Previous Article | Next Article 
Journal of Clinical Microbiology, March 1998, p. 850-851, Vol. 36, No. 3
0095-1137/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
LETTERS TO THE EDITOR
Unexpected High Prevalence of Secondary Bacterial Infection in
Patients with Mycetoma
 |
LETTER |
Mycetoma is a chronic granulomatous infection of the subcutaneous
tissue caused by true fungi or higher bacteria; hence, it is classified
as eumycetoma or actinomycetoma, respectively (5). Mycetoma
is endemic in (sub)tropical areas, and the Sudan seems to be the
mycetoma homeland, with hundreds of new patients attending specialized
clinics each year. Mycetoma pathogens such as the fungus
Madurella mycetomatis can be found in certain types of soil
or as colonizers of plants and show widespread environmental distribution. Infection may be initiated once fungal material is
inoculated into the subcutaneous tissues through minor trauma (7). M. mycetomatis is the main cause of
eumycetoma, being responsible for approximately 70% of all mycetoma
cases in Sudan (2, 6). Mycetoma usually presents as a slowly
progressing subcutaneous nodule which increases in size. Multiple
secondary nodules may evolve as well. The nodules may suppurate, and
characteristic (black) grains as well as purulent material may be
discharged through multiple sinus tracts (Fig. 1 and reference
2). Mycetoma is usually painless (4), but
in some cases, patients seek medical advice because of persisting pain.
The pain may be produced by bone invasion or it may be due to secondary
bacterial infection (SBI) (3). The latter is diagnosed upon
bacterial cultures positive for potentially pathogenic species other
than the microorganisms causing the mycetoma and obtained from deep
within the sinus tracts. Little is known about the incidence of SBI in
mycetoma, the organisms involved, and its potential contribution to
morbidity.
We, therefore, prospectively studied SBIs in mycetoma patients in the
Sudan. Specimens were collected from 98 consecutive patients attending
the Mycetoma Research Centre, Soba University Hospital, University of
Khartoum, Sudan. The mean age of the patients was 23 years (range, 15 to 70 years), and 77 males and 21 females were included, of whom 89 had
eumycetoma and 9 had actinomycetoma. Feet and legs were the limbs most
frequently involved (97%). All patients were receiving treatment,
which in our clinic consists of ketoconazole for eumycetoma and a
combination of streptomycin and dapsone for actinomycetoma, both prior
to eventual surgery. Most of the patients (78 [80%]) were in the
active stage of the disease.
For isolation of bacteria involved in SBI, sterile cotton swabs were
inserted deeply into the sinus tracts. In patients with closed,
inactive fistulae, clinical material was obtained by percutaneous fluid
aspiration from the lesion. In some cases, sinuses were opened with a
sterile hypodermic needle prior to deep insertion of a cotton swab. All
swabs were inoculated directly onto 5% blood agar, MacConkey agar, and
mannitol salt agar plates, which were incubated aerobically at 37°C
for 24 h. It appeared that 62 patients (63%) had SBI caused by
one or more of the following potentially pathogenic microorganisms: 39 (56%) isolates were Staphylococcus aureus, 24 isolates
(34%) were Streptococcus pyogenes, and 7 isolates (10%)
were Proteus mirabilis. All S. aureus strains
were sensitive to amoxicillin-clavulanic acid combination (Augmentin)
and resistant to penicillin, whereas all S. pyogenes
isolates were sensitive to both antibiotics. Some of the P. mirabilis strains were multidrug resistant, which included some
aminoglycosides and broad-spectrum cephalosporins. Overall, SBI was
identified in 59 of 89 of all patients suffering from eumycetoma versus
3 of 9 of the patients with actinomycetoma (P = 0.06).
It was also established that patients with closed inactive sinuses are
less likely than patients with open sinuses to have SBI in their
lesions (P < 0.05).

View larger version (134K):
[in this window]
[in a new window]
|
FIG. 1.
