Failure to observe cross-fertilization between the Echinococcus granulosus G1 and G6 strains after an experimental mixed infection of the definitive host

The classification within Echinococcus granulosus is currently under debate. To assess the reproductive potential between the G1 and G6 strains, an experimental double infection was carried out in a dog. First, two fertile hydatid cysts were collected in Algeria from a cow and a dromedary. They were identified as being G1 and G6 with the markers coxI and nadI. Subsequently, a dog was inoculated with protoscoleces from these two cysts. Sixty days after infection, 85 adult worms were recovered from the intestine of the dog. Then, the two cysts and each of these individual parasites were characterized with the multilocus microsatellite EmsB and compared. For all worms, the scolex and the gravid proglottids, separately analyzed, provided an identical profile: the G1 profile was observed in 70 adults, and the G6 profile in the 15 others. No single worm exhibited a hybrid G1/G6 profile. This result suggests the absence of cross-fertilizing between the two taxa under the given experimental conditions, and so, the presence of a strong cross-reproductive barrier. This observation corroborates with the recent reclassification of G1 and G6 within two distinct species.     

大豆茎生长习性分类方法的研究--有限型与无限型茎顶的特征与识别标记

大豆有限型与无限型茎生长习性主要区别在于：前茎顶有顶生总状花序（或花序轴、或英簇）、三裂苞片、小苞片；后茎顶有复叶及其托叶（2个，生于复叶基部两侧）。针对大豆有限型和无限型茎顶性状发育的不同特点，提出稳定的识别标记及适用时期。     

碱基编辑技术及其在昆虫中的应用和展望

基因编辑是一种能对生物体基因组特定目标基因进行修饰的一种基因工程技术.近年来,基因编辑技术不断突破与发展,以CRISPR编辑系统为基础的单碱基编辑和先导编辑引起了科研人员的关注,随着基因编辑技术的不断成熟,已成功应用到各种动、植物以及其他生物中,为基因治疗和基因功能研究等方面提供了重要的技术支持.本文主要回顾了CRIS...     

Heinz body anemia in a dog that had been sprayed with skunk musk

A 5-year-old pit bull-type dog was examined because of lethargy and black feces, and a presumptive diagnosis of methemoglobinemia was made on the basis of grossly visible brown discoloration of the mucous membranes and urine. Heinz body formation was seen on examination of blood smears, and severe anemia developed 3 days later. The dog did not have any history of exposure to toxins or drugs that have been associated with Heinz body formation. The only remarkable historical finding was that the dog had been wandering loose the day prior to initial examination and returned home smelling strongly of skunk spray. Skunk spray contains thiols and other compounds that are strong oxidizing agents. It was speculated that the methemoglobinemia and Heinz body anemia were a result of exposure to these compounds. Skunk interactions with dogs usually have malodorous but otherwise harmless results. However, findings in this dog suggest that more serious consequences may develop in isolated cases.     

Susceptibility of adult chickens, with and without prior vaccination, to challenge with Marek's disease virus

Marek's disease (MD) outbreaks can occur in previously healthy adult layer or breeder flocks. However, it is not clear whether such outbreaks are caused by recent challenge with highly virulent (vv and vv+) strains of MD virus (MDV; i. e., new infection hypothesis) or by exacerbation of an earlier MDV infection (i. e., old infection hypothesis). To discriminate between these hypotheses, adult White Leghorn chickens of laboratory strains or commercial crosses with or without prior vaccination or MDV exposure were challenged at 18-102 wk of age with highly virulent MDVs, and lesion responses were measured. Horizontal transmission was studied in one trial. Challenge of adult chickens, which were free from prior MDV vaccination or exposure, with highly virulent MDV strains induced transient paralysis or tumors in 60%-100% of 29 groups (mean = 91%), and horizontal spread of virus was detected. The magnitude of the response was similar to that induced by challenge at 3 wk of age. In contrast, comparable challenge of adult chickens, which had been vaccinated or exposed to MDV early in life, induced transient paralysis or tumors in 0%-6% of 12 groups (mean = 0. 5%), although some birds showed limited virologic evidence of infection and transmission of the virus to contacts. The MD responses were influenced by the virulence of the challenge virus strain, and to a lesser extent by virus dose and route of exposure. Strong inflammatory lesions were induced in the brain and nerves of adult specific pathogen-free (SPF) chickens at 9-15 days after infection. The low susceptibility of previously vaccinated and exposed groups to challenge at > or =18 wk of age suggests that late outbreaks of MD in commercial flocks are not likely a result of recent challenge alone and that additional factors could be involved.     

