Abstract:Introduction: Toxic Epidermal Necrolysis (TEN) is primarily associated with medication use. Presented is a patient with likely Mycoplasma pneumoniae infection and progression to TEN. Case: A 19-year-old male presented with 1-week history of pneumonia like symptoms and prescribed antibiotics for suspected community-acquired pneumonia. Onset of a new rash was noted and antibiotics were discontinued less than 24 hours after initiation. The diffuse, maculopapular, bullous rash with mucosal lesions ultimately reach… Show more
“…M. pneumoniae also exerts its toxin-like effects through its metabolites, exotoxin and exotoxin-like toxic substances, lipids, lipopolysaccharides and membrane lipoprotein (28). Following the adherence of M. pneumoniae onto the surface of bronchial cells, with the cytoskeleton rearrangement, M. pneumoniae penetrates through the bronchial mucous membranes and releases nuclease and H2O2, which result in swelling, necrosis and a binding of bronchial epithelial cells, slower microvilli movement, structural deformation, and the termination of swinging, thereby inducing the infiltration of lymphocytes, plasma cells and monocytes (22,29).…”
Mycoplasma are the smallest prokaryotic microbes present in nature. These wall-less, malleable organisms can pass through cell filters, and grow and propagate under cell-free conditions in vitro. Of the pathogenic Mycoplasma Mycoplasma pneumoniae has been examined the most. In addition to primary atypical pneumonia and community-acquired pneumonia with predominantly respiratory symptoms, M. pneumoniae can also induce autoimmune hemolytic anemia and other diseases in the blood, cardiovascular system, gastrointestinal tract and skin, and can induce pericarditis, myocarditis, nephritis and meningitis. The pathogenesis of M. pneumoniae infection is complex and remains to be fully elucidated. The present review aimed to summarize several direct damage mechanisms, including adhesion damage, destruction of membrane fusion, nutrition depletion, invasive damage, toxic damage, inflammatory damage and immune damage. Further investigations are required for determining the detailed pathogenesis of M. pneumoniae.
“…M. pneumoniae also exerts its toxin-like effects through its metabolites, exotoxin and exotoxin-like toxic substances, lipids, lipopolysaccharides and membrane lipoprotein (28). Following the adherence of M. pneumoniae onto the surface of bronchial cells, with the cytoskeleton rearrangement, M. pneumoniae penetrates through the bronchial mucous membranes and releases nuclease and H2O2, which result in swelling, necrosis and a binding of bronchial epithelial cells, slower microvilli movement, structural deformation, and the termination of swinging, thereby inducing the infiltration of lymphocytes, plasma cells and monocytes (22,29).…”
Mycoplasma are the smallest prokaryotic microbes present in nature. These wall-less, malleable organisms can pass through cell filters, and grow and propagate under cell-free conditions in vitro. Of the pathogenic Mycoplasma Mycoplasma pneumoniae has been examined the most. In addition to primary atypical pneumonia and community-acquired pneumonia with predominantly respiratory symptoms, M. pneumoniae can also induce autoimmune hemolytic anemia and other diseases in the blood, cardiovascular system, gastrointestinal tract and skin, and can induce pericarditis, myocarditis, nephritis and meningitis. The pathogenesis of M. pneumoniae infection is complex and remains to be fully elucidated. The present review aimed to summarize several direct damage mechanisms, including adhesion damage, destruction of membrane fusion, nutrition depletion, invasive damage, toxic damage, inflammatory damage and immune damage. Further investigations are required for determining the detailed pathogenesis of M. pneumoniae.
“…Stevens–Johnson syndrome and TEN are mainly believed to be caused by a drug hypersensitivity reaction, and microbial infection is occasionally indicated as a cause of disease . The basic treatment includes discontinuing the culprit drug, giving fluids, providing nutritional support, maintaining the water and electrolyte balance, and handling skin and mucous membrane peeling with care .…”
Section: Discussionmentioning
confidence: 99%
“…Stevens-Johnson syndrome and TEN are mainly believed to be caused by a drug hypersensitivity reaction, 9,10 and microbial infection is occasionally indicated as a cause of disease. 1 The basic treatment includes discontinuing the culprit drug, giving fluids, providing nutritional support, maintaining the water and electrolyte balance, and handling skin and mucous membrane peeling with care. 11 Our study revealed there to be a high rate of suspected infection before the onset of SJS/TEN (40.7% and 50.0% in the low-and high-dose groups, respectively), and the proportion of patients in whom a single causative drug was identified was reduced.…”
Section: Discussionmentioning
confidence: 99%
“…Toxic epidermal necrolysis (TEN) and Stevens–Johnson syndrome (SJS) are severe, life‐threatening, mucocutaneous reactions with high mortality and are currently considered to represent different levels of severity of the same disease. Although most cases of TEN/SJS are thought to be caused by drug reactions, they may also be related to Mycoplasma pneumoniae infection and herpes simplex virus . Both TEN and SJS may cause damage to multiple organ systems and may cause skin pain (erythema, blisters, extensive epidermal exfoliation), eye, mouth and genital mucosa reactions, and multiple organ dysfunction.…”
Section: Introductionmentioning
confidence: 99%
“…Although most cases of TEN/SJS are thought to be caused by drug reactions, they may also be related to Mycoplasma pneumoniae infection and herpes simplex virus. [1][2][3][4] Both TEN and SJS may cause damage to multiple organ systems and may cause skin pain (erythema, blisters, extensive epidermal exfoliation), eye, mouth and genital mucosa reactions, and multiple organ dysfunction. Cases are classified as TEN or SJS according to the degree of epidermal sloughing.…”
Our research supports the use of corticosteroids for the systemic treatment of SJS/TEN. Corticosteroids should be used in a timely manner and in accordance with disease severity, age, underlying diseases, serum albumin level, and concurrent treatment with antimicrobial therapy.
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