Treatment of liver abscess caused by Klebsiella pneumoniae with multi-site infection: a case report

Abstract

Background

Pyogenic liver abscesses are a fatal condition often seen in emergency departments. The major clinical presentations include weakness, anorexia, fever, chills, ventosity and abdominal pain. They occur in immunocompromised individuals who suffer from diabetes mellitus, malignant tumors, hepatocirrhosis, kidney failure, and solid organ transplantation, or those with long-term administration of glucocorticoids. Invasive Klebsiella pneumoniae liver abscess syndrome resulting from hypervirulent Klebsiella pneumoniae often presents with extrahepatic complications such as endophthalmitis, meningitis, brain enlargement, pneumonia, necrotizing fasciitis, and spondylitis. Prompt diagnosis is crucial for the treatment of invasive Klebsiella pneumoniae liver abscess syndrome.

Case report

A 75-year-old Han Chinese female patient who presented to the emergency department primarily for fever accompanied by chills was diagnosed with pyogenic liver abscess complicated with pulmonary infection, involving multiple pus emboli in the branches of the right hepatic vein. The patient accepted intravenous imipenem and cilastatin sodium for anti-infection, and subcutaneous insulin to control hyperglycemia. Percutaneous liver puncture and drainage was performed under ultrasound guidance. During the treatment the patient presented with headache, weakness in both lower limbs and lower back pain. Brain magnetic resonance imaging showed intracranial infection and lumbar magnetic resonance imaging showed infection of the vertebral body, intervertebral disc, and soft tissue. The patient had a liver abscess positive for Klebsiella pneumoniae together with infection of other organs, thus she was eventually diagnosed with invasive Klebsiella pneumoniae liver abscess syndrome. The antibiotics were adjusted according to the site of infection and drug sensitivity test. The patient recovered after percutaneous liver puncture and drainage under ultrasound guidance and anti-infection treatment for 3 months. Reexamination of abdominal computed tomography, chest computed tomography, brain magnetic resonance imaging and lumbar magnetic resonance imaging suggested that the infectious lesions had disappeared.

Conclusion

This medical case report describes a patient with a pyogenic liver abscess caused by Klebsiella pneumoniae who was eventually diagnosed with invasive Klebsiella pneumoniae liver abscess syndrome. Invasive Klebsiella pneumoniae liver abscess syndrome has permanent morbidity, poor quality of life, and lacks warning signs. Despite the complexity of the condition, the patient received effective treatment and the abscess was successfully managed. Through this case, we propose that invasive Klebsiella pneumoniae liver abscess syndrome caused by hypervirulent Klebsiella pneumoniae should be considered for patients with diabetes and fever in the emergency department. Targeted intravenous antibiotics and percutaneous drainage of the abscess are key to the treatment of invasive Klebsiella pneumoniae liver abscess syndrome.

Background

Liver abscesses are pus-filled masses in the liver that are a common intrahepatic infections caused by bacteria, parasites, or fungi. Liver abscesses are mainly divided into pyogenic liver abscesses (PLAs) and amebic liver abscesses. Common causative organisms for PLA are Klebsiella pneumoniae, Escherichia coli, and Staphylococcus aureus [1]. The incidence of PLA varies between Eastern and Western populations [2], which can reach 12–18 cases per 100,000 people per year in Asian countries, with a mortality rate of approximately 2–31% [3]. In 1986, hypervirulent Klebsiella pneumoniae causing various infections was reported in Taiwan [4]. Invasive Klebsiella pneumoniae liver abscess syndrome (IKLAS) is defined as a clinical condition characterized by the presence of a PLA caused by hypervirulent Klebsiella pneumoniae along with such extrahepatic complications as endophthalmitis, meningitis, encephalopyosis, pneumonia, necrotizing fasciitis, and spondylodiscitis [5]. It is now apparent that hypervirulent Klebsiella pneumoniae has spread globally, including India, Europe, Australia, and the USA, and healthcare providers worldwide should recognize the threat of this bacteria [6]. The detection rate of hypervirulent Klebsiella pneumoniae in pyogenic liver abscesses is 40–80% [7]. Herein, we describe a case of PLA caused by Klebsiella pneumoniae resulting in pulmonary infection, pus emboli in the branches of the right hepatic vein, intracranial infection, pyogenic spondylitis, spondylodiscitis, and soft tissue infection, which presented symptoms similar to those seen in IKLAS.

