Pneumonia and influenza mortality among American Indian and Alaska Native people, 1990-2009.

OBJECTIVES: We compared pneumonia and influenza death rates among American Indian/Alaska Native (AI/AN) people with rates among Whites and examined geographic differences in pneumonia and influenza death rates for AI/AN persons. METHODS: We adjusted National Vital Statistics Surveillance mortality data for racial misclassification of AI/AN people through linkages with Indian Health Service (IHS) registration records. Pneumonia and influenza deaths were defined as those who died from 1990 through 1998 and 1999 through 2009 according to codes for pneumonia and influenza from the International Classification of Diseases, 9th and 10th Revision, respectively. We limited the analysis to IHS Contract Health Service Delivery Area counties, and compared pneumonia and influenza death rates between AI/ANs and Whites by calculating rate ratios for the 2 periods. RESULTS: Compared with Whites, the pneumonia and influenza death rate for AI/AN persons in both periods was significantly higher. AI/AN populations in the Alaska, Northern Plains, and Southwest regions had rates more than 2 times higher than those of Whites. The pneumonia and influenza death rate for AI/AN populations decreased from 39.6 in 1999 to 2003 to 33.9 in 2004 to 2009. CONCLUSIONS: Although progress has been made in reducing pneumonia and influenza mortality, disparities between AI/AN persons and Whites persist. Strategies to improve vaccination coverage and address risk factors that contribute to pneumonia and influenza mortality are needed.

Trends in Otitis Media and Myringotomy With Tube Placement Among American Indian and Alaska Native Children and the US General Population of Children After Introduction of the 13-valent Pneumococcal Conjugate Vaccine.

BACKGROUND: American Indian/Alaska Native (AI/AN) children have experienced higher otitis media (OM) outpatient visit rates than other US children. To understand recent trends, we evaluated AI/AN OM rates before and after 13-valent pneumococcal conjugate vaccine introduction. METHODS: We analyzed outpatient visits listing OM as a diagnosis among AI/AN children <5 years of age from the Indian Health Service National Patient Information Reporting System for 2010-2013. OM outpatient visits for the general US child population <5 years of age were analyzed using the National Ambulatory Medical Care and National Hospital Ambulatory Care Surveys for 2010-2011. RESULTS: The 2010-2011 OM-associated outpatient visit rate for AI/AN children (63.5 per 100/year) was similar to 2010-2011 rate for same-age children in the general US population (62.8) and decreased from the 2003 to 2005 AI/AN rate (91.4). Further decline in AI/AN OM visit rates was seen for 2010-2011 to 2012-2013 (P < 0.0001). The AI/AN infant OM visit rate (130.5) was 1.6-fold higher than the US infant population. For 2010-2011, the highest AI/AN OM visit rate for <5 year olds was from Alaska (135.0). CONCLUSIONS: AI/AN <5-year-old OM visits declined by one third from 2003-2005 to 2010-2011 to a rate similar to the US general population <5 years. However, the AI/AN infant OM rate remained higher than the US infant population. The highest AI/AN <5-year-old OM rate occurred in Alaska.

Impact of varicella vaccination on varicella-related hospitalizations among American Indian/Alaska Native people.

BACKGROUND: Routine childhood varicella vaccination, implemented in 1995, has resulted in significant declines in varicella-related hospitalizations in the United States. Varicella hospitalization rates among the American Indian (AI) and Alaska Native (AN) population have not been previously documented. METHODS: We selected varicella-related hospitalizations, based on a published definition, from the Indian Health Service inpatient database for AI/ANs in the Alaska, Southwest and Northern Plains regions (1995-2010) and from the Nationwide Inpatient Sample for the general US population (2007-2010). We analyzed average annual hospitalization rates prevaccine (1995-1998) and postvaccine (2007-2010) for the AI/AN population, and postvaccine for the general US population. RESULTS: From 1995-1998 to 2007-2010, the average annual varicella-related hospitalization rate for AI/ANs in the 3 regions decreased 95% (0.66-0.03/10,000 persons); the postvaccine rate appears lower than the general US rate (0.06, 95% confidence interval: 0.05-0.06). The rate declined in all AI/AN pediatric age groups. Infants experienced the highest prevaccine (14.07) and postvaccine (0.83) hospitalization rates. Adults experienced low rates in both periods. Varicella vaccination rates in 19- to 35-month-old AI/AN children during fiscal years 2008-2010 were 88.1-91.0%. CONCLUSIONS: Widespread use of varicella vaccine in AI/AN children was accompanied by substantial declines in varicella-related hospitalizations consistent with high varicella vaccine effectiveness in preventing severe varicella outcomes.

Navajo neurohepatopathy is caused by a mutation in the MPV17 gene.

Navajo neurohepatopathy (NNH) is an autosomal recessive disease that is prevalent among Navajo children in the southwestern United States. The major clinical features are hepatopathy, peripheral neuropathy, corneal anesthesia and scarring, acral mutilation, cerebral leukoencephalopathy, failure to thrive, and recurrent metabolic acidosis with intercurrent infections. Infantile, childhood, and classic forms of NNH have been described. Mitochondrial DNA (mtDNA) depletion was detected in the livers of two patients, suggesting a primary defect in mtDNA maintenance. Homozygosity mapping of two families with NNH suggested linkage to chromosome 2p24. This locus includes the MPV17 gene, which, when mutated, causes a hepatocerebral form of mtDNA depletion. Sequencing of the MPV17 gene in six patients with NNH from five families revealed the homozygous R50Q mutation described elsewhere. Identification of a single missense mutation in patients with NNH confirms that the disease is probably due to a founder effect and extends the phenotypic spectrum associated with MPV17 mutations.