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512
Brief Reports
CID 1997; 24 (March)
Extragenital Mycoplasma hominis Infection in Two Liver
Transplant Recipients
Reprints or correspondence: Dr. Ulrich Vogel, Institut ftir Hygiene and
Mikrobiologie, Universitat Wiirzburg, Josef-Schneider-Strasse 2, 97080 Wiirzburg, Germany.
Clinical Infectious Diseases 1997; 24:512-3
1997 by The University of Chicago. All rights reserved.
1058-4838/97/2403 —0034$02.00
Figure 1. CT scan demonstrates liver abscess formation (arrow)
due to Mycoplasma hominis in a 29-year-old liver transplant recipient.
M hominis as well as coagulase-negative staphylococci and
Enterococcus faecium were isolated from the swabs. Since the tuf
gene was amplified from suspicious primary colonies and since
subsequent sequence determination allowed M hominis to be identified within 24 hours, treatment with ciprofloxacin [8, 9] was
started immediately and continued for 12 days. Ciprofloxacin was
administered with vancomycin for treatment of infection due to
gram-positive cocci.
Despite initial improvement in the patient's condition, a CT
scan revealed a subcapsular mass of the sixth hepatic segment 15
days after completion of the course of ciprofloxacin therapy (figure
1). Drainage of the abscess yielded 25 mL of pus. Bacteriologic
analysis of the aspirate by initial plating on mycoplasma agar and
sequencing of the tuf gene PCR product from suspicious colonies
revealed intrahepatic M hominis abscess formation. Aerobic and
anaerobic culture of the abscess did not yield any other bacteria.
The patient was then successfully treated with combination antibiotic therapy that included clindamycin and doxycycline [10] for
18 days and by irrigation of the abscess with sodium chloride
solution for 10 days. She was discharged to her home 5 weeks
after completion of the combination therapy, and a control CT
scan was not performed.
Since there are only a few reports on extragenital M hominis
infections in liver transplant recipients, our two cases serve to
emphasize the pathogenic potential of M hominis for these patients. Bacteriological laboratories that perform tests for liver transplant recipients should include mycoplasma agar in their routine
diagnostic program to accelerate the diagnosis of M. hominis infection. Tuf gene amplification [5-7] directly from suspicious colonies followed by sequence determination of the PCR product
allows diagnosis of the species within 24 hours and provides the
diagnostic basis for rapid specific antibiotic therapy. Despite initial
therapy with ciprofloxacin, a liver abscess developed in one patient; this abscess was then successfully treated by drainage and
irrigation and with systemic antibiotic therapy (i.e., clindamycin
combined with doxycycline).
U. Vogel, E. Liineberg, E.-R. Kuse, A. L. Neulinger,
and M. Frosch
Institut fur Medizinische Mikrobiologie and Institut fur Antisthesiologie,
Medizinische Hochschule Hannover, Hannover, Germany
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Mycoplasma hominis has been recognized as an extragenital
pathogen in immunocompromised hosts, including kidney and
heart transplant recipients; patients with systemic autoimmune diseases, lymphomas, or leukemia; and patients who have undergone
cardiac surgery or who have experienced trauma [1, 2]. Liver
transplantation has rarely been reported to increase host susceptibility to intraabdominal M hominis infection [1, 3, 4].
We describe two liver transplant recipients with extragenital
M. hominis infection, and we emphasize the need for physicians to
be aware of the pathogenicity of M. hominis for this group of patients.
The isolation of M. hominis from the pleural space and the abdominal
surgical wound in the first case and from an intrahepatic abscess in
the second one indicates that M hominis infection in sites other than
the peritoneal cavity should be considered. We furthermore propose
the use of sequence determination of the tuf gene [5-7] for rapid
species diagnosis to accelerate clinical decisions.
