Parasites as Drivers and Passengers of Human-Mediated Biological Invasions

We provide an overview of the current state of knowledge of parasites in biological invasions by alien species. Parasites have frequently been invoked as drivers of invasions, but have received less attention as invasion passengers. The evidence to date that parasites drive invasions by hosts is weak: while there is abundant evidence that parasites have effects in the context of alien invasions, there is little evidence to suggest that parasites have differential effects on alien species that succeed versus fail in the invasion process. Particular case studies are suggestive but not yet informative about general effects. What evidence there is for parasites as aliens suggests that the same kind of factors determine their success as for non-parasites. Thus, availability is likely to be an important determinant of the probability of translocation. Establishment and spread are likely to depend on propagule pressure and on the environment being suitable (all necessary hosts and vectors are present); the likelihood of both of these dependencies being favourable will be affected by traits relating to parasite life history and demography. The added complication for the success of parasites as aliens is that often this will depend on the success of their hosts. We discuss how these conclusions help us to understand the likely effects of parasites on the success of establishing host populations (alien or native).

     

The survival and implantation of mouse blastocysts at varying degrees of reduced atmospheric pressure

Pregnant mice were exposed to reduced atmospheric pressures ranging from 630 to 390 mm Hg during the pre-implantation and implantation periods and the numbers of embryos surviving 85 hours post coitum compared with those in litter-mate controls. Even at a pressure of 630 mm Hg (= 1,550 mm Hg) there was a significant fall in numbers of normal blastocysts and rise in abnormal forms before implantation, and implantation sites were reduced in number. The numbers of abnormal forms increased and implantation sites decreased at lower pressures, suggesting strongly that the hypoxia of reduce atmospheric pressure was responsible for the abnormalities observed. The pre-implantation period appears to be one during which the fertilised ovum is at particular risk, both of hypoxic damage and of failure to implant. Implantation may afford a degree of protection against hypoxia.     

Obplacental giant cells of the domestic rabbit: development, morphology, and intermediate filament composition

Obplacental giant cells are large (less than or equal to 210 microns) polyploid cells that appear in the stroma of the pregnant uterus of the rabbit following ovoimplantation. Histological examination of a complete developmental series indicates that obplacental giant cells arise from trophoblastic knobs that have traversed the uterine epithelium during early implantation. During maturation, the cells undergo a massive (approximately 6,000%) increase in volume and penetrate deeply into the uterine stroma and myometrium, where they often become associated with blood vessels and smooth muscle cells. Giant cells at mid-gestation contain one or two large nuclei with prominent nucleoli and appear to be amitotic. They are rich in Golgi complexes, RER, SER, and cortically distributed cytoplasmic filaments, and contain intracellular canaliculi lined by microvilli. Giant cells vary with respect to the occurrence of lipid droplets, phagocytotic inclusions, lysosomal structures, and electron-dense granules. Immunocytochemistry demonstrates that the giant cells exhibit intermediate filaments related to cytokeratin and vimentin, but are negative for desmin and for an endothelial cell marker, Factor VIII-related antigen. The cells are positive for cytokeratin from their inception, but only become vimentin-positive between Days 12 and 15 of pregnancy, a change seemingly related to their detachment from epithelial tissue to take on an independent existence. Our findings indicate that the giant cells originate from obplacental trophoblast and, at maturity, exhibit cytoskeletal characteristics of isolated epithelial cells, as well as a complement of organelles suggestive of synthetic activity.     

Cadmium nephrotoxicity in human proximal tubule cell cultures

Summary Human proximal tubule kidney cells grown in a serum-free tissue culture medium were exposed to concentrations of CdCl₂ in a range of 0.5 to 10μg/ml. Cells were observed from 1 to 20 d upon initiation of cadmium in the culture fluid. Both confluent and subconfluent populations of cells were treated and evaluated for cytotoxicity. Both populations exhibited a concentration-dependent toxicity to ionic cadmium. For cells treated with 2.0 to 10 μg/ml Cd, the decreases in cell numbers were largely irreversible. However, cells treated with Cd in a range of 0.5 to 1.0 μg/ml exhibited a partial recovery of cell number and control morphology. In this range, recovery was more efficient in the subconfluent cultures. Fine structural alterations in Cd-treated tubule cells included condensation of nuclear chromatin, loss of microvilli structure, disorganization of lateral membrane interdigitation, as well as decreased uptake of aminoglycoside antibiotics as evidenced by decreased numbers of myeloid bodies in these cells. The results of this study imply that use of a human proximal tubule culture system has potential in discerning structural and functional effects of cadmium as well as other nephrotoxic metals and compounds on the human kidney. This paper was presented at a Symposium on the Physiology and Toxicology of the Kidney In Vitro co-sponsored by The Society of Toxicology (SOT) and the Tissue Culture Association held at the 27th annual meeting of the SOT in Dallas, Texas in 1988. This work was supported by the Johns Hopkins Center for Alternatives to Animal Testing.     

Abundance-range size relationships in British birds: is unexplained variation a product of life history?

Positive interspecific relationships between local abundance and geographic range size are a common feature of animal assemblages However, range size typically explains only a moderate proportion of the variation m abundance, begging the question of whether species of differing life history deviate from the underlying relationship in any systematic fashion Using data for the avifauna of Britain, and applying a comparative method to control for the effects of phylogenetic association, we demonstrate that this does not appear to be the case Only adult survivorship, age at independence and incubation period explain significant variation in abundance once range size is controlled for statistically, and then only a few percent There are two probable reasons why this result is contrary to general expectation First, although many life history variables are expected to show simple correlations with abundance or range size It is not obvious how these might relate to variation about the abundance–range size relationship Second, intuitive ideas about the form such variation might take may be seriously confounded by phylogenetic non–independence     

Familial Clustering of Abdominal Visceral Fat and Total Fat Mass: The Québec Family Study

The evidence for common familial factors underlying total fat mass (estimated from underwater weighing) and abdominal visceral fat (assessed from CT scan) was examined in families participating in phase 2 of the Québec Family Study (QFS) using a bivariate familial correlation model. Previous QFS investigations suggest that both genetic (major and polygenic) and familial environmental factors influence each phenotype, accounting for between 55% to 71% of the phenotypic variance in fat mass, and between 55% to 72% for abdominal visceral fat The current study suggests that the bivariate familial effect ranges from 29% to 50%. This pattern suggests that there may be common familial determinants for abdominal visceral fat and total fat mass, as well as additional familial factors which are specific to each. The relatively high spouse cross-trait correlations usually suggest that a large percent of the bivariate familial effect may be environmental in origin. However, if mating is not random, then the spouse resemblance may reflect either genetic or environmental causes, depending on the source [i.e., through similar genes or cohabitation (environmental) effects]. Finally, there are significant sex differences in the magnitude of the familial cross-trait correlations involving parents, but not offspring, suggesting complex generation (i.e., age) and sex effects. For example, genes may turn on or off as a function of age and sex, and/or there may be an accumulation over time of effects due to the environment which may vary by sex. Whether the common familial factors are genetic (major and/or polygenic), environmental, or some combination of both, and whether the familial expression depends on sex and/or age warrants further investigation using more complex models.