News|Articles|September 1, 2026

First Report of MOG-IgG in Breast Milk After Severe MOGAD

Author(s)Marco Meglio

A case report documented MOG-IgG antibodies in a mother's breast milk following severe MOGAD, though her breastfed infant's serum tested negative.

A case report describes the first documented detection of myelin oligodendrocyte glycoprotein antibodies (MOG-IgG) in human breast milk, found in a woman who developed a severe, life-threatening manifestation of MOG antibody-associated disease (MOGAD) after an enterovirus infection while she was still breastfeeding. Despite very high antibody titers in her serum, MOG-IgG was not detected in her breastfed infant's blood, according to findings published in Neurology: Neuroimmunology & Neuroinflammation.1

The patient, a 38-year-old woman, presented to the emergency department with acute urinary retention, thermal hypesthesia in her right leg, and bladder dysfunction requiring catheterization. Fourteen days earlier, she had experienced arthralgia, fatigue, and a moderate gastrointestinal infection; stool testing later identified a Coxsackievirus B5 variant. She had been partially breastfeeding her 16-month-old infant at the time of admission.

Cerebrospinal fluid analysis showed marked lymphocytic pleocytosis, and cranial and spinal MRI revealed multiple T2-hyperintense white matter lesions, right optic nerve involvement, and long-extending transverse myelitis with an H-sign in the thoracic spinal cord. Because of this lesion pattern, clinicians included MOGAD as an early differential diagnosis and pursued MOG-IgG testing according to recently proposed international consensus criteria, alongside broad infectious and autoimmune workups.1,2

Within 24 hours, the patient's condition progressed rapidly to coma with nonconvulsive status epilepticus, requiring intensive care admission and an Expanded Disability Status Scale (EDSS) score of 9.5. Serum MOG-IgG returned positive by fixed cell-based assay on hospital day 10 (titer 1:320), and a subsequent live cell-based assay showed markedly higher titers of 1:81,920 in serum and 1:2,048 in cerebrospinal fluid.

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Clinicians initiated high-dose intravenous methylprednisolone followed by 7 cycles of plasma exchange, with meaningful clinical improvement after the third cycle. Long-term immunosuppression with azathioprine was later started given the severity of onset and persistently elevated MOG-IgG titers. At 20-month follow-up, the patient had no further neurologic attacks and an EDSS score of 3.0, though she continued to require intermittent self-catheterization for persistent bladder dysfunction.

Breast milk, collected before the start of immunotherapy, tested positive for MOG-IgG at a titer of 1:64 using the live cell-based assay. The infant's serum, drawn several weeks later, showed no detectable MOG-IgG. Lactation was subsequently discontinued using bromocriptine on clinical recommendation.

"Given the approximately 1,000-fold lower total IgG concentration in breast milk compared with serum, a titer of 1:64 represents a robust, specific response," the study authors wrote.1

The authors, led by corresponding author Stefan Kammermeier, MD, of the Department of Neurology at Ludwig Maximilian University in Munich, Germany, noted that passive transfer of antibodies into breast milk is a facultative process shaped by molecule size, antibody type, and titer. Transfer is facilitated in part by the neonatal Fc receptor and, as recently identified, FcγRIIB-mediated transport across the mammary gland.3

"The very high amount of MOG-IgG in the patient's serum and the very late stage of lactation for the 18-month-old infant probably contributed to the detectability of MOG-IgG in breast milk," the authors wrote, adding that usually only a small amount, if any, of milk antibodies is transferred into infant circulation through breastfeeding.1

The authors also situated the case within broader features of MOGAD, noting that acute symptomatic seizures occur in up to 10% of patients with the disease, with nonconvulsive status epilepticus considered a rare presentation that requires EEG monitoring and seizure-suppressing medication alongside immunotherapy. They cautioned that infectious CNS diseases, including enterovirus-associated encephalomyelitis, can mimic MOGAD and complicate diagnosis, pointing to the case's elevated CSF cell count and preceding gastrointestinal infection as an example.

The authors acknowledged limitations, including that breast milk and infant serum were each sampled only once and that total IgG concentration in the breast milk was not quantitatively measured. "MOG-IgG may be detected in breast milk of lactating woman with MOGAD, but is probably not transmitted to the infant in detectable quantities," they concluded, adding that the finding underscores the value of individualized counseling around breastfeeding in this population.

REFERENCES
1. Kammermeier S, Heck S, Zimmermann H, Engels D, Reindl M, Kümpfel T. Myelin oligodendrocyte glycoprotein antibodies in breast milk in a lactating woman with severe enterovirus-associated MOGAD. Neurol Neuroimmunol Neuroinflamm. 2026;13(5):e200637. doi:10.1212/NXI.0000000000200637
2. Banwell B, Bennett JL, Marignier R, et al. Diagnosis of myelin oligodendrocyte glycoprotein antibody-associated disease: International MOGAD panel proposed criteria. Lancet Neurol. 2023;22(3):268-282. doi:10.1016/S1474-4422(22)00431-8
3. Li X, Du L, Wan Z, et al. FcγRIIB functions as an IgG transporter in the mammary gland. Proc Natl Acad Sci U S A. 2026;123(5):e2522841123. doi:10.1073/pnas.2522841123

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