Granulomatous neck masses are rather common. The differential diagnosis here includes mycobacterial adenitis, sarcoidosis, and cat-scratch disease due to Bartonella henselae. The incidence of mycobacterial lymphadenitis, however, is on the rise among both immunocompromised and immunocompetent individuals. The usual presentation of granulomatous disease in the neck is simply single or matted nodes. Although mycobacterial adenitis can extend to the skin and drain externally, this presentation is rather rare. FNA biopsy is usually the best initial diagnostic approach. Here, cytology, a smear for acid-fast bacilli, a mycobacterial culture, and a sensitivity test can all be done. PCR from FNA is the most sensitive test and is particularly useful when conventional methods have not been diagnostic but the practitioner’s clinical impression remains consistent for tuberculosis infection. While FNA has a high sensitivity (about 88%), its specificity is low (49%) and an excisional biopsy is often required to confirm the diagnosis. For atypical lymphadenopathy, treatment depends on the sensitivity results of the culture. Antibiotics, however, such as isoniazid (six months standard dosage) and rifampin (two months of the standard dosage) tend to be effective.

Normal lymph nodes in the neck are usually less than 1 cm in length. Infections involving the pharynx, salivary glands, and scalp often cause tender enlargement of neck nodes. Indeed, enlarged nodes are common in HIV-infected persons. Except for the occasional node that suppurates and requires incision and drainage, treatment is directed against the underlying infection. An enlarged node (larger than 1.5 cm) or node with a necrotic center that is not associated with an obvious infection should be evaluated further especially if the patient has a history of prior cancer, alcohol use, or smoking. Other common indicators for FNA biopsy of a node include its persistence or continued enlargement. On the other hand, common causes of cervical adenopathy include squamous cell carcinoma, lymphoma, occasional metastases from non-head and neck sites, and infection. While rare, adenopathy can also be caused by Kikuchi disease and autoimmune adenopathy.

Miliaria can typically be found on the patient’s intertriginous areas and trunk. The malady is usually caused by prolonged exposure to a moist, hot environment. Risk of contraction can also be increased by occlusive clothing. Here, the sweat ducts’ ostia are plugged leading to the ultimate rupture of the sweat duct and a stinging, irritating reaction. The typical symptoms are itching and burning. The sweat gland obstruction’s histologic depth determines the clinical presentation. Obstruction in the superficial epidermis, deep epidermis, and dermis is referred to as miliaria crystallina, miliaria rubra, and miliaria profunda respectively. The lesions from this disease are usually non-follicular and between 1 to 3 millimeters in diameter. Miliaria can be prevented with topical antibacterial cream such as chlorhexidine and, if the patient has been hospitalized, miliaria on her back can be reduced by turning her over frequently. For treatment, the patient should be kept cool and wear light clothing. Triamcinolone acetonide, 0.1% in Sarna lotion, or mid-potency corticosteroid lotion or cream can be prescribed for application twice or four times each day. Secondary infections are treated with antistaphylococcal antibiotics (anticholinergic medication can be ordered in severe cases).

Erythema nodosum is a symptom complex characterized by tender erythematous nodules that typically appear on the extensor surfaces of the lower legs (but can appear on the arms, face, and trunk). The lesions should range in color from pink to red and be between 1-10 centimeters in diameter. The malady usually lasts for six weeks and can be associated with pregnancy, oral contraceptive use, primary coccidioidomycosis, streptococcosis, tuberculosis, syphilis, diverticulitis, Y enterocolitica, Yersinia pseudotuberculosis, and other deep fungal infections. Erythema nodosum can also be accompanied by inflammatory bowel disease, Behcet disease, or sarcoidosis. The tender erythematous nodules can be preceded by arthralgia, malaise, and fever. The practitioner should evaluate the patient’s medication exposure history, and conduct a physical examination for a chest radiograph, a PPD, two consecutive ASO/DNAse B titers at 2 to 4 week intervals, diarrheal illness, symptoms of any deep fungal infection specific to the area, and prior upper respiratory infection. In its late stages, erythema nodosum must be distinguished from simple contusions and bruises. The patient can be treated with NSAIDs which typically takes the form of potassium iodide (5-15 drops three times daily), corticosteroid therapy, dapsone, colchicine, or hydroxychloroquine. Complete bed rest should be ordered if the lesions are painful. The reader should note that erythema nodosum differs from other forms of panniculitis in that it does not ulcerate. Erythema induratum from tuberculosis, though, does create lesions on the posterior surface of the legs and can ulcerate.

