(2022) 21:17
Barry et al. Ann Clin Microbiol Antimicrob
https://doi.org/10.1186/s12941-022-00511-9

Annals of Clinical Microbiology
and Antimicrobials
Open Access

CASE REPORT

A fatal case of disseminated nocardiosis
due to Nocardia otitidiscaviarum resistant
to trimethoprim–sulfamethoxazole: case report
and literature review
Mazin Barry1,6,7* , Shahad AlShehri2, Ahlam alguhani3, Mohammad Barry4, Ali Alhijji1,6, Khalifa Binkhamis5,6,
Fahad Al‑Majid1,6, Fatimah S. Al‑Shahrani1,6 and Taim Muayqil6,8

Abstract
Background: Disseminated nocardiosis still causes significant morbidity and mortality and is often caused by Nocardia asteroides, N. basiliensis, and N. farcinica and are often treated with trimethoprim–sulfamethoxazole (TMP–SMX).
Nocardia otitidiscaviarum (N. otitidiscaviarum) rarely causes disseminated disease and resistance to TMP–SMX is even
more rare.
Case presentation: A 37-year-old woman with metastatic breast cancer and right ear deafness with recent occu‑
pational gardening and manipulating soil, presented to the hospital with first time seizure and multiple skin nodules.
Magnetic resonance imaging (MRI) showed ring enhancing lesions, biopsy of the skin and brain lesions grew N.
otitidiscaviarum. She was empirically treated with TMP–SMX and Imipenem–Cilastatin, however, almost three weeks
into therapy, susceptibility results revealed it to be resistant to both antimicrobials, she was subsequently changed to
Amikacin, Linezolid, Moxifloxacin, and Doxycycline but ultimately died.
Conclusions: This case report highlights the importance of suspecting a rare Nocardia species in patients at risk with
proper occupational exposure, moreover, TMP–SMX resistance should be suspected with lack of clinical response, this
may have important implications on clinical practice when facing similar infections.
Keywords: Nocardiosis, Nocardia otitidiscaviarum, Trimethoprim–sulfamethoxazole (TMP–SMX)
Background
Disseminated nocardiosis is a rare disease that can be
fatal and is often attributed to the three more commonly known species: Nocardia asteroides, N. basiliensis, and N. farcinica [1]. N. otitidiscaviarum was first
isolated from the mid-ear of a guinea pig and hence its
name, it was then isolated from humans as well [2, 3].
*Correspondence: mbarry@ksu.edu.sa
1
Division of Infectious Diseases, Department of Internal Medicine, College
of Medicine, King Saud University, PO Box 2925, Riyadh 11461, Saudi Arabia
Full list of author information is available at the end of the article

Trimethoprim–sulfamethoxazole (TMP–SMX) or Linezolid are the backbone of therapy regimens for nocardiosis. However, a combination therapy is usually required.
Resistance to TMP–SMX is rarely reported. We describe
a case of an extensively disseminated infection with N.
otitidiscaviarum, a species that was rarely described as a
significant pathogen in the medical literature.

Case
A 37-year-old woman presented with a generalized
tonic–clonic seizure that spontaneously aborted after
three minutes with post-ictal incontinence. Over the

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Barry et al. Ann Clin Microbiol Antimicrob

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Page 2 of 8

unremarkable. There were multiple nodules in the
extensor area of the right leg and on the surface of her
abdomen measuring 1 × 1 cm in size, they were firm,
non-mobile with an erythematous base and overlying
dark discoloration, they were mildly tender without any
drainage (Fig. 1).
Blood results revealed elevated erythrocyte sedimentation rate (Table 1).
Computed tomography (CT) of the chest showed
right lower lobe consolidation with cavity containing
air-fluid level, with bibasilar atelectatic bands (Fig. 2).
CT brain showed left parietal–temporal hypodensities. Cerebrospinal fluid (CSF) analysis showed no signs
of inflammation and microbiological evaluation including Mycobacterium tuberculosis PCR did not reveal
any pathogen. Magnetic resonance imaging (MRI) of
the Brain showed multiple ring enhancing lesions in
the left frontoparietal region, bilateral frontal regions,

