Common organisms include Group A "Streptococcus" (group A strep), "Klebsiella", "Clostridium", "Escherichia coli", "Staphylococcus aureus," and "Aeromonas hydrophila", and others. Group A strep is considered the most common cause of necrotizing fasciitis.

The majority of infections are caused by organisms that normally reside on the individual's skin. These skin flora exist as commensals and infections reflect their anatomical distribution (e.g. perineal infections being caused by anaerobes).

Sources of MRSA may include working at municipal waste water treatment plants, exposure to secondary waste water spray irrigation, exposure to run off from farm fields fertilized by human sewage sludge or septage, hospital settings, or sharing/using dirty needles. The risk of infection during regional anesthesia is considered to be very low, though reported.

Vibrio vulnificus, a bacterium found in saltwater, is a rare cause.

More than 70% of cases are recorded in people with at least one of the following clinical situations: immunosuppression, diabetes, alcoholism/drug abuse/smoking, malignancies, and chronic systemic diseases. For reasons that are unclear, it occasionally occurs in people with an apparently normal general condition.

The infection begins locally at a site of trauma, which may be severe (such as the result of surgery), minor, or even non-apparent.

In medicine, fasciitis is an inflammation of the fascia, which is the connective tissue surrounding muscles, blood vessels and nerves.

In particular, it often involves one of the following diseases:

- Necrotizing fasciitis

- Plantar fasciitis

- Eosinophilic fasciitis

- Paraneoplastic fasciitis

Purpura fulminans is rare and most commonly occurs in babies and small children but can also be a rare manifestation in adults when it is associated with severe infections. For example, Meningococcal septicaemia is complicated by purpura fulminans in 10–20% of cases among children. Purpura fulminans associated with congenital (inherited) protein C deficiency occurs in 1:500,000–1,000,000 live births.

A recent retrospective study of all cases of Ecthyma gangrenosum from 2004-2010 in a university hospital in Mexico shows that neutropenia in immunocompromised patients is the most common risk factor for ecthyma gangrenosum.

Nodular fasciitis, also known as nodular pseudosarcomatous fasciitis, pseudosarcomatous fasciitis, and subcutaneous pseudosarcomatous fibromatosis, is a benign soft tissue lesion most commonly found in the superficial fascia. The lesion commonly occurs in the first three decades of life. Upper extremities and trunk are the most common affected anatomical sites. Previous history of trauma may be present. Clinically and histologically, nodular fasciitis may be mistaken for a sarcoma.

Until recently, nodular fasciitis have been considered a reactive process of uncertain cause. However, recent findings indicate that nodular fasciitis is a self-limited clonal neoplastic process (see below). Clinically, nodular fasciitis presents as a subcutaneous "growth" over a period of 3–6 weeks that eventually regresses. The lesion usually reaches a size of 2–3 cm. Larger lesions are unusual. Local recurrence has been described after simple surgical excision but it is rare.

While recent case series (n=9-80) studies have found a mortality rate of 20-40%, a large (n=1641) 2009 study reported a mortality rate of 7.5%.

Typical age of onset is around 40 to 50 years. It is not clear whether it is more common in women than men - patient numbers are small and some studies report a preponderance of men and others women. It is also found in children.

Prognosis varies depending on the underlying disorder, and the extent of the intravascular thrombosis (clotting). The prognosis for those with DIC, regardless of cause, is often grim: Between 20% and 50% of patients will die. DIC with sepsis (infection) has a significantly higher rate of death than DIC associated with trauma.

Proliferating angioendotheliomatosis may be divided into the following types:

Due to the rarity of Purpura fulminans and its occurrence in vulnerable patient groups like children research on the condition is very limited and evidence based knowledge is scarce. Currently, there is only one Purpura fulminans related clinical research project, http://www.sapfire-registry.org/, which is registered with clinicaltrials.gov.

Proliferating angioendotheliomatosis has historically been divided into two groups, (1) a reactive, involuting type and (2) a malignant, rapidly fatal type.

The reactive involuting type is uncommon and occurs in patients with various diseases including subacute bacterial endocarditis and end-stage atherosclerotic disease. Patients present with various skin lesions and rashes - mostly commonly on the thighs. Treatment aimed at the underlying condition hastens the resolution of the lesions.