Acute otitis media is a bacterial infection of the temporal bone’s mucosally lined air storage spaces typically caused by Streptococcus pneumoniae, Haemophilus influenzae, or Streptococcus pyogenes. The disease is often accompanied by mastoid tenderness caused by the presence of pus in the mastoid air cells. Here, material forms within the middle ear cleft and the pneumatized mastoid air cells and petrous apex. This disease is usually precipitated by a viral upper respiratory tract infection that obstructs the eustachian tube and results in the accumulation of infected fluid and mucous. Key symptoms include fever, decreased hearing, aural pressure, and otalgia accompanied by a physical finding of erythema and decreased tympanic membrane mobility. With appropriate counseling, spontaneous healing of the tympanic membrane occurs in most cases. If, however, the perforation continues for a prolonged period of time, the patient may develop chronic otitis media. Swelling over the mastoid bone or the association of cranial neuropathies or central findings indicates severe illness requiring urgent care. Acute otitis media can often be treated successfully with a combination of antibiotics and nasal decongestants. The antibiotics of choice are frequently amoxicillin (80-90 mg/kg/day divided twice daily), erythromycin with sulfonamide (50 mg/kg/day and 150 mg/kg/day respectively), cefaclor (20-40 mg/kg/day), and amoxicillin-clavulanate (20-40 mg/kg/day). The practitioner should only resort to surgical drainage of the middle ear when the patient suffers from severe otalgia or otitis complications. Reoccurring acute otitis media can be managed with long-term antibiotic prophylaxis (typically single daily doses of sulfamethoxazole (500 mg) or amoxicillin (250 or 500 mg) over 1 to 3 months). On the other hand, if the otitis media is recurring but the patient is immunocompromised, tympanocentesis can be resorted to.

Pemphigus is an uncommon intraepidermal blistering disease occurring on the skin and mucous membranes. It is caused by autoantibodies to adhesion molecules expressed in the skin and mucous membranes. The cause is unknown. The bullae appear spontaneously and are tender and painful when they rupture. Drug induced pemphigus from penicillamine, captopril, and others have been reported. There are several forms of pemphigus: pemphigus vulgaris and its variant, pemphigus vegetans; and the more superficially blistering pemphigus foliaceus and its variant, pemphigus erythematosus. All forms may occur at any age, but most present in middle age. The foliaceus form is especially apt to be associated with other autoimmune diseases, or it may be drug induced. Paraneoplastic pemphigus, a unique form of the disorder, is associated with numerous types of benign and malignant neoplasms (typically non-Hodgkin lymphoma). Pemphigus is characterized by an insidious onset of flaccid bullae, crusts, and erosions in crops or waves. In pemphigus vulgaris, lesions often appear first on the oral mucous membranes. These quickly become erosive. The scalp is another site of early involvement. Practitioners can rub a cotton swab or finger laterally on the surface of uninvolved skin which may cause easy separation of the epidermis (this is Nikolsky’s sign). The diagnosis is made with light microscopy and by direct and indirect immunofluorescence (IIF) microscopy. Autoantibodies to intercellular adhesion molecules can be detected with ELISA assays and have replaced the use of IIF in some centers. When the condition is severe, patients should be hospitalized at bed rest and given antibiotics/intravenous feedings. Anesthetic troches used before eating ease painful oral lesions. While pemphigus requires systemic therapy as early as possible, ironically, the main morbidity here is side effects from treatment. Initial therapy with systemic corticosteroids can consist of prednisone (60-80 mg daily). In most cases, a steroid sparing agent is added at the beginning at treatment (ex. azathioprine 100-200 mg daily, mycophenolate mofetil 1-1.5 twice daily). Treatment courses can be repeated in patients who do not achieve complete remission or relapse (ex. monthly IVIG at 2 g/kg intravenously over 3-4 days). In refractory cases, cyclophosphamide plus intravenous corticosteroids and plasmapheresis are also used. In patients who have a limited form of the disease, skin and mucous membrane lesions should be treated with topical corticosteroids. Complicating infection requires appropriate systemic and local antibiotic therapy. As far as complications are concerned, secondary infection can occur. This is a major cause of morbidity and mortality. Disturbances of fluid, electrolyte, and nutritional intake can occur as a result of painful oral ulcers. One in three patients will experience remission and, infection from S. aureus is the most frequent fatality cause.

