The abscesses within the muscle must be drained surgically (not all patient require surgery if there is no abscess). Antibiotics are given for a minimum of three weeks to clear the infection.

Pyomyositis, also known as tropical pyomyositis or myositis tropicans, is a bacterial infection of the skeletal muscles which results in a pus-filled abscess. Pyomyositis is most common in tropical areas but can also occur in temperate zones.

The most common clinical sign is subcutaneous edema of the limbs and hemorrhages on mucous membranes. Other clinical signs include depression, anorexia, fever, elevated heart and respiratory rate, reluctance to move, drainage from lymph nodes, exudation of serum from the skin, colic, epistaxis and weight loss. Rarely, horses may also develop disseminated intravascular coagulation (DIC), leading to infarction of various organs, or chronic myositis and muscle atrophy.

Purpura haemorrhagica is a rare complication of equine strangles and is caused by bleeding from capillaries which results in red spots on the skin and mucous membranes together with oedema (swelling) of the limbs and the head. Purpura hemorrhagica is more common in younger animals.

Types of myositis include:

- myositis ossificans

- (idiopathic) inflammatory myopathies

- dermatomyositis

- juvenile dermatomyositis

- polymyositis

- inclusion body myositis

- pyomyositis

Myositis is inflammation or swelling of the muscles. Injury, medicines, infection, or an immune disorder can lead to myositis. It is a documented side effect of the lipid-lowering drugs statins and fibrates.

Secondary peritonitis and intra-abdominal abscesses including splenic and hepatic abscesses generally occur because of the entry of enteric micro-organisms into the peritoneal cavity through a defect in the wall of the intestine or other viscus as a result of obstruction, infarction or direct trauma. Perforated appendicitis, diverticulitis, inflammatory bowel disease with perforation and gastrointestinal surgery are often associated with polymicrobial infections caused by aerobic and anaerobic bacteria, where the number of isolates can average 12 (two-thirds are generally anaerobes). The most common aerobic and facultative bacteria are "Escherichia coli", "Streptococcus" spp. (including Enterococcus spp.), and the most frequently isolated anaerobic bacteria are the "B. fragilis" group, "Peptostreptococcus" spp., and "Clostridium" spp.

Abdominal infections are characteristically biphasic: an initial stages of generalized peritonitis associated with "Escherichia coli" sepsis, and a later stages, in which intra abdominal abscesses harboring anaerobic bacteria ( including "B. fragilis" group ) emerge.

The clinical manifestations of secondary peritonitis are a reflection of the underlying disease process. Fever, diffuse abdominal pain, nausea and vomiting are common. Physical examination generally show signs of peritoneal inflammation, isuch as rebound tenderness, abdominal wall rigidity and decrease in bowel sounds. These early findings may be followed by signs and symptoms of shock.

Biliary tract infection is usually caused by "E. coli, Klebsiella" and "Enterococcus" spp. Anaerobes (mostly "B. fragilis" group, and rarely "C. perfringens") can be recovered in complicated infections associated with carcinoma, recurrent infection, obstruction, bile tract surgery or manipulation.

Laboratory studies show elevated blood leukocyte count and predominance of polymorphonuclear forms. Radiographs studies may show free air in the peritoneal cavity, evidence of ileus or obstruction and obliteration of the psoas shadow. Diagnostic ultrasound, gallium and CT scanning may detect appendiceal or other intra-abdominal abscesses. Polymicrobial postoperative wound infections can occur.

Treatment of mixed aerobic and anaerobic abdominal infections requires the utilization of antimicrobials effective against both components of the infection as well as surgical correction and drainage of pus. Single and easily accessible abscesses can be drained percutaneously.

Affected individuals typically present with sudden painful proptosis, redness, and edema. Proptosis will vary according to the degree of inflammation, fibrosis, and mass effect. Occasionally, ptosis, chemosis, motility dysfunction (ophthalmoplegia), and optic neuropathy are seen. In the setting of extensive sclerosis there may be restriction, compression, and destruction of orbital tissue. Symptoms usually develop acutely (hours to days), but have also been seen to develop over several weeks or even months.Malaise, headaches, and nausea may accompany these symptoms. Other unusual presentations described include cystoid macular edema, temporal arteritis, and cluster headaches.

