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Invasive liver abscess syndrome caused by Klebsiella pneumoniae UpToDate
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Invasive liver abscess syndrome caused by Klebsiella pneumoniae
Authors: WenLiang Yu, MD, YinChing Chuang, MD
Section Editor: Stephen B Calderwood, MD
Deputy Editor: Allyson Bloom, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Feb 2017. | This topic last updated: Oct 29, 2015.
INTRODUCTION — Klebsiella pneumoniae can produce infection at a variety of sites, with the risk being
increased in patients with impaired host defenses (eg, diabetes mellitus, alcoholism, malignancy, chronic
obstructive pulmonary disease, and glucocorticoid therapy). K. pneumoniae is also associated with a community
acquired primary invasive liver abscess syndrome. In addition to liver abscess, some patients develop metastatic
infection at other sites.
Issues related to the K. pneumoniae invasive liver abscess syndrome will be reviewed here. The epidemiology,
clinical features (including the general principles of diagnosis and treatment), microbiology, and pathogenesis of
K. pneumoniae infection are discussed separately. (See "Clinical features, diagnosis, and treatment of Klebsiella
pneumoniae infection" and "Microbiology and pathogenesis of Klebsiella pneumoniae infection".)
DEFINITION — K. pneumoniae primary liver abscess has been variably defined in the literature. In one study, for
example, primary liver abscess was defined as a K. pneumoniae liver abscess occurring in the absence of
predisposing intraabdominal factors, such as hepatobiliary disease, colorectal disease, or a history of
intraabdominal surgery or trauma [1]. In other studies, it has been defined by a monomicrobial K. pneumoniae
isolate, while polymicrobial liver abscess was usually secondary to hepatobiliary disease or intraabdominal
infection [2,3].
We prefer to define K. pneumoniae primary liver abscess (KLA) as liver abscess that occurs in the absence of
hepatobiliary disease. Almost all of these infections are monomicrobial [35]. Although this topic highlights virulent
strains of K. pneumoniae that have the capacity to invade a healthy liver without predisposing anatomical
abnormalities, the rare possibility of concurrent colorectal disease cannot be excluded, as routine colonoscopy is
not generally performed in the setting of KLA. (See "Pyogenic liver abscess", section on 'Association with
colorectal neoplasia'.)
EPIDEMIOLOGY — Most cases of K. pneumoniae primary liver abscess (KLA), particularly those associated
with metastatic infection, have been reported in Taiwan and are communityacquired [112]. In a series of 248
patients with pyogenic liver abscess from Taiwan, for example, K. pneumoniae was responsible for 171 (69
percent) [4].
Communityacquired KLA has also been described in other countries in Asia [7,1317], in Asian patients living in
other countries [1824], and in South Africa [25]. It has less commonly been reported in nonAsian patients in the
United States [19,20,26,27] ( particularly Hispanics [19,27]) and in Europe and Canada [2836]. A report from
New York, for example, evaluated 79 cases of liver abscess [19]. K. pneumoniae was the most commonly
identified pathogen, isolated from 23 of 54 liver abscesses (41 percent) in which an organism was recovered. K.
pneumoniae was more commonly isolated among Asian than nonAsian patients (50 versus 27 percent).
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A minority of patients with KLA, mostly from Taiwan, develops metastatic infection, most commonly manifested as
endophthalmitis and/or meningitis [1,6,8,10,37,38]. The incidence of metastatic infection in the setting of KLA is
about 12 percent in series from Taiwan and is more common in KLA than in liver abscesses of other bacterial
etiology (15 versus 4 percent) [1,3,4]. A somewhat lower rate of metastatic infection (9 percent) was noted in a
series of 290 patients with KLA from Korea [13]. (See 'Metastatic infection' below.)
The findings have been more variable in studies in the United States. There were no cases of metastatic infection
among the 23 patients with KLA in a study from New York [19], whereas a review of 18 cases in the United
States prior to the New York study found metastatic infection in five (28 percent) [20].
In contrast, metastatic infection appears to be a rare complication (2 percent or less) of secondary K.
pneumoniae liver abscess, even in Taiwan [1,3].
Metastatic infection can also occur with K. pneumoniae infections other than liver abscess. These infections are
discussed separately. (See "Clinical features, diagnosis, and treatment of Klebsiella pneumoniae infection",
section on 'Endophthalmitis' and "Clinical features, diagnosis, and treatment of Klebsiella pneumoniae infection",
section on 'Meningitis/brain abscess'.)
PATHOGENESIS AND RISK FACTORS — Klebsiella primary liver abscess (KLA) frequently occurs in patients
with diabetes but can occur in the absence of underlying predisposing medical conditions.
Host factors
Diabetes mellitus — Diabetes mellitus or impaired fasting glucose, present in 70 to 78 percent of patients in
three series from Taiwan, is the major observed risk factor for KLA [36,12,13]. The high prevalence of diabetes
or impaired fasting glucose in patients with KLA is not seen with other causes of liver abscess (5 percent with
polymicrobial liver abscess and 33 percent with nonK. pneumoniae liver abscess in those series) [3,4].
