Streptococcus agalactiae (Group B Strep)

Definitions & Key takeaways

Streptococcus agalactiae, also known as group B streptococcus, is a gram-positive, beta-hemolytic, catalase-negative, and bacitracin-resistant bacterium, which can cause several infections in humans. Most frequently, Streptococcus agalactiae causes neonatal infections like pneumonia, sepsis, meningitis, and septic arthritis. It can also cause chorioamnionitis or cystitis in pregnant females. Treatment involves antibiotics like penicillin G or ampicillin, or Cefazolin and Vancomycin. To prevent Streptococcus agalactiae infections in neonates, intrapartum antibiotic prophylaxis can be administered to vaginally colonized pregnant females.

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With Streptococcus agalactiae 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.
Ok now, a little bit of microbe anatomy and physiology. Strep agalactiae 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.
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. When cultivated on a medium called blood agar, Strep agalactiae colonies cause beta hemolysis, also called complete hemolysis.
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.
With the bacitracin test, a disk of bacitracin is added to the blood agar. Strep agalactiae is bacitracin resistant, so the colonies remain intact, whereas Strep pyogenes is bacitracin sensitive, so the colonies die off.
With the CAMP test, Strep agalactiae is grown with Staphylococcus aureus on the same blood agar. 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.
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.
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.Surprisingly, Strep agalactiae is very common to a level that up to thirty percent of healthy adults are colonized by it, without causing any disease at all.
They mostly colonize the gastrointestinal tract and the vagina. Problems arise in people with a weakened immune system, like newborns, pregnant women and adults with underlying diseases like diabetes mellitus, malignancy, or a preexisting infection like HIV.
Additionally, since the spleen plays an important role in immunity against encapsulated bacteria, Strep agalactiae infections are more common in people who’ve had a splenectomy, meaning their spleen was surgically removed, or in those with sickle cell disease who have functional asplenia.Strep agalactiae can cause a number of infections.
In pregnant women who are colonized with Strep agalactiae, bacteria can ascend from the vagina, through the cervix and get right into the uterus.
From here they can infect the fetal membranes, namely the chorion and amnion, causing chorioamnionitis. When this happens, these membranes can get damaged and then rupture before delivery time, resulting in a miscarriage or a premature delivery.
Sometimes the infection can even spread to the fetus itself, causing intrauterine death. Alternatively, Strep agalactiae can get from the vagina on the perineum, and make their way up the urethra, causing cystitis - which is the inflammation of the urinary bladder.
In pregnant females who are colonized with Strep agalactiae, there’s also a risk that they’ll pass the bacteria to the newborn during natural childbirth.
In newborns, Strep agalactiae is most likely to go down their airways, descend down the respiratory tracts right into the lungs.
This can cause inflammation of the lung tissue, or pneumonia. Occasionally, Strep agalactiae can destroy the baby’s alveolar lining with their beta-hemolysin, and break through the alveoli-capillary wall to get straight into the bloodstream, what’s known as bacteremia.
Bacteremia can cause neonatal sepsis, which is when bacteria trigger a widespread immune reaction that causes vasodilation, hypotension, and hypoperfusion of the baby’s vital organs.
Alternatively, bacteria from the blood can cross the blood-brain barrier, and migrate into the CSF, causing neonatal meningitis.
Less likely, but possible: the bacteria can also travel down the bloodstream to the joints, causing septic arthritis. Treatment for Strep agalactiae requires antibiotics like Penicillin G and Ampicillin.
For penicillin-resistant strains, or in individuals who are allergic to penicillins, Cefazolin or Vancomycin.No vaccine for Strep agalactiae is currently available, so the only way to prevent infection in the newborn is to give colonized mothers intrapartum antibiotic prophylaxis, meaning antibiotics are given a couple of hours before delivery.
##SummaryAlright, as a quick recap, Strep agalactiae, is a gram-positive round bacteria that tend to live in chains. It is beta-hemolytic, non-motile, non-spore forming, catalase negative, hippurate positive, bacitracin-resistant and CAMP positive.
This bacteria can colonize the gastrointestinal tract and vagina asymptomatically. Most frequently, it causes neonatal infections like pneumonia, sepsis, meningitis, and septic arthritis.
But it can also cause chorioamnionitis or cystitis in pregnant females. Treatment relies on penicillin G or ampicillin, but Cefazolin and Vancomycin may be used as alternatives.
To prevent Strep agalactiae infections in neonates, intrapartum antibiotic prophylaxis can be administered to vaginally colonized pregnant