2 Symptoms/signs WBC count, ×103 cells/µL Hemoglobin, g/dL Platelet count, ×103 platelets/µL ESR, mm/h CRP, mg/dL Mycoplasma IgM Other Echo Treatment Case Reports in Medicine Table 1: First hospital admission inpatient course. Day −3 Vomiting, ST∗1, fever, malaise 7.7 12.2 147 RST Neg∗2/MST Neg∗3 Day 0 Fever/rash 10.4 12.4 243 64 14.2 Positive Albumin 2.5 Day 1 Fever/rash 9.3 10.4 256 10.1 Day 4 Afebrile 16.8 8.9 398 145 7.4 Day 6 Fever 92 4.3 Bld cx-neg∗4 Bld cx-neg Dilatation of RCA∗5 New ectasia Tylenol Azithromycin IVIG and ASA∗6 2nd IVIG/ASA Prednisone/ASA Day 9 Afebrile/DC∗7 ASA and prednisone tapering ∗1 sore throat/∗2rapid strept test negative/∗3mononucleosis spot test negative/∗4blood culture negative/∗5right coronary artery/∗6aspirin/∗7discharge. showing mild dilatation of right coronary artery. The patient was immediately started on an IVIG (2 gm/kg) infusion and high-dose aspirin (20 mg/kg/dose every 6 hrs). The patient continued to spike fevers for three days after IVIG infusion. A second dose of 1 gm/kg IVIG infusion was given, but the inﬂammatory markers remained elevated and the patient continued to spike fevers throughout. A repeat echocardiogram on day 6 of hospitalization showed pro- gression of the disease with the addition of left main and proximal left anterior descending artery ectasia. Because of the apparent progression of the disease, pulse therapy with IV methylprednisolone (30 mg/kg) was administered. The patient’s symptoms improved signiﬁcantly with resolution of the fever. The patient was discharged on day 9 of hos- pitalization with aspirin and a prednisone tapering regimen (Table 1). Five days after discharge from the hospital, the patient was readmitted due to recurrence of the fever, malaise, and generalized erythematous rash without any new attributa- ble exposure. Inﬂammatory markers were elevated, but im- proved when compared to previous results. Prior discharge medications, aspirin and prednisone, were continued, and an inﬂiximab infusion (5 mg/kg) was initiated. The patient re- mained febrile, and a second IV methylprednisolone pulse dose (30 mg/kg) was given after which the patient defervesced and improved. The patient was discharged home to continue a prednisone tapering and aspirin regimen (Table 2). The patient was then followed in the outpatient setting and has had no recurrence of symptoms. A repeat echocar- diogram 10 days after discharge showed the diameter of the right coronary artery to be in the upper limits of normal, but the left main and descending arteries were more dilated and prominent. A one-month follow-up echocardiogram showed complete resolution of the coronary arteries. Repeat Myco- plasma IgM serology drawn ten months after discharge was negative (Mycoplasma IgM titer ≤0.90). 2. Discussion Kawasaki disease (KD) is an acute, self-limiting vasculitis of unknown etiology that usually occurs in childhood between the ages of two to ﬁve years old [1]. When untreated, 15 to 25% of patients develop coronary artery aneurysms [2]. It is diagnosed according to the clinical criteria developed by Kawasaki [3], as shown in Table 3. Some patients do not ful- ﬁll the clinical criteria for classic KD and are diagnosed based on echocardiogram ﬁndings. Such patients are diagnosed with “incomplete” KD. Such patients are usually at extreme of ages and are at more risk for developing coronary artery disease. They may also have unusual ﬁndings and manifesta- tions such as thrombocytopenia and hypoalbuminemia. Because of the prolonged history of unexplained fever, rash, bilateral conjunctival injection, and pharyngeal ery- thema, incomplete Kawasaki disease was considered in the case patient. Bilateral lymphadenopathy was present but no cervical lymph node measured 1.5 cm or greater. The patient presented with three out of the ﬁve principal diagnostic criteria along with prolonged fever characteristic of classic Kawasaki disease (Table 3). The diagnosis was conﬁrmed sonographically with involvement of the coronary arteries. Many characteristics of Kawasaki disease suggest that it is caused by an infectious process such as its self-limited, gener- ally nonrecurring nature, fever, and localized outbreaks [2]. It is hypothesized that the vasculitis in KD may be triggered by an immune response to a superantigen (SAg) from an in- fectious pathogen in those who are genetically susceptible [4]. Numerous studies showed a skewed T-cell repertoire in KD patients, and animal models have demonstrated hall- marks of superantigen-mediated response. Many of the in- fectious agents linked to KD such as Staphylococci species share the presence of superantigenic activity [5]. There is limited evidence that Mycoplasma species might be a trigger pathogen, or at least one of them. It has been reported on several occasions that MP infection preceded