Asian Pacific Journal of Tropical Medicine

: 2019  |  Volume : 12  |  Issue : 4  |  Page : 185--194

Disseminated nocardiosis due to Nocardia otitidiscaviarum: A case report and literature review

Shu-Wei Zheng 
 Department of Infectious Diseases, Singapore General Hospital, Singapore

Correspondence Address:
Shu-Wei Zheng
Department of General Medicine, Sengkang General Hospital, 110 Sengkang East Way Singapore 544886


Rationale: Disseminated nocardiosis due to Nocardia otitidiscaviarum is rarely reported in immunocompetent hosts. Patient concerns: A 59 year old male patient complained of painful soft tissue swellings and fever for two days. Diagnosis: Disseminated nocardiosis due to Nocardia otitidiscaviarum. Interventions: Initial antimicrobial therapy with imipenem and trimethoprim/sulfamethoxazole was switched to 6 weeks of trimethoprim/sulfamethoxazole, linezolid and tigecycline after sensitivity test results were available. Thereafter, the patient was switched to maintenance trimethoprim/sulfamethoxazole and moxifloxacin. Prednisolone was gradually tapered. Outcomes: Soft tissue swelling and pain disappeared and the patient was discharged uneventfully. Lessons: Disseminated nocardiosis due to Nocardia otitidiscaviarum should be suspected in immunocompetent hosts with risk factors such as medication with prednisolone. Early identification of the causative species and susceptibility results is crucial given the diverse resistance patterns amongst various Nocardia species.

How to cite this article:
Zheng SW. Disseminated nocardiosis due to Nocardia otitidiscaviarum: A case report and literature review.Asian Pac J Trop Med 2019;12:185-194

How to cite this URL:
Zheng SW. Disseminated nocardiosis due to Nocardia otitidiscaviarum: A case report and literature review. Asian Pac J Trop Med [serial online] 2019 [cited 2023 Jun 5 ];12:185-194
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 1. Introduction

Nocardia spp. is a Gram-positive, weakly acid-fast microorganism that is ubiquitous in the environment with a worldwide distribution. Common factors include long term corticosteroid use, malignancy, human immunodeficiency virus infection and chronic obstructive pulmonary predisposing to Nocardia infectionsdisease[1]. Various Nocardia species differ in their pathogenicity, geographical distribution and antimicrobial susceptibility. Historically, before the advent of molecular techniques and mass spectrometry, biochemical methods were used in the identification of Nocardia species, resulting in only a few known Nocardia species[2]. Matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS) has emerged as a useful tool for the accurate identification of Nocardia species[2],[3],[4].

First recognized in 1924 from a guinea pig with ear disease, Nocardia otitidiscaviarum (N. otitidiscaviarum) has been described as an opportunistic pathogen causing local and disseminated infection in both immunocompetent and immunocompromised hosts[1]. Herein, we describe a case of disseminated N. otitidiscaviarum predisposed by corticosteroid use and a literature review of published case reports and case series of N. otitiscaviarum infections.

 2. Case report

This case report was approved by the local ethics committee of the author’s affiliated institution. The patient provided consent to the use of photographs in the report. Identifying information of the patient was removed.

A 59-year-old man presented with an acute history of painful soft tissue swellings and fever. Upon further questioning, he denied any history of trauma and had been perfectly well 2 d before. He had no cough, hemoptysis, or chest pain. He had a history of hypertension, dyslipidemia, and stage IV chronic kidney disease (baseline serum creatinine ranging 284-313 [μmol/L, reference range, 54-101 μmol/L), secondary to presumptive glomerulonephritis. Two months ago, he had been started on a prednisolone dose of 60 mg daily by his nephrologist for suspected immune-mediated glomerulonephritis. Clinical examination revealed a febrile middle-aged man with discreet tender, warm, and erythematous swellings over his left elbow [Figure 1], right thigh, and right buttock, consistent with cutaneous abscesses. There was no palpable lymphadenopathy. Cardiorespiratory and abdominal examination was unremarkable. He had no focal neurological deficit.{Figure 1}

