Myasthenia gravis (MG) is an autoimmune disease with impaired neuromuscular junction transmission, characterized by fatigue of the affected skeletal muscles. The whole body skeletal muscles can be involved, including the extraocular muscles, pharyngeal muscles, tongue muscles, neck muscles and limb girdle muscles. When the respiratory muscles are weak and cannot maintain normal ventilation, it is called myasthenia gravis crisis. Myasthenia gravis crisis is a dangerous condition with a mortality rate of about 5-8%. For various reasons, MG patients have a much higher chance of developing infections, especially pulmonary infections, than the general population. In turn, infections exacerbate MG symptoms and even trigger critical illnesses. At the same time, more than one antibiotic has been found to aggravate myasthenia gravis symptoms. Clinically, when encountering MG patients with co-infection of the lungs, it is crucial to choose the correct antibiotic quickly. It is important not only to be effective against the underlying pathogen, but also to avoid exacerbating or inducing MG crises. The current guidelines for the treatment of community-acquired pneumonia recommend a starting regimen of respiratory quinolones or beta-lactam antibiotics plus macrolides. So, who is best for MG patients? Fluoroquinolones are very widely used in the clinic, and as early as 1988, ciprofloxacin was reported to cause worsening of MG symptoms, and since then, there have been many articles reporting this side effect. The mechanism by which fluoroquinolones cause worsening of MG is unclear. There are theories that the drug attenuates neuromuscular junction transmission and inhibits presynaptic membrane acetylcholine release through chelation of calcium ions, and there are also theories that the drug has direct toxic effects on acetylcholine channels. From clinical point of view, most of the patients’ symptom aggravation after medication appeared in 24-48 hours, with dyspnea being the most common, followed by weakness and fatigue, while the symptoms were rapidly relieved after stopping the medication, and recovery started in a few hours, and basically improved completely in a few days. MG crisis has also been reported in a small number of cases induced by macrolide antibiotics. Erythromycin-induced MG crisis has been reported in two patients, who recovered after discontinuation of the drug. One of the patients improved and then reintroduced erythromycin at low doses and again developed symptoms of myasthenia gravis. Similar reports have been made with clarithromycin. Telithromycin is a new drug of the ketolactone class, a macrolide antibiotic derivative that is highly effective in drug-resistant community-acquired pneumonia. However, both the raw manufacturer and the FDA warn against its use in patients with MG. Although there are also articles suggesting that exacerbation of MG symptoms may be related to the respiratory infection itself, the evidence is too scant to use them sparingly. Beta-lactams are relatively safe, with occasional reports of myasthenia gravis-like reactions. Two cases of exacerbation of myasthenia gravis symptoms associated with ampicillin have been reported. The authors performed animal experiments and no associated symptoms were induced. One case of carbapenem-cistatin combination has been reported in association. And to date, no exacerbation of MG symptoms has been reported with cephalosporins. When it comes to the relationship between MG symptoms and antibiotics, the notorious and most conclusive ones are the aminoglycosides. Aminoglycoside antibiotics affect both presynaptic acetylcholine release and the function of postsynaptic acetylcholine receptors. As early as 1964, streptomycin was reported to trigger exacerbation of MG symptoms. Neomycin and kanamycin are also included. Aminoglycoside-associated weakness is not unique to patients with MG, and there is also the possibility of critically ill polyneuropathy. The use of such drugs should be highly avoided in patients with MG. Recently, there have been reports of tigecycline. In a patient with MG crisis on previous moxifloxacin and a history of penicillin allergy, excellent results were obtained with the use of tigecycline. Tigecycline is a type of glycylcycline, a derivative of minocycline, which was approved by FDA for skin infections and abdominal infections in 2005 and for community-acquired pneumonia in 2009. As a derivative of the tetracycline family, while tetracycline may induce MG crisis, tigecycline has not been reported as such. When a patient with MG meets a pulmonary infection, the choice of antibiotic is a big challenge. Cephalosporins and penicillins may be preferred, followed by macrolides, and fluoroquinolones with caution. The safety of the drug can be judged by observing clinical symptoms, especially the change of symptoms within 24-48 hours. If there is worsening of symptoms, change promptly. When the efficacy is not good, try new drugs. Relatively contraindicated drugs may be used under close supervision if necessary for pathogenic testing.