Investigators reported severe multiorgan disease in pigs given African swine fever virus–positive spray-dried porcine plasma (SDPP). Gross lesions included marked splenomegaly with hemorrhagic infarction and enlarged, hemorrhagic mandibular, gastrohepatic, and renal lymph nodes with erythema. Tissue samples from organs with visible pathology tested positive for ASFV DNA, the study team observed. The pathological picture matched the clinical course of acute hemorrhagic disease the authors described.
The study group screened 72 SDPP and 219 commercial compound feed (CF) samples collected from affected pig farms. They used suspension in phosphate-buffered saline and real-time PCR for detection; two SDPP and two CF samples yielded detectable ASFV DNA. Virus isolation from feed using primary porcine alveolar macrophages was initially unsuccessful, as the authors reported. For in vivo work, nine healthy 4-week-old Landrace pigs were randomized into three groups (n = 3 each): an SDPP-inoculated group, a CF-fed group, and a negative control group. The SDPP group received a 50% wt/vol SDPP suspension intramuscularly (1 mL per pig) after filtration through a 0.45-µm syringe filter. The CF-fed group received 200 g of the PCR-positive CF once daily for 30 days. Blood, oral, and rectal swabs were collected for real-time PCR monitoring, and animals were housed in ABSL-3 isolators under institutional protocols.
Two SDPP-inoculated pigs developed acute fever (rectal temperature >40.5°C) by 5 days postchallenge (dpc) and the third by 6 dpc. Temperatures peaked at approximately 41.2°C shortly before death. Clinical deterioration was rapid—severe lethargy, anorexia, huddling, and depression were recorded—and all three animals in the SDPP group died, with a mean time to death of 8.0 ±0.8 dpc. The authors detected viremia in whole blood and viral shedding from oral and rectal routes beginning at 4 dpc; blood viral loads exceeded swab loads. By contrast, both CF-fed and control animals remained clinically stable and tested negative for ASFV during the observation period.
Necropsy findings in the SDPP group paralleled the acute clinical syndrome. The study team found extensive congestion and systemic hemorrhage at postmortem examination. Splenic infarction and hemorrhagic lymphadenopathy were prominent. Real-time PCR detected ASFV DNA in postmortem tissues that displayed gross lesions, consistent with disseminated viral infection and systemic replication documented by viremia and shedding.
Although initial virus isolation from feed failed, investigators isolated viable virus from spleen homogenates of the SDPP-inoculated pigs. Next-generation sequencing produced the whole-genome sequence designated ASFV/Korea/SDPP/2026 (GenBank accession PZ617907). Sequence analysis assigned the isolate to p72 genotype II and IGR type I. The genome shared 99.98% nucleotide identity with ASFV/Korea/pig/Dangjin/2025, a strain previously detected at a pig farm. The isolate harbored insertion/deletion polymorphisms, including a 706-bp deletion across MGF 110–7L and 285L and a 9-bp insertion in the MGF 110–10L to 110–14L region; those features were reported by the authors.
Field investigations had associated some outbreaks with PCR-positive feed ingredients. The authors reported that a commercial CF that tested positive for ASFV DNA was produced using SDPP from the same batch as the PCR-positive SDPP sample. The experimental inoculation data demonstrated that SDPP prepared as a suspension and delivered intramuscularly could produce fatal ASFV infection and yield recoverable, farm-related virus. The CF-fed animals in this study did not develop infection under the feeding regimen used; the authors provided those negative-feeding data along with the positive SDPP inoculation results.
The authors noted several critical uncertainties that remain. The source did not report oral dose–response data for SDPP or controlled thermal/chemical inactivation parameters for the implicated SDPP batch, so the minimum infectious dose by feed exposure and the specific steps that would inactivate the product were not established in this report. Initial virus isolation directly from feed samples failed, although viable virus was later recovered from spleen homogenates after experimental infection. The study did not test alternative routes or varied feed processing conditions that might influence infectivity. Given the detection of ASFV DNA in animal-derived feed and the recovery of a genome closely related to a farm outbreak strain, the authors called for strengthened risk management of animal-derived feed ingredients such as SDPP. Specific regulatory or processing milestones were not detailed in the source; remaining questions include quantifying oral infectivity thresholds for SDPP and defining validated processing standards to ensure feed safety.