A review of wildlife diseases from Scandinavia

The epidemiological and historical aspects of some important and representative wildlife diseases from Scandinavia are discussed. In noninfectious diseases, examples include cataract in moose (Alces alces), atherosclerosis in hybrid hares (Lepus timidus X L. europaeus), and ethmoid tumors in moose. The epizootiological and historical aspects of the recent epizootics of myxomatosis in European rabbits (Oryctolagus cuniculus) and rabies and sarcoptic mange in red foxes (Vulpes vulpes) are reviewed. The decline and subsequent increase in population abundances of tetraonids including the capercaillie (Tetrao urogallus), black grouse (Lyrurus tetrix), and hazel hen (Tetrastes bonasia) are discussed, and an hypothesis on predation by foxes is presented as a possible explanation for these population fluctuations. The potential impact of environmental pollution on wildlife populations is emphasized with reference to mercury in wildlife from Sweden and the possible effects of cadmium and selenium resulting from acidification. A bibliography of important references is presented pertaining to these and other diseases of wildlife from Scandinavia.     

Corpora Cardiaca-Allata Complex of the Larvae of the Pink Bollworm,Pectinophora gossypiella. An Ultrastructural Study in Relation to Diapause

Raina, A. K., Borg, T. K. 1980. Corpora cardiaca-allata complex of the larvae of the pink bollworm, Pectinophora gossypiella. An ultrastructural study in relation to diapause. (Department of Entomology, North Dakota State University of South Carolina, School of Medicine, Columbia, U.S.A.) — Acta zool. (Stockh.) 61(2): 65–77. The corpora cardiaca (CC) and corpora allata (CA) of the pink bollworm, Pectinophora gossypiella, were studied at the ultrastructural level during induction maintenance, and termination of larval diapause. The CC is composed of 5–6 intrinsic secretory (IS) cells, glial cells, and axons that carry electron dense (ED) and electron lucent (EL) granules from the brain. The IS cells produce ED granules with an average diameter of 110 ± 26 nm. During diapause, the axons with ED granules showed large accumulations of neurosecretory granules, but the axons with the EL granules contained lesser amounts. The CA is made up of approximately 25 large cells and axons that pass through the CC from the brain. Most of the axons take up a peripheral position. A characteristic feature of CA cells during diapause was the presence of stacks of convoluted tubules of the smooth endoplasmic reticulum (SER) that may be associated with juvenile hormone synthesis. The IS cells of the CC appeared to be inactive during diapause.     

Morphology of connective tissue in skeletal muscle

The arrangement and distribution of connective tissue in six different skeletal muscles and smooth muscle was examined by scanning electron microscopy. The endomysial arrangement of collagen was similar in all types of muscle and consisted of three components: (1) myocyte-myocyte connectives; (2) myocyte-capillary connectives; and (3) a weave network of collagen intimately associated with the basal laminae of the myocytes. The perimysium of the different muscles was qualitatively similar but quantitatively dissimilar. The perimysium consisted of large tendon-like bundles of interwoven collagen which connected with the dense weave collagen that surrounded groups of muscles. The arrangement of the collagen in the perimysium and endomysium would explain differences in the mechanical properties of the different muscle. The contribution of the connective tissue to mechanical properties of muscle is discussed.     

Activation of polyphosphoinositide metabolism at artificial maturation of Patella vulgata oocytes.

The metabolism of polyphosphoinositides (PPI) has been investigated during the meiosis reinitiation of the oocytes of a prosobranch mollusk, the limpet Patella vulgata. Meiosis reinitiation which leads to germinal vesicle breakdown (GVBD) and metaphase-1 spindle formation was artificially induced by treating the prophase-blocked oocytes with 10 mM NH4Cl, pH 8.2. This treatment, which results in a rise in intracellular pH, triggered a general increase in polyphosphoinositide synthesis. Determinations of phosphorus content showed that maturation induced a 30 to 50% increase in both phosphatidylinositol (PI) and phosphatidylinositol-1 monophosphate (PIP) concentrations. Incorporations of 32PO4 and [3H]inositol have been measured in three classes of polyphosphoinositides: PI, PIP, and phosphatidylinositol 4,5-bisphosphate (PIP2). By comparing incorporation rates of the radiolabeled precursors into PPI before and after meiosis reinitiation, we found that artificial maturation by ammonia induced a 50-fold increase in the turnover of these lipids. No significant burst of inositol 1,4,5-trisphosphate (IP3) was observed after maturation. We suggest that modifications in PPI metabolism occurring at maturation of Patella oocytes might ensure the formation of an important stock of PPI that would be available for the profuse production of IP3, the messenger responsible for the Ca2+ signal at fertilization.     

