Treatment of Mycobacterium chelonae-induced skin infection with clarithromycin

Treatment of Mycobacterium chelonae-induced skin infection with clarithromycin

Journal of the American Academy of Dermatology Volume 28, Number 6 Briefcommunications 1019 Treatment of Mycobacterium chelonae-induced skin infecti...

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Journal of the American Academy of Dermatology Volume 28, Number 6

Briefcommunications 1019

Treatment of Mycobacterium chelonae-induced skin infection with cIarithromycin Nathalie Franck, MD,a Andre Cabie, MD,a Beatrice Villette, MD,a Bernard Amor, MD,b Michele Lessana-Leibowitch, MD,a and Jean-Paul Escande, MDa Paris, France Mycobacterium chelonae, one of the Runyon group IV species of mycobacteria, I is ubiquitous in the environment2 and a potent human pathogen. Cutaneous infections have been described after skin injury (injection,3, 4surgery,S, 6 and minortrauma5). Treatment is difficult because of an incomplete response or a relapse. We report the efficacy of clarithromycin in the treatment of M. chelonae skin infection. CASE REPORT A 70-year-old man had nodules and plaques on the left leg; the lesions appeared I month earlier when he was in a spa. He reported a superficial injury to his left foot. He has been treated for years with prednisone (15 mg/day) and intramuscular methotrexate (10 mg/wk) for rheumatoid arthritis. Physical examination revealed numerous, well-demarcated, deep red or purple, hemorrhagic papules and nodules in a sporotrichoid pattern on the left leg (Fig. 1). No inguinal adenopathy was present. The skin reaction to the purified protein derivative test was 4 mm in diameter. A skin biopsy specimen revealed mixed inflammatory cells in the dermis and the hypodermis with pyknotic polymorphonuclear lymphocytes, histiocytes, and rare giant cells. A Fite stain for acid-fast bacilli revealed numerous extracellular organisms. M. chelonae was cultured from the skin biopsy specimen. In vitro sensitivity tests showed resistance to isoniazid, rifampin, ethambutol, f1uoroquinolones, sulfonamides, cyclines, and amikacin but sensitivity to clarithromycin. Cultures of sputum, stool, urine, and blood were negative as was human immunodeficiency virus serology. Oral clarithromycin (500 mg twice daily) was given. Improvement was noted after 10 days. After 6 weeks of

From the Department of Dermatology-Venereology, H6pital TarnierCochin"; and the Department of Rheumatology, H6pital Cochin.b Reprint requests: Nathalie Franck, H6pital Tarnier-Cochin, Pavilion Achard 5° etage, 27 rue du Faubourg St. Jacques, 75014 Paris, France. JAM ACAD DERMATOL 1993;28:1019-21. Copyright © 1993 by the American Academy of Dermatology, Inc. 0190-9622/93 $1.00 +.10 16/54/44450

Fig. 1. Numerous cutaneous abscesses on the left leg. therapy the lesions completely cleared. A skin biopsy specimen revealed the absence ofinflammatory infiltrate, and the Fite stain for acid-fast bacilli was negative. Eight months after the beginning of clarithromycin therapy, no relapse was noted.

DISCUSSION

Rapidly growing mycobacteria are considered to be saprophytes. However, Mycobacterium fortuitum and M. chelonae have been implicated as pathogens in osteomyelitis, cellulitis, soft tissue abscesses,5, 7 postsurgical infections,5 otitis media,8 corneal ulcers,? and pulmonary infections. 5, 9 Primary cutaneous infections appear several weeks or months after skin injury and the evolution is chronic. The sporotrichoid spread of M. chelonae in our patient is unusual 10 compared with skin infection with Mycobacterium marinum and Mycobacterium kansasii. Disseminated infection is rare but has been reported in immunocompromised patients. Therapeutic modalities have included surgical excision,ll localized heating, n and antibiotic therapy with quinoline derivatives, (3-16 c1ofazimine,17 amikacin, 18, 19 sulfonamides)19, 20 and doxycycline,18, 19 The current treatment for disseminated M chelonae disease in immunocompromised patients is a combination of amikacin and cefoxitin,21

