1) Staphylococcus aureus-

1.Staphylococcus aureus, sometimes called staph aureus, is coccal, or round-shaped, and grows in clusters.In fact, its name, broken down, means “golden cluster of grapes”.It sorta starts making sense if you look at it under a microscope - it tends to grow in sticky clusters, and it stains purple when Gram-stained due to its peptidoglycan cell wall, so it’s Gram positive and it resembles grapes..As for its “golden” color, when it’s grown on blood agar plates, the colonies have a distinctive golden-yellow color.

2..Staphylococcus aureus are Gram positive and facultative anaerobes, meaning that they can survive in aerobic and anaerobic environments.They’re non-motile and don’t form spores.

3. Staphylococci produce an enzyme called catalase which converts hydrogen peroxide to water and oxygen.

4.Other common cocci, such as streptococci and enterococci, are catalase negative so they don’t have this ability and we can use a few drops of hydrogen peroxide to differentiate them.

5.Now, a couple of other staphylococci species, like Staph epidermidis and Staph saprophyticus are also catalase positive, so to distinguish between them we can look for another enzyme that’s made by Staph aureus, called coagulase. Coagulase converts fibrinogen into fibrin.

6.So let’s say that we stir up some Staph aureus bacteria in a liquid “emulsion”, and then add a few drops of plasma which contains fibrinogen. The coagulase positive staph aureus will convert the soluble fibrinogen to sticky fibrin, which then visibly clumps up, whereas coagulase negative bacteria won’t.

7.Staph aureus is extremely common and about a quarter of the population is colonized by it, usually in their nostrils, groin, armpits, and other parts of their skin.But, most of the time it’s a normal part of our skin flora, and doesn’t cause trouble.The skin flora is a complex ecosystem of different bacterial species and occasionally, Staph aureus can begin to dominate that ecosystem.

8.In individuals that have staph aureus colonization, a number of factors like the pH, humidity, sweat levels of the skin, as well as presence of other bacteria on our skin, all affect the amount of staph aureus that’s present.If more and more Staph aureus is around on the skin, it begins to penetrate through tiny microfissures in the skin, like you get with eczema, as well as larger breaks in the skin like you might get after shaving.In fact, it’s particularly troublesome in terms of causing wound infections where there is a large break in the skin either from trauma or after a surgery.So low levels of staph aureus with intact skin leads to colonization, whereas high levels of Staph aureus with breaks in the skin lead to infections.When staph aureus invades into the skin it can lead to localized skin infections like a pimple which can evolve into a furuncle, or a boil.

9. A bunch of furuncles clustered together make a carbuncle.There can also be diffuse skin infections, like superficial impetigo which is an infection of the epidermis, or deeper-reaching cellulitis, which is an infection of the dermis and can spread over larger surfaces rapidly.If the infection goes deeper, it can develop into a subcutaneous abscess - a collection of pus that’s walled off and sometimes develops thin walls within it - called septations.

10 These abscesses can occur all over the body including in the mouth where they’re called dental abscesses, and they can develop within various organs like the liver, kidney, spleen, and brain.Now if the infection is overlying a muscle, it can spread into the muscle causing a pyomyositis.If it gets into the bone it can cause osteomyelitis, and if it gets into the joint space it can cause septic arthritis.Finally, if Staph aureus gets into the bloodstream, it can cause a septic thrombophlebitis - an infected blood clot.In addition, bacteria in the blood is called bacteremia, and it can lead to a number of serious problems.

11There’s typically a widespread immune reaction that causes the blood vessels to expand and the blood pressure to fall. The result is hypotension and poor perfusion to various organs - a process called sepsis.y.

12.Now, in addition to invading the body through the skin, Staph aureus can also enter directly into the bloodstream when a person is getting surgery or having dental work done. These events occur infrequently, but when they do come up it’s important to take precautions.For example, individuals at high risk of getting serious disease with Staph aureus - like immunocompromised individuals or those that are at risk for infective endocarditis - should be given antibiotic prophylaxis.Another property of our golden staph is its ability to create biofilm on medical implants like indwelling intravenous catheters, prosthetic heart valves, and artificial joints.The biofilm is, essentially, a layer of “slime” within which the Staph aureus live.

