Accumulation of galactitol has been attributed to many of the negative effects of galactosemia, and high concentrations of galactitol have been found in people with classic galactosemia (GALT deficiency or Galactose-1-phosphate uridylyltransferase deficiency), galactokinase deficiency, and epimerase deficiency with glucose. Oxidation to galactonate
Accumulated galactose can also undergo an alternative reaction: Oxidation to galactonate. The mechanism of galactonate formation is still unclear. However, recent studies suggest that galactose dehydrogenase is responsible for converting galactose to galactonolactone, which then spontaneously or enzymatically converts to galactonate. Once formed, galactonate may enter the pentose phosphate pathway. Thus, Oxidation to galactonate serves as an alternate pathway for metabolizing galactose. This oxidative pathway renders accumulated galactonate less harmful than accumulated galactitol. Diagnosis
In many states throughout the world, infants routinely undergo newborn screening (NBS) for galactosemia. This allows a diagnosis to be made while the person is still an infant. Infants affected by galactosemia typically present with symptoms of lethargy, vomiting, diarrhea, failure to thrive, and jaundice. None of these symptoms are specific to galactosemia, often leading to diagnostic delays. If the family of the baby has a history of galactosemia, doctors can test prior to birth by taking a sample of fluid from around the fetus (amniocentesis) or from the placenta (chorionic villus sampling or CVS). Galactosemia is normally first detected through newborn screening which if available, is able to diagnose the majority of affected infants.
The best mechanism of prevention of A. cantonesis outbreak is to institute an aggressive control of snail and slug population, proper cooking of intermediate and paratenic hosts such as fish, freshwater prawn, frogs, molluscs, and snails along with proper food-handling techniques. The common prevention techniques for diarrheal illness are very effective in preventing A. cantonensis infection. Not much is known about why it targets the brain in humans, but a chemically induced chemotaxis has been implicated recently. Acetylcholine has been previously reported to enhance motility of this worm via nicotinic acetylcholine receptors. Experimental assays in animal models are needed to validate a chemically induced chemotaxis  by use of anticholinergic drugs to prevent cerebral infection following infections by A. cantonesis. Hosts
Intermediate hosts of larvae of for A. cantonensis include:

Land snails: Thelidomus aspera from Jamaica, Pleurodonte sp. from Jamaica, Sagda sp. from Jamaica, Poteria sp. from Jamaica, Achatina fulica, Satsuma mercatoria, Acusta despecta, Bradybaena brevispira, Bradybaena circulus Bradybaena ravida, Bradybaena similaris, Plectotropis appanata and Parmarion martensi from Okinawa and Hawaii, Camaena cicatricosa, Trichochloritis rufopila, Trichochloritis hungerfordianus and Cyclophorus spp.