It is involved in attachment and adherence to host cells as well as natural competence of L. pneumophila.

Over 10% of non-group A beta-hemolytic streptococci (groups C and G) can also show sensitivity.

Pathogenicity

Severalreports stress that inappropriate antibiotics at this stagecould seriously compromise clinical outcome

eutropenic patients with VGS bacteremia.

Dextran production results in glycocalyx deposition that promotes adherence

eptococci can be isolated from the blood, blisterfluid and from cultures of the infe

acteraemia is regu-larly seen in patients with necrotizing fascii

cytokines

ultivation of non-fastidious bacteria

Despite the overall low virulence, they may cause infective endocarditis, contribute to polymicrobic abscess, and invade the bloodstream during the state of neutropenia.

Viridans streptococci represent a group of 24 currently described Streptococcus species that are nutritionally fastidious

approximately 10% of viridans streptococci are bile-esculin positive.

no enzymatic or toxigenic effect has ever been documented as a by-product of alpha hemolysis.

VGS; S. anginosus, S. mutans, and S. sanguinis

bile solubility testing

They differ from pneumococci in that they are optochin resistant and are not bile soluble.

chaining morphology

as many species do not produce any hemolysis on blood agar.

ble 2. Pathogens associated with necrotizing fasciiti

vancomycin is preferred

bacteremia

he oral mucosa is the most common portal of entry

International Journal of Orthodontia and Oral Surgery, Volume 6

Alpha-hemolytic Streptococcus species “Viridans group” streptococci, including species such as the Streptococcus mutans, mitis, and salivarius groups display alpha hemolysis.

Lincosamide for treatment of serious skin and soft-tissue staphylococcal infections

Resistance is obtained as part of a cassette of genetic information, or a transposon, that encodes resistance to multiple antibiotics.

Transposon transfer is thought to be the most likely mechanism in S pneumoniae , although point mutations also occur.

Even cefotaxime and ceftriaxone resistance has been documented

The capsule of S pneumoniae renders it resistant to phagocytosis

cariogenic

Treatment is usually with penicillin. However, strains resistant to penicillin and multiple antibiotics are rapidly emerging. A vaccine is available.

Pneumococci are distinguished from viridans streptococci by the quellung (capsular swelling) reaction, bile solubility, and optochin inhibition.

Vancomycin inhibits the second stage of cell wall synthesis in susceptible bacteria.

Binding to platelets, binding to fibrin, exopolysaccharide production, and binding to fibronectin have been identified as factors associated with virulence of viridans streptococci.

neumolysin is produced as a 52 kDa soluble protein that oligomerizes in the membrane of target cells to form a large ring-shaped transmembrane pore. The pore is 260 Å in diameter and is composed of approximately 40 monomer subunits. During its conversion from a soluble monomer to a membrane-inserted oligomer, pneumolysin undergoes a series of spectacular structural changes42. The oligomers are thought to be responsible for the cytolytic activity of the toxin and the plethora of cell-modulatory activities that are evident at sub-lytic con-centrations. These activities include: inhibition of ciliary beating on respiratory epithelium and brain ependyma; inhibition of the phagocyte respiratory burst; and induc-tion of cytokine synthesis and CD4+ T-cell activation and chemotaxis43,44. Site-directed mutagenesis has shown that pneumolysin activates the classical complement pathway independently of its cell-modulatory activity45

lmost all pneumococcal CPSs are negatively charged, which could increase their repulsion of the sialic acid-rich mucopolysaccharides that are found in mucus12

The pneumococcus resides on the mucosal surface of the upper respiratory tract

one of the common forms of pneumococcal disease, however, promote pneumococcal transmission, which implies that the virulence characteristics of the pneumococcus are prob-ably adaptations that increase its persistence within a host during colonization

Although colonization at this site seems to be asymptomatic, if the organism gains access to the normally sterile parts of the airway a rapid inflamma-tory response ensues that results in disease.

t also has a unique mode of action inhibiting the second stage of cell wall synthesis of susceptible bacteria. There is also evidence that vancomycin alters the permeability of the cell membrane and selectively inhibits ribonucleic acid synthesis.

There has been no increase in resistance to vancomycin during the past three decades.

Briefly, the organism was plated on blood Mueller-Hinton agar and incubated at 35°C in ambient air (preferred), or with CO2 if required for growth, for 20 to 24 h.