Laboratory findings included the following: serum sodium 140 mmol/L (reference range, 136-146 mmol/L), serum potassium 4.5 mmol/L (reference range, 3.6-5.0 mmol/L), serum bicarbonate 24.6 mmol/L (reference range, 19.0-29.0 mmol/L), serum creatinine 332 umol/L, haemoglobin 12.5 g/dL (reference range, 14.0-18.0 g/dL), white blood cell count 15.02 × 109/L (reference range, 4.0-10.0× 109/L), C-reactive protein 86.6 mg/L (reference range, 0.2-9.1 mg/L), serum albumin 31 g/L (reference range, 40-51 g/L), bilirubin 5 [μmol/L (reference range, 7-32 (μmol/L), alkaline phosphatase 51 U/L (reference range, 39-99 U/L), alanine aminotransferase 6 U/L (reference range, 6-66 U/L), and aspartate aminotransferase 17 U/L (reference range, 12-42 U/L). Blood cultures were non-yielding.

A chest radiograph showed a left upper lobe opacity, which was new compared to a previous radiograph taken three months before [Figure 2]A,[Figure 2]B. A computed tomography scan of his thorax revealed a spiculated left upper lobe mass [Figure 2]C corresponding to the opacity detected on the chest radiograph.{Figure 2}

He initially declined surgical drainage. Magnetic resonance imaging (MRI) to delineate the soft tissue abscesses and revealed subcutaneous collections over the left elbow joint, right gluteus maximus, and was right sartorius and iliacus muscle, together with an intramuscular abscess within the right gracilis muscle [Figure 3]A,[Figure 3]B,[Figure 3]C,[Figure 3]D,[Figure 3]E,[Figure 3]F,[Figure 3]G,[Figure 3]H.{Figure 3}

He did subsequently undergo a diagnostic transthoracic needle aspiration of the lung lesion as well as an incision and drainage of the multiple subcutaneous abscesses. Histology of the lung specimen showed acute-on-chronic pneumonitis with microabscess formation. No granulomas or infective organisms were identified and there was no evidence of malignancy. Gram stain, fungal microscopy, acid-fast bacilli stain, and nucleic acid amplification test for Mycobacterium tuberculosis complex were negative.

Eventually, chalky colonies were seen on the blood agar plate several days later [Figure 4]A from both the lung and subcutaneous tissue specimens. On microscopy, beaded Gram-positive rods were seen [Figure 4]B, suspicious for nocardiosis. Antimicrobial therapy was empirically switched to a combination of imipenem and trimethoprim/sulfamethoxazole. The causative microorganism was identified to be N. otitidiscaviarum by the matrix-assisted laser desorption/ionization time-of-flight mass spectrometry.{Figure 4}

An MRI of his brain showed a solitary lesion in the right frontal lobe, consistent with a cerebral abscess [Figure 5]A,[Figure 5]B. Hence, this patient has disseminated nocardiosis resulting in subcutaneous,intramuscular, lung and brain abscesses, predisposed by cortico steroids.{Figure 5}

Susceptibility testing using the broth microdilution method suggested that this isolate was susceptible to amikacin [minimum inhibition concentration (MIC)≤;8 μg/mL], tobramycin (MIC≤4 μg/mL), trimethoprim/sulfamethoxazole (MIC≤2/38 μg/πıL), and linezolid (MIC≤8 μg/mL), intermediate to moxifloxacin (MIC=2 μg/mL), doxycycline (MIC=2 μg/mL), and minocycline (MIC=2 μg/πıL), and resistant to amoxicillin/clavulanic acid (MIC≥32/16 μg/ mL), ceftriaxone (MIC≥64 μg/mL), cefepime (MIC≥32 μg/ mL), imipenem (MIC≥16 μg/mL), ciprofloxacin (MIC≥4 μg/ mL), and clarithromycin (MIC≥8 μg/mL). Tigecycline MIC was tested to be 0.5 μg/mL but without interpretive criteria from the Clinical&Laboratory Standards Institute. Antimicrobial therapy was further switched to trimethoprim/sulfamethoxazole, linezolid and tigecycline. Aminoglycosides were not used in view of his underlying renal disease. He completed 6 weeks of this combination therapy before switching to maintenance trimethoprim/ sulfamethoxazole and moxifloxacin. His prednisolone was gradually tapered and ceased and all his cutaneous lesions were drained surgically. A summary of his clinical progress is shown in [Figure 6].{Figure 6}

