Biology 260: Diseases of the Skin and Eye

Since Meg had recently returned from summer camp in Vermont with the rash, it seems reasonable to assume that the rash was due to an infection picked up at camp. The infection didn't appear to be an infection from the normal skin or eye micro-organisms--Staphylococcus epidermidis, Staphylococcus aureus, Streptococcus pneumoniae, Streptococcus pyogenes, Enterobacteriaceae, Corynebacteria, or Mycobacteria (Todar, 2008)--all of those infections either affected a different part of the body such as the eyes or face or exhibited different symptoms such as lesions (Cowan & Talaro, 2009, p. 538-539).

The immediate suspect for this infection was ringworm of the body (Tinea Corporis). In all likelihood Meg picked up the infection when swimming or in close contact with other adolescents at summer camp. Close contact and shared use of towels and close are excellent ways to transmit a highly contagious infection like Ringworm (Cowan, pp. 559-560). This diagnosis could be partially validated by taking a Gram stain of the skin rash and verifying that the Gram stain was positive (Cowan, p. 566).

Another possible suspect was Lyme disease (B. burgdorferi) that was the cause of the rash because B. burgdorferi, transmitted by ticks from deer and mice, can have somewhat similar symptoms of a circular rash around the bite (Cowan, pp. 619). Also, B. burgdorferi is a serious problem in the Northeas and upper Midwest of the USA ("Map: reported cases," 2004). This was why Meg's doctor asked about aching joints, since Lyme disease can have those symptoms as well as others like dizziness, headache, and fever (Cowan, pp. 619). Fortunately, Meg wasn't displaying any of those symptoms nor mentioned them in the oral history. Nonetheless, checking for a possible Lyme disease infection was good medicine on the part of the doctor.

Ringworm thrives in wet and warm environments and is communicated via direct contact with other people as well as through clothing, bedding and even soil (Cowan, 2009, pp. 559-560). Furthermore, Vermont in the summertime is warm and humid, making it also a great environment for Microsporum. Had Meg attended summer camp in a hot and dry climate such as Arizona, the diagnosis might have been more suspect. One way to prevent ringworm is to keep the skin dry (Cowan, p. 561), which is much easier in a desert climate than a woods climate in the Northeast USA.

Once the diagnosis of ringworm was made, typical treatment is an anti-fungal creams, such a synthetic azoles, other topical anti-fungal (Cowan, p. 561) which halt the growth of the fungus. Azole antifungals work by inhibiting an enzyme (cytochrome P450 enzyme 14-α-sterol-demethylase) ergosterol, an essential molecule of the fungal cell membrane, which arrest fungal growth (Zionos, & Bennet, 2008)). Ringworm feeds on the constantly replenished dead skin in the epidermis and if the fungus cannot grow it is eventually discarded along with