Lymphocutaneous nocardiosis caused by Nocardia otitidiscaviarum: A case report and review of literature
A 60-year-old male with a history of chronic obstructive pulmonary disease (COPD) was admitted to medical ward of our hospital. He presented with a month long history of breathlessness, cough with expectoration (Grade 4), high continuous fever, and ulcers on the right thigh which had been present for 15 days. One month prior, he sustained thorn prick injury while working in the field. An ulcer on right upper third of thigh began as a papule and gradually ulcerated over a period of two weeks. Many erythematous, painful nodules developed on the whole thigh and enlarged inguinal lymph nodes with inflammatory lymphangitic streaks.\nGeneral physical examination revealed mild pallor with clubbing (Grade 3). Vital parameters like blood pressure, pulse rate were within normal limits and respiratory rate was high. Local cutaneous examination revealed two ulcers on the right thigh and inguinal lymph nodes were enlarged and tender. The largest ulcer on the upper third of the right thigh measured 3 × 1.5 cm, excavated 0.5 cm deep with undermined edges with irregular margins. Another ulcer at mid thigh level was covered by scab and an ulcer in evolution was present just above the right knee.\nThe patient presented microcytic hypochromic blood picture and relative neutrophilia with 10.2 gm% hemoglobin. Erythrocyte sedimentation rate was 95 mm at the end of the first hour. Biochemical tests like, blood sugar, urea, creatinine were within normal limits. ELISA for HIV1 and two antibodies were negative. Chest X-ray revealed increased bronchovascular markings in para-hilar region with emphysematous changes. Gram stain of sputum revealed plenty of gram-positive capsulated diplococci and culture on blood agar yielded growth of Streptococcus pneumoniae.\nGram-stained smear from the discharge of ulcerative lesion revealed numerous pus cells and few irregularly stained gram-positive thin branching filaments. Modified Kinyoun's staining demonstrated acid-fast branching filamentous structures. Culture on Sabouraud dextrose agar, blood agar, and Lőwenstein-Jensen media yielded growth after 72 h, showing dry chalky, white-folded colonies with irregular margin. Biochemically, the isolate showed production of urease and reduced nitrates to nitrites. The isolate was identified as nocardia otitidiscaviarum by its ability to digest xanthine, hypoxanthine, and urea but not casein, gelatin, tyrosine.\nThe isolate was sent to Aerobic Actinomycetes Laboratory, Centers for Disease Control and Prevention, Atlanta, Georgia, USA for confirmation and molecular analysis. 16S rRNA gene sequencing was done. Purified genomic DNA was amplified using the Expand High Fidelity PCR System (Roche Diagnostics Corporation, Indianapolis, IN, USA) with primers fL1 5’- CCGAATTCGTCG ACAACA GA GTTTGATCCTGGCTCAG - 3’ and rL1 5’- CCCGGG ATCCAAGC TTACGGCTACCTTG TTA CGACTT -3’.[] Cycle sequencing was performed utilizing 16 universal primers[]; excess dyes were removed with magnetic carboxylate beads (Agencourt Bioscience, Beverly MA) and reactions were sequenced on an ABI 3100 (Applied Biosystems).\nThe 16S rRNA gene sequences were assembled in Accelrys SeqMerge and trimmed to a minimum of two confirming reads. The sequence (>1400 bp) generated was compared to the GenBank database gene sequences derived from related nocardia and submitted by other investigators.\nAnalysis of 16S rRNA gene of the isolate and type strain of N. otitidiscaviarum DSM 43242 showed 100% similarity. The partial gene sequence (1439 bp) was submitted to GenBank, accession number EU031786.\nThe patient was relieved of breathlessness and cough with expectoration, following treatment with amoxicillin and clavulanic acid 625 mg twice daily for eight days. For nocardiosis the patient was initially treated with oral trimethoprim-sulfamethoxazole (TMP-SMX, 80-400 mg), two tablets twice daily for one week with no clinical improvement. Antibiotic susceptibility testing of the isolate by MIC method carried out at CDC Atlanta revealed that it was susceptible only to amikacin (MIC = 4), minocycline (MIC = 1), and linezolid (MIC = 2) and resistant to remaining other routine anti-nocardial drugs. The patient was treated with amikacin and linezolid for four weeks; once a clinical cure was evident the patient was asked to continue linezolid orally for another eight weeks. Four months later, there was no evidence of nocardiosis in the patient.