Puppies are first presented with what appears to be staphylococcal pyoderma. Definitive diagnosis requires cytologic and histopathologic evaluations. Cytologic examination of papulopustular lesions of juvenile cellulitis reveals pyogranulomatous inflammation with no microorganisms and carefully performed cultures are negative. Biopsies of early lesions reveal multiple discrete or confluent granulomas and pyogranulomas consisting of clusters of large epithelioid macrophages with variably sized cores of neutrophils. Cytological analysis of joint fluid often reveals sterile suppurative arthritis.

Diagnosis requires ruling out other potential causes. This includes ruling out vasculitis on skin biopsy.

Large doses of glucocorticoids are the treatment of choice, and are administered until the signs have resolved. In uncomplicated cases, this can take up to a month. If dogs are not treated promptly and with high doses of steroids, severe scarring may occur. If there is evidence of secondary bacterial infection, treatment with antibiotics is required.

Other conditions that may mimic cellulitis include deep vein thrombosis, which can be diagnosed with a compression leg ultrasound, and stasis dermatitis, which is inflammation of the skin from poor blood flow. Signs of a more severe infection such as necrotizing fasciitis or gas gangrene that would require prompt surgical intervention include purple bullae, skin sloughing, subcutaneous edema, and systemic toxicity. Misdiagnosis can occur in up to 30% of people with suspected lower-extremity cellulitis, leading to 50,000 to 130,000 unnecessary hospitalization and $195 to $515 million in avoidable healthcare spending annually in the United States.

Associated musculoskeletal findings are sometimes reported. When it occurs with acne conglobata, hidradenitis suppurativa, and pilonidal cysts, the syndrome is referred to as the follicular occlusion triad or tetrad.

Lyme disease can be misdiagnosed as staphylococcal- or streptococcal-induced cellulitis. Because the characteristic bullseye rash does not always appear in people infected with Lyme disease, the similar set of symptoms may be misdiagnosed as cellulitis. Standard treatments for cellulitis are not sufficient for curing Lyme disease. The only way to rule out Lyme disease is with a blood test, which is recommended during warm months in areas where the disease is endemic.

In those who have previously had cellulitis, the use of antibiotics may help prevent future episodes. This is recommended by CREST for those who have had more than two episodes.

Other conditions that can result in symptoms similar to the common form include contact dermatitis, herpes simplex virus, discoid lupus, and scabies.

Other conditions that can result in symptoms similar to the blistering form include other bullous skin diseases, burns, and necrotizing fasciitis.

Treatment is often with a steroids. This can be either applied as a cream or taken by mouth. As the condition tends to get better on its own taking steroids by mouth should generally only be tried if the rash covers a large area and it does not get better with other measures.

Since the common pathogens involved with impetigo are bacteria naturally found on the skin, most prevention (especially in children), is targeted towards appropriate hygiene, wound cleaning, and minimizing scratching (i.e. by keeping nails trimmed and short). Avoiding close contact and sharing of items such as towels with potentially infected individuals is also recommended.

Impetigo is usually diagnosed based on its appearance. It generally appears as honey-colored scabs formed from dried serum, and is often found on the arms, legs, or face. If a visual diagnosis is unclear a culture may be done to test for resistant bacteria.

Diagnosis is based on two biopsies of the skin, one submitted for routine H&E staining and one for immunofluorescence studies.

Dempster-Shafer Theory is used for detecting skin infection and displaying the result of the detection process.

It is estimated that 2—3 percent of hospitalised patients are affected by a drug eruption, and that serious drug eruptions occur in around 1 in 1000 patients.

Histology of normal epidermal tissue through H&E. Composed of four layers, Stratum basale, Stratum spinosum, Stratum granulosum, and Stratum corneum. Normal pathology of the skin, displaying the dermis which is attached to underlying loose connective tissue which subsequently contains primary adipose tissue.

Histology of Bullous Impetigo through H&E. The cleavage plane can be found either subcorneal or within the upper stratum granulosum. The roof of the pustule is parakeratotic stratum cirneum, and the floor is formed of keratinocytes, which may or may not be acantholytic. Neutrophils begin to fill the pustule. Toxins are produced by S. "aureus" and target desmoglein, which is a desmosomal cell-cell adhesion molecule that is found in the upper levels of the epidermis. Stratum Lucidum is no longer present and can be seen infiltrated with inflammatory cells. This correlates with the subcorneal localization of the bullae.

