屠宰场犬新孢子虫和弓形虫的感染情况调查

<正>犬新孢子虫和弓形虫是呈世界性分布的重要寄生虫^[1]。犬是犬新孢子虫的主要终末宿主，可以排泄出对环境有抵抗力的卵囊。犬新孢子虫是导致牛流产的重要原因^[2-3]。弓形虫病属人兽共患病，由于犬与人及猫的关系密切，因此犬弓形虫病的感染情况可以反映当地弓形虫病的流行特点。犬可以通过吞食被弓形虫卵囊污染的泥土，或采食含弓形虫包囊的生肉而感染弓形虫。犬还可以经机械传播途径将弓形虫卵囊传染给人类^[4]。     

一起规模化猪场母猪群暴发弓形虫病的诊断与控制

<正>弓形虫病是由球虫类原虫—刚第弓形虫(Toxoplasma gondii)引起的一种人畜共患原虫病[1-2]。人或动物通过摄入被刚第弓形虫卵囊污染的食物、饮水或食入含有包囊的肉而被感染。猫(及其它猫科动物)是唯一从粪便排出弓形虫卵囊的动物,在弓形虫病传播中起重要作用[1-2]。猪感染弓形虫病后多呈亚临床症状,规模化养殖场暴发该病的情况较少[1]。2015年4月南方某存栏6 000余头母猪的规模化猪     

水源性弓形虫病的研究进展

弓形虫已对世界范围水源造成潜在威胁,水源性弓形虫病曾在发展中国家和一些发达国家暴发,造成了巨大的经济损失。人和动物感染水源性弓形虫病主要是由于食用含有活组织包囊的生肉或者摄入含有卵囊污染的食物或水而引起的,卵囊感染比组织包囊感染所引起的临床症状更加严重,弓形虫卵囊能够通过多种途径污染水源,传播疾病,对人和动物的健康和水资源的安全卫生造成了威胁。作者就近年来水源性弓形虫病的研究进展作一综述。     

一例猪弓形虫病的诊治报告

弓形体又称弓浆虫病,是由刚第弓形虫寄生于猪牛、羊、猫等动物细胞内引起的以高热、呼吸及神经症状、繁殖障碍为特征的原虫病,猫是传播弓形虫病的最主要感染来源,猫粪中的弓形虫卵囊可保持感染力达数月之久,卵囊可被某些食粪甲虫、蝇、蟑螂和蚯蚓机械性地传播,猪摄食了被卵囊污染的饲料、饮水而被感染。     

犬弓形虫病的病原与诊治

犬弓形虫病由龚地弓形虫引起的人畜及野生动物共患原虫病,主要侵害犬呼吸系统和神经系统。本病发生的原因主要是犬吞食了发育成熟的弓形虫卵囊或含有滋养体的包囊而感染。1病原弓形虫病是由肉孢子虫科弓形虫属的龚地弓形虫引起的人、畜及野生动物共患原虫病。根据其发育阶段的不同可分为滋养体、包囊、裂殖体、配子体和卵囊五型。滋养体和包囊出现在犬及其他中间宿主的体内,裂殖体、配子体和卵囊只出现在猫的体内。     

兔弓形虫病诊治报告

弓形虫病,是由弓形虫引起的一种人畜共患原虫病。据调查,兔弓形虫病的感染发病率在近几年有呈上升趋势。兔急性感染病例,通常死亡率比较高;慢性感染病例,对兔的生长发育及其肉、毛品质都会有不良影响。本病可给养兔生产效益造成严重经济损失。笔者近五年来,共诊治本病460余例,其诊治报告如下:1病因分析引起本病的病原虫是弓形虫。弓形虫的终宿主是猫及其猫科动物,中间宿主是人和各种哺乳动物。弓形虫的有性繁殖阶段主要在猫的小肠上皮细胞内完成,最后形成卵囊而随猫粪排出体外。排出体外的弓形虫卵囊,可在外界环境中再经过孢子增殖发育成为…     

