What Is Causing a Pyogenic Liver Abscess in This Immune-Competent Adult?

Authors:
Mazyar Malakouti, MD, and Sayed K. Ali, MD

Citation:
Malakouti M, Ali SK. What is causing a pyogenic liver abscess in this immune-competent adult? Consultant. 2014;54(9).

A 61-year-old Caucasian male with a past medical history of diabetes mellitus type 2, hyperlipidemia, obstructive sleep apnea, and poor dentition, presented to the emergency room with fevers, malaise, and right upper quadrant pain. His symptoms had been ongoing for about 1 week, except for the right upper quadrant pain that started 2 days ago. He denied any diarrhea, melena, recent travels, or exposure to sick individuals, but stated that he had some mild nausea and was unable to fully tolerate his meals.

Physical examination. The patient had a temperature of 39.5°C, with a blood pressure of 134/77 mm Hg, a heart rate of 122 beats/minute, and oxygen saturation of 97% on room air. He had poor oral hygiene, including gingivitis and multiple cavities, but no visible masses or lesions. No lymphadenopathy was appreciated. 

His heart sounds were normal with no audible murmurs or rubs. His lung fields were clear to auscultation. He had some mild tenderness to palpation in the right upper quadrant, without guarding or rebound. 

The remainder of his physical exam including his skin, palms and eyes were unremarkable. 

Laboratory tests. His white blood cell count was 13,200/mm³ (neutrophils 85%), platelets were 201,000/mm³, hemoglobin was 13.2 g/dL, aspartate aminotransferase and alanine transaminase levels were 22 U/L, total bilirubin was 0.8 mg/dL, and international normalized ratio was 1.1. HIV, hepatitis B, and C/CMV/EBV/influenza A+B tests all were negative.

His chest x-ray showed no infiltrates or effusions and a normal cardiac silhouette. He was started on empiric antibiotics in the emergency room. 

A transthoracic echocardiogram showed trace mitral and tricuspid regurgitation with no bacterial vegetation. This was later confirmed with a transesophageal echocardiogram. To further explore his right upper quadrant pain, an abdominal ultrasound was sought; revealing a hypoechoic fluid collection with internal debris seen on the right lobe of the liver, measuring approximately 6 cm by 5.4 cm by 5.8 cm (Figure 1). This was further verified via CT scan (Figure 2). 

Figure 1. Right, upper quadrant ultrasound showing abscess formation.

Figure 2. CT scan liver, showing abscess formation.

What's your diagnosis?

(Answer and discussion on next page)

Answer: Liver abscess caused by Streptococcus anginosus

History. A 61-year-old Caucasian male with a past medical history of diabetes mellitus type 2, hyperlipidemia,  obstructive sleep apnea, and poor dentition, presented to the emergency room with fevers, malaise, and right upper quadrant pain. His symptoms had been ongoing for about 1 week, except for the right upper quadrant pain that started 2 days ago. He denied any diarrhea, melena, recent travels, or exposure to sick individuals, but stated that he had some mild nausea and was unable to fully tolerate his meals.

Physical examination. The patient had a temperature of 39.5°C, with a blood pressure of 134/77 mm Hg, a heart rate of 122 beats/min, and oxygen saturating of 97% on room air. He had poor oral hygiene, including gingivitis and multiple cavities, but no visible masses or lesions. No lymphadenopathy was appreciated.

His heart sounds were normal with no audible murmurs or rubs. His lung fields were clear to auscultation. He had some mild tenderness to palpation in the right upper quadrant, without guarding or rebound.

The remainder of his physical exam including his skin, palms, and eyes were unremarkable.

Laboratory tests. His white blood cell count was 13,200/mm3 (neutrophils 85%), platelets were 201,000/mm3, hemoglobin was 13.2 g/dL, aspartate aminotransferase and alanine transaminase levels were 22 U/L, total bilirubin was 0.8 mg/dL, and international normalized ratio was 1.1. HIV, hepatitis B, and C/CMV/EBV/influenza A+B tests all were negative.

His chest x-ray showed no infiltrates or effusions and a normal cardiac silhouette. He was started on empiric antibiotics in the emergency room.
A transthoracic echocardiogram (TTE) showed trace mitral and tricuspid regurgitation with no bacterial vegetation. This was later confirmed with atransesophageal echocardiogram (TEE). To further explore his right upper quadrant pain, an abdominal ultrasound was sought; revealing a hypoechoic fluid collection with internal debris seen on the right lobe of the liver, measuring approximately 6 cm by 5.4 cm by 5.8 cm (Figure 1). This was further verified via CT scan (Figure 2).

Diagnosis. Multiple blood cultures, drawn from various site initially grew gram positive cocci, later confirmed as Streptococcus anginosus. CT guided percutaneous drainage of the liver abscess yielded approximately 500 cc of purulent material, which also grew Streptococcus anginosus. This organism later revealed susceptibility to ceftriaxone.

