Common in adults as well as adolescents, acne requires combined medical treatments as well as patient education on home care to control the condition and prevent scars. Dermatologist Timothy Berger, MD, dispels acne myths; clarifies which meds are appropriate for which patients; describes possible underlying issues, such as metabolic syndrome and PCOS; and discusses other serious skin issues, from abscesses to staph infections.
I'm the senior dermatologist here at UCSF. Um, I started practicing dermatology in 1980, so this is my 42nd year. Um, and, uh, I was asked to talk about acne and other, uh, Pustular inflammatory processes in the skin, so that's what we have here today, um. So I'm gonna show just a few cases. A lot of this may be repetition, but I'll try to emphasize, uh, some practical aspects, uh, that are not clearly outlined in the literature. So case 1, 18-year-old healthy adolescent, 2 years of pimples. And here he is with follicular papules, pustules, and he also has prominent Closed and open chmodomes, which distinguishes acne vulgaris from acne rosacea. In adults, that's an important finding because those diseases can overlap. So this would be grade 3 acne, papulopustular acne. It's on the cheeks, and the other aspect of it that is important is it's leaving him with pitted scars. So, um, that makes it more important for us to treat this. So this is an almost universal condition. When they have in large studies followed children through elementary school, the first sign of going through puberty is the development of acne. It precedes everything else. Um, Most cases resolve by age 25, but unfortunately, if you look in women between the ages of 20 and 45, the prevalence of acne does not decrease. So women tend to have more persistent acne, and all dermatologists have practices of middle-aged and professional women with Uh, acne that hangs on. This is not abnormal and doesn't indicate any, uh, significant metabolic problem in most of those patients. All races get it, and there's often a family history. So you get blackheads and whiteheads, those are the chromosomes, then papules and pustules, those are the things with pus, and then inflammatory nodules which go down deep into the fat. The papules, pustules, and cysts can be scarring. So if you biopsy them, this is a bump. Here are a little papule. This is a pustule. Enough neutrophils for this to exude, and then a deep cyst. You can see that in these latter two cases on my right side, the creatinous debris has ruptured outside the hair follicle and it's caused a prominent inflammatory response. So this is how we score acne, grade 1234. This is a patient who has comedonal acne, primarily, uh, with a few pustules. This is called pomade acne and is in part related to the products that are applied uh to the hair. This is grade 2 to 3 acne, papulopustular. This is scarring, grade 4. This is truncal acne, grade 4. This is more common in men. And then here's severe nodular cystic acne. On the trunk. So what elements are important to ask in this case? Well, you want to talk about patient's medications, what about their diet? Weight gaining and other supplements or all of the above, when all of the above is an answer, that's always the answer. So, We will go through these. There's medications that are used fairly regularly that cause acne. Lithium and Dilantin, the anti-seizure medicines, are two of the big ones. Any patients on systemic steroids, they can get acne. Um, and if there's exogenous androgen being taken. And beyond androgen, weight gaining supplements of other types um can cause acne to flare as well. The other, uh, ingestant that worsens acne is iodide. Um, and iodide is found in, uh, seaweed and other products from the ocean. So when I worked in Korea, it was a common problem that people who snacked on a lot of seaweed would get acne. Many multivitamins are made from seaweed or kelp, and so for patients who have acne and are on multivitamins, I have to take the vitamins without minerals, so there's no iodine in there. So why do we get acne? Well, bacteria in the hair follicle, androgens in the circulation, the hair follicle plugging up, and oil. And all of these are a problem. Or a progenitor of the acne. So, you need to have hormones first and those have to be androgens. Um, and those androgens wake up the sebaceous gland. Uh, and produce sebum. The sebum is eaten by the bacteria, and uh they break the sebum, which is a triglyceride, into free fatty acids, and those free fatty acids are what caused the inflammation. And this is all happening behind a plug in the hair follicle, so that this inflammatory process can't exude and instead stays trapped in the hair follicle ruptures. People who have severe scarring acne may also have sort of wimpy follicles, so that with limited inflammation, they rupture more easily and tend to scar. So identifying that patient and being more aggressive in their treatment is important. So what do we use to treat acne? We use oral antibiotics. We use topical benzoyl peroxide, that's over the counter, and topical