Chief of infectious diseases at UBMD discusses viruses, bacteria, antibiotic resistance
By Chris Motola
Q: This tends to be the time of year when people start getting concerned about infectious diseases, your area of expertise. Tell us about what you do.
A: I have significant educational role with educating infectious disease medical students, residents and fellows. I also have an administrative role as chief of the division of infectious diseases, which includes both administrative duties and, lately, answering questions from the media, often about COVID-19. I’m also involved in infectious disease research funded by the Veteran’s Administrative and National Institutes of Health to study and try to treat antimicrobial-resistant bacteria.
Q: What’s your post-mortem analysis of the COVID-19 pandemic? What went well and what could have been done better?
A: I think our greatest achievement was the rapidity with which we got an efficacious vaccine. Imagine if we got that vaccine a year or two years later. It was record time, less than a year. That was the good news. We were, of course, all hoping to have a vaccine that prevents infection, but that’s unrealistic for a respiratory virus vaccine, which is something we also see with the flu vaccines. But it’s been very good at keeping people out of the hospital and having bad outcomes. We took a potentially lethal virus, made it closer to the common cold, and reduced the number of transmissions and infections. Mission accomplished. As for negatives: even though we have the tools, not just the vaccine but antivirals like Paxlovid, we’re not optimally utilizing those tools. It’s almost gotten worse with this season. People aren’t worried about COVID-19, even though it’s likely to get worse. Of course, there’s a stratification of risk to different groups, but no one’s without risk. Only about 14% of adults have gotten the updated COVID vaccine.
Q: What have you found to be the most effective approach to getting patients to consider taking it?
A: I think there have been some misconceptions and, for argument’s sake, let’s stay away from the anti-vaxxer movement. This is just within the context of what’s true. I think people were expecting that vaccination would mean you wouldn’t get infected. What should be expected is prevention of emergency room visits, hospitalizations and deaths. It checks those latter boxes but it’s imperfect at preventing infection. I think that’s one of the issues. The other issue is people saying, “I’ve been vaccinated and-or been infected, I’ve got immunity, I’m safe.” But our immunity wanes over time and the virus continues to evolve. So for optimal protection, we need to go ahead and periodically get updated versions that are a better match to circulating variants. Now, we are still in better shape then we were during the pandemic when no one had any immunity, but individuals who are still at risk of developing significant disease include seniors, those with significant underlying disease and the immunocompromised. Having said that, even in low-risk groups there’s never zero risk of having a bad outcome. And the last point is there’s an increasing body of data that suggests the vaccine decreases your chance of developing long COVID. And that’s important for all age groups, even the ones statistically unlikely to end up hospitalized.
Q: What, exactly, is long COVID? Is it damage resulting from infection? Failure to clear infection? Lingering symptoms? It doesn’t seem like there’s a fully agreed-upon definition.
A: Long COVID is almost a discussion unto itself and you’re right that we don’t yet have a formal definition. Generally the definition is symptoms that persist 30 to 90 days after infection. It’s also more than that. It includes the systemic consequences of being infected. It increases your risk having cardiovascular events, central nervous problems like brain fog, autoimmune issues, clots. These are maximal over the first three months and then hazard ratios decrease over time but may remain elevated even two years out, which is where we are now.
Q: Moving away from COVID-19 and viruses generally, I want to touch on antibiotic resistance. There were some headlines recently about gonorrhea becoming extremely resistant.
A: I don’t specifically work with the bacteria that cause gonorrhea, but the principles of antibiotic resistance apply to all bacteria that cause infections in humans. We’ve been using more and more antibiotics both appropriately and inappropriately, and as a result they’ve become more and more resistant to these antibiotics, in some cases making them very difficult to treat. It’s an ongoing problem and really something that’s mostly on us as healthcare providers. We need to prescribe them only when appropriate and use what we call narrow-spectrum antibiotics against a given infection so we don’t encourage the evolution of resistance. From a personal responsibility side, patients sometimes expect to get a pill when they go to the doctor, even if they have a viral infection. We do have antivirals for things like COVID and the flu, but we don’t want to prescribe antibiotics for viral. Sometimes a patient will come in with a common cold and pressure the physician for antibiotics.
Q: Can you explain narrow-spectrum antibiotics in lay terms?
A: So let’s say you have an antibiotic that’s only effective against three bacteria versus one that’s effective against 10. If the infection you have is among those three, you want to use the first antibiotic rather than second so that you can reserve it for situations where you need something that’s effective against more bacteria and aren’t selecting for resistant bacteria that you aren’t targeting.
Q: On the research side, what’s the strategy for dealing with bacterial infections that are already resistant? How are we keeping up in the arms race?
A: There are multiple strategies. The first strategy what we discussed, using the ones we have more judiciously. The backend is development of new products. That takes a lot of time. There’s a lot of effort going toward that right now, including at our lab at the University at Buffalo, especially bacteria that are common to healthcare settings, which have become very problematic. Other approaches include innovative approaches which could include using them alone or in combination with antibiotics. One example is bacteriophage therapy. The bacteria equivalent of viruses that infect us is called a bacteriophage. So they’re viruses that infect bacteria. Other approaches are developing antibodies. You may remember monoclonal antibodies from the COVID pandemic. The variants eventually became resistant, but this is another area that’s being researched for bacteria. I would add to that that there are vaccination efforts. It’s harder to develop vaccines for bacteria, but in some cases it may be cost effective from a public health point of view for select bacteria that infects broad swaths of the population like gonorrhea, or if you can identify a high-risk population. With new RNA technologies it might get easier to develop efficacious vaccines against bacteria, but that’s still a work in progress.
Lifelines
Name: Thomas A. Russo, M.D.
Position: Division chief, infectious diseases, UBMD Internal Medicine and the Jacobs School of Medicine and Biomedical Sciences at the University at Buffalo; SUNY distinguished professor of medicine, UB
Hometown: Boston, Massachusetts
Education: McGill Medical University
Affiliations: Veteran’s Administration Healthcare System
Organizations: Infectious Disease Society of America, American Association for the Advancement of Science
Family: Wife, three children
Hobbies: Reading, gardening