[Intestinal pseudo-obstruction disclosing digestive anguilluliasis in a non-immunosuppressed patient].
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Various hypotheses have been proposed for the pathogenesis of the neurological signs associated with bovine enteric coccidiosis. We undertook a prospective study of cases of bovine enteric coccidiosis with and without nervous signs to test the validity of these hypotheses and explore other possible pathophysiological mechanisms. Clinical, pathological and toxicological data from 12 calves with, and 15 calves without, neurological signs were compared. Calves with neurological signs had a lower liver Cu concentration (p less than 0.01) and a higher plasma glucose concentration (p less than 0.05) than did calves without neurological signs. Hyperglycemia and Cu deficiency may increase the susceptibility to central nervous system damage, but are not likely to account for the onset of neurological signs in calves with enteric coccidiosis. The results of the study suggest that the following are not involved in the pathogenesis of "nervous coccidiosis": disturbance of serum Na, K, Ca, P, or Mg concentration, vitamin A deficiency, thiamine deficiency, anemia, lead intoxication, uremia, Haemophilus somnus meningoencephalitis, severity of coccidial infection, gross alterations in intestinal bacterial flora and hepatopathy.
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Trichinella nativa and Trichinella pseudospiralis infections in a wild rodent host, the deer mouse (Peromyscus maniculatus), were characterized. Forty-six percent of 400 inoculated T. nativa were recovered on day 4 postinoculation (PI); 77% and 23% were found in the small and large intestines, respectively. Thirty-one percent of the worms recovered on day 4 remained in the large intestine beyond day 20 PI. Worms were embedded in the mucosa of the small intestine, cecum, and colon. Females recovered from the small and large intestines had statistically indistinguishable in vitro larval releases. Distension of the cecum and passage of loose stools were associated with the presence of worms in the large intestine. The ability of T. nativa to establish and thrive in the large intestine of deer mice was confirmed following intracecal implantation of first-stage larvae. On day 4 PI, 35% of 400 inoculated T. pseudospiralis were recovered, with 91% and 9% found in the small and large intestines, respectively. Although T. pseudospiralis established in the large intestine of deer mice, few worms remained beyond day 20. Females recovered from the small and large intestines had statistically indistinguishable in vitro larval releases. Although higher establishments of T. nativa (56% vs. 46%) and T. pseudospiralis (52% vs. 35%) were observed in CD-1 mice than in deer mice on day 4 PI, neither was able to colonize the large intestine of the former. The large intestine may be a more important habitat for adult trichinae than previously recognized.
Complete 18S ribosomal RNA gene sequences were determined for 8 Eimeria species of chickens and for Eimeria bovis of cattle. Sequences were aligned with each other and with sequences from 2 Sarcocystis spp., Toxoplasma gondii, Neospora caninum, and 4 Cryptosporidium spp. Aligned sequences were analyzed by maximum parsimony to infer evolutionary relationships among the avian Eimeria species. Eimecia bovis was found to be the sister taxon to the 8 Eimeria species infecting chickens. Within the avian Eimeria species, E. necatrix and E. tenella were sister taxa: this clade attached basally to the other chicken coccidia. The remaining Eimeria spp. formed 3 clades that correlated with similarities based on oocyst size and shape. Eimeria mitis and Eimeria mivati (small, near spherical oocysts) formed the next most basal clade followed by a clade comprising Eimeria praecox. Eimeria maxima, and Eimeria brumetti (large, oval oocysts), which was the sister group to Eimeria acervulina (small, oval oocysts). The 4 clades of avian Eimeria species were strongly supported in a bootstrap analysis. Basal rooting of E. necatrix and E. tenella between E. bovis and the remaining Eimeria species and the apparent absence of coccidia that infect the ceca of jungle fowl all suggest that E. necatrix and E. tenella may have arisen from a host switch, perhaps from the North American turkey, Meleagris gallopavo.