retinoids. Um, In general, We're gonna try to treat all four of these causes and so we combine agents that work in different ways. So we're gonna use topical antibiotics, for instance, to treat the bacterial component, and we're gonna use topical tretinoin or Retin-A to treat the follicular plugging component. For teenagers, this is a big problem, um, and can generate a fairly poor quality of life. There's a correlation between the mood of a teenager and the presence of their acne, and it's, and it's pretty regular for us to treat teenagers to see a big change in their, uh, well-being when their acne is under much better control. And it's important to recognize that once the scarring occurs, we really don't have that great treatments for it. Um, And so preventing the scarring is really critically important. So what anti antibacterials do you have? Well, topically, we have erythromycin, clindamycin, we have sulfur, just elemental sulfur, benzoyl peroxide. Remember, erythromycin and clindamycin can share resistance, so, uh, if one of these fails, the other may not work. We have anti-roadonal agents, so that tretinoin is the Most commonly used one, adapalene or Differin, which is over the counter. Your patients can just buy it. It's less irritating than Retin-A and works pretty well. And then benzoyl peroxide, in addition to killing the bacteria, also has some anti-roadonal effect. So, um, these are helpful in treating that follicular plugging and then. We have Accutane, which stops the follicular plugging and also markedly reduces semen production. If you biopsy someone's facial skin who's on Accutane, they have no visible sebaceous glands in the biopsy. The stem cells are still there, but the sebaceous glands have just, uh, sort of shrunk up. Uh, and so, uh, that's one of the reasons why the patients have a fairly sustained remission after isotretinoin. Um, benzoyl peroxide now comes in a lot of different combinations. The topical antibiotic with the benzoyl peroxide. Uh, there is a problem if you use a single antibiotic that you get resistance. So it's usually better to use benzoyl peroxide with a topical antibiotic, something like with clindamycin plus benzoyl peroxide. Or erythromycin plus benzoyl peroxide. Uh, there are also combinations of antibiotics with retinoids. You notice that there's no combinations of retinoids and benzoyl peroxide because the two of them inactivate each other. So if your patient is using benzoyl peroxide and also using a retinoid, they have to put them on at separate times because they'll interfere with each other. So, uh, that's why there's no combination of an antibiotic, uh, benzoyl peroxide and a retinoid. The combinations are more expensive, but for kids, they sometimes are a little bit easier as far as compliance is concerned. OK, so acne is not related to skin dirt. Washing more doesn't help. So if the mom's in the room and You know, they're gonna be maybe bugging their teenager. It's always helpful to have the patient's back and say, you know, Mom, really more washing and this cleanliness is not gonna really help the acne. And in fact, excessive scrubbing. Can trigger acne because in those patients who have these fragile follicles, if they start rubbing and scrubbing, they're gonna rupture those follicles under the skin and then get inflammatory lesions. So no scrubs, no mitts, no sponges, just gentle washing. And in fact, friction itself triggers acne. So you see that all the time on the buttocks where people like truck drivers will get uh frictional folliculitis or acne. Uh, you guys may be too young, but Dorothy Hamill, if you remember, who won the Olympic gold medal in figure skating, had this flip of a hairdo like this. So all the girls were brushing their hair like this, and they all got acne on one half of their forehead from the friction of the hair brushing. So, uh, friction is not good for acne. OK. 32-year-old professional woman presents complaining of persistent acne. She had acne in her teens. She took two courses of Accutane. Uh, about 7 or 8 years apart. That's about how long a course of Accutane on average will last. Um, so most people are not cured, but they do get a sustained remission. When asked, she says she has normal menses, and she's frustrated because she still has acne and she's not a teenager anymore. So she's of normal weight, she doesn't have any evidence of hirsutism, no excess hair, um, and she has follicular papules primarily along the jawline and around the mouth, and this is a typical pattern of post-teenage acne. So it sort of starts here in the center face and then sort of moves out and ends up sort of persisting along the jawline and up into the temporal area, uh. Well into the 20s and 30s. So there's a patient who has somewhat that pattern of acne. So when you talk to this patient, several of the lessons I've learned is If the patient says they have regular menses, you actually have to be more clear about that because, um, the patient's normal menstrual cycle may be such that they have a period every 3 months. Uh, so they may actually even meet