Mycoplasma Pneumonia Infection - a Possible unrecognized Cause for Immune Thrombocytopenic Purpura

Mycoplasma pneumonia (M. pneumonia) is usually not considered among the several pathogens that induce immune thrombocytopenic purpura (ITP). We report a case of a child with a clinical diagnosis of severe ITP (as defined by the American Society of Hematology panel guidelines of 1994), that was associated with M. pneumonia pneumonia, and reviewed the few cases described in the English literature. A 7-year-old girl was admitted to the pediatric department with 1 day history of fever, purpura and petechiae on her legs, buttocks, arms, face, hard palate, oral mucous membranes and lips. Crepitations were heard over both lungs’ lower fields. Complete blood count revealed WBC of 22.3×10³/ μL, Hemoglobin of 11.1 gr/dL, and platelet count of 2×10³/μL. Red cells appeared normal on blood film with no features of microangiopathy. A chest X-ray demonstrated right middle lobe infiltrate. Presumptive diagnoses of ITP and RML pneumonia were made and treatment was initiated with one dose of IVIG 0.8 g/kg and daily IV Ceftriaxon at 50 mg/kg. Twelve hours after the IVIG administration, platelet count was 1.2×10³/μL. Bone marrow examination revealed normal cellularity with young megakaryocytes, compatible with the diagnosis of ITP. Since there was no response to IVIG, Methylprednisolone 4 mg/ kg for 4 days was started. An extensive search of the literature for ITP or thrombocytopenia and pneumonia retrieved only 7 case reports. In all cases M. pneumonia was the only identified pathogen. Therefore, clarithromycin 15 mg/kg/d was added to the treatment regimen, prior to obtaining the serology results. Thereafter severe hemoptysis developed; the patient was admitted to the PICU and received 4 units of platelets and a second dose of IVIG. Hemoptysis resolved after another day, when the platelet count started to increase gradually, only to drop after the cessation of steroids. A second course of steroids at the same dose was begun and tapered off gradually over 21 days, while the platelet count steadily increased, exceeding 150×10³/μL at 4 weeks from presentation. A positive Mycoplasma IgM titer at diagnosis and a 1:160 titer at 2 months confirmed the clinical diagnosis. The child is by now 20 months after the event with normal CBC. Several features of the 8 cases described (including our case) distinguish them from “classic” ITP:

1. Thrombocytopenia occurred concomitantly with the infection as opposed to a few days to a few weeks interval between infection and ITP.

2. Severe bleeding in 4 out of 8 patients including 2 with fatal intracranial hemorrhage in contrast to around 3% severe bleeding and around 1‰ fatal intracranial hemorrhage in “classic” ITP.

3. Three of the authors who looked for specific anti-platelet antibodies were unable to demonstrate it, whereas such antibodies are found in many patients with ITP.

Several mechanisms are suggested to explain these differences; though it remains unclear whether Mycoplasma associated thrombocytopenia represents a subset of ITP or constitutes a separate entity. We conclude that M. pneumonia should be looked for in any case of pneumonia and thrombocytopenia or ITP, and early specific anti-Mycoplasma therapy should be initiated to rapidly eliminate the causative agent. This may enhance recovery of the platelet count and decrease the rate of complications.