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  Table of Contents    
CASE REPORT  
Year : 2017  |  Volume : 60  |  Issue : 4  |  Page : 587-589
Pyogenic liver abscess associated with oral flora bacterium, Streptococcus anginosus in a patient with underlying tuberculosis


Department of Microbiology, Indira Gandhi Medical College, Shimla, Himachal Pradesh, India

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Date of Web Publication12-Jan-2018
 

   Abstract 


Streptococcus anginosus forms a part of the commensal flora of the oral cavity. However, it can be aggressive and may lead to gastrointestinal and urogenital infections. We present an interesting case and course in a 38-year-old immunocompetent female patient with pyogenic liver abscess due to S. anginosus infection who had multiple carious teeth and underlying pulmonary tuberculosis.

Keywords: Dental caries, pulmonary tuberculosis Streptococcus anginosus, pyogenic liver abscess

How to cite this article:
Ganju SA, Gautam N, Sharma G. Pyogenic liver abscess associated with oral flora bacterium, Streptococcus anginosus in a patient with underlying tuberculosis. Indian J Pathol Microbiol 2017;60:587-9

How to cite this URL:
Ganju SA, Gautam N, Sharma G. Pyogenic liver abscess associated with oral flora bacterium, Streptococcus anginosus in a patient with underlying tuberculosis. Indian J Pathol Microbiol [serial online] 2017 [cited 2019 Aug 19];60:587-9. Available from: http://www.ijpmonline.org/text.asp?2017/60/4/587/222998





   Introduction Top


Streptococcus anginosus group, earlier referred to as the Streptococcus milleri group comprise of aerobic, Gram-positive bacteria; Streptococcus anginosus, Streptococcus intermedius, and Streptococcus constellatus. These are harmless inhabitants of the human oral cavity but can spread from the oral cavity and colonize the throat, nasopharynx, gastrointestinal tract, and the genitourinary tract [1]S. anginosus is usually β-hemolytic, with a variable carriage of Lancefield group antigen group A, C, F, or G.[2]S. anginosus is frequently isolated from dental abscesses.[3],[4] Other infections caused by the bacterium, within the abdominal cavity include liver abscesses, peritonitis, pelvic and subphrenic abscesses, abdominal wound infections, and cholangitis.[5],[6],[7]

The S. anginosus group, though, closely related have undergone several changes in their nomenclature because of their diverse hemolytic, biochemical, and serological properties. This has led to the underestimation of their clinical significance. High degree of clinical suspicion and microbiological identification is important for treatment and cure of the patient.


   Case Report Top


A 38-year-old female patient was admitted to the medicine department, with the complaints of yellow discoloration of eyes and skin. She complained of dark-colored urine for 5 days and vomiting for the past 1 day. She was diagnosed of tubercular pleural effusion for and put Category 1 antitubercular drugs (ATT); isoniazid (300 mg), rifampicin (450 mg), ethambutol (800 mg), and pyrazinamide (1000 mg) 8 days back. At the time of admission, she was weighing 50 kg, afebrile, pulse rate; 116/min and blood pressure; 110/72 mmHg. Her eyes were icteric. Her oral hygiene was poor; with multiple carious teeth. Respiratory, cardiovascular, and central nervous system examination did not reveal any abnormal finding. Abdominal examination revealed moderate tenderness on palpation at the right upper quadrant and negative Murphy's sign. There was no rebound tenderness, guarding, or hepatosplenomegaly. The relevant laboratory investigations are shown in [Table 1].
Table 1: Laboratory findings

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The chest X-ray was suggestive of the right-sided pleural effusion; however, the pleural tap turned out to be a dry tap, as there was no free fluid in the pleural cavity. A possibility of ATT-induced hepatitis was kept in mind and the ATT drugs were changed to the three-drug regimen; streptomycin, ethambutol, and levofloxacin. The patient was not relieved of tenderness in the right upper abdominal quadrant, and an ultrasonography of abdomen was carried out on the 3rd day of admission. This revealed a hypoechoic lesion (8.4 cm × 5.7 cm) located in Segment V and VI of the liver with multiple air foci suggestive of liver abscess [Figure 1]. Ultrasound-guided pigtail drainage of the liver abscess was conducted on the same day, and the pus was sent to the microbiology laboratory for bacterial, parasitic, and tubercular examination. The patient was empirically started on injectables; ceftriaxone and metronidazole to cover all the possible etiologies. The cytology of the aspirate revealed predominantly degenerated cells, macrophages, lymphocytes, and pus cells. No acid-fast bacilli were detected in the pus smear by the Ziehl–Neelsen staining, and the sample also yielded a negative result for Mycobacterium tuberculosis complex by GeneXpert. The wet mount did not show the presence of organisms suggestive of trophozoites of Entamoeba histolytica. The pus was incubated aerobically in the blood culture bottles in the automated BD BACTEC™ Fx system. The culture was positive after overnight incubation and subjected to Gram staining and inoculation on MacConkey's agar and blood agar. On blood agar with 10% sheep blood [Figure 2] small, 0.5 mm, translucent, circular, and beta-hemolytic colonies were seen. They were both catalase and coagulase negative. The identification of the isolate was carried out in the automated BD Phoenix™ 100 system which identified the isolate to be S. anginosus. The patient responded to penicillin and was discharged on the 9th day after removal of the pigtail and put on oral antibiotics and followed up.
Figure 1: Ultrasonography of liver: Hypoechogenic abscess (between cursors)

