Loma salmonae-associated xenoma onset and clearance in rainbow trout, Oncorhynchus mykiss (Walbaum): comparisons of per os and cohabitation exposure using survival analysis

Survival analysis techniques were used to compare experimental exposure methods of Loma salmonae (Microspora) in rainbow trout (RBT) by measuring xenoma onset and clearance time. Twenty‐eight naive RBT were exposed per os (fed L. salmonae spores) and 28 RBT were exposed by cohabitation with 28 L. salmonae‐infected RBT. Exposed fish were examined once every week (7 days) post exposure (PE). For xenoma onset, the median survival time, the time to first appearance of branchial xenomas, was 6 weeks PE for both per os and cohabitation exposure. For xenoma clearance, the median survival time, the time to total clearance of branchial xenomas, was 10 weeks for per os exposure and 12 weeks for cohabitation exposure. There was a significant difference between the survival curves of per os fish compared with cohabited fish for both xenoma onset and xenoma clearance. The incidence rate of xenoma development was greater for per os exposure (0.1745 cases per fish‐week) compared with cohabitation exposure (0.1342 cases per fish‐week). Similarly, the rate of xenoma clearance was greater for per os exposure (0.1028 cases per fish‐week) compared with cohabitation exposure (0.0885 cases per fish‐week). Differences between exposure methods were attributed to differences in the frequency and duration of exposure to spores. Survival analysis was useful for examining the onset and clearance of L. salmonae and may have applications for understanding disease dynamics in aquaculture.     

Effects of monensin dose and treatment time on xenoma reduction in microsporidial gill disease in rainbow trout, Oncorhynchus mykiss (Walbaum)

The objectives of the study were (1) to determine an acceptable dose of dietary monensin against microsporidial gill disease (MGD) of salmon caused by Loma salmonae and (2) to determine the life stage of L. salmonae at which the action of monensin was most effective at reducing clinical disease. Rainbow trout (RBT) were fed monensin diets at concentrations of 0, 10, 100, 1000 and 5000 ppm starting 1 week before per os exposure to L. salmonae infected gill material. Lethal sampling occurred at weeks 6, 7, 8 and 9 post‐exposure (PE). The acceptable dose of dietary monensin was determined to be 1000 ppm because it was the lowest concentration that produced a significant and constant reduction in xenoma formation. RBT were fed monensin at 1000 ppm beginning at 0, 1, 2 and 3 weeks before exposure and at 1, 2 and 3 weeks after exposure and continuing until week 9 PE. Fish in which treatment was initiated at the time of exposure or 1 week before, showed the greatest reduction in xenoma production when compared with the untreated RBT.     

Whole body net ion fluxes, plasma electrolyte concentrations and haematology during a Loma salmonae infection in juvenile rainbow trout, Oncorhynchus mykiss (Walbaum)

Loma salmonae infections of salmonids culminate in the development of branchial xenomas and subsequent focal hyperplasia of the lamellar or filament epithelium following xenoma rupture and spore release. The effects of this acute branchial disruption upon net ionic flux rates and plasma electrolyte concentrations were determined in juvenile rainbow trout given an experimental oral exposure to L. salmonae. Mean numbers of branchial xenomas peaked at week 5 post-exposure (PE), which coincided with a reduction in the specific growth rate, although there were no significant differences in mass, length or condition of Loma-exposed fish compared with unexposed controls. Following exposure, negative net whole body Na(+) and K(+) fluxes decreased, whereas net Cl(-) fluxes remained unchanged compared with non-exposed control fish. At week 3 PE during the initial branchial xenoma formation stage, there was a significant negative whole body net K(+) flux in Loma-exposed trout compared with other points during the exposure and subsequent infection. Additionally, Loma-exposed fish had marginally elevated plasma Na(+) and Cl(-) concentrations, whilst K(+) levels remained unchanged, compared with control fish. Although there was a progressive decrease in leucocrit, haematocrit remained unchanged over the course of the Loma exposure and subsequent infection. These results suggest that ionic compensation can occur at the gills during the development of xenomas during exposure to L. salmonae and the resultant infection, therefore allowing defence of plasma electrolyte concentrations, unlike the acute ionic disturbances seen with some other parasitic diseases.     

