Lamellar Hyperplasia Research Articles

The influence of etofenprox on narrow clawed crayfish (Astacus leptodactylus Eschscholtz, 1823): Acute toxicity and sublethal effects on histology, hemolymph parameters, and total hemocyte counts

The acute and sublethal effects of etofenprox, a nonester pyrethroid, was determined in narrow-clawed crayfish (Astacus leptodactylus Eschscholtz, 1823). Semistatic bioassay procedures were followed in both experiments, and the 24, 48, 72, and 96 h LC50 values (with 95% confidence limits) of technical etofenprox for crayfish were calculated as 0.68, 0.61, 0.45, and 0.41 µg/L, respectively based on Finney's probit analysis. Two concentrations of etofenprox (0.04 and 0.1 µg/L) were tested to determine sublethal effects due to 96 hours exposure. After exposure to sublethal etofenprox, hemolymph glucose, and lactate levels increased while total hemocyte counts and sodium levels decreased (p < 0.05). Hemolymph calcium, potassium, magnesium, and chloride concentrations did not change significantly. Histological alterations were evident in the gills and hepatopancreas after exposure to sublethal etofenprox concentrations. Lamellar hyperplasia and lining in the afferent and efferent branchial vessels were recorded in gills; whilst tubule necrosis was obvious in hepatopancreas. Etofenprox was found to be very highly toxic to crayfish, a nontarget organism. Exposure to sublethal concentrations for 96 h affected circulating hemocytes and hemolymph stress parameters via histological response, to compansate for the adverse effects of etofenprox. © 2014 Wiley Periodicals, Inc. Environ Toxicol 30: 887-894, 2015.

Histopathological alterations of mercuric chloride toxicity in marine fish (Acanthopagrus latus)

The present study was conducted to understand the mechanisms of mercury toxicity in marine yellowfin seabream, Achanthopagrus latus fish. The histopathological effects of mercuric chloride exposure (10, 20, 40, 80 μg/L), for 3 weeks were studied. Samples of gills, liver, intestine and kidneys were studied by light microscopy. The gill at all doses of HgCl2 showed desquamation, aneurism in secondary lamellae, lifting of the lamellar epithelium, oedema, epithelial hyperplasia and fusion of the secondary lamellae. Degenerative changes in hepatocytes, aggregation of macrophages and focal necrosis were found in the liver in dose dependent manner. Lesions in the kidney were characterized by degeneration in the epithelial cells of renal tubules, dilation of glomerular capillaries, hypertrophy of tuber epithelial cells, narrowing of tubular lumen, and hyaline degeneration. Focal degeneration of villi with swollen tips, increased goblet cells activity, leukocytic infiltration and mast cells aggregation were observed in intestinal folds.

Acute tolerance and histopathological effects of ammonia on juvenile maroon clownfishPremnas biaculeatus(Block 1790)

This study evaluated the median lethal concentration values (LC50) and the histopathological effects of un-ionized ammonia (NH3 - -N) on juvenile maroon clownfish Premnas biaculeatus. After 96 h of exposure to different concentrations of ammonia, juveniles were sampled for histopathological evaluation. The 24 and 96 h LC50 values of NH3 -N determined were 1.68 and 0.89 mg L 1 respectively. Maroon clownfish exposed to different ammonia concentrations displayed histopathological alterations in the gills, kidney, liver and brain. Gill tissue damage included lamellar hyperplasia, lamellar shorting and hyperplasia and hypertrophy of mucous cells. The kidney showed hyperanaemia, enlarged sinusoids within an apparently decreased amount of haematopoietic tissue, oedema on tubular cells and tubular necrosis, and an enlarged Bowman’s capsule. The liver presented dilatation of hepatic sinusoids, fatty deposition in hepatocytes and Mallory bodies. Examination of the brain revealed a proliferation of glial cells, and the Virchow-Robin space indicated a severe perivascular oedema and signs of neuronal suffering with satellitosis. The results of this study indicate that juvenile maroon clownfish are relatively sensitive to ammonia and particular attention must be given to this toxic compound in culture systems.