preceding one month she had noticed multiple nodules
under her skin on the right leg, and over her abdomen.
They were mildly painful, eventually the overlying skin
developed dark discoloration. There was no drainage,
and she did not have similar skin lesions in the past. She
is a known case of stage 4 invasive ductal carcinoma of
the breast with metastasis to the liver, bone, and lungs
that was diagnosed two years prior to the current presentation. She was recently on carboplatin/paclitaxel for a
total of 8 weeks with the last dose given 3 weeks prior to
this presentation. She has not been on corticosteroids in
the preceding three months. Furthermore, over the past
months prior to her current illness, she had been caring
for domestic canaries and gardening frequently without
the use of personal protective equipment nor gloves,
reporting handling dirt and soil with her bare hands with
frequent touching of her face.
On arrival the patient’s vital signs were normal
(Table 1), and her neurological examination was

Fig. 1 Nodular skin lesion overlying patient’s abdomen (left) and leg (right)

Table 1 Clinical and laboratory variables
Laboratory variable

Measurements

Normal value

WBC

9 × ­109/L

3.5–12.0 × ­109/L

Clinical variable

Measurements

Glasgow coma scale

15/15

125 g/L

120–160 g/L

Temperature

37 °C

Haemaocrit %

38%

37–47%

Blood pressure

110/64 mmHg

Platelets

144 × ­109/L

140–450 × ­109/L

Respiratory rate

20 Breaths/minute

0.8–1.3 s

Heart rate

88 Beats/minute

Oxygen saturation

99%

Haemoglobin

International normalized ratio (INR)

0.93 s

Erythrocyte sedimentation rate (ESR)

120 mm/h

0–29 mm/h

C-reactive protein

2.9 mg/L

< 10 mg/L

Creatinine

55 µmol/L

53–115 µmol/L

Barry et al. Ann Clin Microbiol Antimicrob

(2022) 21:17

Fig. 2 Axial CT chest with right lower lobe cavitary lesion containing
air-fluid level (arrow)

Fig. 3 MRI T2 weighted image of brain showing cortical and
subcortical cystic lesions with surrounding vasogenic edema in the
left parietal lobe (arrows)

right parietal lobe and vermis, while T2 weighted image
showed cortical and subcortical cystic lesions (Fig. 3).
A left parietal mini-craniotomy was performed and
frank pus was drained with necrotic tissue. The histopathology showed no evidence for malignancy (metastasis) but histological features consistent with brain
abscess and no granulomas. A modified Kinyoun stain
showed branching bacilli (Fig. 4). The skin lesion punch
biopsy modified Kinyoun stain showed similar result.

Page 3 of 8

Tissue samples from the patient’s brain and skin lesions
were cultured onto different media including sheep
blood agar, chocolate agar, MacConkey agar and Sabouraud Dextrose Agar (Saudi Prepared Media Laboratory
Company Ltd, Riyadh, Saudi Arabia). Initial growth was
observed from both samples after 2 days of incubation
on blood, chocolate and Sabouraud agars. There was only
one colony type observed, the isolate was found to be catalase positive, the colony Gram showed beaded branching Gram-positive bacilli, acid fast stain was negative,
and modified Kinyoun stain was positive. The organism
was identified using Matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF
MS) (bioMerieux, Marcy-l ’Etoile, France) with 99.9%
confidence value as Nocardia otitidiscaviarum. This
was done through an extraction process using the Vitek
MS Mycobacterium/Nocardia kit (bioMerieux, Marcyl ’Etoile, France). Susceptibility testing was referred out
and performed using the Sensititre™ RAPMYCOI panel
(Thermo Fisher Scientific, Massachusetts, United States)
and interpreted using Clinical and Laboratory Standards
Institute interpretive breakpoints (CLSI M24: Clinical
and Laboratory Standards Institute standard M24—Susceptibility Testing of Mycobacteria, Nocardia spp., and
Other Aerobic Actinomycetes).
Upon presentation she was started on Imipenem-Cilastatin 500 mg IV every 6 h and trimethoprim–sulfamethoxazole (TMP–SMX) 15 mg/kg/day of TMP component
IV divided every 8 h, on day 14 of hospital stay she developed a new skin lesion in the abdomen, Amikacin 30/
kg/day IV was added. On day 22 of hospital stay, the susceptibility results returned from the outside referred lab
showing TMP-SMX and Imipenem resistance (Table 2).