The mechanism by which diabetes predisposes to KLA is not well understood. One contributory mechanism may
be that poor glycemic control impairs neutrophil phagocytosis of K1 and K2 capsular serotypes [39]. However,
diabetic patients are also vulnerable to infection caused by nonK1/K2 strains [40]. (See "Microbiology and
pathogenesis of Klebsiella pneumoniae infection", section on 'Association with primary liver abscess'.)
Other host factors — Fatty liver disease has also been more highly associated with KLA compared with liver
abscesses due to other organisms [41].
Although no studies have identified specific human genes that predispose to KLA, the prevalence in Asian
patients has raised the possibility that host genetic factors play a role. As an example, Chinese ethnicity itself
might be a major factor predisposing to intestinal colonization by serotype K1/K2 K. pneumoniae isolates, which
is associated with KLA. In one study that evaluated K. pneumoniae isolates from the stools of healthy adult
Chinese residents of Taiwan, Japan, Hong Kong, China, Thailand, Malaysia, Singapore, and Vietnam, 10 percent
of the isolates were serotypes K1/K2 [42]. (See "Microbiology and pathogenesis of Klebsiella pneumoniae
infection", section on 'Pathogenesis' and "Microbiology and pathogenesis of Klebsiella pneumoniae infection",
section on 'Association with primary liver abscess'.)
Virulence factors — KLA is caused by isolates with an increased number of virulence factors compared with
other K. pneumoniae isolates [13,6,11,25].
In studies from Taiwan, both the K1 capsular serotype and the hypermucoviscosity phenotype are more common
in communityacquired compared with nosocomial K. pneumoniae infections [2,11]. These virulence factors are
also associated with primary liver abscess, and their higher frequency in communityacquired isolates could
explain why isolates from primary liver abscess are almost exclusively acquired in the community [13,6,11,25]. In
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a report from Taiwan of 95 K. pneumoniae isolates from secondary bacteremia with an identified source of
infection, abscess formation in the liver and other sites was much more common with communityacquired than
nosocomial isolates (46 versus 4 percent) [2].
The regional distribution of K. pneumoniae virulence factors also appears to play a significant role in the
geographic restriction of KLA. In a review of 455 consecutive cases of K. pneumoniae bacteremia in seven
countries (Taiwan, South Africa, United States, Australia, Belgium, Turkey, and Argentina), the invasive
communityacquired syndrome of liver abscess, meningitis, or endophthalmitis was only seen in Taiwan and
South Africa [25]. The isolates from Taiwan and South Africa compared with the other countries were much more
likely to have a mucoid phenotype (100 versus 2 percent) and to be rmpApositive (86 versus 7 percent). Other
virulence factors, such as K1 capsular serotype, were common in Taiwan and South Africa but rarely seen in the
other countries.
The role of virulence factors in KLA is discussed in further detail separately. (See "Microbiology and pathogenesis
of Klebsiella pneumoniae infection", section on 'Pathogenesis' and "Microbiology and pathogenesis of Klebsiella
pneumoniae infection", section on 'Association with primary liver abscess'.)
Antibiotic use — Prior antibiotic use also appears to increase the risk of KLA. As an example, in a retrospective
study of 855 patients with KLA and 3400 age and sexmatched controls in Taiwan, ampicillin or amoxicillin
therapy within the prior 30 days was associated with KLA [43]. In an accompanying animal study, ampicillin
administration predisposed K. pneumoniaecolonized mice to increased liver abscess formation.
Risk factors for metastatic disease — Existing published data are conflicting as to whether diabetes is an
independent risk factor for metastatic infection [1,3,6,12,44]. Virulence factors of the isolate have been more
clearly associated with the development of metastatic disease.
The presence of the more virulent K1 serotype is a risk factor for metastatic infection [1,6]. In a report from
Taiwan of patients with primary Klebsiella liver abscess (KLA), septic endophthalmitis was present in infections
with 12 of 85 K1 strains, 2 of 19 K2 strains, and none of 28 nonK1/K2 strains [6]. A similar relationship was seen
in the four patients with other sites of metastatic infection: none occurred in the nonK1/K2 strains. (See
"Microbiology and pathogenesis of Klebsiella pneumoniae infection", section on 'Capsular serotypes'.)
Presence of the magA gene is another risk factor for metastatic infection [8]. Among magApositive isolates,
those that also have the kfu ironuptake system may be particularly associated with metastatic infection [45]. The
rmpA gene also appears to be a significant predictor of metastatic infection [46]. However, the rmpA gene is
almost ubiquitous in KLA strains, thus rmpA could hardly predict metastatic infections among patients with KLA
[47]. (See "Microbiology and pathogenesis of Klebsiella pneumoniae infection", section on 'Siderophores'.)
CLINICAL MANIFESTATIONS — The presenting symptoms and signs of K. pneumoniae liver abscess (KLA)
are similar to those caused by other etiologies of pyogenic liver abscess [3,4,48]. (See "Pyogenic liver abscess",
section on 'Clinical manifestations'.)