Pediatric IOI accounts for about 17% of cases idiopathic orbital inflammation. The most common sign is proptosis, but redness and pain are also experienced. Presentation varies slightly compared to adults with bilateral involvement, uveitis, disc edema and tissue eosinophilia being more common in this population. The presence of uveitis generally implies a poor outcome for pediatric IOI. Bilateral presentation may have a higher incidence of systemic disease.

Anaerobes can be isolated from most types of upper respiratory tract and head and neck and infection and are especially common in chronic ones. These include tonsillar, peritonsillar and retropharyngeal abscesses, chronic otitis media, sinusitis and mastoiditis, eye ocular) infections, all deep neck space infections, parotitis, sialadenitis, thyroiditis, odontogenic infections, and postsurgical and nonsurgical head and neck wounds and abscesses., The predominant organisms are of oropharyngeal flora origin and include AGNB, "Fusobacterium" and Peptostreptococcus spp.

Anaerobes involve almost all dental infections. These include dental abscesses, endodontal pulpitis and periodontal (gingivitis and periodontitis) infections, and perimandibular space infection. Pulpitis can lead to abscess formation and eventually spread to the mandible and other neck spaces. In addition to strict anaerobic bacteria, microaerophilic streptococci and "Streptococcus salivarius" can also be present.

"Fusobacterium" spp. and anaerobic spirochetes are often the cause of acute necrotizing ulcerative gingivitis (or Vincent's angina) which is a distinct form of ulcerative gingivitis.

Deep neck infections that develop as a consequence of oral, dental and pharyngeal infections are generally polymicrobial in nature. These include extension of retropharyngeal cellulitis or abscess, mediastinitis following esophagus perforation, and dental or periodontal abscess.

Idiopathic orbital inflammatory (IOI) disease, or orbital pseudotumor, refers to a marginated mass-like enhancing soft tissue involving any area of the orbit. It is the most common painful orbital mass in the adult population, and is associated with proptosis, cranial nerve (Tolosa–Hunt syndrome), uveitis, and retinal detachment. Idiopathic orbital inflammatory syndrome, also known as orbital pseudotumor, was first described by Gleason in 1903 and by Busse and Hochhmein. It was then characterized as a distinct entity in 1905 by Birch-Hirschfeld. It is a benign, nongranulomatous orbital inflammatory process characterized by extraocular orbital and adnexal inflammation with no known local or systemic cause. Its diagnosis is of exclusion once neoplasm, primary infection and systemic disorders have been ruled-out. Once diagnosed, it is characterized by its chronicity, anatomic location or histologic subtype.

Idiopathic orbital inflammation has a varied clinical presentation depending on the involved tissue. It can range from a diffuse inflammatory process to a more localized inflammation of muscle, lacrimal gland or orbital fat. Its former name, orbital pseudotumor, is derived due to resemblance to a neoplasm. However, histologically it is characterized by inflammation. Although a benign condition, it may present with an aggressive clinical course with severe vision loss and oculomotor dysfunction.

The hallmark of polymyositis is weakness and/or loss of muscle mass in the proximal musculature, as well as flexion of the neck and torso. These symptoms can be associated with marked pain in these areas as well. The hip extensors are often severely affected, leading to particular difficulty in ascending stairs and rising from a seated position. The skin involvement of dermatomyositis is absent in polymyositis. Dysphagia (difficulty swallowing) or other problems with esophageal motility occur in as many as 1/3 of patients. Low grade fever and peripheral adenopathy may be present. Foot drop in one or both feet can be a symptom of advanced polymyositis and inclusion body myositis. The systemic involvement of polymyositis includes interstitial lung disease (ILD) and cardiac disease, such as heart failure and conduction abnormalities.

Polymyositis tends to become evident in adulthood, presenting with bilateral proximal muscle weakness often noted in the upper legs due to early fatigue while walking. Sometimes the weakness presents itself as an inability to rise from a seated position without help or an inability to raise one's arms above one's head. The weakness is generally progressive, accompanied by lymphocytic inflammation (mainly cytotoxic T cells).

Polymyositis and the associated inflammatory myopathies have an associated increased risk of malignancy. The features they found associated with an increased risk of cancer was older age, age greater than 45, male sex, dysphagia, cutaneous necrosis, cutaneous vasculitis, rapid onset of myositis (<4 weeks), elevated creatine kinase, higher erythrocyte sedimentation rate and higher C-reactive protein levels. Several factors were associated with lower-than-average risk, including the presence of ILD, arthritis/arthralgia, Raynaud's syndrome, or anti-Jo-1 antibody. The malignancies that are associated are nasopharyngeal cancer, lung cancer, non-Hodgkin's lymphoma and bladder cancer, amongst others.

