CASE-LETTER
Mycobacterium
kansasii: A Rare
Cause of Brain
Abscess
M
ycobacterium kansasii is a photochromogenic,
slow-growing, nontuberculous mycobacterium
that causes pulmonary disease and dissemi-
nated infection.1 It is a common nontuberculous myco-
bacterial infection, second only to Mycobacterium avium
complex, with an incidence of 2.4 cases per 100,000
adults annually in the United States, with the highest
incidence in the central and southern United States.2,3
Human immunodeficiency virus (HIV) infection is a con-
dition that increases the risk for M kansasii infection.2
The well-recognized risk factors for M kansasii infection
among HIV-negative and HIV-unknown status patients
include preexisting pulmonary disease (pneumoconiosis,
obstructive pulmonary disease), previous mycobacterial
disease, malignancy and alcoholism.2 Despite increasing
reports of extrapulmonary M. kansasii disease in both
HIV-positive and HIV-negative persons, central nervous
system disease is very rare. An extensive literature
review revealed only 4 published cases of proven
M kansasii brain abscess.4,5
A 44-year-old male with advanced HIV (CD4 count of
199 cells/mm3; CD4% of 15.4) presented with a chief
complaint of headache, fever and cough for 1 month.
The patient carried a history of HIV, diagnosed in 1989,
with a history of medication nonadherence. The patient
was recently started on a regimen of combination
antiretroviral therapy. He also had a history of shingles
1 year before presentation, as well as oral candidiasis.
The patient was in his usual state of health until 1 month
before admission, at which time he endorsed onset of
sinus congestion, sore throat, fever, chills and produc-
tive cough with occasional dizziness. He endorsed
coughing for an entire month relentlessly with produc-
tion of quarter-sized amount of yellow sputum. He
reported that his headaches were associated with his
coughing. He described his headache as pounding and
throbbing mostly in the right frontal area, and sometimes
occurring in the frontal regions bilaterally. The patient
noted occasional episodes of lightheadedness. He
denied any weight loss, night sweats, hemoptysis, chest
pain, shortness of breath or sick contacts. Upon pre-
sentation, he had a low-grade fever of 38.31C. Vital signs
were otherwise within normal limits. Cardiopulmonary
examination was unremarkable. No focal findings were
noted on an extensive neurological examination. Glas-
gow Coma Scale was 15 with normal mentation and
90
orientation. Cranial nerves were intact. No focal strength,
sensory or cerebellar abnormalities were noted. Deep
tendon reflexes were 2 of 4 symmetrically throughout.
He had a negative Babinski sign and was negative for
clonus bilaterally. Initial laboratory data revealed a white
blood cell count of 6.2
109 cells/L mm3 (reference
range: 4.5-11.0
109 cells/L mm3) with a normal differ-
ential, as well as a hemoglobin of 8.5 g/dL (reference
range: 12.0-16.0 g/dL) with an mean cell volume of 90.6.
The initial 2-view chest radiograph showed no evidence
of cardiopulmonary disease. A head computed tomog-
raphy (CT) with iodinated contrast revealed a 2.3

1.8 cm2 ring-enhancing hypodensity within the anterior,
right temporal lobe with surrounding edema (Figure).
This finding was not visualized on a noncontrast head
CT 3 months prior. These findings were confirmed and
further characterized on an magnetic resonance imaging
of the brain with gadolinium contrast (Figure). As tox-
oplasmosis was near the top of our differential diagnosis,
Toxoplasma gondii antibodies were obtained. Toxoplasma
IgM antibodies were low at 0.10 IU/mL (reference range
o0.80 IU/mL), as were the IgG antibodies at 0.0 I U/mL
(reference range o7.5 IU/mL), thus making the diagnosis of
toxoplasmosis unlikely. An 18F-fluorodeoxyglucose positron
emission tomography or low-dose CT was performed and
showed that the lesion was hypometabolic compared with
the surrounding brain parenchyma on the positron emission
tomography images, not consistent with lymphoma. Neuro-
surgery was then consulted to obtain a diagnostic brain
biopsy. Open brain biopsy revealed a brain abscess in the
temporal lobe, which was removed and cultured, while the
surrounding area was copiously irrigated. Histology of the
brain biopsy revealed benign brain tissue with reactive
gliosis and chronic inflammation, whereas the removed
mass revealed acute inflammatory cells along with histio-
cytes and lymphocytes associated with large areas of
necrosis, consistent with abscess. The initial stains were
2þ acid-fast bacilli (AFB) positive, with the cultures ulti-
mately growing M kansasii 9 days later. Owing to the
patient's respiratory complaints and despite his negative
chest radiograph, a chest CT with iodinated contrast was
obtained to further evaluate for pulmonary involvement. This
revealed axillary and mediastinal lymphadenopathy, as
well as an 8 mm right middle lobe nodule. Sputum smears
were initially negative for AFB; however, the cultures grew
M kansasii within 24 days. Axillary lymph node biopsies
were negative for mycobacterium or lymphoma. Upon
results of the AFB positive brain lesion, the patient was
initially started on rifampin, isoniazid, pyrazinamide and
ethambutol therapy pending culture results. He was
subsequently placed on isoniazid, rifabutin and ethambu-
tol þ Vitamin B6 once cultures were resulted. The patient
was continued on treatment and repeat brain magnetic
resonance imaging at 10 months and 14 months post-
treatment initiation showed continued improvement of
previous inflammatory abnormalities. Unfortunately, this
THE AMERICAN JOURNAL OF THE MEDICAL SCIENCES
VOLUME 353 NUMBER 1 January 2017

FIGURE. (A) Computed tomography of brain with intravenous contrast showing a 2.3
1.8 cm2 ring-enhancing hypodensity within the anterior
right temporal lobe with surrounding edema. (B) Magnetic resonance T2 image with gadolinium contrast showing a 2.3
1.8 cm2 ring-
enhancing lesion in the right temporal lobe with surrounding edema.
patient succumbed to a separate HIV-associated illness
nearly 15 months after his diagnoses of disseminated
M kansasii.
