The effect of Chattonella exposure on gill histology of yellowtail was examined to clarify the follow ing questions: (1) Is the branchial edema, previously reported as the main branchial lesion in response to Chattonella exposure, truly caused by Chattonella cells or a secondary histological alteration by fatal hypoxemia during the exposure? (2) Is the branchial edema responsible for the rapid decline of blood oxygen levels during the early stages of Chattonella exposure? Fish dying from Chattonella exposure showed many types of lesions, especially severe epithelial separation in the lamellae and filaments. In contrast, the gills of fish dying from environmental hypoxia showed very few lesions and were histologi cally hardly discernible from the control gills. This demonstrated that the branchial edema was induced by Chattonella and not by hypoxemia. On the other hand, the epithelial separation had not developed when the tissues were sampled immediately after the onset of hypoxemia. Therefore, the edema cannot be the cause of hypoxemia. The only histological change observed in the gills sampled at blood oxygen drop was blockade of interfilamental spaces by mucus. Based on these results and the previous findings of oxygen radical production by Chattonella, we hypothesized that oxygen radicals, released from Chat tonella cells, stimulated mucus cells in the gills, and the secreted mucus, possibly plus Chattonella cells trapped within the mucus, destroyed the gas exchange capacity of the gills by shunting respiratory water current away from the lamellae.
The effects of water temperature on the development of the enteric myxosporeans, Enteromyxum fugu and Enteromyxum leei, were investigated in experimentally infected tiger puffer, Takifugu rubripes. After naïve tiger puffer were fed gut tissue infected with both E. fugu and E. leei, they were divided into separate tanks and kept at different constant temperature regimes between 10 and 25 degrees C. Regardless of the water temperature tested, E. fugu was consistently detected with a high prevalence of infection (60-100%), although no sporulation occurred at 10 and 15 degrees C. Development of E. leei and the onset of disease were suppressed by low water temperatures (<15 degrees C). However, a temperature increase to 20 degrees C promoted the development of E. leei, followed by an increase of disease rate in the fish. The present study demonstrates that water temperatures below 15 degrees C have an inhibitory effect on the development of E. fugu and E. leei, resulting in suppression of enteromyxosis at low temperatures.
ABSTRACT-The present study suggests that the myxosporean emaciation disease by enteric infection of Enteromyxum leei disrupts intestinal water uptake of tiger puffer Takifugu rubripes. This idea is based on a significant negative correlation between plasma chloride concentration and condition factor in diseased fish, and significantly higher osmolarity of plasma and major ion concentrations of the intestinal fluid in infected fish than in healthy control fish. Additionally, surgical ligation of the junction between the stomach and the intestine of healthy fish resulted in a 24% drop of body weight within 50 h, and significantly lower water content of the white muscle (operated fish 74 ± 0.5%; sham-operated fish 82 ± 1%). However, in vitro water uptake by isolated intestine sacs was not significantly different between the control and infected fish. Meanwhile, hepatic function appeared to be impaired as evidenced by the significantly lower hepato-somatic index (control fish 8.7 ± 0.8%; infected fish 2.7 ± 0.8%). Plasma activities of LDH, AST and ALT were all significantly lower in the infected fish. We propose that rapid loss of body weight of infected tiger puffer is mainly due to osmoregulatory failure but probably malnutrition is also involved in the pathogenesis.
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