Today, we'll be discussing a case that illustrates

some fundamental principles of host-microbe interaction.

When this 20 year old athlete became the host for

a highly virulent form of bacteria, the result was a painful

reminder of the immune system's ability to wall off infection.

Kahoo was a 20 year old man,

originally from Tonga who was now playing college football in the US.

While travelling with his team for a series of away games,

Kahoo began to experience redness and pain on his right shoulder.

Although he plays a vigorous contact sport,

he didn't remember any particular injury to that area.

Over the following day, his shoulder became increasingly red, warm, and

exquisitely painful.

Kahoo was taken by his athletic trainer

to a local acute care clinic where he was noted to be well appearing,

a large muscular man with no fever and normal vital signs.

On physical exam, the physician observed a three centimeter area

consisting of a central pustule surrounded by a red swollen rim.

The area was warm and tender, and

the lesion was producing a small amount of cloudy discharge.

When the physician applied gentle pressure to the area, she felt a give

suggesting a collection of fluid in the soft tissue underneath the skin.

The redness did not appear to spread beyond the immediate area of the lesion.

Kahoo's lymph nodes in the area were normal

as was the remainder of his physical exam.

The physician explained to Kahoo that he appeared to have an abscess, and then to

treat it, she would need to open the skin to allow the collection of pus to drain.

The process leading to Kahoo's abscess had

most likely begun a few days earlier when a microscopic break

occurred in the skin barrier that usually protects the host from bacterial entry.

This may have happened due to trauma that occurred during a normal football practice

allowing bacterial, which had colonized the skin surface,

to penetrate the skin and enter the subcutaneous tissues.

There, the bacteria produce toxins, which killed nearby cells in the soft tissues.

Kahoo's dying cells released many signalling molecules,

inducing the activation of the innate immune system

to deploy an army of neutrophils to the site of infection.

The neutrophils secreted enzymes to digest the dead cells.

As shown in this scanning electron micrograph of a human neutrophil

ingesting the very same microbe that caused Kahoo's abscess.

Within hours,

a microscopic fluid-filled cavity had formed within Kahoo's subcutaneous tissue.

This fluid, rich in cell debris and neutrophils and

bacteria, is what we know as pus.

Over the next two to three days, the battle between bacteria and

neutrophils continued, and the cavity grew larger.

Meanwhile, local fibroblasts formed a layer of granulation tissue and

a thick layer of collagen rich tissue around the pus filled cavity,

walling off the cavity and the bacteria inside.

This walling off function of the host immune response is life saving, because it

effectively prevents the bacteria from spreading to the rest of Kahoo's body.

This is why he didn't experience any systemic signs of illness like fever,

but, in this case,

Kahoo's immune system was unable to completely eliminate the bacteria.

So the battle continued, and the abscess expanded causing Kahoo's

progressively worsening localized symptoms.

After an abscess has formed, antibiotic medications can't easily

penetrate the pyogenic membrane to kill the bacteria.

So the pus inside the abscess has to be drained either spontaneously or

by a medical procedure, in order for the patient to heal.

In the clinic, the physician washed the affected area with disinfectant soap, and

used a needle and syringe to obtain a sample of the pus inside.

The physician then made an incision into the area

where she had felt the fluid collection.

She thoroughly cleaned and explored the area of incision

to make sure there were no pockets of pus that she had missed.

She then packed the wound with a small piece of gauze, to keep it open so

it would continue to drain, and she applied antibiotic ointment.

She explained to Kahoo and his trainer how to care for the wound,

by gently cleaning it with soap and water, and regularly changing the dressings.

The physician then considered whether she should prescribe oral

antibiotics to Kahoo.

She knew that oral antibiotics alone could not have penetrated the intact abscess.

But after incision and drainage, antibiotics can sometimes be helpful.

She took into account that Kahoo had only a single small lesion, and

the redness and warmth didn't appear to extend beyond the immediate area.

He had no other known medical conditions, was not immunosuppressed, and

had no fever or other signs of systemic infection.

Because of Kahoo's high Body Mass Index and Pacific Islander heritage,

the physician did worry that he was at risk for diabetes,

which can lead to more severe skin infections and poor wound healing.

Fortunately, Kahoo's hemoglobin A1c measured in the clinic was normal,

ruling out diabetes.

Overall, the physician concluded that Kahoo had an uncomplicated abscess, and

she decided not to prescribed oral antibiotics.

The fluid collection in the syringe from Kahoo's abscess

was sent to the microbiology lab for analysis.

Gram stain of the fluid revealed numerous neutrophils and

gram-positive cocci in clusters.

The bacterial culture revealed yellowish colonies with beta

hemolysis on Sheep Blood Agar.

Antibiotics susceptibility testing revealed that bacterial colonies

grew normally in the presence of several beta-lactam antibiotics in

the culture dish.

But the bacterial growth was inhibited by two other antibiotics,

clindamycin and trimethoprim–sulfamethoxazole.

Together, these lab tests confirmed a diagnosis

of community-acquired Methicillin-Resistant Staph Aureus.

Methicillin-Resistant Staph Aureus is an example of how bacteria can

evolve in the presence of antibiotics to develop resistance.

Penicillin and others antibiotics of the beta-lactam family work by

binding to penicillin binding proteins, bacterial proteins,

which are essential for maintaining the bacterial cell wall.

But these bacterial proteins can evolve their structure, so

that they are no longer efficiently bound by beta-lactam antibiotics.

In the case of MRSA, a gene called mecA encodes a particular form of

penicillin-binding protein, PBP2A, which allows the bacteria to grow and

divide in the presence of most beta-lactam antibiotics.

mecA isn't located on the bacterial chromosome.

It's located on a mobile genetic element

called the staphylococcal chromosome cassette, or SCCmec.

This cassette can be passed directly from one bacterium to another through

horizontal gene transfer, which allows the population of

bacteria to develop antibiotic resistance even more rapidly.

MRSA first emerged in healthcare settings in the 1960s,

almost immediately after the development of methicillin and related antibiotics.

But in the 1980s, MRSA also began appearing in young, otherwise,

healthy patients like Kahoo who had no recent exposure to healthcare settings.

This new community acquired MRSA strain was especially virulent

because it had gained the ability to produce a cytotoxin, which forms

pores in the membrane of infected cells causing widespread necrosis.

The gene for

this poor forming cytotoxin is also not located on the bacterial chromosome.

Instead, it's carried on a bacteriophage virus, which infects staph aureus,

another way in which a powerful virulent factor can establish itself widely and

rapidly in the staph aureus population.

The physician called Kahoo to inform him that community acquired MRSA

had been identified as the cause of his abscess.

After learning that Kahoo's infection was caused by this virulent pathogen,

the team athletic trainer researched how he could help prevent the spread of

infection among Kahoo's teammates.

He learned the importance of not sharing items which may become contaminated with

wound drainage, such as towels, clothing, bedding, bar soap, or razors.

And he also disinfected the surfaces in the athletic training room and

in the locker rooms.

Kahoo faithfully cleaned the incision and changed his dressings twice a day.

The redness, swelling, and pain resolved within two days.

And within several days, the wound had healed and

Kahoo could return to full participation in practice and games with his team.

MRSA

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