Discussion and conclusion
In this report, we describe a rare fatal case of disseminated nocardiosis due to N. Otitidiscaviarum resistant to
TMP–SMX in a lady with advanced cancer.
The most common clinical presentation of nocardial
disease is pulmonary due to inhalation of mycelial fragments or via contact with the bacteria by a cut or abraded
skin which may lead to extrapulmonary dissemination
[1]. In our case, the patient’s risk factor was gardening.
N. otitidiscaviarum, formerly called N. caviae, was
first reported in humans in the mid-1960s [2]. It was
previously reported in 1924 after the organism was isolated from a guinea pigs middle ear [3]. Infections with
Nocardia are being increasingly recognized, however,
infections due to N. otitidiscaviarum are reported in only
0.3–2.9% of all Nocardia. infections and remains infrequently reported [4]. In one review only 10 cases of 347
patients infected with Nocardia. in the United States
were identified as N. otitidiscaviarum [5]. In a Japanese

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Fig. 4 Brain tissue: modified Kinyoun stain with branching bacilli

Table 2 Broth microdilution antibiotic susceptibility testing and
interpretation based on CLSI M24
Antibiotic

MIC (μg/mL)

Interpretation

Trimethoprim–sulfamethoxazole

≥ 8/152

Resistant

4.0

Sensitive

≥ 4.0

Resistant

Linezolid
Ciprofloxacin
Imipenem

≥ 64.0

Resistant

2.0

Intermediate

≥ 32.0

Resistant

128

Resistant

≥ 64/32

Resistant

2.0

Sensitive

Ceftriaxone

16.0

Intermediate

Doxycycline

2.0

Intermediate  

Minocycline

2.0

Intermediate

Tigecycline

0.5

Not applicable

Tobramycin

≥ 16.0

Resistant

Moxifloxacin
Cefepime
Cefoxitin
Amoxicillin–Clavulanic acid
Amikacin

Clarithromycin

≥ 16.0

Resistant

report of more than 303 pathogenic Nocardia isolated
from infected patients between 1992 and 2001, only 14
cases were due to N. otitidiscaviarum [6]. More recently,
Chen Liu et al. described a fatal case of severe pneumonia due to N. otitidiscaviarum in an immunocompetent
cotton farmer [7], while Ranjit Sah et al. reported successful treatment of a patient under steroid therapy with
disseminated N. otitidiscaviarum [8]. Moreover, it was
reported to cause disease in both immunocompetent and
immunocompromised hosts in the forms of pulmonary,
cutaneous, central nervous system and lymphocutaneous
infections [4].