Cardiac involvement manifests itself typically as heart failure, and is present in up to 77% of patients.

Interstitial lung disease is found in up to 65% of patients with polymyositis, as defined by HRCT or restrictive ventilatory defects compatible with ILD.

The speed of the progression of JDMS is highly variable. Nearly all JDM patients have some skin involvement. The JDMS rash usually occurs as the initial symptom. Sometimes it is so slight as not to be recognized for what it is until muscle symptoms appear. Sometimes muscle symptoms never appear at all or occur very gradually over the course of months, and sometimes going from normal strength to being unable to walk within days. Usually, muscle symptoms appear weeks to months after the onset of the rash.

The vasculitis caused by JDMS manifests itself predominantly in two ways:

One is a distinctive rash. The rash often affects the face, eyelids, and hands, and sometimes the skin above joints, including the knuckles, knees, elbows, etc. The color of the rash is a pinkish purple, and is called heliotrope (after a flower of the same name with approximately this color). On the hands and face, the rash very closely resembles allergies, eczema, fifth disease, or other more common skin condition, but the heliotrope color is unique to the inflammatory process of JDMS. Some children develop calcinosis, which are calcium deposits under the skin. The rash is the source of the "dermato-" part of the name of the disease.

The second symptom caused by vasculitis is muscle inflammation. This symptom is the source of the "-myositis" part of the name of the disease ("myo" = muscle, "-itis" = inflammation of). Muscle Inflammation causes muscle weakness, which can cause fatigue, clumsiness, not keeping up physically with peers, and eventually inability to perform tasks like climbing stairs, lifting objects, and performing other manual tasks. Other signs may include falling, dysphonia, or dysphagia. The muscle weakness often causes a medical misdiagnosis of muscular dystrophy or other muscle disease. Some patients develop contractures, when the muscle shortens and causes joints to stay bent; exercise, occupational therapy, and physical therapy can prevent this. The muscles first affected tend to be proximal (i.e., neck, shoulders, back, and abdominal). About half of children with JDMS also have pain in their muscles.

Other symptoms may include irritability, weight loss, and mouth ulcers. When a child becomes irritable, fatigued, reluctant to socialize, and the face becomes flushed easily, physicians refer to this constellation of symptoms as "misery."

Around 30% of people have swollen, painful joints, but this is generally mild.

In some people the condition affects the lungs, and they may have a cough or difficulty breathing. If the condition affects the heart, there may be arrhythmias. If it affects the blood vessels in the stomach or intestines, which is more common in juvenile DM, the person might vomit blood, have black, tarry bowel movements, or may develop a hole somewhere in their GI tract.

One form the rashes take is called "heliotrope" (a purplish color) or lilac, but may also be red. It can occur around the eyes along with swelling, but also occurs on the upper chest or back what is called the "shawl" (around the neck) or "V-sign" above the breasts and may also occur on the face, upper arms, thighs, or hands. Another form the rash takes is called "Gottron's sign" which are red, sometimes scaly, papules that erupt on any of the finger joints (the metacarpophalangeal joints or the interphalangeal joints). All these rashes are made worse by exposure to sunlight, and are often very itchy, painful, and may bleed.

If a person exhibits only skin findings characteristic of DM, without weakness or abnormal muscle enzymes, then he or she may be experiencing amyopathic dermatomyositis (ADM, formerly known as "dermatomyositis sine myositis".

MCTD combines features of scleroderma, myositis, systemic lupus erythematosus, and rheumatoid arthritis (with some sources adding polymyositis, dermatomyositis, and inclusion body myositis) and is thus considered an overlap syndrome.

MCTD commonly causes:

- joint pain/swelling,

- malaise,

- Raynaud phenomenon,

- muscle inflammation, and

- sclerodactyly (thickening of the skin of the pads of the fingers)

Masticatory muscle myositis (MMM) is an inflammatory disease in dogs affecting the muscles of mastication (chewing). It is also known as atrophic myositis or eosinophilic myositis. MMM is the most common inflammatory myopathy in dogs. The disease mainly affects large breed dogs. German Shepherd Dogs and Cavalier King Charles Spaniels may be predisposed. There is a similar disease of the eye muscles found in Golden Retrievers. Symptoms of acute MMM include swelling of the jaw muscles, drooling, and pain on opening the mouth. Ophthalmic signs may include third eyelid protrusion, red eyes, and exophthalmos (protruding eyeballs). In chronic MMM there is atrophy of the jaw muscles, and scarring of the masticatory muscles due to fibrosis may result in inability to open the mouth (trismus). The affected muscles include the temporalis, masseter, and pterygoid muscles. The disease is usually bilateral.

