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Mycoplasma-Induced Rash and Mucositis in a Father and Son: A Case Report

Song, Hannah BA*; Huang, Jennifer T. MD; Tan, Jennifer K. MD

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The Pediatric Infectious Disease Journal: July 2018 - Volume 37 - Issue 7 - p e205-e206
doi: 10.1097/INF.0000000000001881
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Abstract

Mycoplasma-induced rash and mucositis (MIRM) is a mucocutaneous blistering eruption that occurs after infection with Mycoplasma pneumoniae. It is characterized by prominent mucositis and sparse skin involvement, typically in younger children. We report 2 cases of recurrent MIRM affecting individuals within the same family.

REPORT OF A CASE

A 42-year-old healthy African American male with a recent upper respiratory illness presented with conjunctivitis, painful erosions on the mucosal membranes and rash on the body that had developed over the past 5 days. There was a remote history of a similar prior episode during childhood, but the patient did not recall the specific diagnosis or associated treatments. There was no exposure to new medications. On physical examination, there was bilateral conjunctivitis, extensive erosions of the oral and genital mucosa and approximately thirty 3- to 8-mm oval atypical targetoid papules and plaques on the trunk. Laboratory studies demonstrated elevated M. pneumoniae immunoglobulin M antibodies at 1.79 U/L (elevated at >0.95 U/L), and histopathology demonstrated interface dermatitis with subepidermal clefting. Clinical and laboratory testing results were most consistent with MIRM. Treatment included supportive management and azithromycin, with resolution of skin lesions after 1 month. Patient-reported sequelae of MIRM included persistent oral pain and phimosis.

Four years later, his 15-year-old son developed fever, dry cough, progressive erosions on the lip and painful rash on the body. There was no exposure to new medications. On physical examination, there was bilateral conjunctivitis, buccal erosions and vesicles along the hard palate, and about 30 vesicles and targetoid papules on the extremities and trunk. M. pneumoniae polymerase chain reaction assay from a nasopharyngeal swab was positive, confirming the diagnosis of MIRM. Treatment included azithromycin and 2 g/kg IVIG, which led to slow improvement over the subsequent month. However, the skin lesions recurred and led to a second admission, where a second course of azithromycin and supportive measures led to dramatic improvement after 1 week. The only noted complication was postinflammatory hyperpigmentation and hypopigmentation on the body.

DISCUSSION

M. pneumoniae infection commonly manifests as an upper or lower respiratory tract infection, with associated fever, dyspnea, cough and coryza. Nevertheless, up to 25% of patients can present with dermatologic findings, including a blistering eruption that can resemble Stevens-Johnson syndrome (SJS).1 However, a recent systematic review of the cases associated with M. pneumoniae concluded that these cases have distinct clinical features and outcome, and proposed reclassifying these cases as “MIRM.”2 Compared with SJS, this condition presents in younger patients with a median age of 12 years and slight male predominance, and a history of preceding upper respiratory infection.2 Furthermore, key distinguishing clinical features of MIRM include prominent mucositis and sparse skin involvement.2–4 Prominent involvement of more than 1 mucosal membrane is common and can present with erosions and hemorrhagic crusting of the lips, oral mucosa, conjunctival membranes and genital region. Skin involvement, when present, typically occurs in an acral distribution. The morphology of the lesions can be pleomorphic and includes vesiculobullous, targetoid, morbilliform and macular or papular lesions2 While common treatment modalities include antibiotics and immunosuppressive regimens, there are no evidence-based guidelines on first-line treatment options.

Household transmission of M. pneumoniae and community outbreaks of MIRM have been well documented.5,6 Furthermore, 2 prior case reports describe M. pneumoniae–induced rash that affected multiple family members, but 1 case report reported erythema multiforme without mucosal involvement in a daughter and mother, and another study reported M. pneumoniae infection in numerous members of the same family where only 1 patient exhibited both skin rash and mucosal involvement.7,8 However, this case report is the first to describe recurrent MIRM affecting individuals within the same family, to our knowledge. The father was confident that the rash from childhood had a similar presentation, suggesting that he may have experienced recurrent MIRM. The son also had recurrent disease that required a second hospitalization.

Prior studies have demonstrated associations between HLA alleles and SJS,9,10 but no comparable studies on MIRM exist in the literature. Though M. pneumoniae is a common bacterial organism that causes community-acquired pneumonia in children, only about 25% of patients with M. pneumoniae infection present with dermatologic manifestations,1 suggesting differences in genetic susceptibility to dermatologic disease. The reported 8% recurrence rate of MIRM in the literature, as well as the presence of recurrent disease in multiple individuals within 1 family, further support the possibility of a genetic susceptibility to this disease entity.2 The family members in our study declined genetic testing. While a small series of patients demonstrated that there may be distinct M. pneumoniae subtypes, based on multilocus variable-number tandem repeat analysis responsible for MIRM,5 further studies elucidating genetic mechanisms, such as HLA alleles that increase susceptibility to disease, may help improve understanding of these disease entity. Improved understanding of these mechanisms may help physicians determine the risk of recurrence, need for longer treatment courses and targeted prophylaxis in select subgroups of patients.

REFERENCES

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3. Schöpf E, Stühmer A, Rzany B, et al.Toxic epidermal necrolysis and Stevens-Johnson syndrome. An epidemiologic study from West Germany. Arch Dermatol. 1991;127:839842.
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8. Balassanian N, Robbins FCMycoplasma pneumoniae infection in families. N Engl J Med. 1967;277:719725.
9. Hung SI, Chung WH, Liou LB, et al.HLA-B*5801 allele as a genetic marker for severe cutaneous adverse reactions caused by allopurinol. Proc Natl Acad Sci U S A. 2005;102:41344139.
10. Man CB, Kwan P, Baum L, et al.Association between HLA-B*1502 allele and antiepileptic drug-induced cutaneous reactions in Han Chinese. Epilepsia. 2007;48:10151018.
Keywords:

Mycoplasma pneumoniae; mucositis; familial rash

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