2) Staphylococcus epidermidis-

1) Staphylococcus epidermidis or simply Staph epidermidis can be broken down into staph which means grapes, coccus which means round shape, and epidermidis referring to the superficial layer of the skin.So, Staphylococcus epidermidis are round bacteria that tend to live clustered together as if they were grapes, and they are part of the skin normal flora even though they may also be found living on the mucosa of the gut.

2).Staph epidermidis has a thick peptidoglycan cell wall, which takes in purple dye when Gram stained - so this is a gram-positive bacteria.It’s non-motile and doesn’t form spores, and also, it’s a facultative anaerobe, meaning that it can survive in both aerobic and anaerobic environments.Staph epidermidis is catalase positive, so it makes an enzyme called catalase.

3)We can use this to differentiate Staph epidermidis from other gram positive cocci, like streptococci and enterococci, which are catalase negative.To test for this, a few drops of hydrogen peroxide are added to the colony of the suspected bacteria.So, if catalase is present, like in staph epidermidis, it makes the hydrogen peroxide dissociate into water and oxygen, causing the mixture to foam.

4)Staph epidermidis is also urease positive, meaning it produces an enzyme called urease that dissociates urea into carbon dioxide and ammonia.This can be tested by transferring a pure sample of bacteria from the culture to a sterile tube containing a mixture of “urea agar” broth and phenol red. Then, the mixture is incubated.So, with Staph epidermidis, urease does it’s thing, making urea dissociate into carbon dioxide and ammonia.Ammonia then makes the mixture change color from orange-yellow to bright pink.This doesn’t happen with urease negative Gram-positive cocci, like Streptococcus pneumoniae or Enterococcus faecalis.

5)Furthermore, unlike many other Staphylococcus species, Staph epidermidis and its close relative, Staph saprophyticus, are both coagulase negative, meaning they don’t produce an enzyme called coagulase.Testing for coagulase is done by transferring a colony of the suspected bacteria in test tube containing fibrinogen-rich plasma.Coagulase-positive bacteria, like Staph aureus, convert the soluble fibrinogen into sticky fibrin, which then visibly clumps up.With coagulase negative species, like Staph epidermidis or Staph saprophyticus, the fibrin doesn’t clump up.

6)Finally, to distinguish Staph epidermidis from Staph saprophyticus, the novobiocin test is done.This is when a disk imbued with Novobiocin, an antibiotic, is added to the culture.

7)Staph epidermidis is novobiocin sensitive, so the colonies will die off, whereas Staph saprophyticus is novobiocin resistant, so the colonies remain intact.

8)Alright, now, Staph epidermidis is actually the most dominant bacteria on the human skin.

9)It colonizes mostly the scalp, the face, the nasal cavities and the axillae, where it lives as an innocent commensal without causing any harm.

3).Staphylococcus saprophyticus-

1)With Staphylococcus saprophyticus, sometimes called Staph saprophyticus, “staph” means grapes, “coccus” means round-shape, while “saprophyticus” refers to organisms that grow on decaying organic material.

So, Staphylococcus saprophyticus are round bacteria that tend to live in grape-like clusters, and are commonly found on contaminated meat products.

2.Staph saprophyticus has a thick peptidoglycan cell wall, which takes in purple dye when Gram stained - so this is a gram-positive bacteria.

3.It’s non-motile and doesn’t form spores, and also, it’s a facultative anaerobe, meaning that it can live with or without oxygen.Staph saprophyticus is catalase positive, so it makes an enzyme called catalase.

4.We can use this to differentiate Staph saprophyticus from other gram positive cocci, like streptococci and enterococci, which are catalase negative.To test for this, a few drops of hydrogen peroxide are added to the colony of the suspected bacteria.So, if catalase is present, like in staph saprophyticus, it makes hydrogen peroxide dissociate into water and oxygen, making the mixture foam.

