A breach of Agreement and the Formation of Staphylococcal Skin Abscess

“We are about to become neighbours, but I can harm you! I do not want this to occur, so let me set my rules while you set yours. Now, this is my only rule in which my many other rules are embedded, and that is, never let me gain entrance into the inner parts of your skin tissues or into your visceral organs. I want you to know that I mean you no harm, but this rule, please abide by it and we will remain friendly neighbours for life”. These were the words of the skin microbiota to its human host at the inauguration of their relationship.

The human host however replied “I accept your rule. It’s not much of a big deal to me to ensure that you remain on the outer part of my skin (the epidermis). As you can see, my skin is tough enough as a barrier to prevent your entrance into my deeper parts, and my skin’s keratinocytes are well able to see to this agreement”.

The human skin and its microbiota had a symbiotic “agreement” that started “almost immediately” after birth. The word symbiotic in this context means an association that involves two parties that one or both members depend on the other. Some of them (skin microbiota) develop a commensal association with human skin and others a mutualistic type, but could turned out to be opportunistic pathogens.

Dohumans keep to this rule? Well, the answer is more of a NO than YES. So what happens when there is a breach of agreement?

Kindly join me as we explore the answers to these questions.

Babies delivered whether vaginally or through Cesarean-section, do have their skins colonized by skin bacteria from their handlers (doctors, midwives, nurses, the happy mother and family).

Recent studies have shown that contrary to the general believe that skin bacteria were entirely pathogenic, some members of the skin microbiota community play essential beneficial roles which include production of certain molecules, such as selective antimicrobial peptides and lantibiotics that prevents the adherence and colonization of the skin by pathogens ^source.

In addition, Nakatsuji, et al. (2013) reported the possibility of skin surface bacterial cells controlling the activities of cells below the surface, as a number of skin bacteria also enters the dermal stroma and interact with specific host cells. They were also found to play significant roles in determining the activities of host immune system.

Members of the skin microbiota, Staphylococcus species in particular can enter into the dermis and deeper subcutaneous tissue if there is a breech on the skin whether as a result of injury to the skin or any other cause.

A break on the skin is “almost” unavoidable by man, and so these microbes usually find their way into inner tissues, and when they do so, they cause different types of skin and soft tissue infections (SSTI).

SSTI include infections that arise from invasion of the skin and soft tissues of the dermis and even deeper layers by opportunistic pathogens among the members of the skin microbiota, and subsequent interaction of these micoorganisms with the host immune system.

Examples of SSTIs include:

• Impetigo (bacterial infection of superficial skin ^source).
• Folliculitis (infection and inflammation of one or more hair follicles
• Furuncles (infection of the hair follicle ^source).
• Carbuncles (a “bunch” of boils interconnected under the skin ^source).
• Cellulitis (bacterial infections involving the inner layers of the skin ^source) among others.

Of major concern to this write up are skin and soft tissue infections caused by a prominent skin bacteria, Staphylococcus aureus, a typical skin commensal bacterium and opportunistic pathogen. They can change the association they have with man from a commensal relationship to a parasitic one where they become pathogens when they find entrance into deeper skin tissues.

This article aims to spotlight the formation of abscesses by S. aureus induced skin and soft tissue infections.

“An abscess is a painful area of inflamed tissue that is filled with pus” – as defined by the Merriam-Webster dictionary.

Abscesses are formed in an attempt to contain an infection of the skin and soft tissue.

It results from the interaction of the causative agent of the infection with the activity of the host immune defence. Among the immune cells that tends to defend the body against Staphylococcal SSTI, the polymorphonuclear leukocytes show more pronounced activity against S. aureus, and they are said to be a major component of abscesses in case of SSTIs and that they perform crucial roles in their (abscesses) formation.

Polymorphonuclear leukocytes also called neutrophils are cells of the innate immune system. They are phagocytes and are among the first responders to foreign invasion, which is one of the reasons they are mostly involved in response to skin invasion by S. aureus.

In my last article, I discussed briefly the phagocytic nature of phagocytes. How they ingest the intruders, “digest” them by releasing certain “killer enzymes” and either release the digested microbes through exocytosis or further process them into antigens and present these antigens to “soldiers” of the adaptive immune system. Neutrophils as phagocytes function in similar way. You can read more here.

Following staphylococcal invasion, keratinocytes of the skin (which are major players in raising a “standard” against skin microbiota) detect the intruders via their pattern recognition receptors, and activate pro-inflammatory response that is followed by an acute inflammation in an attempt to heal up the site of injury (caused by the infection).

The process of inflammation attracts cells of the innate immune system such as macrophages and phagocytes to the site of infection. These cells, together with keratinocytes release chemotactic factors which serve to recruit large numbers of neutrophils to the site of infection. Neutrophils then destroy cells of the invading S. aureus by phagocytosis.

In order to maintain immune “stability”, recruited neutrophils whose lifespan expires at the site of infection undergoes programmed cell death called apoptosis and the debris are cleared off by other phagocytes. This process however, can be hijacked by S. aureus, as this bacterium produces certain molecular toxins such as leukotoxins that induces an undue lysis or death of neutrophils in a process called necrosis.

So the situation at the site of infection is such that, as neutrophils continue to phagocytize staphylococcal cells, they themselves are attacked by toxins produced by their “prey” (S. aureus) and are necrotized.

A whole complex of reactions due to infection and immune activities are taking place at the infection site. In order to contain this infection and eventually eliminate it, the body naturally tends to enclose the site of infection by building a “wall” of fibrous capsule around this area.

This “wall” encircles the necrotized and active neutrophils, other phagocytes, debris of digested or phagocytized Staphylococcal cells, live S. aureus, and other cells and molecules involved in the “immune response-staphylococcal cell” complex of interactions. As the fibrous capsule covering grows and increase in thickness, the young abscess undergoes maturation.

An abscess announces itself with some of these symptoms and signs which include redness, heat, swelling, pain, loss of function and in few conditions fever may also join in.

The use of antibiotics is not recommended for uncomplicated SSTI abscess. Incision and drainage of the abscess is enough treatment to restore the affected skin area back to its normal state. I believe many of us can testify to this. We just try to release the pus in the reddish swollen area on our abscessed skin, then in few days the pain and the abscess is gone.

For the complicated SSTI abscesses caused by S. aureus however, the use of traditional antibiotics such as flucloxacillin or dicloxacillin is recommended. In cases of that caused by the “powerful” methicillin resistant Staphylococcus aureus, MRSA, more complex antibiotics like doxycycline and trimethoprim-sulfamethoxazole are recommended for its treatment.

I must add that S. aureus, known for its capability to develop resistance to antibiotics may evolve to develop resistance to antibiotics (intended to treat complex abscesses), if they (antibiotics) are used outside of due recommendation.

A sole "efficient" preventive measure against Staphylococcal invasion of the soft and underlying tissues of the skin is to prevent their entrance into layers beyond the epidermis. The epidermal layer of the skin was our agreement. That is the apartment we rented out to them, they must not go beyond it.

In summary, S. aureus and other skin microbiota begin to colonize the skin right after birth. They make their bed and remain on the epidermal layer of the skin, and must not be allowed to invade inner tissues. But when invasion occurs, responses and complex reactions occur and all these are enclosed in an abscess so that the infection can be limited to that particular site and not spread to other parts. The abscess can be drained in case of uncomplicated infection, and antibiotics given in case of complex ones. The sure way to prevent all these is to maintain good hygiene and practices that keep these opportunist out of the skin’s inner tissues.

Thanks for reading!!!

References

• Abscess
• Staphyloccal pathogenesis of SSTI abscess
• Skin Microbes an immune system