many people unemployed; this socioeconomic factor may have confounded the study results (Hatchette et al. 2003). Data on comorbidity were unavailable, followup serologic data were incomplete, and the study also may have been limited by participation bias: subjects who continued to have symptoms may have been more likely to participate in both questionnaire surveys.
Later studies have reported differences in immune-response genes among those who report post-Q fever fatigue compared with those who are unaffected (Helbig et al. 2005; Helbig et al. 2003). One hypothesis is that after C. burnetii infection, Coxiella may persist universally in the bone marrow and be regulated by the host’s immune response. A subset of patients with subtle differences in their immune response may later develop post-Q fever fatigue. That and other hypotheses are under active investigation in Australia and the UK.
The committee concludes that there is limited or suggestive evidence of an association between infection by Coxiella burnetii and post-Q fever chronic fatigue syndrome years after primary infection.
The unique properties and history of tuberculosis (TB) led the committee to approach this section differently from the rest of the chapter in two ways. First, initial infection with Mycobacterium tuberculosis (TB infection) is usually asymptomatic, the onset of the disease (TB) is almost always delayed, and relapse of TB may occur years after successful treatment. Thus, TB infection has the potential for delayed long-term adverse health outcomes both because of the onset of clinically evident TB months to decades after initial infection and because of the long-term consequences of acute disease.
Second, TB has a long history of occurrence and transmission in military settings and remains a cause of potential delayed adverse health outcomes in US troops and veterans of the Gulf War, OEF, and OIF—especially those who are or were deployed to regions where TB is highly endemic. The committee discusses TB in the military at the end of this section.
TB is a chronic necrotizing granulomatous infection caused primarily by the acid-fast bacillus Mycobacterium tuberculosis. An obligate aerobe, M. tuberculosis grows best in such tissues with high oxygen tension as the apices of the lung and the renal cortex; this explains why most infections are manifested as pulmonary disease. M. bovis, a related organism, causes a substantial number of TB cases in regions where milk is not routinely pasteurized and where M. bovis-infected cattle are not identified and destroyed.
TB is transmitted primarily through exposure to airborne M. tuberculosis. When an infected person coughs, sneezes, yells, or sings, microscopic droplets containing M. tuberculosis are expelled into the air. Heavier particles quickly settle out of the air, and lighter ones remain suspended, often for several hours. Inhaled droplets of 1-5 µm in diameter are small enough to reach the alveoli, where the mycobacteria colonize and infect the lung tissue of their new hosts (IOM 2000).