5. Staph saprophyticus is also urease positive, meaning it produces an enzyme called urease that dissociates urea into carbon dioxide and ammonia.This can be tested by transferring a pure sample of bacteria from the culture to a sterile tube containing a mixture of “urea agar” broth and phenol red. Then, the mixture is incubated.So, with Staph saprophyticus, urease makes urea dissociate into carbon dioxide and ammonia.Ammonia then makes the mixture change color from orange-yellow to bright pink.

6.This doesn’t happen with urease negative Gram-positive cocci, like Streptococcus pneumoniae or Enterococcus faecalis.

7.Furthermore, unlike many Staphylococcus species, Staph saprophyticus and its close relative, Staph epidermidis, are both coagulase negative, meaning they don’t produce an enzyme called coagulase.

8.Testing for coagulase is done by transferring a colony of the suspected bacteria in test tube containing fibrinogen-rich plasma.Coagulase-positive bacteria, like Staph aureus, convert the soluble fibrinogen into sticky fibrin, which then visibly clumps up.With coagulase negative species, like Staph saprophyticus or Staph epidermidis, the fibrin doesn’t clump up.Finally, to distinguish Staph saprophyticus from Staph epidermidis, the novobiocin test is done.This is when a disk imbued with Novobiocin, an antibiotic, is added to the culture.

4) Streptococcus agalactiae-1)sometimes called Strep agalactiae, strepto means a chain, coccus means round shape, and agalactiae literally means “no milk”.So, Strep agalactiae refers to the round bacteria that grow in chains and that was previously known to infect cattle, resulting in reduced milk production.Later on, Strep agalactiae was found to also be a human potential pathogen responsible for a number of infections that most commonly affect pregnant women and newborns.Strep agalactiae are also called Group B Strep – GBS - in Lancefield classification developed by an American microbiologist Rebecca Lancefield.

2)Strep agalactiae has a thick peptidoglycan cell wall, which takes in purple dye when Gram stained - so this is a gram-positive bacteria.

3)It’s non-motile and doesn’t form spores, and also, it’s a facultative anaerobe, meaning that it can survive in both aerobic and anaerobic environments.

4)Now, a particular trait of Streptococcus species is that they are catalase negative, meaning they do not produce an enzyme called catalase.This is unlike other common gram positive cocci, like Staphylococcus, which are catalase positive.

5)When cultivated on a medium called blood agar, Strep agalactiae colonies cause beta hemolysis, also called complete hemolysisWith the bacitracin test, a disk of bacitracin is added to the blood agar.

6)Strep agalactiae is bacitracin resistant, so the colonies remain intact, whereas Strep pyogenes is bacitracin sensitive, so the colonies die off.

7)With the CAMP test, Strep agalactiae is grown with Staphylococcus aureus on the same blood agar.

8)Both these bacteria are beta-hemolytic, but Strep agalactiae makes a substance called CAMP factor, which enhances the action of staphylococcal beta-hemolysin.This results in greater areas of beta-hemolysis where these colonies cross each other on the blood agar plate.Finally, the hippurate test is based on the fact that Strep agalactiae is the only hippurate positive Strep, because it produces an enzyme called hippuricase or hippurate hydrolase.

9)To test for this, a colony of bacteria is transferred from the culture to a test tube containing a special hippurate medium, and incubated for two hours. Then, a few drops of a substance called ninhydrin are added to the mix.With Strep agalactiae, hippuricase converts hippurate to glycine and benzoic acid - and glycine reacts with ninhydrin, making the mix turn deep blue - or positive.

10)Ok, now, Strep agalactiae has a number of virulence factors, that are like assault weaponry that help it attack and destroy the host cells, and evade the immune system.First, Strep agalactiae is encapsulated, meaning it’s covered by a polysaccharide layer called a capsule.The capsule also has pilli, which are hair-like extensions that help the bacteria attach to a host cell.Additionally, the capsule is rich in sialic acid, which is a substance that can also be found in human cells.