In nature, N otitidiscaviarum is found in soil, decomposing vegetation, and other organic matter, as well as in
fresh and saltwater [9]. A survey of 504 soil samples in
India revealed that N. otitidiscaviarum had a much lower
prevalence compared to other Nocardia which may indicate the reason for its low incidence in clinical practice
[10]. In addition, it was noted to be less pathogenic in
humans when compared to other Nocardia.
Being described as an opportunistic pathogen, individuals with weakened immune system, such as patients
suffering from diabetes mellitus, chronic obstructive pulmonary disease, mixed connective tissue disorder, ulcerative colitis, cirrhosis, human immunodeficiency virus
(HIV) infection, malignancies, those receiving long-term
or large doses of corticosteroid therapy, and stem cell or
solid organ transplant recipients are at higher risk for
infections due to N. otitidiscaviarum [11], similarly, our
case had stage 4 invasive ductal carcinoma of the breast
and was on chemotherapy for eight weeks with the last
dose given three weeks before her presentation.
In a review of the database for N. otitidiscaviarum,
25 cases had been reported between 1997 and 2018 [7,
12–30]. More than half of those cases were reported in
immunocompromised patients. Prolonged use of corticosteroids was a major risk factor in the majority [12,
13, 16, 20, 21, 23, 30, 31]. In other cases, organ transplant
recipients [32], endocrine disorders [26], HIV and rheumatic heart disease were identified as risk factors [18, 20,
25]. On the other spectrum, eight cases were reported in
immunocompetent patients. Four of those were engaged
in gardening or farming and were exposed to dust inhalation similarly to our patient [7, 15, 19, 22]. Only one case

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Page 5 of 8

reported no underlying immunocompromised state nor
any occupational risk factors like farming [13].
It may be challenging to diagnose such patients who
present with many possible differential diagnoses. Conventional evaluation of specimens including wound
drainage, skin and brain lesions biopsies, CSF analysis and cultures along with imaging studies, all remain
the principal diagnostic methods. In the present report,
the species was determined using MALDI-TOF MS.
Although the gold standard for Nocardia species identification is molecular biology with amplification and
sequencing of one or two gene(s) among rrs (i.e. the gene
coding for 16 S rRNA), hsp65, secA1 and sodA, MALDITOF MS is increasingly being used for identifying Nocardia species. MALDI-TOF MS adequately identifies
frequent species in 95–100% of cases, however for cases
of a low identification score molecular biology-based
identification remains important [33]. The isolate in the
current study had a 99.9% confidence value, hence no
molecular sequencing was performed.
Most N. otitidiscaviarum isolates are reported to be
resistant to beta-lactams while usually being susceptible
to Amikacin, Fluoroquinolones [12, 34], and trimethoprim–sulfamethoxazole, hence, Sulfonamides remain
the standard agents for treatment [12]. Meanwhile, some
studies reported N. otitidiscaviarum susceptibility to

Linezolid in-vitro; however, data from in-vivo studies are
still lacking and the risk of haematological toxicity with
prolonged Linezolid therapy is high, hindering its clinical
use [35, 36]. A study that assessed 552 clinical isolates of
Nocardia from six major laboratories in the USA, found
sulfonamide resistance to be only 2%, which is lower than
previously shown [37, 38]. The authors hypothesized
that these discrepancies may be associated with difficulty in the laboratory interpretation of in vitro MICs for
TMP-SMX and SMX and the lack of quality controls for
Nocardia for these agents [39]. The isolate in the current
study showed MIC of ≥ 8/152 for TMP/SMX respectively, which indicates it to be a realistic phenomenon.
However, Imipenem resistance has been more commonly
described [34]. Typical in-vitro antimicrobial susceptibility patterns of various Nocardia species indicates that
N. otitidiscaviarum is usually susceptible to TMP–SMX
(Table 3).
Similarly, in our case combined drug therapy with
Imipenem and TMP-SMX were used for a total of 22
days until the susceptibility result showed resistance
to both agents and treatment with Linezolid, Ceftriaxone, moxifloxacin, doxycycline was used in addition to
Amikacin that was added earlier due to the appearance
of new skin lesions. The delay in obtaining susceptibility results from the outside lab clearly had a negative

Table 3 Typical in-vitro antimicrobial susceptibility patterns of various Nocardia species (Adapted from Manual of clinical microbiology
[40])
Drug