羊弓形虫病的诊断与防治

弓形虫可以感染绝大部分哺乳动物,是一种对人类健康产生巨大威胁的人畜共患性寄生虫病之一。羊弓形虫病不仅可导致羊自身繁殖力下降,人类可能因食含有弓形虫卵囊的肉或奶制品而受感染。基于羊弓形虫病对我国大部分疫区所造成的巨大危害,本文通过对羊弓形虫的病原形态、流行情况、临床症状、病理变化、诊断及防治进行详细阐述,旨在为我国羊弓形虫病的医治与防控提供一定的数据支持。     

猪弓形虫病诊治

弓形虫病是由刚地弓形虫引起的一种人兽共患病,病猪以高热稽留、呼吸困难、皮肤发绀、出现神经症状,患病妊娠母猪以流产、所产胎儿畸形为特征. 1 流行病学 感染弓形虫的患猫和带虫猫(为终末宿主)排出的弓形虫卵囊可污染土壤、饲料和饮水,卵囊在适宜条件下孢子化后,即具有感染性.患病猪、带虫猪及其他被感染动物(中间宿主)的分泌物、排泻物中都含有弓形虫滋养体,其也具有感染性.     

猪弓形体病的防治

猪弓形体病是由弓形虫寄生引起的原虫病。我国各地均有此病。猫在传播上起重要作用。猫是本虫的终末宿主。猪、各种哺乳动物和禽类是本虫的中间宿主。中间宿主吃了猫粪中的弓形虫卵囊而感染。本病     

犬弓形虫病的病原与诊治

<正>犬弓形虫病由龚地弓形虫引起的人畜及野生动物共患原虫病,主要侵害犬呼吸系统和神经系统。本病发生的原因主要是犬吞食了发育成熟的弓形虫卵囊或含有滋养体的包囊而感染。1病原弓形虫病是由肉孢子虫科弓形虫属的龚地弓形虫引起的人、畜及野生动物共患原虫病。根据其发育阶段的不同可分为滋养体、包囊、裂殖体、配子体和卵囊五型。滋养体和包囊出现在犬及其他中间宿主的体内,裂殖体、配子体和卵囊只出现在猫的体内。     

Detection of T. gondii in tissues of sheep and cattle following oral infection.

It has been reported in the literature that cattle are more resistant to toxoplasmosis than sheep. Congenital disease due to T. gondii infection is rarely reported in cattle whereas the parasite is a major cause of abortion and neonatal mortality in sheep. It is believed that sheep remain chronically infected for life. Undercooked meat from infected sheep is an important source of infection for man. In contrast cattle are thought to harbour fewer parasite tissue cysts which may not persist for the lifetime of the host. Therefore, cattle are believed to pose less of a risk for human infection. In this study we examined the presence of T. gondii within a range of tissues in sheep and cattle at 6 weeks and 6 months following oral infection with 10(3) or 10(5) sporulated oocysts of T. gondii. The presence of parasite was determined by bioassay in mice and using polymerase chain reaction (PCR). The results from this study show that T. gondii was more frequently and consistently detected in sheep, in particular within brain and heart tissues, whereas parasites were not detected in the samples of tissues taken from cattle. T. gondii was more frequently detected in sheep given the higher dose of T. gondii. Examination of tissues at either 6 weeks or 6 months after infection did not appear to affect the distribution of T. gondii. The polymerase chain reaction has more specificity and sensitivity when detecting the presence of T. gondii in large animals than histological detection.     

