Complete genomic characteristics and pathogenic analysis of the newly emerged classical swine fever virus in China.

BACKGROUND: Classical swine fever (CSF) is one of the most devastating and highly contagious viral diseases in the world. Since late 2014, outbreaks of a new sub-genotype 2.1d CSF virus (CSFV) had caused substantial economic losses in numbers of C-strain vaccinated swine farms in China. The objective of the present study was to explore the genomic characteristics and pathogenicity of the newly emerged CSFV isolates in China during 2014-2015. RESULTS: All the new 8 CSFV isolates belonged to genetic sub-genotype 2.1d. Some genomic variations or deletions were found in the UTRs and E2 of these new isolates. In addition, the pathogenicity of HLJ1 was less than Shimen, suggesting the HLJ1 of sub-genotype 2.1d may be a moderated pathogenic isolate and the C-strain vaccine can supply complete protection. CONCLUSIONS: The new CSFV isolates with unique genomic characteristics and moderate pathogenicity can be epidemic in many large-scale C-strain vaccinated swine farms. This study provides the information should be merited special attention on establishing prevention and control policies for CSF.

[Haemorrhagic septicaemia in a pig caused by extraintestinal pathogenic Escherichia coli (ExPEC) as a differential diagnosis in classical swine fever--case report and review of the literature]. / Durch Extraintestinal pathogene Escherichia coli (ExPEC) bedingte haemorrhagische Septikaemie beim Schwein als Differentialdiagnose zur Klassischen Schweinepest--Fallbericht und Literaturübersicht.

Domestic pig herds in some regions of Germany are permanently threatened by Classical Swine Fever. In the case of suspicion, a series of infectious and non infectious causes has to be excluded. The present paper describes a case of Escherichia coli septicaemia, with clinical and pathological symptoms that could not be differentiated from European or African Swine Fever. The E. coli strain could not be classified by standard serotyping. Virulence factors common for ETEC (enterotoxic E. coli) or EDEC (edema-disease E. coli) were not detected. Instead, we found P-fimbriae and aerobactin, thus characterising this strain as an extraintestinal pathogenic strain. Such strains have sporadicly been reported as the cause of septicaemia in piglets or weaners, but the present case is the first report of an E. coli-associated septicaemia in an adult pig. This case shows that extraintestinal pathogenic E. coli can be the cause of severe septicaemia and haemorrhagia. They thus have to be considered as a further differential diagnosis in swine fever.

Detection of hog cholera virus antigens in experimentally-infected pigs using an antigen-capture ELISA.

An antigen-capture ELISA was used to detect hog cholera virus (HCV) antigens in blood and tissues taken from pigs infected with 2 different strains of virus. Specific antigens were demonstrated in peripheral blood leucocytes (PBLs) and a wide range of tissue samples 4-6 days after infection of pigs with a moderate-high virulent HCV strain (Weybridge virus). Strong signal to noise (S/N) ratios were obtained in the ELISA for PBLs and lymphoid tissues such as spleen, tonsil and mesenteric lymph nodes at 5-7 days after infection with the Weybridge virus, S/N ratios varying between 8.1-19.7 for blood samples and 4.3-19.1 for spleen samples. High positive ELISA results were also obtained for duodenum and ileum samples (S/N ratios 10.3-18.6) taken from these pigs, reflecting severe pathological changes observed in the gut at post mortem. In contrast, the antigen-capture ELISA gave strong positive results for PBLs and spleen samples only at 7-9 days after infection of pigs with a low virulent strain of HCV (New South Wales virus). The ELISA S/N ratios averaged 9.5 for PBLs and 8.9 for spleen samples in these animals. Although virus isolation detected infection earlier in the infected pigs, the ELISA returned positive results on PBLs and spleen samples around the time all of the animals first showed typical signs of classical swine fever. The technique does not require tissue culture and takes less than 36 h to return a definitive result.