Journal of the Ameril~an Academy of Dermatology June 1993

1020 Brief communications

although tobramycin, erythromycin, and ciprofloxacin have been effective, including one patient with both skin and bone infections.22 The antibiotic susceptibilities of M. fortuitum and M. chelonae are variable and unpredictable. Most isolates are not sensitive to conventional antimycobacterial therapy. Long-term antimicrobial therapy is often necessary and sometimes ineffective with partial response and relapse. 23 Surgical excision 11 and localized heating 12 are not easily performed especially when lesions are numerous. Clarithromycin is a new macrolide with good absorption after oral administration. The concentrations reached in the tissues are several times higher than serum concentration. 24, 25 Clarithromycin is actively concentrated by phagocytes and is a potent intraphagocytic antimicrobial agent. 26 Promising results have been reported by preliminary studies with c1arithromycin as a monotherapy in patients with the acquired immunodeficiency syndrome for the treatment of disseminated Mycobacterium avium infection. 27, 28 Clarithromycin shows in vitro activity against M. kansasii and Mycobacterium xenopi. 29 Brown et al. 7 showed that all isolates of M. chelonae were inhibited in vitro by concentrations of clarithromycin well within achievable levels in serum and tissues. Clarithromycin (l gm/day) rapidly (within 6 weeks) produced a complete recovery in our patient without the withdrawal of the immunosuppressive therapy. This treatment was continued for 6 months and no relapse was observed 2months after cessation of therapy. REFERENCES 1. Runyon EH. Anonymous mycobacteria in pulmonary disease. Med Clin North Am 1959;43:273-96. 2. Goslee S, Wolinsky E. Water as a source of potentially pathogenic mycobacteria. Am Rev Respir Dis 1976; 113:287-92. 3. Gremillion DH, Munsch SB, Lerner CJ. Injection site abscesses caused by Mycobacterium chelonei. Infect Control 1983;4:25-8. 4. Borghans JGA, Stanford JL. Mycobacterium chelonei in abscesses after injection of diphtheria-pertussis-tetanuspolio vaccine. Am Rev Respir Dis 1973;107:1-8. 5. Wallace RJ Jr, Swenson HM, Silcox VA, et al. Spectrum of disease due to rapidly growing mycobacterium. Rev Infect Dis 1983;5:657-79. 6. Safranek TJ, Jarvis WR, Carson LA, et a!. Mycobacterium chelonei wound infections after plastic surgery employing contaminated gentian violet skin-marking solution. N Engl J Med 1987;317:197-201. 7. Brown BA, Wallace RJ Jr, Onyi GO, et al. Activities offour macrolides, including clarithromycin, against Mycobacte-

riumfortuitum, Mycobacterium chelonae, and M. chelonae-like organisms. Antimicrob Agents Chemother 1992;

36:180-4. 8. Lowry PW, Jarvis WR, Oberle AD, et a!. Mycobacterium chelonei causing otitis media in an ear-nose-and-throat practice. N Engl J Med 1988;319:978-82. 9. Wallace RJ Jr. Diagnostic and therapeutic consideration in patients with pulmonary disease due to the rapidly growing mycobacteria. Semin Respir Med 1986;1:230-3. 10. Joff-McKay AG, Randell P. Sporotrichoid cutaneous infection due to Mycobacterium chelonei in a renal transplant patient. Australas J DermatoI1990;31:105-9. II. Madjan DD, Carvallo E, Proper SA, et al. Adjunctive surgical management of cutaneous Mycobacterium fortuitum infection. J Dermatol Surg OncoI1985;11:708-12. 12. Levine N, Rothschild JG. Treatment of Mycobacterium chelonae infection with controlled localized heating. J AM ACAD DERMATOL 1991;24:867-70. 13. Gutknecht DR. TreatmentofdisseminatedMycobacterium chelonae infection with ciproftoxacin. JAM ACAD DERMATOL 1990;23:1179-80. 14. Gay JD, DeYoung DR, Roberts GD. In vitro activities of norfloxacin and ciprofloxacin against Mycobacterium tu-

berculosis, M. avium complex, M. chelonei, M.fortuitum,

15. 16. 17. 18.

19.

20.

21. 22.

23.

24. 25.

26.

and M. kansasii. Antimicrob Agents Chemother 1984; 26:94-6. Texier-Maugein J, Mormede M, Fourche J, et al. In vitro activity of four fluoroquinolones against eighty-six isolates of mycobacteria. Eur J Clin Microbiol 1987;6:584-6. Young LS, Berlin OG, Inderlied CB. Activity of ciprofloxacin and other fluorinated quinolones against mycobacteria. Am J Med 1987;82:23-6. Ausina V, Condom MJ, Mirelis B, et al. In vitro activity of clofazamine against rapidly growing nonchromogenic mycobacteria. Antimicrob Agents Chemother 1986;29:951-2. Dalovisio JR, Pankey GA, Wallace RJ Jr, et al. Clinical usefulness of amikacin and doxycycline in the treatment of infection due to Mycobacteriumfortuitum and Mycobacterium che/onei. Rev Infect Dis 1981;3:1068-74. Swenson NK, Thornsberry C, Silcox VA. Rapidly growing mycobacteria: testing of susceptibility to 34 antimicrobial agents by broth macrodilution. Antimicrob Agents Chemother 1982;22:186-92. Casal M, Rodriguez F. In vitro susceptibility of Mycobacteriumfortuitum and Mycobacterium chelonei to sulfadiazine, sulfisoxazole and sulfathiazole. Eur J Clin Microbiol 1984;3:320-1. Carpenter JL, Troxell M, Wallace RJ. Disseminated disease due to Mycobacterium chelonei treated with amikacin and cefoxitin. Arch Intern Med 1984;144:2063-5. Drabick JJ, Duffy PE, Samlaska CP, et al. Disseminated Mycobacterium chelonae subspecies chelonae infection with cutaneous and osseous manifestations. Arch DermatoI1990;126:1064-7. Wallace RJ Jr, Swenson JM, Silcox VA, et al. Treatment of nonpulmonary infections due to Mycobacterium fortuiturn and Mycobacterium chelonei on the basis of in vitro susceptibilities. J Infect Dis 1985;152:500-14. Davey PG. The pharmacokinetics of clarithromycin and its 14-0H metabolite. J Hosp Infect 1991 ;19(suppl A):29-37. Fraschini F, Scaglione G, Pintucci G, et al. The diffusion of clarithromycin and roxythromycin into nasal mucosa, tonsil and lung in humans. J Antimicrob Chemother 1991;17(suppl A):61-5. Anderson R, Joone G, van Rensburg eEJ. An in vitro