MMM is caused by the presence of 2M fibers in the muscles of the jaw. 2M fibers are not found elsewhere in the body. The immune system recognizes these proteins as foreign to the body and attacks them, resulting in inflammation. Diagnosis of MMM is through either biopsy of the temporalis or masseter muscles or the 2M antibody assay, in which blood serum of the possible MMM-dog is reacted with temporalis tissue of a normal dog, or both. False negatives by the 2M antibody assay may be obtained if MMM is end-stage with destruction of type 2M fibers and marked fibrosis. Treatment is usually with corticosteroids such as prednisone, often with decreasing doses for up to 4–6 months, and in the case of trismus, manual opening of the mouth under anesthesia. Feeding very soft or liquid food during this time is usually necessary. The ultimate degree of recovery of jaw function and muscle mass will depend upon the extent of damage to the muscle tissue. Recurrence of MMM may occur. Misdiagnosis of MMM as a retroorbital abscess based on physical examination and finding of trismus leads to inappropriate treatment with antibiotics, which will not impede the progress of MMM.

Possible symptoms include:

- General symptoms: Fever, weight loss

- Skin: Palpable purpura, livedo reticularis

- Muscles and joints: Myalgia or myositis, arthralgia or arthritis

- Nervous system: Mononeuritis multiplex, headache, stroke, tinnitus, reduced visual acuity, acute visual loss

- Heart and arteries: Myocardial infarction, hypertension, gangrene

- Respiratory tract: Nose bleeds, bloody cough, lung infiltrates

- GI tract: Abdominal pain, bloody stool, perforations

- Kidneys: Glomerulonephritis

Symptoms, if any, can be mild even in the presence of significant swelling or masses.

Lacrimal gland involvement may cause swelling of the upper eyelid, or proptosis if there is severe swelling. Other orbital masses or inflammation can result in visual disturbance (blurred vision, double vision, visual field impairment), restricted eye movements, pain or discomfort, numbness in the distribution of the supraorbital and/or infraorbital nerves, or proptosis.

IgG4-related ophthalmic disease has been estimated to account for approximately 25% of all cases of proptosis, eyelid swelling and other features of orbital swelling.

Myositis ossificans comprises two syndromes characterized by heterotopic ossification (calcification) of muscle.

Mixed connective tissue disease (also known as Sharp's syndrome), commonly abbreviated as MCTD, is an autoimmune disease characterized by the presence of high blood levels of a specific autoantibody, now called anti-U1 ribonucleoprotein (RNP). The idea behind the "mixed" disease is that this specific autoantibody is also present in other autoimmune diseases such as systemic lupus erythematosus, polymyositis, scleroderma, etc. It was characterized in 1972, and the term was introduced by Leroy in 1980.

It is sometimes said to be the same as undifferentiated connective tissue disease, but other experts specifically reject this idea because undifferentiated connective tissue disease is not necessarily associated with serum antibodies directed against the U1-RNP, and MCTD is associated with a more clearly defined set of signs/symptoms.

Many conditions affect the human integumentary system—the organ system covering the entire surface of the body and composed of skin, hair, nails, and related muscle and glands. The major function of this system is as a barrier against the external environment. The skin weighs an average of four kilograms, covers an area of two square meters, and is made of three distinct layers: the epidermis, dermis, and subcutaneous tissue. The two main types of human skin are: glabrous skin, the hairless skin on the palms and soles (also referred to as the "palmoplantar" surfaces), and hair-bearing skin. Within the latter type, the hairs occur in structures called pilosebaceous units, each with hair follicle, sebaceous gland, and associated arrector pili muscle. In the embryo, the epidermis, hair, and glands form from the ectoderm, which is chemically influenced by the underlying mesoderm that forms the dermis and subcutaneous tissues.

