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Year : 2013  |  Volume : 4  |  Issue : 2  |  Page : 119-121

Cryptogenic invasive klebsiella pneumonia liver abscess (cikpla) syndrome

Department of Medicine, Krishna Institute of Medical Sciences University, Karad, Satara, Maharashtra, India

Date of Web Publication16-Sep-2013

Correspondence Address:
Sanket K Mahajan
117, Mahavir Nagar, Bamroli Road, Godhra (Dist: Panchmahals), Gujarat - 389 001
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0975-9727.118244

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Escherichia coli, as the predominant pathogen in pyogenic liver abscess, resulting from underlying ascending hepatobiliary disease is well recognized. Klebsiella pneumoniae is a common pathogen responsible for diverse nosocomial and community-acquired infections, and is the third most common pathogen (10%) found in cases of nosocomial bacteremia, after Escherichia coli (20%) and Staphylococcus aureus (16.5%). Klebsiella pneumoniae has emerged as a major cause of primary or cryptogenic liver abscess with the recognition of the Cryptogenic Invasive Klebsiella Pneumoniae Liver Abscess Syndrome (CIKPLA). The syndrome appears to target populations of Asian descent with underlying disorders reflecting an impaired immunity, and is associated with the K1 hyper viscous serotype of this organism. We report a case of the CIKPLA syndrome, thus highlighting its continued evolution.

Keywords: CIKPLA syndrome, klebsiella, liver abscess, pneumonia

How to cite this article:
Mahajan SK, Kulkarni SS, Chhapra DA. Cryptogenic invasive klebsiella pneumonia liver abscess (cikpla) syndrome. Muller J Med Sci Res 2013;4:119-21

How to cite this URL:
Mahajan SK, Kulkarni SS, Chhapra DA. Cryptogenic invasive klebsiella pneumonia liver abscess (cikpla) syndrome. Muller J Med Sci Res [serial online] 2013 [cited 2023 Mar 20];4:119-21. Available from: https://www.mjmsr.net/text.asp?2013/4/2/119/118244

  Introduction Top

cryptogenic invasive K. pneumoniae-associated liver abscess (CIKPLA) syndrome is typically community-acquired [1] and unrelated to gastrointestinal or hepatobiliary anomalies. Unlike the cryptogenic non-invasive liver abscess syndrome, CIKPLA is highly associated with distant septic seeding and is distinguished by its geographical distribution. It is almost exclusive to Taiwan, [2] where it has been endemic, although a few cases have also been described in China, Korea, Singapore, Japan, India, Thailand, Trinidad, and Jamaica. [3],[4],[5],[6],[7] Compared to the polymicrobial pyogenic liver abscess, CIKPLA has lower mortality (11.3% vs. 41%) and relapse rates (4.4% vs. 41%). [2] We will, hereby, discuss the pathogenesis, clinical picture, and management of such a patient of CIKPLA syndrome.

  Case Report Top

A 56-yrs-old male patient came to Krishna hospital with complaints of breathlessness since 4 days before admission, more in supine position, with no diurnal variation, which was NYHA grade II to start with and was relieved at rest. He also complained of high-grade continuous fever, without chills or rigors since 8 days. Along with pain in right hypochondrium, which was dull aching type, more on coughing and was associated with catch in inspiration. He also had cough with scanty whitish expectoration, non-foul smelling and with no aggravating or relieving factors. There was no history of chest pain, burning micturition, altered bowel habits, or any major illness in the past. He was a chronic alcoholic since 10 yrs (taking daily 90 ml country liquor) and chronic tobacco chewer since 10 yrs (10 pouches per day). On admission, he was averagely built and nourished with a toxic look, restless, pulse-126/min, BP-110/70 mmHg, and respiratory rate- 26 cycles/min. On systemic examination, cardiovascular and central nervous systems were normal. Respiratory system examination revealed reduced breath sounds on right side with bilateral extensive coarse crepitations, more on the right side. His abdomen examination revealed tenderness in right hypochondrium with tender hepatomegaly (2 cms below the right costal margin) with the signs of inflammation over the right hypochondrium. His laboratory reports were as follows:

Hb- 13.4 G%; TLC- 18700/cmm; Platelet count- 4.5 lakh; bleeding time- 2 min; clotting time- 6 min; PT(INR)- 1.4; Random blood sugar- 123 mg/dl; blood urea- 45 mg/dl; serum creatinine- 1.2 mg/dl; serum sodium- 130 mg/dl; serum potassium- 5.4 mg/dl; urine (routine and microscopy)- within normal limits.