The malignant type is an intravascular lymphoma, usually of the diffuse B-cell type. It progresses rapidly through involvement of multiple body systems and mortality occurs in less than a year from the initial diagnosis. The average age of patients newly diagnosed is 55 years. Currently the causative mechanism is unknown. In a few cases treatment with palliative chemotherapy has been effective.

Purpura is a condition of red or purple discolored spots on the skin that do not blanch on applying pressure. The spots are caused by bleeding underneath the skin usually secondary to vasculitis or dietary deficiency of vitamin C (scurvy). They measure 0.3–1 cm (3–10 mm), whereas petechiae measure less than 3 mm, and ecchymoses greater than 1 cm.

Purpura is common with typhus and can be present with meningitis caused by meningococci or septicaemia. In particular, meningococcus ("Neisseria meningitidis"), a Gram-negative diplococcus organism, releases endotoxin when it lyses. Endotoxin activates the Hageman factor (clotting factor XII), which causes disseminated intravascular coagulation (DIC). The DIC is what appears as a rash on the affected individual.

KMS has a mortality rate of about 30%. For patients that survive the acute disease, supportive care may be required through a gradual recovery.

Furthermore, patients may need care from a dermatologist or plastic surgeon for residual cosmetic lesions. On long-term followup, most patients have skin discoloration and/or mild disfiguration from the dormant tumor.

DIC is observed in approximately 1% of academic hospital admissions. DIC occurs at higher rates in people with bacterial sepsis (83%), severe trauma (31%), and cancer (6.8%).

Intravascular papillary endothelial hyperplasia (also known as "Masson's hemangio-endotheliome vegetant intravasculaire," "Masson's lesion," "Masson's pseudoangiosarcoma," "Masson's tumor," and "Papillary endothelial hyperplasia") is a rare, benign tumor. It may mimic an angiosarcoma, with lesions that are red or purplish 5-mm to 5-cm papules and deep nodules on the head, neck, or upper extremities.

Purpura are a common and nonspecific medical sign; however, the underlying mechanism commonly involves one of:

- Platelet disorders (thrombocytopenic purpura)

- Primary thrombocytopenic purpura

- Secondary thrombocytopenic purpura

- Post-transfusion purpura

- Vascular disorders (nonthrombocytopenic purpura)

- Microvascular injury, as seen in senile (old age) purpura, when blood vessels are more easily damaged

- Hypertensive states

- Deficient vascular support

- Vasculitis, as in the case of Henoch–Schönlein purpura

- Coagulation disorders

- Disseminated intravascular coagulation (DIC)

- Scurvy (vitamin C deficiency) - defect in collagen synthesis due to lack of hydroxylation of procollagen results in weakened capillary walls and cells

- Meningococcemia

- Cocaine use with concomitant use of the one-time chemotherapy drug and now veterinary deworming agent levamisole can cause purpura of the ears, face, trunk, or extremities, sometimes needing reconstructive surgery. Levamisole is purportedly a common cutting agent.

- Decomposition of blood vessels including purpura is a symptom of acute radiation poisoning in excess of 2 Grays of radiation exposure. This is an uncommon cause in general, but is commonly seen in victims of nuclear disaster.

Cases of psychogenic purpura are also described in the medical literature, some claimed to be due to "autoerythrocyte sensitization". Other studies suggest the local (cutaneous) activity of tissue plasminogen activator can be increased in psychogenic purpura, leading to substantial amounts of localized plasmin activity, rapid degradation of fibrin clots, and resultant bleeding. Petechial rash is also characteristic of a rickettsial infection.

Most cases of Fournier gangrene are infected by both aerobic and anaerobic bacteria. Resulting mortality increases in individuals lacking access not only to pragmatic resources such as sanitation and medical care, but to psychosocial resources as well.

A 2006 Turkish study reported 46% of those diagnosed with Fourniers had elevated blood sugars. There have been additional findings that seemingly link Fourniers with immunosuppression and alcoholism. One study reported approximately one third of those diagnosed with Fournier had alcoholism with resulting diabetes and malnutrition, while another 10% had been medical immunosuppressed either via chemotherapy, steroids, or malignancy.

