Repeated flood events and fossil forests at Curio Bay (Middle Jurassic), New Zealand

During the Middle Jurassic, the regional environment of Curio Bay, southeast South Island, New Zealand, was a fluvial plain marginal to volcanic uplands. Intermittent flashy, poorly-confined flood events buried successive conifer forests. With the termination of each flood, soils developed and vegetation was reestablished. In most cases, this developed into coniferous forest. In approximately 40 m of vertical section, 10 fossil forest horizons can be distinguished, highlighting a type of fluvial architecture which is poorly documented. Flood-basin material is minimal, but a short-Lived floodbasin lake is inferred to have developed within the interval of study. Paleocurrent indicators suggest enclosure of the basin on more than one side. Sedimentation style suggests a relatively dry (less than humid but not arid) climate with seasonal rainfall. (C) 2001 Elsevier Science B.V. All rights reserved.

N-15 natural abundance of fossil peat reflects the influence of animal-derived nitrogen on vegetation

delta(15)N signatures of fossil peat were used to interpret past ecosystem processes on tectonically active subantarctic Macquarie Island. By comparing past vegetation reconstructed from the fossil record with present-day vegetation analogues, our evidence strongly suggests that changes in the delta(15)N signatures of fossil peat at this location reflect mainly past changes in the proportion of plant nitrogen derived from animal sources. Associated with uplift above sea level over the past 8,500 years, fossil records in two peat deposits on the island chronicle a change from coastal vegetation with fur and elephant seal disturbance to the existing inland herbfield. Coupled with this change are synchronous changes in the delta(15)N signatures of peat layers. At two sites N-15-enriched peat delta(15)N signatures of up to +17parts per thousand were associated with a high abundance of pollen of the nitrophile Callitriche antarctica (Callitrichaceae). At one site fossil seal hair was also associated with enriched peat delta(15)N. Less N-15 enriched delta(15)N signatures (e.g. -1.9parts per thousand to +3.9parts per thousand) were measured in peat layers which lacked animal associated C. antarctica and Acaena spp. Interpretation of a third peat profile indicates continual occupation of a ridge site by burrowing petrels for most of the Holocene. We suggest that N-15 signatures of fossil peat remained relatively stable with time once deposited, providing a significant new tool for interpreting the palaeoecology.

The mitochondrial 12S gene is a suitable marker of populations of Sarcoptes scabiei from wombats, dogs and humans in Australia

We sequenced part of the mitochondrial 12S ribosomal RNA gene of 23 specimens of Sarcoptes scabiei from eight wombats, one dog and three humans. Twelve of the 326 nucleotide positions varied among these mites and there were nine haplotypes (sequences) that differed by 1-8 nucleotides. Phylogenetic analyses indicated that these mites were from two lineages: (1) mites from wombats from Victoria, Australia, and mites from the humans and dog from the Northern Territory, Australia (haplotypes 1-4, 9); and (2) mites from the humans and dog from the Northern Territory (haplotypes 5-8). Mites from the three different hosts (wombats, a dog and humans) had not diverged phylogenetically; rather, these mites had similar 12S sequences. Thus, we conclude that these mites from wombats, humans and a dog are closely related, and that they diverged from a common ancestor relatively recently. This conclusion is consistent with the argument that people and/or their dogs introduced to Australia the S. scabiei mites that infect wombats Australia. So, S. scabiei, which has been blamed for the extinction of populations of wombats in Australia, may be a parasitic mite that was introduced to Australia with people and/or their dogs. These data show that the mitochondrial 12S rRNA gene may be a suitable population marker of S. scabiei from wombats, dogs and humans in Australia.

Long QT syndrome in dogs with tick toxicity (Ixodes holocyclus)

Objective To evaluate cardiac electrical function in dogs with tick toxicity. Design A prospective clinical investigation of 39 client-owned dogs treated for naturally occurring tick toxicity. Procedure An ECG was performed on each dog on several occasions; at admission to hospital with tick toxicity, 24 h later, at discharge from hospital when clinically normal and approximately 12 months later. Results The mean QT interval corrected for heart rate (QTc) was prolonged at admission, 24 h and at discharge compared to the QTc measured 12 months later. T wave morphology was altered in dogs at admission. All other parameters were within normal limits. Conclusions The prolonged QTc interval and altered T wave morphology of dogs with tick toxicity reflects delayed cardiac repolarisation and is comparable with long QT syndrome (LQTS) in people who are predisposed to polymorphic ventricular tachycardia and sudden death. Resolution of ECG changes lagged behind clinical recovery.

Granulomatous meningoencephalomyelitis in dogs

Granulomatous meningoencephalomyelitis (GME) is a morphological description of an inflammatory disorder of the canine central nervous system (CNS). It has been reported in many areas of the world. including Australia, and is one of the more common nervous disorders of dogs. Most breeds of dogs of both sexes and all ages can be affected but young to middle-aged small and terrier breeds have been stated as being more susceptible. There are variable anatomical forms and distribution of the lesions in the CNS; the presenting clinical signs can reflect singly or collectively cerebellar, cerebral, and brain stem dysfunction. Meningeal and spinal cord involvement are also common. There is no specific diagnostic test but a combination of clinical signs, history and cerebro-spinal fluid cytology are useful indicators. However differential diagnosis from other inflammatory disorders of the brain is difficult. No infectious agent aetiology has been established for GME and therefore no satisfactory therapeutic approach is available. The role of the immune system in terms of either initiating or potentiating the lesions in the CNS appears to be the most likely direction for further investigation into the nature of this disorder.