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Year : 2018  |  Volume : 11  |  Issue : 2  |  Page : 41-43
Do we know everything about Streptococcus mitis: From alpha to omega?

1 Department of Microbiology, Dr B C Roy Postgraduate Institute of Pediatrics, Kolkata, West Bengal, India
2 Department of Microbiology, Calcutta National Medical College, Kolkata, West Bengal, India

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Date of Web Publication10-Dec-2019


Background: A 45 year old male was admitted with jaundice, abdominal pain and respiratory distress. He had history of chronic alcoholism. Materials and Methods: Blood tests revealed a raised leucocyte count of 19000/microlitre, high levels of bilirubin, amylase and lipase. Radiological investigations including chest x-ray, USG, CECT, and MRI gave findings of cholelithiasis, pancreatic pseudocyst, left sided pleural effusion and left lower lobe collapse. MRCP diagnosed choledocholithiasis. Pseudocyst fluid was aspirated and sent for culture and sensitivity. Results: Culture yielded pure growth of capsulated gram positive diplococci resembling Streptococcus pneumoniae. However, it was bile-insoluble and hence pure colonies were sent for confirmation by Vitek-2. Vitek-2 confirmed it to Streptococcus mitis sensitive to erythromycin, levofloxacin, linezolid and vancomycin. The patient responded to the antibiotics after surgery and was discharged. Conclusion: Streptococcus mitis is considered to be an oral commensal, sometimes causing infective endocarditis. However, as it contains almost all the virulence factors carried by it's close relative S. pneumoniae, and also can masquerade itself to the latter morphologically and biochemically to a great extent, it seems to walk a thin line between being a harmless commensal and a virulent pathogen. This incidence of infecting a pancreatic pseudocyst should make a microbiologist alert of considering a probability of it's increasing pathogenicity range.

Keywords: Pancreatic pseudocyst, Streptococcus mitis, Streptococcus pneumoniae

How to cite this article:
Chakraborty B, Banerjee D, Mukherjee DM, Bandyopadhyay S, Roy A, Pal S. Do we know everything about Streptococcus mitis: From alpha to omega?. Ann Trop Med Public Health 2018;11:41-3

How to cite this URL:
Chakraborty B, Banerjee D, Mukherjee DM, Bandyopadhyay S, Roy A, Pal S. Do we know everything about Streptococcus mitis: From alpha to omega?. Ann Trop Med Public Health [serial online] 2018 [cited 2021 Jan 26];11:41-3. Available from:

   Introduction Top

Streptococcus mitis is generally considered to be a relatively benign, harmless oral commensal. It belongs to the alpha-hemolytic streptococci and is a member of the mitis group, which also contains a well-recognized dangerous pathogen, Streptococcus pneumoniae, a close relative of S. mitis. However, this interesting member, normally considered to be a harmless oral commensal, is known to cause infective endocarditis and bacteremia and a range of invasive diseases in immunocompromised patients.[1] In fact, the Health Protection Agency studies in the UK have shown that S. mitis bacteremia has surpassed that of Group A or Group B streptococci.

Furthermore, a recent genomic analysis of B6 strain of S. mitis has shown that majority of virulence factors found in its more pathogenic relative are also present in it. Some strains can be optochin sensitive, possess a capsule, and even present as diplococci.[2],[3] Thus, this alpha-hemolytic member of streptococci seems to walk on a thin line between commensalism and pathogenicity, sometimes masquerading its virulent member pneumococcus as well, by simple microscopy and biochemical tests. Keeping this dichotomy in mind, we present possibly the first case of pancreatic pseudocyst infection caused by S. mitis.

   Materials and Methods Top

A 45-year-old Indian male, an agricultural worker by occupation, presented with acute abdomen and jaundice. He also complained of swelling of the abdomen and shortness of breath. He had a history of chronic alcoholism.

Routine blood test, ultrasonography (USG), and chest X-ray were done. Blood examination showed raised leukocyte count of 190,000/μl, bilirubin level of 10.92 mg/dl (conjugated 6.84 mg/dl), and alkaline phosphatase level of 912.5 U/L. The values of amylase (403.2 U/L) and lipase (197.5 U/L) were also raised. X-ray revealed left-sided pleural effusion whereas USG showed contracted gall bladder with thick walls and a cystic SOL in the epigastric region anterior to the body of the pancreas.

He was given conservative treatment and referred to the surgical department.

A contrast-enhanced computed tomography was done. It showed a low-attenuation collapse in the left pleural sac with a patch of consolidation in the left lower lobe. The gallbladder was indistinct with foci of calcification in the neck region. A thick-walled SOL of low attenuation (20 cm × 11 cm) was observed anterior to the body of the pancreas. No solid component, septa, or calcification was seen. A diagnosis of pancreatic pseudocyst with cholelithiasis, left pleural effusion with left lower lobe consolidation, was made.

Magnetic resonance cholangiopancreatography also revealed calculus in mid-CBD (common bile duct) with proximal biliary dilatation.

Surgical intervention was done and the fluid from the pancreatic pseudocyst was sent for culture and sensitivity.