So inexperienced immune cells, like that of a newborn, may confuse Strep agalactiae with self cells, allowing it to survive inside the body.And finally, Strep agalactiae makes beta-hemolysin, which destroys the host’s tissues and causes hemolysis, meaning it destroys red blood cells.That’s because Strep agalactiae makes a toxin called beta-hemolysin, that causes complete lysis of the hemoglobin in the red blood cells, making them blood agar change color from red to transparent yellow around the colonies.However, other Streptococcus species, like Strep pyogenes, are also beta hemolytic.So to identify Strep agalactiae specifically, the bacitracin test, the hippurate test, or the CAMP test can be done.

5)Streptococcus pyogenes-Streptococcus pyogenes, sometimes called Strep pyogenes, can be broken down into “strepto” which means chain, “coccus”, which refers to round shape, “pyo” which means pus, and “genes” which refers to forming.So, Strep pyogenes are round bacteria that grow in chains, responsible for a number of infections that often present with pus. Strep pyogenes are also called Group A Strep – GAS - in Lancefield classification developed by American microbiologist Rebecca Lancefield.

2)Ok now, Strep pyogenes has a thick peptidoglycan cell wall, which takes in purple dye when Gram-stained - so this is a gram-positive bacteriat.

3)It’s non-motile and doesn’t form spores, and it’s also a facultative anaerobe, meaning it can survive in both aerobic and anaerobic environments.Finally, Strep pyogenes is catalase negative, meaning it doesn’t make an enzyme called catalase.

4)However, unlike other common cocci like Enterococci, Strep pyogenes is pyrrolidonyl arylamidase positive, because it makes an enzyme called L-pyrrolidonyl arylamidase.

5)To test for this, a small sample is taken from a suspected bacterial colony, and then inoculated to a disk pad that’s embedded with pyrrolidonyl beta naphthylamide - another joy of a word.With Strep pyogenes, pyrrolidonyl arylamidase hydrolyzes pyrrolidonyl beta—naphthylamide to produce beta-naphthylamide.try saying that 3 times fast! Finally, another reagent called N-methylamino-cinnamaldehyde is added to the disk, and it reacts with beta—naphthylamide, resulting in a bright red color that confirms Strep pyogenes is pyrrolidonyl arylamidase positive.

6)When cultivated on a medium called blood agar, Strep pyogenes colonies cause beta-hemolysis, also called complete hemolysis. That’s because Strep pyogenes makes toxins known as streptolysins, which hydrolyze the hemoglobin in red blood cells to transparent yellow color byproducts.

7)But some other Streptococcus species, like Strep agalactiae, are also beta-hemolytic. So a bacitracin test is done to distinguish Strep pyogenes.That’s when a disk of bacitracin is added to the blood agar. Strep pyogenes is bacitracin sensitive, so the colonies die off, whereas with Strep agalactiae, the colonies remain intact.

8)Now, Strep pyogenes has a number of virulence factors, that are like assault weaponry that help it attack and destroy the host cells, and evade the immune system.So first, Strep pyogenes is encapsulated, meaning it’s covered by a polysaccharide layer called a capsule.And on the capsule, there are adherence proteins such as lipoteichoic acid, Streptococcus fibronectin binding protein - or Sfbl for short, and M protein, which help Strep pyogenes attach to the host cells, like those in the skin or the pharyngeal mucosa. Then, Strep pyogenes uses toxins like hyaluronidase, which destroys hyaluronic acid, a cement substance that keeps cells of the connective tissues and blood vessels tightly linked.

9)Destruction of hyaluronic acid results in local inflammation, and enables the bacteria to spread to the bloodstream.In the bloodstream, Strep pyogenes uses streptolysin O and S, which are toxins that cause hemolysis, or red blood cell destruction.

10)It also uses erythrogenic toxins, that are also called Streptococcal Pyrogenic Exotoxins, or Spe for short, which come in 3 flavors: SpeA, SpeB, and SpeC.

11)This leads to increased hemolysis in the dermal and submucosal blood capillaries. What is more, SpeA and SpeC are superantigens, meaning they don’t need to be eaten up and processed by an antigen-presenting cell such as a macrophage to generate an immune response from T-cells.