Outcome of the case. The patient’s antibiotics were immediately switched to ceftriaxone. The remainder of his hospital course was unremarkable and he gradually recovered with complete resolutions in his symptoms. A repeat CT scan of his liver showed marked improvement in the size of the abscess. Repeat blood cultures were reported as negative. The patient was discharged home to complete an 8-week course of ceftriaxone and was advised to follow with the infectious disease clinic. It was postulated that his poor oral hygiene compromised his mucosal membrane, resulting in his infection and abscess formation. He was strongly advised to follow up with his dentist on a regular basis and to practice good oral hygiene.

Discussion. In 1956, Guthof, a German microbiologist, discovered a new species of bacteria within the Streptococcus viridans group. He named it Streptococcus milleri in honor of Willioughby D. Miller (1853-1907), an American dentist and first oral microbiologist.^1,2 The S. milleri group is now known as the Streptococcus anginosus group and is a subgroup of viridans streptococci with 3 distinct species: S. anginosus, Streptococcus intermedius, and Streptococcus constellatus.^3,7

Members of the S. anginosus group are common flora and usually found in the oropharyngeal, gastrointestinal, and genitourinary tracts. They can become pathogenic and causes infections, including abscesses, once the integrity of the mucosa is compromised.^1,4,7 Systemic infections in adults and children can include oral, endodontic, head, neck, thoracic, and abdominal infections with a high rate of morbidity if not identified early.⁴ However, infective endocarditis is rare. Abscess formations are a unique characteristic of the S. anginosus group and are generally purulent, but infrequent in immune-competent patients.^5-7

The classification of this group based on hemolysis patterns and Lancefield antigens are challenging due to variability of these properties. Hence a combination of rapid tests, though not sensitive, can be used for identifying S. anginosus group.⁸ In addition, the advent of technology has recently improved better identification and classification of these organisms.

Due to pathogenicity and ability of S. anginosus to form abscesses, early recognition and treatment is crucial.⁹ Drainage of the abscess is paramount and should be immediately considered. This group of microorganisms is largely susceptible to penicillin, but specific treatment should be chosen based on results of the culture and antimicrobial susceptibility testing.^7,8,10
 
This case highlights the importance of considering this common pathogen as a culprit in healthy patients who presents with fevers and abscess in the setting of poor oral hygiene. In addition, positive blood cultures for this pathogen should alert the provider on the high likelihood of an underlying abscess that often need percutaneous or surgical drainage.

References:

1. Guthof O. Pathogenic strains of Streptococcus viridans; streptocci found in dentalabscesses and infiltrates in the region of the oral cavity. Zentralbl Bakteriol Orig. 1956;166:553.
2. Terzic A, Scolozzi P. Deep neck space abscesses of dental origin: the impact of Streptococcus group Milleri. Eur Arch Otorhinolaryngol. 2014;271(10):2771-2774.
3. Siegman-Igra Y, Azmon Y, Scwart D. Milleri group streptococcus—a stepchild in the viridian family. Eur J Clin Microbiol Infec Dis. 2012;31:2453-2459.
4. Mutneja R, Shah M, Silverstein N. Concomitant lung and brian abscesses: a rare presentation of a common bacteria. Conn Med. 2014;78(1):25-27.
5. Claridge JE 3rd, Attorri S, Musher DM, et al. Streptococcus intermedius, Streptococcus constellatus, and Streptococcus anginosus (“Streptococcus milleri group”) are of different clinical importance and are not equally associated with abscess. Clin Infect Dis. 2001;32(10):1511-1515.
6. Nagashima H, Takao A, Maeda N. Abscess forming ability of streptococcus milleri group: synergistic effect with Fusobacterium nucleatum. Microbiol Immunol. 1999;43(3):207-216.
7. Giuliano S, Rubini G, Conte A, et al. Streptococcus anginosus group disseminated infection: case report and literature review. Infez Med. 2012;20(3):145-154.
8. Whiley RA, Fraser H, Hardie JM, Beighton D. Phenotypic differentiation of Streptococcus intermedius, Streptococcus constellatus, and Streptococcus anginosus strains within the “Streptococcus milleri group.” J Clin Microbiol. 1990;28(7):1497-1501.
9.  Spellerberg B, Brandt C. Streptococcus. In: Murray PR, Baron EJ, Jorgenson JH, et al. Manual of Clinical Microbiology. 9th ed, Vol 1. Washington, DC: ASM Press; 2009.
10. Tracy M, Wanahita A, Shuhatovich Y, et al. Antibiotic susceptibilities of genetically characterized Streptococcus milleri group strains. Antimicrob Agents Chemother. 2001;45(5):1511-1514.