 3. Discussion

A computerized search for publications on N. otitidiscaviarum in the Medline database of the National Library of Medicine was conducted for the literature review. Only reports available in English, published in the last 25 years, were included. Articles were identified through screening of titles and their abstracts to determine final eligibility. Key words used include “Nocardia otitidiscaviarum”.

The search terms yielded a total of 106 articles, in which 49 articles were included[5],[6],[7],[8],[9],[10],[11],[12],[13],[14],[15],[16],[17],[18],[19],[20],[21],[22],[23],[24],[25],[26],[27],[28],[29],[30],[31],[32],[33],[34],[35],[36],[37],[38],[39],[40],[41],[42],[43],[44],[45],[46],[47],[48],[49],[50],[51],[52],[53]. One article was excluded in view of inconsistently reported results. One article[43] was reviewed from its abstract only, as the full manuscript was not available. A total of 141 cases of N. otitidiscaviarum infections, including our case, were collated. Their clinical features and antimicrobial susceptibilities were shown in [Table 1]. The median age was 57 years, and 69.2% were males. The commonest risk factors reported included corticosteroids use (n=11), chronic lung disease (n=12), solid organ transplant (n=8), underlying human immunodeficiency virus (n=4) and solid organ malignancy (n=3). Eighteen patients did not appear to have any underlying medical conditions. Mortality occurred in 8 out of 49 cases reported (16.3%). Seventy-two cases had their sites of infection stated. The commonest clinical infective syndrome included pneumonia (n=35, 48.6%), skin and soft tissue infection (n=34.7%), brain abscess (n=8, 11.1%), parapneumonic effusion/empyema (n=7, 9.72%), lymph nodal involvement (n=3, 4.17%), septic arthritis (n=3, 4.17%), ocular infection (n=3, 4.17%), osteomyelitis (n=1, 1.39%), extraperitoneal mass (n=1, 1.39%) and bacteremia (n=1, 1.39%). 7 patients (9.72%) presented with disseminated disease.{Table 1}

[Table 2] shows the commonest antimicrobial agents tested. We included agents with at least 20 isolates tested, where susceptibilities were reported specifically to be sensitive, intermediate or resistant only. The most susceptible agents included linezolid (n=47, 100.0%), amikacin (n=55, 96.5%), trimethoprim/sulfamethoxazole (n=82.8%), gentamicin (n=21, 72.4%) and tobramycin (n=26, 72.2%). Beta-lactam antimicrobial agents exhibited high rates of resistance against this species, with 98.6% for amoxicillin clavulanic acid, 93.2% for cefotaxime, 89.0% for imipenem and 86.1% for ceftriaxone.{Table 2}

In one of the largest retrospective study of nocardiosis with 113 patients proven with Nocardial infections, the commonest implicated species included Nocardia brasilensis (n=54, 47.8%), Nocardia asteroides (n=36, 31.8%), Nocardia farcinica (n=7, 6.2%), Nocardia flavorosea (n=4, 3.5%), and N. otitidiscaviarum (n=3, 2.7%). Cutaneous infection was the commonest presentation in 64 patients (56.6%), followed by pulmonary infection in 38 (33.6%) and brain abscesses in 7 patients (6.2%). Eight patients (7.1%) presented with disseminated infection, with 5 secondary to Nocardia asteroides and 3 secondary to Nocardia farcinica. Mortality in this series was 8.0%[19]. We report the largest series of cases of N. otitidiscaviarum infection reported over the course of 25 years, in which pulmonary involvement appear the commonest. The case fatality rate in our series appears much higher at 16.3%, likely due to more cases of pneumonia and brain abscesses reported. Indeed, amongst the eight cases of mortality in our series, six patients had pulmonary involvement only and two had brain abscesses.

