Haemostatic abnormalities in African swine fever a comparison of two virus strains of different virulence (Dominican Republic '78 and Malta '78).

African swine fever (ASF) virus strains cause haemorrhage by producing a variety of defects, which vary in severity from strain to strain. To distinguish the main haemostatic defects leading to haemorrhage, two groups of pigs were infected with moderately virulent (Dominican Republic '78) and less virulent (Malta '78) ASF virus strains. Mortality rate and severity of clinical observations were greater in pigs infected with DR '78 virus compared with pigs infected with Malta '78 virus. The animals became febrile from day 3 to 4 onwards at a time when the viraemia was high (10(7) to 10(8) HAD50/ml). No difference was found during the period observed in their pattern of viraemia or pyrexia. Thrombocytopenia developed in both groups but with different kinetics, suggesting two different mechanisms of sequestration of platelets. When coagulation tests were performed, significant abnormalities were found, including evidence for disseminated intravascular coagulation. These abnormalities were much less pronounced in the group infected with Malta '78. Antithrombin III activity did not change significantly in either group. Decreased plasminogen activity was found in the early phase of disease in DR '78 infected pigs. These results indicate that when haemorrhage does occur in DR '78 infected pigs, it is a consequence of more pronounced degrees of haemostatic impairment probably due to a marked endothelial injury and/or generation of procoagulant activity.

Moderately virulent African swine fever virus infection: blood cell changes and infective virus distribution among blood components.

Blood samples of pigs infected with a moderately virulent African swine fever virus (ASFV) isolate, obtained from the Dominican Republic (DR-II), were monitored temporally for viremia, infective ASFV association with major blood components, differential changes in blood cell composition, and plasma antibodies to ASFV. After intranasal/oral virus inoculation, pigs underwent acute infection and illness that resolved. Acute illness began on postinoculation day (PID) 4 and continued to PID 11, and pigs were febrile, with maximal infective ASFV titers detected in blood. By PID 11, initial antibody titers to ASFV antigens were detected in plasma. The WBC numbers were maintained near preinoculation counts; however, lymphocyte counts decreased slightly with a compensatory increment in neutrophil and monocyte numbers. From PID 11 to PID 25, rectal temperatures gradually returned to preinoculation values, titers of viremia began to decrease, plasma antibody to ASFV antigens increased to peak titers, and WBC numbers increased slightly. Percentages of lymphocytes returned to preinoculation values, neutrophil percentages decreased to slightly below preinoculation values, monocyte percentages were mildly increased, and eosinophil percentages were unaffected. From PID 25 to PID 46, titers of viremia further decreased, and plasma titers of antibodies to ASFV antigens remained high. In pigs with DR-II viremia (PID 4 to PID 46), most viral infectivity (greater than 95%) was RBC associated. Plasma contained less than 1% infectivity, and less than 0.1% of virus was in the WBC fraction (monocytes, lymphocytes, and granulocytes). After PID 46, viremia was no longer detectable.

Clinical and immunologic responses of pigs to African swine fever virus isolated from the Western Hemisphere.

Pigs in the United States were exposed to African swine fever (ASF) virus isolated from pigs in Brazil and the Dominican Republic. The former were examined for clinical response, lesions, viremia, and antibody response. Sequential blood samples were tested for the presence of ASF virus by the hemadsorption test (in swine buffy coat cell culture) and for antibody to ASF virus by the enzyme-linked immunosorbent assay. The incubation period was 3 to 5 days; inoculated pigs had fever for 8 to 16 days (mean 12.5 days) and viremia at 3 to 35 days after inoculation and few died. Inoculated pigs developed antibodies at 7 days after inoculation which were detectable until the termination of the experiment (10th month). Reinoculation of some of the surviving pigs with the homologous isolate at approximately 6 months after exposure did not induce clinical response, viremia, nor anamnestic antibody response. In contrast, challenge exposures of convalescent pigs with the Lisbon-60 viral strain approximately 5 weeks after exposure to the Brazilian strain produced death, in spite of an anamnestic antibody response.

Virulence in African swine fever: its measurement and implications.

A method of measuring and expressing the virulence of African swine fever virus in numerical terms was developed. Seventeen viruses (13 hemadsorbing and 4 nonhemadsorbing) were tested and classified into 3 groups: highly infectious and highly virulent, highly infectious and moderately virulent, and slightly infectious and slightly virulent. This classification was based on the number of 50% hemadsorption unit (HA50) or TCID50 required to produce 1 LD50 for swine, the number of HA50 or TCID50 required to produce one 50% pig infectious dose (PID50), and the number of PID50 required for each LD50. The virulent virus (group 1) required less than or equal to 10 virus units (HA50 or TCID50) for 1 PID50 and LD50 (highly infectious and highly lethal), respectively, and had a ratio of 1.0 for PID50/LD50, ie, all infected pigs died from acute African swine fever. Tengani, L'60, and DR-I isolants and nonhemadsorbing viruses of Haiti-1 isolant belong to this group. The moderately virulent virus (group 2) required less than 10 virus units for 1 PID50 and 20 to 562 virus units for 1 LD50 (highly infectious and moderately lethal), respectively, and recoveries from the clinical disease and immunologic deaths were frequent. Madrid '75, Haiti-1, DR-II, and BR-I isolants belong to this group. The slightly virulent virus (group 3) required 56 to 10,000 virus units for 1 PID50 and 56,200 to 3,120,000 virus units for 1 LD50 (slightly infectious and less lethal).(ABSTRACT TRUNCATED AT 250 WORDS)