[Asymptomatic carriage of Pestivirus in ruminants]. / Le portage asymptomatique des Pestivirus chez les ruminants.

Pestiviruses are enveloped single-chain ribonucleic acid viruses with a positive polarity. Pestiviruses include the viruses of classical swine fever (hog cholera), Border disease of sheep, mucosal disease of cattle, and isolates obtained from wild animals, such as red deer (Cervus elaphus). Among ruminants, pestiviruses have developed a remarkable strategy for assuring their persistence. Through epigenetic transmission, they lead to the birth of asymptomatic carrier animals harbouring non-cytopathic variants, which become immunotolerant to the strain of virus present. The presence of a small number of asymptomatic carriers enables the virus to circulate within a herd by horizontal transmission, leading to the birth of a new generation of asymptomatic carriers.

A comparison of the pathogenicity of two strains of hog cholera virus. 1. Clinical and pathological studies.

The virulence of a strain of hog cholera virus isolated during an outbreak of mild disease in pigs in New South Wales in 1960/61 (the NSW strain) was compared over 11 days with that of a virulent strain by inoculating 8 pigs with each virus and comparing the ensuing clinical signs and pathology. Both viruses caused persistent pyrexia and leukopenia, the NSW strain 4 to 5 days and the virulent strain 3 days, after inoculation. Few other clinical signs were observed in the pigs inoculated with the NSW strain. In contrast, all pigs inoculated with the virulent strain became progressively depressed and incoordinated, and were killed between days 6 and 9. Bronchopneumonia and swollen, reddened lymph nodes were observed in pigs inoculated with both viruses. Few other gross lesions were observed with the NSW strain, but some pigs receiving the virulent strain had pustules in the tonsil and the anterior oesophagus, petechial haemorrhages in the kidney, and small infarcts at the margins of the spleen. There were marked differences in the histopathology, both in the variety of organs affected and the severity of lesions in individual organs. Suppurative bronchopneumonia occurred in both groups. Other changes in the pigs affected with the NSW strain were colitis, mild cerebral vasculitis, necrosis, haemorrhage and neutrophil infiltration in some lymph nodes and spleens. In pigs infected with virulent virus the cerebral vasculitis was so severe that there was necrosis of cells within the vessel walls.(ABSTRACT TRUNCATED AT 250 WORDS)

A comparison of the pathogenicity of two strains of hog cholera virus. 2. Virological studies.

Quantitative and qualitative differences were demonstrated in the amount of virus in a range of tissues from pigs infected with either the Weybridge or New South Wales (NSW) strains of hog cholera (HC) virus. The titre of the Weybridge strain in samples, as assessed by either virus titration in cell culture or by the density of specific fluorescing cells in tissue sections, was higher than that for the NSW strain. This correlated with the greater severity of the clinico-pathological syndrome induced by the Weybridge strain. The implications of the differences in the virus content of tissues in the diagnosis of HC is discussed as is the use of monoclonal antibodies to differentiate HC and bovine virus diarrhoea viruses.

Survival of hog cholera virus (HCV) in sausage meat products (Italian salami).

Survival of hog cholera virus (HCV) was determined in several sausage meat products (Italian salami) prepared with meats from experimentally infected hogs slaughtered at the peak of disease. Meats were processed following the technology applied by the main factories of the typical Italian production. The survival of HCV was assessed through inoculation in both PK 15 cell monolayers and fully susceptible piglets. In all types of sausages examined HCV was detected up to 75 days of curing by piglet inoculation. This technique was much more sensitive than use of cell culture.

Pathogenesis of classical swine fever: B-lymphocyte deficiency caused by hog cholera virus.