12)Instead, they interact immediately with the class II MHC molecule on the surface of the macrophage, forming a superantigen-MHC complex, which then interacts with the T-cell receptor and stimulates up to 30% of the entire T- cell population.This is 300 times powerful the conventional antigens, and it stimulates the release of a whole bunch of inflammatory cytokines.Specifically, this is called a cytokine storm, and it can result in toxic shock syndrome or TSS, which happens when a such cytokine storm triggers widespread systemic vasodilation, making blood pressure drop, which leads to poor perfusion of vital organs.

13)From the bloodstream, strep pyogenes bacteria can spread to other organs, like the lungs, causing pneumonia or lung abscesses, or the heart, where they form clumps called vegetations on the heart valves, causing infective endocarditis.Alternatively, if they spread to central nervous system, they can cause brain abscesses, or meningitis.Surprisingly, despite all that powerful arsenal, Strep pyogenes can actually peacefully colonize the skin, the mucosa of the pharynx or throat, the femal reproductive part , and the rectum.It doesn’t do any harm so long as the immune system keeps them in check, restricting their growth and preventing them from spreading somewhere else in the body.

14)Problems arise in individuals with weaker immune systems, like infants and the elderly. Other immune-weakening conditions include HIV infection, diabetes, or a malignancy.In these cases, Strep pyogenes usually gets in the bloodstream through a breach on the skin, a mucosal laceration, or following surgery. Most often, Strep pyogenes causes strep pharyngitis also called strep throat, which is the inflammation of the pharyngeal mucosa and tonsils.Strep pharyngitis may also be associated with scarlet fever, which is when intracapillary hemolysis results in a bright-red skin rash.When Strep pyogenes infects the epidermis, it causes impetigo, which are superficial skin lesions that look like honey clusters.

6).Streptococcus pneumoniae- 1)Streptococcus pneumoniae or Strep. pneumoniae can be broken down into strepto- which means chain, -coccus, which means round shape, and pneumoniae, which refers to the fact that it causes pneumonia - no surprises there.So, Strep pneumoniae are round bacteria that tend to grow in chains, usually in lancet-looking pairs called diplococci.They’re the most common cause of community-acquired pneumonia - meaning pneumonia acquired somewhere other than the hospital.

2)Strep pneumoniae has a thick peptidoglycan cell wall, which takes in purple dye when Gram stained - so this is a gram-positive bacteria.

3)They’re non-motile and don’t form spores, and also, they’re facultative anaerobes, meaning that they can survive in both aerobic and anaerobic environments.Finally, they’re catalase negative - which means they don’t produce an enzyme called catalase.

4)Ok, now, when cultivated on a medium called blood agar, Strep pneumoniae colonies cause alpha hemolysis, also called green hemolysis, because they produce hydrogen peroxide, which partially oxidizes initially red hemoglobin in the blood agar to green methemoglobin.

5)Other Streptococcus species, like Strep viridans, are also alpha hemolytic.So, an optochin test is done to distinguish Strep pneumoniae. That’s where a few drops of optochin are added to the culture.

6)Strep pneumoniae are optochin sensitive, meaning the bacteria dies after adding optochin, whereas Strep viridans are optochin resistant - meaning they survive.

7)Now, Strep pneumoniae has a number of virulence factors, that are like assault weaponry that help it attack and destroy the host cells, and evade the immune system.So first, Strep pneumoniae is encapsulated, meaning it’s covered by a polysaccharide layer called a capsule.The capsule has pili and fimbriae, which are hair-like extensions that help it attach to a host cell.Once attached to a mucosal surface like in the nasopharynx or the middle ear, Strep pneumoniae can multiply and produce biofilms.

8)A biofilm is basically a layer of goop-like material made of exopolysaccharides or EPS, within which Strep pneumoniae bacteria live and reproduce.Comparing a biofilm to strawberry jam, the seeds would be the bacteria and the rest of the jam would be the EPS.