Case report

A 75-year-old Han Chinese female was admitted to our emergency department (ED) after 5 days of fever accompanied by chills, with the maximum body temperature being 38.5 °C. She presented with symptoms of somnolence and weakness. Her physical examination revealed a blood pressure of 85/55 mmHg, a heart rate of 134 beats/minute, and a respiratory rate of 24 beats/minute. She had no abdominal pain, lumbago, headache, dizziness, and visual impairment. She had a history of type 2 diabetes mellitus (T2DM) for 20 years, regularly taking melbinum and insulin therapy. She had no history of smoking or alcohol abuse. In the ED, a blood culture was collected and the results of laboratory tests are shown in Table 1. Abdominal ultrasound demonstrated a low echoic area of the right lobe of the liver, which was considered to be a liver abscess.

Table 1.

Laboratory test results of the patient

Laboratory findings	Value	Reference range
White blood cell count (109/L)	13.39 ↑	4–10
Neutrophils (%)	85.6 ↑	40–75
Platelets (109/L)	7 ↓	100–300
Hemoglobin (g/L)	141	115–150
Procalcitonin (ng/mL)	8.91 ↑	0.04–0.50
C-reactive protein (mg/L)	169.18 ↑	0–10
Interleukin-6 (pg/mL)	23.68 ↑	0–10
Glycosylated hemoglobin (%)	11.70 ↑	4–6
Creatinine (μmol/L)	64	41–81
Albumin (g/L)	21 ↓	40–55
Alanine aminotransferase (U/L)	168 ↑	0–40
Aspartate aminotransferase (U/L)	109 ↑	0–40
Alkaline phosphatase (U/L)	169 ↑	50–135
Glutamyl aminotransferase (U/L)	37	7–45
Total bilirubin (μmol/L)	15.1	0–21
Direct bilirubin (μmol/L)	6.5	0–7
Lactic acid (mmol/L)	1.6 ↑	0.6–1.4
D-dimer (ng/mL)	4400 ↑	0–500
Glycated hemoglobin A1c (%)	11.7 ↑	4–6

Upon admission, chest computed tomography (CT) and an abdominal contrast enhanced CT were performed. The chest CT showed the multiple patchy and nodular consolidation in both lungs (Fig. 1), which was considered the pulmonary infection. The abdominal enhanced CT confirmed the diagnosis of the liver abscess with multiple pus emboli in the branches of the right hepatic vein (Figs. 2 and 3). The patient accepted the intravenous infusion of the broadspectrum carbapenem antibiotics imipenem and cilastatin sodium (1 g once every 8 hours), albumin and platelets to help prevent the progression of the disease, and subcutaneous insulin to control the hyperglycemia. Five days after anti-infective treatment, abdominal ultrasound revealed that the liver abscess had liquefied. A percutaneous liver puncture and drainage tube was placed under ultrasound guidance. Both blood culture and liver abscess drainage cultures showed Klebsiella pneumoniae, and the drug sensitivity test displayed the bacteria was sensitive to cephalosporins, penicillin, quinolones, and carbapenems antibiotics. Ten days into the hospitalization, body temperature, blood platelet count, inflammatory indicators, and albumin all returned to normal ranges. The abdominal ultrasound detected that the size of abscess had decreased. Unfortunately, the patient complained of headache and weakness in both lower limbs. Brain magnetic resonance imaging (MRI) showed multiple enhancement lesions in the bilateral frontal, parieto-occipital lobe, and the right cerebellar hemisphere, which were considered as intracranial infections (Fig. 4). According to the drug sensitivity test, the patient was switched to intravenous meropenem (2 g once every 8 hours) as antibiotic therapy. On the 15th day, Lumbar MRI was performed because the patient had lower back pain. Lumbar MRI showed infection of the lumbar 4 vertebra, lumbar 5 vertebra, lumbar 4/5 intervertebral discs, and their surrounding soft tissues (Figs. 5 and 6).

