Journal of Medical Sciences

: 2014  |  Volume : 34  |  Issue : 3  |  Page : 133--136

Recurrent serotype K1 Klebsiella pneumoniae liver abscess: A single or different pathogen?

Wen-Sen Lai1, Jung-Chung Lin2,  
1 Department of Otolaryngology-Head and Neck Surgery, Division of Infectious Diseases and Tropical Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan; Department of Otolaryngology-Head and Neck Surgery, Taichung Armed Forces General Hospital, Taichung, Republic of China
2 Department of Internal Medicine, Division of Infectious Diseases and Tropical Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, Republic of China

Correspondence Address:
Assoc. Prof. Jung-Chung Lin
Division of Infectious Diseases and Tropical Medicine, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, No. 325, Sec. 2, Cheng-Gong Road, Taipei 114, Taiwan
Republic of China


We report a case of an 81-year-old woman who had a history of type 2 diabetes mellitus with the presentation of a recurrent community-acquired liver abscess caused by capsular serotype K1 Klebsiella pneumoniae after a previous liver abscess had been cured. With regards to the serotype K1 K. pneumoniae strains, the molecular genome of the recurrent strain differed completely from the strain that had caused the primary community-acquired liver abscess even though the antibiogram was the same. This case attempts to highlight that capsular serotype K1 could be an important factor influencing liver abscess formation and its subsequent recurrence.

How to cite this article:
Lai WS, Lin JC. Recurrent serotype K1 Klebsiella pneumoniae liver abscess: A single or different pathogen?.J Med Sci 2014;34:133-136

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Lai WS, Lin JC. Recurrent serotype K1 Klebsiella pneumoniae liver abscess: A single or different pathogen?. J Med Sci [serial online] 2014 [cited 2021 Mar 1 ];34:133-136
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Full Text


The epidemiology, management, and mortality in patients with pyogenic liver abscess, a potentially life-threatening intra-abdominal infection, have changed dramatically over the last two decades. In the past, Escherichia coli was the predominant causative agent. However, recent reports indicate that the incidence of Klebsiella pneumoniae has surpassed that of E. coli in Asia and western countries. The early use of broad-spectrum antibiotics plus drainage is the gold standard to control morbidity and mortality. [1],[2],[3],[4]

A recurrent K. pneumoniae liver abscess (KLA) has seldom been reported, [5],[6] and a recurrent liver abscess with the same pathogen, but different molecular pattern even less so. Herein, we describe a case of a liver abscess caused first by K. pneumoniae, and then unusually a recurrent liver abscess 4 months later caused again by K. pneumonia in which the strain shared the same capsular serotype and antibiogram with the first K. pneumoniae strain.

 Case Report

An 81-year-old woman presented with a history of type 2 diabetes mellitus and hypertension, which had been controlled by regular oral medications for >10 years. Her first admission to our department was on May 30, 2010, because of poor appetite and general malaise for 1-week. At the emergency department, laboratory examinations showed leukocytosis and elevated C-reactive protein. Accordingly, abdominal ultrasonography was performed, which disclosed multiple hypoechoic lesions over the inferior portion of the lateral segment (S3), medial segment of the left hepatic lobe (S4) and inferior portion of the anterior segment of the right hepatic lobe (S5), which were seen as multi-lobulated cystic lesions on abdominal computed tomography, with the largest being about 5 cm × 2 cm in size over segment 4 [Figure 1]. Mild anemia and positive stool occult blood test were also noted. A liver abscess was confirmed by fine needle aspiration with pinkish pus from the hepatic lesions. She was treated with percutaneous transhepatic abscess drainage and parenteral antibiotics with third generation cephalosporin during hospitalization. The drained abscess culture showed serotype K1 K. pneumoniae with positive magA and rmpA genes on June 6, 2010, which was susceptible to the antibiotics we had administered. After discharge, an oral antibiotic regimen was employed for a total of 4 weeks. One month after discharge, follow-up abdominal sonography showed no focal lesions of the liver parenchyma [Figure 2].{Figure 1}{Figure 2}

Unexpectedly, the patient developed another episode of a liver abscess in the following 3 months. She presented with intermittent fever with chills and fatigue for 5 days, and visited our emergency department again on October 3, 2010. Complete blood count showed more severe leukocytosis and a higher level of C-reactive protein than during the previous admission, and a positive stool occult blood test was also noted. Abdominal ultrasonography and noncontrast abdominal computed tomography both disclosed an irregular hypoechoic lesion (size: About 4.2 cm) over the superior portion of the anterior segment of the right hepatic lobe (S8), which was different from the first episode [Figure 3]. A liver abscess was diagnosed by fine needle aspiration of the S8 lesion. An aspirated pus culture showed E. coli, however blood cultures revealed ampicillin-resistant serotype K1 K. pneumoniae positive for the magA and rmpA genes, but with a different type of pulse-field gel electrophoresis [Figure 4]. The patient then received 4 weeks of antibiotic treatment, after which no complications including metastatic foci infection of the endophthalmitis or brain abscess were noted from the recurrent liver abscess. The characteristics and demographic data of the primary and recurrent KLA are shown in [Table 1].{Figure 3}{Figure 4}{Table 1}


A pyogenic liver abscess may be caused by hematogenous dissemination or via the portal vein from a gastrointestinal infection by disseminated sepsis. [7] The disease can also arise from surgical or penetrating wounds and occasionally tissue super-infections. The pathogenesis leading to a major liver abscess is polymicrobial, and mixed enteric facultative and anaerobic pathogens are the most common. The typical clinical manifestations are fever, abdominal pain, nausea, vomiting, anorexia, and malaise, however these are nonspecific. In the current report, the antibiogram of the recurrent K1 KLA strain remained uniquely resistant to ampicillin, which was the same as the strain of the primary K1 KLA. From the view point of the genome, a different molecular pattern was demonstrated between the primary KLA and the recurrent strain. The most probable explanation why K. pneumoniae lead to the recurrent liver abscess is that it had colonized the intestinal tract or previously been seeded on the portal venous system.

Community-acquired pyogenic liver abscesses caused by K. pneumoniae has become an important health issue in Taiwan and the USA. One report indicated that the annual incidence of pyogenic liver abscesses has increased steadily from 11.15/100,000 population in 1996 to 17.59/100,000 in 2004. [8] Risk factors include diabetes mellitus, gastrointestinal malignancy, hepato-biliary pathology and renal diseases. In one case-control study, patients with diabetes had a 3.6-fold increased risk of experiencing a pyogenic liver abscess. [9] Abscesses caused by K. pneumoniae have been reported to be more strongly associated with diabetes or impaired fasting glucose than liver abscesses caused by non-K. pneumoniae. [10]

Poor glycemic control with a higher level of glycosylated hemoglobin A1c leads to a higher risk of KLA and recurrent liver abscesses. We assume that diabetes mellitus is also a risk factor for recurrence. However, recurrent liver abscesses have been reported to occur in different hepatic segments resulting from common pathogens with K. pneumoniae. [11] Good glycemic control can increase the ability of neutrophil phagocytosis and prevent recurrent pyogenic liver abscesses.


Serotype K1 K. pneumoniae more easily causes liver abscesses and thus recurrence, especially in patients with diabetes and poor glycemic control.


This work was supported by grants from Tri-Service General Hospital, National Defense Medical Center (C03-01 and C03-02), Taiwan.


The authors have no financial conflicts of interest.


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