Cutaneous leishmaniasis in Texas

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REFERENCES 1. Gathers RC, Lim HW. Centrifugal cicatricial alopecia, past, present and future. J Am Acad Dermatol 2009;60:660-8. 2. Gathers RC, Jankowski M, Eide M, Lim HW. Hair grooming practices and central centrifugal cicatricial alopecia. J Am Acad Dermatol 2009;60:574-8. 3. Khumalo NP, Jessop S, Gumedze F, Ehrlich R. Hairdressing is associated with scalp disease in African schoolchildren. Br J Dermatol 2007;157:106-10. 4. Khumalo NP, Jessop S, Gumedze F, Ehrlich R. Hairdressing and the prevalence of scalp disease in African adults. Br J Dermatol 2007;157:981-8. 5. Khumalo NP, Pillay K, Ngwanya RM. Acute ‘relaxer’-associated scarring alopecia: a report of five cases. Br J Dermatol 2007;156:1394-7. 6. Nnoruka NE. Hair loss: is there a relationship with hair care practices in Nigeria? Int J Dermatol 2005;44(suppl 1):13-7. doi:10.1016/j.jaad.2009.08.012

Goeckerman treatment: Neglected in the consensus approach for critically challenging case scenarios in moderate to severe psoriasis To the Editor: We note that Goeckerman treatment (ultraviolet light phototherapy plus crude coal tar) was considered as one of the top 10 options for managing moderate to severe psoriasis for only six (including three that concerned its use in pregnancy) of the 32 critically challenging case scenarios in the consensus statement recently published in the Journal.1 In contrast, at Mayo Clinic, Goeckerman treatment is one of our top considerations (and often the top choice) for managing the vast majority of scenarios described in this article. Goeckerman treatment has been well documented for decades to be extraordinarily effective, safe, and associated with long-lasting remission2,3; it is also cost effective (current cost, approximately $10000-12000)3 and is associated with a low incidence of adverse effects. There are no absolute contraindications. As a skindirected therapy, it is particularly useful in the described critically challenging case scenarios. Although topical tar and ultraviolet B light are both known carcinogens, the risk of developing nonmelanoma skin cancer has been documented to be low.4,5 Given the riskebenefit ratio of Goeckerman therapy, we believe that it should be included as a top option for managing moderate to severe psoriasis in the vast majority of the scenarios illustrated in this publication. Mark D.P. Davis, MD, Marian T. McEvoy, MD, Michael Camilleri, MD, Alina G. Bridges, MD, Lawrence E. Gibson, MD, and Rokea A. elAzhary, MD

Department of Dermatology, Mayo Clinic, Rochester, Minnesota Funding sources: None. Conflicts of interest: None declared. Correspondence to: Mark D. P. Davis, MD, Department of Dermatology, 200 First St SW, Rochester, MN 55905 E-mail: [email protected] REFERENCES 1. Strober B, Berger E, Cather J, Cohen D, Crowley JJ, Gordon KB, et al. A series of critically challenging case scenarios in moderate to severe psoriasis: a Delphi consensus approach. J Am Acad Dermatol 2009;61(1 suppl. 1):S1-S46. 2. Muller SA, Perry HO. The Goeckerman treatment in psoriasis: six decades of experience at the Mayo Clinic. Cutis 1984;34:265-8, 270. 3. de Miguel R, el-Azhary R. Efficacy, safety, and cost of Goeckerman therapy compared with biologics in the treatment of moderate to severe psoriasis. Int J Dermatol 2009;48:653-8. 4. Stern RS, Zierler S, Parrish JA. Skin carcinoma in patients with psoriasis treated with topical tar and artificial ultraviolet radiation. Lancet 1980;1:732-5. 5. Pittelkow MR, Perry HO, Muller SA, Maughan WZ, O’Brien PC. Skin cancer in patients with psoriasis treated with coal tar: a 25-year follow-up study. Arch Dermatol 1981;117:465-8. doi:10.1016/j.jaad.2009.08.027

Cutaneous leishmaniasis in Texas To the Editor: Wright et al1 documented nine cases of cutaneous leishmaniasis acquired in Texas between 2005 and 2007 and offered suggestions for the apparent movement of the disease into northeast Texas. Their statement, however, that all 30 previously reported cases were in south-central Texas is incorrect. McHugh et al2 documented one case in Brown County in Central Texas with a date of onset of June 1988 and another in the same county with a date of onset of 1992. One in Albany, Shackelford County, Texas—approximately 132 miles due west of the DallaseFort Worth metroplex—had a date of onset of November 1994 (this case was incorrectly reported in Fig 1 of Wright et al1 as occurring with the other two cases in Brown County, 70 miles to south). So there are some historic data indicating a northward trend in the distribution of human cases in Texas, almost as far north as the cases in the present report, by the mid-1990s. Based on the ranges of the three Neotoma species—N micropus, N albigula, and N floridana— implicated as vertebrate hosts for Leishmania mexicana, McHugh et al3 predicted that leishmaniasis could occur over much of the southern United States from southern California in the west to Florida in the

