Reproductive cycle of yellow sea bream <Emphasis Type="Italic">Dentex tumifrons</Emphasis> in Wakasa Bay,the Sea of Japan off central Honshu

ABSTRACT:   To determine the spawning season and reproductive cycle of the yellow sea bream, Dentex tumifrons , in Wakasa Bay, in the Sea of Japan off central Honshu, seasonal change in the gonadosomatic index ( GSI ) was examined and histological observations of both ovaries and testes were conducted. The female GSI gradually increased from May, maintained a high level between August and October and then rapidly decreased. The histological observations of the ovary showed that vitellogenesis began from May and developed until September. Spent fish began to be observed in October and all the fish collected in December were spent. There was only one peak in the seasonal change in GSI of males and females in Wakasa Bay. Thus, yellow sea bream spawn only in autumn in Wakasa Bay. Differences in the reproductive cycle and number of spawning seasons were found between the two different latitudinal areas, Wakasa Bay and the East China Sea (low latitudinal area) where the spawning seasons were spring and autumn. An increase in water temperature is an important factor to initiate gonadal maturation (recrudescence) and is terminated by the short day-length in Wakasa Bay.     

Association between preoperative characteristics and risk of anaesthesia-related death in dogs in small-animal referral hospitals in Japan

Objective

To explore the major risk factors linking preoperative characteristics and anaesthesia-related death in dogs in referral hospitals in Japan.

Feline demodicosis caused by an unnamed species

A case of feline demodicosis is described in this report. A 13-year-old spayed female domestic short hair cat weighing 4.5 kg was being treated with cefovecin and alternately with prednisone or methylprednisolone. On further physical examination, the cat showed mild erythema and hair loss on the bridge of the nose, around the eyes, on the chin, on the side part of the breast and on the abdomen. A large number of Demodex mites were found in deep skin scrapings from the affected areas. The cat was then treated with ivermectin at 600 μg/kg administered SC daily. After 4 weeks of treatment, the cat was clinically normal with no mites detected in the skin scrapings from the face or breast areas. The mite responsible may represent a previously seen but as yet unnamed new species. This is third report that describes a case of feline demodicosis caused by a different, unnamed mite species that has different morphological characteristics to those of known Demodex mites and may represent a previously seen but as yet unnamed species.     

Scanning electron microscopy of root resorption of feline teeth

Scanning electron microscopy was carried out on 10 feline extracted permanent teeth from 3 cases with root resorption. Various-sized resorption lacunae were well defined, showing an etched pattern and configuration as shown in human deciduous teeth. In cats, regardless of the shape and depth of lacunae, the resorption lacunae showed opening dentinal tubules in the wall with or without cement matrix apperring only in the deep and round lacunae of human cases. Some specific process of mineralization for repairing dental root resorption was suggested in cats.     

Origin and evolution of highly pathogenic H5N1 avian influenza in Asia

Outbreaks of highly pathogenic avian influenza caused by H5N1 viruses were reported almost simultaneously in eight neighbouring Asian countries between December 2003 and January 2004, with a ninth reporting in August 2004, suggesting that the viruses had spread recently and rapidly. However, they had been detected widely in the region in domestic waterfowl and terrestrial poultry for several years before this, and the absence of widespread disease in the region before 2003, apart from localised outbreaks in the Hong Kong Special Autonomous Region (SAR), is perplexing. Possible explanations include limited virus excretion by domestic waterfowl infected with H5N1, the confusion of avian influenza with other serious endemic diseases, the unsanctioned use of vaccines, and the under-reporting of disease as a result of limited surveillance. There is some evidence that the excretion of the viruses by domestic ducks had increased by early 2004, and there is circumstantial evidence that they can be transmitted by wild birds. The migratory birds from which viruses have been isolated were usually sick or dead, suggesting that they would have had limited potential for carrying the viruses over long distances unless subclinical infections were prevalent. However, there is strong circumstantial evidence that wild birds can become infected from domestic poultry and potentially can exchange viruses when they share the same environment. Nevertheless, there is little reason to believe that wild birds have played a more significant role in spreading disease than trade through live bird markets and movement of domestic waterfowl. Asian H5N1 viruses were first detected in domestic geese in southern China in 1996. By 2000, their host range had extended to domestic ducks, which played a key role in the genesis of the 2003/04 outbreaks. The epidemic was not due to the introduction and spread of a single virus but was caused by multiple viruses which were genotypically linked to the Goose/GD/96 lineage via the haemagglutinin gene. The H5N1 viruses isolated from China, including the Hong Kong SAR, between 1999 and 2004 had a range of genotypes and considerable variability within genotypes. The rising incidence and widespread reporting of disease in 2003/04 can probably be attributed to the increasing spread of the viruses from existing reservoirs of infection in domestic waterfowl and live bird markets leading to greater environmental contamination. When countries in the region started to report disease in December 2003, others were alerted to the risk and disease surveillance and reporting improved. The H5N1 viruses have reportedly been eliminated from three of the nine countries that reported disease in 2003/04, but they could be extremely difficult to eradicate from the remaining countries, owing to the existence of populations and, possibly, production and marketing sectors, in which apparently normal birds harbour the viruses.     

Effects of butorphanol and carprofen on the minimal alveolar concentration of isoflurane in dogs

OBJECTIVE: To evaluate the effects of butorphanol and carprofen, alone and in combination, on the minimal alveolar concentration (MAC) of isoflurane in dogs. DESIGN: Randomized complete-block crossover study. ANIMALS: 6 healthy adult dogs. PROCEDURE: Minimal alveolar concentration of isoflurane was determined following administration of carprofen alone, butorphanol alone, carprofen and butorphanol, and neither drug (control). Anesthesia was induced with isoflurane in oxygen, and MAC was determined by use of a tail clamp method. Three hours prior to induction of anesthesia, dogs were fed a small amount of canned food without any drugs (control) or with carprofen (2.2 mg/kg of body weight [1 mg/lb]). Following initial determination of MAC, butorphanol (0.4 mg/kg [0.18 mg/lb], i.v.) was administered, and MAC was determined again. Heart rate, respiratory rate, indirect arterial blood pressure, endtidal partial pressure of CO2, and saturation of hemoglobin with oxygen were recorded at the time MAC was determined. RESULTS: Mean +/- SD MAC of isoflurane following administration of butorphanol alone (1.03 +/- 0.22%) or carprofen and butorphanol (0.90 +/- 0.21%) were significantly less than the control MAC (1.28 +/- 0.14%), but MAC after administration of carprofen alone (1.20 +/- 0.13%) was not significantly different from the control value. The effects of carprofen and butorphanol on the MAC of isoflurane were additive. There were not any significant differences among treatments in regard to cardiorespiratory data. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that administration of butorphanol alone or in combination with carprofen significantly reduces the MAC of isoflurane in dogs; however, the effects of butorphanol and carprofen are additive, not synergistic.