• Journal of agricultural medicine and community health
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• v.5 no.1
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• pp.5-15
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• 1980

The first recorded trypanosomiasis epidemic in Uganda took place at the beginning of this century in the islands and in a strip along the northern shores of Lake Victoria, which resulted in deaths of 1/3 million people. The disease was partly controlled by early 1930's and continued to occur sporadically in certain localized foci. The disease has however flared up in an explosive outbreak in Busoga district along Lake Victoria since 1977. The incidence of disease in northern district adjacent to Southern Sudan is also increasing lately. This paper describes the three month observation on the surveillance and control activities in the epidemic areas and of various health units including the Vector Control Division, the Tsetse fly Control Division, Tororo Trypanosomiasis Research Institute, medical units in Busoga, and Acholi districts. Data analysis and review were made of disease information so far collected by various health units in the Ministry of Health and district health offices. The findings may be summarized in the following: 1) A total of 12, 100 patients and 38 deaths: have occured in Busoga district since 1977 onward, and over 100 cases of diseases arc occuring in the Northern region bordering Southern Sudan. 2) the distribution of trypanosomiasis is characterized with two district patterns. The disease caused by Trypanosoma rhodesiense occurs in Busoga and is transmitted by Glossina palpalis, G. fuscipes infested in the islands and in the northern shore of forests of Lake Victoria. Another type caused by Trypanosoma gambiense occurs in Madi and Acholi in the north and is transmitted by Glossina morsitans in Savannah. 3) The house survey in Rusoga indicated that most of patients keep domestic animals in their house premises, and are engaging in either farming or fishing. Practically all the patients remembered that they had been bitten by tsetse in the field. 4) The routine diagnostic methods in the hospital laboratory is carried out through the microscopic examination of trypanosome with Giemsa stain of blood and cerebro-spinal fluid, The measurement of ESR and IgM has been used by Tororo Tryponosomiasis Research Institute for field screening.

• Parasites, Hosts and Diseases
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• v.49 no.2
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• pp.115-123
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• 2011

Toxoplasma gondii Korean isolate (KI-1) tachyzoites were inoculated intraduodenally to BALB/c mice using a silicon tube, and the course of infection and immune responses of mice were studied. Whereas control mice, that were infected intraperitoneally, died within day 7 post-infection (PI), the intraduodenally infected mice survived until day 9 PI (infection with $1{\times}10^5$ tachyzoites) or day 11 PI (with $1{\times}10^6$ tachyzoites). Based on histopathologic (Giemsa stain) and PCR (B1 gene) studies, it was suggested that tachyzoites, after entering the small intestine, invaded into endothelial cells, divided there, and propagated to other organs. PCR appeared to be more sensitive than histopathology to detect infected organs and tissues. The organisms spread over multiple organs by day 6 PI. However, proliferative responses of splenocytes and mesenteric lymph node (MLN) cells in response to con A or Toxoplasma lysate antigen decreased significantly, suggesting immunosuppression. Splenic $CD4^+$ and $CD8^+$ T-Iymphocytes showed decreases in number until day 9 PI, whereas IFN-${\gamma}$ and IL-10 decreased slightly at day 6 PI and returned to normal levels by day 9 PI. No TNF-${\alpha}$ was detected throughout the experimental period. The results showed that intraduodenal infection with KI-1 tachyzoites was successful but did not elicit significant mucosal immunity in mice and allowed dissemination of T. gondii organisms to systemic organs. The immunosuppression of mice included reduced lymphoproliferative responses to splenocytes and MLN cells to mitogen and low production of cytokines, such as IFN-${\gamma}$, TNF-${\alpha}$, and IL-10, in response to T. gondii infection.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.3 no.2
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• pp.151-159
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• 2000

Purpose: Recently, a wide application of gastrofiberscopy in the pediatric group have revealed that nodular duodenitis is not an uncommon disease in children and is suspected to be associated with H. pylori infection. The aim of this retrospective study was to investigate the clinical and histopathologic features in children with nodular duodenitis, and to assess the correlations beween both. Methods: During a period of 5 years (Jan. 1995~Dec. 1999), we investigated clinical, endoscopic and histopathologic features of 39 consecutive patients diagnosed as having nodular duodenitis at Pediatric department of Seoul Red Cross Hospital. In 35 children with nodular duodenitis endoscopic biopsy specimens were stained with Hematoxylin & Eosin and Giemsa's stain, and were graded according to the criteria outlined by Triadafilopoulos, Whitehead et al., and Prieto et al.. Statistical analyses were performed with Graph PAD InStat. Results: The prevalence rate of nodular duodenitis was 17.1% and the most frequent chief complaint was abdominal pain (69.2%). Endoscopically grade 1 was the most common (45.7%) and nodular gastritis was coexistent in 28.3%. The most common histology of the duodenum was grade 2 (54.3%), and the most common histologic score of the stomach was 2 (42.9%). H. pylori was found in the duodenum in 37.1%, and in the stomach in 31.4%. The correlation coefficient between the endoscopic grade and the histologic grade of nodular duodenitis was 0.3983 (p=0.0178). And the correlation coefficient between the histologic grade and the grade of H. pylori colonization in the duodenum was 0.5154 (p=0.0018). Conclusion: There was significant correlation between the endoscopic grade and the histologic grade of nodular duodenitis, and was also significant correlation between the histologic grade and the grade of H. pylori colonization in the duodenum. Therfore H. pylori infection should be regarded as an etiologic factor of nodular duodenitis.