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east, beyond the Four Corners region into southern Colorado and Utah, into southern Nebraska in the mideUnited States, and to the southern tip of North Carolina in the east. The cases reported by Wright et al1 support our hypothesis. Wright et al1 suggest that this apparent northward movement in distribution is real and may depend on the presence of vertebrate hosts other than woodrats such as opossums, armadillos, and cotton rats. Through the mid-1990s we screened, from various locations in Texas, at least 106 hispid cotton rats— with a prevalence rate of 0%. We screened at least 60 opossum—with a prevalence rate of 0%. We screened at least 20 armadillos—this is admittedly a low number, but the prevalence rate was also 0% (McHugh, unpublished data). The role of the hispid cotton rat (Sigmodon hispidusas) as host has a particularly interesting history in the scientific literature. Disney4 determined that just one of 43 rats was positive ( prevalence, 2.3%) for L mexicana and realized that it was an accidental host. Williams5 concurred, noting that ‘‘cotton rats prefer open grassy places and avoid dense forest,’’ which is the primarily ecologic setting for leishmaniasis in Belize. Bray6 elevated the role of the cotton rat from ‘‘accidental host’’ to ‘‘host,’’ and Shaw et al7 uncritically called it a ‘‘sylvatic reservoir of cutaneous leishmaniasis in endemic areas’’ despite its grassland habitat. Since that time, failure to read the original literature has led a succession of authors to refer to cotton rat as a possible reservoir host, the most recent before Wright et al1 being Furner.8 In any event, hispid cotton rat populations undergo a boom or bust cycle with peak populations about every 10 years in Central Texas,9 making it an unreliable host for blood-feeding insects. Wright et al1 also suggests a shift, presumably to the north, of the habitat of woodrats and sand flies. This is possible, but unlikely. The 1974 edition of Davis9 and the 1997 revision10 indicate that the distribution of woodrats has been historically stable and already includes the entire area where cases occurred. Unfortunately, the historic and present distribution of sand flies in the United States is imperfectly known and really reflects the distribution of collectors and not that of the flies themselves. Another possibility is a shift—or expansion—of the range of the parasite. This is not uncommon with insect-borne pathogens—witness the amazingly fast movement of West Nile virus across much of the United States. In a 19-month study, Raymond et al11 documented, on a small scale, the movement of L mexicana through a population of N micropus in south-central Texas,

suggesting that this could be occurring on a larger scale. The new distribution of cases may also reflect increased clinical suspicion. If so, it would still be unclear if these cases are truly novel or just documenting a historic, enzootic cycle. For that reason, it would be interesting to retrospectively review additional cases before 2005. If the new cases really represent novel infections, perhaps the most plausible explanation is the intrusion of humans into established foci. This could occur as larger agricultural properties are subdivided to accommodate population increases in counties surrounding the DallaseFort Worth metroplex. This could also occur if residents create situations that draw pre-existing foci into close proximity to the case residence. This includes having debris around the house that creates suitable woodrat habitats or having acceptable hosts for sand flies, such as rabbits or pigs, near the house. In particular, we have observed rabbits near several case residences in south-central Texas and southeastern Oklahoma and pigs at one residence in Texas (McHugh, unpublished data). Unfortunately, the historic range of the enzootic cycle is unknown and unknowable. Perhaps the best way to determine the present distribution is to collect on a corridor of land from within the range of the present cases some distance to the north. The corridor could be limited to habitat favored by woodrats, most likely mixed hammock and river bottoms in northeast Texas and Oklahoma. The distribution of woodrats, sand flies, and L mexicana could be plotted and the northernmost extent of enzootic foci noted. Two caveats: the collections would have to be conducted during the peak of sand fly activity—late May through late September in southcentral Texas,12 but unknown in northeast Texas and Oklahoma—and the distribution would apply to only the corridor sampled, not the entire United States. Chad P. McHugh, MPH, PhD Epidemiology Consult Service, US Air Force School of Aerospace Medicine, Brooks City-Base, Texas The opinions and assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the US Air Force or the Department of Defense. Funding sources: None. Conflicts of interest: None declared. Reprint requests: Chad P. McHugh, MPH, PhD, US Air Force School of Aerospace Medicine,