Effect of water temperature manipulation on a thermal unit predictive model for Loma salmonae

Loma salmonae is an important microsporidian pathogen affecting the mariculture of Pacific salmon, Oncorhynchus tshawytscha (Walbaum). Clinical signs associated with infection arise when the parasite enters sporogony and forms xenoparasitic complexes (xenomas) within the gill. The present study tested a thermal unit (TU) model, which was devised to predict the timing of xenoma formation, under conditions in which water temperature changed during the course of infection. In vivo trials with juvenile trout showed that the model TU for xenoma onset= (days post exposure) (C above 7C) accurately predicted the onset time for xenomas when fish were moved from either 11 or 5C to 15C at various intervals after exposure. These findings suggest that the TU model may allow aquaculturists to predict disease onset. However, the model failed when fish were moved from 15 to 5C at intervals after exposure. This finding suggests that the temperature-constrained phase of the life-cycle of L. salmonae occurs early on after the spore is ingested by the fish.     

Chicken-derived IgY recognizes developing and mature stages of Loma salmonae (Microsporidia) in Pacific salmon, Oncorhynchus spp.

A polyclonal IgY preparation, purified from yolk of immunized hens, is shown to be useful for the detection of Loma salmonae in Pacific salmon. Purity of the IgY was confirmed by SDS-PAGE and western blots of yolk protein extracts. Reactivity of the IgY preparation to L. salmonae was determined through indirect-fluorescent antibody tests on purified spores and by immunohistochemistry. Developing xenomas in histological sections of heart and gill tissue of infected chinook salmon (Oncorhynchus tshawytscha) were visualized as early as 4 weeks post-exposure (PE). Non-lethal detection of L. salmonae was obtained by indirect-fluorescent microscopy of acetone-fixed gill smears. The IgY preparation was shown to react with another Loma sp., L. branchialis. In contrast, no reactivity was observed with other microsporidian parasites of fish such as Pseudoloma neurophilia and Glugea anomala. Yolk derived IgY may be useful in the detection of other fish pathogens.     

The transmission potential of Loma salmonae (Microspora) in the rainbow trout, Oncorhynchus mykiss (Walbaum), is dependent upon the method and timing of exposure

The ability of a parasite to transmit from one fish to another is important in the dissemination of disease. Groups of 25 naive rainbow trout (RBT), Oncorhynchus mykiss (Walbaum), were exposed to Loma salmonae by feeding on the viscera (gills, hearts and spleens) from L. salmonae -infected donor RBT (DRBT) or by cohabitation with infected DRBT. Exposure occurred 3, 7, 11 and 15 weeks after the DRBT were infected. All naive RBT were examined 7 weeks post-exposure (PE) to the DRBT. Naive RBT, exposed to DRBT at week 3 PE, by feeding on viscera or by cohabitation, failed to develop visible branchial xenomas. Cohabiting naive RBT with DRBT, at week 7 PE and week 11 PE, resulted in the development of branchial xenomas. Xenomas failed to develop in naive RBT exposed via cohabitation to week 15 PE DRBT. Naive RBT, exposed by feeding on the viscera of DRBT at week 7 PE, week 11 PE and week 15 PE, developed branchial xenomas. The transmission potential of viscera from L. salmonae -infected DRBT at week 15 and week 20 PE was also examined. Naive RBT, fed with viscera free of visible branchial xenomas, from DRBT at week 15 PE and week 20 PE, developed branchial xenomas by week 7 PE. A polymerase chain reaction (PCR) was used to detect L. salmonae DNA from the water and sediments of a tank of L. salmonae -infected RBT at week 7 PE. The method and timing of exposure of naive fish to L. salmonae -infected fish are important in disease transmission and may be useful in predicting and preventing disease outbreaks in aquaculture.     

Evaluating protection against Loma salmonae generated from primary exposure of rainbow trout, Oncorhynchus mykiss (Walbaum), outside of the xenoma-expression temperature boundaries

A series of challenge and re-challenge studies was conducted in which juvenile rainbow trout were exposed to the pathogen Loma salmonae , a microsporidian which typically causes xenoma formation during sporogony and inflammation in the gills as the xenomas undergo dissolution. The specific goal was to determine if a primary exposure, conducted at a water temperature outside of the range which permits the parasite to undergo sporogony and form branchial xenomas, would stimulate a protective response in the fish to a later challenge conducted under temperature conditions optimal for the parasite. Primary challenge of fish to L. salmonae at 7 °C or 21 °C blocked or limited xenoma formation, as discussed in a previous study. However, these fish had a relative percentage protection (RPP) against a second optimized exposure which matched, or was not significantly less than, the degree of protection (100%) that developed in other groups of fish that received a primary exposure throughout the range of water temperatures which permits xenoma formation. When the primary exposure was conducted at 5 °C, the RPP against the second exposure was adversely affected and declined to 61%. These findings have application to the control of L. salmonae within aquaculture, in that it may be possible to expose hatchery stocks of susceptible salmonid species to spores of L. salmonae when hatchery water temperature is at 7 °C. At this temperature, the risks of disease stemming from this primary exposure appear minimal, since xenomas fail to form. However, the degree of protection appears promising, and may be sufficient to protect fish from spore exposure occurring at netpen marine sites where the parasite may be endemic.     

