Asymptomatic Visceral Leishmania infantum Infection in US Soldiers Deployed to Iraq.

BACKGROUND: Visceral leishmaniasis (VL), due to Leishmania infantum, is a persistent intracellular parasitic infection transmitted by the bite of infected sand flies. Symptomatic VL has been reported in U.S. soldiers with Iraq deployment. Untreated symptomatic VL can be fatal; asymptomatic VL (AVL) may establish a lifelong risk of reactivation. We report prevalence and AVL risk factors in Operation Iraqi Freedom (OIF) deployers during 2002-11. METHODS: Healthy soldiers exposed to VL endemic areas in Iraq and 50 controls who never traveled to endemic regions were recruited through military healthcare facilities (2015-17). Responses to a risk factor survey and blood samples were obtained. Leishmania research diagnostics utilized included enzyme-linked immunosorbent assay (ELISA), rk39 test strips, quantitative polymerase chain reaction (PCR), and interferon gamma release (IGRA) assays. Statistical analyses included Fisher exact test, Pearson χ2 test, Mann-Whitney U test, and logistic regression. RESULTS: 200 deployed subjects were enrolled, mostly males (84.0%), of white ethnicity (79.0%), and median age 41 (range 24-61) years. 64% were seropositive for Phlebotomus alexandri saliva antibodies. Prevalence of AVL (any positive test result) was 39/200 (19.5%, 95% confidence interval 14.4%-25.8%). Two (1.0%) PCR, 10 (5%) ELISA, and 28 (14%) IGRA samples were positive. Travel to Ninewa governorate increased risk for AVL (P = .01). CONCLUSION: AVL was identified in 19.5% of OIF deployers; travel to northwest Iraq correlated with infection. Further studies are needed to inform risk for reactivation VL in US veterans and to target additional blood safety and surveillance measures.

In vivo effect of wood smoke on the expression of two mucin genes in rat airways.

A short-term, time-dependent smoke exposure of rats in a nose-only chamber to burning wood and 24-h recovery time revealed inflammation of the airways with varying degrees of injury from loss of cilia, degeneration of epithelium, and squamous metaplasia to submucosal edema. These histological changes were reflected in variable expression of the secretory Muc5AC and low expression of membrane-associated Muc4 mucin genes. 20-min smoke exposure in extended recovery experiments showed marked disorder of tracheal epithelium for up to 72 h of recovery with a return to normal by 7 days. Gene expressions were elevated at 24 and 48 h of recovery. 30-min smoke exposure showed a more severe degeneration of the epithelium and a longer recovery time. Muc5AC expression decreased after 72 h of recovery, while there was upregulation of Muc4 gene from 48 through 96 h. Because Muc4 upregulation and histological results correlate and it has reportedly been associated with epithelium renewal, Muc4 gene may be a useful marker for the regeneration of tracheal epithelium.