Dual Sarcocystis neurona and Toxoplasma gondii infection in a Northern sea otter from Washington state, USA

Dual Sarcocystis neurona and Toxoplasma gondii infection was observed in a Northern sea otter from Washington, USA. The animal was found stranded, convulsed, and died shortly thereafter. Encephalitis caused by both S. neurona and T. gondii was demonstrated in histological sections of brain. Immunohistochemical examination of sections with S. neurona specific antisera demonstrated developmental stages that divided by endopolygeny and produced numerous merozoites. PCR of brain tissue from the sea otter using primer pairs JNB33/JNB54 resulted in amplification of a 1100 bp product. This PCR product was cut in to 884 and 216 bp products by Dra I but was not cut by Hinf I indicating that it was S. neurona [J. Parasitol. 85 (1999) 221]. No PCR product was detected in the brain of a sea otter which had no lesions of encephalitis. Examination of brain sections using T. gondii specific antisera demonstrated tachyzoites and tissue cysts of T. gondii. The lesions induced by T. gondii suggested that the sea otter was suffering from reactivated toxoplasmosis. T. gondii was isolated in mice inoculated with brain tissue. A cat that was fed infected mouse brain tissue excreted T. gondii oocysts which were infective for mice. This is apparently the first report of dual S. neurona and T. gondii in a marine mammal.     

Fatal toxoplasmosis in brown hares (Lepus europaeus): possible reasons of their high susceptibility to the infection

Brown hares (Lepus europaeus) trapped in the countryside and domestic rabbits were experimentally infected with Toxoplasma gondii (K7 strain) oocysts. Hares (n=12) were divided into groups of 4 and infected with 10, 10(3) and 10(5) oocysts. Rabbits (n=12) were infected in the same way. The experimentally infected animals were monitored for 33 days after infection (p.i.). Most of the infected hares demonstrated behavioural changes, and all of them died between 8 and 19 days p.i. Three of the rabbits demonstrated only clinical changes related to the concurrent pasteurellosis. The typical pathological finding in the hares were haemorrhagic enteritis, enlargement and hyperaemia of mesenteric lymph nodes, splenomegaly and multiple miliary necrotic lesions in the parenchyma of the liver and other organs. Pathological changes in the rabbits were less pronounced than in the hares. In rabbit brains, tissue cysts of the T. gondii were found. The incidence of T. gondii antibodies both in the hares and the rabbits was first ascertained on day 7 p.i. On day 12 p.i., antibodies were already found in all the animals infected. Antibody titres in indirect fluorescence antibody test (IFAT) using the anti-rabbit conjugate were markedly higher in rabbits than in hares. In all hares, T. gondii was isolated post mortem from the liver, brain, spleen, kidney, lung, heart and skeletal muscles. Although T. gondii was also isolated in all rabbits, it was not always isolated in all their organs. In all hares, parasitemia was demonstrated on days 7 and 12 p.i. The percentage of rabbits with detected parasitemia was lower. In hares, a decrease in the numbers of leukocytes during the infection was observed. No such decrease was observed in the rabbits. The lymphocyte activity after the stimulation with non-specific mitogens showed significant differences between the hares and the rabbits even before the infection. After the infection, the hares infected with 10(3) and 10(5) doses and in rabbits infected with a 10(5) dose showed a decrease of lymphocyte activity. Rabbits infected with a 10(3) dose showed an increase of the lymphocyte activity. While in hares toxoplasmosis was an acute and fatal disease, the infection in rabbits had subclinical manifestations only and easily passed to a latent stage. The different courses of toxoplasmosis in the hare and the rabbit may be due to the differences in the natural sensitivity of the two species to the T. gondii infection or a negative impact of stress to the immune status of hares.     

Comparative infectivity of oocysts and bradyzoites of Toxoplasma gondii for intermediate (mice) and definitive (cats) hosts