Fig. 1.

Chest computed tomography detected multiple patchy and nodular consolidations in both lungs, which suggested an infectious lesion

Fig. 2.

Abdominal enhanced computed tomography showed a liver abscess in the right lobe of the liver (red circles)

Fig. 3.

Abdominal enhanced computed tomography showed bacterial emboli in the branches of the right hepatic vein (red arrow)

Fig. 4.

Diffusion-weighted imaging sequences showed high signals in the left occipital lobe (left red arrow), and enhanced T1 sequences showed nodular enhancement (right red arrow), which suggested an infectious lesion

Fig. 5.

Sagittal T2 fat sequences showed heterogeneous high-signal-intensity infectious lesions of L4 and L5 vertebrae, as well as the 4/5 lumbar intervertebral disc (red circles)

Fig. 6.

Sagittal T2 fat sequence showed high-signal-intensity infectious lesions in the soft tissue of the lower back (red arrow)

The patient was immunocompromised and had multiple organ infections, therefore she was diagnosed with IKLAS after a multi-disciplinary team discussion (infectious diseases department, neurosurgery department, orthopedics department, hepatological surgery department, and medical imaging department). There was no surgical indication for the patient, and conservative anti-infection treatment was continued. Two weeks after the application of meropenem, the patient’s vital signs and routine blood tests were normal; inflammatory factors were decreased and the antibiotic treatment was changed to intravenous ceftriaxone (2 g once every 12 hours). After a month of hospitalization, the patient was transferred to the community hospital and subsequently took intravenous ceftriaxone. After antibiotic treatment for 3 months, the patient’s body temperature, routine blood, and inflammatory factors were normal, and the patient had no headache or lower back pain but still had weakness in both lower limbs. Reexamination of abdominal CT, chest CT, brain MRI, and lumbar MRI suggested that the infectious lesions had disappeared.

Discussion

We successfully managed a patient with poorly controlled T2DM who developed IKLAS. Klebsiella pneumoniae caused PLAs through the biliary tract, the portal vein, the hepatic artery, and direct infection from adjacent infected foci [8]. Sometimes the infection pathways of PLA were not clear, and it was defined as cryptogenic infection. In China, data shows that the main etiology of PLA has shifted from biliary to cryptogenic, and that the bacteria causing PLA have changed from Escherichia coli to Klebsiella pneumoniae [2, 9]. Recently IKLAS has been increasingly reported all over the world, especially in the Asia–Pacific region, and has high morbidity and mortality [5]. The causative organism of IKLAS is hypervirulent Klebsiella pneumoniae and the most typical symptoms are endophthalmitis, meningitis, and brain abscesses [10]. Hypervirulent Klebsiella pneumoniae occurs in more than 80% of patients with PLA in South Asia and is strongly associated with right liver abscess, a size of abscess > 5 cm, and diabetes mellitus [11]. Hypervirulent Klebsiella pneumoniae liver abscesses have the following characteristics: a single bacterial infection accompanied by extrahepatic multiple site infections, and most patients have no history of biliary tract disease [6]. Hypervirulent Klebsiella pneumoniae strains are more resistant to phagocytosis by macrophages and neutrophils, prevent complement-mediated bactericidal effect, proliferate faster in humans, and show stronger virulence in various infection models. Hypervirulent Klebsiella pneumoniae exhibit increased virulence by expressing rmpA and/or rmpA2 to produce more capsular polysaccharides [12].

