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The digenetic trematode Bolbophorus damnificus is a significant hindrance to the production of farm‐raised catfish in the southeastern USA. Severe infections with Bolbophorus damnificus can result in death, but the real damage lies in mild to moderate infections, which can go unnoticed by producers. Research has shown even mild infections can inhibit production to the point of operating at a net loss. The ramshorn snail Planorbella trivolvis is the first intermediate host for Bolbophorus damnificus and is prevalent in most commercial catfish ponds in the Southeast. Management practices aimed at controlling Bolbophorus damnificus infections primarily focus on reducing snail populations in ponds. Other aquatic snail species are also commonly associated with commercial catfish ponds, although little is known about their contributions to trematode infections in catfish. In the summer of 2014, 804 snails Biomphalaria havanensis (synonym: Biomphalaria obstructa) were collected from a single commercial catfish pond and screened for trematode infections. Seven of these snails (0.81%) were actively releasing cercariae identified molecularly as Bolbophorus damnificus. These cercariae were subsequently used in infectivity trials with Channel Catfish Ictalurus punctatus fingerlings (5–8 cm). Seven days postchallenge, fish were examined histologically for the presence of metacercariae, which were present in 13 of 15 (86.67%) surviving fish. This is the first report of naturally occurring infections of Bolbophorus damnificus in another snail species.

Bolbophorus damnificus (Digenea: Bolbophoridae) causes significant economic losses in catfish aquaculture in the southeastern USA. To determine mortality trends associated with B. damnificus exposure, three separate disease challenges were conducted. The first challenge exposed channel catfish, Ictalurus punctatus, fingerlings (7–13 cm) to approximately 285 B. damnificus cercariae/L, while the second exposed fish to approximately 215 cercaria/L. Fish were monitored for morbidity and mortality for 28 d. In both studies, mortality first occurred 8 d postchallenge (PC) and peaked at 9 and 10 d PC, respectively. Mortality had subsided by 14 d PC, with only sporadic mortality occurring >15 d PC. Dead and moribund fish presented with lesions consistent with B. damnificus infection. A third challenge was performed to record histological changes associated with parasite development from initial exposure up to the cessation of mortality. Catfish (2–5 cm) were exposed as described above to a range covering 0, 35, 70, 100, 150, 175, and 215 cercariae/L. Each day, two fish were sampled from each treatment. Mortality trends were consistent with previous challenges. The mortality window coincided with parasite encapsulation, neovascularization, and development of the host‐derived cyst, suggesting that morbidity and mortality are linked to host pathophysiological changes in response to metacercariae encapsulation.

The smallmouth buffalo Ictiobus bubalus Rafinesque (Catostomidae) is native to North American waterways and occasionally grown in pond aquaculture. Species of Myxobolus Bütschli, 1882 have been reported from the gills, integument, and intestinal tract of buffalo fish, although there is ambiguity in some host records. In the summer of 2013, thirteen adult smallmouth buffalo were seined from a 0.1-acre (0.04-hectare) experimental research pond at the Thad Cochran National Warmwater Aquaculture Center in Stoneville, Mississippi, USA, and examined for the presence of parasitic infection. Two previously unknown species of Myxobolus were observed parasitising the gills. Plasmodia of the two species differed from each other in both size and shape. Morphologically the two species were distinct from one another and from other Myxobolus spp. previously reported from buffalo fish. Myxospores of Myxobolus ictiobus n. sp. were spherical and measured 12.7-14.5 (13.9 ± 0.4) µm in length and 10.7-13.6 (12.5 ± 0.7) µm in width with a thickness of 10.3-14.8 (12.6 ± 2.3) µm. Polar capsules measured 5.6-7.4 (6.6 ± 0.4) µm in length and 3.7-4.9 (4.5 ± 0.8) µm in width and each contained a coiled polar filament with 5-6 turns. Myxospores of Myxobolus minutus n. sp. were circular in shape and measured 7.4-9.6 (8.6 ± 0.7) µm in length and 7.5-9.9 (8.8 ± 0.7) µm in width with a thickness of 6.5-7.3 (6.7 ± 0.3) µm. Polar capsules measured 3.6-4.9 (4.3 ± 0.3) µm in length and 2.8-3.8 (3.3 ± 0.3) µm and each contained a coiled polar filament with 5-6 turns. Supplemental 18S rRNA gene sequencing identified unique sequences for each isolate. Phylogenetic analysis of 18S rRNA sequences demonstrated a strong clustering of both isolates with other species of Myxobolus from cypriniform fish.

