Tropical liver fluke‐induced stress in experimentally infected and immunised buffaloes

Abstract

Disease-related stress associated with Fasciola gigantica infection was investigated in 16 male, yearling Murrah buffaloes. The animals were randomly assigned to one of four groups. Animals in groups 1 and 2 were vaccinated subcutaneously with 4.8 mg of excretory-secretory antigen (group 1) or 1300 μg infection-specific antigen (group 2), in three doses. Subsequently, all the animals in groups 1, 2 and 3 were infected orally with 800 viable F gigantica metacercariae (bubaline origin) on week 6 of the experiment. The animals in group 4 served as healthy controls. The clinical progress of the disease with respect to the adrenocortical response to infection was assessed periodically. The infected animals in group 3 developed characteristic signs of the disease and had the highest in situ fluke population (mean [se] 331.8 [19.5] ). One of the four animals in group 3 died on day 110 postinfection (PI). Animals that had been immunised before infection (groups 1 and 2) acquired adequate levels of immunity, were comparatively healthier and had significantly lower (P<0.05) fluke populations (mean [se] 194.3 [11.8] in group 1 and 164.5 [9.2] in group 2). Throughout the course of the disease, the group 3 animals had significantly higher cortisol levels than those in groups 1 and 2 (P<0.01) from week 4 PI onward. Although animals in the immunised groups (groups 1 and 2) had increased hormone levels, they were not significantly different from those in the control animals in group 4. Cortisol levels were higher during the early prepatency phase (weeks 1 to 6 PI) than during the late prepatency and/or patency phases of the disease. Cortisol levels in the healthy control animals in group 4 remained within the normal range.

Epizootiology, pathogenesis and immunoprophylactic trends to control tropical bubaline fasciolosis: an overview

“…Like other metazoan diseases, the Okao (1984) and Fabiyi (1987) Ethiopia 30-90 Fabiyi (1987) severity and the course of the disease in buffaloes vary with the dose of MC ingested, in a primary single massive dose or perpetual and recurrent lower doses, over a shorter or a prolonged period. A primary infection dose of 800-1000 F. gigantica MC caused acute disease with pathognomic clinical manifestations synchronous with growth and maturation of the infection dose and was incidental to 20-33.3% mortality in Murrah buffalo yearlings (Yadav et al 1999b;Edith et al 2010c). The prepatent period of F. gigantica in riverine buffaloes is longer (92-97 days) than F. hepatica (50-70 days) in large ruminants.…”

“…The Murrah buffalo yearlings, infected with 800/1000 F. gigantica MC, persistently had elevated hormone activity in the circulation indicated variable degree and magnitude of the adrenocortical response to the in situ distome population (Ganga et al 2007;Edith et al 2010c). The response was, however, variable in severity depending upon the clinical phase of the disease, in situ activities and location of the F. gigantica adolescercariae or adult fluke population.…”

Magnetic resonance imaging and spectroscopy for differential assessment of liver abnormalities induced by Opisthorchis felineus in an animal model

“…There are some publications about elevation of plasma cortisol in animals infected by parasitic worms [86,87]. This glucocorticoid(-s) has several effects on metabolism, in particular, it provokes mobilization of non-hexose substrates from extrahepatic tissues and stimulates synthesis of glucose in the liver.…”

Outbreak of Fatal Subacute Bubaline Fasciolosis in Wayanad, Kerala, India

“…Tropical fasciolosis caused by F. gigantica, an inhabitant of hepatobiliary system of domestic ruminants was reported previously from fourteen Indian states and Union territories [11][12][13]. In India, prevalence of fasciolosis in buffaloes varies from 10 to 100% [3].…”

“…Death occurs suddenly or after several days. Mortality of 20-33% of Murrah buffaloes due to experimental infection with 800-1000 metacercariae was recorded [13,23]. Freshwater aquatic snails of the family Lymnaeidae are the snail vectors for this disease.…”