Case Report

Bartholins abscess caused by hypermucoviscous

Klebsiella pneumoniae
Benjamin A. Pinsky,
1
Ellen J. Baron,
1,2
J. Michael Janda
3
and Niaz Banaei
1,2
Correspondence
Benjamin A. Pinsky
[email protected]
1
Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA
2
Clinical Microbiology Laboratory, Stanford Hospital and Clinics, Palo Alto, CA 94304, USA
3
Microbial Diseases Laboratory, California Department of Public Health, Richmond, CA 94804,
USA
Received 19 September 2008
Accepted 11 January 2009
Klebsiella pneumoniae serogroups displaying the hypermucoviscosity phenotype are associated
with a distinct clinical syndrome characterized by liver abscesses, bacteraemia and metastatic
lesions. We describe here what we believe to be the first reported case of hypermucoviscous K.
pneumoniae causing a superficial Bartholins abscess in the absence of systemic involvement.
Case report
In April 2008, an otherwise healthy 36-year-old Asian
American woman presented to her gynaecologist with a
3-day history of vulvar swelling. She reported a similar
episode in 2002 that resolved with antibiotic treatment.
Her medical and surgical history was otherwise unremark-
able. The patient was born in Vietnam and emigrated to
the United States as a child but denied any recent travel to
Asia.
On physical exam, she had a firm, left-sided Bartholins
abscess and no other abnormal findings. At this initial visit,
she was prescribed a 7-day course of ciprofloxacin, 500 mg
per day, and was scheduled to return to the clinic for
incision and drainage 2 days later. At that time, a swab of
the abscess material was sent for routine bacteriological
work up. The patients abscess healed well following the
drainage procedure and completion of the course of
ciprofloxacin. On follow-up, she had no signs or symptoms
of local or disseminated recurrence of infection.
Culture of the abscess material on blood agar revealed
numerous large, dull-grey, hypermucoid colonies positive
for the string test (Fig. 1). Growth on MacConkey agar
indicated lactose fermentation. Identification and anti-
biotic susceptibility testing by microdilution performed on
the MicroScan Walkaway (Siemens, Dade-Behring) iden-
tified Klebsiella pneumoniae resistant to ampicillin and
susceptible to cefazolin, pipericillin/tazobactam, gentami-
cin, ciprofloxacin, trimethoprimsulfamethoxazole and
levofloxacin. Serological testing revealed that the isolate
had the K2 capsule type, and PCR evaluation indicated that
the strain carried the plasmid-encoded regulator of mucoid
phenotype A (rmpA) gene. Consistent with the serogroup-
ing results, the mucoviscosity-associated gene A (magA), a
marker of the K1 serotype, was not present. The causative
agent of this Bartholins gland abscess was therefore K.
pneumoniae expressing the K2 capsular serotype and the
hypermucoviscosity phenotype.
Discussion
Hypermucoviscous K. pneumoniae is a virulent Klebsiella
subtype that was first recognized in Taiwan and is now an
emerging cause of community-acquired invasive infections
worldwide (Fang et al., 2004; McIver & Janda, 2008;
Nadasy et al., 2007; Wang et al., 1998). In particular, this
organism is associated with pyogenic liver abscesses in both
immunocompetent and diabetic patients often without
apparent underlying hepatobiliary disease (Lee et al., 2006).
This invasive syndrome can result in numerous metastatic
complications, including endophthalmitis, suppurative
meningitis and pleural empyema (Chen et al., 2004; Lee
et al., 2006; Liu et al., 1986; Wiskur et al., 2008; Yang et al.,
2007). We present here a case of Bartholins gland abscess
with hypermucoviscous K. pneumoniae. While commun-
ity-acquired extra-hepatic abscess with hypermucoviscous
K. pneumoniae has been described (Ku et al., 2008), to our
knowledge, this is the first reported case of an isolated,
superficial infection with this organism.
Bartholins glands are located bilaterally at the posterior
introitus and provide lubrication for the vaginal vestibule.
