Brändli, Otto

Pfyffer, Gaby E.

Shang, Helena

Strässle, Anni

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219CID 1998;26 (January) Brief ReportsReferencesdecreases in HIV-1 replication that would reduce the level of tatgene expression, and this reduced level of expression could induce1. Beral V. Epidemiology of Kaposi’s sarcoma. Cancer Surveys 1991;10:neither angiogenesis nor malignant transformation of endothelial5–22.cells by tat-induced cytokines [3]. Third, the use of antiretroviral 2. Chang Y, Cesarman E, Pessin M, et al. Identification of herpes virus–likeagents could be associated with an improvement in the immune DNA sequences in AIDS-associated Kaposi’s sarcoma. Science 1994;response, enabling control of tumor progression. 266:1865–9.Further studies are needed to better determine the therapeutic 3. Barillari G, Buonaguro L, Fiorelli V, et al. Effects of cytokines from acti-vated immune cells on vascular cell growth and HIV-1 gene expression.effects of antiretroviral therapy on the progression of KS in HIV-J Immunol 1992;149:3727–34.infected patients. Combinations of these drugs could become alter-4. Krown SE, Metroka C, Wernz JC, et al. Kaposi’s sarcoma in acquirednatives to the conventional treatment of AIDS-related KS.immunodeficiency syndrome: a proposal for a uniform evaluation, re-sponse and stating criteria. J Clin Oncol 1989;7:1201.5. Kern D, Collins M, Fultz T, et al. An enhanced-sensitivity branched-DNARicardo Parra, Manuel Leal, Juan Delgado, Juan MacıB as, assay for quantification of human immunodeficiency virus type 1 RNAAmalia Rubio, Fernando Go´mez, Vicente Soriano, in plasma. J Clin Microbiol 1996;34:3196–202.Armando Sanchez-Quijano, Juan Antonio Pineda, 6. Mitsuyasu RT. Clinical aspects of AIDS-related Kaposi’s sarcoma. Currand Eduardo Lissen Opin Oncol 1993;5:835–44.7. Langford A, Ruf B, Kunze R, Pohle H-D, Reichart P. Regression of oralViral Hepatitis and AIDS Study Group, Virgen del RocıB o UniversityKaposi’s sarcoma in a case of AIDS on zidovudine (AZT). Br J DermatolHospital, Seville; and Service of Infectious Diseases, Instituto de SaludCarlos III, Madrid, Spain 1989;120:709–13.isoniazid, rifampin, and streptomycin. Treatment with isoniazid,Three Episodes of Tuberculosis—To Multidrugrifampin, ethambutol, pyrazinamide, and ciprofloxacin was started;Resistance and Back to Susceptibilitytherapy with the latter three drugs was continued for 12 months.After she recovered, she traveled several times to India betweenWe report the case of a patient who had three episodes of tuber-1990 and 1993 and subsequently worked as an assistant nurse atculosis; two of these episodes were due to resistant strains ofthe University Hospital in Zurich. In the fall of 1995, she com-Mycobacterium tuberculosis, and one was due to a susceptibleplained of pain under the right scapula and developed a productivestrain.cough, malaise, fever, and night sweats. An infiltrate was observedA 31-year-old Tibetan woman who was born in India developedon a chest radiograph, and pulmonary TB with right-sided cervicalsmear-positive tuberculosis (TB) of the lung in 1987, 1990, andlymphadenitis was diagnosed (episode 3). For the third time, cul-1995. Upon immigration to Switzerland in 1984, findings on hertures were positive, but surprisingly, the M. tuberculosis isolatechest radiograph were normal. Three years later, progressive, cav-was fully susceptible to all first-line drugs.ernous TB of the left upper lobe was diagnosed (episode 1).This finding prompted us to study all isolates at the molecularM. tuberculosis was isolated from sputum and gastric fluid speci-level to better understand this case. By using PvuII as the restrictionmens, and primary resistance to isoniazid was detected. The patientenzyme and IS6110 as a probe [1], we found two different patternswas hospitalized and treated with isoniazid, rifampin, and pyra-of restriction fragment length polymorphism (RFLP): the isolateszinamide for 2 months, followed by a regimen of rifampin andrecovered during episode 1 and episode 2 had identical DNA fin-ethambutol for 4 months. After 14 weeks of treatment, culturesgerprints, whereas