Risk factors for hospitalization among adults aged ≥65 years with non-typhoidal Salmonella infection linked to backyard poultry contact.

OBJECTIVE: We describe the epidemiology of live poultry-associated salmonellosis (LPAS) and investigate potential risk factors associated with hospitalization among adults aged ≥65 years in the United States during 2008-2017. LPAS is a public health concern in the United States, especially among people with increased risk for hospitalization, such as older adults. SAMPLE: We analysed data from people aged ≥65 years with non-typhoidal salmonellosis who reported live poultry contact within seven days prior to illness onset. PROCEDURE: We used logistic regression to estimate the odds of hospitalization associated with several risk factors including types of live poultry contact exposures. RESULTS: LPAS among older adults in this analysis resulted in high hospitalization rates. Salmonella Hadar infection was associated with increased hospitalization. Among older adults with LPAS, 109 individuals of 127 (86%) reported contact with live poultry at their or someone else's residence, and 85 of 105 with available information (81%) reported owning poultry. CONCLUSIONS AND CLINICAL RELEVANCE: Additional infection prevention information and education targeted at poultry-owning older adults are needed to prevent illness and hospitalization.

Angiotensin II acts through the angiotensin 1a receptor to upregulate pendrin.

Pendrin is an anion exchanger expressed in the apical regions of B and non-A, non-B intercalated cells. Since angiotensin II increases pendrin-mediated Cl(-) absorption in vitro, we asked whether angiotensin II increases pendrin expression in vivo and whether angiotensin-induced hypertension is pendrin dependent. While blood pressure was similar in pendrin null and wild-type mice under basal conditions, following 2 wk of angiotensin II administration blood pressure was 31 mmHg lower in pendrin null than in wild-type mice. Thus pendrin null mice have a blunted pressor response to angiotensin II. Further experiments explored the effect of angiotensin on pendrin expression. Angiotensin II administration shifted pendrin label from the subapical space to the apical plasma membrane, independent of aldosterone. To explore the role of the angiotensin receptors in this response, pendrin abundance and subcellular distribution were examined in wild-type, angiotensin type 1a (Agtr1a) and type 2 receptor (Agtr2) null mice given 7 days of a NaCl-restricted diet (< 0.02% NaCl). Some mice received an Agtr1 inhibitor (candesartan) or vehicle. Both Agtr1a gene ablation and Agtr1 inhibitors shifted pendrin label from the apical plasma membrane to the subapical space, independent of the Agtr2 or nitric oxide (NO). However, Agtr1 ablation reduced pendrin protein abundance through the Agtr2 and NO. Thus angiotensin II-induced hypertension is pendrin dependent. Angiotensin II acts through the Agtr1a to shift pendrin from the subapical space to the apical plasma membrane. This Agtr1 action may be blunted by the Agtr2, which acts through NO to reduce pendrin protein abundance.