the criteria for PCOS even though they feel that's normal menses for them. Uh, I think that you can identify those patients who have Uh, androgen excess, uh, or excess androgen effect if they have an oily T-zone. So those are the patients who say that they have to use an astringent on their nose or it gets shiny by the afternoon. And if they, if this person goes on Accutane, that's one of the first things they'll notice it gets better. You need to think about pregnancy if you're going to treat a woman who potentially can become pregnant. And then I will often have the patient bring in all their stuff and you'd be surprised what you'll find and then get rid of all the irritating things um in that bucket. So topical antibiotics, I think work really well in this group in uh sort of women past teenage years, and I think clindamycin is more effective than erythromycin, and you can add benzoyl peroxide to that. Topical retinoids are good for this group, but their skin tends to be a little bit more sensitive. And so I start off very slowly. So I'll give the patient The topical retinoid and have them use a thin, small amount twice a week to start and then build up. If they use it every day right from the beginning, they may get a flare. Azeleic acid is good for mild acne, but for patients who have uh natural skin pigmentation, persons of color, the azelaic acid tends to diminish the post-inflammatory hyperpigmentation. So it's really a good product for persons who have mild acne, but that's leading to pigmentary change. And, uh, lastly, topical sulfur is safe to use, um, in everyone, um, and has some good activity against acne, just a little smelly. Uh, topical retinoids have never been shown to cause any kind of fetal problems, but they are not recommended during pregnancy. Benzoyl peroxide is safe. OK, and then if the patient doesn't respond or has grade 3 or 4 acne, we'll give oral antibiotics. Doxycycline works better than tetracycline. It's easier to take. Um, and so that's where we usually start. Minocycline is more effective than doxycycline. It gets pushed into the hair follicle a little bit better. Minocycline does have a higher rate of causing lupus. And minocycline also causes Uh, an inflammatory vasculitis that's identical to polyarteritis nodosa. So, um, you can get those unusual side effects from the minocycline, and it also causes hyperpigmentation because it's deposited in the skin with this gray color, so you have to watch for that. Um, in my experience, if you treat patients like this with isotretinoin, as opposed to getting that 7 to 8-year free period that happens with teenage acne, and these patients, while they're on Accutane, they're great. When they go off Accutane for 6 months, they're great, and then it comes right back. So, um, I have to have another strategy to deal with them. Uh, I do two things. Uh, one is hormonal therapy, which we'll talk about, and the other is, uh, in patients who can't become pregnant, I may put them on low-dose Accutane chronically. And I have patients who take one Accutane pill every 2 weeks. So 2 pills a month, uh, completely controls their acne, costs 10 bucks. It's the cheapest treatment that works for this refractory acne. So, uh, that you can do. It's just if the woman is a, a childbearing potential, the system doesn't accommodate for chronic accutane therapy, and so it's problematic. What I usually do is write for a year's worth and then put them back on iPledge again. So It's pretty clear. That most women who have acne after teenage years have some form of hormonal imbalance, and there are different types of that. But those things, that hormonal imbalance, which we'll talk about the different types. All respond to this strategy. So you can give an oral contraceptive and the estrogens reduce semen production, or my favorite, spironolactone. So spironolactone, uh, It was noted when it was made in the 50s that women who had fine hair on their upper lip, that it got much less prominent while they were on spironolactone, and they then documented that it has an anti-androgen effect directly on the sebaceous gland. And the dose you need is somewhere between 25 and 100 mg a day. Um, and this is my favorite acne treatment for women who have chronic acne in this, uh, post-teenage year. Side, side effects are totally minimal. Uh, there's now good evidence that you don't have to monitor potassium. Uh, and you can add Aldactone to an oral contraceptive, uh, to suppress the hormones more. Uh, or this hormonal effect more. Uh, most people on Aldactone don't get hypotension. I, I do have marathoners and other people who might be doing exercise where they're gonna replace a large portion of their body fluids, and they may replace those with pota high potassium drinks. So I do have them stop their spironolactone the day of A sporting event where they're gonna sweat 2 3 4 L maybe. Uh, but otherwise, I don't monitor. The patients don't really have any side effects and it's a great drug for controlling this and much easier for patients to take and avoids the difficulties of