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Editorial Response: Is Mycobacterium xenopi an Emerging Pathogen?
Mycobacterium xenopi is an unusual microorganism, even
among the mycobacteria referred to as opportunistic pathogens.
The original description of M xenopi [1] detailed its isolation
from an abscess under the skin (probably in the dorsal lymph
sac) of a South African toad that had been born and maintained
in a laboratory in Great Britain. This isolation was, therefore,
considered to be an example of a mycobacterial disease in a
cold-blooded animal. Extensive literature on this subject had
already been published [2], and Schwabacher [1] pointed out
that in 1889 Sibley had described subcutaneous mycobacterial
nodules in a snake who had died in captivity.
Despite the fact that M xenopi caused infection in a coldblooded animal, the optimum temperature for the growth of
this organism is 43°C, thus making it a thermophile. Although
it was not stated in the original or subsequent reports, the toad
probably was being used for pregnancy tests and had been
injected with human urine. The usual cause of cold-blooded
mycobacteriosis is Mycobacterium fortuitum or other rapidly
growing mycobacteria that grow well at room or lower temperatures.
See the article by Jiva et al. on pages 226-32.
M xenopi is also one of the two mycobacterial species that
may be found in tap water or water contained in pipes or tanks
that is to be used for drinking or washing. The other species
is Mycobacterium kansasii [3].
M xenopi is not difficult to identify in the laboratory. Acidfast staining of growing colonies reveals long, slender, tapering,
and palisading cells that present in an interwoven pattern. Colonies on corn meal agar have prominent filaments protruding
from the main growth [4]. Sophisticated molecular techniques,
although helpful, are not necessary for the identification of this
organism.
In this issue of Clinical Infectious Diseases, Jiva et al. [5]
investigated M xenopi on the basis of a retrospective review
of the microbiology laboratory records from a group of hospitals and at least one tuberculosis clinic in the city of Rochester,
New York. During a 3-year period, specimens containing the
organism were obtained from 103 persons. In only 10% of
these individuals was M. xenopi considered to be a pathogen.
Positive samples were almost always sputum or other respiratory tract specimens; the organism was isolated from extrapul-
Received 7 October 1996.
Reprints or correspondence: Dr. Emanuel Wolinsky, Division of Infectious
Diseases, Department of Medicine, 2500 MetroHealth Medical Center, Cleveland, Ohio 44109-1998.
Clinical Infectious Diseases 1997; 24:233-4
0 1997 by The University of Chicago. All rights reserved.
1058-4838/97/2402 —0023$02.00
monary sites in only nine individuals. Five of the 10 individuals
with M xenopi disease were HIV-negative, older than 50 years
of age, and white and had chronic obstructive pulmonary disease. PPD skin tests were not helpful in distinguishing disease
from colonization in these five infected patients and in the
colonized patients.
The other five patients with M xenopi disease were young
HIV-infected men; two had pulmonary disease, and three had
disseminated disease. Of the 43 HIV-positive patients who
were colonized with M xenopi, 41 had AIDS, and seven had
disseminated Mycobacterium avium complex infection. The
PPD skin tests again were not helpful in distinguishing disease
from colonization. Cultures of stool specimens from three colonized patients yielded M xenopi.
The study by Jiva et al. illustrates many of the important
aspects of M xenopi disease. It is usually an indolent pulmonary infection involving cavity formation in adults with wellestablished chronic obstructive pulmonary disease who have
apparently normal immune functions. It is not readily distinguishable from M avium complex disease or any other mycobacterial infection by clinical or radiological means. M xenopi
disease also may be seen in young immunocompromised patients who have opportunistic infections that are usually localized to the lungs but are occasionally disseminated. Disseminated M xenopi disease may occur in HIV-infected patients,
but the frequency of this disease is much less than that of
M avium complex or M kansasii infection.
The frequency of M. xenopi in the respiratory tracts of HIVpositive patients may be high because they are more likely to
be hospitalized and their specimens are sent more often for
culture; therefore, there is a better chance for contamination in
the laboratory and for nosocomial acquisition from potable
water contaminated with M xenopi.
There is no doubt about the danger of nosocomial acquisition
of M xenopi infection; several reports have been published
since Lelieur's doctoral thesis in 1968, which was later published in full in 1970 [6], and probably many other smaller
outbreaks have gone unreported. Lelieur described an outbreak
of M xenopi infection in a hospital in Le Havre, France, in
his thesis. The organism was isolated from 345 patients from
1960 through 1967; —10% of these patients were considered
to have disease associated with M xenopi.
