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We describe five patients who were initially thought to have Crohn's disease and were treated accordingly. The original diagnosis was based upon clinical presentation, roentgenograms, and histological examination, but subsequent follow-up showed that diagnosis to be in error. The following diagnoses were established instead: tuberculosis, Actinomyces Israeli infection, reaction to gold therapy, metastatic cancer, and linitis plastica. We stress the importance of considering conditions that can mimic Crohn's disease.
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In a landmark lecture on this disease, the author presents his experience with some 8,000 cases of regional enteritis and 4,000 of granulomatous colitis. The paper is divided into sections on the history, pathology, pathogenesis, roentgen findings, and course of the disease. The main thrust of the paper is the extensive roentgen analysis of granulomatous disease, with a discussion of differential diagnosis, especially from ulcerative colitis. Through the years, the author has been impressed with certain clinical and roentgen features of this malady (his Ten Principles of Crohn's Disease) which are carefully reviewed.
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The study was performed in 24 children aged 2 months to 6 years, without intestinal or immunological diseases. Intestinal biopsies were obtained by a Crosby's capsule, pediatric size. The number of immunoglobulin forming cells of lamina propria was measured by planimetry. Under 12 months of age there are increased levels of IgM forming cells and a low IgA forming cells/IgM forming cells quotient, but over 1 year the difference disappears. This suggests that the maturity process is very rapid. There are no correlation between serum IgA, IgM, and IgG levels and its respective forming cells number of lamina propria. It seems to support that the participation of intestinal lymphoid tissue in serum pool of immunoglobulin is very poor and that systemic and intestinal immunity maturation are completely independent.
Intestinal secretion rates of albumin, hyaluronan, and beta 2-microglobulin (beta 2-micro) were determined under basal conditions and after gliadin challenge of coeliac patients and healthy controls by the use of a jejunal perfusion technique. A new tube system was used where a jejunal segment is isolated between balloons and then perfused with a balanced salt solution. Under basal conditions the secretion rate of albumin was similar in the patients and controls while the secretion rate of the glycosaminoglycan hyaluronan, a high molecular weight connective tissue component, was increased more than two times in coeliac patients. Beta 2-micro was secreted in on average three-fold rates in coeliacs compared with controls. All three substances were secreted at a higher rate in patients with active disease than in those with inactive disease defined by morphological damage in small bowel biopsies. The concentrations in jejunal perfusion fluids relative to serum levels in the coeliac patients were for albumin 0.0007, beta 2-micro 0.10, and for hyaluronan 1.94. Challenge with a single dose of gliadin into the jejunal segment gave within 60 min a significant, about two-fold, increase of the secretion rates of all three measured substances. The appearance of hyaluronan could reflect a gliadin induced mucosal oedema with an enhanced leakage from the interstitial/lymph fluid, rich in this glycosaminoglycan. The observed parallel increases in the jejunal secretion of albumin and beta 2-micro after gliadin challenge are best explained by a similar mechanism.
The histology from rectal biopsy specimens taken 1980-1990 on 131 occasions from 116 horses, age 1-18 years, with clinical signs of intestinal disease was evaluated and classified retrospectively. In 40 horses, autopsy results were studied for comparison. Biopsy specimens (21 horses) and post mortem rectal tissue (9 horses) from 30 healthy horses, age 4-22 years, were used as controls. In 105 clinical cases, a biopsy was performed on only one occasion, while repeat biopsy was performed in 11 cases. Specimens showed pathological changes in 60 horses. The findings were classified into acute, chronic or chronic active simple proctitis, granulomatous enteritis, eosinophilic granulomatosis/gastroenteritis, eosinophilic proctitis, erosive/ulcerative proctitis, pseudomembranous proctitis, proctitis with vasculitis and malignant lymphoma. Mild scattered neutrophil infiltration in the lamina propria was found in controls, but neutrophils in crypt or surface epithelia were abnormal findings. Depletion or hyperplasia of goblet cells sometimes accompanied inflammation. Simple proctitis occurred in association with malignant lymphoma and various inflammatory disorders of the gastrointestinal tract apparent at autopsy. Eosinophilic granulomatosis/gastroenteritis and granulomatous enteritis were diagnosed from biopsy specimens in 6 of 12 and 4 of 9 cases, respectively, of these diseases confirmed at autopsy. Reduction of acid mucins in goblet cells was a prominent feature of eosinophilic granulomatosis. Rectal biopsy was found to be a useful adjunct for evaluation of intestinal disease in the horse.
