Ichthyophthirius multifiliis impairs splenic enzymes of the phosphoryl transfer network in naturally infected Rhamdia quelen: effects on energetic homeostasis

Abstract

Its integrated energetic and metabolic signaling roles place the phosphoryl transfer network, through the enzymes creatine kinase (CK), adenylate kinase (AK), and pyruvate kinase (PK), as a regulatory system coordinating components of the cellular bioenergetics network. Analysis of these enzymes provides new information and perspectives with which to understand disturbances in energetic metabolism between sites of adenosine triphosphate (ATP) generation and utilization. Thus, the aim of this study was to evaluate the involvement of the phosphoryl transfer network in splenic tissue linked with the pathogenesis of silver catfish naturally infected with Ichthyophthirius multifiliis. Splenic cytosolic and mitochondrial CK activities decreased in infected animals compared to uninfected animals, as was also observed for splenic PK activity and splenic ATP levels. In contrast, splenic AK activity increased in infected animals compared to uninfected animals. Based on this evidence, the inhibition and absence of efficient communication between CK isoenzymes cause the impairment of splenic bioenergetics, which is in turn compensated by the augmentation of splenic AK activity in an attempt to restore energy homeostasis. The inhibition of splenic PK activity impairs communication between sites of ATP generation and ATP utilization, as corroborated by splenic ATP depletion. In summary, these alterations contribute to disease pathogenesis linked to spleen tissue in animals infected with white spot disease.

Creatine Kinase Activity as an Indicator of Energetic Impairment and Tissue Damage in Fish: A Review

“…Similar results were found in other fish species affected by different diseases, such as the inhibition of splenic cytosolic and mitochondrial CK activities in silver catfish naturally infected by the parasite Ichthyophthirius multifiliis [8], the inhibition of cerebral cytosolic and mitochondrial CK activities in silver catfish experimentally infected by Streptococcus agalactiae [9], the inhibition of branchial cytosolic and mitochondrial CK activities in Nile tilapia (Oreochromis niloticus) experimentally infected with Providencia rettgeri [10], and the inhibition of branchial cytosolic and mitochondrial CK activities in grass carp naturally infected by Saprolegnia parasitica [11]. In summary, the detrimental involvement of CK activity in energetic homeostasis in fish that are naturally or experimentally infected by bacterial, fungal, or parasitic diseases is clear, as is its contribution to the pathophysiology of diseases.…”