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Skin and soft tissue infections
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Infections due to rapidly growing mycobacteria. , disseminated infection to soft tissue after systemic steroid use; , abscess after injection with contaminated adrenal cortex solution; , breast reduction—associated infection; , pedicure-associated infection; , cosmetic surgery—associated facial infection.

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Infections due to rapidly growing mycobacteria. , disseminated infection to soft tissue after systemic steroid use; , abscess after injection with contaminated adrenal cortex solution; , breast reduction—associated infection; , pedicure-associated infection; , cosmetic surgery—associated facial infection.

Furunculosis after whirlpool footbaths has received much attention [ 21 ]. In one outbreak, risk included microabrasion from shaving the legs before the footbath [ 22 ]. Typing of strains of M. fortuitum in one case and Mycobacterium mageritense in another case obtained from the footbath and the patient revealed identical patterns. In these instances, it was concluded that contamination resulted from municipal water, which supplied the footbath. It was speculated that further growth on sloughed skin and other organic debris present in the drain resulted in high numbers of organisms. Infections ranged from mild to severe. Most patients were treated with antimicrobials, and the infection resolved in all, although some were left with disfigurement. It is important to note that new skin lesions can occur even during appropriate therapy.

Cosmetic surgery has emerged as an important source of rapidly growing mycobacterial infection [ 23 ]. Facial procedures, abdominoplasty, liposuction, breast reduction or augmentation, mammoplasty, and nipple piercing have all been associated with cases of postprocedure infection with rapidly growing mycobacteria. Contributing factors may include increased use of alternative medicine providers and increased numbers of procedures performed in freestanding surgical centers that are not routinely monitored by infection-control committees or equivalent oversight bodies. The recent outbreak of infection due to rapidly growing mycobacteria after cosmetic surgery done in the Dominican Republic and Venezuela underscores this issue [ 24 ]. To prevent skin and device-related infections, strict avoidance of tap (nonsterile) water for medical procedures and instrument cleaning is recommended.

Postsurgical wound infections have also been reported after the use of contaminated solutions, instrumentation, and implants (e.g., gentian violet, ice, lacrimal duct probes, tympanostomy tubes, epidural catheters, graft materials). There are also reports of postsurgical infections associated with contaminated suture material causing prolonged postoperative healing, wound breakdown, and intra-abdominal fistula formation. Mediastinitis and sternal wound infections due to M. fortuitum or M. chelonae have been reported after cardiothoracic surgery [ 25 ]. Skin infections due to rapidly growing mycobacteria usually produce painful red to violaceous nodules that can drain serosanguinous material, ulcerate, spread to deeper tissues, and form fistulous tracts. Culture material frequently yields negative results on smear testing for acid-fast bacilli and reveals abundant neutrophils [ 26 , 27 ]. Granulomas may be caseating or noncaseating. The immunocompromised person may not display the typical histopathologic findings. Frequently a patient will present with an indolent inflammatory lesion that is partially or entirely unresponsive to antimicrobials commonly used for treatment of cellulitis. Corticosteroids are often administered before the definitive diagnosis is made, which may delay the diagnosis of rapidly growing mycobacterial infection because of their potent anti-inflammatory action and temporary relief of signs and symptoms of localized infection.


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Without or without insurance, medical debt can be a huge burden. Hospital and doctor’s bills can be extremely high and sometimes impossible to pay without a plan.

Even if you have an insurance plan, you can quickly get overloaded with co-pays, deductibles, and prescriptions.

Unpaid healthcare expenses are easily one of the largest debts that people can face in their lives, and knowing where to turn for help can be a challenge. That’s added on top of your other bills and expenses you have to pay each month.

What’s more, sometimes health care bills are hard to decipher and can even be inaccurate, so it’s important to be cautious whenever dealing with them. It’s also useful to know what options are available to you to make it easier to manage your medical debt. We’ve got all the information you need below.

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Are your medical bills accurate?

When you’re dealing with medical debt, it can be hard to determine what you are being charged for. Depending on your insurance (assuming you have insurance) it isn’t always clear in the first place just how much you might owe.

Services might sometimes overlap or be described in technical language, and there can be billing for any variety of tests, medicine, use of equipment, or time spent with doctors or specialists.

Hospital bills can be particularly hard to break down. Sometimes insurance companies won’t pay what they said they would, and doctors or hospitals will bill you for unexpected items you thought were supposed to be covered by your healthcare plan.

There can also be issues of duplicate billing and other mistakes that are hard to track down. Plus, your bills might be staggered so that you don’t actually know the total cost of what you owe.

For all these reasons, it’s crucial to be very careful and thorough when dealing with your medical bills to ensure that you aren’t paying more than you should be. Unfortunately, this can mean a lot of time on the phone clarifying every potential issue as it arises.

Otherwise, these issues can be buried in paperwork. It’s also essential to keep thorough and accurate records so you have a reference point whenever a new question arises.

One of the best things to do is familiarize yourself with your insurance plan’s explanation of benefits (EOB). This isn’t always clear, but you can get a better understanding of the types of procedures you’re covered for.

You can also find out what percentage you’re responsible for, and what medical providers are considered in-network versus out-of-network, or Tier 1 versus Tier 2. If you’re confused, call your healthcare company for clarity.

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surrounding medical bills were weighed the same as credit card or any other type of debt.