Bullous pemphigoid may be self-resolving in a period ranging from several months to many years even without treatment. Poor general health related to old age is associated with a poorer prognosis.

Drug eruptions are diagnosed mainly from the medical history and clinical examination. However, they can mimic a wide range of other conditions, thus delaying diagnosis (for example, in drug-induced lupus erythematosus, or the acne-like rash caused by erlotinib). A skin biopsy, blood tests or immunological tests can also be useful.

Drug reactions have characteristic timing. The typical amount of time it takes for a rash to appear after exposure to a drug can help categorize the type of reaction. For example, Acute generalized exanthematous pustulosis usually occurs within 4 days of starting the culprit drug. Drug Reaction with Eosinophilia and Systemic Symptoms usually occurs between 15 and 40 days after exposure. Toxic epidermal necrolysis and Stevens-Johnson syndrome typically occur 7–21 days after exposure. Anaphylaxis occurs within minutes. Simple exanthematous eruptions occur between 4 and 14 days after exposure.

TEN and SJS are severe cutaneous drug reactions that involve the skin and mucous membranes. To accurately diagnose this condition, a detailed drug history is crucial. Often, several drugs may be causative and allergy testing may be helpful. Sulfa drugs are well-known to induce TEN or SJS in certain people. For example, HIV patients have an increased incidence of SJS or TEN compared to the general population and have been found to express low levels of the drug metabolizing enzyme responsible for detoxifying sulfa drugs. Genetics plays an important role in predisposing certain populations to TEN and SJS. As such, there are some FDA recommended genetic screening tests available for certain drugs and ethnic populations to prevent the occurrence of a drug eruption. The most well known example is carbamezepine (an anti-convulsant used to treat seizures) hypersensitivity associated with the presence of HLA-B*5801 genetic allele in Asian populations.

DIHS is a delayed onset drug eruption, often occurring a few weeks to 3 months after initiation of a drug. Interestingly, worsening of systemic symptoms occurs 3-4 days after cessation of the offending drug. There are genetic risk alleles that are predictive of the development of DIHS for particular drugs and ethnic populations. The most important of which is abacavir (an anti-viral used in the treatment of HIV) hypersensitivity associated with the presence of the HLA-B*5701 allele in European and African population in the United States and Australians.

AGEP is often caused by antimicrobial, anti-fungal or antimalarial drugs. Diagnosis is often carried out by patch testing. This testing should be performed within one month after resolution of the rash and patch test results are interpreted at different time points: 48 hours, 72hours and even later at 96 hours and 120 hours in order to improve the sensitivity.

Diagnosis is by complete blood count (CBC). However, in some cases, a more accurate absolute eosinophil count may be needed. Medical history is taken, with emphasis on travel, allergies and drug use. Specific test for causative conditions are performed, often including chest x-ray, urinalysis, liver and kidney function tests, and serologic tests for parasitic and connective tissue diseases. The stool is often examined for traces of parasites (i.e. eggs, larvae, etc.) though a negative test does not rule out parasitic infection; for example, trichinosis requires a muscle biopsy. Elevated serum B or low white blood cell alkaline phosphatase, or leukocytic abnormalities in a peripheral smear indicates a disorder of myeloproliferation. In cases of idiopathic eosinophilia, the patient is followed for complications. A brief trial of corticosteroids can be diagnostic for allergic causes, as the eosinophilia should resolve with suppression of the immune over-response. Neoplastic disorders are diagnosed through the usual methods, such as bone marrow aspiration and biopsy for the leukemias, MRI/CT to look for solid tumors, and tests for serum LDH and other tumor markers.

Antibiotics are aimed at gram positive bacteria. Medical attention should be sought if symptoms persist beyond 2–3 days.

Clinical examination alone cannot distinguish between a response caused by infection, such as cellulitis, and skeeter syndrome. However, skeeter syndrome usually progresses over the course of hours versus cellulitis, which typically will evolve over the course of several days. As such, accurate history is imperative when making the diagnosis. Since IgE and IgG are key players in mosquito allergy, diagnosis can be confirmed by an immunosorbent assay measuring IgE and IgG to mosquito saliva antigens.

Bacterial infections of the orbit have long been associated with a risk of catastrophic local

sequelae and intracranial spread.

The natural course of the disease, as documented by Gamble (1933), in the pre-antibiotic era,

resulted in death in 17% of patients and permanent blindness in 20%.

Immediate treatment is very important for someone with orbital cellulitis. Treatment typically involves intravenous (IV) antibiotics in the hospital and frequent observation (every 4–6 hours). Along with this several laboratory tests are run including a complete blood count, differential, and blood culture.

