Original Article
Nontuberculous mycobacterial infection of the
musculoskeletal system in immunocompetent hosts
Manit K Gundavda, Hitendra G Patil, Vikas M Agashe, Rajeev Soman1, Camilla Rodriques2, Ramesh B Deshpande3
Abstract
Background: Nontuberculous mycobacteria (NTM) were considered saprophytic organisms for many years but now are recognized
as human pathogens. Although humans are routinely exposed to NTM, the rate of clinical infection is low. Such infections usually
occur in the elderly and in patients who are immunocompromised. However, there has been an increasing incidence in recent
years of infections in immunocompetent hosts. NTM infections in immunocompetent individuals are secondary to direct inoculation
either contamination from surgical procedures or penetrating injuries rather than hematogenous dissemination. Clinically and on
histopathology, musculoskeletal infections caused by NTM resemble those caused by Mycobacterium tuberculosis but are mostly
resistant to routine antituberculosis medicines.
Materials and Methods: Six cases of NTM infection in immunocompetent hosts presenting to the department from 2004 to 2015 were
included in study. Of which two cases (one patella and one humerus) of infection were following an open wound due to trauma while
two cases (one hip and one shoulder) of infection were by inoculation following an intraarticular injection for arthrogram of the joint, one
case was infection following arthroscopy of knee joint and one case (calcaneum) was infection following local injection for the treatment
of plantar fasciitis. All patients underwent inaging and tissue diagnosis with samples being sent for culture, staining, and histopathology.
Results: Clinical suspicion of NTM inoculation led to the correct diagnosis (four cases with culture positive and two cases with
histopathological diagnosis). There treatment protocol for extrapulmonary NTM infection was radical surgical debridement and
medical management based on drug sensitivity testing in culture positive cases. At a mean follow up of 3 years (range1–9 years)
all patients had total remission and excellent results.
Conclusions: Whenever a case of chronic granulomatous infection is encountered that does not respond to standard
anti-tuberculous treatment, with a history of open trauma, surgical intervention, or injection as shown in this study, a possible
NTM infection should be considered and managed appropriately.
Key words: Atypical mycobacteria, chronic granulomatous inflammation, immunocompetent hosts, infection by inoculation,
musculoskeletal system
MeSH terms: Musculoskeletal system, immunocompetence, mycobacterium infections, atypical, chronic, granulate disease
Introduction
T
he nontuberculous mycobacteria (NTM) are a group
of Mycobacterium species other than the obligate
pathogens Mycobacterium tuberculosis complex
Departments of Orthopaedics, 1Infectious Diseases, 2Microbiology and 3Pathology,
Hinduja Hospital and Medical Research Center, Mumbai, Maharashtra, India
Address for correspondence: Dr. Manit K Gundavda,
B/204, Hilton CHS, Shastri Nagar, Andheri West, Mumbai - 400 053,
Maharashtra, India.
E-mail: manit.gundavda@gmail.com
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DOI:
10.4103/0019-5413.201718
© 2017 Indian Journal of Orthopaedics | Published by Wolters Kluwer ‑ Medknow
and Mycobacterium leprae. The American Thoracic
Society in their statement endorsed the name NTM.1,2
These organisms were typically regarded as nonpathogenic
because of their low virulence until 1950, but they are
now recognized as opportunistic pathogens and important
causes of human disease.3,4 NTM are ubiquitous in nature
and widely distributed in water and soil. These are the
main sources of infection in humans.5 Clinically and
histopathologically, musculoskeletal infections caused by
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How to cite this article: Gundavda MK, Patil HG, Agashe VM,
Soman R, Rodriques C, Deshpande RB. Nontuberculous
mycobacterial infection of the musculoskeletal system in
immunocompetent hosts. Indian J Orthop 2017;51:205-12.
205
Gundavda, et al.: Musculoskeletal infections with NTM following inoculation in immunocompetent hosts
NTM resemble those caused by M. tuberculosis, i.e., chronic
granulomatous infection, although the overall course of
NTM disease is often milder than that of tuberculosis.6 The
clinical significance of diagnosing NTM infection is that
they are mostly resistant to routine antituberculosis drugs.1
Although immunocompromised patients are usually more
susceptible to these infection,7 there has been an increasing
incidence of infections caused by NTM in recent years in
both immunocompromised and normal hosts,3 leading to
significant confusion as regards diagnosis, leading to delay
in treatment. NTM infection in nonimmunocompromised
individuals is secondary to direct inoculation either
contamination from surgical procedures or penetrating
injuries rather than hematogenous dissemination (that is
common in immunocompromised individuals).6,8
We report six cases of NTM infection treated in our institute
since March 2004 to 2015 to create awareness about the
diagnosis of NTM infections in the musculoskeletal system.
