Aggravation of pathogenesis mediated by ochratoxin A in mice infected with Trypanosoma brucei rhodesiense.

作者: J. K. KIBUGU , J. J. N. NGERANWA , J. N. MAKUMI , J. K. GATHUMBI , J. M. KAGIRA

DOI: 10.1017/S0031182008005386

关键词:

摘要: Mice fed 1.5 mg ochratoxin A (OTA) per kg body weight and infected with Trypanosoma brucei rhodesiense were compared trypanosome-infected placebo-fed uninfected OTA-fed controls. Uninfected mice showed fever, lethargy, facial eyelid oedemas, mild hepatitis nephritis, high survival. Infected controls had mean pre-patent period (PPP) of 3.26 days, dyspnoea, scrotal oedema, survival 33-65 reduced red cell counts (RCC: 10.96-6.87x106 cells/microl blood), packed volume (PCV: 43.19-26.36%), haemoglobin levels (Hb: 13.37-7.92 g/dL) corpuscular (MCV) 37.96-41.31 fL, hepatosplenomegaly, generalized heart congestion, nephritis. Compared to controls, significantly (P<0.05) shorter PPP (2.58 days), (6-47 more pronounced fever dyspnoea. The latter RCC (10.74-4.56x106 PCV (43.90-20.78%), Hb (13.06-5.74 g/dL), increased MCV (39.10-43.97 fL), severe haemorrhages, hepatic haemosiderosis, hepatitis, endocarditis, pericarditis exclusively, splenic macrophage giant hyperplasia, expanded pulp erythrophagocytosis. It was concluded that OTA aggravated the pathogenesis T. b. infection in mice, should therefore be taken into consideration during trypanosomosis control programmes.

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