Worms usually appear in the anterior chamber and vitreous and can sometimes be removed surgically. Incubation period
The incubation period in humans is usually from 1 week to 1 month after infection, and can be as long as 47 days. This interval varies, since humans are accidental hosts and the life cycle does not continue predictably as it would in a rat. Cause
Transmission
Transmission of the parasite is usually from eating raw or undercooked snails or other vectors. Infection is also frequent from ingestion of contaminated water or unwashed salad that may contain small snails and slugs, or have been contaminated by them. Reservoirs
Rats are the definitive host and the main reservoir for A. cantonensis, though other small mammals may also become infected. While Angiostrongylus can infect humans, humans do not act as reservoirs since the worm cannot reproduce in humans and therefore humans cannot contribute to their life cycle. Vectors
Angiostrongylus cantonensis has many vectors among invertebrates, with the most common being several species of snails, including the giant African land snail (Achatina) in the Pacific islands and apple snails of the genus Pila in Thailand and Malaysia. The golden apple snail, Pomacea canaliculata, is the most important vector in areas of China. Freshwater prawns, crabs, or other paratenic, or transport, hosts can also act as vectors. Organism
Morphology
A. cantonensis is a nematode roundworm with 3 outer protective collagen layers, and a simple stomal opening or mouth with no lips or buccal cavity leading to a fully developed gastrointestinal tract. Males have a small copulatory bursa at the posterior.
Milk fever, postparturient hypocalcemia, or parturient paresis is a disease, primarily in dairy cattle but also seen in beef cattle and non-bovine domesticated animals, characterized by reduced blood calcium levels (hypocalcemia). It occurs following parturition, at onset of lactation, when demand for calcium for colostrum and milk production exceeds the bodys ability to mobilize calcium. "Fever" is a misnomer, as body temperature during the disease is generally not elevated. Milk fever is more commonly seen in older animals (which have reduced ability to mobilize calcium from bone) and in certain breeds (such as Channel Island breeds). Clinical signs
The clinical signs of milk fever can be divided into three distinct stages:

Stage 1
Cows are mobile but show signs of hypersensitivity and excitability such as restlessness, tremors, ear twitching, head bobbing, and mild ataxia. If not treated, symptoms usually progress to stage 2. Stage 2
Cows can no longer stand and present in sternal recumbency. Tachycardia, weakened heart contraction and peripheral pulses. Cows appear dull, have dry muzzles, cold extremities and a lower than normal body temperature. Smooth muscle paralysis can cause bloat, and the inability to urinate or defecate. Cows often tuck their heads into their flanks. Stage 3
Lateral recumbency, muscle flaccidity, unresponsiveness to stimuli, and loss of consciousness progressing to coma. Heart rate can approach 120 bpm, with peripheral pulses  becoming undetectable. If untreated, progression will continue to death.