A 48-year-old male patient underwent orthotopic liver transplantation for treatment of hepatocellular carcinoma and liver cirrhosis associated with hepatitis B virus. The patient developed
fever, pleural effusions, and signs of abdominal surgical wound
infection in the fifth week after transplantation. The results of
standard bacteriologic examination of the pleural fluid and of
wound swabs were unremarkable; after 3-4 days, translucent pinpoint colonies appeared on Columbia agar and on chocolate agar.
Subculture on supplemented mycoplasma agar (Oxoid, Basingstoke, UK) revealed colonies with the "fried-egg" appearance that
is typical for mycoplasmas after 2 days.
Before specific antibiotic therapy could be initiated, the patient
developed fulminant and fatal Klebsiella oxytoca pneumonia that
did not respond to initial treatment with piperacillin and tobramycin. The mycoplasma isolates were nonglycolytic and hydrolyzed arginine. The isolates were confirmed to be M hominis
by amplification of the gene encoding the elongation factor Tu
(tuf) and by direct sequence determination of the PCR product as
described previously [5-7].
Although the clinical relevance of the pleural and wound infection remained unclear in this patient's case, our experience
prompted us to culture relevant extragenital specimens obtained
from liver transplant recipients in mycoplasma agar (this agar was
used in addition to standard diagnostic culture media). The value
of using this agar was confirmed since 2 months later M hominis
was isolated from swab specimens from the peritoneal cavity of
a female 29-year-old drug addict who had heptitis B virus—induced
acute liver failure that had been treated by liver transplantation.
Peritonitis and fever had developed 4 weeks after transplantation
due to partial necrosis of the bile duct, which was treated surgically
by a hepatojejunostomy.
CID 1997;24 (March)
References
1. Meyer RD, Clough W. Extragenital Mycoplasma hominis infections in
adults: emphasis on immunosuppression. Clin Infect Dis 1993; 17 (Suppl
1):S243-9.
2. Madoff S, Hooper DC. Nongenitourinary infections caused by Mycoplasma hominis in adults. Rev Infect Dis 1988;10:602-13.
3. Jacobs F, Van de Stadt J, Gelin M, et al. Mycoplasma hominis infection
of perihepatic hematomas in a liver transplant recipient. Surgery 1992;
111:98-100.
4. Haller M, Forst H, Ruckdeschel G, Denecke H, Peter K. Peritonitis due to
Mycoplasma hominis and Ureaplasma urealyticum in a liver transplant
recipient [letter]. Eur J Clin Microbiol Infect Dis 1991; 10:172.
5. Ltineberg E, Jensen JS, Frosch M. Detection of Mycoplasma pneumoniae
by polymerase chain reaction and radioactive hybridization in microtiter
plates. J Clin Microbiol 1993;31:1088-94.
Active tuberculosis in patients with prior tuberculous infection
can occur after endogenous reactivation or exogenous reinfection.
Endogenous reactivation results from reactivation of viable tubercle
bacilli in dormant foci that persist after primary infection. Exogenous
reinfection results from inhalation of new bacilli, causing active disease. Since the publication of Stead's article in 1967 [1], exogenous
reinfection has not been considered a significant cause of tuberculosis
in individuals known to have had previous tuberculin reaction in the
United States and other developed countries.
However, recent reports from the United States have documented exogenous reinfection with resistant Mycobacterium tuberculosis in patients with advanced HIV infection, alcoholism, and
malnutrition [2-5]. We describe a diabetic patient with a history
of tuberculosis who is receiving treatment for multidrug-resistant
tuberculosis (MDRTB) apparently acquired through exogenous reinfection.
A 60-year-old Peruvian man was treated for pulmonary tuberculosis in 1951 with collapse therapy and intramuscular streptomycin.
He moved to New York in 1953 and has worked in our hospital's
housekeeping department since 1971. In 1974, he underwent a tine
test done at the employee health service, which was positive. Other
than adult-onset diabetes mellitus, well controlled with oral hypoglycemic agents, he had no other illnesses and took no other medications.