In a review of 160 cases from Taiwan, the most common clinical features and their frequencies are listed below
[3]:
● Fever (93 percent)
● Right upper quadrant tenderness (71 percent)
● Nausea, vomiting, diarrhea, or abdominal pain (38 percent)
● Leukocytosis (70 percent)
● Elevations in serum alanine and aspartate aminotransferases (59 and 68 percent)
● Elevations in alkaline phosphatase (78 percent)
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● Elevations in bilirubin (26 percent)
In contrast to liver abscesses caused by other organisms, those due to K. pneumoniae are more likely to be
solitary and more likely to be monomicrobial [35]. In a report from Taiwan, for example, 65 of 68 were
monomicrobial [5].
Certain imaging findings have been reported more commonly with KLA compared with liver abscesses of other
bacterial etiology. On ultrasonography, KLA often have a predominantly solid appearance and, compared with
other causes of bacterial liver abscess, have a much smaller quantity of pus at initial aspiration [49]. On CT scan,
monomicrobial KLA tends to be single, unilobular, and multiloculated [50]. When compared with abscesses
caused by other bacteria, KLA is more likely to be solid, thinwalled, without rim enhancement, and associated
with thrombophlebitis [50,51].
Metastatic infection — A minority of patients with primary liver abscess has concurrent evidence of or develops
metastatic infection at other sites [1,3,4,6,8,10,12,13,20,37,38,45,5254]. The most common manifestations of
metastatic infection are endophthalmitis, meningitis and brain abscess [1,3,12]. Other manifestations include
lumbar or cervical spondylitis and discitis, septic pulmonary emboli, lung abscess, psoas abscess, splenic
abscess, necrotizing fasciitis, neck abscess, and osteomyelitis [1,3,12,18,55]. (See "Clinical features, diagnosis,
and treatment of Klebsiella pneumoniae infection", section on 'Endophthalmitis' and "Clinical features, diagnosis,
and treatment of Klebsiella pneumoniae infection", section on 'Meningitis/brain abscess'.)
DIAGNOSIS — Similar to the diagnosis of pyogenic liver abscesses, the diagnosis of primary liver abscess due to
K. pneumoniae (KLA) is made when K. pneumonia is isolated from the abscess aspirate or blood of a patient with
imaging findings consistent with a liver abscess in the absence of underlying hepatobiliary disease. (See
"Pyogenic liver abscess", section on 'Diagnosis'.)
Ultrasonography and computed tomography (CT) are the imaging methods of choice when liver abscess is part of
the differential diagnosis in patients with the above clinical manifestations and laboratory abnormalities (image 1).
Imaging for liver abscess may also be warranted in patients who present with K. pneumoniae bacteremia and
have persistent fever despite appropriate antibiotic therapy. Some radiographic findings have been associated
with KLA compared with liver abscesses due to other pathogens, but these findings alone are not diagnostic of
KLA. (See 'Clinical manifestations' above.)
Following radiologic identification of a possible liver abscess, imageguided diagnostic aspiration should be
performed to confirm a pyogenic process. Specimens should be sent for Gram stain and both aerobic and
anaerobic culture. Blood cultures should be obtained from all patients with known or suspected liver abscess
since KLA may be associated with bacteremia [10,11,25].
DIFFERENTIAL DIAGNOSIS — The differential diagnosis of fever and right upper quadrant abdominal pain
includes other hepatobiliary disease, colitis, or pneumonia. This topic is reviewed in detail separately.
The differential diagnosis of patients presenting with a focal liver lesion is broad and includes both malignant and
infectious etiologies. Imaging studies (ultrasound or computed tomography [CT]) can usually differentiate abscess
from malignancy. In some instances, however, a multilobulated abscess may mimic the heterogeneity of hepatic
tumor (image 2). Conversely, necrosis of hepatic tumor can appear similar to a highly suppurative abscess on
CT. In these diagnostic difficulties, diffusionweighted magnetic resonance imaging may be useful to differentiate
between hepatic abscess and necrotic liver tumor [56,57]. However, it is possible that K. pneumoniae could be
isolated from an infected and necrotic hepatic tumor [58,59]. In such a situation, the diagnosis is extremely
difficult and may require tissue biopsies. This is a particular consideration in the setting of a nonresolving liver
abscess. (See "Solid liver lesions: Differential diagnosis and evaluation".)
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In a patient with imaging findings consistent with a liver abscess, many different microbiological etiologies are
possible and cannot be distinguished without culture or serological data. (See "Pyogenic liver abscess", section
on 'Microbiology'.)
TREATMENT — Treatment of primary Klebsiella liver abscess (KLA) involves drainage and systemic antibiotic
therapy.
Drainage — Percutaneous drainage guided by imaging (either ultrasonography or computed tomography [CT]) is
used for both diagnosis and treatment and is preferred over surgical drainage. Percutaneous drainage for
treatment is recommended even in patients in whom the diagnosis has been made on the basis of positive blood
cultures.
In some cases, the abscess may not be amenable to immediate drainage, for example, if it is still in an immature
form. Two options are to postpone drainage and monitor closely until the abscess has matured and can then be
drained or to insert the drain and retain the tubing so that the abscess can drain once it becomes liquefied.
Surgical resection may be warranted in some instances, such as when the abscess is multiloculated, it fails to
liquefy, or there is delayed resolution and a protracted course of fever. (See "Pyogenic liver abscess", section on
'Drainage'.)