Materials and Methods
All cases with a history of open trauma or invasive
intervention that developed chronic infection not responding
to empirical chemotherapy were evaluated for the possibility
of NTM infection. Six patients (5:1 male:female) averaging
33 years in age (range 15–44 years) meeting the above
criteria were included in the study. All patients underwent
radiological (X-rays and magnetic resonance imaging [MRI])
and tissue diagnosis with samples being sent for culture,
staining, and histopathology. Accompanied clinical data and
good communication between the clinician and microbiologists
were essential to optimize culture conditions to increase the
sensitivity of culture and laboratory diagnosis of NTM disease.
Samples were inoculated onto at least one solid medium for
quantitative as well as species diagnosis. Susceptibility of rapid
growing mycobacteria for eight antimicrobial agents2 [Table 1]
was advocated in culture-positive cases.
debridement, which was performed in all cases and
appropriate medical therapy was decided and monitored
by the infectious disease specialists at our institution.
Cases
Six cases of chronic infection postintervention/open trauma
were diagnosed and treated at musculoskeletal NTM
infections [Table 2].
Cases were divided into two groups: Group A: NTM infection
following open trauma, Case A1: Open facture, humerus
[Figure 1], Case A2: Open fracture, patella [Figure 2];
Group B: NTM infection following invasive intervention,
Case B1: Intraarticular injection for arthrogram, hip
[Figure 3], Case B2: Intraarticular injection for arthrogram,
shoulder, Case B3: Local injection for plantar fasciitis,
calcaneum [Figure 4], Case B4: Arthroscopy, knee [Figure 5].
Clinical description of 1 case from each group is described
below:
Case A1: The open fracture with wound contamination
A 32-year-old male sustained an open comminuted fracture
of the left middle 1/3rd humerus after a road traffic accident
in March 2004. No surgical treatment had been given until
arrival to our hospital six days after the injury, with obvious
signs of infection. Radical debridement was performed,
infected material and several foreign bodies were removed
and external fixator applied [Figure 1a and b]. Initial
a
As there is no available guideline or treatment protocol
for extrapulmonary NTM infection2,7 except for radical
Table 1: Susceptibility testing of antimicrobial agents and
therapeutic doses
Antimicrobial agent
Amikacin
Cefoxitin
Clarithromycin
Ciprofloxacin
Doxycycline
Linezolid
SMX (TMP‑SMX)
Tobramycin
Therapeutic dose for NTM infection
6-7.5 mg/kg/day
2 g IV QDS
500 mg B.D.
750 mg B.D.
200 mg B.D.
600 mg O.D.
1-1.5 g B.D.
3-5 mg/kg/day
TPM=Trimethoprim, SMX=Sulfamethoxazole, NTM=Nontuberculous mycobacteria,
IV=Intravenous
206
c
b
Figure 1: (Case A1) (a) Peroperative photograph showing, open
wound, extensive contamination of open fracture wound taken up
for debridement. (b) Radiograph of humerus anteroposterior view
showing external fixator in situ (c) Clinical photograph showing final
range of motion
Indian Journal of Orthopaedics | Volume 51 | Issue 2 | March‑April 2017
Gundavda, et al.: Musculoskeletal infections with NTM following inoculation in immunocompetent hosts
Table 2: Case summary and clinical implications
Case
Age, (years)
Sex
Local
complaints
NTM
inoculation
A1
32
Male
March 2004:
Open fracture of
the left humerus
with wrist drop
Wound
contamination
Mean duration 6 weeks
time from
first event to
diagnosis
Presentation of Chronic
NTM infection
discharging
sinus with
foul smelling
discharge
Involved bone/ Humerus
joint
Acid‑fast smear Positive
Culture positive Atypical
mycobacteria
Pathology
CGI with AFB
A2
15
Male
December 2012:
Open fracture of
the right patella
following RTA
Wound
contamination
B1
42
Male
Right hip pain on
exertion since 2007
2 months
7 months
3 discharging
sinuses around
knee with knee
swelling and
painful range of
motion
Patella
Chronic discharging
sinus following
arthrogram
Painful active
Discharging sinus
Dull aching knee pain
range of motion with serosanguinous and thigh abscess
of the shoulder discharge
with swelling
and warmth
Hip
Shoulder
‑
‑
‑
‑
Atypical mycobacteria ‑
January 2011:
MR arthrogram
CGI without AFB CGI without AFB
Mycobacterium
fortuitum
‑
Mycobacterium
chelonae
Surgery
Application of
external fixator
Debridement
four to five times
Radial nerve
exploration and
release
Drainage of
loculated fluid
from arm
Amikacin 1 g
Clarithromycin
500 mg B.D.
