Four cotton-top tamarins (Sanguinus oedipus oedipus) and one emperor tamarin (S imperator subgrisescens) housed in a zoo became depressed, anorexic, paraparetic and eventually paralysed. The animals died within 5 days to 18 months of the appearance of clinical signs. Histological examination showed nonsuppurative and eosinophilic meningoencephalitis, and metastrongyle nematode larvae were found within subarachnoid spaces of all animals and within the spinal cord of one. Intact larvae with features consistent with Angiostrongylus cantonensis were recovered from the brain of one animal. This parasite is the classical cause of eosinophilic meningoencephalitis in many parts of the world and the diagnosis can be strongly suspected on clinical grounds. In endemic areas like south-east Queensland, protection of captive animals against infection with A cantonensis is a difficult balance between providing a stimulating, natural setting and eliminating potentially infectious definitive, intermediate and paratenic hosts. This is the first report of cerebrospinal angiostrongyliasis in tamarins and nonhuman primates in Australia.
Lecithocladium invasor n.sp. is described from the oesophagus of Naso annulatus, N. tuberosus and N. vlamingii on the Great Barrier Reef, Australia. The worms penetrate the oesophageal mucosa and induce chronic transmural nodular granulomas, which expand the full thickness of the oesophageal wall and protrude both into the oesophageal lumen and from the serosal surface. We observed two major types of lesions: large ulcerated, active granulomas, consisting of a central cavity containing a single or multiple live worms; and many smaller chronic fibrous submucosal nodules. Small, identifiable but attenuated, worms and degenerate worm fragments were identified within some chronic nodules. Co-infection of the posterior oesophagus of the same Naso species with Lecithocladium chingi was common. L. chingi is redescribed from N. annulatus, N. brevirostris, N. tuberosus and N. vlamingii. Unlike L. invasor n.sp., L. chingi was not associated with significant lesions. The different pathenogenicity of the two species in acanthurid fish is discussed.
We have identified a population of Caucasians with a defined past history of infection with Plasmodium vivax malaria. Using purified synthetic peptides overlapping the sequence of the circumsporozoite protein, we determined the percentage of individuals whose T cells proliferated or secreted IFN-gamma in response to peptide stimulation, for both this population and a population of nonmalaria-exposed control individuals. A number of peptides were recognized by both groups, but 11 peptides were uniquely recognized by the exposed population, and thus represented malaria-specific T cell epitopes. CD4 T cells were found to be responsible for the proliferative response. Humans last exposed to vivax sporozoites as long ago as 49 yr responded as well or better to these malaria-specific epitopes as individuals exposed within the previous month. Since such malaria-induced memory response may not be a feature of Plasmodium falciparum infections, and since P. falciparum does not have a persisting hypnozoite stage, our data argue that the persistence of T cell memory to vivax epitopes may result from antigenic persistence in the liver.
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