Antibiotic choice — Treatment of KLA requires parenteral antibiotic therapy in addition to drainage. Generally,
communityacquired KLA isolates remain susceptible to cephalosporins [14,60]. Resistant isolates, including
those that produce extendedspectrum betalactamases (ESBL), have been rarely reported [61,62]. Initial
therapy for KLA may be administered as outlined for empiric management of pyogenic liver abscess, which
generally should include coverage for gramnegative and anaerobic organisms (table 1). (See "Pyogenic liver
abscess", section on 'Antibiotics'.)
Subsequent antibiotic therapy should be tailored to results of antibiotic susceptibility testing. In reports from
Taiwan and Korea, antibiotic regimens have included extended spectrum betalactams and cephalosporins with
or without aminoglycosides [1,3,14,20].
There is disagreement regarding the selection of early or late generation cephalosporins. Many favor use of first
generation cephalosporins (with or without an aminoglycoside) given their relatively low cost and apparent
efficacy with respect to rates of mortality, metastatic infection, and complications [46]. However, others have
reported higher metastatic infection rates among patients treated with cefazolin compared with those treated with
a second or third generation cephalosporin, both with or without an aminoglycoside (37 versus 6 percent) [63].
In regions where third generation cephalosporins are much more costly than first generation cephalosporins,
cefazolin with or without an aminoglycoside may be the favored antibiotic regimen. However, third generation
cephalosporins are favorable if costs are not prohibitive and/or in the setting of severe infection.
Although aminoglycosides penetrate abscess cavities poorly, in theory they may eradicate bloodstream
organisms early in the course of infection, potentially decreasing risk for metastatic complications. However, this
benefit is unproven and may be outweighed by the toxicity of aminoglycosides. (See "Aminoglycosides".)
Duration of therapy — For most cases, antibiotic therapy should be administered for four to six weeks. Longer
courses of treatment may be warranted for patients requiring subsequent drainage procedures or with persistent
radiographic evidence of abscess. Parenteral antibiotics may be administered for the first two to three weeks until
the patient has improved systemically and drainage is complete; the remainder of the course can be completed
with oral agents.
Followup imaging should be used to monitor the response to therapy, to determine the duration of antibiotics,
and to assess the need for further aspiration. In general, treatment should be continued until CT imaging
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demonstrates complete or near complete resolution of the abscess cavity. Some abscesses with a thick capsule
may leave a CT abnormality remaining after the infection has been eradicated, and other clinical findings, such as
normalization of inflammatory markers, sterile cultures, and the finding of a clear cavity without debris or other
content on imaging, can be helpful to distinguish this from persistent infection.
Treatment of metastatic infection — In addition to systemic antibiotics, local therapy or debridement may be
required in patients with metastatic infection. As an example, patients with Klebsiella endophthalmitis should
receive intravitreal antibiotics and vitrectomy. Management of the metastatic complications is discussed further in
the topic reviews on those clinical syndromes.
PROGNOSIS — The prognosis of K. pneumoniae liver abscess (KLA) is good overall, but the metastatic
complications can cause significant morbidity. The largest published experience comes from Taiwan:
● In a review of 160 cases of KLA (all but one were primary), the mortality rate was 11 percent and relapse
occurred in 4.4 percent [3]. Among the 18 patients who died, the main causes of death were fulminant sepsis
in nine (all with inadequate or delayed drainage of the abscess), metastatic infection in four (meningitis in
two, brain and lung abscess in one, and necrotizing fasciitis in one), and rupture of the abscess in two. The
mortality rate was significantly higher (41 percent) in 22 patients with polymicrobial liver abscess, all but one
of whom had a biliary tract stone or intraabdominal malignancy. Sepsis was the only cause of death in these
patients.
● A later study evaluated 248 patients with pyogenic liver abscess (171 due to K. pneumoniae and 77 to other
bacteria) [4]. The mortality rate was significantly lower in patients with K. pneumoniae infection (4.1 versus
20.8 percent), while the relapse rate was the same in the two groups (6.5 versus 6.4 percent).
Although the mortality rate is relatively low, the morbidity in patients with metastatic endophthalmitis is often high
despite aggressive therapy, as many patients have impaired vision or blindness [1,54,6467]. In addition, patients
with meningitis may have persistent neurologic abnormalities [1,68], particularly if they have substantial
neurologic impairment prior to the onset of antibiotic therapy [68]. (See "Bacterial endophthalmitis", section on
'Endogenous bacterial endophthalmitis' and "Gramnegative bacillary meningitis: Treatment".)
The frequency of adverse outcomes was illustrated in a report of 23 patients with KLA who had metastatic
infection involving the eye or central nervous system [1]. Sixteen had severe irreversible disability, including loss
of vision, quadriplegia, paraparesis, or impaired higher cortical function. Good vision at presentation and early
therapy have been associated with a higher likelihood of maintenance of vision [64,65]. (See "Clinical features,
diagnosis, and treatment of Klebsiella pneumoniae infection", section on 'Endophthalmitis' and "Clinical features,
diagnosis, and treatment of Klebsiella pneumoniae infection", section on 'Meningitis/brain abscess'.)