Hog cholera, also known as classical or European swine fever, is caused by hog cholera virus, a member of the genus Pestivirus. It is shown here that the end stage of lethal infection in the natural host is associated with a dramatic depletion preferentially of B lymphocytes in the circulatory system as well as in lymphoid tissues. Already at the onset of disease, viral replication in lymphoid tissues demarcates the germinal centers, and the viral genome remains localized to that site as the disease progresses even after morphologic disintegration of the follicular structure. A block in B-lymphocyte maturation by infection and destruction of germinal centers is discussed as a key event in the pathogenesis of acute, lethal hog cholera.

Characterization and pathogenicity for pigs of a hog cholera virus strain isolated from wild boars.

One hog cholera virus strain isolated from an outbreak of the disease in a wild boar breeding herd in Brittany (France) in 1990 has been characterized with a panel of monoclonal antibodies to hog cholera virus and ruminant pestiviruses: the strain was found to be indistinguishable from that of other domestic pig isolates. The pathogenicity of the strain to domestic pigs was evaluated by infecting intranasally, intramuscularly and by contact 17 specific pathogen-free 6-week- and 12-week-old pigs. Sixteen of the 17 pigs showed symptoms of hog cholera. The virus was detected in the blood of the 16 pigs during all phases of hyperthermia which persisted up to death or the terminal phase, ie between 16 and 29 days post-infection. One animal recovered after presenting a mild form of the disease. This pig was the only one which raised antibodies to the virus. Typical hog cholera lesions were observed in 2 pigs only; the other animal showed very few pathological changes. No relationship between intensity or duration of the disease and pathological changes could be established.

Clinical, post mortem and virological findings after simultaneous inoculation of pigs with hog cholera and bovine viral diarrhoea virus.

The clinical course, post mortem lesions as well as virological and serological results after simultaneous intranasal inoculation of pigs with bovine viral diarrhoea virus (BVDV) and hog cholera virus (HCV) are described. Five groups of four weaners received constant doses of BVDV strain OSLOSS/2482 and tenfold decreasing doses of HCV strain ALFORT/187. Doses of 1,000 and 100 TCID50 of HCV in groups A and B of pigs led to fever and severe clinical signs in all animals of two groups, whereas at higher dilution of inoculum two, three or four animals survived without any clinical signs in the respective groups (C-E). Leucocyte samples taken from febrile animals and from normal pigs on five consecutive days were inoculated into both fetal calf kidney (FCK) and PK (15) cell cultures. Virus isolates were differentiated with BVDV and HCV specific monoclonal antibodies. HCV viraemia was detected in febrile animals exclusively, and BVDV viraemia occurred in not affected animals on days 3 to 7 post inoculation. Neutralizing antibodies (nab) against BVDV appeared before HCV nab in surviving animals of groups C and D after receiving low doses of HCV (10 or 1 TCID50). No BVDV nab were detected in group E that had received such a high dilution of HCV in addition to BVDV that theoretically no HCV was applied.

A survey of wild swine in the United States for evidence of hog cholera.

The results of surveillance for hog cholera (HC) in wild swine (Sus scrofa) collected from throughout the United States from 1979 to 1987 are presented. Sera collected from 1,218 wild swine and tissues from 637 were evaluated for HC antibodies and virus, respectively. Included within this surveillance were samples from Santa Cruz and Santa Rosa Islands, California, where HC virus had been deliberately introduced into wild swine during the 1950's in attempts to eradicate these animals. All evaluations were considered negative for HC. It appears that the HC virus does not maintain itself in dispersed swine populations and that wild swine have not remained a reservoir of HC since its eradication in domestic swine in the United States.

Classical swine fever: virulence and tissue distribution of a 1986 English isolate in pigs.

Following the recurrence of classical swine fever in the United Kingdom in 1986, a virus isolated from a single outbreak was studied. A major factor in the spread of this disease is considered to be the presence of infectious virus in tissues taken from animals at certain stages of infection, although their condition may escape detection by routine inspection either before or after slaughter. Intranasal inoculation of the isolate into eight-week-old pigs reproduced the acute form of the disease. The pigs were killed or died between seven and 25 days after inoculation. The virus concentration was determined in a wide range of tissues taken at different stages of infection. Infectious virus was present at high concentrations in all the tissues taken and at all stages of infection. Any porcine tissue is therefore a potential source of infection even when it is taken either before the animal displays detectable signs of disease of after it develops serum neutralising antibodies.

