Freshwater snails: Pila spp., Pomacea canaliculata, Cipangopaludina chinensis, Bellamya aeruginosa and Bellamya quadrata
Slugs: Limax maximus, Limax flavus Deroceras laeve, Deroceras reticulatum, Laevicaulis alte, Sarasinula plebeia, Vaginulus yuxjsjs, Lehmannia valentiana, Phiolomycus bilineatus, Macrochlamys loana, Meghimatium bilineatum and probably other species of slugs.Definitive hosts of A. cantonensis include wild rodents, especially the brown rat (Rattus norvegicus) and the black rat (Rattus rattus).Paratenic hosts of A. cantonensis include the predatory land flatworm Platydemus manokwari and the amphibians, Bufo asiaticus, Rana catesbeiana, Rhacophorus leucomystax and Rana limnocharis.In 2004, a captive yellow-tailed black cockatoo (Calyptorhynchus funereus) and two free-living tawny frogmouths (Podargus strigoides) suffering neurological symptoms were shown to have the parasite. They were the first avian hosts discovered for the organism. In 2018, in Mallorca two North African hedgehogs with signs of acute neurological disease were found to have A. cantonensis in their brains, one of them with a gravid female. It was the first report of hedgehogs as hosts of Angiostrongylus.The Hawaiʻi Dept. of Health states that fresh water opihi can carry the parasite, as well as other aquatic organisms such as prawns, frogs, and water monitor lizards. House pets may interact with A. cantonensis-carrying animals yet not well studied. Cats are known to carry and spread feline lungworm in rat and snail interactions. Pathogenesis of human angiostrongylosis
The presence of parasitic worms burrowed in the neural tissue of the human central nervous system (CNS) causes complications.
All of the following result in damage to the CNS:
Direct mechanical damage to neural tissue from the worms motion
Toxic byproducts such as nitrogenous waste
Antigens released by dead and living parasites

Eosinophilic meningitis
Although the clinical disease caused by Angiostrongylus invasion into the CNS is commonly referred to as "eosinophilic meningitis", the actual pathophysiology is of a meningoencephalitis with invasion not just of the meninges, or superficial lining of the brain, but also deeper brain tissue. Initial invasion through the lining of the brain, the meninges, may cause a typical inflammation of the meninges and a classic meningitis picture of headache, stiff neck, and often fever. The parasites subsequently invade deeper into the brain tissue, causing specific localizing neurological symptoms depending on where in the brain parenchyma they migrate. Neurologic findings and symptoms wax and wane as initial damage is done by the physical in-migration of the worms and secondary damage is done by the inflammatory response to the presence of dead and dying worms. This inflammation can lead in the short term to paralysis, bladder dysfunction, visual disturbance, and coma and in the long term to permanent nerve damage, mental retardation, nerve damage, permanent brain damage, or death.Eosinophilic meningitis is commonly defined by the increased number of eosinophils in the cerebrospinal fluid (CSF). In most cases, eosinophil levels rise to 10 or more eosinophils per μl in the CSF, accounting for at least 10% of the total CSF leukocyte (white blood cell) count.