It is estimated that 2 % of all women will develop a
Bartholins duct cyst or gland abscess in their lifetime,
making the diagnosis and treatment of this infection a
relatively common occurrence in gynaecological practice
(Omole et al., 2003). In a recent study of the microbiota of
Bartholins gland abscess in Asia, Klebsiella species
accounted for only a small fraction of cases (7/224,
~3 %) and the presence of hypermucoviscosity was not
noted (Tanaka et al., 2005). As the klebsiellae are members
of the Enterobacteriaceae, it is probable that this patients
Journal of Medical Microbiology (2009), 58, 671673 DOI 10.1099/jmm.0.006734-0
006734 Printed in Great Britain 671
infection arose from faecal contamination. Given her
history of a previous incidence of the same syndrome, we
hypothesize that the patient and/or her sexual partner
carried this organism in their gastrointestinal tract.
The majority of invasive infections with hypermucoviscous
K. pneumoniae have been reported in Asia and in Asian
patients living abroad (Kawai, 2006). Consistent with this,
our patient was Vietnamese. While these observations
suggest that Asian ancestry may be an important risk factor
for both invasive and superficial disease, the basis for this
apparent ethnic specificity remains unknown. Host genetic
susceptibility, limited geographical distribution of hyper-
mucoviscous subtypes, or contamination of unique dietary
elements may all play a role in the epidemiology of this
infection.
The hypermucoviscosity phenotype is thought to contrib-
ute to invasive virulence by impairing phagocytosis and
enhancing resistance to serum killing (Fang et al., 2004).
The underlying molecular mechanism involves multiple
factors, including the antigenicity of the capsule itself, in
particular the K1 and K2 serotypes (Chuang et al., 2006;
Fang et al., 2004; Struve et al., 2005; Yeh et al., 2006, 2007),
as well as the expression of the rmpA gene, whose protein
product positively regulates extra-capsular polysaccharide
synthesis (Nassif et al., 1989; Yu et al., 2006, 2008).
Although the K. pneumoniae strain isolated in our case
expressed the K2 capsule and carried the plasmid-borne
rmpA gene, the patient showed no signs or symptoms of
systemic illness. It may be that this isolate lacks additional
virulence factors important for invasive disease (Yu et al.,
2008). Alternatively, it is possible that the Bartholins gland
represented the primary focal abscess and only rapid
identification and treatment prevented this infection from
further spread.
It is our hope that this case report heightens awareness of
hypermucoviscous K. pneumoniae as a cause of superficial
infection. While this patient did not progress to invasive
disease, identification of this organism from an isolated site
should suggest the potential for spread and prompt a
thorough clinical evaluation for systemic involvement.
Acknowledgements
We thank Dr Mary Margaret ONeill for generously providing patient
information.
References
Chen, Y. J., Kuo, H. K., Wu, P. C., Kuo, M. L., Tsai, H. H., Liu, C. C. &
Chen, C. H. (2004). A 10-year comparison of endogenous
endophthalmitis outcomes: an East Asian experience with Klebsiella
pneumoniae infection. Retina 24, 383390.
Chuang, Y. P., Fang, C. T., Lai, S. Y., Chang, S. C. & Wang, J. T. (2006).
Genetic determinants of capsular serotype K1 of Klebsiella pneumo-
niae causing primary pyogenic liver abscess. J Infect Dis 193, 645654.
Fang, C. T., Chuang, Y. P., Shun, C. T., Chang, S. C. & Wang, J. T.
(2004). A novel virulence gene in Klebsiella pneumoniae strains
causing primary liver abscess and septic metastatic complications. J
Exp Med 199, 697705.
Kawai, T. (2006). Hypermucoviscosity: an extremely sticky phenotype
of Klebsiella pneumoniae associated with emerging destructive tissue
abscess syndrome. Clin Infect Dis 42, 13591361.
Ku, Y. H., Chuang, Y. C. & Yu, W. L. (2008). Clinical spectrum and
molecular characteristics of Klebsiella pneumoniae causing commun-
ity-acquired extrahepatic abscess. J Microbiol Immunol Infect 41, 311
317.
Lee, H. C., Chuang, Y. C., Yu, W. L., Lee, N. Y., Chang, C. M., Ko, N. Y.,
Wang, L. R. & Ko, W. C. (2006). Clinical implications of
hypermucoviscosity phenotype in Klebsiella pneumoniae isolates:
association with invasive syndrome in patients with community-
acquired bacteraemia. J Intern Med 259, 606614.