Normal and aberrant tissue distribution of Loma salmonae (Microspora) within rainbow trout, Oncorhynchus mykiss (Walbaum), following experimental infection at water temperatures within and outside of the xenoma-expression temperature boundaries

Temperatures above 20 °C or below 9 °C interrupt the life cycle of the gill intracellular microsporidian parasite Loma salmonae (Microspora) prior to sporogony, inhibiting the production of xenomas. This study intended to characterize this life-cycle failure. Juvenile rainbow trout, Oncorhynchus mykiss (Walbaum), were experimentally infected with L. salmonae spores, and the effect of water temperature on the progress of infection, as determined by polymerase chain reaction, was compared for fish held at water temperatures of 5, 15 and 21 °C. At 15 °C, parasite DNA was first detected in the heart (3 days post-exposure [PE]), and then in the gills and spleen (2 weeks PE). Branchial xenomas developed by week 4 PE. In contrast, at 5 °C, the arrival of the parasite in the heart was delayed until 7 days PE. However, even though parasite DNA was detected in the gills at 7 days PE, xenomas failed to form in the gill, and by week 4 PE, parasite DNA was no longer detected. In fish held at 21 °C, parasite DNA was detected in the heart, gills and spleen by 3 days post-infection, and similar results were observed at 7 days PE. Xenomas also failed to form in these fish and parasite DNA was no longer detected by week 2 PE. Within the range of temperatures tested in this study, spore germination and delivery of their DNA into the host through the intestinal wall was not blocked by temperature. At 5 or 21 °C, migration to the heart and gills occurred, but at aberrant periods of time. The normal life cycle of L. salmonae may depend on the completion of relatively lengthy, but yet unknown, stages of development within the heart, prior to reaching the gill. This development may be adversely affected by temperature, and explain the temperature limits of this parasite.     

Altered tissue distribution of Loma salmonae: effects of natural and acquired resistance

This study compared and contrasted the fate of the microsporidian Loma salmonae , a branchial pathogen of salmonids of the genus Oncorhynchus , upon exposure of (1) naive susceptible rainbow trout (RT) O. mykiss , (2) naive RT passively immunized with sera from RT previously exposed to L. salmonae , (3) previously exposed and resistant RT and (4) two species believed to be innately resistant to the parasite, Atlantic salmon (AS) Salmo salar and brook trout (BT) Salvelinus fontinalis . The fish were infected per os with viable L. salmonae spores. The infection was followed in the fish by detection of parasite DNA by polymerase chain reaction (PCR) at several times post-infection. Spore germination and intestinal invasion by the parasite occurred in all groups of fish. In the susceptible RT, parasite DNA was detected in the heart by day 3 post-exposure (PE), followed by the gill at 2 weeks PE, whereas visible xenoparasitic complexes (xenomas) were detected by week 4 PE. In the passively immunized RT, the parasite's fate was similar to that of controls, however, its arrival in the heart was delayed by 1 week. A delay was also detected in RT which had been previously exposed to L. salmonae and then recovered from disease. In these resistant fish, the parasite was able to reach the heart by week 3 PE, however, it failed to reach the gill and form xenomas. In AS and BT, the parasite reached the heart and gills quickly, where it remained for 2 weeks before being cleared; xenomas never formed. We speculate that failure to complete the life cycle in AS, BT and resistant fish might be because of interference by the immune system in the development of the parasite, resulting in the absence of disease in these fish.     