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Figure 2: Blood agar plate: β- hemolytic colonies of Streptococcus anginosus (blue arrows)

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   Discussion Top


We report an unusual case the pyogenic liver abscess caused by S. anginosus. The first cases of S. anginosus group causing hepatic abscesses were reported in 1975.[8]S. anginosus group organisms are frequently encountered in purulent infections of the mouth and in dental abscesses.[9] The pathogenesis of pyogenic liver abscess possibly could be due to the blood-borne bacteria reaching the liver either by way of the portal vein, biliary tree or hepatic artery or by direct extension from infection in adjacent organs. Normally, in an immunocompetent individual, the hepatic reticuloendothelial system removes and destroys such bacteria efficiently keeping the healthy human liver sterile.[10],[11] Any factor decreasing the hepatic resistance locally may contribute to localizing the bacteria and abscess formation. Active tuberculosis could have led to decrease in the immune status in our patient with invasion of S. anginosus which was already colonizing the carious teeth. As the patient was started on ATT approximately 8 days back, hepatitis and/or paradoxical immune-mediated hepatic abscess is a possibility. In this case, hematogenous dissemination of S. anginosus has led to localization and abscess formation in liver as has been observed in cases due to bacteremia secondary endocarditis and pyelonephritis.[12] The liver abscess associated with S. anginosus is generally monomicrobial, as was seen in the present case. Liver abscesses associated with other microorganisms usually have a polymicrobial etiology. The patient was discharged after 9 days. A longer duration of the symptoms are noted in a liver abscess associated with S. anginosus in comparison to the liver abscess associated with other microorganisms.[13]

Pyogenic liver abscess can be a potentially life-threatening disease, and the clinical diagnosis is a problem as the presenting complaints are nonspecific. This case highlights the fact that patients on ATT can develop hepatitis and/or paradoxical immune-mediated hepatic abscess, but due to a compromised immune status, commensal bacteria of the mouth, especially in caries teeth can disseminate to liver and cause pyogenic abscesses.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Mirzanejad Y, Stratton CW. Streptococcus anginosus group. In: Mandell GL, Bennett JE, Dolin R, editors. Principles and Practice of Infectious Diseases. Philadelphia: Elsevier Churchill Livingstone; 2005. p. 2451-5.  Back to cited text no. 1
    
2.
Spellerberg B, Brandt C. Streptococcus. In: Versalovic J, Carroll KC, Funke G, Jorgensen JH, Landry ML, Warnock DW, editors. Manual of Clinical Microbiology. 10th ed. Washington DC: ASM Press; 2011. p. 331-49.  Back to cited text no. 2
    
3.
Molina JM, Leport C, Bure A, Wolff M, Michon C, Vilde JL, et al. Clinical and bacterial features of infections caused by Streptococcus milleri. Scand J Infect Dis 1991;23:659-66.  Back to cited text no. 3
    
4.
Robertson D, Smith AJ. The microbiology of the acute dental abscess. J Med Microbiol 2009;58:155-62.  Back to cited text no. 4
    
5.
Gossling J. Occurrence and pathogenicity of the Streptococcus milleri group. Rev Infect Dis 1988;10:257-85.  Back to cited text no. 5
    
6.
Murray HW, Gross KC, Masur H, Roberts RB. Serious infections caused by Streptococcus milleri. Am J Med 1978;64:759-64.  Back to cited text no. 6
    
7.
Hardwick RH, Taylor A, Thompson MH, Jones E, Roe AM. Association between Streptococcus milleri and abscess formation after appendicitis. Ann R Coll Surg Engl 2000;82:24-6.  Back to cited text no. 7
    
8.
Bateman NT, Eykyn SJ, Phillips I. Pyogenic liver abscess caused by Streptococcus milleri. Lancet 1975;1:657-9.  Back to cited text no. 8
    
9.
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;28:1497-501.  Back to cited text no. 9
    
10.
Sayek I, Onat D. Pyogenic and amebic liver abscess. In: Holzheimer RG, Mannick JA, editors. Surgical Treatment: Evidence-Based and Problem-Oriented. Munich: Zuckschwerdt; 2001. Available from: https://www.ncbi.nlm.nih.gov/books/NBK6955/. [Last accessed on 2016 Dec 16].  Back to cited text no. 10
    
11.
Meena M, Gupta N, Kewlani J, Kumararesan SH. Hepatic abscess as a paradoxical response to antituberculous chemotherapy for tubercular lymphadenitis. BMJ Case Rep 2015;2015. pii: bcr2015211936.  Back to cited text no. 11
    
12.
Murarka S, Pranav F, Dandavate V. Pyogenic liver abscess secondary to disseminated Streptococcus anginosus from sigmoid diverticulitis. J Glob Infect Dis 2011;3:79-81.  Back to cited text no. 12
    
13.
Yılmaz H, Yılmaz EM, Karadag A, Esen S, Sunbul M, Leblebicioglu H. Liver abscess associated with an oral flora bacterium Streptococcus anginosus. J Microbiol Infect Dis 2012;2:33-5.  Back to cited text no. 13
    

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Correspondence Address:
Sunite A Ganju
Department of Microbiology, Indira Gandhi Medical College, Shimla, Himachal Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/IJPM.IJPM_842_16

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