Infection of rats with the enteric, lumen-dwelling tapeworm Hymenolepis diminuta causes electric changes in host intestinal smooth muscle and decreased luminal transit. The mechanisms that stimulate host intestinal alterations during this nontissue invasive infection may include the tapeworm's biomass, its diurnal migratory behavior, a host immune-mediated response, or direct parasite stimulation of host motor activity. In vivo intestinal myoelectric activity was monitored to evaluate the following: (1) that reinfection with H. diminuta is influenced by host immune regulation and (2) that administration of tapeworm fractions to never-before-infected rats initiates an alteration of enteric smooth muscle activity. To address the first hypothesis, we determined that altered intestinal myoelectric activity patterns were no different and did not occur earlier in a second infection with H. diminuta than in a primary infection. The lack of either a change in myoelectric pattern or an earlier onset of intestinal myoelectric changes indicates that tapeworm-induced myoelectric activity is not anamnestically stimulated by host immunomodulatory mechanisms. Consistent with the second hypothesis, administration of either H. diminuta carcass homogenate or tegument-enriched fractions directly into the intestinal lumen of tapeworm-naive rats initiated myoelectric patterns previously characteristic of chronic H. diminuta infection. Additionally, the appearance of characteristic nonmigrating myoelectric patterns in uninfected rats administered tapeworm fractions indicates that a substance from H. diminuta acts as the triggering signal molecule for intestinal myoelectric alterations. These findings also indicate that neither the tapeworm's biomass nor its diurnal movement is required for initiation of H. diminuta-altered myoelectric patterns. We have shown that H. diminuta possess a signal molecule(s) that alters host enteric electric activity, and we suggest that these alterations may play an important role in the symbiotic rat-tapeworm interrelationship.
Cells containing somatostatin immunoreactivity were localized in the alimentary tract of parasite-free sheep by indirect immunocytochemistry, using an antiserum raised to ovine somatostatin. Nerve fibres showing somatostatin-like immunoreactivity were identified in the oesophagus, reticulum wall and groove, rumen pillar and wall, omasum sulcus and abomasum. Varicose fibres were found in the myenteric plexuses of the duodenum, jejunum, ileum and colon. The greatest distribution of endocrine cells (99 cells mm-2) was found in the antrum of the abomasum with 47, 29, 12 and 6 cells mm-2 respectively in the fundus, the first part of the duodenum, mid-jejunum and ileum. Some of the parasite-free sheep which had never experienced infection with larvae of the abomasal nematode, Haemonchus contortus, were paired with similar sheep in an experiment to investigate the effect of parasitism on nitrogen metabolism in the small intestine. The protocol of this experiment required observations before and after parasite infection, with final observations 2 weeks after removal of the infection by treatment with an anthelmintic drug. The sheep were then killed and tissues taken from each paired animal. Tissues from the recently parasitized sheep showed increases of D cells in the fundus and antrum of the abomasum. At present it is not clear if these increases were related to parasitism, per se, or were the post-treatment indicators of healing and recovery from infection with parasite larvae.
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An epizootic disease characterized by failure to gain weight, lethargy, enteropathy, and death developed in weanlings from a production colony of NIH/Nmri CV mice. Light microscopic and scanning electron microscopic examination of the intestine revealed large numbers of protozoan parasites identified as Spironucleus (Hexamita) muris. The extensive, entangled mass of organisms in the intestinal lumen enveloped the villi and continued deep within the crypts of Lieberkühn. Inflammation and significant intestinal lesions were not observed. The scanning electron microscopic appearance of the small intestine in spironucleosis gives credence to a pathogenesis of malabsorption with subsequent, severe malnutrition and death in weanling mice.
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The large intestine of a rat has been neglected almost completely as a site of Strongyloides sp. infection. We reported that adult Strongyloides ratti remained in the large intestine for more than 80 days, producing more number of infective larvae than small intestine adults, and therefore hypothesized that parasitism in this site could be a survival strategy. In wild rats, however, no study has focused on large intestine infections of Strongyloides. The present study revealed that 32.4% of 68 wild rats, Rattus norvegicus, had the infection of S. ratti in the large intestine, with an average of 4.7 worms. These worms harbored normal eggs in the uterus. In a laboratory experiment with S. ratti and Wister rats, daily output of infective larvae by 4.7 females in the large intestine was estimated to be 4,638.4, suggesting that a few parasites could play a role in the parasite transmission. Five species of nematode found in the wild rats showed seasonality in infection intensity, with highest intensities in March-May. The number of S. ratti in the large intestine was also highest in these months.