those recovered during episode 3 differed con-became negative.siderably from the initial strains. On probing AluI-digested DNAAfter the patient recovered clinically, she traveled to India andwith the polymorphic GC-rich repetitive sequence [2], bandingNepal in 1989; however, upon her return in 1990, she developedpatterns for the isolates from episodes 1 and 2 were again founda cough and night sweats, and cavernous TB of the left upper lobe,to differ from those of episode 3.with laryngeal and endobronchial involvement, was diagnosed (ep-On the basis of this case, three major conclusions can be drawn:isode 2). The M. tuberculosis isolate proved to be resistant to(1) Of the two episodes of TB in 1990 and 1995, only one was atrue relapse, probably caused by inadequate drug therapy. Con-versely, episode 3 was due to exogenous reinfection. (2) Treatmentof TB after episode 2 was successful, as indicated by the significantReprints or correspondence: Dr. Gaby E. Pfyffer, Swiss National Center for improvement in the patient’s condition and the numerous culture-Mycobacteria, Department of Medical Microbiology, University of Zurich,negative follow-up specimens that were obtained. (3) A mixed-Gloriastrasse 30, 8028 Zurich, Switzerland.strain infection during episode 3 can be safely ruled out, not onlyClinical Infectious Diseases 1998;26:219–20on account of the DNA fingerprinting results but also becauseq 1998 by The University of Chicago. All rights reserved.1058–4838/98/2601–0054$03.00 of the isolate’s susceptibility pattern (fully susceptible), which220 Brief Reports CID 1998;26 (January)excludes the presence of the previous strains (resistant to isoniazid for TB control must be aimed primarily at minimizing transmis-sion, i.e., eliminating M. tuberculosis in such environments.and to multiple drugs).Since the strain recovered from the patient’s sister, who hadGaby E. Pfyffer, Anni Stra¨ssle, Otto Bra¨ndli,active TB in 1984, was not available for typing, it is not clearand Helena Shangwhether the patient became infected via her sister or whether sheSwiss National Center for Mycobacteria, Department of Medicalwas infected while living in Tibet. The latter scenario is quiteMicrobiology, University of Zurich, Zurich; and Zu¨rcher Ho¨henkliniklikely, since the incidence of TB among Tibetan immigrants livingWald, Faltigberg, Switzerlandin Switzerland is very high (384 cases per 100,000 persons;P. Helbling, Swiss Federal Office of Public Health, personal com- Referencesmunication). In addition, the time of reinfection with the fully1. Van Embden JDA, Cave MD, Crawford JT, et al. Strain identification ofsusceptible strain is not known.Mycobacterium tuberculosis by DNA fingerprinting: recommendationsExogenous reinfection has been demonstrated conclusively infor standardized methodology. J Clin Microbiol 1993;31:406–9.patients with advanced HIV infection [3], but such reinfection 2. Poulet S, Cole ST. Repeated DNA sequences in mycobacteria. Arch Micro-has also been reported among immunocompetent individuals with biol 1995;163:79–86.either alcoholism [4] or diabetes [5] as risk factors. The patient 3. Small PM, Shafer RW, Hopewell PC, et al. Exogenous reinfection withmulti-drug resistant Mycobacterium tuberculosis with advanced HIV in-described herein had neither underlying disease nor other knownfection. N Engl J Med 1993;328:1137–44.risk factors. To our knowledge, this is the first well-documented4. Shafer RW, Singh SP, Larkin C, Small PM. Exogenous reinfection withcase demonstrating that both relapse of TB, with progression tomulti-drug resistant Mycobacterium tuberculosis in an immunocompetentmultidrug-resistant TB, followed by exogenous reinfection andpatient. Tuber Lung Dis 1995;76:575–7.development of active disease within a short period (8 years) is5. Turett GS, Fazal BA, Justman JE, Alland D, Duncalf RM, Telzak EE.possible within the same patient. A history of frequent travel to Exogenous reinfection with multidrug-resistant Mycobacterium tubercu-areas where TB is highly prevalent supports the assumption that losis. Clin Infect Dis 1997;24:513–4.in such countries, exogenous