SUMMARY
● Klebsiella pneumoniae primary liver abscess (KLA) occurs in the absence of hepatobiliary disease and is
almost always monomicrobial. Most cases have been reported from Asia or in patients of Asian origin. (See
'Definition' above and 'Epidemiology' above.).
● Diabetes mellitus or impaired fasting glucose is the most important host risk factor for primary KLA. (See
'Host factors' above.)
● The Klebsiella isolates that cause KLA have an increased number of virulence factors compared with other
Klebsiella isolates and appear to be restricted geographically. (See 'Virulence factors' above.)
● In addition to the manifestations typical of pyogenic liver abscess, such as fever, leukocytosis, right upper
quadrant tenderness, and elevated liver enzymes, a minority of patients with primary KLA can develop
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metastatic infections at other sites. The most common sites for metastatic infections are the eye, meninges,
and brain. (See 'Clinical manifestations' above.).
● Imaging should be performed in patients with signs and symptoms of a liver abscess or in patients with K.
pneumoniae bacteremia who have persistent fevers despite appropriate antibiotic therapy. Diagnosis of
primary KLA is made by detection of a liver abscess on imaging (ultrasound or computed tomography [CT])
followed by aspiration of the lesion for Gram stain and aerobic and anaerobic culture. (See 'Diagnosis'
above.)
● Treatment of KLA requires parenteral antibiotic therapy in addition to drainage, optimally percutaneous.
Antibiotic choice should be based upon the results of antibiotic susceptibility testing. A thirdgeneration
cephalosporin is preferable if the isolate is susceptible and cost is not prohibitive. Antibiotics should be given
for at least four to six weeks, depending on abscess resolution as determined by imaging findings. (See
'Antibiotic choice' above and 'Duration of therapy' above.)
● The reported mortality rate has ranged from 4 to 11 percent. Metastatic disease to the eyes or brain can
cause significant longterm morbidity. (See 'Prognosis' above.)
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REFERENCES
1. Fang CT, Lai SY, Yi WC, et al. Klebsiella pneumoniae genotype K1: an emerging pathogen that causes
septic ocular or central nervous system complications from pyogenic liver abscess. Clin Infect Dis 2007;
45:284.
2. Yu WL, Ko WC, Cheng KC, et al. Association between rmpA and magA genes and clinical syndromes
caused by Klebsiella pneumoniae in Taiwan. Clin Infect Dis 2006; 42:1351.
3. Wang JH, Liu YC, Lee SS, et al. Primary liver abscess due to Klebsiella pneumoniae in Taiwan. Clin Infect
Dis 1998; 26:1434.
4. Yang CC, Yen CH, Ho MW, Wang JH. Comparison of pyogenic liver abscess caused by nonKlebsiella
pneumoniae and Klebsiella pneumoniae. J Microbiol Immunol Infect 2004; 37:176.
5. Chan KS, Chen CM, Cheng KC, et al. Pyogenic liver abscess: a retrospective analysis of 107 patients
during a 3year period. Jpn J Infect Dis 2005; 58:366.
6. Fung CP, Chang FY, Lee SC, et al. A global emerging disease of Klebsiella pneumoniae liver abscess: is
serotype K1 an important factor for complicated endophthalmitis? Gut 2002; 50:420.
7. Yeh KM, Kurup A, Siu LK, et al. 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
2007; 45:466.
8. Fang CT, Chuang YP, Shun CT, et al. A novel virulence gene in Klebsiella pneumoniae strains causing
primary liver abscess and septic metastatic complications. J Exp Med 2004; 199:697.
9. Chuang YP, Fang CT, Lai SY, et al. Genetic determinants of capsular serotype K1 of Klebsiella
pneumoniae causing primary pyogenic liver abscess. J Infect Dis 2006; 193:645.
10. Ko WC, Paterson DL, Sagnimeni AJ, et al. Communityacquired Klebsiella pneumoniae bacteremia: global
differences in clinical patterns. Emerg Infect Dis 2002; 8:160.
11. Tsay RW, Siu LK, Fung CP, Chang FY. Characteristics of bacteremia between communityacquired and
nosocomial Klebsiella pneumoniae infection: risk factor for mortality and the impact of capsular serotypes as
https://www.uptodate.com/contents/invasiveliverabscesssyndromecausedbyklebsiellapneumoniae/print
7/14
3/10/2017
Invasive liver abscess syndrome caused by Klebsiella pneumoniae UpToDate
a herald for communityacquired infection. Arch Intern Med 2002; 162:1021.
12. Cheng DL, Liu YC, Yen MY, et al. Septic metastatic lesions of pyogenic liver abscess. Their association with
Klebsiella pneumoniae bacteremia in diabetic patients. Arch Intern Med 1991; 151:1557.
13. Chung DR, Lee SS, Lee HR, et al. Emerging invasive liver abscess caused by K1 serotype Klebsiella
pneumoniae in Korea. J Infect 2007; 54:578.
14. Kang CI, Kim SH, Bang JW, et al. Communityacquired versus nosocomial Klebsiella pneumoniae
bacteremia: clinical features, treatment outcomes, and clinical implication of antimicrobial resistance. J
Korean Med Sci 2006; 21:816.
