At this point, does anyone really need a reason to quit smoking or even start for that matter? Well, just in case you have been cut off from communication for the last decade or so and are unaware of the dangers associated with cigarette smoke, here is a new one that might stop some in their tracks. A team of investigators led by scientists at the University of Bath has just published new data showing that cigarette smoke can make Methicillin-Resistant Staphylococcus aureus (MRSA) bacterial strains more resistant to antibiotics. Findings from the new study were published recently through an article titled “Cigarette smoke exposure redirects Staphylococcus aureus to a virulence profile associated with persistent infection.”
Moreover, the researchers found that cigarette smoke exposure can make some strains of S. aureus—which is present in 30–60% of the global population and responsible for an array of diseases, some fatal—more invasive and persistent, although the effect is not universal across all strains tested.
“We expected some effects, but we didn’t anticipate smoke would affect drug-resistance to this degree,” noted senior study investigator Maisem Laabei, PhD, a lecturer in the department of biology and biochemistry at the University of Bath.
The researchers believe the stress cigarette smoke causes to S. aureus sparks an emergency “SOS” response, which increases the rate of mutation in microbial DNA, resulting in hardy and persistent variants better able to resist antibiotics.
“We recognize that exposure in a lab is different from inhaled smoke over a long time, but it seems reasonable to hypothesize, based on our research and others’ that stressful conditions imposed by smoking induce responses in microbial cells leading to adaptation to harsh conditions, with the net effect of increasing virulence and/or potential for infection,” Laabei added.
Previous studies had attributed smokers’ increased susceptibility of infection to the damaging effects of smoke on our immune system, but this study shows that it may also be changing the DNA and characteristics of pathogenic microbes as well.
In a series of lab-based experiments, the researchers exposed six reference strains of the most important “superbug” MRSA clones to cigarette smoke.
“We investigated the impact of cigarette smoke (CS) on specific virulence phenotypes important in S. aureus pathogenesis,” the authors wrote. “We observed strain-dependent differences following exposure to CS, namely growth inhibition, augmented biofilm formation, increased invasion of, and persistence within, bronchial alveolar epithelial cells. Additionally, we confirm the critical role of a functional accessory gene regulator (Agr) system in mediating increased biofilm development and host cell invasion and persistence following CS exposure. Furthermore, CS exposure resulted in reduced toxin production. Importantly, exposure of S. aureus to CS accelerated the frequency of mutations and resulted in a significant increase in gentamicin-resistant small colony variant (SCV) formation.”
The strains were known to cause conditions ranging from skin infections to pneumonia and endocarditis and were chosen for their clinical relevance and genetic diversity. Although not all responded to cigarette smoke, in the same way, some, including those known to cause invasive infections, showed increased resistance to the antibiotic rifampicin and increased invasiveness and persistence. Resistance to other antibiotics is also likely to be affected.
“Smoking is the leading cause of preventable death worldwide, and cigarette smoke has over 4,800 compounds within it,” Laabei explained. “We wanted to study S. aureus because it’s so common in humans and it can cause a range of diseases, so we wanted to see what happened when we exposed it to smoke.”
Interestingly the current study links these changes to the emergence of SCVs—hardy sub-populations that are adapted to harsh conditions. SCVs have been linked to chronic infections in smokers in previous research. The scientists are now interested in studying how air pollution, from diesel exhaust fumes and other sources, might affect the microbes in our nasal passages as many of the pollution compounds are the same as in cigarette smoke.
“These small colony variants are highly adhesive, invasive, and persistent,” Laabei concluded. “They can sit around for a long time, are difficult to kick out, and are linked to chronic infections. We hope that our work provides another reason for people not to smoke and for current smokers to quit.”