Cantonal tubeworm disease (angiostrongyliasis cantonensis) is a parasitic infection with acute meningitis as the main manifestation, which is characterized by a significant elevation of eosinophils in the cerebrospinal fluid (CSF). Eosinophilic meningitis (eosinophilic meningitis) is almost synonymous with guangdong tuberous nematode disease. The disease is more common in Southeast Asia and the southeast coast of China, and was first identified in the lungs of rats in Guangzhou by Chen Xintao in 1933 and named after him, and cases of CSF larvae detected in Taiwan were reported in 1945. The main intermediate hosts are freshwater snails, mainly the brown onyx snail and the “Fortuna snail” in China. snail), originally an introduced species for artificial breeding, is now multiplying in the field in the south of China. After the eggs are produced, the stage 1 larvae hatch in the capillaries of the lungs and are discharged from the body to develop into stage 3 larvae in mollusks such as snails. After the mollusks are swallowed by the end hosts such as rats, the stage 3 larvae enter the blood circulation through the digestive tract, enter the liver, heart and central nervous system, and finally return to the pulmonary artery through the veins to develop into adults. Humans are incidental hosts, mostly infected by eating freshwater snails containing larvae of this stage. The larvae of the Cantonal tuberous nematode migrate within the human body and generally fail to develop into adults. The larvae invade the central nervous system, involving the meninges, brain and spinal cord parenchyma. Larval migration and dead worms cause tissue damage and inflammatory reactions, with large numbers of eosinophilic infiltrates, which can also form granulomas. Clinical manifestations: The disease can occur in “gourmets” and travelers in endemic areas who prefer freshwater fresh food. The disease can also occur in endemic areas when contaminated raw vegetables and fruit and vegetable juices are consumed. In non-endemic areas (where no natural host animals are found in the natural environment), infection is often caused by ingestion of contaminated food from endemic areas. The disease usually starts acutely, with patients presenting with fever and headache. The headache is often severe and persists without relief. Symptoms of meningeal irritation such as cervical resistance, positive Kernig’s sign, and increased intracranial pressure such as nausea, vomiting, and optic papilledema may be seen. There may be signs of focal damage to the brain or spinal cord parenchyma, with limb paralysis and pathological signs. Cranial nerve involvement may also be involved, such as facial nerve palsy, oculomotor nerve palsy, and hearing impairment. Patients often have the so-called “triple pain” symptoms of headache, muscle pain, and skin tingling [3]. There may be painful sensory abnormalities in the limbs or symptoms like occipital neuralgia. Diffuse enhancement of the soft meninges is seen on cephalometric magnetic resonance imaging (MRI) plus enhancement, suggesting meningitis; in the case of parenchymal damage, long T1 and long T2 signals are seen in punctate patches in the brain and spinal cord, and sometimes abnormal linear-like signals are seen, which are thought to be possible tunnels for worm migration and surrounding tissue edema. Patients may also have manifestations of other systemic damage, such as cough. In some cases, patchy lung images are found on chest radiographs and/or chest CT. The cerebrospinal fluid in patients in the acute phase is markedly altered, with elevated pressure, elevated protein, and more common hypoglycemia, and a moderately elevated white blood cell count of tens to hundreds of ×106/L. Cerebrospinal fluid cytology reveals a significantly elevated percentage of eosinophils, often above 50%. Peripheral blood generally also has an elevated eosinophil ratio. This is important for diagnosis. In a very few cases, tubeworms can be detected in the cerebrospinal fluid. Positive blood and cerebrospinal fluid antibodies against C. cantonensis are of diagnostic significance. Treatment: Glucocorticoids can effectively relieve symptoms and reduce the percentage of eosinophils in the cerebrospinal fluid and peripheral blood. Albendazole treatment can shorten the course of the disease. A combination treatment regimen of albendazole and glucocorticoids is available. The prognosis of the disease is generally good.