Aquaculture is an increasingly important food resource, but its sustainability is often limited by disease. In Scombridae fishes, puffy snout syndrome (PSS) is a debilitating condition where tumor-like collagenous growths form around the eyes, nares, and mandibles which impair vision and feeding and frequently lead to mortality. While PSS is considered an infectious or metabolic disease, no disease agents or promoters have been identified. Here, we used electron microscopy (EM) to describe the cellular pathology and search for etiological agents of PSS in Pacific mackerel Scomber japonicus, the first use of this approach for PSS. We examined aquaculture specimens across a range of apparent PSS severity, comparing the results to both wild and aquaculture asymptomatic mackerel. EM imagery consistently revealed viral-like particles in PSS samples, as well as the uniform absence of bacteria, protists, fungi, and other multicellular parasites. In addition to viral-like particles, symptomatic fish had a higher mean percentage of swollen and disintegrating mitochondria than both asymptomatic aquaculture and wild mackerel. This suggests that degraded mitochondria may be related to PSS and could be important to further understanding the origin, promoters, and prevention of PSS. This study serves as a first step in identifying the etiological agents of PSS.

Scombrids represent some of the most economically important fisheries globally. However, increased interest in creating aquaculture systems for these fish has increased the risk of disease emergence. One such disease, Puffy Snout Syndrome (PSS), causes collagenous tissue growths on the face, in numerous scombrid taxa. PSS has only been documented in captive-held fish populations and can lead to high mortality rates. Despite this, little is known about PSS's causative agent(s) and the immune response they elicit. Therefore, we leveraged metatranscriptomic data of symptomatic-captive, asymptomatic-captive, and healthy-wild Pacific Mackerel (Scomber japonicus) to evaluate the physiological characteristics of PSS infections and identify a mechanism of disease. PSS symptomatic-captive and asymptomatic-captive mackerel showed distinct gene expression patterns from their wild counterparts. Genes involved in tumorigenesis, immune response, and pathophysiology were over-expressed in captive-held fish. In particular, the Wnt9 pathway was increased by more than 2 orders of magnitude in captive fish, potentially representing a diagnostic feature of this disease. Together, these host physiological data and our past visual identification of RNA virus-like particles in afflicted tissues suggest that viral-mediated oncogenesis may be driving PSS in captive mackerel.

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