Poisoning in Ferrets by Tissues of Alkyl Mercury-Fed Chickens

Chickens were fed alkyl mercury-dressed wheat (mercury content about 8 mg/kg) for 35–44 days and were then immediately sacrificed. No signs of untoward effects were observed. Muscle of the chickens, and a minor proportion of liver, were fed to two groups of two ferrets (Mustela furo L. × M. putorius L.), the mercury content of the diet being 7 and 5 mg/kg, respectively. The ferrets of the first group died after 35 and 36 days and those of the second after 58 days. The experimental ferrets showed a marked weight loss, attributable to muscular atrophy in addition to a reduced food intake. Clinical signs appeared in two to three weeks and were primarily neurological such as ataxia, trembling and paralysis. The signs could be correlated with pronounced degenerative changes of the central and peripheral nervous systems involving mainly the cerebellum and peripheral nerves and, to a lesser extent, the cerebrum and the spinal cord. Hypoplasia of the lymphatic tissue of the spleen and degeneration of the graafian follicles were seen as well. High mercury levels were found in the kidneys, liver and brain and also in skeletal muscle and the gonads of the ferrets (Table 2). Methyl mercury constituted the major part of the tissue mercury in the ferrets (as well as in the chickens). The results provide direct evidence of the transfer and accumulation of alkyl mercury in a toxic form through a food chain. The ecological implications are discussed.     

An EG-VEGF-Dependent Decrease in Homeobox Gene NKX3.1 Contributes to Cytotrophoblast Dysfunction: A Possible Mechanism in Human Fetal Growth Restriction

Idiopathic fetal growth restriction (FGR) is frequently associated with placental insufficiency. Previous reports have provided evidence that endocrine gland–derived vascular endothelial growth factor (EG-VEGF), a placental secreted protein, is expressed during the first trimester of pregnancy, controls both trophoblast proliferation and invasion, and its increased expression is associated with human FGR. In this study, we hypothesize that EG-VEGF-dependent changes in placental homeobox gene expressions contribute to trophoblast dysfunction in idiopathic FGR. The changes in EG-VEGF-dependent homeobox gene expressions were determined using a homeobox gene cDNA array on placental explants of 8–12 wks gestation after stimulation with EG-VEGF in vitro for 24 h. The homeobox gene array identified a greater-than-five-fold increase in HOXA9, HOXC8, HOXC10, HOXD1, HOXD8, HOXD9 and HOXD11, while NKX 3.1 showed a greater-than-two-fold decrease in mRNA expression compared with untreated controls. Homeobox gene NKX3.1 was selected as a candidate because it is a downstream target of EG-VEGF and its expression and functional roles are largely unknown in control and idiopathic FGR-affected placentae. Real-time PCR and immunoblotting showed a significant decrease in NKX3.1 mRNA and protein levels, respectively, in placentae from FGR compared with control pregnancies. Gene inactivation in vitro using short-interference RNA specific for NKX3.1 demonstrated an increase in BeWo cell differentiation and a decrease in HTR-8/SVneo proliferation. We conclude that the decreased expression of homeobox gene NKX3.1 downstream of EG-VEGF may contribute to the trophoblast dysfunction associated with idiopathic FGR pregnancies.     

Intracellular degradation of insulin and crinophagy are maintained by nitric oxide and cyclo-oxygenase 2 activity in isolated pancreatic islets

BACKGROUND INFORMATION: Pancreatic beta-cells require an optimal insulin content to allow instantaneous secretion of insulin. This is maintained by insulin biosynthesis and intracellular degradation of insulin. Degradation may be effected by crinophagy, i.e. the fusion of secretory granules with lysosomes. IL-1beta (interleukin 1beta) induces distinct changes of beta-cell lysosomes. To study the mechanisms for intracellular insulin degradation and crinophagy, isolated mouse pancreatic islets were exposed to IL-1beta and known pathways for IL-1beta actions were blocked. Intracellular insulin degradation was determined by following the fate of radioactively labelled insulin. Crinophagy was studied by ultrastructural analysis. The effects of blocking pathways for IL-1beta were monitored by measurements of nitrite and PGE(2) (prostaglandin E(2)). RESULTS: IL-1beta caused an enhancement of islet intracellular insulin degradation and an increase in the lysosomal incorporation of beta-cell secretory granules. The effects of IL-1beta were abolished by aminoguanidine, a selective inhibitor of inducible NOS (nitric oxide synthase), or by rofecoxib, a specific inhibitor of COX-2 (cyclo-oxygenase 2). In the absence of IL-1beta, nitroarginine, which is a selective inhibitor of constitutive NOS, caused a decrease in intracellular degradation of insulin in parallel with a decreased production of NO and PGE(2) by the islets. CONCLUSIONS: The correlation between the enhanced intracellular insulin degradation and lysosomal changes caused by IL-1beta suggests that insulin degradation may be effected by crinophagy. Under physiological conditions, significant beta-cell degradation of insulin may depend on the activity of COX-2, possibly stimulated by endogenous NO.