Journal of Acute Care
Volume 1 | Issue 3 | Year 2022

A Case Report of Necrotic Lung Abscess due to Nocardia Otitidiscaviarum

Owais Tisekar1https://orcid.org/0000-0003-3751-469X, Ajith Kumar AK2https://orcid.org/0000-0001-5134-1698, Justin A Gopaldas3https://orcid.org/0000-0002-0420-6925, Rajeev C Mathews4, Ranjeeta Adhikary5https://orcid.org/0000-0003-4695-0135

1-3Department of Critical Care Medicine, Manipal Hospital, Bengaluru, Karnataka, India

4Department of Internal Medicine, Manipal Hospital, Bengaluru, Karnataka, India

5Department of Laboratory Medicine–Microbiology, Manipal Hospital, Bengaluru, Karnataka, India

Corresponding Author: Owais Tisekar, Department of Critical Care Medicine, Manipal Hospital, Bengaluru, Phone: +91 9773841038, e-mail: waistisekar@gmail.com

Received on: 01 October 2022; Accepted on: 13 February 2023; Published on: 03 May 2023


Nocardia is a cause of localized or disseminated infection in humans. Nocardia otitidiscaviarum (N. otitidiscaviarum) is an infrequent cause of nocardiosis, accounting for <5% of the cases. N. otitidiscaviarum primarily affects the lungs, skin, and brain, with the lungs being the most common site. Diagnosis can be a challenge, and it requires a high index of suspicion among clinicians. A 52-year-old gentleman presented to our hospital with a 2-month history of fever, cough, and progressive breathlessness. He was started on a high-flow nasal cannula (HFNC) for respiratory failure. The positron emission tomography (PET) showed a left lower lobe mass lesion with a maximum standardized uptake value (SUV) of 17.4. The histopathological findings of the computed tomography (CT)-guided mass biopsy were consistent with an abscess. The identification of Nocardia species was made by Kinyoun staining after decolorization with 1% of sulfuric acid. According to the drug-sensitivity test, the patient was started on trimethoprim/sulfamethoxazole along with imipenem/cilastatin. There was clinical improvement in 3–4 days and the patient was weaned off the HFNC support. Nocardiosis should be an essential consideration for the differential diagnosis of many bacterial, fungal, and viral infections, even in immunocompetent individuals. Early diagnosis and treatment help to improve survival.

How to cite this article: Tisekar O, Ajith Kumar AK, Gopaldas JA, et al. A Case Report of Necrotic Lung Abscess due to Nocardia Otitidiscaviarum. J Acute Care 2022;1(3):163-167.

Source of support: Nil

Conflict of interest: Dr Ajith K, Dr Justin A Gopaldas and Dr Ranjeeta Adhikary are associated as the Editorial board members of this journal and this manuscript was subjected to this journal’s standard review procedures, with this peer review handled independently of these Editorial board members and their research group.

Patient consent statement: The author(s) have obtained written informed consent from the patient for publication of the case report details and related images.

Keywords: Immunocompetent, Lung abscess, Nocardia, Otitidiscaviarum.


Nocardia, an Actinomycetales, causes localized and disseminated infection in humans. To date, over 50 species of the family, Nocardiaceae, are clinically significant, asteroids being the most frequent.1 It is a rare cause of opportunistic infection in immunosuppressed and healthy individuals. N. otitidiscaviarum most commonly affects the lungs via inhalation.1 CT chest plays an important role in diagnosis; however, findings are nonspecific and require microbiological confirmation.2 Diagnosis can be a challenge, and it requires a high index of suspicion among clinicians. We describe a case of N. otitidiscaviarum affecting the lungs in an immunocompetent individual with an emphasis on the approach for its diagnosis.


