AIRCRAFT VENTILATION CAN RESTRICT TRANSMISSION OF INFECTIOUS DISEASES

Increasing ventilation within aircraft cabins can reduce the spread of infectious diseases in-flight, according to a report in the March 12 Lancet. Alexandra Mangili, MD, and Mark A. Gendreau, MD, reviewed data from studies focusing on transmission of diseases during commercial airline travel. They found that while commercial airlines are a suitable environment for the spread of pathogens carried by passengers or crew, the environmental control systems used in commercial aircraft seem to restrict the spread of airborne pathogens.

Although risk of disease transmission is difficult to determine, “data suggest that risk of disease transmission to other symptom-free passengers within the aircraft cabin is associated with sitting within two rows of a contagious passenger for a flight time of more than eight hours,” said Drs. Mangili and Gendreau. This association is mainly based on studies focusing on in-flight transmission of tuberculosis; however, it is believed to be relevant to other airborne infectious diseases.

In addition, Drs. Mangili and Gendreau found that the risk of in-flight disease transmission was apparantly associated with the aircraft’s type of cabin ventilation. “One air exchange removes 63% of airborne organisms suspended in that particular space,” they said.

“Further assessment of risk through mathematical modeling is needed and will provide insight into disease transmission within the aircraft cabin as well as control of outbreaks of different diseases,” Drs. Mangili and Gendreau commented. Until then, “the aviation industry and medical community should educate the general public on health issues related to air travel and infection control.”

In an accompanying editorial, David Ozonoff, MD, and Lewis Pepper, MD, of Boston University School of Public Health, stated that although most commercial aircraft recirculate 50% of the air delivered to the passenger cabin, only 85% of US commercial aircraft carrying more than 100 passengers are equipped with high-efficiency particulate air (HEPA) filters. “Many fewer of the smaller regional jets that recirculate cabin air use HEPA filters,” they added. Drs. Ozonoff and Pepper concluded, “Regulations requiring HEPA filters for any airplane that recirculates air should be seriously considered.”

Mangili A, Gendreau MA. Transmission of infectious diseases during commercial air travel. Lancet. 2005;365:989-996.
Ozonoff D, Pepper L. Ticket to ride: spreading germs a mile high. Lancet. 2005;365:917-919.

FURTHER EVIDENCE THAT SMOKING CESSATION PROGRAMS CAN REDUCE MORTALITY RATES

Smoking cessation intervention programs have a substantial effect on subsequent mortality, according to a 14.5-year study involving 5,887 middle-aged smokers. Results of the Lung Health Study, conducted by Nicholas R. Anthonisen, MD, and colleagues, were published in the February 15 Annals of Internal Medicine.

Participants “were smokers who did not consider themselves ill but had evidence of airway obstruction and little evidence of other disease,” the researchers said. “The intervention was a 10-week smoking cessation program that included a strong physician message and 12 group sessions using behavior modification and nicotine gum, plus either ipratropium or a placebo inhaler.”

At the five-year follow-up, 21.7% of intervention participants had stopped smoking, compared with 5.4% of usual care participants. The researchers found that at the 14.5-year follow-up, 731 patients had died: 240 of lung cancer, 77 of coronary heart disease, 163 of cardiovascular disease, 154 of cancer of organs other than the lungs, 57 of respiratory disease other than cancer, and 17 of unknown causes. Mortality was higher in the usual care group than in the intervention group (10.38 per 1,000 person-years vs 8.83 per 1,000 person-years).

The researchers noted that the effects of cessation were probably due to the absence of further insult due to smoking rather than to reversal of existing disease.

In an accompanying editorial, Jonathan M. Samet, MD, MS, stated that the results of the Lung Health Study “provide further ‘proof,’ based on experiment rather than observation, that smoking is causally responsible for the increased risk for death in smokers.” He added that “interventions by clinicians do increase the rates of successful quitting, and clinicians should follow recommended guidelines by obtaining a smoking history from all patients and assisting smokers in quitting.”

In a separate but related study published in the February 24 American Journal of Medicine, researchers found that immediate and long-term mortality rates were lower among individuals receiving inpatient smoking cessation counseling. Results were based on data collected from the medical records of 16,743 smokers 65 and older who were admitted to the hospital with a documented acute myocardial infarction.

According to Thomas K. Houston, MD, MPH, and colleagues, 41% of the study subjects had medical record documentation of smoking cessation counseling during their admission. Results indicated that patients who received smoking cessation counseling had lower 30-day, 60-day, and two-year mortality, compared to those who did not receive counseling. The greatest reduction in mortality, 19%, was seen within 30 days.

“The positive association of smoking cessation counseling with survival that we observed provides evidence for an association suggested, but not directly demonstrated, by previous reports on the impact of counseling on cessation and the impact of cessation on mortality,” concluded the researchers.

Anthonisen NR, Skeans MA, Wise RA, et al. The effects of a smoking cessation intervention on 14.5-year mortality. Ann Intern Med. 2005;142:233-239.
Houston TK, Allison JJ, Person S, et al. Post-myocardial infarction smoking cessation counseling: associations with immediate and late mortality in older Medicare patients. Am J Med. 2005;118:269-275.
Samet JM. Smoking kills: experimental proof from the Lung Health Study. Ann Intern Med. 2005;142:299-301.

RPF PROTEINS COULD LEAD TO THE TREATMENT FOR DORMANT TUBERCULOSIS

Researchers have discovered the structure of a resuscitation-promoting factor domain, called RpfBc, which signals Mycobacterium tuberculosis to exit dormancy. According to a report published in the March Nature Structural & Molecular Biology, this discovery might lead to the development of drugs that would enable treatment of dormant and multidrug-resistant tuberculosis.

The researchers used nuclear magnetic resonance spectroscopy to determine the structure of RpfBc. They found that these proteins resembled a hybrid of bacterial soluble lytic transglycosidase proteins and c-type lysozymes, suggesting that RpfBc cleave oligosaccharides. A conserved active site glutamate, “combined with a clear binding pocket for a large molecule that undergoes rearrangement in presence of a polysaccharide, strongly suggests that the function of resuscitation-promoting factors is to cleave oligosaccharide and this is responsible for their role in revival of dormant bacteria,” noted the researchers.

Their discovery will improve the present understanding of the functional activity of resuscitation-promoting factors and “could allow the development of methods to ‘wake up’ all dormant bacteria in a patient, allowing antibiotics to kill the bacteria and cure the disease,” said John Ward, of the Department of Biochemistry and Molecular Biology, University College London.

“Although active tuberculosis is quickly treated, the remaining dormant tuberculosis bacteria are very hard to reach, and take six months to treat with antibiotics. But if we can find a way of copying resuscitation-promoting factor as a drug, and delivering it into the system so that it wakes up all of the tuberculosis bacteria, treatment will be faster and more effective,” added Brian Henderson, of the Division of Microbial Diseases, Eastman Dental Institute, also in London.

Cohen-Gonsaud M, Barthe P, Bagnéris C, et al. The structure of a resuscitation-promoting factor domain from Mycobacterium tuberculosis shows homology to lysozymes. Nat Struct Mol Biol. 2005;12:270-273.

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