Liu, Y. C., Cheng, D. L. & Lin, C. L. (1986). Klebsiella pneumoniae liver
abscess associated with septic endophthalmitis. Arch Intern Med 146,
19131916.
McIver, C. J. & Janda, J. M. (2008). Pathogenesis and laboratory
identification of emerging hepatovirulent Klebsiella pneumoniae. Clin
Microbiol Newsl 30, 127131.
Nadasy, K. A., Domiati-Saad, R. & Tribble, M. A. (2007). Invasive
Klebsiella pneumoniae syndrome in North America. Clin Infect Dis 45,
e25e28.
Nassif, X., Fournier, J. M., Arondel, J. & Sansonetti, P. J. (1989).
Mucoid phenotype of Klebsiella pneumoniae is a plasmid-encoded
virulence factor. Infect Immun 57, 546552.
Omole, F., Simmons, B. J. & Hacker, Y. (2003). Management of
Bartholins duct cyst and gland abscess. Am Fam Physician 68, 135
140.
Struve, C., Bojer, M., Nielsen, E. M., Hansen, D. S. & Krogfelt, K. A.
(2005). Investigation of the putative virulence gene magA in a
worldwide collection of 495 Klebsiella isolates: magA is restricted to
the gene cluster of Klebsiella pneumoniae capsule serotype K1. J Med
Microbiol 54, 11111113.
Tanaka, K., Mikamo, H., Ninomiya, M., Tamaya, T., Izumi, K., Ito, K.,
Yamaoka, K. & Watanabe, K. (2005). Microbiology of Bartholins
gland abscess in Japan. J Clin Microbiol 43, 42584261.
Fig. 1. The patients K. pneumoniae isolate was string test
positive (.5 mm string length).
B. A. Pinsky and others
672 Journal of Medical Microbiology 58
Wang, J. H., Liu, Y. C., Lee, S. S., Yen, M. Y., Chen, Y. S., Wang, J. H.,
Wann, S. R. & Lin, H. H. (1998). Primary liver abscess due to Klebsiella
pneumoniae in Taiwan. Clin Infect Dis 26, 14341438.
Wiskur, B. J., Hunt, J. J. & Callegan, M. C. (2008). Hypermucoviscosity
as a virulence factor in experimental Klebsiella pneumoniae
endophthalmitis. Invest Ophthalmol Vis Sci 49, 49314938.
Yang, C. S., Tsai, H. Y., Sung, C. S., Lin, K. H., Lee, F. L. & Hsu, W. M.
(2007). Endogenous Klebsiella endophthalmitis associated with
pyogenic liver abscess. Ophthalmology 114, 876880.
Yeh, K. M., Chang, F. Y., Fung, C. P., Lin, J. C. & Siu, L. K. (2006).
magA is not a specific virulence gene for Klebsiella pneumoniae strains
causing liver abscess but is part of the capsular polysaccharide gene
cluster of K. pneumoniae serotype K1. J Med Microbiol 55, 803804.
Yeh, K. M., Kurup, A., Siu, L. K., Koh, Y. L., Fung, C. P., Lin, J. C., Chen,
T. L., Chang, F. Y. & Koh, T. H. (2007). Capsular serotype K1 or K2,
rather than magA and rmpA, is a major virulence determinant for
Klebsiella pneumoniae liver abscess in Singapore and Taiwan. J Clin
Microbiol 45, 466471.
Yu, W. L., Ko, W. C., Cheng, K. C., Lee, H. C., Ke, D. S., Lee, C. C.,
Fung, C. P. & Chuang, Y. C. (2006). Association between rmpA and
magA genes and clinical syndromes caused by Klebsiella pneumoniae
in Taiwan. Clin Infect Dis 42, 13511358.
Yu, W. L., Ko, W. C., Cheng, K. C., Lee, C. C., Lai, C. C. & Chuang, Y. C.
(2008). Comparison of prevalence of virulence factors for Klebsiella
pneumoniae liver abscesses between isolates with capsular K1/K2 and
non-K1/K2 serotypes. Diagn Microbiol Infect Dis 62, 16.
Superficial hypermucoviscous K. pneumoniae
http://jmm.sgmjournals.org 673