Journal of the American Academy of Dermatology Volume 28, Number 6 evaluation of the cellular uptake and intraphagocytic bioactivity of clarithromycin (A-56268, TE-03I), a new macrolide antimicrobial agent. J Antimicrob Chemother 1988; 22:923-33. 27. Dautzenberg B, Truffot C, Legris S, et al. Activity of clarithromycin against Mycobacterium avium infection in patients with the acquired immune deficiency syndrome. Am Rev Respir Dis 1991;144:564-9.

Brief communications 1021 28, Weits J, Sprender HG, Ilic P, et al. Clarithromycin monotherapy of MAC-Mycobacteriosis in AIDS. Neth J Moo 1991 ;39: 126-8. 29. Berlin OGW, Young LS, Floyd-Reising SA, et al. Comparative in vitro actj.,5ty of the new macrolide A-56268 against mycobacteria. Eur J MicrobioI1987;4:486-7.

Purpuric pityriasis rosea Joseph C. Pierson, MD,a Jacob W. E. Dijkstra, MD,a and MAl Dirk M. Elston, Me, USAb

Cleveland, Ohio Pityriasis rosea (PR) is a common self-limited exanthem of unknown cause. The typical presentation of PR is easily recognized. Clinical variants include papular PR, vesicular PR, pustular PR, inverse PR, cephalic PR, PR gigantea, PR urticata, and purpuric (hemorrhagic) PR. I We report an example of purpuric PRo CASE REPORT

An ll-year-old girl noticed several asymptomatic spots on her abdomen. The eruption spread to the remainder of her trunk and proximal extremities during the next 3 weeks. Physical examination revealed multiple, nonscaling petechiae and ecchymoses oriented along Langer's lines on the neck, trunk, and proximal extremities. Complete blood cell count, prothrombin time, partial thromboplastin! time, 16-variable automated chemistry panel and urinalysis were all normal. Antinuclear antibody, rapid plasma reagin, rickettsial profile, and streptococcal antibody titers were unremarkable. A skin biopsy specimen demonstrated a superficial and mid-dermal perivascular mononuclear cell infiltrate with erythrocyte extravasation, No foci of parakeratosis or spongiosis were seen, and there was no evidence ofvascuFrom the Departments of Dermatology" and Dermatopathology,b Cleveland Clinic Foundation. Reprint requests: Joseph C. Pierson, MD, Department of Dermatology, A61, Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland, OH 44195, JAM ACAD DERMATOL 1993;28:1021. Copyright @ 1993 by the American Academy of Dermatology, Inc, 0190-9622/93 $1.00

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litis. Direct immunofluorescence testing of the skin was negative, A diagnosis of purpuric PR was made. The eruption began to fade 6 weeks after onset. DISCUSSION

Hartman2 first described a patient with purpuric PR in 1944. Including our report, there are 10 cases in the literature. 2-4 Although Paller et al. 4 used the term hemorrhagic PR, we prefer purpuric PR as an earlier review suggested. 3 Children and adults have been equally affected, and the course of the disease has been similar to typical PR with no change in prognosis. Histopathologic examination of purpuric PR reveals extravasation of erythrocytes into the papillary dermis without evidence of vasculitis. 3 Other features of typical PR such as focal parakeratosis, spongiosis, and a superficial lymphocytic perivascular infiltrate may be present. The differential diagnosis includes hematologic disease, vasculitis, and a pigmented purpuric dermatosis. REFERENCES 1. Bjornberg A. Pityriasis rosea, In: Fitzpatrick TB, Eisen AZ, WolffK, et al., eds. Dermatology in general medicine. 3rd ed. New York: McGraw-Hill 1987:984. 2. Hartman MS. Pityriasis rosea, Arch DermatoI 1944;50:201. 3. Verbov 1. Purpuric pityriasis rosea. Dermatologica 1980: 160:142-5. • 4, Paller AS, Esterly NB, Lucky AW, et al. Hemorrhagic pityriasis rosea: an unusual variant. Pediatrics 1982;70:357-9.