Scarlet Fever: A Razorback House Divided
Stevens-Johnson syndrome Toxic epidermal necrolysis. Atypical target lesions with central dusky purpura; bullae and blister formation; fever, malaise, headache, cough, and conjunctivitis 3 days before rash; hypotension; involvement of palms and soles; mucosal involvement; painful burning; positive Nikolsky sign exfoliation of skin when rubbed ; sloughing and erosion; spreads from face downwards to entire body; tachycardia.
Bullous pemphigoid; drug-induced hypersensitivity syndrome; erythema multiforme; febrile drug reaction; Kawasaki disease; staphylococcal scalded skin syndrome; urticaria; vasculitis. Clinical signs, symptoms, and history; histology; immunofluorescence; laboratory testing lymphopenia, neutropenia, thrombocytopenia, elevated serum transaminase and BUN levels, elevated erythrocyte sedimentation rate ; skin biopsy.
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Antibiotic therapy only if signs of infection Discontinue causative drug Fluid resuscitation, nutritional supplementation Hospital admission Intravenous immune globulin some benefit noted Ophthalmology consultation 10 — 12 Wound care. Hospital admission for supportive therapy Hydration Penicillinase-resistant antibiotics Vasopressors Wound care.
Information from references 1 through Key findings in patients with Rocky Mountain spotted fever include history of a tick bite, fever, and a characteristic rash. Between 60 and 75 percent of patients with this condition are given an alternate diagnosis at the initial physician visit. Rocky Mountain spotted fever is the most common rickettsial disease in the United States. It has an overall mortality rate of 5 to 10 percent.
Cases of Rocky Mountain spotted fever are most often reported in American Indians, whites, males, and children. Rocky Mountain spotted fever is transmitted by Rickettsia rickettsii , a small gram-negative bacterium that grows in eukaryotic cells. The natural hosts for this organism consisting of the wood tick Dermacentor andersoni in the western United States and the dog tick Dermacentor variabilis in the eastern United States.
Ultimately, R. Clinical Findings. The diagnosis of Rocky Mountain spotted fever is primarily clinical. The classic triad of symptoms associated with the disease includes fever, headache, and rash in a person with a history of tick bite or exposure to ticks. The rash appears two to five days after the onset of fever in 80 to 90 percent of patients.
The rash begins as small, blanching, nonpruritic macules that develop into a maculopapular rash and progress after several days to petechial lesions. The classic spotted appearance occurs when the petechial lesions coalesce and form ecchymosis Figure 1.
The early rash of Rocky Mountain spotted fever mimics many infectious and noninfectious diseases that have an associated maculopapular rash.
The face is usually spared. A rash on the palms and soles is a distinct distribution that occurs in approximately 40 percent of patients with Rocky Mountain spotted fever. Petechial lesions on the leg of a patient who developed Rocky Mountain spotted fever after a tick bite. Cutaneous vasculitis. The Color Atlas of Family Medicine. Laboratory Testing.
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Basic laboratory tests that should be ordered in patients with suspected Rocky Mountain spotted fever include a complete blood count and blood chemistry profile, including measurement of electrolytes and creatinine, and liver function tests. Laboratory findings may include thrombocytopenia, hyponatremia, and elevated hepatic transaminase levels with a normal white blood cell count.
Cerebrospinal fluid analysis can be performed if neurologic symptoms are present. If a rash is present, direct immunofluorescence of a punch biopsy fixed in special media can detect rickettsial organisms within the vascular endothelium. A standard punch biopsy fixed in formalin may show necrotizing vasculitis. Treatment for Rocky Mountain spotted fever should begin immediately after diagnosis, and cases must be reported to the state health department. Patients treated more than five days after the onset of symptoms have a mortality rate three times greater than that in patients treated earlier.
Tetracycline is an alternative in adults and children older than eight years, and chloramphenicol is preferred in pregnant women.
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Necrotizing fasciitis has a mortality rate of 25 percent, and up to 70 percent in patients who develop sepsis. There are two types of necrotizing fasciitis, which are grouped according to etiology and infectious pathogen. Type I, polymicrobial necrotizing fasciitis, is usually preceded by trauma or surgery. The most common pathogens are Streptococci non-group A , Bacteroides , Enterobacteriaceae, and Pepto-streptococcus. The most common pathogens associated with this type include group A beta-hemolytic streptococci and Staphylococcus aureus.