15. Okano H, Shiraki K, Inoue H, et al. Clinicopathological analysis of liver abscess in Japan. Int J Mol Med
2002; 10:627.
16. Siu LK, Fung CP, Chang FY, et al. Molecular typing and virulence analysis of serotype K1 Klebsiella
pneumoniae strains isolated from liver abscess patients and stool samples from noninfectious subjects in
Hong Kong, Singapore, and Taiwan. J Clin Microbiol 2011; 49:3761.
17. Lee KH, Hui KP, Tan WC, Lim TK. Klebsiella bacteraemia: a report of 101 cases from National University
Hospital, Singapore. J Hosp Infect 1994; 27:299.
18. Nadasy KA, DomiatiSaad R, Tribble MA. Invasive Klebsiella pneumoniae syndrome in North America. Clin
Infect Dis 2007; 45:e25.
19. Rahimian J, Wilson T, Oram V, Holzman RS. Pyogenic liver abscess: recent trends in etiology and mortality.
Clin Infect Dis 2004; 39:1654.
20. Lederman ER, Crum NF. Pyogenic liver abscess with a focus on Klebsiella pneumoniae as a primary
pathogen: an emerging disease with unique clinical characteristics. Am J Gastroenterol 2005; 100:322.
21. Fang FC, Sandler N, Libby SJ. Liver abscess caused by magA+ Klebsiella pneumoniae in North America. J
Clin Microbiol 2005; 43:991.
22. Fierer J, Walls L, Chu P. Recurring Klebsiella pneumoniae pyogenic liver abscesses in a resident of San
Diego, California, due to a K1 strain carrying the virulence plasmid. J Clin Microbiol 2011; 49:4371.
23. McCabe R, Lambert L, Frazee B. Invasive Klebsiella pneumoniae infections, California, USA. Emerg Infect
Dis 2010; 16:1490.
24. Anstey JR, Fazio TN, Gordon DL, et al. Communityacquired Klebsiella pneumoniae liver abscesses an
"emerging disease" in Australia. Med J Aust 2010; 193:543.
25. Yu VL, Hansen DS, Ko WC, et al. Virulence characteristics of Klebsiella and clinical manifestations of K.
pneumoniae bloodstream infections. Emerg Infect Dis 2007; 13:986.
26. Harris PJ, Laczek JT, Polish RD, Fraser SL. Two cases of Klebsiella pneumoniae primary liver abscesses;
an emerging clinical entity among diabetics. Hawaii Med J 2005; 64:306.
27. Braiteh F, Golden MP. Cryptogenic invasive Klebsiella pneumoniae liver abscess syndrome. Int J Infect Dis
2007; 11:16.
28. Gomez C, Broseta A, Otero JR, et al. Primary pyogenic liver abscess cause by magA+ Klebsiella
pneumoniae in Spain. Clin Microbiol Newsl 2007; 29:13.
29. Karama EM, Willermain F, Janssens X, et al. Endogenous endophthalmitis complicating Klebsiella
pneumoniae liver abscess in Europe: case report. Int Ophthalmol 2008; 28:111.
30. Keynan Y, Karlowsky JA, Walus T, Rubinstein E. Pyogenic liver abscess caused by hypermucoviscous
Klebsiella pneumoniae. Scand J Infect Dis 2007; 39:828.
https://www.uptodate.com/contents/invasiveliverabscesssyndromecausedbyklebsiellapneumoniae/print
8/14
3/10/2017
Invasive liver abscess syndrome caused by Klebsiella pneumoniae UpToDate
31. Hsu CR, Lin TL, Chen YC, et al. The role of Klebsiella pneumoniae rmpA in capsular polysaccharide
synthesis and virulence revisited. Microbiology 2011; 157:3446.
32. Vila A, Cassata A, Pagella H, et al. Appearance of Klebsiella pneumoniae liver abscess syndrome in
Argentina: case report and review of molecular mechanisms of pathogenesis. Open Microbiol J 2011;
5:107.
33. Sobirk SK, Struve C, Jacobsson SG. Primary Klebsiella pneumoniae Liver Abscess with Metastatic Spread
to Lung and Eye, a NorthEuropean Case Report of an Emerging Syndrome. Open Microbiol J 2010; 4:5.
34. Decré D, Verdet C, Emirian A, et al. Emerging severe and fatal infections due to Klebsiella pneumoniae in
two university hospitals in France. J Clin Microbiol 2011; 49:3012.
35. Merlet A, Cazanave C, Dutronc H, et al. Primary liver abscess due to CC23K1 virulent clone of Klebsiella
pneumoniae in France. Clin Microbiol Infect 2012; 18:E338.
36. Moore R, O'Shea D, Geoghegan T, et al. Communityacquired Klebsiella pneumoniae liver abscess: an
emerging infection in Ireland and Europe. Infection 2013; 41:681.
37. Lee HC, Chuang YC, Yu WL, et al. Clinical implications of hypermucoviscosity phenotype in Klebsiella
pneumoniae isolates: association with invasive syndrome in patients with communityacquired bacteraemia.
J Intern Med 2006; 259:606.