Linezolid
600 mg O.D.
Exploration and
debridement
Insertion of
biodegradable
vancomycin
impregnated
cement beads
Debridement and hip
excision arthroplasty
Tobramycin antibiotic
cement beads
insertion
Amikacin 1 g
Clarithromycin
500 mg B.D.
Linezolid
600 mg O.D.
9 years
9 months
Amikacin 1 g
Clarithromycin
500 mg B.D.
Linezolid 600 mg O.D.
Clofazimine
100 mg O.D.
15 months
Followup
B4
30
Male
February 2014:
Twisting injury of right
knee with complete
ACL tear
October 2010: January 2010 : Local February 2014:
MR arthrogram steroid injection
Arthroscopic ACL
and diagnostic thrice over a period reconstruction with
arthroscopy
of 6 months
semitendinosus graft
2 months
8 months
6 months
CGI without
AFB
‑
Mycobacteria
Chemotherapy
B2
44
Male
Pain in the left
shoulder since
2008
B3
36
Female
Pain in right heel
with localised
swelling since 2009
Calcaneum
Knee
Positive
Atypical
mycobacteria
CGI with AFB
Positive
Atypical mycobacteria
CGI with AFB
Rapid growing
Mycobacterium
(chelonae/fortuitum/
abscessus)
Open
Excision of lower
exploration and 1/3 right calcaneum
synovectomy
Rapid growing
Mycobacterium
(chelonae/fortuitum/
abscessus)
Right thigh abscess
drainage, excision
of ACL graft and
interference screw
Debridement of
femoral tunnel
Clarithromycin
500 mg B.D.
Clofazimine
100 mg O.D.
Amikacin 1 g
Clarithromycin
500 mg B.D.
Linezolid
600 mg O.D.
Amikacin 1 g
TPM+SMX ‑ 800+160
Doxycycline 100 mg
3 years
3 years
1 year
Acid‑fast smear and mycobacterial culture for specimens from large joints. AFB=Acid‑fast Bacilli, CGI=Caseating granulomatous inflammation, GI=Granulomatous inflammation,
NTM=Nontuberculous mycobacteria, , ACL=Anterior cruciate ligament, MR=Magnetic resonance, TPM=Trimethoprim, SMX=Sulfamethoxazole, RTA=Road Traffiic Accident
cultures were suggestive of acute infection by Enterococci
and Gram-negative bacilli and hence treatment started
with susceptible antibiotics (ciprofloxacin 750 mg B.D.,
and co-amoxiclav 1.2 g B.D.). Over the next 2 weeks,
the wound was debrided twice as the infection was
not coming under control. Histopathology done at two
weeks revealed a dense inflammatory exudate with
granulomas. The intraoperative tissue cultures grew
the NTM (Mycobacterium fortuitum, rapid-growing
Mycobacterium). The patient was started on combination
Indian Journal of Orthopaedics | Volume 51 | Issue 2 | March‑April 2017
therapy of amikacin 1 g intravenous. daily for 6 weeks,
linezolid 600 mg O.D., and clarithromycin 500 mg B.D., for
6 months based on the antibiotic sensitivity report. Renal
profile was periodically monitored while on injectable
amikacin therapy. The wound improved immediately
and secondary suturing was done 2 weeks after starting
the treatment. The external fixator was removed after
3 months and “U” slab was given for support for 4 weeks.
The fracture united uneventfully with a full range of
movements at the elbow and shoulder [Figure 1c].