The epidermis is the most superficial layer of skin, a squamous epithelium with several strata: the stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale. Nourishment is provided to these layers by diffusion from the dermis, since the epidermis is without direct blood supply. The epidermis contains four cell types: keratinocytes, melanocytes, Langerhans cells, and Merkel cells. Of these, keratinocytes are the major component, constituting roughly 95 percent of the epidermis. This stratified squamous epithelium is maintained by cell division within the stratum basale, in which differentiating cells slowly displace outwards through the stratum spinosum to the stratum corneum, where cells are continually shed from the surface. In normal skin, the rate of production equals the rate of loss; about two weeks are needed for a cell to migrate from the basal cell layer to the top of the granular cell layer, and an additional two weeks to cross the stratum corneum.

The dermis is the layer of skin between the epidermis and subcutaneous tissue, and comprises two sections, the papillary dermis and the reticular dermis. The superficial papillary dermis with the overlying rete ridges of the epidermis, between which the two layers interact through the basement membrane zone. Structural components of the dermis are collagen, elastic fibers, and ground substance. Within these components are the pilosebaceous units, arrector pili muscles, and the eccrine and apocrine glands. The dermis contains two vascular networks that run parallel to the skin surface—one superficial and one deep plexus—which are connected by vertical communicating vessels. The function of blood vessels within the dermis is fourfold: to supply nutrition, to regulate temperature, to modulate inflammation, and to participate in wound healing.

The subcutaneous tissue is a layer of fat between the dermis and underlying fascia. This tissue may be further divided into two components, the actual fatty layer, or panniculus adiposus, and a deeper vestigial layer of muscle, the panniculus carnosus. The main cellular component of this tissue is the adipocyte, or fat cell. The structure of this tissue is composed of septal (i.e. linear strands) and lobular compartments, which differ in microscopic appearance. Functionally, the subcutaneous fat insulates the body, absorbs trauma, and serves as a reserve energy source.

Conditions of the human integumentary system constitute a broad spectrum of diseases, also known as dermatoses, as well as many nonpathologic states (like, in certain circumstances, melanonychia and racquet nails). While only a small number of skin diseases account for most visits to the physician, thousands of skin conditions have been described. Classification of these conditions often presents many nosological challenges, since underlying etiologies and pathogenetics are often not known. Therefore, most current textbooks present a classification based on location (for example, conditions of the mucous membrane), morphology (chronic blistering conditions), etiology (skin conditions resulting from physical factors), and so on. Clinically, the diagnosis of any particular skin condition is made by gathering pertinent information regarding the presenting skin lesion(s), including the location (such as arms, head, legs), symptoms (pruritus, pain), duration (acute or chronic), arrangement (solitary, generalized, annular, linear), morphology (macules, papules, vesicles), and color (red, blue, brown, black, white, yellow). Diagnosis of many conditions often also requires a skin biopsy which yields histologic information that can be correlated with the clinical presentation and any laboratory data.

Calcification is typically depicted 2 weeks earlier by ultrasound (US) when compared to radiographs. The lesion develops in two distinct stages with different presentations at US. In the early stage, termed immature, it is depicts a non-specific soft tissue mass that ranges from a hypoechoic area with an outer sheet-like hyperechoic peripheral rim to a highly echogenic area with variable shadowing. In the late stage, termed mature, myositis ossificans is depicted as an elongated calcific deposit that is aligned with the long-axis of the muscle, exhibits acoustic shadowing, and has no soft tissue mass associated. US may suggest the diagnosis at early stage, but imaging features need to evolve with successive maturation of the lesion and formation of the characteristic late stage changes before they become pathognomonic.

The differential diagnosis includes many tumoral and nontumoral pathologies. A main concern is to differentiate early myositis ossificans from malignant soft-tissue tumors, and the latter is suggested by a fast-growing process. If clinical or sonographic findings are dubious and extraosseous sarcoma is suspected, biopsy should be performed. At histology, detection of the typical zonal phenomenon is diagnostic of myositis ossificans, though microscopic findings may be misleading during the early stage.

IgG4-related ophthalmic disease (IgG4-ROD) is the recommended term to describe orbital (eye socket) manifestations of the systemic condition IgG4-related disease, which is characterised by infiltration of lymphocytes and plasma cells and subsequent fibrosis in involved structures. It can involve one or more of the orbital structures.

Frequently involved structures include the lacrimal glands, extraocular muscles, infraorbital nerve, supraorbital nerve and eyelids. It has also been speculated that ligneous conjunctivitis may be a manifestation of IgG4-related disease (IgG4-RD).

As is the case with other manifestations of IgG4-related disease, a prompt response to steroid therapy is a characteristic feature of IgG4-ROD in most cases, unless significant fibrosis has already occurred.