Reproduction of postweaning multisystemic wasting syndrome in pigs by prenatal porcine circovirus 2 infection and postnatal porcine parvovirus infection or immunostimulation

Postweaning multisystemic wasting syndrome (PMWS) was reproduced in prenatally porcine circovirus 2 (PCV2)-infected pigs by either postnatal infection with porcine parvovirus (PPV) or by immunostimulation. Twenty-four randomly selected piglets from 3 sows, which had been experimentally infected during gestation with PCV2, were randomly divided into 3 groups; group 1 (prenatal PCV2 infection, with postnatal PPV infection), group 2 (prenatal PCV2 infection, with postnatal keyhole limpet hemocyanin, emulsified in incomplete Freund's adjuvant [KLH/ICFA] injection), and group 3 (prenatal PCV2 infection only). Twenty-four randomly selected piglets from 3 uninfected sows were randomly divided into 3 groups; group 4 (no prenatal infection, with postnatal PCV2 and PPV infection), group 5 (no prenatal infection, with postnatal PCV2 infection), and group 6 (negative control pigs). Body weight in negative control pigs (group 6) was increased significantly compared with pigs in groups 1, 2, and 4 at 49, 52, 56, 59, and 63 days of age. The granulomatous inflammatory reaction and lymphoid depletion that are typical lesions in pigs with PMWS were observed in the lymph node of piglets in groups 1, 2, and 4 at 63 days of age. Pigs in group 3 had significantly fewer PCV2-positive cells than those from groups 1, 2, 4, or 5. When the prenatally PCV2-infected pigs were infected with PPV or injected with immunostimulant in the postnatal period, they developed PMWS. Thus, factors that potentiate the progression of prenatal PCV2 infection to PMWS are postnatal infection with PPV or immune stimulation.     

Feline leukaemia. ABCD guidelines on prevention and management

OverviewFeline leukaemia virus (FeLV) is a retrovirus that may induce depression of the immune system, anaemia and/or lymphoma. Over the past 25 years, the prevalence of FeLV infection has decreased considerably, thanks both to reliable tests for the identification of viraemic carriers and to effective vaccines.InfectionTransmission between cats occurs mainly through friendly contacts, but also through biting. In large groups of non-vaccinated cats, around 30–40% will develop persistent viraemia, 30–40% show transient viraemia and 20–30% seroconvert. Young kittens are especially susceptible to FeLV infection.Disease signsThe most common signs of persistent FeLV viraemia are immune suppression, anaemia and lymphoma. Less common signs are immune-mediated disease, chronic enteritis, reproductive disorders and peripheral neuropathies. Most persistently viraemic cats die within 2–3 years.DiagnosisIn low-prevalence areas there may be a risk of false-positive results; a doubtful positive test result in a healthy cat should therefore be confirmed, preferably by PCR for provirus. Asymptomatic FeLV-positive cats should be retested.Disease managementSupportive therapy and good nursing care are required. Secondary infections should be treated promptly. Cats infected with FeLV should remain indoors. Vaccination against common pathogens should be maintained. Inactivated vaccines are recommended. The virus does not survive for long outside the host.Vaccination recommendationsAll cats with an uncertain FeLV status should be tested prior to vaccination. All healthy cats at potential risk of exposure should be vaccinated against FeLV. Kittens should be vaccinated at 8–9 weeks of age, with a second vaccination at 12 weeks, followed by a booster 1 year later. The ABCD suggests that, in cats older than 3–4 years of age, a booster every 2–3 years suffices, in view of the significantly lower susceptibility of older cats.