isotretinoin. If the patient is frankly here's to the female patient, then you need an endocrine workup. Um, Which would include free and total testosterone and the DHEAS. If the patient's menstrual cycles are irregular, you might wanna work them up for PCOS. But by far the most common reason that people have persistent acne after teenage years is that they have metabolic syndrome. Um, and What happens is in metabolic syndrome, as you know, there's progressive insulin resistance, and so insulin resistance uh leads to higher insulin levels. And those higher insulin levels induce epidermal growth factor, which enhances follicular plugging. So the type 2 diabetes metabolic syndrome, like polycystic ovarian syndrome, is associated with acne. Um, and there's some interesting dietary information which we'll talk about. So, what about stress and diet and acne? Um, That there's now very good studies that stress triggers flares of acne. Uh, it increases follicular keratinization and it changes inflammation. So, uh, people often have flares of acne with stress. High glycemic diets. Uh, which is essentially the normal young adult teenage US diet. Uh, will worsen acne. And I, I was in Okinawa when I was a teenager in the Boy Scouts, and we would have native Okinawan young men. Join our scout troop for camp. And half of those people had to be sent back home because when they switched from their Japanese diet to our Western diet, they got fulminant acne and had to go back home. So, I, I personally had seen this, and now the, the mechanism of all this is kind of understood. So a high BMI is associated with worse acne if you're past the age of 18. And this again has to do with this insulin resistance, and in addition to causing follicular plugging, high levels of insulin increase androgen production and reduce sex hormone binding globulin, so you have more free androgen. So as I tell patients, you know, your mom is right. The hamburger is bad, but it's not the greasy hamburger, it's the bun and the fries that are the problem. So, In Australia, they did this study. Where they had 2 cafeterias in 2 dorms at a university. And they randomized the students. So that what they did is they changed the food they offered them in the cafeteria. The kids were able to eat as much as they want, take as much as they want, but in one cafeteria, all the food had a low glycemic load, and in the other, they had just like the regular diet. And um those. Mostly boys who were on the low glycemic diet had a much more rapid improvement of their acne. Now, all of the patients were counseled about the study, and in acne studies, what happens is people get better because they Take care of their skin a little bit more. They sort of pay attention. They may be on medicines which they then begin to use. So there was this fairly marked reduction, and it turns out going on a low glycemic diet for a young man is as effective as going on an oral antibiotic for treating acne. And here are some before and after pictures. Before, after, before, after, before, after, it's not perfect, but that's, that's pretty good result for essentially just being on the right diet to be healthy, right? So, so I do counsel young men about what they eat, um. The other, uh, complicating factor is that way, which is in, um, A lot of uh weight gaining products, WHEY, which is the protein from milk, also uh has an adverse effect on acne. So, uh, that's another dietary thing to be discussed. What about cosmetics? Cosmetics get tested for chromatogenicity, so whether they make acne, um, and, but they don't label them. Because if they labeled them non-communogenic, then people would say, well, what about this over here? It doesn't have that label. Does that make acne? And then, of course, what are you going to say, so the companies don't do that. Um, but if you notice that the patient is having acne in areas where they're applying makeup, you may want to talk to them about asking specifically for, uh, non-commutogenic. Uh, products. Sunblocks and moisturizers, uh, in addition, should be non-comedogenic. Again, scrubbing makes acne worse. OK, so what do we do? We take a menstrual history, we do a dietary history, especially in males who are over the age of 18, although I, I didn't mention one thing. In um the low glycemic diet study. Boys under the age of 18 didn't benefit from the low glycemic diet. Only the boys over 18, over the age of 18. So there appears to be a change. So when you're going through puberty, your hormone levels are really high, and then as you get older, if your acne is persisting, it becomes more. Uh, related to these other factors that increase, uh, your hormone levels. So take a dietary history, look for hirsutism in women, talk about metabolic syndrome and weight. If you're gonna use a topical antibiotic, use it with benzoyl peroxide, and remember, Aldactone, uh, in the woman who's failing, uh, oral antibiotics or doesn't want to take chronic oral antibiotics, which in my experience is, this has saved my behind many, many times. Retinoids, topical retinoids are great, but start really slow, um, and stop rubbing and picking. OK, so now we're gonna talk uh a little bit about pyodermis in the skin. Uh, most pyodermas in the skin are due to staph aureus. Uh, 5% of people carry Staph aureus. 