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Epidemiology Consult Service, 2513 Kennedy Circle, Brooks City-Base, TX, 78235 E-mail: [email protected] REFERENCES 1. Wright NA, Davis LE, Aftergut KS, Parrish CA, Cockerell CJ. Cutaenous leishmaniasis in Texas: a northern spread of endemic areas. J Am Acad Dermatol 2008;58:650-2. 2. McHugh CP, Melby PC, LaFon SG. Leishmaniasis in Texas: epidemiology and clinical aspects of human cases. Am J Trop Med Hyg 1996;55:547-55. 3. McHugh CP, Thies ML, Melby PC, Yantis LD Jr, Raymond RW, Villegas MD, et al. Short report: a disseminated infection of Leishmania mexicana in an eastern woodrat, Neotoma floridana, collected in Texas. Am J Trop Med Hyg 2003;69:470-2. 4. Disney RHL. Observations on a zoonosis: leishmaniasis in British Honduras. J Appl Ecol 1968;5:1-59. 5. Williams P. Phlebotomine sandflies and leishmaniasis in British Honduras. Tran Roy Soc Trop Med Hyg 1970;64:317-60.

RESEARCH Dermatitis herpetiformis exacerbated by cornstarch To the Editor: Dermatitis herpetiformis (DH) is related to gluten sensitivity, especially to gliadin protein. Wheat, rye, and barley, but not corn or rice, contain gluten. We report the cases of two patients with DH who described significant flares after ingestion of cornstarch. Both followed a strict gluten-free diet with good symptom control, only requiring occasional dapsone after unavoidable gluten ingestion. Case 1. A 71-year-old man described flares of DH whenever he ate cornflakes or corn flour, with symptoms completely resolving on avoidance. The same occurred within 48 hours of taking co-proxamol ( for arthralgia), subsiding within days after discontinuing treatment. Separate challenges with co-proxamol and with cornflakes induced DH with a rise in IgA-negative tissue-transglutaminase (TTG) antibody titers. The pharmaceutical manufacturer confirmed that the tablets contained cornstarch but not gluten. Avoidance of cornstarch-containing products produced symptomatic control and undetectable antibody titers. Case 2. An 84-year-old man developed flares of DH after eating cornflakes, which resolved on avoidance. Cornflake challenge caused DH lesions and increased antibody titers. Symptoms were also provoked by coated piroxicam tablets (Pfizer, New York, NY), a nonsteroidal anti-inflammatory drug (NSAID) for osteoarthritis, again confirmed by re-challenge. This did not occur with the soluble form. The

6. Bray RS. Leishmania. Annu Rev Microbiol 1974;28:189-217. 7. Shaw PK, Quigg LT, Allain DS, Juranek DD, Healy GR. Autochthonous dermal leishmaniasis in Texas. Am J Trop Med Hyg 1976;25:788-96. 8. Furner BB. Cutaneous leishmaniasis in Texas: report of a case and review of the literature. J Am Acad Dermatol 1990;23:36871. 9. Davis WB. The mammals of Texas. Austin: Texas Parks and Wildlife Department; 1974. 10. Davis WB, Schmidly DJ. The mammals of Texas—online edition. Lubbock: Texas Tech University; 1997. 11. Raymond RW, McHugh CP, Witt LR, Kerr SF. Temporal and spatial distribution of Leishmania mexicana infections in a population of Neotoma micropus. Mem Inst Oswaldo Cruz 2003;98:171-80. 12. McHugh CP, Ostrander BF, Raymond RW, Kerr SF. Population dynamics of sand flies (Diptera: Psychodidae) at two foci of leishmaniasis in Texas. J Med Entomol 2001;38:268-77. doi:10.1016/j.jaad.2009.08.034

LETTERS manufacturer confirmed that the tablets were gluten free but contained cornstarch, while the soluble form did not. Our patients demonstrated a clear link between ingestion of cornstarch and DH flares, with associated antibody titer elevation (IgA-TTG). In patient 1, corn flour was not tested for contamination with wheat; however, in both patients the cornflakes and the ingested tablets were gluten free. Some NSAIDs may exacerbate DH and celiac disease; however, this was unlikely to be relevant in patient 2 as he was completely asymptomatic with the piroxicam formulation that did not contain cornstarch. Co-proxamol contains paracetamol and dextropropoxyphene; there are no reported cases of DH or celiac disease provoked by these or related agents, and the generic brand used was gluten free. This apparently previously unreported association is unexpected as corn (maize) is considered a ‘‘nontoxic’’ cereal in DH and celiac disease. The mechanism has not been investigated specifically in DH, but laboratory evidence supports cross-reactivity between soluble corn prolamines and gliadin protein. Antibodies against gliadin may target an amino-acid sequence that is homologous in ‘‘non-toxic’’ cereals (corn and rice).1,2 This is supported by animal studies; rabbits immunized with gliadin produced high-titer antibodies against barley, oats, and corn prolamines.3 Similar results were found in guinea pigs.4 These experiments suggest the possibility that immunogenic