reinfection may be a common mecha- 6. Styblo K. Epidemiology of tuberculosis. Bull Int Union Tuberc 1978;53:141–52.nism by which clinical TB develops [6]. If so, global strategiescrotic areas (figure 1). There was no fever or inguinal lymphadenopa-Inflammatory Tinea Corporis Due to Trichophytonthy. Results of a complete blood count and blood chemistry evaluationverrucosumwere normal, and the erythrocyte sedimentation rate was 13 mm/h.Repeated skin biopsy was performed, and results of gram and acid-A recent report by Sabota et al. describes tinea barbae due to Tricho- fast stains as well as routine bacterial and mycobacterial cultures werephyton verrucosum in dairy farmers [1]. T. verrucosum may also cause negative. Histopathologic evaluation demonstrated a mixed inflamma-other infections including tinea corporis [2, 3], and other animals, such tory cell infiltrate and a fungal spore (figure 1). After 2 weeks’ incuba-as horses, may be the source of infection [4, 5]. We describe a patient, tion at 307C, T. verrucosum was isolated. Oral itraconazole (200 mgb.i.d.) was administered for 12 weeks, and the leg lesion resolvedwith horse contact, who developed inflammatory tinea corporis due tocompletely.T. verrucosum, confirmed by histopathology and culture results.Chronic tinea corporis is uncommon and is usually due to eitherA 54-year-old man, whose work involved riding horses in ruralTrichophyton mentagrophytes or T. verrucosum [4]. T. verrucosum isareas, presented with left leg tenderness and erythema; he had no feverdistributed globally [5], and human infection has been reported pre-or other systemic symptoms. There was no response to treatment withviously from Australasia [6, 7]. T. verrucosum usually infects cows,oral flucloxacillin and roxithromycin. A biopsy of the leg lesion wasbut it is also isolated frequently from horses [4]. In the current case,performed. A gram stain of the specimen was negative, but coagulase-the lesion was on the patient’s leg, where there had been direct contactnegative staphylococci were isolated, and histopathology demonstratedwith a common site of horse ringworm [4]. Zoophilic dermatophytesnonspecific chronic inflammatory changes with folliculitis. Treatmentlike T. verrucosum may produce inflammatory disease that can bewith flucloxacillin (1 g q6h iv) and oral ciprofloxacin (750 mg b.i.d.)mistaken for bacterial infection [1, 5, 8]. Tinea corporis due to zoophilicwas begun, but there was no improvement in the patient’s condition.dermatophytes may resolve spontaneously, but systemic antifungalSeven weeks after his initial presentation, he was referred to ourtherapy is usually required [5, 9].institution for consideration of hyperbaric oxygen therapy for ‘‘celluli-In cases of tinea corporis, biopsies may demonstrate cylindricaltis’’ that was not responding to therapy with antibacterial agents. Exam-fungal filaments, or rounded arthroconidia [10], which are characteristi-ination of the medial aspect of the left leg revealed a 15 1 6-cm,cally large in T. verrucosum infection [3]. In inflammatory tinea corpo-erythematous, indurated plaque, containing pustular lesions with ne-ris caused by zoophilic dermatophytes such as T. verrucosum, hypersen-sitivity reactions may produce vesicles and papules accompanied bydermal infiltrates [10], or vasculitis characterized by small follicularpapules with necrotic areas [3]. Histopathologic features of hypersensi-tivity reactions include infiltration of lymphocytes, plasma cells, neutro-Reprints or correspondence: Dr. Tony Korman, Department of Microbiol-phils, and eosinophils into the dermis [10].ogy, Monash University, Clayton Victoria 3168 Australia.Tinea corporis due to T. verrucosum should be included in theClinical Infectious Diseases 1998;26:220–1differential diagnosis of chronic inflammatory skin lesions in patientsq 1998 by The University of Chicago. All rights reserved.1058–4838/98/2601–0055$03.00 with a history of contact with animals, including cows and horses.

Three Episodes of Tuberculosis—To Multidrug Resistance and Back to Susceptibility

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