Latent tuberculosis infection prevalence in second generation immigrants from high to low TB burden countries.

BACKGROUND: Latent tuberculosis infection (LTBI) diagnosis in a country with a low tuberculosis burden is complicated. Since the prevalence of LTBI in second generation immigrants has not been well recognized, we conducted a cross-sectional study which aimed to explore the differences in LTBI prevalence between offspring of immigrants from high tuberculosis (TB) burden countries and those whose parents were born in countries with a low TB burden. METHODS: Between May 2014 and April 2018 young native Israelis who were required to perform pre-occupational tuberculin skin tests (TST) (medical and paramedical personnel or teaching assistants of immigrants from high TB burden countries) and who had a TST result of 10mm and above were tested for QuantiFERON-TB In Tube (QFT-GIT). Statistical comparisons were made between second generation immigrants and those with both parents from a low TB burden country. RESULTS: Of 102 patients, 71 were born to parents both of whom were from low-risk countries, 14 to one parent from a high-risk country and 17 to parents both of whom were from a high-risk country. The odds ratio for LTBI was 4.5 (95% CI, 1.2...17.2; p=0.03) if both parents were born in a high-risk country compared to both parents being from a low-risk country and 4.01 (95% CI, 1.12...14.3; p=0.03) higher compared to persons for whom at least one parent was born in a low-risk country. CONCLUSION: The risk for latent TB is significantly higher in second generation immigrants if both parents were born in a high-risk country. IGRA should be considered before treatment to patients with a positive TST if at least one parent was born in a low-risk country in order to confirm LTBI.

Antibodies against Mac-1 attenuate neutrophil accumulation after traumatic brain injury in rats.

Neutrophils (PMN) accumulate and are associated with cerebrovascular disturbances after experimental traumatic or ischemic brain injury, and meningitis. We hypothesized that posttraumatic PMN accumulation in brain is mediated by the PMN adhesion receptor Mac-1 (CD11b/CD18). Anesthetized rats were randomized to receive 2 mg/kg intravenously of murine monoclonal antibody to rat Mac-1 (1-B6) or anti-Mac-1 F(ab)2' [1-B6F(ab)2'] fragment (Repligen Corp., Cambridge, MA). Control rats were treated with isotype matched control antibody. Rats were subjected to percussive trauma to the right parietal cortex 30 min after treatment. Rats were killed 24 h posttrauma, and PMN accumulation was assessed by myeloperoxidase (MPO) activity. The presence of 1-B6F(ab)2' bound to PMN in brain after trauma was assessed by immunohistochemistry. Complete blood cell counts were obtained before treatment and 24 h after trauma. Brain MPO activity was reduced by 43% in the 1-B6-treated rats vs. controls (0.31 +/- 0.09 vs 0.55 +/- 0.10 U/g, n = 6/group, p = 0.013) and by 34% in the 1-B6F(ab)2'-treated rats vs. controls (0.43 +/- 0.10 vs. 0.65 +/- 0.09 U/g, n = 6/group, p = 0.006). Systemic neutropenia developed in the 1-B6-treated rats (absolute PMN count decreased by 73% vs. baseline) but not in rats treated with 1-B6F(ab)2' (absolute PMN count increased by 26 and 25% vs. baseline in treated and controls, respectively). Immunohistochemical staining showed 1-B6F(ab)2' on the surface of infiltrated PMN 24 h after trauma. Mac-1 mediates posttraumatic PMN accumulation in brain. This accumulation can be attenuated by 34%, without reducing circulating PMN, using an anti-Mac-1 F(ab)2' fragment; however, some PMN coated with 1-B6F(ab)2' still infiltrate into traumatized tissue. These results are similar to those reported in models of cerebral ischemia, and suggest the participation of multiple PMN adhesion pathways after ischemic and traumatic brain injury.