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Gundavda, et al.: Musculoskeletal infections with NTM following inoculation in immunocompetent hosts
Nearing 10 years postcompletion of treatment, he has
no evidence of recurrence/re-activation of disease and
excellent function.
Case B1: Inoculation by intraarticular injection
a
b
Figure 2: (Case A2) (a) Clinical photograph showing multiple
discharging sinuses around the knee. (b) postoperative radiograph
of the knee joint lateral view showing bio-degradable cement beads
(arrows)
a
A 42-year-old male, presented with intermittent dull aching
pain in the right hip since 2007, which was aggravated
on exertion. Since there was no relief of symptoms with
medications and physiotherapy, an MRI arthrogram was
performed. One month following arthrogram, the pain in
the right hip exacerbated and was associated with swelling,
induration, and intermittent fever. Empirical antibiotics were
tried before a computed tomography-guided aspiration
for obtaining material was performed at another hospital
prior to presentation at our institute which revealed
granulomatous infection on histopathology, while there was
no growth on culture. The patient was started on four drug
c
b
d
e
Figure 3: (Case B1) (a) Radiograph of the right hip at presentation, showing decreased joint space and destructive changes in the right hip (arrow)
(b) Magnetic resonance imaging with gadolinium contrast of the right hip showing periarticular soft tissue and intraarticular involvement with
destruction of the femoral head (c) Intraoperative photograph showing destroyed and irregular femoral head (d) Histopathology: microphotograph
showing granulomatous inflammation with the presence of acid-fast Bacilli (arrow). (e) postoperative radiograph hip with thigh lateral view showing
excision of damaged femoral head and insertion of antibiotic cement beads
a
b
c
Figure 4: (Case B3) (a) Clinical photograph showing, discharging sinus and old surgical scar in the inner aspect of heel. (b) Magnetic resonance
imaging of calcaneum with gadolinium contrast showing marrow edema and soft tissue involvement along the plantar fascia. (c) Histopathology
microphotograph showing granulomatous inflammation with the absence of caseating necrosis
208
Indian Journal of Orthopaedics | Volume 51 | Issue 2 | March‑April 2017
Gundavda, et al.: Musculoskeletal infections with NTM following inoculation in immunocompetent hosts
Renal profile was periodically monitored while on injectable
amikacin therapy. The wound healed almost immediately
following appropriate antibiotic therapy and insertion of
cement beads. One year since the first visit and 5 months since
the last surgery, the patient was admitted for removal of the
antibiotic cement beads, as the wound had healed well and
with no fresh complaints. An intraoperative sample was sent
for culture but showed no growth. Two years after completion
of the treatment, his total hip arthroplasty (THA) was done
and he is totally asymptomatic at 6 months post-THA.
Results
Figure 5: (Case B4) Magnetic resonance imaging showing thigh
abscess
antitubercular treatment (ATT). In spite of 3 months of ATT,
the pain worsened significantly and the patient presented
to our institute with systemic symptoms, toxic appearance,
leukocytosis and raised erythrocyte sedimentation rate. The
radiograph [Figure 3a] at presentation showed decreased
joint space and destructive changes in the right hip,
while MRI [Figure 3b] with contrast suggested significant
soft tissue and joint involvement and destruction of the
femoral head and joint effusion. In view of the presentation
of severe infection and extensive bone and cartilage
destruction [Figure 3c], an excision arthroplasty was
performed. The tissue samples were cultured specifically for
M. tuberculosis and tissue was also sent for histopathology.
Histopathology [Figure 3d] indicated granulomatous
inflammation with the presence of acid-fast Bacilli (AFB)
and cultures grew NTM (Mycobacterium chelonae; rapidgrowing Mycobacterium) sensitive to linezolid, amikacin,
and clarithromycin. In consultation with a pulmonologist
in view of mycobacterial infection, appropriate antibiotics
were started based on the sensitivity pattern with amikacin
750 mg injected 3 times a week, clarithromycin 500 mg,
B.D., and linezolid 600 mg, O.D. In spite of starting the
treatment, the wound did not completely heal and a chronic
discharging sinus from the surgical site persisted. The sinus
was traced by performing a sinogram and excised but the
infection persisted.