38. Yu WL, Fung CP, Ko WC, et al. Polymerase chain reaction analysis for detecting capsule serotypes K1 and
K2 of Klebsiella pneumoniae causing abscesses of the liver and other sites. J Infect Dis 2007; 195:1235.
39. Lin JC, Siu LK, Fung CP, et al. Impaired phagocytosis of capsular serotypes K1 or K2 Klebsiella
pneumoniae in type 2 diabetes mellitus patients with poor glycemic control. J Clin Endocrinol Metab 2006;
91:3084.
40. Yu WL, Chan KS, Ko WC, et al. Lower prevalence of diabetes mellitus in patients with Klebsiella
pneumoniae primary liver abscess caused by isolates of K1/K2 than with nonK1/K2 capsular serotypes.
Clin Infect Dis 2007; 45:1529.
41. Li J, Fu Y, Wang JY, et al. Early diagnosis and therapeutic choice of Klebsiella pneumoniae liver abscess.
Front Med China 2010; 4:308.
42. Lin YT, Siu LK, Lin JC, et al. Seroepidemiology of Klebsiella pneumoniae colonizing the intestinal tract of
healthy Chinese and overseas Chinese adults in Asian countries. BMC Microbiol 2012; 12:13.
43. Lin YT, Liu CJ, Yeh YC, et al. Ampicillin and amoxicillin use and the risk of Klebsiella pneumoniae liver
abscess in Taiwan. J Infect Dis 2013; 208:211.
44. Sheu SJ, Kung YH, Wu TT, et al. Risk factors for endogenous endophthalmitis secondary to klebsiella
pneumoniae liver abscess: 20year experience in Southern Taiwan. Retina 2011; 31:2026.
45. Ma LC, Fang CT, Lee CZ, et al. Genomic heterogeneity in Klebsiella pneumoniae strains is associated with
primary pyogenic liver abscess and metastatic infection. J Infect Dis 2005; 192:117.
46. Lee SS, Chen YS, Tsai HC, et al. Predictors of septic metastatic infection and mortality among patients with
Klebsiella pneumoniae liver abscess. Clin Infect Dis 2008; 47:642.
47. Chuang YC, Lee MF, Tan CK, et al. Can the rmpA gene predict metastatic meningitis among patients with
primary Klebsiella pneumoniae liver abscess? J Infect 2013; 67:166.
48. Chan KS, Yu WL, Tsai CL, et al. Pyogenic liver abscess caused by Klebsiella pneumoniae: analysis of the
clinical characteristics and outcomes of 84 patients. Chin Med J (Engl) 2007; 120:136.
49. Hui JY, Yang MK, Cho DH, et al. Pyogenic liver abscesses caused by Klebsiella pneumoniae: US
appearance and aspiration findings. Radiology 2007; 242:769.
https://www.uptodate.com/contents/invasiveliverabscesssyndromecausedbyklebsiellapneumoniae/print
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50. Alsaif HS, Venkatesh SK, Chan DS, Archuleta S. CT appearance of pyogenic liver abscesses caused by
Klebsiella pneumoniae. Radiology 2011; 260:129.
51. Lee NK, Kim S, Lee JW, et al. CT differentiation of pyogenic liver abscesses caused by Klebsiella
pneumoniae vs nonKlebsiella pneumoniae. Br J Radiol 2011; 84:518.
52. Kawai T. Hypermucoviscosity: an extremely sticky phenotype of Klebsiella pneumoniae associated with
emerging destructive tissue abscess syndrome. Clin Infect Dis 2006; 42:1359.
53. Chou FF, Kou HK. Endogenous endophthalmitis associated with pyogenic hepatic abscess. J Am Coll Surg
1996; 182:33.
54. Sheu SJ, Chou LC, Hong MC, et al. Risk factors for endogenous endophthalmitis secondary to Klebsiella
pneumoniae liver abscess. Zhonghua Yi Xue Za Zhi (Taipei) 2002; 65:534.
55. Keynan Y, Rubinstein E. Endogenous endophthalmitis caused by hypermucoviscous Klebsiella
pneumoniae: an emerging disease in Southeast Asia and beyond. Curr Infect Dis Rep 2008; 10:343.
56. Awaya H, Ito K, Honjo K, et al. Differential diagnosis of hepatic tumors with delayed enhancement at
gadoliniumenhanced MRI: a pictorial essay. Clin Imaging 1998; 22:180.
57. Chan JH, Tsui EY, Luk SH, et al. Diffusionweighted MR imaging of the liver: distinguishing hepatic abscess
from cystic or necrotic tumor. Abdom Imaging 2001; 26:161.
58. Huang CI, Wang LY, Yeh ML, et al. Hepatocellular carcinoma associated with liver abscess. Kaohsiung J
Med Sci 2009; 25:537.
59. Chong VH, Lim KS. Pyogenic liver abscess as the first manifestation of hepatobiliary malignancy.
Hepatobiliary Pancreat Dis Int 2009; 8:547.
60. Lin TL, Tang SI, Fang CT, et al. Extendedspectrum betalactamase genes of Klebsiella pneumoniae
strains in Taiwan: recharacterization of shv27, shv41, and tem116. Microb Drug Resist 2006; 12:12.