Based on a Spanish series of 35 strains of N. otitidiscaviarum, beta-lactam resistance rates appeared to be high, which is consistent with our series. Among three beta-lactams tested, including amoxicillin/clavulanate, cefotaxime, and imipenem, resistance ranged from 82.9% to 100.0%. This contrasts with other commoner Nocardial species that are relatively more beta-lactam susceptible. For example, Nocardia cyriacigeorgica, which is the commonest Nocardial isolate in this series, exhibits resistance to cefotaxime and imipenem in only 2.8% of the cases[53]. Given the significant associated morbidity and mortality, and that susceptibility results take time to return, early identification of the causative Nocardial species plays a huge role in targeting an appropriate initial empiric therapy. In general, the treatment of disseminated nocardiosis entails a combination systemic antimicrobial therapy for a protracted duration. Currently, no prospective trials are available to guide effective therapy. For severe infections secondary to N. otitidiscaviarum, we suggest initial combination therapy with linezolid, amikacin and trimethoprim/sulfamethoxazole until susceptibility results return.

There are current no interpretative breakpoints from the Clinical &Laboratory Standards Institute for the use of tigecycline for nocardiosis. In a case series of fifteen cases of nocardiosis reported by Maraki et al[24] the minimal inhibitory concentration (MIC90) range of all isolates are at most 0.19 g/mL, including four isolates of N. otitidiscaviarum. In Lai et al's study, tigecycline appears most effective for Nocardia brasiliensis and Nocardia puris, with MIC values of ≤ 8 μg/mL against all of the tested isolates[51]. Our patient received tigecycline together with linezolid and trimethoprim/sulfamethoxazole as part of a combination therapy for disseminated nocardiosis with clinico-radiological improvement. These emerging data potentially suggests tigecycline as a possible option in the treatment of nocardiosis.

We present an interesting case of disseminated nocardiosis secondary to a rare species of Nocardia, treated with combination tigecycline, linezolid and trimethoprim/sulfamethoxazole. Awareness of the possible risk factors for this infection is crucial to suspecting this disease, which can present in a widely diverse manner, virtually involving any organ. Early identification of the causative species and susceptibility results is crucial given the diverse resistance patterns amongst various Nocardia species.[54]

Conflict of interest statement

We declare that we have no conflict of interest.