An infectious disease specialist was consulted who adjusted
the dose and frequency of amikacin – 1 g intravenously daily
instead of thrice a week for 1 month followed by 5 times a
week for the next 5 months. Clofazimine (100 mg tablet, O.D.)
was added while continuing clarithromycin and linezolid as
before, also a reexploration and extensive debridement with
obtaining sample for culture and histopathology along with
insertion of tobramycin antibiotic cement beads (based on
the antibiotic sensitivity report) were performed [Figure 3e].
Indian Journal of Orthopaedics | Volume 51 | Issue 2 | March‑April 2017
Six (5:1 male:female) immunocompetent patients with
a history of invasive procedures in four cases and open
trauma in two cases presenting with chronic infections
not responding to routine chemotherapy were evaluated
radiologically and by tissue diagnosis. Average time
to diagnosis from inoculation: 4 months (6 weeks to
8 months), Histopathological diagnosis based on chronic
granulomatous inflammation: 100% cases (6/6 cases),
Culture growth with mycobacterial species identification:
66.6% (4/6 cases), AFB positive on smear: 50% (3/6 cases).
Based on clinical profile, histopathology, drug sensitivity
reports and opinion of infectious disease consultant,
chemotherapy consisted of a combination of (A) Amikacin
+ clarithromycin + linezolid was administered in three
patients (B) Amikacin + clarithromycin + linezolid +
clofazamine in one patient who had not responded to ATT as
well as treatment for NTM (C) Clarithromycin + clofazimine
in one patient (patient had been treated empirically by
ATT prior to presentation to our institute) (D) Amikacin
+ trimethoprim-sulfamethoxazole + doxycycline was
administered in one patient.
Injection amikacin was administered for a maximum
duration of 6 weeks while oral therapy for a minimum
duration of 6 months in all patients while monitoring blood,
renal and liver profiles for toxicity.
At a mean follow up of 3 years (range1–9 years) all
patients (6/6) had total remission and good function.
Discussion
NTM have been recognized as saprophytic organisms for
many years until the 1950s when they were recognized as
human pathogens.9 To date, more than 125 species have
been identified and about sixty are known to cause clinically
significant disease.4,10 Traditionally, NTM have been grouped
into four broad categories according to the Runyon system.
In this classification, NTM are divided by growth rates and
209
Gundavda, et al.: Musculoskeletal infections with NTM following inoculation in immunocompetent hosts
pigment production. Groups I, II, and III are slow-growing
NTM, and Group IV are fast growers (i.e., detectable in
culture within 7 days). The slow-growing NTM are subdivided
into Group I photochromogens (pigment producers in the
presence of light), Group II scotochromogens (pigment
producers in the absence of light), and Group III
nonchromogens (not producing pigments).3,10
NTM are ubiquitous in nature and widely distributed in
water, soil, and animals. Water (natural as well as reservoirs)
and soil are the main sources of infection in human.11,12
They can also be found as colonizers of medical equipment
such as endoscopes and surgical solutions.13 Human-tohuman transmission has not yet been reported.14,15 Biofilm
formation is a successful survival strategy for these very
hydrophobic organisms. Dispersal from biofilms may be a
mechanism of shedding from a device or water pipe to infect
the patient.16-18 They are difficult to eradicate with common
decontamination practices and are relatively resistant to
standard disinfectants such as chlorine, organomercurials,
and alkaline glutaraldehydes.19 There is a wide spectrum of
clinical diseases caused by NTM, which can be divided into
chronic pulmonary infections, superficial lymphadenitis,
skin and skeletal infections, and disseminated disease.3,4
As culture with strict criteria is still not routinely done in
most parts of India, there is a tendency to ignore such
isolates as contaminants, so it is difficult to comment on
the exact magnitude of the problem.20 Clinically important
species by group include Mycobacterium kansasii and
Mycobacterium marinum (Group I); Mycobacterium
gordonae and Mycobacterium scrofulaceum (Group II);
Mycobacterium avium intracellulare and Mycobacterium
ulcerans (Group III); and M. fortuitum, M. chelonae,
Mycobacterium abscessus (Group IV).3,11 Out of these,
NTM strains often acquired by trauma are M. fortuitum,
M. chelonae, and M. marinum.2,21
Clinically, musculoskeletal infections caused by atypical
mycobacteria often resemble those caused by M. tuberculosis,
i.e., chronic granulomatous infection,22 although the overall
course of atypical mycobacterial disease is often milder than
that of tuberculous infection.6 The histopathology is often
suggestive of a granulomatous lesion.23 Thus, these cases are