Induced resistance in rainbow trout, Oncorhynchus mykiss (Walbaum), to gill disease associated with the microsporidian gill parasite Loma salmonae

Branchial xenomas were detected by week 5 and disappeared by week 10 after naive juvenile rainbow trout, held at 14.5 °C, were fed or intubated with Loma salmonae ‐infected gill tissue preparations. Upon re‐challenge with L. salmonae , these fish were protected from disease and branchial xenomas did not develop. Branchial xenomas were never detected in naive fish held at 10 °C and exposed to L. salmonae . When these fish were re‐challenged with L. salmonae at 14.5 °C, they were also protected from the disease. Branchial xenomas also developed after naive fish, held at 14.5 °C, were injected intraperitoneally with a semipurified preparation of fresh spores, but generally did not develop after intraperitoneal injection with a preparation of spores subjected to freezing and thawing before use. Fish that had received fresh spores intraperitoneally were completely resistant to disease when re‐challenged via oral delivery of spores, whereas those that had received frozen spores were incompletely, but significantly, protected from disease compared with naive fish. We conclude that infection with L. salmonae induces strong protection towards the disease upon re‐exposure to spores, and that the protection does not depend on the completion of the parasite's life cycle, thus establishing the basis for further research on vaccine development for this disease.     

Interaction of water temperature and challenge model on xenoma development rates for Loma salmonae (Microspora) in rainbow trout, Oncorhynchus mykiss (Walbaum)

This study evaluated the regulatory effects of water temperature on the development of branchial xenomas caused by Loma salmonae using a high-dose per os-challenge model compared with a low-dose cohabitation-challenge model. Approximately 275 juvenile rainbow trout (RBT), Oncorhynchus mykiss, were randomly distributed to six tanks with two tanks each maintained at 11, 15 and 19 degrees C. Fish in one tank from each temperature setting were exposed per os to macerated L. salmonae-infected gill material and fish in the other tank from each temperature setting were exposed to L. salmonae using the cohabitation-challenge model. Fish were monitored for the development of branchial xenomas beginning at day 21 post-exposure. Survival analyses were used to evaluate the effect of water temperature and challenge model on the number of days until the first visible branchial xenoma was detected. The survivor curves for the per os-challenge model revealed that there was at least one significant difference, whereas the cohabitation challenge did not reveal any significant differences amongst the temperature settings. The proportional hazards model revealed a significant interaction between the challenge model used and water temperature. This indicated that the effect of water temperature was different depending on challenge model. Additionally, from the mean xenoma intensities, on average, the per os-challenged fish showed higher xenoma intensity compared with the cohabitation-challenged fish. Overall, the impact of water temperature on disease pathogenesis was greater when the RBT were per os challenged compared with using the cohabitation model.     

Influence of feeding ratio and size on susceptibility to microsporidial gill disease caused by Loma salmonae in rainbow trout, Oncorhynchus mykiss (Walbaum)

Two trials were designed to quantify the effect of feeding ratio and fish size on the cohabitation transmission of Loma salmonae, the causative agent of microsporidial gill disease (MGD) in salmonids, Oncorhynchus spp. To evaluate the effect of feeding ratio on disease onset, groups of 45 rainbow trout, O. mykiss (Walbaum) (RBT), were fed daily at 1% (low), 2% (medium) or 4% (high) of the fish biomass in the tank. There were three tanks at each feeding level: two tanks were exposed to the pathogen and one was a control. For the second objective, 300 RBT were separated into seven tanks so that the weight classifications were small (17-23 g), medium (32-38 g) and large (57-63 g). Each size class was done in duplicate with one control tank containing medium-sized fish. Separately for each trial, on day 0 post-exposure (PE) five highly infectious RBT were added to each tank (not including the control tanks) to begin the cohabitation exposure period. Beginning on day 21 PE and continuing biweekly until days 70 and 77 PE for the feeding and fish size trials, respectively, each fish was evaluated for visible branchial xenomas to determine disease onset time. Using survival analysis, the survival curves for the low, medium and high feedings were not significantly different from each other. However, there were significant differences amongst the small, medium and large weight classes in the size trial. The median numbers of days to the development of branchial xenomas was 31, 38 and 42 for small, medium and large size fish, respectively. On any given day, a medium or large sized fish had a hazard ratio for developing branchial xenomas of 0.66 and 0.63, respectively, compared with a small fish. In addition to host species and host strain differences, fish size is now considered a host risk factor for the development of MGD.     