1Brown-Elliott BA, Brown JM, Conville PS, Wallace RJ Jr. Clinical and laboratory features of the Nocardia spp. based on current molecular taxonomy. Clin Microbiol Rev 2006; 19(2): 259-282.
2Conville PS, Brown-Elliot BA, Smith T, Żelazny AM. The complexities of Nocardia taxonomy and identification. J Clin Microbiol 2017; 56(1): e01419-17.
3Marin M, Ruiz A, Iglesias C, Quiroga L, Cercenado E, Martin-Rabadan P, et al. Identification of Nocardia species from clinical isolates using MALDI-TOF mass spectrometry. Clin Microbiol Infect 2018; 24(12): 1342.e5-1342.e8.
4Xiao M, Pang L, Chen SC, Fan X, Zhang L, Li HX, et al. Accurate identification of common pathogenic Norcadia species: Evaluation of a multilocus sequence analysis platform and matrix-assisted laser desorption isonization-time of flight mass spectrometry. PLoS One 2016; 11(1): e0147487.
5Princess I, Ebenezer R, Ramakrishnan N, Nandini S. Pulmonary nocardiosis and scrub typhus in an immunocompromised host. J Glob Infect Dis 2018; 10(2): 108-111.
6Thirouvengadame S, Muthusamy S, Balaji VK, Easow JM. Unfolding of a clinically suspected case of pulmonary tuberculosis. J Clin Diagn Res 2017; 11(8): 1-3.
7Liu C, Feng M, Zhu J, Tao Y, Kang M, Chen L. Severe pneumonia due to Nocardia otitidiscaviarum identified by mass spectrometry in a cotton farmer. A case report and literature review. Medicine (Baltimore) 2017; 96(13): e6526.
8Sadamatsu H, Takahashi K, Tashiro H, Komiya K, Nakamura T, Sueoka-Aragane N. Successful treatment of pulmonary nocardiosis with fluoroquinolone in bronchial asthma and bronchiectasis. Respirol Case Rep 2017; 5(3): e00229.
9Mahgoub A, Gumaa SA, Joseph MR, Saleh MS, Elsheikh AH, Elkhalifa Al, et al. Pulmonary nocardiosis caused by Nocardia otitidiscaviarum in an adult asthmatic female patient: The presence of acid-fast branching filaments is always significant, S Afr Med J 2016; 107(1): 43-45.
10Jiang Y, Huang A, Fang Q. Disseminated nocardiosis caused by Nocardia otitidiscaviarum in an immunocompetent host: A case report and literature review. Exp Ther Med 2016; 12(5): 3339-3346.
11Deepa R, Banu ST, Jayalakshmi G, Parveen JD. Pleuropulmonary nocardiosis due to Nocardia otitidiscaviarum in a debilitated host. Indian J Pathol Microbiol 2016; 59(2): 240-242.
12Eren E, Ulu-Kilic A, Atalay A, DemiraslanH, Parkan O, Koc N. Report of an immunocompetent case with disseminated infection due to Nocardia otitidiscaviarum: Identification by 16S rRNA gene sequencing. Infez Med 2016; 24(1): 71-76.
13Ishihara M, Takada D, Sugimoto K, Oguro H, Gonoi T, Akiyama Y et al. Primary brain abscess caused by Nocardia otitidiscaviarum. Intern Med 2014; 53(17): 2007-2012.
14Huang CH, Hsueh PR, Chen YH. Empyema thoracis due to Nocardia otitidiscaviarum. J Microbiol Immunol Infect 2015; 48(5): 580-581.
15Shahapur PR, Peerapur BV, Honnutagi RM, Biradar MS. Lymphocutaneous nocardiosis caused by Nocardia otitidiscaviarum: A case report and review of literature. J Nat Sci Biol Med 2014; 5(1): 197-201.
16Taj-Aldeen SJ, Deshmukh A, Doiphode S, Wahab AA, Allangawi M, Almuzrkchi A, et al. Molecular identification and susceptibility pattern of clinical Nocardia species: Emergence of Nocardia crassostreae as an agent of invasive nocardiosis. Can J Infect Dis Med Microbiol 2013; 24(2): e33-e38.
17Ramamoorthi K, Pruthvi BC, Rao NR, Belle J, Chawla K. Pulmonary nocardiosis due to Nocardia otitidiscaviarum in an immunocompetent host- A rare case report. Asian Pac J Trop Med 2011; 4(5): 414-416.