Microbiological water quality and gill histopathology of fish from fish farming in Itapecuru-Mirim County, Maranhão State

The present study evaluated the microbiological water quality and tissue lesions in gills from Nile tilapia (Oreochromis niloticus) and hybrid tambacu (Colossoma macropomum female x Piaractus mesopotamicus male). For this, water and gills were collected from fish farming at six locations in Itapecuru- Mirim County, Maranhao State. Microbiological water analyses revealed contamination by total coliforms, Escherichia coli and heterotrophic bacteria. In the gills, we observed a diversity of Gram-positive and Gram- negative bacteria. The tissue lesions were: lamellar fusion, interlamellar hyperplasia, sub-epithelial edema and telangiectasia. Inflammatory lesions were not observed. Significant statistical difference (p > 0.05) was not detected when comparing different gills lesions during rainy and dry season. The correlation between lesion and pond type was statistically different (p < 0.05) for lamellar fusion and interlamellar hyperplasia which occurred more frequently at ground ponds. Regarding the frequency of lesions in the different fish species, there was statistical difference (p < 0.05), and the tambacu was more sensitive to lamellar fusion while tilapia was more sensitive for the other lesions. In relation to the sampling stations, there was statistical difference for all the gill lesions. In conclusion, tissue lesions are nonspecific and function as a defense mechanism against polluted aquatic environments, without infectious character.

Development of a novel histopathological gill scoring protocol for assessment of gill health during a longitudinal study in marine-farmed Atlantic salmon (Salmo salar)

Gill health and disease in farmed Atlantic salmon (Salmo salar) were studied at a marine site on the west coast of Ireland. Fish were sampled on a regular basis during the summer and autumn of 2009. A novel histopathological scoring system was devised to give a semi-quantitative measure of gill pathology. The index criteria for gill histopathology were lamellar hyperplasia, lamellar fusion, circular anomalies (necrosis or sloughing) and lamellar oedema, a score from 0 to 3 being assigned for each parameter. Ancillary criteria, such as hypertrophy, haemorrhage and the presence of specific pathogens, were assigned a score of 0 or 1. Environmental monitoring undertaken included zooplankton and phytoplankton sampling, as well as temperature and oxygen recordings for the site. Epitheliocystis was frequently observed at low levels but was not associated with any significant gill pathology. Clinically significant gill pathology was observed on one occasion during the sampling period, coinciding with the occurrence of Pelagia noctiluca, Muggiaea atlantica and Solmaris corona. Throughout the longitudinal study, the scoring system provided an accurate and effective means of assessing gill health, demonstrating the ability of this practical tool to be used in future studies of gill health and disease.

Toxic Effect of Brewery Effluent on Fingerlings of Clarias gariepinus

Background: The indiscriminate discharge of waste-water (effluent) as influenced by industrialization and development create significant pollution problems to normal flora and fauna of the ecosystem. Toxicity of brewery effluent remain unknown, particularly its implications on histopathology of fish under continous exposure. The study unravels the effects of brewery effluent on fingerlings of Clarias gariepinus under laboratory conditions. Materials and Methods : Fingerlings of Clarias gariepinus (of mixed sex) (5.20×0.42g) were exposed to various concentrations of brewery effluent in five treatment (in duplicate) 15, 20, 25, 30, 35% and 0.00% for control The Toxicity and histopathology of the gills and liver of fish exposed were observed under laboratory conditions. Result : Acute concentrations had adverse effects on mortality and oxygen consumption. The 96-h LC 50 of brewery effluent was 23.99ml/l with upper and lower confidence limits of 29.478ml/l and 18.324ml/l respectively. Symptoms of toxicity include restlessness, air gulping, loss of equilibrium, exhaustion and death. Exposure of the Clarias gariepinus fingerlings to various lethal concentrations of the brewery effluent were implicated in the histopathological examinations of gills which showed mutilations of gill filament, Oedema, fusion of central venous sinus, swelling, necrosis of various degrees and total lamellar hyperplasia. The liver showed evidence of necrosis and vacuolation of liver cells whereas control group showed both normal gill and liver section. Conclusion . The indiscriminate or deliberate discharge of industrial effluent (brewery effluent) directly into the aquatic environment without any form of treatment is a common sight in many industrial cities of Nigeria today; therefore, creating awareness for environmental protection through sustainable production processes is of utmost significant.

