Abstract
An article recently published by Dr Nicole Andenmatten and coworkers in Nature Methods 1 reveals the existence of an intriguing pathway of host-cell invasion used by Toxoplasma gondii, an apicomplexan protozoan parasite infecting a range of hosts worldwide, including several aquatic mammal species, in which it may cause abortion and lethal systemic disease. 4 Free-ranging bottlenose dolphins (Tursiops truncatus) 4 and striped dolphins (Stenella coeruleoalba) 2 rank among T. gondii– susceptible hosts, with both cetacean species inhabiting the Mediterranean Sea and many other marine ecosystems worldwide. More in detail, T. gondii is believed to be a pathogen of concern for the 2 aforementioned species, with a documented potential to affect their already threatened health and conservation status, as clearly highlighted by the prominent subacute-to-chronic, nonsuppurative meningoencephalitis lesions reported in several striped dolphins found stranded between 2007 and 2008 along the Ligurian Sea coast of Italy. 2 The brain tissue from these animals showed immunohistochemical and biomolecular evidence of T. gondii in close association with the above inflammatory lesions, 2,3 with the brain parenchyma from 3 dolphins also scoring positive for the protozoan B1, uprt, and gra6 genes, which subsequently allowed classification of the concerned T. gondii isolates as a genotype II and as 2 “atypical” genotype II strains, respectively. 3
Interestingly enough, although the bottlenose dolphin—a coastal species—is believed to acquire T. gondii infection through fecal oocyst contamination flowing from land to sea, this appears much less plausible for the striped dolphin, a typically pelagic species. 5 Indeed, the biological, eco-pathological, and epidemiological features of T. gondii infection among striped dolphins (as well as in other susceptible cetacean species living offshore) could not entirely reflect those characterizing T. gondii infection among bottlenose dolphins and, more in general, in terrestrial mammals. Therefore, an “open sea T. gondii life cycle” involving striped dolphins and other pelagic cetaceans, and thereby existing independently from the land and the benthic protozoan cycle(s), should not be ruled out. Furthermore, T. gondii strains infecting striped dolphins and other susceptible cetacean hosts living in the open sea could display a pathogenetic behavior not completely overlapping that of the protozoan isolates infecting bottlenose dolphins as well as terrestrial mammals. In this respect, differences in genes coding for virulence factors, such as those crucially involved in host-cell colonization, may account for a pathogenetic behavior of T. gondii among striped dolphins distinct from that of the protozoan isolates infecting bottlenose dolphins and land mammals.
On the basis of what has been described above, T. gondii strains obtained from stranded cetaceans, with special emphasis on those recovered from striped dolphins and other offshore species, should be considered a potentially valuable source of information for comparative studies addressing, in the future, the protozoan genes and factors involved in host-parasite interaction and host-cell invasion.