18Betran A, Villuendas MC, Rezusta A, Moles B, Rubio MC, Revillo MJ, et al. Cavitatory pneumonia caused by Nocardia otitidiscaviarum. Braz J Microbiol 2010; 41(2): 329-332.
19Tan CK, Lai CC, Lin SH, Liao CH, Chou CH, Hsu HL, et al. Clinical and microbiological characteristics of Nocardiosis including those caused by emerging Nocardia species in Taiwan, 1998-2008. Clin Microbiol Infect 2010; 16(7): 966-972.
20Reddy AK, Garg P, Kaur I. Speciation and susceptibility of Nocardia isolated from ocular infections. Clin Microbiol Infect 2010; 16(8): 1168-1171.
21Minero MV, Marin M, Cercenado E, Rabadan PM, Bouza E, Munoz P. Nocardiosis at the turn of the century. Medicine (Baltimore) 2009; 88(4): 250-261.
22Chawla K, Mukhopadhyay C, Payyanur P, Bairy I. Pulmonary nocardiosis from a tertiary care hospital in Southern India. Trop Doct 2009; 39(3): 163-165.
23Pelaez AI, Garcia-Suarez MDM, Manteca A, Melon O, Aranaz C, Cimadevilla R, et al. A fatal case of Nocardia otitidiscaviarum pulmonary infection and brain abscess: Taxonomic characterization by molecular techniques. Ann Clin Microbiol Antimicrob 2009; 8: 11.
24Maraki S, Scoulica E, Nioti E, Tselentis Y. Nocardial infection in Crete, Greece: Review of fifteen cases from 2003 to 2007. Scan J Infect Dis 2009; 41(2): 122-127.
25Thoms KM, Zimmermann O, Schupp P, Thorns S, Emmert S. Nocardia otitidiscaviarum: Cause of long-term cutaneous abscesses on the leg of an immunocompetent man. Arch Dermatol 2007; 143(8): 1086-1087.
26Munoz J, Mirelis B, Aragon LM, Gutierrez N, Sanchez F, Espanol M, et al. Clinical and microbiological features of nocardiosis 1997-2003. J Med Microbiol 2007; 56(Pt 4): 545-550.
27Bonifaz A, Flores P, Saul A, Carrasco-Gerard E, Ponce RM. Treatment of actinomycetoma due to Nocardia spp. with amoxicillin-clavulanate. Br J Dermatol 2007; 156(2): 308-311.
28Fabre S, Gibert C, Lechiche C, Jorgensen C, Sany J. Primary cutaneous Nocardia otitidiscaviarum infection in a patient with rheumatoid arthritis treated with infliximab. J Rheumatol 2005; 32(12): 2432-2433.
29Yoshida K, Bandoh S, Fujita J, Tokuda M, Negayama K, Ishida T. Pyothorax caused by Nocardia otitidiscaviarum in a patient with rheumatoid vasculitis. Intern Med 2004; 43(7): 615-619.
30Hemmersbach-Miller M, Martel AC, Benítez AB, Sosa AO. Brain abscess due to Nocardia otitidiscaviarum: Report of a case and review. Scand J Infect Dis 2004; 36(5): 381-384.
31Kageyama A, Yazawa K, Ishikawa J, Hotta K, Nishimura K, Mikami Y. Nocardial infections in Japan from 1992 to 2001, including the first report of infection by Nocardia transvalensis. Eur J Epidemiol 2004; 19(4): 383-389.
32Sharma M, Gilbert BC, Benz RL, Santoro J. Disseminated Nocardia otitidiscaviarum infection in a woman with sickle cell anemia and end-stage renal disease. Am J Med Sci 2007; 333(6): 372-375.
33Shivaprakash MR, Rao P, Mandal J, Biswal M, Gupta S, Ray P, et al. Nocardiosis in a tertiary care hospital in North India and review of patients reported from India. Mycopathologia 2007; 163(5): 267-274.
34Dikensoy O, Filiz A, Bayram N, Balci I, Zer Y, Celik G, et al. First report of pulmonary Nocardia otitidiscaviarum infection in an immunocompetent patient from Turkey. Int J Clin Pract 2004; 58(2): 210-213.
35Wada A, Matsuda S, Kubota H, Miura H, Iwamoto Y. Primary lymphocutaneous nocardiosis caused by Nocardia otitidiscaviarum. Hand Surg 2002; 7(2): 285-287.
36Mari B, Monton C, Mariscal D, Lujan M, Sala M, Domingo C. Pulmonary nocardiosis: Clinical experience in ten cases. Respiration 2001; 68(4): 382-388.
