Early ocean distribution of juvenile Chinook salmon in an upwelling ecosystem

Extreme variability in abundance of California salmon populations is often ascribed to ocean conditions, yet relatively little is known about their marine life history. To investigate which ocean conditions influence their distribution and abundance, we surveyed juvenile Chinook salmon (Oncorhynchus tshawytscha) within the California Current (central California [37°30′N) to Newport, Oregon (44°00′N]) for a 2‐week period over three summers (2010–2012). At each station, we measured chlorophyll‐a as an indicator of primary productivity, acoustic‐based metrics of zooplankton density as an indicator of potential prey availability and physical characteristics such as bottom depth, temperature and salinity. We also measured fork lengths and collected genetic samples from each salmon that was caught. Genetic stock identification revealed that the majority of juvenile salmon were from the Central Valley and the Klamath Basin (91–98%). We constructed generalized logistic‐linear negative binomial hurdle models and chose the best model(s) using Akaike's Information Criterion (AIC) to determine which covariates influenced the salmon presence and, at locations where salmon were present, determined the variables that influenced their abundance. The probability of salmon presence was highest in shallower waters with a high chlorophyll‐a concentration and close to an individual's natal river. Catch abundance was primarily influenced by year, mean fork length and proximity to natal rivers. At the scale of sampling stations, presence and abundance were not related to acoustic indices of zooplankton density. In the weeks to months after ocean entry, California's juvenile Chinook salmon population appears to be primarily constrained to coastal waters near natal river outlets.     

Progression of aflatoxicosis in growing barrows

The progression of aflatoxicosis was evaluated in growing crossbred barrows given 0, 1, 2, 3, or 4 mg of aflatoxin (AF)/kg of feed for 28 days (6 to 10 weeks of age). On day 28, pigs were euthanatized and necropsied, and tissues were removed for histologic examination. Body weight gains were decreased in barrows fed 2 mg of AF/kg after 7 days and in barrows fed 1 mg of AF/Kg after 14 days. By 28 days, all barrows fed AF had decreased body weights and weight gains. Compared with decreased in all barrows fed AF. Neither liver weights nor bone ash values were altered, although liver lipid values were increased in barrows fed AF. Serum aspartate transaminase, gamma-glutamyl transferase, and alkaline phosphatase activities were increased in barrows fed AF, whereas creatine kinase activity was decreased. Aflatoxin diets resulted in decreases in serum concentrations of urea nitrogen, phosphorus, cholesterol, albumin, and total protein. Histologic alterations in liver included interlobular fibrosis, periportal lipidosis, bile duct hyperplasia, and periportal lymphocytic infiltration. Lymphocytes in the thymus were depleted, and numbers of granulocytic cells in the bone marrow were reduced. The frequency and severity of lesions increased with increased doses of AF.     

Mycotoxin interactions in poultry and swine

Mycotoxins are toxic compounds produced by fungi. When one mycotoxin is detected, one should suspect that others also are present in a contaminated feed ingredient or finished feeds. The toxicity and clinical signs of observed in animals when more than one mycotoxin is present in feed are complex and diverse. Some mycotoxins, such as the combination of aflatoxin with either ochratoxin A or T-2 toxin, interact to produce synergistic toxicity in broiler chicks. The effects observed during multiple mycotoxin exposure can differ greatly from the effects observed in animals exposed to a single mycotoxin. For example, fatty livers in poultry are used for presumptive diagnostic identification of aflatoxicosis. However, simultaneous presence of ochratoxin A prevents fatty livers. Of the mycotoxin combinations that have been investigated in poultry and swine, the aflatoxin + ochratoxin A and aflatoxin + T-2 toxin interactions appear to be the most toxic.     

Spatial variability in ocean‐mediated growth potential is linked to Chinook salmon survival

Early ocean survival of Chinook salmon, Oncorhynchus tshawytscha, varies greatly inter‐annually and may be the period during which later spawning abundance and fishery recruitment are set. Therefore, identifying environmental drivers related to early survival may inform better models for management and sustainability of salmon in a variable environment. With this in mind, our main objectives were to (a) identify regions of high temporal variability in growth potential over a 23‐year time series, (b) determine whether the spatial distribution of growth potential was correlated with observed oceanographic conditions, and (c) determine whether these spatial patterns in growth potential could be used to estimate juvenile salmon survival. We applied this method to the fall run of the Central Valley Chinook salmon population, focusing on the spring and summer period after emigration into central California coastal waters. For the period from 1988 to 2010, juvenile salmon growth potential on the central California continental shelf was described by three spatial patterns. These three patterns were most correlated with upwelling, detrended sea level anomalies, and the strength of onshore/offshore currents, respectively. Using the annual strength of these three patterns, as well as the overall growth potential throughout central California coastal waters, in a generalized linear model we explained 82% of the variation in juvenile salmon survival estimates. We attributed the relationship between growth potential and survival to variability in environmental conditions experienced by juvenile salmon during their first year at sea, as well as potential shifts in predation pressure following out‐migration into coastal waters.     

Endocrine responses in mares and geldings with high body condition scores grouped by high vs. low resting leptin concentrations

Previous observations from this laboratory indicated that horses with high BCS could have resting plasma leptin concentrations ranging from low (1 to 5 ng/mL) to very high (10 to 50 ng/mL). To study the possible interactions of leptin secretion with other endocrine systems, BCS and plasma leptin concentrations were measured on 36 mares and 18 geldings. From mares and geldings that had a mean BCS of at least 7.5, five with the lowest (low leptin) and five with the highest (high leptin) leptin concentrations were selected. Jugular blood samples were collected twice daily for 3 d from the 20 selected horses to determine average resting hormone concentrations. Over the next 12 d, glucose infusion, injection of thyrotropin-releasing hormone (TRH), exercise, and dexamethasone treatment were used to perturb various hormonal systems. By design, horses selected for high leptin had greater (P < 0.0001) leptin concentrations than horses selected for low leptin (14.1 vs. 2.8 +/- 0.92 ng/mL, respectively). In addition, mares had greater (P = 0.008) leptin concentrations than geldings. Horses selected for high leptin had lower (P = 0.027) concentrations of GH but higher (P = 0.0005) concentrations of insulin and thriiodothyronine (T3) than those selected for low leptin. Mares had greater (P = 0.0006) concentrations of cortisol than geldings. There was no difference (P > 0.10) in concentrations of IGF-1, prolactin, or thyroid-stimulating hormone (TSH). Horses selected for high leptin had a greater (P = 0.0365) insulin response to i.v. glucose infusion than horses selected for low leptin. Mares had a greater (P = 0.0006) TSH response and tended (P = 0.088) to have a greater prolactin response to TRH than geldings; the T3 response was greater (P = 0.047) in horses selected for high leptin. The leptin (P = 0.0057), insulin (P < 0.0001), and glucose (P = 0.0063) responses to dexamethasone were greater in horses selected for high leptin than in those selected for low leptin. In addition, mares had a greater (P < 0.0001) glucose response to dexamethasone than geldings. Cortisol concentrations were decreased (P = 0.029) by dexamethasone equally in all groups. In conclusion, differences in insulin, T3, and GH associated with high vs. low leptin concentrations indicate a likely interaction of these systems with leptin secretion in horses and serve as a starting point for future study of the cause-and-effect nature of the interactions.