All 50 strains were susceptible to vancomycin

based on alpha-hemolysis, gram-positive reaction, coccus morphology in chains, negative catalase test, and exclusions of pneumococci and enterococci by routine biochemical tests (optochin test, bile solubility, and PYR [N,N-dimethylaminocinnamaldehyde] test).

nutritionally fastidious and mainly alpha-hemolytic on sheep blood agar

Sequencing analysis of the 16S rRNA gene has become an essential part of bacterial taxonomy

Colonies of viridans streptococci on blood agar surroundend by a wide zone of alpha-hemolysis.

clindamycin

One hundred thirty-eight strains(33.6%) were resistant to penicillin

The susceptibility rates for S. sanguis were: penicillin, 74%; amoxicillin, 84%; ceftriaxone, 94%; clindamycin, 87%, and vancomycin, 100%. The susceptibility rates for S. mitis were: penicillin, 42%; amoxicillin, 67%; ceftriaxone, 58%; clindamycin, 100%; and vancomycin, 100%. The susceptibility rates for S. milleri were: penicillin, 100%, amoxicillin. 100%; ceftriaxone, 100%, clindamycin, 100%; and vancomycin, 100%.

omorbidity was diabetes mellitus

viridans streptococcus  any of a group of streptococci with no defined Lancefield group antigens but not Streptococcus pneumoniae, usually α-hemolytic; part of the normal flora of the respiratory tract but also causing dental caries, bacterial endocarditis, and other disorders in immunocompromised hosts

Morphology: cocci in Chains

Penicillins, but resistance reported among beta hemolytic streptococci

Shows key test in the differentiation of the virdidans streptoco

A,C,G, F, none

Viridans streptococci: most strains are α-hemolytic on blood agar media, are usually neither susceptible to optochin or bile soluble.

all viridans species are PYR negative

all strains of viridans streptococci have been sensitive to vancomycin

10% of viridans streptococci are bile-esculin positive

Viridans streptococci, mutans group Streptococcus mutans (human plaque) Streptococcus cricetus (rodent plaque, human) Streptococcus downei (monkey plaque) Streptococcus ferus(rodent plaque) Streptococcus macaccae (monkey plaque) Streptococcus ratti(rodent, human plaque) Streptococcus sobrinus(human plaque) Viridans streptococci, oral groupStreptococcus salivarius (human) Streptococcus vestibularius(human) Streptococcus sanguinis(human) Streptococcus parasanguinis(human) Streptococcus gordonii(human) Streptococcus anginosus(human) Streptococcus constellatus(human) Streptococcus intermedius(human) Streptococcus mitis(human) Streptococcus oralis(human) Streptococcus crista(human) Streptococcus infantis(human) Streptococcus perois (human)

viridans Streptococcus, or of unknown identity (basically includes all cultures other than pneumococci, ß-hemolytic streptococci, and nutritionally variant streptococci), inoculate the following media. Inoculate a trypticase soy 5% sheep blood agar plate by streaking a heavy inoculum onto one-fourth of the plate and streak the remaining portion for isolated colonies. Place a vancomycin disk on the heaviest part of the inoculum, and put the plate into a candle extinction jar or a CO2 incubator for 18 to 24 h at 35C.

enicillin susceptibility cannot be assumed

biotic usage drives resistance holds true for VGS, and there are numerous studies that have shown direct correlations between both penicillin and macrolide usage and the development of resistance in VGS.

pyrrolidonylarylamidase negative, and do not grow in 6.5% NaCl, and almost all species are negative for growth on bile esculin agar.

eucine aminopeptidase positive

catalase-negative,

heterogeneous group of organisms that can be both commensal flora and pathogens in humans

GS, the rates and patterns of antimicrobial resistance vary greatly depending upon the species identification and the patient populatio

The VGS are a group of catalase-negative, Gram-positive cocci with a chaining morphology on microscopic examination.

commensal flora

VGS can cause invasive disease, such as endocarditis, intra-abdominal infection, and shock.

Conventional tests cannot identify most species of the viridans streptococci.

These bacteria can be found in the mouth, gastrointestinal tract and vagina of healthy humans,

Alpha-hemolytic streptococci cause a partial or “greening” hemolysis around the colony, associated with the reduction of red cell hemoglobin.

nonhemolytic

VGS are presumed to be uniformly susceptible to penicillin

Viridans streptococci are usually organisms of low virulence

Although little is known about the transmission of viridans streptococci, studies of S. mutans passage within families indicates that intra-family transmission is common

Viridans streptococci are the predominant species of the human oral flora and commonly inhabit other areas of the upper respiratory, gastrointestinal, and female genital tracts. Viridans streptococci are occasionally found in the skin flora.

Streptococci are Gram-positive spherical or ovoid bacteria

oral mucosa is the most common portal of entry