Pyogenic Liver Abscess Secondary to Staphylococcus aureus Infection Without Primary Source of Infection

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Introduction

Intra-abdominal abscesses often follow an episode of peritonitis that commonly arises from perforations of the bowel or biliary tree.  The liver is the most commonly involved organ when a visceral abscess occurs. Pyogenic liver abscesses are potentially life threatening and early diagnosis is often challenging. The most common source of a pyogenic liver abscess is the biliary tree, accounting for 40-60 percent of cases. The two major mechanisms for the development of pyogenic liver abscesses are local spread from contiguous infections within the biliary tree or peritoneal cavity, and hematogenous seeding. When the biliary tree is the source of infection enteric gram negative aerobic bacilli and Enterococci are common isolates. Among liver abscesses arising from pelvic and other intraperitoneal sources, mixed aerobic and anaerobic organisms (esp. Bacteroides fragilis) are more common. Staphylococcus Aureus and Streptococcal species are most common with hematogenous spread. Klebsiella pneumoniae has been described as a cause of primary liver abscess in Taiwan and Candida species has been reported in patients who have received chemotherapy.

Case Report

A 46 year old African-American male, migrated from Africa 14 years ago, presented with chief complaint of productive cough for 2 months, associated with pleuritic chest pain, fever for 3 days, night sweats, mild shortness of breath, and loss of appetite.  The patient denied hemoptysis, weight loss, recent travel, sick contacts, and had no similar episodes in the past. His past medical history was significant only for GERD.  He reported a history of Penicillin allergy. He lives with his family and denied any pets in the house. He is a smoker, but denied alcohol or drug use. His vital signs were Temp of 103F, Pulse 130/min, Respiratory rate 28/min, Blood pressure 140/75 mmHg and oxygen saturation was 98% on room air. Lab values were significant for WBC of 11.7, Hemoglobin/hematocrit of 14.4 gm/dl/41%, Platelet count of 319. Blood cultures done on admission were negative. Liver function tests were elevatedl (refer to trend in LFTs given below) and chemistry was normal. He was admitted with the impression of Pneumonia and started on intravenous Levofloxacin. Chest x-ray revealed no active pulmonary disease. On Day 3 the patient had a temperature spike of 102.6F and pancultures were negative. Hepatitis B and C serology was negative except for reactive Anti-Hepatitis B core antibody.  Repeat CBC showed a slight decrease in the WBC count but the LFTS remained elevated. Infectious Disease was consulted. HIV testing was negative (HIV 1 and HIV 2) and the LFTS and now the WBC count continued to increase. CT of chest with contrast showed scarring at the right lung apex and cystic changes in the right middle lobe. A large mass in the right lobe of the liver (7cm) was noted and subsequent ultrasound revealed a hypoechoeic 6.3 x 4.4 cm mass in the right lobe of the liver. Triple phase Liver Scan was done which showed a 7-8 cm fluid filled abscess and a GI evaluation was requested. Initial impression was Echinococcus infection. Serology testing for Echinococcus granulosus and E. histolytica were negative.

Radiological guided drainage of the liver abscess was performed which showed a purulent material with cell count as follows: WBC 285000, RBC 57500, Neutrophils 27, Lymphs 65. Cytology showed predominantly neutrophils. Gram stain of the fluid showed Gram Positive cocci in clusters and the culture grew methicillin resistant Staphylococcus aureus. The patient was treated with Vancomycin and the WBC and LFTs started to decrease. Whole body Gallium Scan was negative and Echocardiography didn’t show any vegetations. The patient was discharged home on oral Clindamycin. The patient was seen in clinic for follow up and reported complete improvement in symptoms and repeat CT scan showed resolution of the Liver abscess.