Effects of some pesticides on the vital organs of juvenile rainbow trout ( Oncorhynchus mykiss)

Gill, trunk kidney, spleen, and liver of rainbow trout ( Oncorhynchus mykiss) were examined after exposure to different sublethal concentrations of carbosulfan (25, 50 and 200 μg L −1), propineb (3, 6 and 24 mg L −1), and benomyl (2, 5 and 20 mg L −1) for 14 days. Lesions were observed in gill, trunk kidney, spleen, and liver of rainbow trout exposed to either concentration of pesticides. The most important lesions were determined in the highest concentrations of pesticides. Lamellar fusion, lamellar hyperplasia, epithelial lifting, vacuolization of epithelial tissue, epithelial necrosis, hypertrophy and sloughing of epithelium were observed on fish exposed to carbosulfan, propineb and benomyl. Fish had cell necrosis, degeneration and oedemas in liver, trunk kidney and spleen. None of these lesions were seen in control fish.

Assessment of acute toxicity and histopathology of the fungicide captan in rainbow trout

Acute toxicity of the fungicide, captan, to juvenile rainbow trout was evaluated under static-renewal test condition. Actual concentrations of captan ranged from 0.05 to 1.00 mg/L. The concentrations of captan that killed 50% of the rainbow trout (3.11±0.8 g) within 24 (24 h; LC(50)), 48, 72 and 96 h were 0.57±0.09, 0.49±0.10, 0.44±0.11 and 0.38±0.13 mg/L (95% confidence limits), respectively. None of the unexposed control fish died and the first fish died 6 h after exposure to captan (≥0.65 mg/L). Hypertrophy, separation of epithelium from lamellae, lamellar fusion, and epithelial cell necrosis were observed on captan exposed fish. Gills also had scattered areas of focal lamellar hyperplasia. Fish exposed to fungicide had inflammation and necrosis in liver, trunk kidney and spleen. In order, the most affected organs were gill, trunk kidney and liver.

Aqua-toxicological Effects of Water Soluble Fractions (WSF) Of Diesel Fuel On O. Niloticus Fingerlings

Five concentrations of water soluble fraction (WSF) of diesel fuel (1.6 ppm, 3.2ppm, 6.4ppm, 12.3ppm and 19.2ppm) were made. To each of the concentrations of the WSF, ten fingerlings of O. niloticus with an average weight of 3g were incubated for 96hours. The 96hour LC50 was determined (8.08ppm). Histopathological examination of the fish gills following exposure to the LC50 and LC100 concentrations of the WSF showed gill elongation and lamellar hyperplasia respectively. There was reduction of dissolved oxygen content (from 7.2 to 4.5 mg/l) caused by diesel that dissolved in water. This was below acceptable levels for the sustenance of aquatic life (i.e. 6.0 – 8.0 mg/L). However, the pH reading was not adversely affected. The result tended to suggest that the death of the fingerlings might be related to the decreased dissolved oxygen content of the water due to the presence of diesel. The structural changes of the gills observed may be an adaptation by the fingerlings to oxygen stress

Histopathological changes induced by maneb and carbaryl on some tissues of rainbow trout, Oncorhynchus mykiss

Acute toxicity of the pesticides, maneb and carbaryl, to juvenile rainbow trout were evaluated under static-renewal test conditions. Actual concentrations of maneb ranged from 0.10 mg/L to 2.00 mg/L and carbaryl ranged from 0.20 mg/L to 3.90 mg/L. The concentrations of maneb that killed 50% of the rainbow trout (3.27 ± 0.9 g) within 24-h (24-h; LC 50), 48-h, 72-h and 96-h were 1.19 ± 0.12, 1.04 ± 0.11, 0.92 ± 0.12 and 0.81 ± 0.14 mg/L (95% confidence limits), respectively. LC 50 values of carbaryl for 24-h, 48-h, 72-h and 96-h were 2.52 ± 0.71, 2.16 ± 0.63, 1.71 ± 0.46 and 1.39 ± 0.15 mg/L, respectively. None of the unexposed control fish died and the first fish died 6 h after exposure to maneb (≥1.30 mg/L), and carbaryl (≥2.60 mg/L). Lamellar edema, separation of epithelium from lamellae, lamellar fusion, swelling of the epithelial cells and epithelial cell necrosis were observed on maneb and carbaryl exposed fish. Gills also had scattered areas of focal lamellar hyperplasia. Fish exposed to pesticides had inflammation and focal necrosis in liver, trunk kidney and spleen. Maneb and carbaryl had similar histopathological lesions. In order, the most affected organs were gill, trunk kidney and liver.