Recent studies have already shown that capsules, siderophores, and lipopolysaccharide may be contribute to the pathogenicity of hypervirulent Klebsiella pneumoniae [13]. The chromosomes or large virulence plasmids or both are responsible for the hypervirulence of Klebsiella pneumoniae [14]. Bacteria need iron for metabolism, and synthesize siderophores to obtain iron for growth in low iron environments [15]. Bacterial virulence is closely related to the expression of the capsule. Glucose, which acts as a kind of environmental signal, increases capsule production [16]. Hypermucoviscosity is the most critical virulent factor and hypermucoviscosity strains appear more immune tolerant to peripheral blood mononuclear cells [17]. Another feature of hypervirulent Klebsiella pneumoniae is colibactin, which grows faster in malnourished individuals and expresses enhanced virulence [18]. Unfortunately, IKLAS is prone to misdiagnosis due to atypical presentations, nonspecific symptoms, and overlapping clinical conditions. Immunocompromised individuals, such as those with diabetes mellitus, cancer, hepatobiliary diseases, and solid organ transplantation, are more susceptible to IKLAS. A recent study showed that the incidence of liver abscesses in patients with diabetes was over three times more than that of healthy individuals [19]. It is generally accepted that hyperglycemia can diminish phagocyte adhesion, chemotaxis, phagocytosis, and bactericidal activity to reduce the ability to kill bacteria and increase the severity of the infection [11, 20]. In recent years, multidrug resistant Klebsiella pneumoniae infections have been reported, and the drug resistance of bacteria is becoming increasingly more serious [21].

The patient in this case was diagnosed with PLA in the ED. After admission, the patient received percutaneous liver puncture and drainage and anti-infective therapy with imipenem and cilastatin sodium. The cultures of the blood and drainage fluid were positive for Klebsiella pneumoniae that was non-drug resistant. Ten days after treatment, she had developed neurologic symptoms of headache and weakness in both lower limbs. Brain MRI confirmed the diagnosis of intracranial infection. Klebsiella pneumoniae, which caused the liver abscesses, had spread to the central nervous system. Anti-infective treatment was continued with meropenem, which can penetrate the blood–brain barrier. On the 15th day of treatment, the patient underwent lumbar MRI for lower back pain, which revealed infection of the vertebrae, lumbar intervertebral discs, and their surrounding soft tissues. The patient had a liver abscess of Klebsiella pneumoniae with infection of other organs and so was eventually diagnosed with IKLAS. On the 24th day of treatment, her symptoms improved, and the antibiotics were de-escalated to ceftriaxone. The patient recovered after 3 months of the treatment with anti-bacterial agents and strict glycemic control.

Owing to the microbiology laboratory not being able to identify hypervirulent Klebsiella pneumoniae, it was difficult to diagnose whether the liver abscesses were caused by hypervirulent Klebsiella pneumoniae and whether it was accompanied by extrahepatic migrating infected lesions. When patients with liver abscesses have other clinical symptoms, the infection of hypervirulent Klebsiella pneumoniae should be considered, and imaging examination should be conducted to find dormant infected lesions, which are conducive to targeted selection of antibiotics [6]. The consensus for the treatment of PLA is the combination of percutaneous drainage or open surgical drainage of the abscess and the prompt administration of appropriate antibiotics. Owing to the advancement of interventional radiology and minimally invasive surgery, percutaneous drainage has became more widespread and provides effective source control for liver abscesses. Recently, percutaneous drainage under ultrasound or CT guidance combined with long-term antibiotic therapy has replaced traditional surgical drainage [22]. Thanks to the advancements in treatment approaches, the mortality rate associated with PLA has sharply declined in recent years.

Conclusion

The final diagnosis consisted of IKLAS and T2DM. The patient benefited from the targeted intravenous broad-spectrum antibiotics, strict blood glucose control with intensive insulin, and early percutaneous drainage of the abscess. Except for weakness in both lower limbs, the patient had no discomfort and could take care of herself. When the patient developed new clinical symptoms, we examined the cause and gave targeted treatment. Clinically, patients with diabetes and liver abscesses caused by Klebsiella pneumoniae should be considered susceptible to other sites of infection. We have delivered this report to improve clinician’s awareness of IKLAS. Targeted intravenous antibiotics and percutaneous drainage of the abscess are the key to the treatment of IKLAS.

Author contributions

All authors discussed the results and contributed to the final manuscript. QW collected the data. YG and SS wrote the paper, and conceived and designed the analysis. YJ performed the analysis.

Funding

No funding.

Data availability

The data that support the findings of this study are available on request from the corresponding author, YG

Declarations

Ethical approval and consent to participate

Not applicable.

Consent for publication

Written informed consent was obtained from the patient’s legal guardian for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Competing interests

The authors declare no competing interests.