A 52-year-old cotton farmer was admitted to our hospital with fever, productive cough, and gradually progressive breathlessness for 2 months. There was no history of night sweats or weight loss, nor any history of tuberculosis. There was no other significant comorbid illness. Physical examination on admission showed a pulse rate of 96/minute, blood pressure of 112/78 mmHg, a skin temperature of 37.8°C with a room air saturation of 92%, and a respiratory rate of 30 cycles/minute. There were early to mid inspiratory crepitations in the left infrascapular area on auscultation. A complete hemogram showed a hemoglobin of 13.4 g/dL (normal range—13.5–18 g/dL), white cell count of 23030/μL (normal range—4000–11000/μL) with 86.4% neutrophils (normal range—45–76%), and 7.6% lymphocytes (normal range—17–44%). Screening for human immunodeficiency virus infection and diabetes mellitus was negative. The chest radiograph showed bilateral ill-defined nodular shadows with the largest coalescent opacity in the left lower zone. Blood and sputum cultures were sent for analysis, and cultures were negative. We started him on ceftriaxone and azithromycin empirically. On day 5 of the illness, we started him on HFNC for hypoxemic respiratory failure, not amenable to oxygen supplementation. Given the suspicion of tuberculosis versus malignancy, a PET-CT was undertaken. PET-CT (Fig. 1) showed a 9 × 7 cm heterogeneously enhancing mass lesion in the left lower lobe with internal hypodense areas, likely an abscess. The maximum SUV of the abscess was 17.4. There was no other lesion on PET-CT. We did a CT-guided biopsy from the left lower lobe necrotic mass from the most fluorodeoxyglucose (FDG) avid area. Histopathology revealed an acute inflammatory collection of many neutrophils, histiocytes, and extensive necrosis with few foreign body giant cells. Gram stain on the specimen revealed many branching, filamentous, and gram-positive bacteria, which were positive with Kinyoun staining for acid-fast bacteria after decolorization with 1% sulfuric acid (Fig. 2). The culture of the specimen grew N. otitidiscaviarum on 5% sheep and chocolate agar with species identification by matrix-assisted laser desorption/ionization-time of flight (MALDI-TOF) spectrometry (Fig. 3). The isolate was susceptible to sulfamethoxazole-trimethoprim and aminoglycoside and resistant to amoxicillin/clavulanate as per the susceptibility testing by broth dilution method. Hence, we started the patient on trimethoprim/sulfamethoxazole (160/800 mg) thrice daily with imipenem/cilastatin 500/500 mg 4 times per day. Over the next 3–4 days, his symptoms gradually improved, and he got weaned off from the HFNC and was transferred to the ward. At 3 weeks of treatment for nocardiosis, imipenem/cilastatin was stopped, and he was discharged on trimethoprim/sulfamethoxazole (160/800 mg) every 8 hours. The patient was asked to review after four weeks; however, he was lost to follow-up. At the time of discharge, he had a clinical resolution of symptoms with a room air saturation of 96%.

Fig. 1: Chest radiograph demonstrates coalescent mass lesion in the left lower zone (black arrow) with nodular shadows bilaterally (red arrow)

Fig. 3: Left lower lobe heterogeneous mass with multiple internal necrotic areas and adjacent air bronchogram. There is right lower lobe mucous plugging and associated bronchiectasis

Fig. 2: Modified Kinyoun stain showing branching acid-fast bacilli after decolourization with 1% sulfuric acid


  1. Enumerate the opportunistic pathogens affecting the lungs?

    The following list of pathogens is considered in the differential diagnosis of infections when there is a loss of host immune responses (Table 1).

    Table 1: List of the common opportunistic pathogens seen in the immunocompromised host
    Bacteria Nocardia, actinomycosis
    Viruses Respiratory viruses like influenza, adenovirus, parainfluenza, respiratory syncytial virus, and human metapneumovirus
    Human herpes virus
    Fungi Pneumocystis jirovecii
    Aspergillus species
    Candida species
    Cryptococcus neoformans
    Molds like mucor and rhizopus
    Endemic mycosis
    Other filamentous fungi (Fusarium and Scedosporium)
  2. Classify the immune defects and the typical organisms associated with the immune defects (See Table 2).