9)The bacteria in the biofilm hide from the host's immune system and antibiotics, and even exchange resistance genes. Sneaky...As if that wasn’t enough, Strep pneumoniae also produces toxins, and the most important ones are IgA protease and pneumolysin.IgA protease destroys Immunoglobulin A or IgA, which normally binds invading bacteria, so neutrophils can destroy them. That’s like a computer virus first taking over the antivirus software!And then there’s pneumolysin, which activates the host’s complement system – a set of plasma proteins involved in immunity.This results in a local inflammation which not only destroys the bacteria, but also the host tissues - like alveolar capillaries and pneumocytes.

10)And here’s the most interesting part. Strep pneumoniae can actually peacefully colonise the nasal cavities and sinuses, where it doesn’t do any harm so long as the immune system keeps them in check, restricting their growth and preventing them from spreading somewhere else in the body.Problems arise in individuals with weaker immune systems, like infants and the elderly.Other immune-weakening conditions include an HIV infection, diabetes, malignancy, or alcohol abuse.

11)Additionally, some toxic compounds in cigarette smoke can weaken the local respiratory defense mechanisms, making individuals more susceptible to Strep pneumoniae infections.Strep pneumoniae can cause a number of infections.One example is rhinosinusitis, which is when the mucous membrane lining the nose and the paranasal sinuses gets inflamed, resulting in fever, facial pain, and headaches.Sometimes, when the walls of the paranasal sinuses are very thin, and Strep pneumoniae can get into the cranial cavity - resulting in meningitis.With meningitis, people develop a fever, neck stiffness, and a headache.Strep pneumoniae can also invade the Eustachian tube, and cause an infection of the middle ear - or otitis media, which causes pain and an earache.Chronic otitis media can spread to the mastoid antrum behind the ear, where it causes mastoiditis.

7)Enterococcus-1)With Enterococcus, entero- refers to the intestines, while -coccus means round shape.So Enterococcus is a genus of round bacteria that commonly colonizes the gut of humans and animals.

2)Enterococcus is also called Group D streptococcus in Lancefield classification developed by an American microbiologist Rebecca Lancefield.

3)There are two species that can cause infections in humans and these are Enterococcus faecalis, amounting for the majority of infections, and Enterococcus faecium, which causes disease more rarely.

4)Now, looking at an individual bacterium, Enterococcus has a thick peptidoglycan cell wall, which takes in purple dye when Gram stained - so this is a gram-positive bacteria.When there’s more of them, Enterococci grow in short chains, usually in pairs.

5)They’re non-spore forming, facultative anaerobes, meaning that they can survive in both aerobic and anaerobic environments and catalase negative, which means they don’t produce an enzyme called catalase.

6)Enterococci also can tolerate extreme environmental conditions including high sodium chloride concentrations, high pH and even high temperatures.They can survive at 60 degrees Celsius for up to 30 minutes!

7)Ok, now, enterococcus is pyrrolidonyl arylamidase positive, because it makes an enzyme called L-pyrrolidonyl arylamidase.To test for this, a small sample is taken from a suspected bacterial colony, and then inoculated to a disk pad that’s embedded with pyrrolidonyl beta naphthylamide - another joy of a word.With Enterococcus, pyrrolidonyl arylamidase hydrolyzes pyrrolidonyl beta-naphthylamide to produce beta-naphthylamide.Try saying that 3 times fast! Finally, another reagent called N-methylamino-cinnamaldehyde is added to the disk, and it reacts with beta-naphthylamide, resulting in a bright red color that confirms Enterococcus is pyrrolidonyl arylamidase positive.

8)Now, most commonly, Enterococci are gamma hemolytic which means that when cultivated on blood agar they don’t induce hemolysis, so the agar under and around the colony remains unchanged.

