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Results for “FASCIOLIASIS”

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At least 1,315 records · Page 73Linked to original sources
PubMed2004

Coinfection of chronic hepatitis B and fasciolosis.

Chronic hepatitis B and fasciolosis are associated with the induction of T-cell responses polarized to the Th2 subtype. Interferon-alpha enhances innate immunity as well as Th1 immune response. We present a male patient with chronic hepatitis B and fasciolosis who responded to chronic hepatitis treatment with hepatitis B virus (HBV) vaccine, interferon-alpha-2b and lamivudine.

Adult↗
PubMed1992

Factors affecting morbidity and mortality on-farm and on-station in the Ethiopian highland sheep.

Factors affecting morbidity and mortality of the Ethiopian highland sheep were studied both on-farm and on-station at Debre Berhan between 1989 and 1990. Primary causes of infectious origin resulted in high proportional morbidity (88.4% on-farm) and mortality (72.9% on-farm and 71.8% on-station) rates. Nutritional and managemental factors were also responsible for mortalities in lambs. The most frequent secondary causes of morbidity and/or mortality were ectoparasites and nasal myiasis. Health management interventions on-station were not high enough to produce performance improvements above the on-farm levels. However, the occurrence of gastrointestinal parasites significantly (P < 0.05) differed between the two management systems. The frequency of some of the major causes of morbidity and mortality such as pneumonia, fasciolasis and enteritis were significantly (P < 0.01) affected by season and age of an animal. In order to alleviate the major health constraints identified in this study, a proper health management intervention involving vaccination, strategic anthelmintic treatment and feeding management are suggested.

Age Factors↗
PubMed1994

Characterization of the oligomycin-sensitivity properties of the F1F0-ATPase in mitochondria from rats infected with the liver fluke Fasciola hepatica.

The F1F0-ATPase activity of liver mitochondria isolated from rats infected with Fasciola hepatica at 3 and 4 weeks post-infection showed a marked loss of sensitivity to oligomycin and to N,N'-dicyclohexylcarbodiimide. A loss of sensitivity to diethylstilbestrol was also demonstrated at 4 weeks post-infection. Recovery was apparent in most cases by 6 weeks post-infection. No significant difference in latent ATPase activity was observed between mitochondria from control and infected livers at any stage of the infection. The mitochondria from infected livers were therefore considered to have a full complement of the F1 moiety of the F1F0-ATPase complex. Purification of the mitochondrial ATPase from 4-week infected livers resulted in a very low yield of an oligomycin-insensitive complex. This was due to a failure to enrich specific activity during purification. The evidence presented indicates that infection with Fasciola hepatica gives rise to alterations in the function of the host liver mitochondrial ATPase, namely loss of inhibitor sensitivity and apparent structural alterations of the ATPase complex.

Animals↗