1152

Mycobacterium genavense Infection Presenting as a Solitary Brain Mass in a
Patient with AIDS: Case Report and Review
Stephen M. Berman, Ronald C. Kim, Dennis Haghighat,
Maury E. Mulligan, Joshua Fierer, and Frederic C. Wyle

Departments of Medicine and Pathology. Veterans Affairs Medical
Center, Long Beach; University of California, Irvine; and Veterans
Affairs Medical Center. La Jolla, California

Patients with AIDS develop numerous opportunistic infections and are particularly prone to infections caused by
Mycobacterium tuberculosis and by organisms belonging to
the Mycobacterium avium complex (MAC). Most MAC infections are disseminated, and the patients usually present
with chronic fevers and weight loss and often with anemia
[1]. Recently there have been several reports ofdisseminated
infection due to Mycobacterium genavense. a new member of
the genus Mycobacterium [2-5]. All of the patients described
in these reports presented with signs and symptoms similar to
those seen in patients with disseminated MAC infection [1].
We describe a patient with AIDS who presented after having
a seizure; he was found to have a cerebral mass lesion that
was caused by infection with M. genavense. We believe that
this is the first patient with infection due to this organism to
present in such a fashion.

Case Report
On 30 November 1992 a 50-year-old male homosexual
was admitted to the Long Beach Veterans Affairs Medical
Center after having a grand mal seizure. He had tested positive for infection with the human immunodeficiency virus
(HIV) in May 1992. At that time his CD4 lymphocyte count
was 84/mm 3 . He was treated with zidovudine, trimethoprimsulfamethoxazole (three times per week), and fluconazole
for oral candidiasis. Questioning of the patient revealed that
he had had two episodes of right arm tremor within the previous month, right arm paresthesias and weakness for 2

Received I February 1994; revised 26 April 1994.
Reprints or correspondence: Dr. Stephen M. Berman, 590 I East Seventh
Street, 111-10. Long Beach. California 90822.
Clinical Infectious Diseases 1994;19:1152-4
© 1994 by The University of Chicago. All rights reserved.
1058-4838/94/1906-0026$02.00

weeks, and memory impairment and confusion over the
month preceding admission.
Physical examination was remarkable for multiple lesions
of molluscum contagiosum and several lesions of Kaposi's
sarcoma on both lower extremities. Slight weakness of the
right side, a mild sensory deficit in the right upper extremity,
and slightly slurred speech were noted. A computed tomographic scan (without contrast medium) of the patient's head
showed a large area of cerebral edema with mild mass effect
in the upper left parietal lobe. Enzyme immunoassay revealed serum IgG (218 IU/L) to Toxoplasma. He was empirically treated with pyrimethamine and sulfadiazine for possible toxoplasmosis of the CNS despite the fact that the
radiological findings were atypical for this infection.
Seven days later he had another grand mal seizure. Magnetic resonance imaging (MRI) showed a solid, enhancing,
peripheral left parietal mass (2 em wide X 1.3 ern thick) that
abutted onto the dura; there was slight meningeal enhancement and an 8-cm area of surrounding edema (figure 1). The
patient was given dexamethasone to reduce the edema and
underwent a stereotactic CT-guided needle biopsy of the
mass. Histopathological examination of the biopsy specimen
showed a scattered, sometimes perivascular lymphohistiocytic inflammatory infiltrate in the cerebral cortex and white
matter, but there was no evidence ofgranulomata or multinucleated giant cells. Ziehl-Neelsen staining ofthe biopsy specimen revealed clusters of acid-fast bacilli (AFB). Therapy
with isoniazid, rifampin, pyrazinamide, clarithromycin, and
ciprofloxacin was initiated to treat infection due to M. tuberculosis and M. avium. Eventually culture of the biopsy specimen yielded M. genavense. Therapy was changed to that with
clarithromycin, ciprofloxacin, and ethambutol. The dosage
ofdexamethasone was slowly tapered over a l2-week period.
Repeated MRI performed 6 months after the diagnosis
was made showed a marked decrease in the size of the mass
and decreased edema. The patient did well clinically while

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Patients with AIDS are prone to developing infections with opportunistic pathogens. Recently, a
new mycobacterium, Mycobacterium genavense, has been found to cause infection in patients
with AIDS. Previously published reports indicate that patients who are infected with this organism present with the same clinical features as do patients with disseminated infection due to
organisms of the Mycobacterium avium complex. We describe an unusual case of a patient with
AIDS who presented with grand mal seizures and a mass lesion in his brain, which was found to
be caused by infection with M. genavense. No evidence of disseminated infection could be found
in this patient. We discuss the microbiology of this organism and review the literature on M.
genavense infections. Clinicians should be aware of this organism so that efforts at culture and
identification will be made.

CID 1994;19 (December)

Brain Mass Due to Mycobacterium genavense

1153

subcultured on Middlebrook 7H II agar supplemented with
2 Ilg of mycob actin J (Allied Laboratories, Fayette, MO) and
on Lowenstein-Jensen culture medium supplemented with
human blood. Colonies grew slowly and were dysgonic and
nonpigmented after 6 weeks. They were negative for niacin
production and nitrate reduction and positive for urease production, characteristics consistent with those of M. genavense
[6,7].

Discussion and Literature Review

genavense.

receiving the above-described regimen plus phenytoin (not
including dexamethasone); he did not have any seizures for
several months. MRI performed I year after he started receiving therapy showed complete resolution of the mass lesion and the edema.
We were unable to detect or isolate AFB from blood, bone
marrow, stool, or sputum, and examination of the bone
marrow did not reveal any evidence of granulomatous infection.