Cell and tissue reactions of turbot Scophthalmus maximus (L.) to Tetramicra brevifilum gen. n., sp. n. (Microspora)

Abstract. Tetramicra brevifilum gen, n. sp, n. is described from the connective tissues throughout the body musculature of turbot Scophthalmus maximus (L.). Uninucleate spores (4.8·2 μm) are characterized by a large posterior vacuole, electron dense inclusion bodies in cytoplasm and nucleus and short filaments with 3–5 coils (50 μm extruded). Sporogony is apansporoblastic and tetrasporoblastic, within a host vacuole. Features of the xenoma (2 mm diameter) include a microvillous surface layer with microtubules and microfilaments and a reticulate nucleus with numerous nucleoli. Adherence between adjacent xenomas results in composite cysts of various sizes and shapes depending on site, being dendritic in the myomeres, arms extending between the fibres. Effects on the host, other than eventual destruction of the host cell, include displacement of muscle fibres in myomeres with loss of attachment to myocommata. Breakdown of the xenoma with release of spores into the connective tissue matrix was associated with a localized necrosis affecting surrounding muscle fibres, with leucocyte infiltration and collagen deposition. Spores phagocytosed by macrophages were destroyed in vacuoles, some with multi-laminate walls. Experimental infections established by intramuscular injection at marked sites remained localized, which suggested that xenomas afford sufficient scope for spore production without the need of secondary invasion. The swimming efficiency of turbot would be impaired in severe infections leading to lowered growth rates and increased mortality in wild populations due to predation and starvation. Feeding hierarchies exist in turbot and the disease could prove significant in farming conditions.     

In vitro and in vivo effects of rabbit anti-thymocyte serum on circulating leucocytes and production of complement fixing antibodies in thymectomized Oncorhynchus mykiss (Walbaum) infected with Cryptobia salmositica Katz 1951

Rabbit anti-thymocyte serum (RATS) against thymocytes of rainbow trout was toxic to leucocytes from intact and thymectomized rainbow trout at 10 °C under in vitro conditions. The total number of leucocytes decreased significantly in 24 h after RATS was injected intraperitoneally into intact rainbow trout, but the number returned to pre-injection level within 1 week. RATS destroyed a lower percentage of leucocytes in thymectomized fish than in intact fish under both in vitro and in vivo conditions and the recovery in the number of leucocytes was slower in thymectomized fish. The parasitaemia, packed cell volume and production of complement fixing antibody in thymectomized and intact fish (injected with RATS before Cryptobia salmositica infection) were not significantly different from control fish (not injected with RATS), and they both acquired protective immunity against cryptobiosis on recovery. This indicates that RATS is not cytotoxic to B-like cells in the lymphoid tissue which produce complement fixing antibody against C. salmositica and that the protective antigen in C. salmositica seems to be thymus-independent.     

Spraguea (Microsporida: Spraguidae) infections in the nervous system of the Japanese anglerfish, Lophius litulon (Jordan), with comments on transmission routes and host pathology

Anglerfish from the genus Lophius are a globally important commercial fishery. The microsporidian Spraguea infects the nervous system of these fish resulting in the formation of large, visible parasitic xenomas. Lophius litulon from Japan were investigated to evaluate the intensity and distribution of Spraguea xenomas throughout the nervous system and to assess pathogenicity to the host and possible transmission routes of the parasite. Spraguea infections in L. litulon had a high prevalence; all fish over 403 mm in standard length being infected, with larger fish usually more heavily infected than smaller fish. Seventy percent of all fish examined had some gross visible sign of infection. The initial site of development is the supramedullary cells on the dorsal surface of the medulla oblongata, where all infected fish have parasitic xenomas. As the disease progresses, a number of secondary sites typically become infected such as the spinal, trigeminal and vagus nerves. Fish with infection in the vagus nerve bundles often have simultaneous sites of infection, in particular the spinal nerves and along the ventral nerve towards the urinary bladder. Advanced vagus nerve infections sometimes form xenomas adjacent to kidney tissue. Spraguea DNA was amplified from the contents of the urinary bladders of two fish, suggesting that microsporidian spores may be excreted in the urine. We conclude that supramedullary cells on the hindbrain are the primary site of infection, which is probably initiated at the cutaneous mucous glands where supramedullary cells are known to extend their peripheral axons. The prevalence of Spraguea infections in L. litulon was very high, and infections often extremely heavy; however, no associated pathogenicity was observed, and heavily infected fish were otherwise normal.     