10% of us carry Staph aureus because we're healthcare workers. Uh, and Staph aureus lives. In your Place where you live. So, um, more and more over time as I've practiced. I'm treating larger and larger segments. Of people around people who have recurrent staph infections, and we'll talk about that. OK, so first case here, 35 year old male, 2 weeks of blisters on the legs which itch a little. And you see these. Little bumps that start around the hair follicle here, which is usually the ingress point of the staff. And then they formed this flaccid blister that ruptured. So this is classic bullissimpetigo. And bullus impetigo in temperate climates is due to staph. In tropical climates, it's due to strep. So, uh, there's different bacteria that cause the same. Uh, pathogenic condition, whether you're in the tropics or in, uh, temperate climates. That's bullis impetigo. And these are the bacterial infections we think of primarily with staph, impetigo, folliculitis, abscesses, ecyma, we'll talk about, then cellulitis, necrotizing fasciitis, and then toxic shock syndromes, which can occur from the toxins that staph makes. There are a few interesting things about staph when staph colonizes, uh, dermatitis. It causes the immune cells in the dermatitis to lose their steroid receptors. So if you have a patient who has eczema and they suddenly are getting worse, one of the reasons can be that their eczema is infected with staph. You have normally antimicrobial peptides that your body makes. And these things uh prevent staph. Those antimicrobial peptides are packaged in the oil that goes to the surface of your skin. And that oil delivery to the surface of your skin in that packaging is vitamin D dependent. So if you have low vitamin D, you can get recurrent infections, and if you have eczema and low vitamin D, your eczema does worse and you get more infections. So one of the things that I check and monitor and treat is vitamin D in patients who are having recurrent infections. The Nobel Prize was given in 2006. For the concept of sending people with tuberculosis to sanitaria high in altitude or in the south. And what happened, of course, when you did that is they got more sunlight, so their vitamin D went up and their tuberculosis did better. So it took us from 1906 to 2006 to figure out why that was the case, but uh the Nobel Committee was correct. OK, this is also a patient with impetigo, and in the center, it's crusted, but you can see here this superficial blister, and this is where you wanna take a culture, uh, so you can identify the infectious organism. This is folliculitis, a superficial folliculitis, so you can see that the staff likes to go down the hair follicle. The groin is another place where staph is carried. Anyone who is culture positive in the groin is usually culture positive from the nose, so we think the nares are the primary place where staph lives when we acquire it. If you take healthcare workers and you have them stick their hand in a plastic bag with, you know, culture media, so you can grow out the staff if they have it, if you treat the patient's nose. Their hands become culture negative without treating their hands. So it really does suggest that the Neres is where staph lives. Most antibiotics do not penetrate the nares. Uh, except for rifampin. So, uh, and long-term clindamycin. So, uh, if you have a patient with recurrent diseases we'll talk about, you really need to pick antibiotics that are going to get rid of the or do something to get rid of the nasal carriage. OK. This is ecthyma. Eczema in the tropics is due to strep. Eczema in temporal, temperate climates is due to staph. It looks like it's punched out ulcer. Patient may or may not say that it started like an impetigo lesion. Um, these are pretty difficult to treat. The course of antibiotics is long, um, and the patients tend to be recurrent visitors to your clinic. So, um, it's a little bit more of a difficult to manage thing. So you definitely wanna know what the culture and sensitivity is because you're gonna be on antibiotics for some time. This is an abscess or furuncle, a carbuncle. Uh, on the back Cellulitis So, inflammation that then causes erythema usually moves from distal to proximal. Patients can have systemic symptoms and elevated white count. And this is cellulitis with purpura and bullae. Uh, in a study that they did at Harvard, They looked at patients who were diagnosed with bilateral cellulitis. All those patients had stasis dermatitis, none of them had cellulitis. So if you see what looks like cellulitis on both legs. Think of another diagnosis. Um, And if the patient's gonna be admitted to the hospital unless they have an elevated white count or toxic, you may not need to give them antibiotics, because usually it's a fluid problem. And this is necrotizing fasciitis, so an area of deep infection with