Tinea versicolor is a mild, superficial Malassezia infection of the skin. The condition has a high reoccurrence rate after treatment. Patients often report the malady after discovering an area of their skin that will not tan and, mistaken the disease as well as the resulting hypopigmentation for vitiligo. A few patients will also present with itching and velvety, tan, pink, or white macules or thin papules. Large, blunt hyphae, and thin walled budding spores will appear on the KOH. The patient can be treated with selenium sulfide lotion (applied from neck to waist every day and left on for five to fifteen minutes for seven days). This treatment is repeated weekly for a month and then monthly for maintenance. Ketoconazole shampoo (1% or 2%) lathered on the chest and back and left on for five minutes can also be used for treatment. Two doses of oral fluconazole (300 mg) fourteen days apart is the first-line treatment. Imidazole creams, solutions, and lotions are quite effective for localized areas but are too expensive for use over large areas such as the chest and back.

Patients with pompholyx, or vesiculobullous dermatitis of the palms and soles, will typically present with small clear vesicles resembling grains of tapioca on the skin at the side of the fingers and the palms. The vesicles may be associated with intense itching and then become dry, scaly and fissured. The patient can be treated with topical and systemic corticosteroids. Typically, the practitioner will order a topical corticosteroid to ameliorate the flare and avoid pruritus. The patient should also avoid any skin irritants and wear cotton gloves when performing wet chores. Some patients have responded to PUVA therapy.

Tinea pedis (commonly known as athlete’s foot) is an acute or chronic dermatosis. Most infections are caused by the Trichophyton species. The patient will present with itching, burning, or stinging. Pain here may indicate secondary infection with complicating cellulitis. Interdigital tinea pedis is the most common predisposing cause of lower extremity cellulitis in healthy individuals. On the sole and heel, tinea may appear as chronic noninflammatory scaling occasionally with thickening or fissuring. This may extend over the sides of the feet in a moccasin distribution. The KOH preparation is usually positive. Tinea pedis can also present as scaling or fissuring in the toe webs with maceration. As the web spaces become more macerated, the KOH preparation and fungal culture have a lower tendency to return positive results because bacterial species begin to dominate. The malady can be treated with aluminum subacetate solution soaks for 20 minutes twice daily. Broad spectrum antifungal creams and solutions will help combat dipheriods and other gram-positive organisms. If topical imidazoles fail, one week of topical allylamine treatment will often result in clearing. Itraconazole (200 mg daily for two weeks or 400 mg daily for one week) can be used in refractory cases.

The primary symptoms of herpes simplex are burning and stinging. Neuralgia may precede or accompany attacks. The lesions consist of small, grouped vesicles on an erythematous base that can occur anywhere. Most cases occur on the patient’s vermillion lip border, the penile shaft, labia, perianal skin, and the rear end. The regional lymph nodes may be swollen and tender. The lesions usually crust and heal in one week. Immunosuppressed patients may also present with verrucous or nodular herpes lesions at the aforementioned sites of involvement. Herpes simplex lesions must be distinguished from chancroid, syphilis, pyoderma, and trauma. Direct fluorescent antibody slide tests offer a rapid means of diagnosis. The malady can be treated with acyclovir, valacyclovir, and famciclovir. Only the first drug is available for intravenous administration. For the initial clinical episode of herpes simplex, the patient is provided with acyclovir (400 mg orally, five times a day), valacyclovir (1000 mg orally twice every day), and famciclovir (250 mg orally three times every day). The duration of treatment is for seven to ten days typically.