N.
abscessus

N.
brasiliensis

N. brevicatena N. cyriacigeorgica N.
farcinica
and N.
paucivorans

N. nova
complex

N. otitidiscaviarum N.
pseudobrasiliensis

N. transvalensis
complex

Amoxicil‑
lin–Clavu‑
lanic Acid

S

S

S

R

R

–

Amikacin

R

–

R

S

–

S

S

S

S

S

–

R

Ceftriaxone S

–

S

S

R

S

R

–

S

Ciprofloxa‑
cin

R

R

S

R

S

–

S

S

S

Clarithro‑
mycin

R

R

R

R

R

S

–

S

R

Gen‑
tamicin

–

–

R

–

R

–

S

–

R

Imipenem

R

–

R

S

S

S

R

–

S

Linezolid

S

S

S

S

S

S

S

S

S

Minocy‑
cline

–

S

–

–

–

–

–

R

–

Sulfameth‑
oxazole

–

S

–

–

–

–

S

S

–

Tobramy‑
cin

–

–

–

–

R

–

–

–

R

S susceptible, R Resistant
The optimal antimicrobial management for N. otitidiscaviarum is still not clearly defined, however, combined treatment is suggested for disseminated and severe
disease. In our case, the isolated N. otitidiscaviarum was susceptible to Linezolid and Amikacin and was resistant to TMP-SMX, Ciprofloxacin, Imipenem, Cefepime,
Cefoxitin, Amoxicillin-Clavulanic acid, Clarithromycin and Tobramycin. Seven cases were similarly reported with resistance to TMP-SMX [17, 19, 21, 24, 28, 30] with four
cases reported in immunocompetent patients [17, 19, 24], and one infecting a farmer [19], details of these studies are described in Table 4

69M

41F

79M

2004

Mahgoub et al. [17] 2016

2017

2018

2020

2020

Yoshida et al. [30]

Candel et al. [13]

Princess et al. [21]

Saksena et al. [24]

Saksena et al. [24]

Immunocompetent

Immunocompetent

On Corticosteroid therapy

On Corticosteroid therapy

Immunocompetent

On Corticosteroid therapy

TMP-SMX à Clarithromycin + Amikacin

Treatment

Resistant to: Ampicillin, Amoxicillin-Clavulanate,
Erythromycin, TMP-SMX and imipenem. Susceptible to:
Amikacin, Linezolid, Ciprofloxacin, and Gentamicin

Resistant to: Ampicillin, Amoxicillin-Clavulanate,
Erythromycin, TMP-SMX and imipenem. SusceptibleTo:
Amikacin, Linezolid, Ciprofloxacin, and Gentamicin

Resistant to: TMP-SMX, Amoxicillin, Clavulanate. Suscep‑
tible to: Amikacin, Ciprofloxacin, Linezolid, Imipenem
and Ceftriaxone

Resistant to: TMP-SMX. Susceptible to Aminoglycosides,
Beta-lactams and Carbapenem

Resistant to: Azithromycin, Ceftazidime, Penicillin,
Rifampicin and TMP-SMX. Susceptible to: Amikacin,
Ciprofloxacin, Meropenem and Streptomycin

Died

Recovered

Recovered

Recovered

Outcome

Meropenem + Colistin à TMP-SMX added

Amoxicillin-Clavulanate + Azithromycin à TMP-SMX

Died

Died

Azithromycin + Doxycycline à TMP-SMX + Imipenem Died

Levofloxacin + Vancomycin + Tobramycin

TMP-SMX + Amikacin + Imipenem à Ceftriaxone +
Amikacin + Ciprofloxacin

Resistant to: Ampicillin, Piperacillin, Cefazolin, Imipenem, Imipenem + TMP-SMX à TMP-SMX + Gentamicin
minocycline, Vancomycin, TMP-SMX, Erythromycin. Sus‑
ceptible to: Levofloxacin, Gentamicin and Levofloxacin

M, male; F, female; TMP-SMX, trimethoprim–sulfamethoxazole; GCS, Glasgow coma scale

