Derma-Bacterial

• Pyodermas: impetigo, ecthyma, folliculitis, furuncle, carbuncle.
• Soft tissue infections: cellulitis, erysipelas.
• Gram positive infections associated with toxin production: Staphylococcal Scalded Skin Syndrome, Toxic Shock Syndrome, Scarlet Fever.
• Pyodermas include impetigo, ecthyma, folliculitis, furuncle, and carbuncle.
• Soft tissue infections include cellulitis and erysipelas.
• Carbuncle is a more extensive, deeper, communicating, and infiltrated lesion that develops when suppuration occurs in thick inelastic skin when multiple, closely set furuncles coalesce.
• Nasal decolonization is recommended for recurrent furunculosis.
• Erysipelas is caused by a breach in the skin barrier and is usually associated with group A beta hemolytic Streptococcus.
• Systemic host factors, such as obesity, blood dyscrasias, and defects in neutrophil function, are associated with furunculosis.
• Treatment for furunculosis includes local application of moist heat, systemic antibiotic, and incision and drainage.
• Cellulitis usually, but not always, follows some discernible wound and is caused by a breach in the skin barrier that provides a portal of entry.
• Furuncle is a deep-seated inflammatory nodule that develops around a hair follicle.
• Diffuse dermal infiltration is manifested by enlargement of ear lobes, widening of the nasal root, fusiform swelling of the fingers, and the skin being thrown into folds.
• Nerve trunk palsies occur in Lepromatous Leprosy (LL).
• Reactional states in Lepromatous Leprosy (LL) include Reversal Reaction (Jopling’s Type I Reaction), which is a delayed-type hypersensitivity (DTH) response, and Erythema Nodosum Leprosum (ENL)/Jopling’s Type II Reaction, which is characterized by crops of painful and tender, bright pink, dermal and subcutaneous nodules in clinically normal skin.
• Hair loss is most common in Lepromatous Leprosy (LL), affecting the eyebrows.
• Hypotension is a common feature of TSS.
• Forschheimer spots are petechiae and punctate red macules on the soft palate and uvula.
• Complications of Lepromatous Leprosy (LL) include peripheral nerve injury, venous insufficiency secondary to endothelial involvement of deep vein valves, scarring, destruction of joints (Charcot joints), and sympathetic nerve involvement, which results in decreased hidrosis, leading to dry palms and soles, leg ulcers, and collapse of the nose.
• The clinical features of acute onset include fever, sore throat, myalgia, diarrhea, vomiting.
• Loss of eccrine sweating (dry palms and soles) is common in Lepromatous Leprosy (LL).
• Treatment for severe or recalcitrant cases of TSS includes intravenous immunoglobulin to neutralize antibodies against toxins.
• Pastia’s sign is when the rash becomes more intense around skin folds.
• Clinical features of Lepromatous Leprosy (LL) include diminished CMI toward M. leprae, leading to unrestricted bacillary replication and widely disseminated disease.
• Oral findings in scarlet fever include edematous, erythematous tonsils sometimes covered with a yellow, gray, or white exudate.
• Non-menstrual TSS can be caused by surgical wounds, sinusitis, osteomyelitis, influenza, intravenous drug use, burn wounds, and gynecologic infection.
• Clinical features of Lepromatous Leprosy (LL) also include skin folding and nodule formation, which is referred to as leonine facies.
• The clinical findings of scarlet fever include prodrome, exanthem, pastia’s sign, and generalized exanthem.
• Menstruation-associated TSS is caused by the use of highly absorbent tampons.
• The incidence of nonmenstrual TSS is higher than menstrual-associated TSS.
• The tongue in scarlet fever can be either white or red, with the white tongue appearing on the first 2 days of the disease.
• Treatment for TSS is supportive, and involves intensive care in an eradication of the offending S. aureus.
• Scarlet fever is caused by group A Streptococcal pyrogenic exotoxin (SPEA).
• Erythematous macules to patches on the trunk and extremities desquamate within 1–2 weeks after it appears.
• Phenolic glycolipid I is a major species-specific and immunogenic constituent of the highly nonpolar outer layer of the bacillus, facilitating its entry into nerves.
• Peripheral Nerve Changes in Hansen’s Disease (Leprosy) include nerve enlargement, sensory impairment in skin lesions, and nerve trunk palsies.
• Stocking-glove pattern of sensory impairment (S-GPSI) is a late complication of Hansen’s Disease (Leprosy), involving a slow loss of type C fibers, involving heat and cold discrimination, leading to loss of pain or light touch, beginning in acral areas.
• If allergic to penicillin, treatment includes Cephalexin, Clindamycin, Azithromycin.
• Diagnosis of Hansen’s Disease (Leprosy) is made through clinical signs and a rapid streptococcal test or throat culture.
• Etiology and pathogenesis of Hansen’s Disease (Leprosy) involve Mycobacterium leprae, the cause of leprosy, which is a non-cultivable, Gram-positive, obligate intracellular, acid-fast bacillus.