Acute massive intestinal bleeding from Crohn disease occurred in 1.4% of 503 patients undergoing treatment at the New York Hospital-Cornell Medical Center over a 43-year period. Of the entire series, 31% had clinically evident rectal bleeding, while 13% had occult bleeding. Combined with previously reported series, onset of massive bleeding was not influenced by age of patient, duration of Crohn disease, use of corticosteroids, or activity of disease. Surgical therapy gave satisfactory results in patients with life-threatening hemorrhage.
Salmonella species cause a wide range of disease in multiple hosts. Salmonella enterica serovar Typhimurium causes self-limited intestinal disease in humans and systemic typhoid-like illness in susceptible mice. The prevailing dogma in murine S. enterica serovar Typhimurium pathogenesis is that distinct virulence mechanisms-Salmonella pathogenicity islands 1 and 2 (SPI1 and SPI2)-perform distinct roles in pathogenesis, the former being important for invasion and intestinal disease and the latter important for intracellular survival and systemic persistence and disease. Although evidence from bovine infections has suggested that SPI2 has a role in ileal disease, there is no evidence that SPI2 is important for inflammation in a disease that more closely recapitulates human colitis. Using S. enterica serovar Typhimurium strains that lack functional type III secretion systems, we demonstrate that SPI2 is essential for complete virulence in murine infectious enterocolitis. Using a recently characterized murine model (M. Barthel,S. Hapfelmeier, L. Quintanilla-Martinez, M. Kremer, M. Rohde, M. Hogardt, K. Pfeffer, H. Russmann, and W. D. Hardt, Infect. Immun. 71:2839-2858, 2003), we demonstrate that SPI1 mutants are unable to cause intestinal disease 48 h after infection and that SPI2-deficient bacteria also cause significantly attenuated typhlitis. We show that at the peak of inflammation in the cecum, SPI2 mutants induce diminished intercellular adhesion molecule 1 expression and neutrophil recruitment but that wild-type and mutant Salmonella are similarly distributed in the lumen of the infected organ. Finally, we demonstrate that attenuation of intestinal inflammation is accompanied by resolution of typhlitis in the mutant, but not wild-type, infections. Collectively, these results indicate that SPI2 is needed for enterocolitis, as well as for systemic disease.
Our objectives were to assess the prevalence of intestinal parasitic infections in Riyadh and to determine associated sociodemographic and environmental factors. The study was conducted through a household survey. Three health centres were chosen from each of the five Riyadh urban regions and 15 from rural areas. Based on the average family size, a random sample of households were chosen. All household members were asked to participate in the study. Data were collected using a pre-designed questionnaire eliciting data on sociodemographic and environmental factors. A stool specimen of each individual was examined microscopically for the presence of trophozoites and cysts. Six thousand and twelve participants with a mean age of 23.3 +/- 17.4 (median 19 years, 48.6% males) were studied and 32.2% were infected. The infection rate was high in urban areas (33.3%), among children < 12 years (34.4%), non-Saudis (42.2%), single persons (34.9%), illiterate individuals (33.8%), those who obtained drinking water from tankers (36.1%) and those who disposed of sewage in open channels (47.1%). Stratified analysis showed that for Saudis <12 years parasitic infections were significantly higher among tanker users (39.5%) and septic tank users (36.8%). For Saudis> or =12 years low education, water storage and open sewage disposal were statistically associated with parasitic infections (P < 0.05). Among expatriates, infections were high among males (47.6%), urban residents (48.3%), single persons (46.9%), tanker users (39.5%) and septic tank users (78.6%). Multivariate logistic regression analysis showed that age < 12 years, non-Saudi nationalities, educational level below secondary school, tanker as source of water and open sewage disposal were independently associated with high intestinal parasitic infection.
Although improved sanitation in the United States has resulted in a general diminution in the prevalence of intestinal parasitic infections, some, such as enterobiasis, are not reduced by improved environmental or water sanitation and others, such as amebiasis and hookworm infection, persist in foci. Other infections, notably giardiasis, have increased due to the travels of American tourists in other countries where environmental sanitation is poor. North American physicians, therefore, may expect at some time to have to treat parasitic infections. Favored chemotherapeutic agents currently are: for amebiasis--metronidazole and diiodohydroxyquin; for giardiasis--metronidazole; for tapeworm infections--niclosamide; for enterobiasis--pyrantel pamoate, piperazine citrate, or pyrvinium pamoate; for ascariasis--piperazine citrate; for stronglyoidiasis--thiabendazole; for trichuriasis--mebendazole; for hookworm infection--pyrantel pamoate; for schistosomiasis japonica--tartar emetic; and for schistosomiasis mansoni--niridazole.