- Antibiotic therapy – Since orbital cellulitis is commonly caused by "Staphylococcus" and "Streptococcus" species both penicillins and cephalosporins are typically the best choices for IV antibiotics. However, due to the increasing rise of MRSA (methicillin-resistant "Staphylococcus aureus") orbital cellulitis can also be treated with Vancomycin, Clindamycin, or Doxycycline. If improvement is noted after 48 hours of IV antibiotics, healthcare professions can then consider switching a patient to oral antibiotics (which must be used for 2–3 weeks).

- Surgical intervention – An abscess can threaten the vision or neurological status of a patient with orbital cellulitis, therefore sometimes surgical intervention is necessary. Surgery typically requires drainage of the sinuses and if a subperiosteal abscess is present in the medial orbit, drainage can be performed endoscopically. Post-operatively, patients must follow up regularly with their surgeon and remain under close observation.

The diagnosis of Ludwig's angina is clinical. History and physical examination are usually enough to establish the diagnosis.

Tuberculous cellulitis is a skin condition resulting from infection with mycobacterium, and presenting as cellulitis.

The best imaging modality for idiopathic orbital inflammatory disease is contrast-enhanced thin section magnetic resonance with fat suppression. The best diagnostic clue is a poorly marginated, mass-like enhancing soft tissue involving any area of the orbit.

Overall, radiographic features for idiopathic orbital inflammatory syndrome vary widely. They include inflammation of the extraocular muscles (myositis) with tendinous involvement, orbital fat stranding, lacrimal gland inflammation and enlargement (dacryoadenitis), involvement of the optic sheath complex, uvea, and sclera, a focal intraorbital mass or even diffuse orbital involvement. Bone destruction and intracranial extension is rare, but has been reported. Depending on the area of involvement, IOI may be categorized as:

- Myositic

- Lacrimal

- Anterior – Involvement of the globe, retrobulbar orbit

- Diffuse – Multifocal intraconal involvement with or without an extraconal component

- Apical – Involving the orbital apex and with intracranial involvement

Tolosa–Hunt syndrome is a variant of orbital pseudotumor in which there is extension into the cavernous sinus through the superior orbital fissure. Another disease variant is Sclerosing pseudotumor, which more often presents bilaterally and may extend into the sinuses.

CT findings

In non-enhanced CT one may observe a lacrimal, extra-ocular muscle, or other orbital mass. It may be focal or infiltrative and will have poorly circumscribed soft tissue. In contrast-enhanced CT there is moderate diffuse irregularity and enhancement of the involved structures. A dynamic CT will show an attenuation increase in the late phase, contrary to lymphoma where there is an attenuation decrease. Bone CT will rarely show bone remodeling or erosion, as mentioned above.

MR findings

On MR examination there is hypointensity in T1 weighted imaging (WI), particularly in sclerosing disease. T1WI with contrast will show moderate to marked diffuse irregularity and enhancement of involved structures. T2 weighted imaging with fat suppression will show iso- or slight hyperintensity compared to muscle. There is also decreased signal intensity compared to most orbital lesions due to cellular infiltrate and fibrosis. In chronic disease or sclerosing variant, T2WI with FS will show hypointensity (due to fibrosis). Findings on STIR (Short T1 Inversion Recovery) are similar to those on T2WI FS. In Tolosa–Hunt syndrome, findings include enhancement and fullness of the anterior cavernous sinus and superior orbital fissure in T1WI with contrast, while MRA may show narrowing of cavernous sinus internal carotid artery (ICA).

Ultrasonographic findings

On grayscale ultrasound there is reduced reflectivity, regular internal echoes, and weak attenuation, in a way, similar to lymphoproliferative lesions.

Tufted folliculitis presents with doll's hair-like bundling of follicular units, and is seen in a wide range of scarring conditions including chronic staphylococcal infection, chronic lupus erythematosus, lichen planopilaris, Graham-Little syndrome, folliculitis decalvans, acne keloidalis nuchae, immunobullous disorders, and dissecting cellulitis.

Skeeter syndrome (papular urticaria) is a localized allergic reaction to mosquito bites, consisting of inflammation and sometimes fever. It is caused by allergenic polypeptides in mosquito saliva and is therefore not contagious.

Taking oral Cetirizine regularly has been known to help those who suffer from skeeter syndrome.

Although the term seems informal, it has appeared in the published literature.