There have been no reported cases of patient’s developing post-infectious myasthenia gravis from COVID-19, but cases of co-existing COVID-19 with pre-existing MG have been published[7, 9].
In our brief literature review, we reviewed 17 patients with known MG that were infected with COVID-19. All patients except one  were sero-positive myasthenic patients on varying immunosuppressive therapies (majority on at least 2 agents, including pyridostigmine), and with varying disease status at the time of infection[7-9, 11-13]. The patients were either continued on the same medication regimen during their COVID-19 infection or given an extra pulse dose of steroids or IVIG, depending on whether or not they were suffering from acute worsening of bulbar respiratory symptoms warranting further aggressive therapy. Majority of patients were able to be discharged to home or rehab facility, with two patients however remained on mechanical ventilation[2, 7] (refer table 1).
The patient suffered from ocular symptoms, and showed with improvement with pyridostigmine trial, which further indicates that these findings are secondary to myasthenia, with an indirect perpetuation from COVID-19. During the COVID-19 pandemic, it has been established that neurological complications in form of autoimmune reactions such as GBS and MG may be provoked. Along with the patient’s underlying predilection for the disease due to genetic factors, environmental factors may also play a role, which was further instigated by the viral infection.
While the underlying mechanism of disease pathology has not been clearly established, and would need further investigation. However, it is well known that there is a decrease in the availability of AchRs at the post-synaptic neuromuscular junction due to destruction by the antibodies and the inflammatory response, plays a key role in the pathogenesis . Antibodies produced by an inflammatory reaction to an external agent such as a virus, can result in a triggered immune response that cross reacts with the AchRs due to molecular resemblance leading to damage. COVID-19 has affinity to ACE-2 receptors directly causing formation of autoantibodies leading to a significant inflammatory cascade . The ACE-2 receptor is expressed in multiple different organs such as the lungs, kidneys, and liver. This produces proinflammatory cytokines and chemokines along with B and T-cell depletion with increased levels of interleukins and TNF-a which correlates with disease severity, and increased risk of cross-reactive autoimmune attack against our own body’s receptors .Myasthenia gravis antibody production is a B cell dependent process and plays an important role in loss of self-tolerance and dysregulation . IL-6 is an inflammatory marker that is found in COVID-19 and MG, and can be associated with higher mortality rate in COVID-19 . In our case, patient had mild to moderate COVID-19 symptoms based off of ATS/IDSA guidelines . The ongoing inflammatory response along with production of destructive reactive oxygen species can lead to ARDS and long-term pulmonary fibrosis.
There have also been reported cases of post-infectious myasthenia gravis that developed weeks after initial infection, associated with Varicella zoster, West Nile Virus, Zika virus[18-20]. In the literature review, post-COVID-19 infection, neuromuscular manifestations have been found after a 1 to 3 weeks [6, 21].Our case had neuromuscular manifestation after 2 weeks of viral prodromal symptoms.
Treatment is targeted at symptomatic improvement with pyridostigmine and with immunosuppressive therapies (corticosteroids and long-term steroid-sparing agents) to control the production of antibodies and decrease the severity of disease [2, 4, 9].Current guidelines from a panel of MG experts recommend tailoring treatment according to each individual patient with underlying comorbidities with the primary care provider and specialists, however, it is encouraged to continue standard MG protocol during hospitalizations and continue immunosuppressive therapy[2, 4].