Point-of-care sonographic detection of intestinal ascaris lumbricoides in the pediatric emergency department.

Point-of-care ultrasound use is rapidly growing in acute-care settings such as pediatric emergency departments, and new applications are continually being explored. This is especially true in the developing world where the World Health Organization estimates that 75% of people have no access to any imaging or availability of more costly imaging technology may be limited (Essential Health Technologies Strategy 2004-2007). We report a case of intestinal roundworm infection in a 3-year-old boy and describe the ultrasound findings of Ascaris lumbricoides.

Alterations of the myenteric plexus of the ileum and the descending colon caused by Toxoplasma gondii (genotype III).

Alterations caused by a genotype III strain of Toxoplasma gondii were assessed with respect to the number and the morphometry of the myenteric neurons in the terminal ileum and the descending colon. Eighteen rats were divided into four groups: Acute Control Group (ACG, n=4); Acute Experimental Group (AEG, n=4); Chronic Control Group (CCG, n=5) and Chronic Experimental Group (CEG, n=5). NaCl solution was administered through gavage to the animals in the ACG and CCG. Toxoplasma gondii tachyzoites (10(4)) from a genotype III strain were orally administered to the AEG and CEG. Acute Groups were died after 24 hours, and the Chronic Groups after 30 days. Neuronal loss was not observed in both organs. The neurons atrophied in the terminal ileum as the opposite occurred with the neurons at the descending colon during the chronic phase of infection. In the terminal ileum, the neurons atrophied during the chronic phase of the infection as no alteration was found during the acute phase. For the descending colon, the neurons became hypertrophic during the chronic infection in opposition to the atrophy found during the acute phase.

Alterations of the myenteric plexus of the ileum and the descending colon caused by Toxoplasma gondii (genotype III) / Alterações do plexo mientérico do íleo e cólon descendente causadas por Toxoplasma gondii (genótipo III)

Alterations caused by a genotype III strain of Toxoplasma gondii were assessed with respect to the number and the morphometry of the myenteric neurons in the terminal ileum and the descending colon. Eighteen rats were divided into four groups: Acute Control Group (ACG, n=4); Acute Experimental Group (AEG, n=4); Chronic Control Group (CCG, n=5) and Chronic Experimental Group (CEG, n=5). NaCl solution was administered through gavage to the animals in the ACG and CCG. Toxoplasma gondii tachyzoites (10(4)) from a genotype III strain were orally administered to the AEG and CEG. Acute Groups were died after 24 hours, and the Chronic Groups after 30 days. Neuronal loss was not observed in both organs. The neurons atrophied in the terminal ileum as the opposite occurred with the neurons at the descending colon during the chronic phase of infection. In the terminal ileum, the neurons atrophied during the chronic phase of the infection as no alteration was found during the acute phase. For the descending colon, the neurons became hypertrophic during the chronic infection in opposition to the atrophy found during the acute phase.

Objetivou-se avaliar as alterações causadas por uma cepa genótipo III de Toxoplasma gondii, sobre o número e a morfometria de neurônios mientéricos, do íleo terminal e do cólon descendente. Dividiu-se dezoitos ratos em quatro grupos: controle agudo (GCA, n=4), experimental agudo (GEA, n=4), controle crônico (GCC, n=5) e experimental crônico (GEC, n=5). Os animais do GCA e GCC receberam solução de NaCl por gavagem, e os animais do GEA e GEC 10(4) taquizoítos de uma cepa genótipo III de T. gondii por via oral. Os grupos agudos após 24 horas foram mortos e os crônicos após 30 dias. Observou-se que não houve perda neuronal em ambos os órgãos. No íleo terminal, os neurônios atrofiaram-se na fase crônica da infecção, enquanto nenhuma alteração ocorreu na fase aguda. Já no cólon descendente, os neurônios tornaram-se hipertróficos na fase crônica da infecção, em oposição à atrofia observada na fase aguda.