The prevalence and pathogenic effects of trypanosomosis were determined in cattle, goats and pigs reared in Kasese, Jinja and Rakai districts, Uganda; presence of trypanosomes was detected by buffy coat technique (BCT). The overall prevalence of trypanosomosis in cattle was 7.6% (144/1,891), 0.7% in goats (4/573) and 2.3% in pigs (9/386). Internal transcribed spacer 1 (ITS1) of ribosomal DNA polymerase chain reaction was utilised to identify trypanosomes to species level and revealed infections in 108 of the 144 trypanosome-positive cattle while all infected goats and pigs gave amplicons. Trypanosoma vivax was the most prevalent trypanosome species in cattle in single and mixed infections compared to infections involving Trypanosoma congolense and Trypanosoma brucei; in pigs, eight were mixed infections with one single T. vivax infection. No predominant trypanosome species was detected in goats. Anaemia, the main trypanosomosis pathological feature, was investigated by determining packed cell volume (PCV). Mean PCV values by t test in infected individuals were significantly lower than non-infected individuals (P<0.05) for all animal species. However, the proportion of anaemic animals was not significantly different in infected and non-infected individuals. In addition, the percent of infected animals by Fisher's exact test depended on district of origin and species but not sex. These findings show that trypanosomosis is a major cause of anaemia in livestock in endemic areas. Cattle were the major animal species affected by trypanosomosis; similar genotypes of trypanosomes were detected in the three animal species. BCT was more effective than ITS1 rDNA detecting trypanosomes in naturally infected cattle.

Rift Valley fever (RVF) virus is caused by a zoonotic arbovirus that is endemic to eastern and southern Africa. It has also been reported in West and North Africa, Madagascar and the Arabian Peninsula. The virus is transmitted by mosquitoes, but people can also become infected while handling blood or other body fluids of animals and humans with RVF. In 2007, there was a large outbreak of RVF in Kenya, Tanzania, Sudan and Somalia. Outbreaks were also reported in South Africa in 2008–2011. The epidemiology of RVF and factors for disease occurrence in Rwanda are neither clear nor documented. Therefore, we conducted a cross-sectional study from December 2012 to March 2013 to generate baseline information on RVF in cattle. Purposive sampling of cattle (n = 595) was done in six districts, and serum samples were screened with competitive enzyme-linked immunosorbent assay (ELISA). We performed a statistical analysis on the generated data, and risk factors associated with RVF seroprevalence were determined by a simple logistic regression. Overall, RVF seroprevalence was 16.8% (95% confidence interval [CI] [13.8% – 20.0%]). The highest seroprevalence was recorded in Kirehe district (36.9%) followed by Ngoma (22.3%), and the least was recorded in Nyagatare (7.9%). RVF was more likely to occur in adult cattle (19.9% [odds ratio {OR} = 1.88, 95% CI {0.98–3.61}]) compared to young cattle (10.5% [OR = 0.47, 95% CI {0.26–0.83}]). Pure exotic or cross-breeds were significantly exposed to RVF virus (seroprevalence 22.9% [OR = 4.26, 95% CI {1.82–9.99}]) in comparison to 14.1% (OR = 0.55, 95% CI [0.35–0.86]) in local breeds. Sex differences were not statistically significant. These findings indicated that cattle have been exposed to RVF virus in six districts in Rwanda with a significant risk in adult, exotic or cross-breeds in Kirehe district.

Rift Valley fever (RVF) virus is caused by a zoonotic arbovirus that is endemic to eastern and southern Africa. It has also been reported in West and North Africa, Madagascar and the Arabian Peninsula. The virus is transmitted by mosquitoes, but people can also become infected while handling blood or other body fluids of animals and humans with RVF. In 2007, there was a large outbreak of RVF in Kenya, Tanzania, Sudan and Somalia. Outbreaks were also reported in South Africa in 2008–2011. The epidemiology of RVF and factors for disease occurrence in Rwanda are neither clear nor documented. Therefore, we conducted a crosssectional study from December 2012 to March 2013 to generate baseline information on RVF in cattle. Purposive sampling of cattle (n = 595) was done in six districts, and serum samples were screened with competitive enzyme-linked immunosorbent assay (ELISA). We performed a statistical analysis on the generated data, and risk factors associated with RVF seroprevalence were determined by a simple logistic regression. Overall, RVF seroprevalence was 16.8% (95% confidence interval [CI] [13.8% – 20.0%]). The highest seroprevalence was recorded in Kirehe district (36.9%) followed by Ngoma (22.3%), and the least was recorded in Nyagatare (7.9%). RVF was more likely to occur in adult cattle (19.9% [odds ratio {OR} = 1.88, 95% CI {0.98–3.61}]) compared to young cattle (10.5% [OR = 0.47, 95% CI {0.26–0.83}]). Pure exotic or cross-breeds were significantly exposed to RVF virus (seroprevalence 22.9% [OR = 4.26, 95% CI {1.82–9.99}]) in comparison to 14.1% (OR = 0.55, 95% CI [0.35–0.86]) in local breeds. Sex differences were not statistically significant. These findings indicated that cattle have been exposed to RVF virus in six districts in Rwanda with a significant risk in adult, exotic or cross-breeds in Kirehe district.

Limited pharmacological studies have been conducted on plant species used against poultry helminths. The objective of this study was to provide a basis for plant based anthelmintics as possible alternatives against poultry anthelmintic resistance. The study justified the need for alternative anthelmintics. The study places emphasis on the increasing anthelmintic resistance, mechanism of resistance, and preparational protocols for plant anthelmintics and their associated mechanism of action. Pharmaceutical studies on plants as alternative therapies for the control of helminth parasites have not been fully explored especially in several developing countries. Plants from a broad range of species produce a wide variety of compounds that are potential anthelmintics candidates. Important phenolic acids have been found in Brassica rapa L. and Terminalia avicenniodes Guill. and Perri that affect the cell signaling pathways and gene expression. Benzo (c) phenanthridine and isoquinoline alkaloids are neurotoxic to helminths. Steroidal saponins (polyphyllin D and dioscin) interact with helminthic mitochondrial activity, alter cell membrane permeability, vacuolation and membrane damage. Benzyl isothiocyanate glucosinolates interfere with DNA replication and protein expression, while isoflavones from Acacia oxyphylla cause helminth flaccid paralysis, inhibit energy generation, and affect calcium utilization. Condensed tannins have been shown to cause the death of nematodes and paralysis leading to expulsion from the gastro-intestinal tract. Flavonoids from Chenopodium album L and Mangifera indica L act through the action of phosphodiesterase and Ca2+-ATPase, and flavonoids and tannins have been shown to act synergistically and are complementary to praziquantel. Artemisinins from Artemisia cina O. Berg are known to disrupt mitochondrial ATP production. Terpenoids from Cucurbita moschata L disrupt neurotransmission leading to paralysis as well as disruption of egg hatching. Yeast particle encapsulated terpenes are effective for the control of albendazole-resistant helminths.

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