74F

74M

51F

Drug Susceptibility

Immunocompetent (Farmer) Resistant to: TMP-SMX, Penicillin, Piperacillin, Imipenem,
Ceftazidime. Susceptible to: Amikacin, Minocycline,
Clarithromycin

2000

Matsu et al. [19]

74M

Years Age/gender Immune Status

References

Table 4 Case studies of N. otitidiscaviarum resistant to TMP-SMX

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Barry et al. Ann Clin Microbiol Antimicrob

(2022) 21:17

impact on patient outcome, such cases would advocate
for wider availability of such testing and higher turnaround time.
Mortality due to disseminated Nocardiosis is high,
therefore early diagnosis and initiation of therapy
are of vital importance in Nocardial infections. In
our case, the patient was started on empirical treatment for Nocardiosis that was later adjusted according to the susceptibility results, however, the delay in
administering proper antimicrobials and her pre-existing advanced malignancy may have attributed to her
mortality.
In conclusion, N. otitidiscaviarum infection though
rare may have considerable mortality; early diagnosis and
susceptibility testing are crucial in avoiding similar devastating outcomes. In addition, surveillance for emerging
TMP-SMX resistance should be closely monitored.
Abbreviations
TMP–SMX: Trimethoprim–sulfamethoxazole; WBC: White blood cells; ESR:
Erythrocyte sedimentation rate; CRP: C-reactive protein; CT: Computed
tomography; CSF: Cerebrospinal fluid; AFB: Acid-fast bacilli; M. tb: Mycobacte‑
rium tuberculosis; PCR: Polymerase chain reaction; MRI: Magnetic resonance
imaging; GMS: Grocott methenamine silver; PAS: Periodic acid–Schiff;
MALDI-TOF MS: Matrix-assisted laser desorption ionization-time of flight mass
spectrometry; MIC: Minimum inhibitory concentration; CLSI M24: Clinical
and Laboratory Standards Institute standard M24—Susceptibility Testing of
Mycobacteria, Nocardia spp., and Other Aerobic Actinomycetes.; HIV: Human
immunodeficiency virus.
Acknowledgements
None.
Author contributions
All authors contributed equally to Conceptualization, Validation, Investiga‑
tion, Resources, Writing - Original Draft, Writing - Review & Editing, Visualiza‑
tion, Supervision, Project administration, Methodology.All authors read and
approved the final manuscript.
Funding
This research did not receive any specific Grants from any funding agencies in
the public, commercial, or not-for-profit sector.
Availability of data and materials
All the data for this study will be made available upon reasonable request to
the corresponding author.

Declarations
Ethics approval and consent to participate
The study was approved by King Saud University IRB No. 21-1509E. Next of kin
consented to the publication of this report.
Competing interests
None declared.
Author details
1
Division of Infectious Diseases, Department of Internal Medicine, College
of Medicine, King Saud University, PO Box 2925, Riyadh 11461, Saudi Arabia.
2
Infectious Diseases Unit, Internal Medicine Department, Prince Sultan
Military Medical City, Riyadh, Saudi Arabia. 3 Infectious Diseases Unit, Internal
Medicine Department, King Abdullah Medical City National Guard, Riyadh,
Saudi Arabia. 4 Medical Imaging Department, King Abdullah bin Abdulaziz

Page 7 of 8

University Hospital, Riyadh, Saudi Arabia. 5 Department of Pathology, College
of Medicine, King Saud University, Riyadh, Saudi Arabia. 6 King Saud University
Medical City, King Saud University, Riyadh, Saudi Arabia. 7 Division of Infectious
Diseases, Faculty of Medicine, University of Ottawa, Ottawa, Canada. 8 Division
of neurology, Department of Internal Medicine, College of Medicine, King
Saud University, Riyadh, Saudi Arabia.
Received: 24 November 2021 Accepted: 6 May 2022

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