    Table 2: Immune defects and the organisms commonly associated with them
    Neutropenia Medications (methotrexate, valganciclovir, sulfamethoxazole, azathioprine, everolimus, antineoplastic agents)Hematological malignancies
    Bone marrow suppression
    Opportunistic pathogens like cytomegalovirus, cryptosporidium, parvovirus, Pneumocystis jirovecii
    Neutrophil functional defect Chronic granulomatous disease
    Chronic exocrine insufficiency
    Chronic liver disease
    Gram-positive cocci (Staphylococcus and Streptococcus)
    Gram-negative bacilli like E. coli, Klebsiella
    Fungi like Candida, Mucormycosis, and Aspergillus
    T-cell defect Organ transplantation like kidney, liver, heart
    Bone marrow transplant
    Hematological malignancies
    T-cell-depleting drugs like tacrolimus, everolimus, and cyclosporin
    Community-acquired respiratory viruses
    Cytomegalovirus and varicella zoster virus
    Nocardia and ActinomycosisPneumocystis jirovecii
    Mycobacterial tuberculosis
    B-cell defect B-cell-depleting drugs like mycophenolate mofetil, rituximab, bortezomib
    Chronic leukemia and lymphomas
    Encapsulated bacteria like H. influenza Human herpes virus
    Complement abnormalities Drug-induced like Eculizumab and Carfilzomib
    Systemic lupus erythematosus
    Encapsulated bacteria
    Asplenia Postsplenectomy Encapsulated bacteria
  3. What are the most common nocardial species affecting the human population?

    Nocardia is an anaerobic, filamentous, gram-positive, and weak acid-fast bacillus. Species most commonly causing human infection include Nocardia asteroids, Nocardia transvalensis, Nocardia brasiliensis, N. otitidiscaviarum, and Nocardia cyriacigeorgica.3 N. otitidiscaviarum accounts for roughly 2.9% of all Nocardia infections.4

  4. What are the predisposing risk factors for Nocardiosis?

    One-third of the cases are seen in immunocompetent individuals.7 In immunocompetent individuals, infection is mostly self-limiting.

    Risk factors predisposing to infection are described below (Table 3).5

    Table 3: Predisposing risk factors for nocardiosis
    Acquired immune deficiency syndrome with CD4 counts <50 Lymphoproliferative diseases and carcinomas
    Chronic steroid therapy Liver cirrhosis
    Solid organ transplant, especially lungs Intravenous drug abuse
    Bone marrow organ transplant Chronic lung disease
    Table 4: Common bacterial, fungal, and viral organisms coinfecting patients with Nocardia
    Klebsiella pneumoniae Coagulase negative Staphylococcus aureus Escherichia coli
    Pseudomonas Tuberculosis Aspergillus
    Candida Herpes Cytomegalovirus
    Table 5: Nocardial species and the corresponding antibiotic sensitivity pattern
    N. abscessus Sensitive to penicillins, cefalosporins, linezolid, and aminoglycosides.
    Resistant MICs for macrolides, carbapenems, etc.
    N. otitidiscaviarum Sensitive to aminoglycoside, sulfamethoxazole, and fluoroquinolone.
    Resistant to β-lactam antibiotics.
    N. pseudobrasiliensis Sensitive to penicillin, macrolide, and sulfamethoxazole.
    Resistant to aminoglycoside and minocycline
    N. brasiliensis Sensitive to penicillins, minocycline, and sulfamethoxazole
    Resistant to fluoroquinolone, aminoglycoside, and macrolide.
    N. asteroides complex Sensitive to ceftriaxone, carbapenems, and aminoglycoside
    Resistant to penicillins and macrolide
    N. farcinica Sensitive to fluoroquinolones, linezolid, and carbapenems
    Resistant to penicillins, cephalosporins, and macrolide
    N. transvalensis complex Sensitive to linezolid, fluoroquinolones, and carbapenems
    Resistant to macrolides and aminoglycosides
    N. nova complex Sensitive to ampicillin, macrolides, and linezolid
    Resistant to amoxicllin-clavulanate

    MIC, minimum inhibitory concentration

  5. Describe the clinical features of Nocardiosis?

    Nocardiosis affects people between 20 and 60 years of age. Males are more frequently affected than females and are predominantly a disease in rural areas. Infection is acquired either through traumatic cutaneous inoculation or through inhalation (67% of cases). The cutaneous lymphocutaneous form arises through the skin, whereas the pleuropulmonary form arises via inhalation. Either of these two forms can lead to hematogenous dissemination to the pleura, brain, or abdominal organs like the liver.5