USG abdomen and pelvis [Figure 1]→ Enlarged liver (16.5 cm) with heterogenic cystic lesion of size 7 x 5.5 x 6 cm in right lobe, posterior superior segment suggestive of liver abscess.
Figure 1: Ultrasonography of abdomen showing liver abscess in right lobe of liver

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Chest X-Ray AP View [Figure 2]→ Suggestive of right-sided massive lobar pneumonia.
Figure 2: Chest X-ray suggestive of massive lobar pneumonia in right lung

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He was immediately started on injectable ceftriaxone 2 gm IV q 12 th hourly and injectable metronidazole 500 mg IV q 8 th hourly along with other supportive care. Meanwhile, USG-guided aspiration of liver abscess was performed on emergency basis, and 100 ml of anchovy-sauce aspirate was removed and sent for analysis, which showed TLC- 2000 cells/hpf (100% polymorphs) with Proteins- 1 gm/dl, Sugar- 35 mg/dl. The aspirated pus was also sent for culture and sensitivity. Ceftriaxone and metronidazole were continued for 14 days and, meanwhile, the culture report of the aspirated pus showed growth of Klebsiella sensitive to ciprofloxacin, amikacin, and cefoxitin. Meanwhile, sputum was also sent for culture and sensitivity studies, which showed growth of Klebsiella. Respecting the culture and sensitivity report and the severity of the disease, injectable ciprofloxacin 200 mg IV q 12 th hourly along with injectable amikacin 500 mg IV OD were started and continued for complete 7 days, followed by a course of oral ciprofloxacin for next 7 days. This treatment resulted in complete resolution of liver abscess, as confirmed by repeat ultrasonography of abdomen, and the chest x-ray also showed signs of resolution of pneumonia. He was later on discharged after 15 days of hospital stay in a hemodynamically stable condition and was advised to follow up after 7 days with a chest x-ray PA view, ultrasonography of abdomen, and liver function tests, which were all eventually within normal limits.

  Discussion Top

K. pneumoniae is an encapsulated Gram-negative bacillus belonging to the family of Enterobacteriaciae. Important geographical differences exist in its clinical presentation in different parts of the world. CIKPLA syndrome is a community-acquired, mostly monomicrobial, solitary liver lesion frequently associated with diabetes mellitus and classically complicated by one or more septic conditions (e.g., meningitis, endophthalmitis, lung abscess, or necrotizing fasciitis). The CIKPLA cases reported have previously only been documented in patients of Asian origin. [8] According to Ko et al., more than 900 cases of K. pneumoniae-associated liver abscess syndrome have been reported from Asian countries in the last decade; fewer than 23 cases were reported from regions outside Asia. [1]

Previous studies in Taiwan have demonstrated that the CIKPLA syndrome appeared to be common in middle-aged men who had concomitant diabetes mellitus. [9],[10] This has been attributed to the impaired phagocytosis of the capsulated Klebsiella organism due to the presence of diabetes mellitus; however, the CIKPLA syndrome has also been documented in patients who were not diabetic, suggesting that there are intrinsic virulence factors in the organism that convey a predilection to escape the host's immune response. [9],[10]

magA and rmpA are good markers to diagnose liver abscess in Klebsiella bacteremia. K. pneumoniae serotypes isolated in Taiwanese patients with CIKPLA had a high prevalence of capsular polysaccharide serotypes K1 and K2 and an increased resistance to phagocytosis and intracellular killing. Resistance to phagocytosis and bacterial death in human serum observed in the invasive strains has been linked to the virulence gene magA, which encodes the outer membrane protein of a mucoviscous exopolysaccharide web.

A few poor prognostic features have been documented in the CIKPLA syndrome, namely a Glasgow Coma Scale <7 on initiation of treatment, [11] high white blood cell count, thrombocytopenia, and low glucose in the CSF. [12] Although the organism appears to be more virulent, it remains sensitive to a prolonged course of intravenous cephalosporins (three weeks) and drainage of the abscess. [13] ESBL-producing K. pneumoniae is rarely isolated from the aspirates of monomicrobial liver abscesses (invasive or noninvasive), which are commonly community-acquired conditions (4.3%). [10] Therefore, the treatment of choice would be a third generation cephalosporin, preferably ceftriaxone, because it accumulates in the vitreous fluid and CSF at therapeutic concentrations, [14] thus preventing the other complications of Klebsiella bacteremia, just as in our case.

