Streptococcus viridans characteristics, life cycle and symptoms

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Philip Kelley

Streptococcus viridans It is a heterogeneous group composed of about 20 species of streptococcal bacteria that are commensal, mainly, of the oropharyngeal cavity and genital tract of mammals, of low pathogenicity and devoid of Lancefield antigens..

Because it is a pseudotaxonomic name, many authors prefer to use the terms viridans group streptococci (SGV), viridian streptococci, or viridian streptococcal species..

Photomicrograph of the bacterium Streptococcus viridans grown in a blood culture

In the past, the terminology applied to SGVs was confusing and inconsistent. The term viridans refers to the fact that some of the members of the group are α-hemolytic that produce a green color on blood agar plates, however other SGVs are non-hemolytic..

Although SGVs are commensal of the oral cavity, upper respiratory tract, female genital tract, the entire gastrointestinal tract, and even the skin of humans, they can cause significant infections when the oral mucosa is significantly damaged and the mechanisms of defense are engaged.

Article index

  • 1 Taxonomy
  • 2 Biological and physiological characteristics
  • 3 Life cycle
  • 4 How it is spread and symptoms
    • 4.1 Mouth infections
    • 4.2 Neonatal infections
  • 5 Treatment
  • 6 References

Taxonomy

One of the first attempts to classify SGVs was made in 1906 by Andrewes and Horder, who first described the species, named by them, Streptococcus mitis, S. salivarius and S. anginosus..

Today, it has been recognized that the last of these species actually formed a heterogeneous group with at least four other species (Streptococcus milleri, S. constellatus, S. intermedius and the S. milleri group).

In the 1970's, two different classification schemes were proposed:

That of Colman and Williams, who suggested the separation into five species: Streptococcus mutans, S. milleri, S. sanguis, S. salivarius and S. mitior, which was followed by European researchers.

That of Facklam, which recognized 10 physiological species (Streptococcus sanguis I and II, S. mitis, S. salivarius, S. mutans, S, uberis, S, acidominimus, S. morbillorum, S. anginosus-constellatus and S. MG- intermedius), followed by American researchers.

Today, the ability to make comparisons of genetic material has allowed taxonomists to classify bacteria on the basis of not only phenotypic but also genetic similarities..

It is currently preferred to define species as a group of genetically related bacteria. Based on these criteria, at least 19 species included in six major groups are recognized: Streptococcus mutans group, S. salivarius group, S. anginosus group, S. mitis group, S. sanguinis group and S. bovis group. 

Biological and physiological characteristics

SGVs are chain-type coco-type bacteria, gram-positive catalase-negative, leucine aminopeptidase positive, pyrrolidonylarylamidase negative and do not grow on bile esculin agar or 6.5% NaCl (4).

They inhabit as commensals of the oropharyngeal cavity, genital tract of mammals, where their presence and physiology lead to the acidification of their nearby environment, thus hindering the colonization and infection of such sites by other pathogens, for example Haemophilus influenza..

S. salivarius has been shown to protect humans from invasion of the mucosa of the upper respiratory tract by Candida albicans, the fungus responsible for candidiasis.

Lifecycle

SGVs reproduce asexually by binary fission. The acquisition of SGV by humans begins from the moment of their birth.

Colonization by microorganisms originates from the mother's vagina, the mother's upper respiratory tract, milk or water that the baby ingests. It can also come from the saliva of individuals close to the baby.

The mouth of a newborn is practically sterile, however, with the first feedings, the mouth is regularly inoculated with microorganisms, including SGV.

By one month of birth, virtually all children are colonized by at least one species of SGV.

Once the new being is colonized, the SGVs begin to grow and reproduce until reaching an equilibrium in which they are generally not pathogenic, however, if the appropriate conditions are established, such as immunocompromised states of the host, they can acquire high levels of pathogenicity..

How it spreads and symptoms

SGVs are commensals of mammals where they can live without causing damage, but in case of infections in the mucous membranes, in immunocompromised states and in cases where they enter the bloodstream, they can become highly pathogenic.

SGVs are more abundant in the mouth and main components of dental plaque.

Mouth infections

One of the members of the viridans group, S. mutans, is the cause of dental caries in most cases and populations, and is involved in the pathogenesis of certain cardiovascular diseases, being the most prevalent bacterial species detected in valve tissues. cardiac excised.

Others may be involved in other oral or gingival infections, such as pericoronitis. They are the most common cause of subacute bacterial endocarditis, and it occurs when bacteria enter the bloodstream through placement of access routes or any dental, respiratory tract, or gastrointestinal tract surgical procedure..

Neonatal infections

SGVs have been identified in cases of neonatal infections and are responsible for bacteremia in patients with neutropenia, as well as spontaneous bacterial peritonitis in terminal patients with liver disease.

Symptoms will vary depending on the SGV species or species involved and the type of infection, from acute pain in teeth with cavities (S. mutans), to abdominal pain, ileus, fever and encephalopathy in the case of peritonitis spontaneous bacterial.

Subacute endocarditis can manifest itself through moderate fevers, weight loss, anemia, rashes, excessive sweating, and other symptoms that can make it difficult to detect and even be mistaken for viral syndromes and other trivial diseases..

Some neonatal bacterial infections can be asymptomatic and, if not detected and treated in time, lead to sepsis, meningitis or endocarditis.

Treatment

The effects of (S. mutans) can be prevented with good oral hygiene and mechanical cleaning. Other more serious infections can be treated with different antimicrobial agents, such as ciprofloxacin, levofloxacin and cefuroxime, cefotaxime and doxycycline..

Due to the resistance of SGVs to a wide variety of antimicrobial agents, susceptibility to penicillin cannot be assumed.

References

  1. Nakajima T., Nakanishi S., Mason C., Montgomery J., Leggett P., Matsuda M., and others. Population structure and characterization of viridans group streptococci (VGS) isolated from the upper respiratory tract of patients in the community. The Ulster Medical Journal. 2013; 82 (3), 164-168.
  2. Viridans streptococci. On Wikipedia. Retrieved on October 17, 2018 from en.wikipedia.org.
  3. Tunkel A., Sepkowitz A. Infections caused by viridans streptococci in patients with neutropenia. Emerging Infections. 2002; 34, 1524-1529.
  4. Menon T. Understanding the viridians group streptococci: Are we there yet? Indian Journal of Medical Microbiology. 2016; 34: 421-6.
  5. Coykendall A. Classification and Identification of the Viridans Streptococci. Clinical Microbiology Reviews. 1989; 2 (3), 315-328.
  6. Dhotre S., Suryawanshi N., Selkar S., Nagoba B. Viridans group streptococci and the oral ecosystem. European Journal of General Medicine. 2015; 13 (2), 145-148.
  7. Streptococcus mutans. On Wikipedia. Retrieved on October 17, 2018 from en.wikipedia.org.
  8. Bert F., Valla D., Moreau R, Nicolas-Chanoine M.H., Viridans group streptococci causing spontaneous bacterial peritonitis and bacteremia in patients with end-stage liver disease. Liver Transplantation. 2008; 14, 710-711.
  9. Heffner J. Extracardiac Manifestations of bacterial endocarditis. The Western Journal of Medicine. 1979; 131, 85-91.
  10. Molinaro J., Cohen G., Saudek K. 2014. Streptococcus infection in a newborn. Wisconsin Medical Journal. 2014; 113 (5), 202-203.

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