A 21‐year‐old local college student with no medical history presented with progressive odynophagia, dysphagia, and facial swelling. Her symptoms started 1 week prior to admission with a progressive cough, purulent yellow expectorate, and fevers up to 38.3°C. Two days prior to admission, she noted difficulty in swallowing, with the development of multiple painful mouth sores. She denied rash, genital ulcers, sexual activity, or any prior eruption. She noted recent ibuprofen and acetaminophen use but denied other medications, smoking, alcohol, or illicit drugs. On the day of admission she developed fever up to 39.3°C. Her cheeks and neck appeared swollen, with tender bilateral submandibular lymphadenopathy. Multiple, dime‐sized, white‐tinged ulcerations, about 5 mm deep, tender, and with an erythematous base, were scattered across her buccal mucosa, gums, lips, palate, and posterior pharynx. The remainder of the physical examination was unremarkable. Laboratory studies revealed an elevated white cell count with predominant neutrophilia and an elevated erythrocyte sedimentation rate, with normal serum electrolytes, liver, and renal function test results. Direct laryngoscopy showed lesions confined to the upper pharynx, sparing the epiglottis, esophagus, and trachea. She was initially treated with parenteral fluids, acyclovir, azithromycin, and ampicillin/sulbactam. Blood and throat bacterial cultures were negative, and after 48 hours ampicillin/sulbactam was discontinued. A buccal punch biopsy showed generalized neutrophilic inflammation without giant cells (Fig. 1). A mononucleosis antibody titer was negative, and acyclovir was discontinued. On the second day, there was improvement in neck swelling, but marked dysphagia persisted. Subsequent serology showed markedly elevated mycoplasma IgM titers (2830 U/mL) on hospital day 6 and herpes simplex, cytomegalovirus, HIV, syphilis, and antinuclear antibody studies were negative. The patient was discharged after a 7‐day course of azithromycin with marked improvement in her oral lesions.
Figure 1. Oral ulcer with mild inflammation and granulation tissue – no evidence of giant cells organisms. 1A. Haematoxylin and eosin stain – 40X IB. Giemsa stain ‐ 40X 1C. Rickettsial stain – 40X.
Stomatitis and oral lesions have a broad differential that includes Mycoplasma pneumoniae infection. The pathogenesis of M. pneumoniae stomatitis is controversial, and it probably has an immu‐nologic basis. Mycoplasma species, including M. pneumoniae, can non‐specifically stimulate B lymphocytes, which form antibodies against glyco‐lipid antigens of M. pneumoniae. These, in turn, may act as autoanti‐bodies. Current diagnostic methods primarily rely on serologic confirmation. Culture of respiratory or blood samples, although time consuming and variable in yield, remains the gold standard for diagnosis. The IgM enzyme‐linked immunosorbent assay (ELISA) is the most sensitive and specific method for diagnosis and mycoplasma‐specific antibody detection. Acute and convalescent IgM titers are required, although a single titer > 1:64 is suggestive of an acute infection. Newer diagnostic techniques such as mycoplasma antigen detection using antigen capture‐enzyme immunoassay and PCR are being evaluated. Mycoplasma‐associated stomatitis responds to supportive care and antibiotic therapy, preferably with macrolides.
In summary, M. pneumoniae should be considered when evaluating patients with a respiratory prodrome and unexplained oral ulcerations. Extrapulmonary abnormalities are an important part of mycoplasma disease and may suggest the diagnosis.
H. S. Singh, None; J. Chadha Singh, None; P. J. Rosenthal, None.
To cite this abstract:Singh H, Singh J, Rosenthal P. An Unusual Case of Stomatitis with a Usual Pathogen. Abstract published at Hospital Medicine 2007, May 23-25, Dallas, Texas Abstract 1002. Journal of Hospital Medicine. 2007; 2 (suppl 2). https://www.shmabstracts.com/abstract/an-unusual-case-of-stomatitis-with-a-usual-pathogen/. Accessed April 10, 2020.