Angiostrongylus cantonensis3
History of discovery
Nematodes suspected to be
A. cantonensis
were first identified in the cerebrospinal fluid of a patient with eosiniphilic meningitis by Nomura and Lim in Taiwan in 1944. They calledthe parasite
Haemostrongylus ratti
, and noted that raw food eaten by the patient may havebeen contaminated by rats. Their paper, however, was not translated from the original Japanese into English until just after the parasite had been recognized in 1964, so theirdiscovery was not widely recognized.In 1955, Mackerass and Sanders identified the life cycle of the worm in rats, defining snailsand slugs as the intermediate host and noting the path of transmission through the blood,brain, and lungs in rats.In 1961, an epidemiological study of eosiniphilc meningitis in humans was conducted byRosen, Laigret, and Bories, who hypothesized that the parasite causing these infections wascarried by fish. However Alicata noted that raw fish was consumed by large numbers of people in Hawaii without apparent consequences, and patients presenting with meningitissymptoms had a history of eating raw snails or prawns in the weeks before presenting withsymptoms. This observation along with epidemiology and autopsy of infected brainsconfirmed
A. cantonensis
infection in humans as the cause of the majority of eosiniphilicmeningitis cases in Southeast Asia and the Pacific Islands.
[4]
Clinical presentation in humans
In humans, Angiostrongylus is the most common cause of eosiniphilic meningitis.
[1]
Frequently the infection will resolve without treatment or serious consequences, but incases with a heavy load of parasites the infection can be so severe it can cause permanentdamage to the CNS or death.
[5]
Early symptoms
Infection first presents with severe abdominal pain, nausea, vomiting, and weakness, whichgradually lessens and progresses to fever, and then to CNS symptoms and severe headacheand stiffness of the neck.
Severe/
CNS infection
CNS symptoms begin with mild cognitive impairment and slowed reactions, and in a verysever form often progress to unconsciousness.
[2]
Patients may present with neuropathicpain early in the infection. Eventually severe infection will lead to ascending weakness,quadriparesis, areflexia, respiratory failure, and muscle atrophy, and will lead to death if not treated. Occasionally patients present with cranial nerve palsies, usually in nerves 7and 8, and rarely larvae will enter ocular structures.
[6]
Even with treatment, damage to theCNS may be permanent and result in a variety of negative outcomes depending on thelocation of the infection, and the patient may suffer chronic pain as a result of infection.
[2]
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