Characterization of a monoclonal antibody against the 47- kDa antigen of Cryptobia salmositica Katz and its use in an antigen-capture enzyme-linked immunosorbent assay for detection of parasite antigen in infected rainbow trout, Oncorhynchus mykiss (Walbaum)

A monoclonal antibody (designated MAb-007) was produced against the pathogenic haemoflagellate Cryptobia salmositica Katz. This IgG3 antibody recognized the 47-kDa antigenic polypeptide of C. salmositica (SDS-PAGE and Western immuno-blotting). The antibody did not agglutinate live parasites, and there was no change in the staining intensity of the 47-kDa band on Western immunoblots after immunoabsorption of MAb-007 with live intact parasites. The 47-kDa antigen recognized by MAb-007 was localized in the cytoplasm of the parasite (immunogold labelling and electron microscopy). The monoclonal antibody cross- reacted with the 47-kDa polypeptides of C. bullocki Srrout and C. catostomi Bower & Woo. It was used in an antigen-capture ELISA for the detection of parasite antigen in the plasma of rainbow trout inoculated with the parasite, or with an attenuated vaccine strain of C. salmositica. All pre-infection plasma were negative while all infected fish with detectable parasitaemias were positive for antigen at 1–9 weeks after infection. Parasite antigen was even detected in vaccinated fish that were negative for parasites using the wet mount microscopic technique. The antigen-capture ELISA detected C, salmositica antigen in whole cell lysate preparations at concentrations as low as 0.5 μg ml^-1. Fifty microlitres of fish plasma was required in the antigen-capture ELISA, and the use of a plate reader and 96-well plates facilitated rapid analysis of a large number of plasma samples. The sensitivity of the assay makes it a potentially useful tool for detection of Cryptobia infections.     

Cloning and expression of a surface immunogenic protein in Streptococcus dysgalactiae isolated from fish and its application in enzyme‐linked immunosorbent assays to diagnose S. dysgalactiae infections in fish

Lancefield group C Streptococcus dysgalactiae (GCSD) causes severe necrotic lesions in the caudal peduncle in the genus Seriola farmed in Japan. To develop a sero‐diagnostic method for GCSD infection in farmed fish, we attempted to identify a surface immunogenic protein that induces an antibody after infection with GCSD by immunoblot analysis using sera collected from infected fish. A protein obtained from sodium dodecyl sulfate (SDS) extracts of GCSD was identified as S. dysgalactiae surface immunogenic protein (Sd‐Sip). Sd‐Sip exhibited more than 94% homology with a surface antigen or a hypothetical protein from S. dysgalactiae mammalian isolates at the nucleotide sequence level. Expression of the recombinant Sd‐Sip (rSd‐Sip) was confirmed by immunoblot analysis, that is, its reactivity to GCSD‐infected sera. Antibody detection ELISA using rSd‐Sip and their usefulness for diagnosis of GCSD infection were examined. GCSD‐infected sera collected from farmed amberjack, Seriola dumerili (Risso), showed strong reaction with immobilized rSd‐Sip. Meanwhile, sera immunized by other pathogenic bacteria of fish were showed ELISA values similar to those of non‐infected sera. These results of this study suggest that the antibody detection ELISA using rSd‐Sip is an effective diagnostic method for GCSD infection in fish.     

A Preliminary Study on the Effects on Growth,Condition, and Feeding Indexes in Channel Catfish,Ictalurus punctatus,after the Prophylactic Use of Potassium Permanganate and Oxytetracycline

The prophylactic use of potassium permanganate (KMnO₄) and oxytetracycline and its effects on catfish growth were assessed. For eleven weeks, healthy channel catfish, Ictalurus punctatus, juveniles were exposed to KMnO₄ and oxytetracycline. KMnO₄‐treated fish were exposed to 1 ppm twice a week for 1 h, while oxytetracycline‐treated fish received a 50 mg/kg dose in the feed (35 fish per tank, two tanks per treatment). Assessed parameters included body weight and length, specific growth rate (SGR), feed intake (FI), condition, and feed conversion index (FCI). Potassium permanganate did not have a suppressive effect on growth, while oxytetracycline significantly enhanced growth on channel catfish (weight and length), as they were heavier (12.5%) than KMnO₄‐treated fish and controls at the end of the trial. SGR (%/d), FI, and FCI were not significantly different (P > 0.05) among the three groups of fish. Condition index (K) was significantly higher (ANOVA, P < 0.05) in the oxytetracycline‐treated fish. The present study suggests that, at concentrations commonly used in aquaculture, exposure of healthy channel catfish to oxytetracycline enhanced growth, while KMnO₄ does not induce growth suppression.