Pyoderma and Gangrenosum Pyoderma: Symptoms, Diagnosis and Treatment

What is Piodermitis?

The skin has resident bacteria, which live as commensal bacteria and transient bacteria that can occasionally colonize the skin.

Pyodermitis is defined as primary infections of the skin caused mainly by pyogenic bacteria of the genera Staphylococcus and Streptococcus.

Causes

Among the staphylococci is the most important pathogen, causing superficial or deep infections and diseases related to the action of their toxins.

The skin is the natural habitat of many species of staphylococci. There is permanent colonization with aureus in the anterior nostrils of 20% of the population.

Approximately 60% of healthy individuals have occasional colonization with aureus somewhere in the body, especially in the armpit, perineum, pharynx, hands, and nostrils (nostrils).

The primary defense against staphylococci is the phagocytosis of neutrophils.

 

Conditions predisposing to the colonization of the skin due to low resistance to the agent include atopic dermatitis, diabetes, dialysis, intravenous drug use, liver dysfunction, and HIV infection.

Streptococci almost always participate in the microbiota of the oral or gastrointestinal tract and are among the most common agents of human diseases.

Streptococcus pyogenes is responsible for most infections caused by bacteria of the family Streptococcaceae, which are found in the oropharynx of 10% of the general population.

Only 1% of people have it on normal skin. The most virulent streptococci belong to group A and have the M protein on their surface, protecting against phagocytosis and increasing adherence to epithelial tissues.

Infections with S. pyogenes are more common in childhood and adolescence. This is because subsequent conditions, symptomatic or not apparent, with serotypes prevalent in the community, confer lasting and specific immunity against this pathogen.

The frequency of pyodermitis varies depending on several factors; In general, they affect around 7% of the population.

The summer season favors skin infections since it facilitates the installation and maintenance of the microclimate, heat, and humidity necessary for developing infectious agents.

In the pathogenesis of pyoderma, we must consider the factors of the host: the presence of resident flora that makes colonization with other bacteria difficult.

This produces unsaturated fatty acids that form a chemical and mechanical barrier, the moisture content of the skin; the more significant the humidity, the easier it is the bacterial multiplication and an alkaline pH that facilitates the bacterial colonization and the immune competence of the individual.

The degree of pathogenicity and virulence is considered about the microorganism, which basically derives from the invasive potential determined by the presence of antiphagocytic elements on the bacterial surface and the capacity to produce toxins.

Pyoderma gangrenous

Another condition related to skin infections is pyoderma gangrenosum, a chronic, neutrophilic, and progressive skin necrosis of unknown etiology, often associated with systemic diseases and, sometimes, skin lesions.

The etiology is unknown, but pyoderma gangrenosum can be associated with various systemic diseases, including vasculitis, gammopathies, leukemia, lymphoma, infection with hepatitis C virus, etc.

It is thought to be mediated by an abnormal immune response. The majority of patients are between 25 and 55 years old. It can manifest itself in several subtypes.

Pyoderma gangrenosum ulcerations occur after trauma or injury to the skin in approximately 30% of patients.

symptom

Often, pyoderma gangrenosum begins as an inflamed erythematous papule, pustule, or nodule.

The lesion, which may resemble a boil or an arthropod bite at this stage, then ulcerates and expands rapidly, developing a swollen necrotic base and a raised, dark to the violaceous border.

An undercut edge (i.e., loss of underlying support tissue at the border) is standard. Systemic symptoms such as fever and malaise are common.

The symptoms and signs may vary with the subtype:

Ulcerative subtype (classic):  In this most common subtype, ulcers are formed as described above, most often in the lower extremities or the trunk, particularly the buttocks and the perineum.

Bullous (atypical)  subtype: This less common subtype often develops in patients with hematologic disorders.

The lesions usually begin as bullae that erode and turn into superficial ulcers. Arms and faces are more frequently involved.

Pustular subtype: This subtype tends to develop during exacerbations of inflammatory bowel disease.

Painful pustules develop, surrounded by erythema; arthralgias are common.

Vegetative subtype (superficial granulomatous pyoderma):  In this subtype, it occurs most frequently in the head or neck.

Diagnosis

The diagnosis is clinical and is a diagnosis of exclusion after other causes of ulceration have been ruled out. The expansion of ulceration after surgical debridement strongly suggests pyoderma gangrenosum.

Biopsies of injuries are often not diagnostic, but they can be supportive; 40% of the biopsies of a leading-edge show vasculitis with neutrophils and fibrin in superficial vessels.

Treatment

The treatment includes:

  • Wound care
  • Corticosteroids
  • TNF-alpha inhibitors
  • Sometimes other anti-inflammatory or immunosuppressive medications
  • Avoid surgical debridement

Wound healing can be promoted with occlusive dressings that retain moisture for less exudative wounds and absorbent dressings for highly exudative wounds.

Wet to dry dressings should be avoided. Topical therapy with high potency corticosteroids or tacrolimus may help with superficial and early lesions.

Surgical treatments are avoided due to the risk of wound extension.