Coculture assay

Inhibition of viral attachment Virus was preincubated with heparin or d -mannose, at 37°C for 60 min, and was added to Ect1 cell monolayer. The culture was washed 5 times the next day and lysed immediately, and p24 was determined. For treatment with heparitinase, the cells were pretreated with 0.1 U of heparitinase III (Sigma-Aldrich) for 60 min at 37°C, followed by exposure to virus for 16 h. The cells were then thoroughly washed and lysed for determination of p24. Cells without treatment served as controls

Inhibition of viral attachment

HIV-1 infection of epithelial cells The generation and characterization of the Ect1 cell line have been reported elsewhere [ 17 ]. Our preliminary results indicated that the epithelial cells were resistant to cell-free HIV-1 infection. To determine whether the epithelial cells require higher viral input to become infected, Ect1 cells were exposed to an increasing viral input, and the culture supernatants were monitored for production of p24 over a period of up to 13 days after exposure to virus. Figure 1A and 1B show the supernatant viral p24 in Ect1 cells exposed to either RF (a CXCR4-using, synctium-inducing [SI] virus) or BaL (a CCR5-using, non–synctium-inducing [NSI] virus) at increasing viral inputs. With a viral input of 10 or 20 ng/mL p24, which nevertheless resulted in a productive infection of H9 cells or PBMCs (data not shown), there was no appreciable level of p24 detected during the entire period of culture (up to 13 days after exposure to virus). However, with higher viral inputs, we consistently observed increasing levels of p24 in the Ect1 culture, levels that peaked around 9 days after exposure to virus. For example, with RF virus input at 250 ng/mL, the level of p24 increased during the culture period and reached ∼2.3 ng/mL at the peak, 9 days after exposure to virus. We also tested another CCR5 isolate, ADA, and a dual-tropic isolate, 89.6, and found that the profiles of p24 in the culture supernatants, during the time, did not appear to have any relationship with the viral phenotypes (data not shown). Consistent with all the virus isolates tested the levels of p24 were generally significantly lower than those for the input virus, even at the peak

HIV-1 infection of epithelial cells
Figure 1
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Viral production in Ect1 cells or primary keratinocytes. Ect1 cells and or primary keratinocytes were exposed to increasing amounts of RF and or BaL virus overnight at 37°C. The viral production was monitored by measuring supernatant p24 at the indicated time points. Each data point represents mean of duplicate wells, and each virus was repeated at least 3 times. Viral input: RF and ○, 10 ng/mL; ▪, 50 ng/mL; ▴, 250 ng/mL; BaL ○, 20 ng/mL; ▪, 100 ng/mL; ▴, 500 ng/mL

Figure 1
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Viral production in Ect1 cells or primary keratinocytes. Ect1 cells and or primary keratinocytes were exposed to increasing amounts of RF and or BaL virus overnight at 37°C. The viral production was monitored by measuring supernatant p24 at the indicated time points. Each data point represents mean of duplicate wells, and each virus was repeated at least 3 times. Viral input: RF and ○, 10 ng/mL; ▪, 50 ng/mL; ▴, 250 ng/mL; BaL ○, 20 ng/mL; ▪, 100 ng/mL; ▴, 500 ng/mL

To investigate whether this is a phenomenon specifically associated with transformed epithelial cells, monolayers of human primary foreskin keratinocytes were exposed to 10 and 250 ng/mL p24 of RF virus. Again, the profile of production of p24 was similar to that of Ect1 cells, except that much higher levels of p24 were detected in the culture supernatant ( figure 1C ). For example, at 9 days after exposure to virus, 12 ng/mL p24 was detected in Ect1 cell culture exposed to 250 ng/mL p24 of virus. Because of the limited life span of the primary cells, we did not obtain p24 values from cultures >9 days after exposure to virus

But what about the time cost of diversification? Underwriting new investments takes time away from underwriting the existing ones. This might seem like a problem that could be solved by adding resources, say by hiring analysts to process more potential investments. But I don’t buy this approach. In my model, certain aspects of the investment process are too critical to be delegated: To do so might lower the quality of the work or, at the very least, my confidence in the conclusion. On paper a value range is a value range.

In practice, the skill and experience of the analyst matters. Since I will always be the primary capital allocator in my model, adding analysts or other resources cannot resolve all the inherent bottlenecks of assessing potential investments. However, this factor is also environment-dependent. As a professional investor who has been valuing companies for 17 years, I know quite a few firms and industries.

So in an environment in which many industries and companies are deeply undervalued, I would not need much time to value additional companies and add them to the portfolio. On the other hand, when opportunities are scarce and scattered in various pockets of the market, my learning curve on a potential new investment will likely be much steeper.

So diversification is worthwhile in environments where potential investments offer similar prospective returns or where undervaluation is widespread.

On the other hand, increased concentration is the logical course in environments where the opportunity cost — in both returns and time — of adding new investments to the portfolio is high. I set the upper bound for the number of investments at 20 under normal circumstances, which is consistent with my typical “small” position size of 5%.

Thus the portfolio will have between 10 and 20 investments under normal circumstances. The precise level of concentration within that range depends on the environment and the available opportunities.

So to return to the free lunch, the old adage holds true in investing and in life: There is no such thing — not even diversification.

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All posts are the opinion of the author. As such, they should not be construed as investment advice, nor do the opinions expressed necessarily reflect the views of CFA Institute or the author’s employer.

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an investment firm with a concentrated long-term intrinsic value strategy. Prior to founding the firm in 2016, Mishuris was a managing director at Manulife Asset Management. From 2004 through 2010, he was a vice president at Evergreen Investments. Mishuris began his career at Fidelity as an equity research associate. Mishuris received an S.B. in computer science and an S.B. in economics from the Massachusetts Institute of Technology (MIT).

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