Chronic infections of the small intestine.

PURPOSE OF REVIEW: Chronic infections of the small intestine cause significant morbidity and mortality globally. This review focuses on the recent advances in the field of our understanding of selected intestinal infections. RECENT FINDINGS: Primary and secondary immunodeficiency increase the susceptibility to many chronic intestinal infections. Endoscopy and intestinal biopsies are central to establishing a diagnosis of these conditions. Tuberculosis (TB) remains a major global health challenge. Emerging therapeutic agents to counteract multidrug-resistant strains have shown clinical efficacy, but concerns regarding mortality remain. PCR-based diagnostic TB tests have the potential to reduce diagnostic delays, but remain to be validated for intestinal infections. Adjunctive diagnostic imaging modalities can differentiate infections from Crohn's disease with increasing accuracy. Whipple's disease remains rare, but there have been substantial advances in our understanding of the causative organism Tropheryma whipplei. Extended treatment with broad-spectrum antibiotics is effective in most cases. The narrow therapeutic window and limited armamentarium for treating invasive filamentous fungal infections contribute to their significant morbidity and high rates of mortality. SUMMARY: The speed and accuracy of diagnosing chronic intestinal infections have improved with recent imaging and laboratory methodologies. Significant research opportunities remain for clinicians and scientists to improve the diagnostic accuracy and clinical outcomes of chronic intestinal infections.

HLA and tropical sprue.

In 27 Puerto Rican patients with tropical sprue proven by intestinal biopsy and clinical response to folic acid, HLA type was determined with a microcytotoxicity assay. 25 of these patients had at least one antigen of the Aw-19 series (p = 10(-10)). The strongest association was with Aw-31, for which the relative risk was 10.6 (p = 1.2 X 10(-6)). The absence of a B-locus or haplotype effect suggests a marker association only, rather than an immune association.

Autoantibodies to duodenal gastric-inhibitory-peptide (GIP) cells and to secretin (S) cells in patients with coeliac disease, tropical sprue and maturity-onset diabetes.

The presence of autoantibodies detected by immunofluorescence to single endocrine cells, of human duodenum is described in three groups of patients and two control groups. Of 173 coeliac cases, four had GIP cell antibodies, one had secretin cell antibodies and twenty-one reacted with both cell types. Of twelve tropical sprue sera, four reacted with the same two cells. Among fifty elderly diabetics treated with hypoglycaemic drugs, seven sera gave a positive cytoplasmic IFL on duodenal substrate. Four were identified as GIP cells by use of the appropriate hormone antiserum and three reactions were against cells distinct from those stained by anti-GIP, -secretin, -somatostatin, -glucagon and -gastrin. Additional gut hormone antisera will have to be tested to identify these APUD cells. Thirty blood donors and seventy-three sera from autoimmune endocrine patients gave entirely negative results on unfixed cryostat sections of duodenal mucosa. Although impaired GIP and secretin responses have been reported in coeliac disease, and abnormal GIP values were found in Type II diabetes, there is as yet no data to correlate these metabolic dificiencies with the presence of endocrine cell antibodies in the serum. These studies are in progress.