Clinical Presentation and Pathogens in Foot Abscesses with No Accompanying Wound

Amanda Killeen, DPM, shares background and additional details from her research article, “Foot Abscesses With No Accompanying Wound: Clinical Presentation and Pathogens.” Additional coauthors include Katerina Grigoropoulos, DPM; Mehmet Suludere, MD; Peter Andrew Crisologo, DPM; and Lawrence A. Lavery, DPM, MPH. Read the full article here.
 

Transcript:

Hi, my name is Amanda Killeen, I'm a podiatrist and an assistant professor in the Department of Plastic Surgery at UT Southwestern in Dallas. We function as a small diabetic limb salvage group within the plastic surgery organization. So my paper is about foot abscesses with no accompanying wounds. This may sound like a fairly superficial topic, but there is nothing else in the literature that we could find about this specific patient population.

I practice at both a county hospital and a university hospital, and the difference in socioeconomic status couldn't be further apart. What we did was we tracked patients who had an abscess with no apparent wound, no known injury for about 3 years. And during that time, we compiled 20 patients. Half of those patients happened to have diabetes and half of them did not. So we essentially tracked them from admission to their surgeries, which was 2.4 on average, and then followed up the cultures afterward.

The most interesting part of this paper is that all of the infections that we cultured came back as mono microbial, which seems to be at odds with the expectation and what has been published in the literature because in the past it's been basically understood that polymicrobial infections exist in the diabetic foot. What we're finding with the advent of better culturing techniques and especially molecular and genomics work through people like Sue Gardner and Lindsey Kalin who are looking at the microbiome of the foot and especially the diabetic foot, is that there are tons of bacteria, way more than we ever cultured appropriately when we were using simple methods, but we are still unsure which of those present bacteria are actually the pathogenic ones.

Typically, it's staph and strep that are usually the drivers, and that's what we saw in this series. Of the 20 patients, 10 of them had staph, which you would expect, and the other 8 who had culture positive results were strep species. Two of them actually had no bacterial growth at all from the abscess when we went into surgery. But the interesting thing too is that of these subjects, the patients with diabetes tended to have higher inflammatory markers on admission.

Now, if you're assuming that patients with diabetes had a much higher rate of neuropathy, you'd be correct. In this study, it was about 45% overall. But when we looked at the group separately, 90% of patients with diabetes had neuropathy, but even still with no known injury, no known wound, and nothing leading up to this abscess, those patients still had a higher inflammatory response and showed up sooner than the patients who did not have diabetes at all.

I think necessity is the mother of invention, and it's no different when we're talking about clinical research. While this seems like 20 patients may not be life shattering in the rest of published literature, 20 patients still took us 3 years to collect, and this is at thousand-bed hospitals. The county hospital has a thousand beds, the university has 883, and we have anywhere between 10 to 15 consults a day on one and 5 to 10 at the other. So we have an extremely high volume, and even here in this setting still only found a low number of these subjects.

So this may be something that is occurring other places, but at such a low rate that other people haven't been able to quantify these data before. So we're hoping that this published report, while it is small and it's only 20 and it's descriptive, statistics may be something foundational for something in the future where people who are looking to better treat these patients or looking to see what to expect could use our pieces of data here and hopefully have that help them in the patient care course.

The most surprising thing is just the mono microbial nature of the cultures that we got, and especially because a lot of these patients came in with moderate to severe signs of infection according to the Infectious Diseases Society of America and the International Working Group on the Diabetic Foot criteria. So we're seeing things like local cellulitis greater than two centimeters. We're seeing pain, we're seeing purulence, sometimes only in the operating room once that abscess had been opened. Some actually just opened up bedside.

But for the patients who had systemic symptoms, most of those patients were the patients with diabetes, which is also not what we typically see. We typically don't see a great immune response in people with diabetes when we're comparing to their counterparts that don't have diabetes. But there is the question that may lead to further research on this topic of the way we cultured these abscesses. When we do a deep culture in the operating room, of course the skin has been prepped and everything is sterile. We take deep cultures and send a piece of tissue.

But the question remains, if we're just doing plating for these bacterial cultures, are we missing something like are we not capturing all anaerobes that could have been there, or are things just not growing as well on the plates that we typically use? If we're expecting it to be staph and strep, then maybe blood agar was not what we needed to be growing for X bacteria. We needed something different.

So that's always a question, and I think that there's going to be, in the next 5 or 10 years, probably a nice interaction between this type of culturing that's standard and cheap and easy and moving into the more genomics work where we can see is there something else there. But then also finding out what exactly was contributing to this infection and to the symptoms that the patient presented with.

I think another avenue for research is linking what is present in the wound to what is pathogenic and then what actually shows up in the patient's presentation. I think in a lot of places we are so worried about resistant bacteria that we cover for them all the time. In our hospital, our rate of methicillin-resistant staph aureus is very low in the diabetic foot compared to nares swabs or incidence of MRSA and the diabetic foot in other locations in the country, let alone compared to other countries in the world.

So I think if we're able to identify which of those pathogens are actually causing the severity of the symptoms or the recurrence of symptoms when patients have recurrent infections, I think that is a really interesting field of inquiry that we really haven't elucidated fully. So in our study we had seven patients who had methicillin-sensitive staph aureus, and then we had three that had methicillin-resistant.

Unfortunately, in our facilities, there's not a defined timeline for when we take off precautions. So if a patient had culture positive nares swab, for example, with a resistant bug 3 years ago or 5 years ago, they will always be in isolation and then they may culture out sensitive bugs in the future. So we could see whether the outcomes and the severity of those outcomes have to do with a sensitive or resistant bug, and if our view and our dogma on that actually matches what happens clinically.