The patient was well until September 1994, when he developed a
persistent productive cough and lost 20 pounds over the ensuing 2
months. In November 1994 a chest radiograph revealed patchy nodular infiltrates of the right lung and left-sided pleural thickening. No
previous radiograph was available for review. He denied all risk
factors for HIV infection and tested negative for antibodies to the
virus. Multiple sputum specimens were smear positive for acid-fast
Reprints or correspondence: Dr. Glenn S. Turett, Bronx-Lebanon Hospital
Center, 8th Floor, Department of Medicine, 1650 Grand Concourse, Bronx,
New York 10457.
© 1997 by The University of Chicago. All rights reserved.
1058-4838/97/2403 — 0035$02.00
6. Berg S, Liineberg E, Frosch M. Development of an amplification and
hybridization assay for the specific and sensitive detection of Mycoplasma fermentans DNA. Mol Cell Probes 1996; 10:7-14.
7. Liineberg E, Kamla V, Hadding U, Frosch M. Sequence and expression
in Escherichia colt of a Mycoplasma hominis gene encoding elongation
factor Tu. Gene 1991; 102:123-7.
8. Haller M, Forst H, Ruckdeschel G, Pratschke E. Mycoplasma hominis in
liver transplantation [letter]. Surgery 1993; 113:359 —60.
9. Gass R, Fisher J, Badesch D, et al. Donor-to-host transmission of Mycoplasma hominis in lung allograft recipients. Clin Infect Dis 1996;22:
567-8.
10. McMahon DK, Dummer JS, Pasculle AW, Cassell G. Extragenital
Mycoplasma hominis infection in adults. Am J Med 1990;89:
275 —81.
bacilli, and cultures yielded M tuberculosis that was resistant to seven
antituberculous drugs, including all five first-line agents. Restriction
fragment length polymorphism (RFLP) analysis revealed that this
strain's pattern was identical to that of a strain responsible for many
MDRTB cases in New York City (Public Health Research Institute
Tuberculosis Center [New York City] strain W) [6].
In January 1997 the patient was completing his 24th month of
directly observed therapy, which consisted of daily oral ofloxacin,
cycloserine, p-aminosalicylic acid, and pyridoxine; intramuscular
capreomycin was included in this regimen during the first 6
months. His compliance with this regimen has exceeded 90%.
After he started receiving this therapy, his sputum smears and
cultures converted to negative within 2 months, and he had an
excellent clinical and radiographic response.
The findings in this case illustrate probable exogenous reinfection of a diabetic man with MDRTB. Despite lack of culture confirmation of our patient's original episode of tuberculosis, much
evidence supports prior infection, including his description of a
clinical picture consistent with tuberculosis, previous surgical and
medical treatment for tuberculosis, and a positive tine test in 1974.
In 1994 he had culture-confirmed tuberculosis, probably caused
by a strain of M. tuberculosis different from that which caused his
initial infection. His job involved cleaning respiratory isolation
rooms of patients with suspected and known tuberculosis, including some patients with MDRTB whose isolates had a strain W
pattern. Strain W, which apparently dates back to the 1980s, has
been recovered primarily in New York City and has caused many
cases of MDRTB, including nosocomial outbreaks [6]. This strain
first appeared at our institution in November 1992. The RFLP
pattern of the isolate from the patient described herein matched
the pattern of isolates from other patients seen at our hospital.
This case, as well as those previously reported [2-5], demonstrates
that prior tuberculous infection or disease does not provide all patients
with adequate protective immunity to reinfection with a different
strain of M. tuberculosis. These patients were all in groups considered
to be at high risk of developing active disease after tuberculous
infection [7]. The factors that make such patients more likely to
develop disease when they are infected may also put them at greater
risk of reinfection when exposed again to M tuberculosis.
Exogenous reinfection is believed to be a significant cause
of tuberculosis in developing countries and other areas where
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Exogenous Reinfection with Multidrug-Resistant
Mycobacterium tuberculosis
Clinical Infectious Diseases 1997; 24:513-4
513
Brief Reports