Mycetoma lesions on the sole of a foot. The picture
clearly shows the severity of the lesions, which rendered the patient
invalid. Closed as well as open sinuses are visible. Note the shedding
of purulent material and the characteristic black grains consisting of
fungus from the open sinuses.
|
|
Our findings indicate that most of the patients with mycetoma,
especially those with eumycetoma, are susceptible to SBI in their
lesions. These results contradict the previous impression that the
sinuses' discharge is usually sterile due to antibiotics produced by
the fungi (1). Upon testing the M. mycetomatis strains for antibiotic production, no such inhibitory compounds to
which standard clinically relevant bacterial species were susceptible were detected (data not shown). S. aureus appeared to be the
most-common pathogen in this type of infection. Although the number of
patients with actinomycetoma included in the present study is small,
SBI might be less common in this group because these patients receive streptomycin as part of antimicrobial therapy.
In conclusion, a high prevalence of secondary bacterial infection has
been found in lesions of patients suffering from various types of
mycetoma. SBI appears to be a serious problem in mycetoma. It may cause
pain and increased disability. Moreover, some superinfected patients
develop concomitant bacteremia or septicemia which incidentally results
in death (7). The clinical significance of our present findings with respect to patient management needs to be assessed in
future case control studies.
 |
REFERENCES |
| 1.
|
Fahal, A. H., and A. M. El Hassan.
1992.
Mycetoma.
Br. J. Surg.
79:1138-1141[Medline].
|
| 2.
|
Fahal, A. H., and S. H. Suliman.
1994.
Clinical presentation of mycetoma.
Sudan Med. J.
32:46-66.
|
| 3.
|
Fahal, A. H.,
A. R. Sharfi,
A. M. El Hassan, and E. S. Mahgoub.
1996.
Internal fistula formation: an unusual complication of mycetoma.
Trans. R. Soc. Trop. Med. Hyg.
90:550-552[Medline].
|
| 4.
|
Fahal, A. H.,
E. A. El Toum,
S. A. Gumaa,
E. S. Mahgoub, and A. M. El Hassan.
1994.
A preliminary study on the ultrastructure of Actinomadura pelletieri and its host tissue reaction.
J. Med. Vet. Mycol.
32:343-348[Medline].
|
| 5.
|
Fahal, A. H.,
E. A. El Toum,
S. A. Gumaa,
E. S. Mahgoub, and A. M. El Hassan.
1995.
Host tissue reaction to Madurella mycetomatis: new classification.
J. Med. Vet. Mycol.
33:15-17[Medline].
|
| 6.
|
Gumaa, S. A.
1994.
The aetiology and epidemiology of mycetoma.
Sudan Med. J.
32:14-22.
|
| 7.
|
Magana, M.
1984.
Mycetoma.
Int. J. Dermatol.
23:221-236[Medline].
|
| | | | |
Abdalla O. A. Ahmed
El Sir A. M. Abugroun
College of Medical Laboratory Sciences P.O. Box 11018
|
| | | | |
Ahmed H. Fahal
Department of Surgery P.O. Box 102
|
| | | | |
Ed E. Zijlstra
Institute of Endemic Diseases P.O. Box 102 University of Khartoum Khartoum, Sudan
|
| | | | |
Alex van Belkum
Henri A. Verbrugh
Department of Medical Microbiology and Infectious Diseases University Hospital Rotterdam Dr. Molewaterplein 40 3015 GD Rotterdam The Netherlands
|
Journal of Clinical Microbiology, March 1998, p. 850-851, Vol. 36, No. 3
0095-1137/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
This article has been cited by other articles:
-
Ahmed, A. O. A., Mukhtar, M. M., Kools-Sijmons, M., Fahal, A. H., de Hoog, S., van den Ende, B. G., Zijlstra, E. E., Verbrugh, H., Abugroun, E. S. A. M., Elhassan, A. M., van Belkum, A.
(1999). Development of a Species-Specific PCR-Restriction Fragment Length Polymorphism Analysis Procedure for Identification of Madurella mycetomatis. J. Clin. Microbiol.
37: 3175-3178
[Abstract]
[Full Text]