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Case 22: A Blistering Rash
Published in Layne Kerry, Janice Rymer, 100 Diagnostic Dilemmas in Clinical Medicine, 2017
An id reaction is an eczematous, autoimmune response to an underlying infection, which is typically fungal in nature, but can be bacterial. Treatment should target the underlying infection (i.e. antifungal/antibiotic therapy), followed by topical or oral steroids for the rash related to the id reaction.
The Histopathology of Eczema
Published in Donald Rudikoff, Steven R. Cohen, Noah Scheinfeld, Atopic Dermatitis and Eczematous Disorders, 2014
Cynthia M. Magro, A. Neil Crowson, Molly E. Dyrsen, Martin C. Mihm
The id reaction case is a form of sensitization in which distant lesions occur, cognate to a primary infective site in the case of certain forms of viral, fungal, or bacterial infection, or to a primary hypersensitivity site in the case of prior contact sensitization. Various provocative or causal factors, when known, give specific pathophysiological import to the designations, eg, a tuberculid is an inflammatory process at a distant, sterile site, which is cognate to a primary infection of the gut or lung by Mycobacterium spp. (Choudhri et al. 1994). A fungid will reflect an inflammatory response distant to a site of a deep, or more commonly a superficial, fungal infection such as a dermatophytosis. Finally, a bacterid is characterized by an inflammatory process at a sterile site distant from a bacterial infection, usually arising in oropharyngeal, respiratory, gastrointestinal, or cutaneous sites, which could be designated infectious id panniculitis when involving subcutaneous fat (Magro et al. 2008).
Atypical systemic and dermatologic loxoscelism in a non-endemic region of the USA
Published in Clinical Toxicology, 2021
John W. Downs, Kevin T. Gould, Ryan C. Mclaughlin, Kirk L. Cumpston, S. Rutherfoord Rose
On post-bite Day 7, the patient noted extension of a petechial rash onto the palms and soles (Figure 5). He returned to the tertiary medical center and was found to have a temperature of 102.6 °F, a heart rate of 130 beats per minute, and was hypotensive with systolic blood pressures ranging from 80 to 90 mmHg. His examination was now notable for non-blanching petechiae and purpura of the distal upper and lower extremities (Figure 6), with desquamation of the right thigh. A skin biopsy revealed epidermal spongiosis and acanthosis with focal parakeratosis containing neutrophils. These findings were interpreted as consistent with an “id reaction,” also known as an autoeczematization reaction, a dermatitis developing at a site distant to a primary inflammatory or infectious skin insult. Laboratory evaluation was remarkable for a white blood cell (WBC) count of 13,400 cells/µL and mild hepatic enzyme elevation of AST 83 IU/L and ALT 115 IU/L. Blood cultures were obtained but showed no growth. Over the next three days, the hemoglobin remained consistent at 11.4 to 11.7 g/dL. However, the WBC count rose to over 28,500 cells/µL. Haptoglobin ranged from 248 to 322 mg/dL (normal 35–200 mg/dL) and lactate dehydrogenase ranged from 291 to 399 U/L (normal 0–250 U/L). Total bilirubin remained less than 1.1 mg/dL. The combination of the absence of hemolysis, the atypical appearance of the bite site, the presence of three of four systemic inflammatory response syndrome (SIRS) criteria with infectious concerns, and non-endemic geography all cast doubt on the diagnosis of LX. The patient did report a recent history of outdoor work. As such, antibiotic coverage for rickettsial diseases was initiated, and he was admitted. After considering this may be an atypical presentation of LX, corticosteroids were then increased to methylprednisolone 1 mg/kg every 6 h until the patient had been afebrile for at least 24 h. The patient’s condition slowly improved over the next 72 h and he was discharged on post-bite Day 10 with a slow oral corticosteroid taper for an additional 14 days.