Intact humoral immunity is essential for enterovirus immune defense. Severe enteroviral infections can occur in patients with humoral immunodeficiencies. We report a case of a neonate who presented with enterovirus meningitis and myocarditis in the setting of intrauterine Rituximab and maternal enterovirus meningitis exposure, found to have absent B cells.
A two-week-old full-term male presented with hypothermia, hypoglycemia, seizures, respiratory failure, and myocarditis. Family history was significant for mother with granulomatosis with polyangiitis and rheumatoid arthritis, who received Rituximab at seven months gestational age. On the infant’s fourth day of life, his mother was hospitalized for seizures due to enteroviral meningitis.
The patient’s initial workup was notable for elevated troponin, rhinovirus/enterovirus on Respiratory Pathogen Panel, and enterovirus on Meningitis/Encephalitis CSF PCR Panel. Transthoracic echocardiogram showed reduced biventricular function with left ventricular ejection fraction (LVEF) 30%. He was intubated and required pressor support. He was treated with antibiotics, intravenous immunoglobulin (IVIG), steroids, and pocapavir. His hospital course was also notable for necrotizing enterocolitis and MSSA bacteremia. He improved after seven weeks and was discharged on room air with improved LVEF.
His inpatient immune workup after initiation of IVIG and steroids was notable for decreased T cells, absent B cells, and low NK cells. Immunoglobulin G (IgG) levels remained normal throughout his hospitalization. Repeat labs at 39 weeks old demonstrated near normal T cell, B cell, and NK cell counts with normal IgG level. Genetic testing is currently pending.
Here we report a disseminated enteroviral infection in a newborn and his mother following third trimester exposure to Rituximab. Absent B cells at birth with subsequent improvement is consistent with Rituximab effect on B cells. However, primary immune defects, such as leaky X-linked hypogammaglobulinemia and NK cell defects, are currently being investigated with further genetic testing.
Both primary and secondary immune defects should be considered in patients with severe enteroviral infections.