M kansasii's major reservoir is tap water and local
water supplies.2 The mode of transmission of M kansasii
infection is most likely via ingestion or inhalation from the
gastrointestinal or respiratory tract.2 There is no evidence
to support person-to-person transmission of M kansasii.2
Cases of M kansasii infection have been well docu-
mented in both immunocompetent and immunocompro-
mised patients. The infection typically manifests clinically
with bronchopulmonary symptoms and chest radio-
graphic findings similar to pulmonary Mycobacterium
tuberculosis infection.2 Disseminated infection can also
commonly occur and typically affect immunocompro-
mised individuals such as HIV-infected patients, solid-
organ transplant recipients, patients with hematologic
malignancy or patients on chronic steroid regimens.2
The most frequent presentation of clinical M kansasii is
that of a pulmonary infection with nearly identical symptoms
and radiographic findings to that of M tuberculosis.2 The
pulmonary symptoms of nontuberculous mycobacterium
(NTM) infection are nonspecific and typically include chronic
cough, sputum production, fever, dyspnea and malaise.2
Radiographically, NTM pulmonary disease may present
either as cavitary or nodular. Although subtle radiographic
differences may exist, none are specific enough to exclude
M tuberculosis from the differential diagnosis, and thus
isolation of M kansasii from expectorated sputum or
bronchial lavage is necessary for the diagnosis.2 When
evaluating for NTM pulmonary infections, multiple samples
should be obtained to decrease the likelihood of a false-
positive or a contaminated specimen. The American Thora-
cic Society and the Infectious Disease Society of America
recommend that the evaluation of patients with suspected
pulmonary NTM should include, at the minimum, chest
imaging, 3 or more sputum specimens for acid fast bacilli
analysis, and exclusion of other pulmonary disorders such
as M tuberculosis and lung malignancy.2
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Mycobacterium kansasii Brain Abscess
In patients with advanced HIV, the clinical presentation
of disseminated NTM if fairly nonspecific. M kansasii is the
second most prevalent disseminated NTM in HIV-infected
patients, less common only than M avium complex
(MAC).2 In contrast to MAC, most patients with dissemi-
nated M kansasii also have active pulmonary disease, and
central nervous system involvement is rarely described.6
Although pulmonary M kansasii should be diagnosed with
the methods previously described, disseminated infec-
tions should be isolated from the particular site of involve-
ment. In a study by Campo and Campo of 46 sequential
patients with M kansasii infections, 21.7% had dissemi-
nated disease. Extrapulmonary isolates were obtain from
several sources, including pleural fluid, pericardial fluid,
stool, lymph nodes, blood and bone.6 In our reported
case, confirmation of central nervous system involvement
was obtained by direct biopsy.
As there are no randomized trials of the treatment of
M kansasii, recommendations for treatment regimens
have been based on retrospective data.2 Initial reports
of treatment regimens before the use of rifampin showed
low sputum conversion rates and a high incidence of
relapsing infection. Later studies using rifampin-based
regimens reported sputum conversion rates near 100%
and a very low relapse rate, usually due to rifampin
resistant organisms.7 The currently recommended
regimen for treatment of pulmonary M kansasii includes
rifampin 600 mg per day, isoniazid 300 mg per day, and
ethambutol 15 mg/kg per day for at least 12 months
of continuously negative sputum cultures.2 There is
no surgical role in treatment of routine pulmonary
M kansasii.2 The treatment regimen for patients with
disseminated M kansasii infections is typically the same
as for those with pulmonary disease.2 The treatment
regimen for HIV-infected patients should be constructed
with an infectious disease specialist as to best avoid
interactions with antiretroviral therapy. The duration
of treatment for patients with disseminated M kansasii is
the same as the recommended duration for disseminated
91
Onor et al
MAC, and there are no recommends for prophylaxis
against M kansasii.5
M kansasii is a common NTB infection seen in the HIV
population, most commonly presenting with a broncho-
pulmonary infection similar to that of M tuberculosis.
Although it is the second most common cause of
disseminated NTB, focal brain abscess is a rare pre-
sentation. We present this case as evidence that
M kansasii should remain in the differential for an immu-
nocompromised patient with a ring-enhancing brain lesion.
IfeanyiChukwu O. Onor, PharmD
Meagan E. Piazza, PharmD
Mona F. Khashan, Pharm D
Seema Walvekar, MD
*Shane G. Guillory, MD
Department of Internal Medicine, Division of Hospital Medicine,
Louisiana State University Health Sciences Center,
New Orleans, Louisiana
*E-mail: sguil1@lsuhsc.edu
The authors have no financial or other conflicts of interest to disclose.
92
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6. Campo RE, Campo CE. Mycobacterium kansasii disease in patients
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1233–8.
7. Ahn CH, Lowell JR, Ahn SS, et al. Short-course chemotherapy for
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VOLUME 353 NUMBER 1 January 2017