Serratia marcescens

Definitions & Key takeaways

Serratia is a genus of gram-negative, facultatively anaerobic, endospore-forming, rod-shaped bacteria of the Enterobacteriaceae family. It is known to cause a variety of infections, such as urinary tract infections, pneumonia, bacteremia, and other forms of nosocomial infections.

The symptoms of a Serratia marcescens infection can vary depending on the type of infection but may include fever, pain, redness, swelling at the site of the infection, and other symptoms. Serratia infections can be diagnosed by identifying the bacteria in culture from blood, sputum, urine, or CSF and are treated with antibiotics like aminoglycosides, antipseudomonal beta-lactams, fluoroquinolones, and carbapenems.

Watch video only
Serratia marcescens is a Gram-negative bacteria which belongs to a family of bacteria called the Enterobacteriaceae. Now, the genus consists of at least 20 species, of which eight are known to have caused infections in humans, with Serratia marcescens being the main human pathogen.
Serratia marcescens is widely distributed in water, soil and plants and it causes a variety of hospital-acquired infections.
Now, Serratia marcescens has a thin peptidoglycan layer, so it doesn’t retain the crystal violet dye during Gram staining.
Instead, like any other Gram-negative bacteria, it stains pink with safranin dye. And since it’s a Gram-negative bacillus, it looks like a little pink rod under the microscope.
Ok, now Serratia marcescens is motile and also facultative anaerobic which means it can survive in both aerobic and anaerobic environments.
It’s urease positive which means it can produce 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 Serratia marcescens, urease makes urea dissociate into carbon dioxide and ammonia.
Ammonia then makes the mixture change color from orange-yellow to bright pink. Also, it’s catalase positive which means it can produce an enzyme called catalase.
To test for this, a few drops of hydrogen peroxide are added to the colony of the suspected bacteria. So, if catalase is present, it makes the hydrogen peroxide dissociate into water and oxygen, causing the mixture to foam.
Furthermore, it produces another three enzymes, DNase, lipase, and gelatinase, which are unique to Serratia and this can help easily differentiate it from other Enterobacteriaceae.
Finally, Serratia marcescens grows well on MacConkey agar which is a medium that contains a pH sensitive dye and lactose.
This medium helps identify whether Gram-negative bacteria are lactose fermenters or not. Some bacteria, like Klebsiella, Enterobacter and Escherichia coli can ferment lactose, which results in the production of acid, that makes the pH sensitive dye turn pink - so their colonies will be pink.
Others, like Salmonella, Yersinia and Shigella can’t ferment lactose so their colonies will be colorless. Now, Serratia marcescens and also Citrobacter are slow lactose fermenters, so they are a bit lazy, but eventually ferment lactose.
So at first, the colonies appear colorless but 48 hours later, they turn pink. Finally, some strains of Serratia marcescens make a characteristic red pigment, called prodigiosin, that is typically found staining showers, toilet bowls, and around wetted tiles.
Production of this pigment can lead to the formation of red colonies on agar, if the plate is incubated at 25 degrees Celsius.
Ok, now Serratia marcescens has very few notable virulence factors such as fimbriae to attach to host cells and hemolysins which cause formation of tiny holes in the cell membrane, leading to cell damage.
However, it can form adherent biofilms on medical equipment such as respiratory equipment, intravenous and urinary catheters and contact lenses.
A biofilm is basically a layer of “slime” made of exopolysaccharides or EPS, within which Serratia 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.
Biofilms make it difficult for antibiotics to reach the bacteria, so the infection is more difficult to treat. So in hospitalized individuals, it can cause a number of hospital-acquired infections.
And the risk is higher in immunocompromised individuals, like those who are HIV-positive, or have an underlying condition like diabetes or malignancy.
So, in people who are mechanically ventilated, it can cause pneumonia. In those with urinary catheters, it may cause urinary tract infections, or UTIs.
In people with a blood vessel catheter, or in those who inject intravenous drugs, it may cause bloodstream infections like bacteremia or sepsis.
From the bloodstream, bacteria may also get to the heart, causing endocarditis. In those who have undergone neurological instrumentation, like a ventriculoperitoneal shunt used to divert cerebrospinal fluid away from the brain ventricles into the peritoneum, to lower intracranial pressure, it may cause central nervous system infections like meningitis or cerebral abscesses.
In people with burns or with surgical wounds it can produce skin and soft tissue infections such as cellulitis, fasciitis, which is inflammation of the connective tissue surrounding muscles, blood vessels and nerves, myositis, which is inflammation of the muscles, and skin abscesses.
Finally, eye infections include conjunctivitis, which is inflammation of the conjunctiva and keratitis, which is the inflammation of the cornea.
Symptoms are usually nonspecific and depend upon the type of infection. So, pneumonia can present with fever, chills, cough and chest pain.
A urinary tract infection can develop with dysuria which is pain during urination, urinary frequency and urinary urgency.
With skin and soft tissue infections, people may present with swelling, erythema, tenderness and pain. In a bloodstream infection there may be fever, chills, hypotension and tachycardia, and with endocarditis, there may also be new heart murmurs on auscultation.
With meningitis and cerebral abscesses, there may be fever, headaches and vomiting. Next up, skin infections.
With cellulitis there may be swelling, erythema, tenderness and purulent drainage. Skin abscesses associate with redness, heat, swelling and pain.
Fasciitis symptoms include fever, swelling and excessive pain, and with myositis there’s muscle weakness. Finally, conjunctivitis symptoms include eye redness, pain and burning in the eye and keratitis develops with eye redness, pain and photophobia which is eye pain due to light exposure.
Serratia marcescens can be identified in a culture from blood, sputum, urine or CSF depending on the type of infection. For UTIs, a urinalysis should be done, and it may show bacteriuria, or the presence of bacteria in the urine, as well as pyuria, which is the presence of white blood cells in the urine.
A chest X-ray may be done to diagnose pneumonia, a brain CT scan and a lumbar puncture can help diagnose central nervous system infection and echocardiography can be done for endocarditis..
Now, Serratia marcescens is often resistant to commonly used antibiotics such as ampicillin, macrolides and first-generation cephalosporins.
So, treatment requires aminoglycosides with antipseudomonal beta-lactams such as piperacillin-tazobactam and ticarcillin-clavulanate and if the infection persists, with fluoroquinolones or carbapenems.
For abscesses, the collection should also be drained. Alright, as a quick recap, Serratia marcescens is a Gram-negative bacillus from the family Enterobacteriaceae.
It is motile, facultative anaerobic, urease and catalase positive, slow lactose fermenter which grows into pink colonies on MacConkey agar.
It’s an opportunistic pathogen which causes a wide variety of hospital-acquired infections such as pneumonia, UTIs, ocular and central nervous system infections and endocarditis.
Serratia infections can be diagnosed by identifying the bacteria in a culture from blood, sputum, urine or CSF and is treated with aminoglycosides, antipseudomonal beta-lactams, fluoroquinolones and carbapenems.