[Swine fever: a changing clinical picture]. / Varkenspest: een veranderend ziektebeeld.

Signs of disease typical of classical swine fever are often absent in outbreaks caused by virus strains of low virulence. The clinical picture and epizootiology of these strains causing swine fever in the Netherlands are elucidated on the basis of experimentally induced infections and outbreaks in the field respectively. Strains of both high and low virulence are involved in the present epizootic. The absence of symptoms hampers early detection in the field. Intra-uterine infections may occur in a large proportion of the pregnant sow population. On one farm, 43 per cent of these sows showed intra-uterine infection. Piglets born of these sows may live for weeks and occasionally months without showing any marked symptoms, as a result of which the virus may persist over prolonged periods even in vaccinated herds.

[Demonstration of the swine fever virus by the infection of cell cultures of lymphocytes and lysed red blood cells]. / Dokazvane na virusa na chumata po svinete chrez zaraziavane na kletuchni kulturi s limfotsiti i lizirani cherveni kruvni kletki.

A method was worked out for the diagnosing of swine fever by means of infecting sensitive cell cultures on lamellae with lyzed red blood cells and lymphocytes, the demonstration being performed through immunofluorescence. The new method made it possible to avoid killing of suspected animals for diagnostic purposes (in order to prepare suspensions of parenchymal organs and isolate the virus) while the characteristic morphologic changes were still not well manifested.

Properties of hog cholera viruses recently isolated in Japan.

Hog cholera (HC) viruses newly isolated in Japan in 1980 and 1981 were examined for pathogenicity and serological properties by the neutralization test with antisera against bovine viral diarrhea-mucosal disease (BVD . MD) and HC viruses. Five of 23 isolates examined were neutralized poorly by BVD . MD antibody, but well by HC antibody. On the contrary, 15 isolates were neutralized readily and two isolates moderately by BVD . MD antibody. The other one reacted poorly with either HC or BVD . MD antibodies. The isolate neutralized poorly by BVD . MD antibody was more highly pathogenic than those neutralized readily. It was concluded that the antigenic properties and pathogenicity of the HC viruses were not monotype , and that HC viruses varying in antigenicity and pathogenicity were present in the field.

Congenital tremor in pigs farrowed from sows given hog cholera virus during pregnancy.

At different stages of gestation, 3 groups of pregnant sows were inoculated with a strain of hog cholera virus (HCV). After the infection, clinical signs of hog cholera were not observed in the sows. Pigs from the sows infected on day 22 or 43 of gestation showed varying degrees of muscular tremor, ataxia, splayleg, and suckling inability. Of the pigs with tremor, 83% had cerebellar hypoplasia. Surviving pigs demonstrated persistent viral infection and continued to shed HCV, but did not have antibodies to HCV. Sows infected at 72 days of gestation farrowed numerous mummified and stillborn pigs. Signs of tremor were not seen in any pigs from these sows.

Atypical hog cholera infection: viral isolation and clinical study of in utero transmission.

Sows in different stages of pregnancy were inoculated with a low-virulence hog cholera strain. Clinical signs of disease were not observed in the sows during pregnancy, but most of their pigs were splaylegged and had nervous disorders; perinatal mortality was high. A few pigs from sows that were inoculated during the 1st trimester of pregnancy survived and remained inapparent carriers of virus, without developing antibodies. Seemingly, these pigs were immunotolerant. Virus was transmitted from immunotolerant pigs to susceptible pigs by contact 5 weeks after farrowing, but not 3 months after farrowing, despite the persistence of the virus at a high concentration in the blood and in the organs of the immunotolerant pigs.