CORRECT DIAGNOSIS:
Erythema Induratum caused by Mycobacterium chelonei
DISCUSSION:
Erythema induratum (EI) was first described in 1855 by Bazin prior to the identification of tuberculids.1,2 Although initially associated with pulmonary tuberculosis, there has been much debate over the role of Mycobacterium tuberculosis in the pathogenesis of EI. In the early 1900s, Whitfield3,4 and Galloway5 distinguished cases of EI unrelated to Mycobacterium tuberculosis infection as a separate clinical entity from those associated with tuberculosis. Four decades later in 1945, Montgomery6 proposed the term nodular vasculitis to describe cases of EI lacking evidence of tuberculin origin. The relationship of EI with Mycobacterium tuberculosis has since been solidified by isolation of mycobacterial deoxyribonucleic acid (DNA) from EI biopsies via polymerase chain reaction (PCR), yet most clinicians use the term EI and nodular vasculitis interchangeably regardless of etiology.7 Today, cases of EI are most prevalent in populations with a higher incidence of tuberculosis.8
The clinical picture of EI is characterized by tender, violaceous nodules and plaques most commonly affecting the posterior lower legs of adolescent or perimenopausal women.2,7 Lesions have a tendency to ulcerate and drain. Spontaneous resolution of lesions is common within a few months leaving areas of postinflammatory hyper-pigmentation and atrophic scarring.8 EI runs a chronic, recurrent course in which lesions return every 3 to 4 months over the span of many years.8 Histopathological examination of EI demonstrates a predominant lobular panniculitis with granulomatous inflammation. A neutrophilic vasculitis is usually present and affects contiguous small and medium-sized vessels.7,9,10 Necrosis of fat lobule adipocytes may also be present and occasionally form palisading granulomas.8-10
Despite the current support for the tuberculous origin of EI, many authors believe other etiopathogenic factors should be considered. Previous cases have reported an association of EI with infectious disorders caused by Nocardia, Pseudomonas, Fusarium, Hepatitis C, and Hepatitis B.7 Several cases have also been linked to autoimmune disease and propylthiouracil therapy.11 A recent study examined the possibility that atypical mycobacteria may cause EI, but failed to isolate atypical species from lesions via PCR.12 Interestingly, the same study looked for DNA from 11 different atypical mycobacterial species, but did not test for the presence of Mycobacterium chelonei.
Mycobacterium chelonei is a rapidly growing atypical mycobacterium belonging to the Runyon group IV classification.13 Although originally isolated from the sea turtle, Chelona corticata, Mycobacterium chelonei is found ubiquitously in the environment in soil, water, and dust particles.14 Cultures between 25 and 40°C form nonpigmented colonies with either a rough or smooth surface.15 Clinically, Mycobacterium chelonei is rare, but can cause disseminated disease in patients immunosuppressed by organ transplantation,16 collagen vascular disease,17 malignancy, or corticosteroid therapy.18 Localized infection may occur due to implantation into the skin following surgery, injections, or trauma.15 Following inoculation, it is likely Mycobacterium chelonei remains localized in these patients because their immune system is strong enough to mount a cell-mediated immune response against the bacterium. Treatment of Mycobacterium chelonei infection is challenging. In the few cases of Mycobacterium chelonei infection found in the literature, antimicrobial therapy was complicated due to the highly resistant nature of Mycobacterium chelonei to standard antibiotics.12 Clarithromycin has been found to be effective against 100 percent of isolates in vitro,15 but monotherapy is ill advised due to the rapid development of resistance via a point mutation in the gene coding for the 23S rRNA molecule.12 To avoid the development of resistance in the patient in this case, the authors elected to supplement 500mg clarithromycin therapy twice daily with 100mg doxycycline twice daily, shown to treat 25 percent of Mycobacterium chelonei isolates.14 Other antibiotics effective against Mycobacterium chelonei are tobramycin, amikacin, imipenem, and ciprofloxacin.19
TREATMENT:
500mg clarithromycin twice daily and 100mg doxycycline twice daily with resolution after four months of therapy.
REFERENCES:
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4. Whitfield A. A further contribution to our knowledge of erythema induratum. Br J Dermatol. 1905;15:241–247.
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19. Iseman MD. Group IV Rapid growing mycobacteria. In: Yu VI, Merigan TC Jr, Barriere SL, editors. Antimicrobial Therapy and Vaccines. Baltimore: Williams and Wilkins; 1999. pp. 494–497.