First detection of Echinococcus granulosus sensu stricto (G1) in dogs in central Sudan.

Eighty-four stray dogs shot as a part of a governmental rabies control program in two neighboring towns of central Sudan were examined for the presence of Echinococcus spp. and other intestinal helminths. Echinococcus worms were identified to species level by PCR and gene sequencing. For comparative reasons, rectal content of the necropsied dogs was examined for helminth eggs and subjected to copro-PCR for Echinococcus. At necropsy, 51.2% (43/84) of the dogs harbored Echinococcus canadensis (G6/7) worms with worm burdens ranging from 22,000 to 80,000. Dipylidiun caninum was found in 53.6% of the dogs. At coproscopy, taeniid eggs were found in 37 of the 43 dogs which were positive for Echinococcus at necropsy, but none in the 41 necropsy-negative dogs. In addition, 58% of the rectal samples contained eggs of Toxocara spp., 34.5% eggs of Trichuris spp. (34.5%), and 26% eggs of Ancylostoma caninum. Copro-PCR gave positive results for E. canadensis with 97.5% (39/40) of nonhibiting samples from the necropsy positive dogs; the one remaining dog tested positive for E. granulosus sensu stricto (G1), whose partial cox1 and nad1 sequences showed a 100% identity with various reference sequences of the G1 genotype. 100% of 38 non-inhibited samples taken from the necropsy-negative dogs were also negative in copro-PCR. This is the first study which combines prevalence and genetic identification of Echinococcus spp. in dogs of Sudan. Together with a recent report from cattle, it confirms the autochthonous presence, at low level, of E. granulosus sensu stricto in Central Sudan.

Defining the role of pneumococcal neuraminidases and O-glycosidase in pneumococcal haemolytic uraemic syndrome.

The host and bacterial factors that lead to development of pneumococcal haemolytic uraemic syndrome (pHUS) remain poorly defined; however, it is widely believed that pneumococcal exposure of the Thomsen-Friedenreich antigen (T-antigen) on host surfaces is a key step in pathogenesis. Two enzymatic activities encoded by pneumococci determine the level of T-antigen exposed. Neuraminidases cleave terminal sialic acid to expose the T-antigen which is subsequently cleaved by O-glycosidase Eng. While a handful of studies have examined the role of neuraminidases in T-antigen exposure, no studies have addressed the potential role of O-glycosidase. This study used 29 pHUS isolates from the USA and 31 serotype-matched controls. All isolates contained eng, and no significant correlation between enzymatic activity and disease state (pHUS and blood non-pHUS isolates) was observed. A prior study from Taiwan suggested that neuraminidase NanC contributes to the development of pHUS. However, we observed no difference in nanC distribution. Similar to previously published data, we found no significant correlation between neuraminidase activity and disease state. Accurate quantification of these enzymatic activities from bacteria grown in whole blood is currently impossible, but we confirmed that there were no significant correlations between disease state and neuraminidase and O-glycosidase transcript levels after incubation in blood. Genomic sequencing of six pHUS isolates did not identify any genetic elements possibly contributing to haemolytic uraemic syndrome. These findings support the hypothesis that while exposure of T-antigen may be an important step in disease pathogenesis, host factors likely play a substantial role in determining which individuals develop haemolytic uraemic syndrome after pneumococcal invasive disease.

Malignant tumors of upper urinary tract - an experience in Benghazi.

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