HISTOLOGICAL CHANGES INDUCED BY LEAD NITRATES IN THE GILLS OF GRASS CARP, Ctenopharyngodon idelia (Val.) JUVENILES

The present study showed that the lead had toxic effects on the gill structures of the grass carp (Ctenopharyngodon idella) juveniles such as clubbing molting of epithelial cells, epithelial separation, necrosis, fusion of adjacent lamellar epithelium and hyperplasia of secondary lamellar epithelium, destruction of epithelial cells, curved of epithelial, loose in regular shape of epithelium, bite and bleeding tissues through exposure for 48 hrs. All these histological changes depended on lead concentration and exposure period.

TOXIC EFFECT OF MALATHION IN TILAPIA NILOTICA

Toxic effect of malathion in Tilapia nilotica fish after short (one month) and long (5 months) term exposure as well as reversibility of the lesions were investigated. The result showed malthion has adverse effect on all vital organs of T. nilotica fish at both levels of exposure. Necrobiotic changes in the parenchyma of liver, kidney and heart Lamellar hyperplasia with lamellar fusion in gills and neuronal injuries and edema were all detected. Most of the lesions observed have been almost completely disappeared by 4weeks of withdrawal of malathion but the brain still showed focal subependymal edema accompanied with neuronal injury and edema of the nerve tract.

Experimental induction of gill disease in Atlantic salmon Salmo salar smolts with Tenacibaculum maritimum

An experimentally induced bacterial infection of marine Atlantic salmon Salmo salar smolt gills was developed using strains of Tenacibaculum maritimum originally isolated from disease outbreaks in Tasmania. The gills of salmon were inoculated with a high concentration of bacteria (4 x 10(11) cells per fish) of either strain 00/3280 or 89/4747 T. maritimum. Gentle abrasion of the gills was used to enhance the progression of gill disease. One strain (00/3280) was highly pathogenic, causing morbidity and mortality within 24 h post-inoculation, and produced acute focal branchial necrosis associated with significant increases in plasma osmolality and lactate concentration compared with controls (non-inoculated) or strain 89/4747-inoculated fish. There were no differences in the whole body net ammonium flux between control (non-inoculated) and strain 00/3820-inoculated fish. Gill abrasion resulted in acute telangiectasis and focal lamellar hyperplasia in all fish regardless of bacterial inoculation. This work provides the basis of a challenge model suitable for investigating the pathophysiological processes associated with acute branchial necrosis in marine fish, suggesting that osmoregulatory and possibly respiratory dysfunction are the primary consequences of infection.

Contents and organ distribution of pantothenic acid in maturing turbot (Psetta maxima )

Contents and organ distribution of pantothenic acid in maturing turbot (<i>Psetta maxima</i> )

Histopathological effects of crude oil on Atlantic cod following chronic exposure

To assess the long-term effect on the tissues of marine fish, Atlantic cod, Gadus morhua L., were exposed to water-soluble fractions of Venezuelan and Hibernia crude oils at concentrations of 50–300 ppb for 12–13 weeks in a flow-through seawater system. Histopathological changes in oil-exposed fish included increased numbers of mucus-producing epithelial cells, capillary dilation, lamellar hyperplasia, and fusion of adjacent filaments in gills, microvesicular formation in hepatocytes, delayed spermatogenesis with intratubular multinucleated giant cells, and an increase of melanomacrophage centers in the spleen and kidney. Lesions were more prevalent and severe in fish exposed to Hibernia crude than to Venezuelan crude at a similar concentration.

Development of lamellar epithelial hyperplasia in gills of pantothenic acid‐deficient rainbow trout, Salmo gairdneri Richardson

Two semisynthetic diets differing in the levels of pantothenic acid (PA) supplementation (0 or 40 mg kg−1 diet) were fed to rainbow trout, Salmo gairdneri Richardson, initially weighing 0.7 g fish−1. Each diet was fed to two tanks of fish and, at the start of the feeding trial, each tank contained 200 animals. The experiment was conducted for 28 days during which time, every 2 days, gill tissue was sampled and food consumption was determined. Lamellar hyperplasia was first detected in the gills of deficient fish on the 12th day sample, while reduced feed intake was first manifest at 16 days. Hyperplasia first appeared in the distal regions of the gill filaments, but the lesion rapidly progressed in a proximal direction and 35 of 40 fish examined on days 22–28 exhibited hyperplasia on more than 75% of the filament surface. Gill lamellar hyperplasia is a sensitive indicator of PA deficiency in the rainbow trout. Moreover, the lesion is specific to PA deficiency since its developmental pattern differs histologically from the lamellar hyperplasia of the non‐nutritional gill diseases.