    Nocardia can have an acute, subacute, or chronic suppurative presentation. Symptoms include fever, chills, night sweats, cough, and breathlessness which are usually seen to last from a few days to weeks.3

  6. Why is N. otitidiscaviarum infrequently detected compared to other nocardial species?

    The low incidence of N. otitidiscaviarum is attributed to the lower prevalence in soil and reduced pathogenicity requiring repeated inhalation or inoculation of large doses for causing disease besides infrequent reporting of cases.3

  7. Describe the radiological features of N.otitidiscaviarum?

    No characteristic radiological feature can be ascribed to nocardiosis. Radiologically, it presents in the respiratory tract as pneumonia, pleural effusion, abscess, cavitary, or nodular masses mimicking either infection or malignancy.2

    PET-CT shows high uptake in the infected area with an SUV over 2.5.8 Biopsy commonly shows necrosis with neutrophils, macrophages, and lymphocytes in the acute or subacute phase. Fibrosis predominates in the chronic phase.3

  8. Which organisms are frequently isolated from Nocardia species?

    Concurrent infection is seen in 17% of cases, mainly with other bacteria, fungi, or viruses.6

  9. How is the confirmatory diagnosis of Nocardiosis made?

    Diagnosis is made by microscopic identification by Gram stain or modified Kinyoun stain. Microscopically, it is gram-positive, beaded, and branching filament, which is 1% acid-fast. Colonies on culture are chalky white or cotton ball-like.3

  10. Which method is used for accurate diagnosis of N. otitidiscaviarum species?

    Molecular techniques are now preferred for accurate species determination. Species identification is done by the MALDI-TOF mass spectrometry method, which has an accuracy of 95.9% in species identification.9 In addition, it helps in the identification of important Nocardia species.

    Other molecular methods available are polymerase chain reaction, DNA sequencing, and restriction fragment length polymorphism.3

  11. Describe the standard therapy for N. otitidiscaviarum and how does it differ from other Nocardia species?

    The initial antibiotic most commonly used is trimethoprim + sulfamethoxazole monotherapy combination, which is similar to other Nocardia species. The isolate of N. otitidiscaviarum is frequently resistant to sulfonamides. The antibiotic pattern of N. otitidiscaviarum includes resistance to beta-lactams, cephalosporins, and carbapenems. However, isolates are usually sensitive to amikacin, fluoroquinolones, and first-line drug sulfonamide.3,10 Indication for antibiotic susceptibility includes lack of response to initial therapy, relapse after therapy, contraindication to sulfonamide, or strains resistant to sulfonamides like Nocardia farcinica and N. otitidiscaviarum.5,11 The duration of treatment for the pulmonary disease is at least 6 months, which can be extended up to 12–18 months in immunosuppressed patients. In critical patients, combination drugs are used initially for 3–6 weeks. A longer duration of therapy is used in relapsed cases.12

  12. How much time does it take to see a response in a patient on appropriate antibiotic therapy?

    The response is seen in 8–10 days and in cases of combination therapy, the antibiotic is de-escalated to monotherapy after 3–6 weeks of initial therapy.12 Radiological follow-up with a CT scan may be warranted every 2–3 months and before the stoppage of medication.


Though the case is uncommon and the work-up detailed, a more comprehensive approach in the discussion will increase the value of the report, which at this time is just a narrative of the clinical course.

Immunosuppressive therapy should be reduced or discontinued in patients at risk of Nocardia infection. Secondary prophylaxis with daily double-strength TMP-SMX may be considered in patients with prior nocardiosis infections who are on immunosuppressive therapy that cannot be discontinued.12


Although nocardiosis is considered an opportunistic infection in immunosuppressed individuals, physicians should consider it as a differential diagnosis even in immunocompetent individuals. Radiological techniques like CT chest and PET scans are valuable aids in diagnosis, but microbiological confirmation is the rule. Early detection and prompt treatment can reduce mortality rates, especially in cases of severe or disseminated nocardiosis.


Owais Tisekar https://orcid.org/0000-0003-3751-469X

Ajith Kumar AK https://orcid.org/0000-0001-5134-1698

Justin A Gopaldas https://orcid.org/0000-0002-0420-6925

Ranjeeta Adhikary https://orcid.org/0000-0003-4695-0135


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