necrosis of the overlying skin. So the correct treatment for an abscess is? IND, right? If there's pus, get it out and In many studies that have been done. Additional antibiotics in immunocompetent people and even in patients with HIV do not improve the outcome. So the treatment is I&D. Antibiotics alone are not the treatment for loculated. Um, areas of infection, so you need to get it out. OK. What's the most common cause of cellulitis in the lower extremity in a healthy person if they don't have a leg ulcer? Pretty healthy person comes in, they got cellulitis. They didn't have an injury, they don't have an ulcer. The problem is athlete's foot, so they get athlete's foot in between the toes. The bacteria overgrowing there, they kind of cause a little crack, and then the strep get in there and so, um. In the like basic training at uh Uh, in San Antonio, for instance, they, you know, screen all the young guys when they come. They give them a talk about looking in between their toes. They give them powder or other things to treat any athlete's foot that's there, and they reduce the number of admissions of these young recruits into the hospital just by that kind of intervention. So, uh, look in between the toes for, uh, we had a Poor young girl who had She was a teenager, and so the pediatricians didn't pick up. She had bad athlete's foot. She'd been admitted 6 times for cellulitis. She had a course of oral rebenafine, and that was it. She was not in the hospital anymore. OK. What about treating community-acquired MRSA? What antibiotics do we use? This is one of the reasons now that I more and more want culture patients cause I wanna know what their sensitivities are, because I'm gonna take antibiotics and they may end up with recurrent infections. So I wanna know what antibiotics their bug is sensitive to. Whatever antibiotic your community uses as first line for staph, what will happen over time is that, that it'll become resistant. So when I was practicing in the late 80s here in San Francisco, I was at San Francisco General Hospital. We had a huge HIV population. Um and many of those patients were on sulfamethoxazole, trimethoprim for PCP prophylaxis. You guys may remember those days. Um, and all the staff that we cultured was sulfamethoxazole trimethoprim resistant. Now, because everybody uses doxycycline because they're worried about MRSA. All we're culturing is doxycycline resistant staff, and all the staff in the community is now sensitive to sulfamethoxazole trimethoprim. So there's antibiotic pressure from the application of antibiotics to the population and however, the treating healthcare workers in the community are using antibiotics that will determine the sensitivity of staff in your community. So you kind of need to monitor that. And know what that is. The hospital has that data usually posted somewhere, um, and, you know, once every 6 months to 1 year, I look at that, uh, just to know if there's been a shift in the antibiotic profile of staff in our environment. OK, so we can use doxycycline that's become relatively standard. It's really a good drug and it's, it's cheap now. Uh, sulfamethoxazole, dermatologists are always afraid of the sulfa drugs cause they cause bad drug rashes. Quinolones, we've had 3 ruptured Achilles tendons in our department, so Cipro's gotten a bad name, but, uh, other than that, Clinda. I like, but remember, if the staph comes back as erythromycin resistant, then it has some likelihood that there'll be an inducible clindamycin resistance, so you don't want to use clina if the sensitivity says it's erythromycin resistant. OK. What's the most common cause of recurrent staph aureus infections? So being a nasal carrier, right? So activities that lead to the nasal carriage. Intravenous drug users. If you get allergy shots, your rate of staph carriage goes up. If you are injecting insulin, your rate of staph carriage goes up. If you have atopic dermatitis, if you're a healthcare worker, so all these things that break the skin barrier or that expose you to staph increase your risk for carrying staph, and that carriage is the source of infections, and they did a study where they took patients who are going into the operating room. And they just swabbed and cultured their noses before they went in. And then they looked. After, and they looked at the patients who got wound infections, you know, got infections of their wound, surgical wound, right? It was the staff that they took into the OR. They didn't pick it up from the doctors or from the equipment. It was their own staff that was the problem. So if you have a patient who's had problems with recurrent nasal, I mean with recurrent staph infections, and they're going to have surgery, you probably want to try to eradicate that staph infection. Um, And treatment of nasal carriage is required to stop these recurrent episodes. So just giving antibiotics doesn't solve the problem. You got to get rid of the carriage, uh, and we'll talk about that. The other thing is that some persons are susceptible to staph. If you have atopic dermatitis, if you're immune deficient, I have a patient who's a fireman who got trapped in a building and had 80% 2nd degree burns, so he just has essentially scar for skin. And he gets recurrent staph infections because he has no Sebaceous glands. He has no natural protection, plus he keeps his skin covered, so he's vitamin D deficient. So, uh, he's getting recurrent staph infections, but he's not the carrier. Then, and he was sent to me because they kept culturing his ear he's not finding anything. But then when I treated his dog, his wife, and his son, he did much better. OK. So if someone has recurrent staph infections, culture the lesions, get sensitivities. If it's staph. Give 5 days of rifampin with your appropriate oral antibiotic. 