Myelin oligodendrocyte glycoprotein antibody–associated disease (MOGAD) is a distinct neuroinflammatory disorder that may be preceded by infections. The potential for transmission of disease-associated antibodies from mother to infant via lactation has not been well documented. The authors describe a case in which a lactating woman developed severe, enterovirus-associated MOGAD and investigators measured MOG-IgG in maternal breast milk and in the serum of the breastfed infant.
The patient was a 38-year-old woman who was partially breastfeeding at the time of illness onset. She had experienced enterovirus gastroenteritis prior to the neurologic presentation. Clinically, the disease manifested as a severe, progressive episode of central nervous system inflammation affecting the optic nerve, brain, and spinal cord. The clinical picture rapidly worsened to coma with status epilepticus, necessitating admission to the intensive care unit for critical care management.
At presentation the patient had high serum MOG-IgG titers, consistent with active MOGAD. The investigators also tested the patient’s breast milk and the serum of the breastfed infant for MOG-IgG. The patient’s breast milk tested positive for MOG-IgG, whereas the infant’s serum tested negative for these antibodies. The abstract does not report assay methods, specific titer values, timing of sample collection relative to symptom onset, or longitudinal antibody measurements.
Immediate attack therapy was initiated following diagnosis. The acute immunotherapy regimen included high-dose glucocorticosteroids followed by plasma exchange. Following this intervention the patient experienced rapid clinical improvement. The abstract reports that prompt therapeutic intervention at acute onset of MOGAD was important for achieving attack remission. Details such as duration of steroid therapy, number of plasma exchange sessions, intensive care measures, anticonvulsant management, or long-term neurologic outcome beyond the stated rapid improvement were not provided in the abstract.
Testing detected MOG-IgG in breast milk from the lactating patient. Despite presence of antibody in the milk, the serum of the breastfed infant was negative for MOG-IgG, indicating that in this single case there was no detectable transmission to the infant bloodstream. The abstract does not provide additional data on the infant’s clinical status, timing of breastfeeding relative to sampling, or follow-up testing to assess later seroconversion.
This case report highlights several points relevant to clinicians managing acute neuroinflammatory disease in lactating women. First, infections such as enterovirus gastroenteritis may precede the onset of MOGAD. Second, rapid clinical deterioration, including coma and status epilepticus, can occur and may require intensive care and aggressive immunotherapy. Third, MOG-IgG can be detected in human breast milk during active disease.
Importantly, detection of antibody in milk in this instance did not correlate with detectable antibody in the infant’s serum. From the data presented in the abstract, it is not possible to conclude whether antibodies in milk pose a clinical risk to the infant, whether they are biologically active after ingestion, or whether different sampling timing or assay sensitivity might change the findings. The report underlines that early diagnosis and prompt treatment are critical for attack remission in acute MOGAD, but leaves open questions about transmission risk through lactation and the need for routine infant monitoring when maternal antibodies are present in milk.
In a lactating 38-year-old woman who developed severe enterovirus-associated MOGAD, investigators documented high serum MOG-IgG and presence of MOG-IgG in breast milk, while the breastfed infant’s serum was negative for these antibodies. Early recognition and prompt immunotherapy were associated with rapid clinical improvement for the patient. The case indicates that MOG-IgG may be present in breast milk during active disease but suggests that transmission to the infant in detectable quantities did not occur in this reported instance. The abstract does not provide assay specifics, quantitative titers, or extended infant follow-up; therefore further data are required to define the clinical significance of antibody detection in breast milk.