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Combined polyvinyl chloride microplastic exposure and Vibrio parahaemolyticus challenge are associated with hepatopancreatic injury and production losses in Pacific white shrimp
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Shrimp exposed to microplastic particles and a common bacterial pathogen together suffered more liver and gut damage, and died at much higher rates, than shrimp exposed to either alone. This suggests microplastic pollution in shrimp farms could worsen disease outbreaks, potentially affecting seafood supply and safety, though more testing is needed to confirm the particles involved and their exact role.
Microplastic particles and bacterial pathogens can co-occur in shrimp-production systems, but experimental designs without particle-only treatments cannot establish a statistical interaction between these stressors. This study therefore evaluated biological outcomes during combined polyvinyl chloride microplastic (PVC-MP) exposure and Vibrio parahaemolyticus challenge in Pacific white shrimp ( Litopenaeus vannamei ). Five treatments, each with three replicate containers, comprised an unexposed negative control (KN), a bacterial-challenge control (KP), and combined treatments containing nominal PVC-MP concentrations of 3, 30, or 300 mg L −1 (P1-P3) followed by a 10 4 CFU mL −1 immersion challenge. PVC-MP pre-exposure lasted 15 days and survival was recorded for 7 days after challenge. Light-microscopy counts after hydrogen-peroxide digestion increased from 17.66 to 18.14 particles g −1 in the controls to 74.28, 171.28, and 217.44 particles g −1 in P1-P3. These values are reported as putative digestive particle counts because recovered-particle identity was not confirmed by FTIR or Raman spectroscopy and analytical recovery was not validated. Survival declined from 83.33% in KN and 66.67% in KP to 48.33%, 26.67%, and 21.67% in P1-P3. Representative histology showed increasingly severe tubule dilation, degeneration, epithelial cytolysis, abnormal lumina, B-cell enlargement, and hemocytic infiltration in the combined-exposure groups. FCR, not corrected for mortality, increased, while SGR, container-level net biomass gain, and length gain declined. These findings support a dose-linked, treatment-associated pattern of putative digestive particle counts, hepatopancreatic injury, and production loss under bacterial challenge. Interpretation is limited by the absence of PVC-only treatments, FTIR/Raman confirmation, particle-recovery controls, mortality-corrected FCR, and direct quantification of V. parahaemolyticus on PVC surfaces.
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