A high index of suspicion for CIKPLA in any patient with Klebsiella bacteremia needs to be considered, as the condition can be fatal if not appropriately managed. The empirical treatment in such cases should be an injectable third generation cephalosporin along with metronidazole for minimum 14 days along with the drainage of the abscess, and the treatment needs to be changed depending on the sensitivity of the organism grown on culture from the sputum and the aspirates of liver abscess.

  References Top

1.Ko WC, Paterson DL, Sagnimeni AJ, Hansen DS, Von Gottberg A, Mohapatra S, et al. Community-acquired Klebsiella pneumoniae bacteremia: Global differences in clinical patterns. Emerg Infect Dis 2002;8:160-6.  Back to cited text no. 1
2.Wang JH, Liu YC, Lee SS, Yen MY, Chen YS, Wann SR, et al. Primary liver abscess due to Klebsiella pneumoniae in Taiwan. Clin Infect Dis 1998;26:1434-8.  Back to cited text no. 2
3.Ohmori S, Shiraki K, Ito K, Inoue H, Ito T, Sakai T, et al. Septic endophthalmitis and meningitis associated with Klebsiella pneumoniae liver abscess. Hepatol Res 2002;22:307-12.  Back to cited text no. 3
4.Naito T, Kawakami T, Tsuda M, Ebe T, Sekiya S, Isonuma H, et al. A case of endophthalmitis and abscesses in the liver and the lung caused by Klebsiella pneumoniae. Kansenshogaku Zasshi 1999;73:935-8.  Back to cited text no. 4
5.Valabhji J, Robinson S, Elkeles RS. Hepatic abscess in a diabetic patient. Postgrad Med J 2000;76:797-8.  Back to cited text no. 5
6.Barton EN, Daisley H, Gilbert DT, Roberts L. Diabetes mellitus and Klebsiella pneumoniae liver abscess in adults. Trop Geogr Med 1991;43:100-4.  Back to cited text no. 6
7.Gaskin DA, Bodonaik NC, Williams NP. Hepatic abscesses at the University Hospital of the West Indies. A 24-year autopsy review. West Indian Med J 2003;52:37-40.  Back to cited text no. 7
8.Braiteh F, Golden M. Cryptogenic invasive Klebsiella pneumoniae liver abscess syndrome. J Infect Dis 2007;11:16-22.  Back to cited text no. 8
9.Cheng DL, Liu YC, Yen MY, Liu CY, Wang RS. Septic metastatic lesions of pyogenic liver abscess: Association with Klebsiella pneumoniae bacteraemia in diabetic patients. Arch Intern Med 1991;151:1557-9.  Back to cited text no. 9
10.Ko WC, Paterson DL, Sagnimeni AJ, Hansen DS, Von Gottberg A, Mohapatra S, et al. Community acquired Klebsiella pneumoniae bacteraemia: Global differences in clinical patterns. Emerg Infect Dis 2002;8:160-6.  Back to cited text no. 10
11.Fang CT, Chen YC, Chang SC, Sau WY, Luh KT. Klebsiella pneumoniae meningitis: Timing of antimicrobial therapy and prognosis. QJM 1993;1:45.  Back to cited text no. 11
12.Huang CR, Lu CH, Chang HW, Lee PY, Lin MW, Chang WN. Community acquired spontaneous bacterial meningitis in adult diabetic patients: An analysis of clinical characteristics and prognostic factors. Infection 2002;30:346-50.  Back to cited text no. 12
13.Casella F, Finazzi L, Repetti V, Rubin G, Dimarco M, Mauro T, et al. Liver abscess caused by Klebsiella pneumoniae: Two case reports. Cases J 2009;2:6879.   Back to cited text no. 13
14.Wang FD, Wang LS, Liu YC, Liu CY, Lin CL, Wong WW. Successful treatment of metastatic endophthalmitis. Case reports. Ophthalmologica 1989;198:124-8.  Back to cited text no. 14


  [Figure 1], [Figure 2]


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