Liver Abscess Seen in initial CT Scan
Liver Abscess Seen in initial CT Scan
Trend of CBC
CELL COUNT DAY 1 DAY 12 DAY 15 DAY 16 DAY 20 DAY 21
White Cell Count (per mm3 ) 11.7 12.3 16.1 10.0 9.8 8.4
Neutrophils ( per mm3 ) 78.4 75.7 85.3 66.4 66.7 59.0
Hemoglobin( gm/dl ) 14.7 12.7 13.0 13.8 14.2 13.7
Hematocrit ( % ) 43.3 38.0 38.3 40.5 42.0 39.9
Platelets ( per mm3 ) 319 289 490 500 505 477
Trend of LFT
COMPONENTS DAY 1 DAY 3 DAY 8 DAY 12 DAY 20
Albumin ( gm/dl ) 3.5 2.6 2.7 2.9 3.0
Total Protein ( gm/dl ) 6.8 5.7 5.8 6.2 6.7
ALT ( IU/L) 59 43 93 60 26
AST ( IU/L) 46 31 67 37 21
Total Bilirubin ( mg/dl) 1.0 0.7 1.0 0.7 0.8
Direct Bilirubin ( mg/dl ) 0.3 0.2 0.2 0.1 0.1
Alkaline Phosphatase ( U/L ) 192 186 267 263 185

Discussion

The most common clinical features for pyogenic liver abscess are fever, chills and abdominal pain. Other non specific symptoms are anorexia, weight loss, nausea and vomiting, weakness and malaise. Patients can have symptoms and signs localized to the right upper quadrant. Only about one half of patients have hepatomegaly, right upper quadrant tenderness or jaundice. Laboratory abnormalities are usually non-specific.  An elevated serum alkaline phosphatase level is the most common laboratory abnormality, followed by a leukocytosis. A chest radiograph may show an elevation of the right hemidiaphragm, right basilar infiltrate, or a unilateral pleural effusion. A complete history and physical examination, evaluation of lab abnormalities and prompt arrangement for imaging studies including ultrasonography and computed tomography will lead to diagnosis. Once the diagnosis of pyogenic liver abscess is established, a potential source should be sought. The aggressive performance of image guided catheter drainage and appropriate administration of antibiotics may reduce the mortality rate of pyogenic liver abscess. Empiric antibiotic therapy should include broad spectrum antibiotics until culture results of fluid obtained by percutaneous aspirate or surgical drainage are available. The duration of antibiotic therapy is usually four to six weeks. Parenteral antibiotics are often given for initially for two to three weeks and remainder of the course is completed with oral agents. Follow-up imaging is used to monitor response to therapy. In general treatment should be continued until CT scan shows complete or near complete resolution of the abscess cavity. The most striking point in this case is there was no primary source of infection from Staphylococcus aureus found.  Liver abscess due to Staphylococcus aureus has been described most commonly secondary to spread of infection from another primary source.

References

  1. Rahimian J, Wilson T, Oram V, Holzman RS. Pyogenic liver abscess: recent trends in etiology and mortality. Clin Infec Dis 2004; 39:1654-1659.

  2. Kasper DL, Zaleznik DF. Intra-abdominal Infections and Abscesses. In: Kasper DL (eds), et al. Harrison’s Principles of Internal Medicine. 16th ed. McGraw-Hill, New York 2005: 749.

  3. Wang JH, Liu YC, Lee SS, Yen MY, Chen YS, Wang JH, Wann SR, Lin HH.Primary liver abscess due to Klebsiella pneumoniae in Taiwan. Clin Infect Dis 1998; 26:1434-1438.

  4. Huang CJ, Pitt HA, Lipsett PA, Osterman FA, Lillemoe KD, Cameron JL, Zuidema GD. Pyogenic hepatic abscess. Changing trends over 42 years. Ann Surg 1996; 223:607-609.

  5. Maher JA, Reynolds TB, Yellin AE. Successful medical treatment of pyogenic liver abscess. Gastroenterology 1979; 77: 618-622.

  6. Reynolds, TB. Medical treatment of pyogenic liver absess. Ann Intern Med 1982; 96:373-374.

  7. Mohsen AH, Green ST, Read RC, Mckendrick MW. Liver abscess in adults: ten years experience in a UK centre. QJM 2002; 95:797-802.