Clinostomum spp. (Digenea: Clinostomidae) are a group of trematodes commonly found in the buccal cavity and oesophagus of a variety of piscivorous birds. The metacercariae, colloquially known as "yellow grubs," have been reported from a diverse group of freshwater fishes worldwide. In the catfish farming region of the southeastern USA, piscivorous birds present a continuous challenge for aquaculturists in the form of fish depredation and the introduction of trematodes into these static, earthen pond systems. Clinostomum spp. are commonly encountered in farm-raised catfish. While generally considered pests of minimal importance, heavy infections can result in unmarketable fillets. Of the piscivorous birds that frequent catfish aquaculture operations in the southeastern US, the double-crested cormorant (Phalacrocorax auritus Lesson) is one of the most damaging, although reports of Clinostomum spp. from P. auritus are limited. In this study, adult trematodes morphologically consistent with Clinostomum sp. were found in the trachea of a double-crested cormorant captured in Lowndes Co., Mississippi, USA. These specimens differed from other recognised Clinostomum spp. in several key morphological characters. Moreover, sequence data of mitochondrial cytochrome c oxidase subunit 1 gene (cox1), nicotinamide adenine dinucleotide dehydrogenase subunit 1 gene (nad1) and ribosomal internal transcribed spacer (ITS) regions did not match any known Clinostomum sp. for which sequence data are available. While genetically similar to C. marginatum and C. album Rosser, Alberson, Woodyard, Cunningham, Pote & Griffin, 2017 reported from the great egret Ardea alba L. in Mississippi, these adult clinostomids were larger in size and limited to the trachea, whereas both C. marginatum Rudolphi, 1819 and C. album are found in the oral cavity and esophagus. Given these distinct morphological and molecular characters we propose a new member of the genus, known hereafter as Clinostomum poteae n. sp. Additionally, larval stages in the life-cycle of C. album are morphologically and molecularly identified for the first time from ramshorn snails Planorbella trivolvis Say and fathead minnows Pimephales promelas Rafinesque.

Restrictive cardiomyopathy (RCM), a potentially devastating heart muscle disorder, is characterized by diastolic dysfunction due to abnormal muscle relaxation and myocardial stiffness resulting in restrictive filling of the ventricles. Diastolic dysfunction is often accompanied by left atrial or bi-atrial enlargement and normal ventricular size and systolic function. RCM is the rarest form of cardiomyopathy, accounting for 2-5% of pediatric cardiomyopathy cases, however, survival rates have been reported to be 82%, 80%, and 68% at 1-, 2-, and 5-years after diagnosis, respectively. RCM can be idiopathic, familial, or secondary to a systemic disorder, such as amyloidosis, sarcoidosis, and hereditary hemochromatosis. Approximately 30% of cases are familial RCM, and the genes that have been linked to RCM are cTnT, cTnI, MyBP-C, MYH7, MYL2, MYL3, DES, MYPN, TTN, BAG3, DCBLD2, LNMA, and FLNC. Increased Ca 2+ sensitivity, sarcomere disruption, and protein aggregates are some of the few mechanisms of pathogenesis that have been revealed by studies utilizing cell lines and animal models. Additional exploration into the pathogenesis of RCM is necessary to create novel therapeutic strategies to reverse restrictive cardiomyopathic phenotypes.

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