An important risk factor for M xenopi infection was repeated
admission to the pulmonary department, although M xenopi
was not isolated from the hospital environment. One of the
largest and most persistent outbreaks of M xenopi disease
occurred on the pulmonary service at the Veterans Administration hospital in West Haven, Connecticut [7]; cultures of one
or more specimens from >600 patients yielded M xenopi.
However, pulmonary disease due to the organism was diagnosed for only 19 patients. Extensive and prolonged contamination of the hot water supply was documented.
234
Wolinsky
These [6, 7] and other studies have demonstrated that hot
water storage tanks may be contaminated and that a culture of
a specimen from a faucet yielding hot water is more likely to
be positive than a culture of a specimen from a faucet yielding
cold water. These findings are in keeping with the thermophilic
nature of M xenopi.
I agree with the authors of these studies that the most likely
pathway of M xenopi infection involves aerosols of contaminated potable water that are inhaled during showering by individuals who have well-established chronic lung disease. The
mechanism by which piped water becomes contaminated is not
known, because M xenopi is very rarely recovered from natural
waters or soil. The early British and French researchers who
investigated M xenopi speculated that the natural hosts were
seabirds since the organism was found mainly in coastal areas
of England and Europe and since it was thermophilic. However,
further studies produced no direct evidence for this speculation,
and I believe that it has been abandoned.
Rochester now must be added to West Haven in the United
States, Toronto and Ontario in Canada, London and the southeast coast of England, and the northwest coast of Europe as
places where M xenopi contamination of potable water is likely
to occur. Does that mean that water taps and holding tanks in
all hospitals should be examined carefully for mycobacteria?
I do not believe that this is necessary, unless there is an unusual
prevalence of M. xenopi isolations from patient specimens. Is
M xenopi an emerging pathogen? I think that it is not, but
only time will tell.
Cases of disseminated M xenopi disease in patients with
AIDS have been rare and are not increasing in number. Unlike
Mycobacterium genavense (a recently recognized species of
mycobacteria that is now commonly reported as producing
disseminated disease in patients with AIDS), M xenopi is easily
grown in culture and is easily recognized. In various reports
from several countries, 10%-40% of M xenopi isolates (usually from respiratory secretions) were indicators of significant
CID 1997;24 (February)
disease. In addition, about one dozen cases of skeletal (commonly the spine) infection due to M xenopi have been reported
[8]. In at least two cases, infection of the spine was traced
directly to contaminated hospital water [9].
The warning to clinicians and laboratorians not to discard
an isolate of M xenopi as a contaminant is a good one to
remember. It applies equally as well to any mycobacterial species cultured from human specimens, no matter how benign it
looks on paper.
Emanuel Wolinsky
Division of Infectious Diseases, Department of Medicine, MetroHealth
Medical Center, Cleveland, Ohio
References
1. Schwabacher H. A strain of mycobacterium isolated from skin lesions of
a cold-blooded animal, Xenopus laevis, and its relation to atypical acidfast bacilli occurring in man. J Hyg (Lond) 1959; 57:57-67.
2. Thoen CO, Schliesser TA. Mycobacterial infections in cold-blooded animals. In: Kubica GP, Wayne LG, eds. The mycobacteria, a source book.
New York: Marcel-Dekker, 1984:1297-311.
3. Collins CH, Grange JM, Yates MD. Mycobacteria in water. J Appl Bacteriol
1984; 57:193 —211.
4. Runyon EH. Serial hyphae of Mycobacterium xenopi. J Bacteriol 1968; 95:
734-5.
5. Jiva TM, Jacoby HM, Weymouth LA, Kaminski DA, Portmore AC. Mycobacterium xenopi: innocent bystander or emerging pathogen? Clin Infect
Dis 1997; 24:226 —32.
6. Desbordes-Lize J, Fouye G, Lelieur GM. Contribution a l'etude de Mycobacterium xenopi, a l'occasion d'une importante endemie hospitaliere.
Poumon Coeur 1970; 26:1141 —82.
7. Costrini AM, Mahler DA, Gross WM, Hawkins JE, Yesner R, D'Esopo
ND. Clinical and roentgenographic features of nosocomial pulmonary
disease due to Mycobacterium xenopi. Am Rev Respir Dis 1981; 123:
104-9.
8. Miller WC, Perkins MD, Richardson WJ, Sexton DJ. Pott's disease caused
by Mycobacterium xenopi: case report and review. Clin Infect Dis 1994;
19:1024-8.
9. Froideveaux D, Claudepierre P, Brugieres P, Larget-Piet B, Chevalier X.
Iatrogenically induced spondylodiskitis due to Mycobacterium xenopi in
an immunocompetent patient [letter]. Clin Infect Dis 1996; 22:723 —4.