describe the change in LRTI-associated hospitalization rates for AI/AN children and for the general US child population aged <5 years. Methods. A retrospective analysis of hospitalizations with discharge ICD-9-CM codes for LRTI for AI/AN children and for the general US child population <5 years during 2009–2011 was conducted using Indian Health Service direct and contract care inpatient data and the Nationwide Inpatient Sample, respectively. We calculated hospitalization rates and made comparisons to previously published 1998–1999 rates prior to pneumococcal conjugate vaccine introduction. Results. The average annual LRTI-associated hospitalization rate declined from 1998–1999 to 2009–2011 in AI/AN (35%, p<0.01) and the general US child population (19%, SE: 4.5%, p<0.01). The 2009–2011 AI/AN child average annual LRTI-associated hospitalization rate was 20.7 per 1,000, 1.5 times higher than the US child rate (13.7 95% CI: 12.6–14.8). The Alaska (38.9) and Southwest regions (27.3) had the highest rates. The disparity was greatest for infant (<1 year) pneumonia-associated and 2009–2010 H1N1 influenza-associated hospitalizations. Conclusions. Although the LRTI-associated hospitalization rate declined, the 2009–2011 AI/AN child rate remained higher than the US child rate, especially in the Alaska and Southwest regions. The residual disparity is likely multi-factorial and partly related to household crowding, indoor smoke exposure, lack of piped water and poverty. Implementation of interventions proven to reduce LRTI is needed among AI/AN children. © 2015 Eric M. Foote et al.

Neil K.P.,Epidemic Intelligence Service | Neil K.P.,Centers for Disease Control and Prevention | Sodha S.V.,Centers for Disease Control and Prevention | Lukwago L.,Ministry of Health | And 17 more authors.
Clinical Infectious Diseases | Year: 2012

Background. Salmonella enterica serovar Typhi (Salmonella Typhi) causes an estimated 22 million typhoid fever cases and 216 000 deaths annually worldwide. In Africa, the lack of laboratory diagnostic capacity limits the ability to recognize endemic typhoid fever and to detect outbreaks. We report a large laboratory-confirmed outbreak of typhoid fever in Uganda with a high proportion of intestinal perforations (IPs).Methods.A suspected case of typhoid fever was defined as fever and abdominal pain in a person with either vomiting, diarrhea, constipation, headache, weakness, arthralgia, poor response to antimalarial medications, or IP. From March 4, 2009 to April 17, 2009, specimens for blood and stool cultures and serology were collected from suspected cases. Antimicrobial susceptibility testing and pulsed-field gel electrophoresis (PFGE) were performed on Salmonella Typhi isolates. Surgical specimens from patients with IP were examined. A community survey was conducted to characterize the extent of the outbreak. Results. From December 27, 2007 to July 30, 2009, 577 cases, 289 hospitalizations, 249 IPs, and 47 deaths from typhoid fever occurred; Salmonella Typhi was isolated from 27 (33%) of 81 patients. Isolates demonstrated multiple PFGE patterns and uniform susceptibility to ciprofloxacin. Surgical specimens from 30 patients were consistent with typhoid fever. Estimated typhoid fever incidence in the community survey was 8092 cases per 100 000 persons. Conclusions. This typhoid fever outbreak was detected because of an elevated number of IPs. Underreporting of milder illnesses and delayed and inadequate antimicrobial treatment contributed to the high perforation rate. Enhancing laboratory capacity for detection is critical to improving typhoid fever control. © 2012 The Author.

Jentes E.S.,Centers for Disease Control and Prevention | Blanton J.D.,NCEZID | Johnson K.J.,Centers for Disease Control and Prevention | Petersen B.W.,NCEZID | And 8 more authors.
Journal of Travel Medicine | Year: 2014

We assessed rabies vaccine (RV) and immune globulin (RIG) availability on the local market by querying US Embassy medical staff worldwide. Of 112 responses, 23% were from West, Central, and East Africa. RV and RIG availability varied by region. Possible rabies exposures accounted for 2% of all travelers' health inquiries. © Published 2013. This article is a U.S.Government work and is in the public domain in the USA.

Singleton R.,055 Tudor Center Dr | Singleton R.,Centers for Disease Control and Prevention | Gessner B.D.,Epidemiology and Vaccinology Consulting | Bulkow L.,Centers for Disease Control and Prevention | And 3 more authors.
Journal of Pediatric Endocrinology and Metabolism | Year: 2015

Background: Rickets and vitamin D deficiency appeared to increase in Alaskan children starting in the 1990s. We evaluated the epidemiology of rickets and vitamin D deficiency in Alaska native (AN) children in 2001-2010. Methods: We analyzed 2001-2010 visits with rickets or vitamin D deficiency diagnosis for AN and American Indian children and the general US population aged <10 years. We conducted a case-control study of AN rickets/vitamin D deficient cases and age- and region-matched controls. Results: In AN children, annual rickets-associated hospitalization rate (2.23/100,000 children/year) was higher than the general US rate (1.23; 95% CI 1.08-1.39). Rickets incidence increased with latitude. Rickets/vitamin D deficiency cases were more likely to have malnutrition (OR 38.1; 95% CI 4.9-294), had similar breast-feeding prevalence, and were less likely to have received vitamin D supplementation (OR 0.23; 95% CI 0.1-0.87) than controls. Conclusions: Our findings highlight the importance of latitude, malnutrition, and lack of vitamin D supplementation as risk factors for rickets. © 2015 by De Gruyter.

Dauphin L.A.,Centers for Disease Control and Prevention | Marston C.K.,NCEZID | Bhullar V.,Centers for Disease Control and Prevention | Baker D.,Centers for Disease Control and Prevention | And 5 more authors.
Journal of Clinical Microbiology | Year: 2012

The clinical laboratory diagnosis of cutaneous anthrax is generally established by conventional microbiological methods, such as culture and directly straining smears of clinical specimens. However, these methods rely on recovery of viable Bacillus anthracis cells from swabs of cutaneous lesions and often yield negative results. This study developed a rapid protocol for detection of B. anthracis on clinical swabs. Three types of swabs, flocked-nylon, rayon, and polyester, were evaluated by 3 extraction methods, the swab extraction tube system (SETS), sonication, and vortex. Swabs were spiked with virulent B. anthracis cells, and the methods were compared for their efficiency over time by culture and real-time PCR. Viability testing indicated that the SETS yielded greater recovery of B. anthracis from 1-day-old swabs; however, reduced viability was consistent for the 3 extraction methods after 7 days and nonviability was consistent by 28 days. Real-time PCR analysis showed that the PCR amplification was not impacted by time for any swab extraction method and that the SETS method provided the lowest limit of detection. When evaluated using lesion swabs from cutaneous anthrax outbreaks, the SETS yielded culture-negative, PCR-positive results. This study demonstrated that swab extraction methods differ in their efficiency of recovery of viable B. anthracis cells. Furthermore, the results indicated that culture is not reliable for isolation of B. anthracis from swabs at ≥7 days. Thus, we recommend the use of the SETS method with subsequent testing by culture and real-time PCR for diagnosis of cutaneous anthrax from clinical swabs of cutaneous lesions. Copyright © 2012, American Society for Microbiology. All Rights Reserved.

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