5 days is enough to clear nasal carriage. It's pretty well tolerated. Remember the rifampin. Um, interacts with cytochrome P450 and is the one drug that really breaks down drugs quickly. So if you have a patient who's on methadone, they'll go through opiate withdrawal if you put them on revampin. If you have a woman on oral contraceptives, she might become pregnant, uh, because of the loss of efficacy. So you, you have to pay attention to that, but, uh, the risks are easy to avoid and the benefits are great. And so in the person who has recurrent infections, I'm going to culture their nares, but I'm also going to be thinking about this group of people around them who may intermittently brings staff into their living space and then infect this person. Uh, and especially that's true if this is an immunosuppressed host and the people coming from outside maybe just delivering the staph. So if you look at kids who have recurrently infected eczema, 60% of the time, one of the parents will be a chronic staph carrier. So, uh, do that. Dogs, cats, and many other pets carry staph. I did have a patient who was having recurrent boils and the pediatricians couldn't figure it out. And so then I went in and I was talking to her, and I said, do you have a dog at home? She said, yeah, and I said, well, where's the dog sleep? She said, oh, the dog sleeps in my bed. So they took the dog to the veteran, if the dog was carrying staph. They treat the dog and her abscesses go away. So you have to think of a broader circle than just the person. So over time I've changed my approach to staph in that staph infections are not the person with the staph infection, but the environment in which the staph infection is occurring. OK. Clindamycin orally will clear nasal carriage, but you have to do it for a long time. Um, mupirocin. I think is a good drug. We use it a lot. Um, about 25% of community, uh, staff are resistant. And there's only one place where that rate is higher, and in New Zealand, 50% of all staff are resistant to mupirocin. And that's because New Zealand is the only country where mupirocin is sold over the counter, and so it's overused and all the staff are essentially resistant. So, um, we like mupirocin for the most refractory can't clear the carriage problem. 1.5% gentian violet, one time painted in the nose, gone. So, in a patient where you can't give revampen, the Bactroban hasn't worked. That's your backup strategy. It always works. You just have to be careful that it doesn't drip down on the patient's lip when they're putting it in their nose, cause otherwise they'll have a purple lip for a while. Um, gentian violet is great for, uh, Clearing up staph like in between the toes and people with recurrent cellulitis, especially people who can't treat themselves very often. Like people who are homebound and have a healthcare worker come once a week, or a, a nurse's aide, and once a week, somebody can put that gentian violet in between their toes. It'll dry everything up. It kills the fungus, it kills the bacteria, and uh stops these recurrent infections and cellulitis. OK, what's the sign on physical exam that a cellulitic lesion could be neck fas? So this is the one thing you're always afraid of, right? This is cellulitis. Is it down in that deep compartment? Is it really necrotizing fasciitis and, and that's going to be really serious. So if it's if the tissue is necrotic, that's obviously a concern, right? Something wiped the blood vessels out. So If the patient's hypotensive, septic, if there's evidence of rhabdomyolysis, DIC. If there's sort of just the tissue has died and the epidermis is sloughing off, if you feel air in the tissue, but often the first thing is that there's anesthesia, that the Infection as it clears through this space right over the fascia, it's knocking off the sensory nerves that go to that skin and the area becomes numb. We had a, a lawsuit at UCSF where. The patient had cellulitis, was not getting better, and the medical student kept asking the attendings and writing in the chart. The patient can't feel on this spot. Cellulitis is supposed to be sore. And he kept asking this question, he kept asking this question. After 3 days when the patient tubed, then somebody said, ah, this was neck fascia all along, right? So, um, so that's a good clue to avoid missing that diagnosis.