Necrotizing fasciitis of the genital and perineal areas is called Fournier gangrene. In all types, bacterial infection leads to edema, vascular occlusion, ischemia, tissue necrosis, and, if not treated promptly, sepsis. Patients with necrotizing fasciitis often have a history of a wound or trauma.
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Common symptoms include fever and chills, with heat, erythema, edema, and pain over a focal area of skin Figure 2. Erythema, swelling, and bullae on the leg and groin of a patient with necrotizing fasciitis. Reprinted with permission from Dufel S, Martino M. Simple cellulitis or a more serious infection? J Fam Pract. The erythematous skin develops a dusky blue discoloration. Yellow vesicular and bullous lesions form over the erythematous skin, with some serosanguineous drainage. Impetigo, cellulitis, and toxic shock syndrome can mimic these lesions. After four to five days, the bullae become violaceous, and the skin becomes gangrenous.
Anesthesia, another key feature of necrotizing fasciitis, develops as a result of infarction of cutaneous nerves. The black eschar that is formed sloughs off by day Crepitus also occurs in 35 percent of patients. Laboratory Testing and Imaging. There is no specific diagnostic test for necrotizing fasciitis. Common nonspecific findings include a white blood cell count greater than 14, cells per mm 3 These parameters can help distinguish necrotizing fasciitis from other soft tissue infections.
Histology and culture of deep tissue biopsy are essential; surface cultures cannot be relied on alone. Gram staining of the exudate may provide clues about the pathogens while the physician awaits culture results. Radiography, computed tomography, ultrasonography, and magnetic resonance imaging can be used to detect pyomyositis or gas within soft tissues or muscles.
First-line treatment for necrotizing fasciitis is immediate hospitalization, surgical debridement, and antibiotic therapy. Although they are controversial, hyperbaric oxygen therapy and intravenous immune globulin may have a role as adjunct therapies. Toxic epidermal necrolysis and Stevens-Johnson syndrome are acute hypersensitivity cutaneous reactions that present as dermatologic emergencies.
They are thought to be severe presentations of erythema multiforme. In the United States, Stevens-Johnson syndrome and toxic epidermal necrolysis most often occur during early spring and winter. Most affected patients are 20 to 40 years of age, and the male-to-female ratio is Approximately 50 percent of cases of Stevens-Johnson syndrome and 80 to 90 percent of cases of toxic epidermal necrolysis are drug induced. The exact pathogenesis of these conditions is unknown. After one to three weeks of exposure to the causative agent, a prodrome of fever, malaise, headache, cough, and conjunctivitis develops Figure 3.
The bullae coalesce, forming flaccid blisters with full-thickness epidermal necrosis.
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Patients with toxic epidermal necrolysis have large areas of epidermal detachment sloughing and erosions, which increase the risk of blood and fluid loss, and of superinfection Figure 5. The palms and soles become painful, erythematous, and edematous. Mucosal involvement occurs in almost all affected patients.
The most common sequelae are ocular scarring and blindness.
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Skin lesions in a year-old boy who developed Stevens-Johnson syndrome after taking penicillin for pneumonia. There is no specific diagnostic test for Stevens-Johnson syndrome or toxic epidermal necrolysis. Lymphopenia may be present, as well as neutropenia 30 percent of patients , thrombocytopenia 15 percent of patients , elevated erythrocyte sedimentation rate, and elevated serum transaminase and blood urea nitrogen levels. Clinical findings and a skin biopsy are useful in diagnosis.
Frozen section analysis can facilitate rapid diagnosis and, in combination with immunofluorescence, can exclude other diagnoses. Patients with Stevens-Johnson syndrome or toxic epidermal necrolysis should be admitted to an intensive care or burn unit immediately, because rapid deterioration is possible.
Antibiotics should be used only if there is evidence of infection. Intravenous immune globulin has been incorporated into some treatment protocols. Already a member or subscriber? Log in. Address correspondence to Richard P. Reprints are not available from the authors. American Academy of Dermatology. Cutaneous anthrax management algorithm. Accessed July 5, Anthrax as a biological weapon: medical and public health management. Practice guidelines for the diagnosis and management of skin and soft-tissue infections [published corrections appear in Clin Infect Dis.
Clin Infect Dis. Centers for Disease Control and Prevention. Group A streptococcal GAS disease. Accessed July 1, Value of standard laboratory tests for the early recognition of group A beta-hemolytic streptococcal necrotizing fasciitis. Tickborne rickettsial diseases: Rocky Mountain spotted fever.