started on ATT either empirically or after histopathology. The
microbiological diagnosis of rapidly growing mycobacteria
infections includes direct microscopic observation of the
microorganism in the samples,10,24 culture in selective media,
and identification of the isolated species by phenotypic,
biochemical, molecular, and chromatographic techniques.25
The finding of AFB in stained smears by the Ziehl–Neelsen
or auramine techniques examined under a microscope is the
first evidence of the presence of mycobacteria in a clinical
specimen. On histopathological examination, a spectrum
210
of inflammatory changes has been reported including
granulomatous lesions with or without caseation. 26-28
Accompanied by clinical data, i.e., history of open wound
or surgical procedure or injections, it can help to establish
the presumptive diagnosis of NTM infection. However,
the gold standard in diagnosis is the identification of
Mycobacterium species in culture.7,10 Besides confirming
diagnosis, it allows us to do drug sensitivity so that
appropriate drug regimen can be selected, as NTM are
usually resistant to routine antitubercular medicines and
there is variability in susceptibility among species. 1,24
However, it is important to have a good communication
between the clinicians and microbiologists to optimize
culture conditions and to increase the sensitivity of culture
and laboratory diagnosis of NTM disease. Samples should
be inoculated onto at least one solid medium (Lowenstein–
Jensen or Middlebrook 7H10 and 7H11) and into a liquid
culture system (BACTEC 460, MGIT, MB9000, MB BacT,
ESP). The latter systems permit more rapid culture and
isolation of a greater range of species than the use of solid
media alone, but solid culture permits quantification of
the isolated Mycobacterium.29,30 The optimal temperature
for most cultures for NTM is between 28°C and 37°C.23
All skin specimens should be cultured at 28°C–30°C and
at 35°C–37°C, both are essential for optimal recovery.31
Many NTM grow within 2–3 weeks on subculture, but
M. ulcerans or Mycobacterium genavense cultures should
be incubated for at least 8–12 weeks. Rapidly growing
mycobacteria usually grow within 7 days of subculture.32
When NTM infection is suspected, it is important to inform
the microbiologist accordingly.
As far as treatment is concerned, there is no firmly established
standardized treatment regimen.33 Treatment is usually
guided by the drug sensitivity report. If there is no growth on
culture but diagnosis of NTM is suspected based on clinical
history and histopathology findings (as in cases A2 and B2),
treatment has to be started on the basis of the susceptibility
results published in the literature.31 Agents which can be used
for treating NTM infections are macrolides (clarithromycin,
azithromycin); rifampin or rifabutin; ethambutol;
doxycycline; quinolones (ciprofloxacin, moxifloxacin,
and gatifloxacin); sulfonamides; amikacin; streptomycin;
isoniazid; ethionamide; cefmetazole; and imipenem.34
The number of agents required for effective treatment
is not clear, although three drug regimens are often
adopted.4 For most NTM infections, macrolide-based
drug regimens are an effective option.4 Furthermore, the
optimal duration of therapy is unknown, although courses
of 6–12 months are generally used guided by clinical and
radiologic improvement on therapy.31 All patients have to
be monitored for possible adverse drug effects of individual
and combination antibiotic therapies.
Indian Journal of Orthopaedics | Volume 51 | Issue 2 | March‑April 2017
Gundavda, et al.: Musculoskeletal infections with NTM following inoculation in immunocompetent hosts
Conclusions
NTM are now recognized as opportunistic but true
pathogens and are an important cause of human disease.3,4,7
There has been an increasing incidence of infections caused
by NTM in recent years in both immunocompromised and
normal hosts.3 Whenever a case of chronic granulomatous
infection is encountered, that does not respond to standard
anti-tuberculous treatment, with a history of open trauma,
and surgical intervention or injection, there should be clinical
suspicion of a possible NTM infection.2,23 It is important
to have a good communication between clinicians and
microbiologists so as to optimize culture conditions. This
will increase the sensitivity of culture so that antimicrobial
susceptibility testing can be performed. In case there is no
growth on culture and still diagnosis of NTM is suspected
based on clinical history and histopathology findings (as in
cases A2 and B2), treatment has to be started on the basis
of the susceptibility results published in the literature.12,17,22
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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Indian Journal of Orthopaedics | Volume 51 | Issue 2 | March‑April 2017