Tachyzoites, bradyzoites (in tissue cysts), and sporozoites (in oocysts) are the three infectious stages of Toxoplasma gondii. The prepatent period (time to shedding of oocysts after primary infection) varies with the stage of T. gondii ingested by the cat. The prepatent period (pp) after ingesting bradyzoites is short (3-10 days) while it is long (18 days or longer) after ingesting oocysts or tachyzoites. The conversion of bradyzoites to tachyzoites and tachyzoites to bradyzoites is biologically important in the life cycle of T. gondii and it has been proposed that the pp can be used to study stage conversion. In the present study, infectivity of oocysts and bradyzoites released from tissue cysts of a recent isolate of T. gondii, TgCkAr23, to cats and mice was compared. Ten-fold dilutions of oocysts or bradyzoites were administered orally to cats, and orally and subcutaneously to mice. Of the 29 cats each fed 1-10 million oocysts only one cat shed oocysts and the pp was 23 days; all cats remained asymptomatic. In contrast, all mice administered the same 10-fold dilutions of oocysts either orally or subcutaneously died of toxoplasmosis. The results confirm that infectivity of the oocysts to cats is lower than for mice and that oocysts are non-pathogenic for cats. Of the 41 cats each fed 1-1,000 free bradyzoites, 15 shed oocysts with a short pp of 4-9 days, and all remained asymptomatic. The infectivity of bradyzoites to mice by the oral route was approximately 100 times lower than that by the subcutaneous route. The results confirm the hypothesis that the pp in cats is stage and not dose dependent, and that transmission of T. gondii is most efficient when cats consume tissue cysts (carnivory) or when intermediate hosts consume oocysts (fecal-oral transmission).     

Correlation of tissue infection and serologic findings in pigs fed Toxoplasma gondii oocysts

Each of thirteen 6-week-old pigs was inoculated per os with 10,000 sporulated oocysts of Toxoplasma gondii. By postinoculation day (PID) 13, pigs were seropositive by the indirect fluorescent antibody test. Beginning on PID 13 and every 7 days thereafter through PID 97, 1 pig was killed and 6 tissues were examined for T gondii. Of the 13 pigs, 11 were infected, including the 1st pig killed on PID 13, although none of the pigs had gross lesions of toxoplasmosis. Tissues harboring T gondii most frequently were the heart and brain; organisms were detected less frequently in the longissimus muscles, diaphragm, and liver. Toxoplasma gondii was not detected in the bronchial lymph nodes. There was good correlation between antibody and presence of T gondii in these pigs. One additional pig, maintained as a noninfected control, remained seronegative and had no evidence of infection when killed on PID 97.     

Serodiagnosis of acute toxoplasmosis in macropods

The sera of 34 Australian macropods, the brains of which had been bioassayed for Toxoplasma gondii, were used to establish that a titre greater than 1/32 was significant for a direct agglutination test against toxoplasmosis. In addition, the concentration of 2-mercaptoethanol required to destroy the IgM fraction of macropod serum was confirmed in a modified direct agglutination test. To further validate the tests, the serological responses of three eastern grey kangaroos (Macropus giganteus) dosed orally with T. gondii oocysts and one M. giganteus injected with T. gondii cysts were studied. The tests were then used to investigate a diagnosis of acute toxoplasmosis in four Tasmanian pademelons (Thylogale billardierii) clinically suspected of acquiring toxoplasmosis naturally. One hundred and fifty-one Bennett's wallabies (Macropus rufogriseus rufogriseus) and 85 T. billardierii were also tested to determine the prevalence of acute toxoplasmosis of macropods in the wild. Four percent of M. r. rufogriseus and 1.2% of T. billardierii possessed T. gondii-specific IgM in their sera.     

Acute primary toxoplasmic hepatitis in an adult cat shedding Toxoplasma gondii oocysts

A 3-year-old 4-kg neutered male domestic shorthair cat died within 5 days after onset of fever and respiratory distress. At necropsy, all tissues were icteric, and the liver had a diffuse reticular pattern. Histologically, hepatitis and encephalitis were associated with Toxoplasma gondii tachyzoites. Toxoplasma gondii female gamonts and oocysts were found in epithelial cells of intact villi and in epithelial cells desquamated into the lumen. Finding of acute hepatitis and T gondii oocysts in an adult cat without detectable immunodeficiency is unusual, because adult cats rarely have clinical signs of toxoplasmosis during the oocyst-shedding phase.     

