Reactive infectious mucocutaneous eruption (RIME) is a relatively uncommon mucocutaneous condition resulting from
Mycoplasma pneumoniae infection and, less commonly, other viral and bacterial infections. It is characterized by prominent mucositis. Initially, RIME was designated as MIRM (
Mycoplasma-induced rash and mucositis), given that all then-recognized cases were associated with
M pneumoniae. With the recognition that other infectious agents (including
Chlamydia pneumoniae,
human parainfluenza virus 2,
rhinovirus,
adenovirus,
enterovirus,
human metapneumovirus, and
influenza B virus) can cause a similar clinical picture, the term RIME was adopted. A case of RIME induced by
COVID-19 (SARS-CoV-2 infection) has been reported.
RIME secondary to
M pneumoniae (ie, MIRM):
- Usually seen in children and adolescents (mean age of approximately 12 years); however, adults of middle age and younger individuals may also be affected.
- Cases occur more commonly in males than females (ratio of 2:1).
- Prodromal symptoms of cough, fever, and malaise precede mucocutaneous manifestations by approximately a week. Mucositis is a prominent feature and is usually associated with a sparse, polymorphic eruption.
- Complications may include hematemesis, epiglottitis, subcorneal pustulosis, pneumomediastinum, pericardial effusion, and hepatitis.
- Ocular sequelae include conjunctival shrinkage, corneal ulceration, blindness, synechiae, dry eyes, and loss of eyelashes. Oral or urogenital adhesions are less common. Pulmonary complications such as restrictive lung disease and chronic obliterative bronchitis have also been observed in MIRM patients.
- MIRM is very rarely fatal and has a reported mortality rate of 3%, occurring in cases with significant respiratory disease. Most patients make a full recovery, and both long-term complications and recurrences are infrequent.
The pathophysiology underlying RIME remains poorly defined. Direct cytotoxic injury, autoimmune-mediated injury, and immune complex-mediated vascular injury have all been proposed as potential etiological mechanisms. It is speculated that a genetic predisposition is also important. Of note, it has been postulated that autoantibodies produced as a result of molecular mimicry between
M pneumoniae and endogenous proteins cross-react with specific self-antigens that are most abundant in mucous membranes. This theory helps explain why mucositis is such a salient feature.