Microbiology
The initial fluorochrome smear of the brain biopsy specimen revealed numerous AFB. The tissue was inoculated directly into BACTEC 12B broth (Becton Dickinson, Towson,
MD) and onto Middlebrook 7H II agar. There was no
growth on the agar. Growth in the BACTEC 12B broth increased slowly for the first 2 weeks and then began to decrease; numerous AFB were apparent in the bottle at this
time. Subculture of the broth in another BACTEC-12B bottle did not produce growth. However, the organism grew
slowly in BACTEC 12B broth supplemented with 10%brainheart infusion medium (Difco, Detroit). The isolate was sent
to Dr. Erik Bottger who identified it as M. genavense on the
basis ofanalysis of the 16S rRNA [3]. The organism was also

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Figure 1. Magnetic resonance imaging scan with gadolinium
showing a solid, enhancing mass (2 em X 1.3 em) in the left parietal
area of a patient with AIDS and infection due to Mycobacterium

A fatal infection with an unidentified AFB recently occurred in a patient with AIDS [2]. The organism could not be
grown in culture, and nucleic acid analysis indicated that the
organism was not M. avium or Mvcobacterium leprae. Bottger
et al. [3] later described 18 patients with advanced HIV infection who had similar illnesses. The authors were able to
grow AFB in liquid medium only. With use of DNA amplification techniques, they determined that the organism was a
new member of the genus Mvcobacterium, and they named it
M. genavense. All 18 patients whom they described presented
with fever, diarrhea, and marked weight loss. Subsequently,
Wald et al. [4] described seven patients with AIDS who had
similar symptoms; cultures of blood from these patients
yielded M. genavense. The authors were able to culture the
organism only on Middlebrook 7H 11 agar supplemented
with mycobactin J (2 Ilg/mL); however, there was never
enough growth for standard biochemical analysis and drug
susceptibility testing.
More recently, Pechere et al. [5] reviewed the clinical features of 44 cases (including some of the cases mentioned
herein) of M. genavense infection that occurred in six countries; 74% of the patients had wasting, 50% had diarrhea, 26%
had abdominal pain, and virtually all had fevers and/or night
sweats. The estimated mortality rate was 68% at 12 months
after diagnosis. It is significant that patients who received
medication that was effective against mycobacteria (especially M. aviunis survived for markedly longer periods than
those who did not receive therapy.
M. genavense has recently been isolated and characterized
in the laboratory by use of a variety of techniques [6]. However, there are no data on the organism's antibiotic susceptibility patterns. Bottger et al. [7] believed that regimens for M.
avium infection may be effective in treating patients with M.
genavense infection because the clinical features of patients
infected with either organism are similar; our case supports
this belief because the patient responded to treatment with
agents that are frequently used to treat M. avium complex
infections [8].
To our knowledge, this is the first case of infection with M.
genavense presenting as a mass lesion in the brain with no
other signs of disseminated infection. We were unable to find

1154

Berman et al.

evidence of the organism in any other site outside the brain.
The findings in this case illustrate the value of aggressive
intervention (including biopsy of mass lesions in the eNS of
HIV-infected patients) when there is no response to antitoxoplasmal therapy. The findings also point out the difficulty
of identifying fastidious mycobacteria and selecting appropriate therapy. To increase the diagnostic yield for cases of
infection with M. genavense, consideration should be given to
inoculating all liquid cultures that are positive for AFB onto
Lowenstein-Jensen agar supplemented with human blood or
onto Middlebrook 7H II agar containing mycobactin J. Finally, further work needs to be done in the laboratory to
facilitate antibiotic susceptibility testing of this organism.

The authors thank Dr. Erik Bottger and his laboratory staff for
their assistance in definitively identifying the isolate as M. gena-

vense.

References
I. Hawkins CC, Gold JWM. Whimbey E, et al. Mycobacterium avium
complex infections in patients with the acquired immunodeficiency
syndrome. Ann Intern Med 1986; 105: 184-8.
2. Hirschel B. Chang HR. Mach N. et al. Fatal infection with a novel.
unidentified mycobacterium in a man with the acquired immunodeficiency syndrome. N Engl J Med 1990; 323: 109-13.
3. Bottger EC, Teske A. Kirschner p. et al. Disseminated "Mycobacterium
genavense" infection in patients with AIDS. Lancet 1992; 340:76-80.
4. Wald A, Coyle MB. Carlson LC, Thompson RL. Hooton TM. Infection
with a fastidious mycobacterium resembling Mycobacterium simiae in
seven patients with AIDS. Ann Intern Med 1992; 117:586-9.
5. Pechere M, Emler S, Wald A, et al. Infection with Mycobacterium genavense (MG): clinical features in 44 cases [abstract no. WS-B10-2]. In:
Program and abstracts of the 9th International Conference on AIDS
(Berlin). 1993.
6. Coyle MB, Carlson LC, Wallis CK. et al. Laboratory aspects of "Mycobacterium genavense, "a proposed species isolated from AIDS patients. J
Clin Microbiol 1992; 30:3206-12.
7. Bottger E, Hirschel B. Coyle MB. M. genavense sp. nov. Int J Syst BacterioI1993;43:841-3.
8. Chiu J, Nussbaum J. Bozzette S, et al. Treatment ofdisseminated Mycobacterium avium complex infection in AIDS with arnikacin, ethambutol, rifarnpin, and ciprofloxacin. Ann Intern Med 1990; 113:358-61.

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Acknowledgments

CID 1994; 19 (December)