Serological evidence of Toxoplasma gondii infection in captive marine mammals in Mexico

Toxoplasma gondii infection in marine mammals is important because they are considered as a sentinel for contamination of seas with T. gondii oocysts, and toxoplasmosis causes mortality in these animals, particularly sea otters. Serological evidence of T. gondii infection was determined in 75 captive marine mammals from four facilities in southern and central geographical regions in Mexico using the modified agglutination test (MAT). Antibodies (MAT, 1:25 or higher) to T. gondii were found in 55 (87.3%) of 63 Atlantic bottlenose dolphins (Tursiops truncatus truncatus), 3 of 3 Pacific bottlenose dolphins (Tursiops truncatus gillii), 2 of 4 California sea lions (Zalophus californianus), but not in 3 West Indian manatees (Trichechus manatus), and 2 Patagonian sea lions (Otaria flavescens). Seropositive marine mammals were found in all 4 (100%) facilities sampled. All marine mammals were healthy and there has not been any case of clinical toxoplasmosis in the facilities sampled for at least the last 15 years. The seroprevalence of T. gondii infection in marine mammals of the same species did not vary significantly with respect to sex and age. This is the first report on the detection of antibodies to T. gondii in marine mammals in Mexico.     

Enrofloxacin is able to control Toxoplasma gondii infection in both in vitro and in vivo experimental models

Currently, toxoplasmosis is treated with sulfadiazine and pyrimethamine. However, this treatment presents several adverse side effects; thus, there is a critical need for the development and evaluation of new drugs, which do not present the same problems of the standard therapy. Enrofloxacin is a fluoroquinolone antibiotic known to control infection against several bacteria in veterinary medicine. Recently, this drug has demonstrated protective effects against protozoan parasites such as Neospora caninum. The present study aimed to determine the effect of enrofloxacin in the control of Toxoplasma gondii infection. For this purpose, human foreskin fibroblast (HFF) cells were infected with T. gondii RH strain and treated with sulfadiazine, penicillin/streptomycin, pyrimethamine, or enrofloxacin. Following treatment, we analyzed the infection index, parasite intracellular proliferation and the number of plaques. Additionally, tissue parasitism and histological changes were investigated in the brain of Calomys callosus that were infected with T. gondii (ME49 strain) and treated with either sulfadiazine or enrofloxacin. Enrofloxacin was able to reduce the infection index, intracellular proliferation and the number of plaques in HFF cells infected by T. gondii in comparison with untreated or penicillin/streptomycin-treated ones. Enrofloxacin was more protective against T. gondii in HFF infected cells than sulfadiazine treatment (P<0.001). In addition, pyrimethamine, enrofloxacin or the associations of sulfadiazine plus pyrimethamine, enrofloxacin plus sulfadiazine or enrofloxacin plus pyrimethamine-treatments were able to reduce the plaque numbers in HFF cells infected by T. gondii when compared to medium, penicillin/streptomycin or sulfadiazine alone. In vivo experiments demonstrated that enrofloxacin diminished significantly the tissue parasitism as well as the inflammatory alterations in the brain of C. callosus infected with T. gondii when compared with untreated animals. Based on our findings, it can be concluded that enrofloxacin is a potential alternative drug for the treatment of toxoplasmosis.     

The influence of colostrum on infection of calves around 7 months of age with Schistosoma mattheei

Thirty red-legged partridges (Alectoris rufa), 5-month-old, were orally inoculated with oocysts of the OV-51/95 strain of Toxoplasma gondii. Birds were distributed into five groups and received, respectively, 10 (group A, 4 birds), 50 (group B, 14 birds), 10(2) (group C, 4 birds), 10(3) (group D, 4 birds) and 10(4) (group E, 4 birds) oocysts. One partridge from group B and one from group E died suddenly of acute toxoplasmosis at 7 day after inoculation (DAI) with demonstrable T. gondii in several tissues. The rest of birds remained clinically normal until killed at 44, 58, 65, 72, 79 or 100 DAI. Brain, heart, liver and skeletal muscle from these partridges were bioassayed individually in mice; T. gondii was demonstrated in all these tissues, except in heart of three birds inoculated, respectively, with 10, 50 and 10(2) oocysts. Lesions were not seen in histologic sections of tissues from surviving partridges. These results suggest that red-legged partridges are resistant to clinical toxoplasmosis.