61. Li W, Sun G, Yu Y, et al. Increasing occurrence of antimicrobialresistant hypervirulent (hypermucoviscous)
Klebsiella pneumoniae isolates in China. Clin Infect Dis 2014; 58:225.
62. Su SC, Siu LK, Ma L, et al. Communityacquired liver abscess caused by serotype K1 Klebsiella
pneumoniae with CTXM15type extendedspectrum betalactamase. Antimicrob Agents Chemother 2008;
52:804.
63. Cheng HP, Siu LK, Chang FY. Extendedspectrum cephalosporin compared to cefazolin for treatment of
Klebsiella pneumoniaecaused liver abscess. Antimicrob Agents Chemother 2003; 47:2088.
64. Chen YJ, Kuo HK, Wu PC, et al. A 10year comparison of endogenous endophthalmitis outcomes: an east
Asian experience with Klebsiella pneumoniae infection. Retina 2004; 24:383.
65. Tan YM, Chee SP, Soo KC, Chow P. Ocular manifestations and complications of pyogenic liver abscess.
World J Surg 2004; 28:38.
66. Yoon YH, Lee SU, Sohn JH, Lee SE. Result of early vitrectomy for endogenous Klebsiella pneumoniae
endophthalmitis. Retina 2003; 23:366.
67. Ang M, Jap A, Chee SP. Prognostic factors and outcomes in endogenous Klebsiella pneumoniae
endophthalmitis. Am J Ophthalmol 2011; 151:338.
68. Fang CT, Chen YC, Chang SC, et al. Klebsiella pneumoniae meningitis: timing of antimicrobial therapy and
prognosis. QJM 2000; 93:45.
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GRAPHICS
Liver abscess
A contrastenhanced CT scan of the upper abdomen demonstrates a large gas
containing abscess in the right lobe of the liver. This location is easily amenable
to percutaneous CTguided drainage.
CT: computed tomography.
Courtesy of Jonathan Kruskal, MD, PhD.
Graphic 61510 Version 3.0
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Klebsiella pneumoniae liver abscess
Computed tomography (CT) of a primary liver abscess due to Klebsiella pneumoniae. The
multiloculated appearance can make radiographic distinction from a hepatic tumor
difficult. In such cases, diffusionweighted magnetic resonance imaging may be helpful to
better differentiate between abscess and tumor.
Courtesy of WenLiang Yu, MD and YinChing Chuang, MD.
Graphic 83712 Version 1.0
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Empiric antibiotic therapy for gramnegative and anaerobic pathogens
Regimen
Dose (adult)*
First choice
Monotherapy with a betalactam/betalactamase inhibitor:
Ampicillinsulbactam ¶
3 g IV every six hours
Piperacillintazobactam Δ
3.375 or 4.5 g IV every six hours
Ticarcillinclavulanate
3.1 g IV every four hours
Combination third generation cephalosporin PLUS metronidazole:
Ceftriaxone plus
1 g IV every 24 hours or 2 g IV every 12 hours for CNS infections
Metronidazole
500 mg IV every eight hours
Alternative empiric regimens
Combination fluoroquinolone ◊ PLUS metronidazole:
Ciprofloxacin or
400 mg IV every 12 hours
Levofloxacin plus
500 or 750 mg IV once daily
Metronidazole
500 mg IV every eight hours
Monotherapy with a carbapenem §:
Imipenemcilastatin
500 mg IV every six hours
Meropenem
1 g IV every eight hours
Doripenem
500 mg IV every eight hours
Ertapenem ￥
1 g IV once daily
* Antibiotic doses should be adjusted appropriately for patients with renal insufficiency or other doserelated consideration.
¶ E coli resistance to Ampicillinsulbactam is emerging in some areas; check local susceptibility data.
Δ Some clinicians use 4.5 g every eight hours for empiric therapy since the percent time above the MIC is similar between
the regimens for most pathogens; however, this regimen is NOT recommended for nosocomial pneumonia or Pseudomonas
coverage. Please refer to UpToDate topics on the "Treatment of hospitalacquired, ventilatorassociated, and healthcare
associated pneumonia in adults" and "Treatment of Pseudomonas aeruginosa infections".
◊ Fluoroquinolones are generally avoided in pregnant women due to potential fetal toxicity.
§ Use carbapenems cautiously in patients with immediatetype hypersensitivity to betalactams.
￥ Ertapenem lacks activity against Acinetobacter and Pseudomonas and is not an appropriate choice for severe or
nosocomial infection.
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Contributor Disclosures
Wen-Liang Yu, MD Nothing to disclose Yin-Ching Chuang, MD Nothing to disclose Stephen B
Calderwood, MD Patent Holder: Vaccine Technologies Inc [Vaccines (Cholera vaccines)]. Equity
Ownership/Stock Options: Pulmatrix [Infectious diseases (Inhaled antimicrobials)]; PharmAthene
[Anthrax (Antibody therapies)]. Allyson Bloom, MD Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these
are addressed by vetting through a multi-level review process, and through requirements for references
to be provided to support the content. Appropriately referenced content is required of all authors and
must conform to UpToDate standards of evidence.
Conflict of interest policy
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