   Results Top

Gram stain from smear directly showed Gram-positive capsulated cocci in pairs. Culture on blood agar showed pure growth of capsulated Gram-positive diplococci, sensitive to optochin, suggesting the presence of pneumococcus [Figure 1]. However, it was not bile soluble and hence pure growth of colonies on blood agar was sent for Vitek. Vitek confirmed the presence of S. mitis, an alpha-hemolytic Streptococcus. Antibiotic sensitivity testing was done conforming to the CLSI guidelines.[4] The strain was found to be sensitive to erythromycin, levofloxacin, linezolid, and vancomycin, while showing resistance to ceftriaxone and cefotaxime.
Figure 1: Streptococcus mitis colony on BA showing clear zone around optochin disk

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The patient was put on total parenteral nutrition and antibiotics after surgery. Gradually, there was improvement of symptoms; jaundice decreased and finally the patient was discharged.

   Discussion Top

The physiological similarity between S. mitis and S. pneumoniae has come up in different articles. However, the genetic basis for this has been looked into recently.[5],[6],[7],[8] As mentioned earlier, it has been shown that genetic analysis of S. mitis B6 strain showed almost all the arsenals common to S. pneumoniae required to produce virulence.[2] Thus, the question arises why this similar group of arsenals in S. mitis fail to overwhelm the host immune system. The plausible explanation is absence of genes for producing a polysaccharide capsule in S. mitis B6 strain renders it vulnerable to neutrophil killing, thus taking away its virulence potential, and is a critical distinguishing feature between the two bacteria. In the same tune, it must be mentioned that studies regarding pathogenic potential of capsulated strains of S. mitis have not been thoroughly investigated. Interestingly enough, the strain causing the infection in pancreatic pseudocyst in this study was a capsulated one.

As far as morphological similarity is concerned, a tragic resemblance exists. S. mitis cells are arrow headed in shape, which under a microscope can very well look like lanceolate in shape. Moreover, they grow in pairs or in short chains.[9] Again, a trap is laid for a naïve superficial microbiological examination.

As if that is not enough to mislead a microbiologist, comes the optochin test. Classically, S. mitis are said to be optochin resistant, and in most countries, optochin susceptibility test remains the only biochemical test done to identify S. pneumoniae.[10] However, in a study, eight optochin-susceptible alpha-hemolytic (viridians) Streptococcus isolates were subjected to molecular level study. They turned out to be S. mitis, and the biochemical clue behind suspicion was their uniform bile insolubility.[3] The S. mitis strain in our study also lacked bile solubility and led us wondering about its true nature.

Thus, S. mitis, a normal oral commensal, has been known to be an opportunistic pathogen in immunocompromised patients and in those undergoing chemotherapy. In healthy children and adults, it causes bacteremia and infective endocarditis and has infrequently been reported with meningitis, eye infections, and pneumonia.

   Conclusion Top

Thus, one should be ever vigilant keeping in mind its increasing pathogenicity spectrum and its close similarity to S. pneumoniae morphologically and to a great extent biochemically, to avoid wrong diagnosis, which is due to lack of experience or sophisticated instruments.

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


Conflicts of interest

There are no conflicts of interest.

   References Top

Marron A, Carratalà J, González-Barca E, Fernández-Sevilla A, Alcaide F, Gudiol F. Serious complications of bacteremia caused by Viridans streptococci in neutropenic patients with cancer. Clin Infect Dis 2000;31:1126-30.  Back to cited text no. 1
Denapaite D, Brückner R, Nuhn M, Reichmann P, Henrich B, Maurer P, et al. The genome of Streptococcus mitis B6-what is a commensal? PLoS One 2010;5:e9426.  Back to cited text no. 2
Balsalobre L, Hernández-Madrid A, Llull D, Martín-Galiano AJ, García E, Fenoll A, et al. Molecular characterization of disease-associated streptococci of the mitis group that are optochin susceptible. J Clin Microbiol 2006;44:4163-71.  Back to cited text no. 3
Clinical and Laboratory Standards Institute. Performance Standards for Antimicrobial Susceptibility Testing; Twenty-fifth informational supplement. M100-S25. Wayne, PA: Clinical and Laboratory Standards Institute; 2015.  Back to cited text no. 4
Johnston C, Hinds J, Smith A, van der Linden M, Van Eldere J, Mitchell TJ. Detection of large numbers of pneumococcal virulence genes in streptococci of the mitis group. J Clin Microbiol 2010;48:2762-9.  Back to cited text no. 5
Kilian M, Poulsen K, Blomqvist T, Håvarstein LS, Bek-Thomsen M, Tettelin H, et al. Evolution of Streptococcus pneumoniae and its close commensal relatives. PLoS One 2008;3:e2683.  Back to cited text no. 6
Romero P, Croucher NJ, Hiller NL, Hu FZ, Ehrlich GD, Bentley SD, et al. Comparative genomic analysis of ten Streptococcus pneumoniae temperate bacteriophages. J Bacteriol 2009;191:4854-62.  Back to cited text no. 7
Siboo IR, Bensing BA, Sullam PM. Genomic organization and molecular characterization of SM1, a temperate bacteriophage of Streptococcus mitis. J Bacteriol 2003;185:6968-75.  Back to cited text no. 8
Mitchell J. Streptococcus mitis: Walking the line between commensalism and pathogenesis. Mol Oral Microbiol 2011;26:89-98.  Back to cited text no. 9
Lund E, Herichsen J. Laboratory diagnosis, serology and epidemiology of Streptococcus pneumoniae. Methods Microbiol 1978;12:241-62.  Back to cited text no. 10

Correspondence Address:
Dibyendu Banerjee
27H, Rajkrishna Street, Uttarpara - 712 258, West Bengal
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ATMPH.ATMPH_190_17

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