The elderly and those with a weakened immune system are especially vulnerable to contracting cellulitis. Diabetics are more susceptible to cellulitis than the general population because of impairment of the immune system; they are especially prone to cellulitis in the feet, because the disease causes impairment of blood circulation in the legs, leading to diabetic foot or foot ulcers. Poor control of blood glucose levels allows bacteria to grow more rapidly in the affected tissue, and facilitates rapid progression if the infection enters the bloodstream. Neural degeneration in diabetes means these ulcers may not be painful, thus often become infected. Those who have suffered poliomyelitis are also prone because of circulatory problems, especially in the legs.

Immunosuppressive drugs, and other illnesses or infections that weaken the immune system, are also factors that make infection more likely. Chickenpox and shingles often result in blisters that break open, providing a gap in the skin through which bacteria can enter. Lymphedema, which causes swelling on the arms and/or legs, can also put an individual at risk.

Diseases that affect blood circulation in the legs and feet, such as chronic venous insufficiency and varicose veins, are also risk factors for cellulitis.

Cellulitis is also common among dense populations sharing hygiene facilities and common living quarters, such as military installations, college dormitories, nursing homes, oil platforms, and homeless shelters.

The pathogenesis of this disease is unclear. Arteriosclerosis obliterans has been postulated as the cause, along with errors of the clotting and fibrinolytic pathways such as antiphospholipid syndrome.

Warfarin necrosis usually occurs three to five days after drug therapy is begun, and a high initial dose increases the risk of its development. Heparin-induced necrosis can develop both at sites of local injection and - when infused intravenously - in a widespread pattern.

In warfarin's initial stages of action, inhibition of protein C and Factor VII is stronger than inhibition of the other vitamin K-dependent coagulation factors II, IX and X. This results from the fact that these proteins have different half-lives: 1.5 to six hours for factor VII and eight hours for protein C, versus one day for factor IX, two days for factor X and two to five days for factor II. The larger the initial dose of vitamin K-antagonist, the more pronounced these differences are. This coagulation factor imbalance leads to paradoxical activation of coagulation, resulting in a hypercoagulable state and thrombosis. The blood clots interrupt the blood supply to the skin, causing necrosis. Protein C is an innate anticoagulant, and as warfarin further decreases protein C levels, it can lead to massive thrombosis with necrosis and gangrene of limbs.

Notably, the prothrombin time (or international normalized ratio, INR) used to test the effect of warfarin is highly dependent on factor VII, which explains why patients can have a therapeutic INR (indicating good anticoagulant effect) but still be in a hypercoagulable state.

In one third of cases, warfarin necrosis occurs in patients with an underlying, innate and previously unknown deficiency of protein C. The condition is related to purpura fulminans, a complication in infants with sepsis (blood stream infection) which also involves skin necrosis. These infants often have protein C deficiency as well. There have also been cases in patients with other deficiency, including protein S deficiency, activated protein C resistance (Factor V Leiden) and antithrombin III deficiency.

Although the above theory is the most commonly accepted theory, others believe that it is a hypersensitivity reaction or a direct toxic effect.

Cellulitis in 2015 resulted in about 16,900 deaths worldwide, up from 12,600 in 2005.

The organism enters directly through the breakdown of mechanical defense barriers such as mucosa or skin. Immunocompromised conditions make the patient more susceptible to this infection and septicemia. In case of septicemia, the bacteria reaches the skin via the bloodstream. Defective humoral or cellular immune system increases the risk because the organism is not able to be cleared from the bloodstream. The main mechanism of the organism that is causing the typical skin lesions is the invasion of the organism into the arteries and veins in the dermis and subcutaneous tissues of the skin. This perivascular invasion leads to nodular formation, ulceration, vasculitis and necrosis due to impaired blood supply. Perivascular involvement is achieved by direct entry of bacteria through the skin or hematogenous spreading in case of sepsis.

Vitamin K reactions occur after injection with vitamin K, and there are two patterns of presentation, (1) a reaction may occur several days to 2 weeks after inection with skin lesions that are pruritic, red patches and plaques that can deep-seated, involving the dermis and subcutaneous tissue, or (2) with subcutaneous sclerosis with or without fasciitis, that appears at the site of injection many months after treatment. The latter pseudosclerodermatous reaction has been termed Texier's disease and lasts several years.