37Saarinen KA, Lestringant GG, Czechowski J, Frossard PM. Cutaneous nocardiosis of the chest wall and pleura-10-year consequences of a hand actinomycetoma. Dermatology 2001; 202(2): 131-133.
38Duran E, Lopez L, Martinez A, Comunas F, Boiron P, Rubio MC. Primary brain abscess with Nocardia otitidiscaviarum in an intravenous drug abuser. J Med Microbiol 2001; 50(1): 101-103.
39Hartmann A, Halvorsen CE, Jenssen T, Bjorneklett A, Brekke IB, Bakke SJ, et al. Intracerebral abscess caused by Nocardia otitidiscaviarum in a renal transplant patient-cured by evacuation plus antibiotic therapy. Nephron 2000; 86(1): 79-83.
40Taniguchi H, Mukae H, Ashitani J, Ihi T, Sakamoto A, Kohno S, et al. Pulmonary Nocardia otitidiscaviarum infection in a patient with chronic respiratory infection. Intern Med 1998; 37(10): 872-876.
41Sandre RM, Summerbell RC. Disseminated Nocardia otitidiscaviarum in a patient with AIDS. Can J Infect Dis 1997; 8(6): 347-350.
42Mereghetti L, van der Mee-Marquet N, Dubost AF, Boiron P. Nocardia otitidiscaviarum infection of a traumatic skin wound. Eur J Clin Microbiol Infect Dis 1997; 16(5): 383-384.
43Freland C, Fur JL, Nemirovsky-Trebucq B, Lelong P, Boiron P. Primary cutaneous nocardiosis caused by Nocardia otitidiscaviarum: two cases and a review of the literature. J Trop Med Hyg 1995; 98(6):395-403.
44Poonwan N, Kusum M, Mikami Y, Yazawa K, Tanaka Y, Gonoi T, et al. Pathogenic Nocardia isolated from clinical specimens including those of AIDS patients in Thailand. Eur J Epidemiol 1995; 11(5): 507-512.
45Suzuki Y, Toyama K, Utsugi K, Yazawa K, Mikami Y, Fujita M, et al. Primary lymphocutaneous nocardiosis due to Nocardia otitidiscaviarum: the first case report from Japan. J Dermatol 1995; 22(5): 344-347.
46Clark NM, Braun DK, Pasternak A, Chenoweth CE. Primary cutaneous Nocardia otitidiscaviarum infection: Case report and review. Clin Infect Dis 1995; 20(5): 1266-1270.
47Castelli L, Zlotnik H, Ponti R, Vidotto V. First reported Nocardia otitidiscaviarum infection in an AIDS patient in Italy. Mycopathologia 1994; 126(3): 131-136.
48Wei M, Wang P, Qu J, Li R, Liu Y, Gu L, et al. Identification and antimicrobial susceptibility of clinical Nocardia species in a tertiary hospital in China. J Glob Antimicrob Resist 2017; 11: 183-187.
49Hakawi AM, Al Rabiah FA. Clinical pattern of nocardiosis in Saudi Arabia: A case series. East Mediterr Health J 2018; 14(4): 966-971.
50McTaggart LR, Doucet J, Witkowska M, Richardson SE. Antimicrobial susceptibility among clinical Nocardia species identified by multilocus sequence analysis. Antimicrob Agents Chermother 2015; 59(1): 269-275.
51Lai CC, Liu WL, Ko WC, Chen YH, Tan HR, Huang YT, et al. Multicenter study in Taiwan of the in vitro activities of nemonoxacin, tigecycline, doripenem, and other antimicrobial agents against clinical isolates of various Nocardia species. Antimicrob Agents Chermother 2011; 55(5): 2084-2091.
52Hashemi-Shahraki A, Heidarieh P, Bostanabad SZ, Hashemzadeh M, Feizabadi MM, Schraufnagel D, et al. Genetic diversity and antimicrobial susceptibility of Nocardia species among patients with nocardiosis. Sci Rep 2015; 5: 17862.
53Valdezate S, Garrido N, Carrasco G, Medina-Pascual MJ, Villalon P, Navarro AM, et al. Epidemiology and susceptibility to antimicrobial agents of the main Nocardia species in Spain. J Antimicrob Chemother 2017; 72: 754-761.
54Lalitha P, Tiwari M, Prajna M, Gilpin C, Prakash K, Srinivasan M. Nocadia keratitis: Species, drug sensitivities, and clinical correlation. Cornea 2007; 26(3): 255-259.