9)But sometimes, they can induce alpha hemolysis, also called partial hemolysis, which means that the agar under the colony turns dark and greenish.Finally, it can grow on bile salts, which is very useful to differentiate Enterococci from non-enterococcus group D streptococci.This can be demonstrated with the Bile-Esculin test, that can be done on tubes or plates and uses a medium that contains peptone, beef extract, bile, esculin, ferric citrate and agar.So, in the presence of bile, Enterococcus can hydrolyze esculin into glucose and esculetin.Then, esculetin reacts with the ferric ions supplied by ferric citrate and form a black diffusible complex.So, after 24 to 48 hours, Enterococci cause a diffuse blackening of more than half of the tube or black halos around colonies on plates.

10)Now, Enterococci are opportunistic pathogens which causes a wide variety of hospital-acquired infections, particularly in people with underlying cardiovascular conditions, or in people with immunosuppressive conditions, like an HIV infection.

11)They also cause disease in people who have been hospitalized for long periods of time and received multiple antibiotic treatments, or in people with indwelling medical devices such as central venous catheters or urinary catheters.Under these circumstances, Enterococcus mainly causes infective endocarditis - in fact, Enterococcus is the second most common cause of infective endocarditis overall.

8) S. viridans- 1)The term “streptococcus viridans”, refers to five groups of Streptococci that include Streptococcus anginosus group, mitis group, sanguinis group, salivarius group, and finally the mutans group.And each of these groups has approximately 30 species that can cause disease in humans.So the more correct term would be “viridans streptococci”, to reflect that there’s more than one of them.

2)Generally speaking, viridans streptococci can’t be assigned to a Lancefield group based on their cell wall antigens.

3)However, in the Streptococcus anginosus group, some species can be assigned to Lancefield groups A, C, F or G.

4)Now, viridans streptococci have a thick peptidoglycan cell wall, which takes in purple dye when Gram stained - so they’re gram-positive bacteria.

5)They’re also catalase negative - which means they don’t produce an enzyme called catalase. Ok, now, when cultivated on a medium called blood agar, viridans streptococci colonies cause alpha hemolysis, also called green hemolysis, because they produce hydrogen peroxide, which partially oxidizes initially red hemoglobin in the blood agar to green methemoglobin.

6)One way to remember this is to think that 'viridans’ means ‘green’ in Latin.Some species in the Streptococcus anginosus group, however, can also be beta-hemolytic or nonhemolytic.These guys are special little snowflakes.Now, other Streptococcus species, like Streptococcus pneumoniae, are also alpha hemolytic.So, an optochin test is done to distinguish them.That’s where an optochin-containing paper disc is placed on a plate of blood agar that has been inoculated with the bacteria.

7)With Strep pneumoniae, the growth of the bacteria is inhibited in the zone that surrounds the optochin disc, meaning that Strep pneumoniae is optochin sensitive.On the flip side, viridans streptococci are optochin resistant - meaning there’s no inhibition of the growth around the optochin disc.

8)Another test that can be used to distinguish Strep viridans from Strep pneumoniae is the bile solubility test, which can be done in a test tube, or more commonly, by dripping drops of bile on bacterial colonies.Strep pneumoniae is bile soluble, meaning that the bile salts will promote the lysis of the bacteria; whereas viridans streptococci are bile insoluble, or bile resistant.

Finally, viridans streptococci also lack the polysaccharide-based capsule typical of Streptococcus pneumoniae.

9)Viridans streptococci are commensal organisms that reside in the oropharynx, epithelial surfaces of the oral cavity, teeth, skin, the gastrointestinal and genitourinary tract.

So, they live alongside their host without causing harm unless there’s a change in their environment.

10)Inside the mouth, viridans streptococci like Streptococcus mutans, and Streptococcus mitis adhere to tooth enamel with the help of a dextran polysaccharide, and aggregate, forming dental plaques which can lead to dental caries, dental caries, and gum disease.

In contrast, Streptococcus sanguinis promotes dental health by inhibiting the growth of Streptococcus mutans.

However, when dental work is done, like a tooth extraction, viridans streptococci can enter the bloodstream and cause bacteremia.

From there, they can make their way to the heart, where they may stick to a thrombus - an aggregate of platelets, red blood cells, and a mesh of cross-linked fibrin protein - on a damaged or prosthetic heart valve and cause subacute valve endocarditis.

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