Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:036187 (gut)
 73,132 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The spontaneous production of botulinum toxin in the infant gut by ingested Clostridium botulinum organisms is the underlying cause of infant botulism, recognised as an infectious disease only in late 1976. Because of the recognition of the pathophysiology of this disease and because the known potency and action of botulinum toxin can lead to rapid respiratory arrest, it appeared possible that the in-vivo production of botulinum toxin could cause the sudden death of some infants. To test this hypothesis, serum, selected tissues, and bowel contents from 280 dead infants were examined for the presence of C. botulinum toxin and/or organsisms. We found C. botulinum organisms in 10 infants, all of whom died suddenly and unexpectedly. 9 of these deaths were classified by the forensic pathologist as sudden infant death syndrome (S.I.D.S. or crib death). In 2 of these 10 sudden deaths both C. botulinum organisms and botulinum toxin were identified, and from the spleen of 1, C. botulinum organisms were isolated. Faecal specimens from 160 age-matched healthy infants who served as controls in studies of inpatient infant botulism cases were negative for both C. botulinum organisms and toxin, except for one specimen that contained only C. botulinum type A organisms. The 9 S.I.D.S. cases with evidence of C. botulinum infection comprised 4.3% of the 211 S.I.D.S. cases examined over 12 months. These findings suggest that intestinal production of botulinum toxin by C. botulinum is one cause of S.I.D.S. The strikingly similar age-distribution of 62 inpatient infant botulism cases and the 211 S.I.D.S. cases is also consistent with this concept. The possibility that in-vivo production of botulinum toxin may account for a larger proportion of S.I.D.S. cases is discussed.
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PMID:Intestinal infection and toxin production by Clostridium botulinum as one cause of sudden infant death syndrome. 7 45

Experimental infection of 2-day-old gnotobiotic lambs with lamb astrovirus produced mild diarrhoea after an incubation period of about 48 hours. No other clinical symptoms developed. Infection was studied by immunofluorescent and histological examination of tissues from the lambs. Astroviruses infected only mature villus epithelial cells and subepithelial macrophages in the small intestine, where they produced partial villus atrophy. Infected enterocytes were replaced with cuboidal cells from the crypts, and the lesion gradually healed by 5 days after infection. No serological relationship was detected by immunofluorescence between lamb astrovirus antigen in gut sections and antisera to either calf or human astrovirus.
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PMID:Pathogenesis of diarrhoea caused by astrovirus infections in lambs. 11 23

The pathogenicity of Entamoeba histolytica is discussed from an immunologic point of view. The evidence that there is some "trigger" mechanism which converts a commensal dwelling organism into a tissue invasive pathogen is rejected as inadequate. The number of liver abscess cases in comparison with the number of intestinal amebic infections in a population is so low that this in itself suggests that tissue invasion is a rare event in the life history of the ameba. A review is made of the experimental evidence that some type of sensitization is necessary before ameba can invade tissue. In postulating an immunologic basis for the pathogenicity of ameba, a parallel between the behavior of malignant cells in the body and an amebic infection in the gut is made. An appealing hypothesis which deserves further research effort is that an altered immune response is the basis for the pathogenic mechanism in the host.
Infection 1975
PMID:Pathogenicity of entamoeba histolytica. 17 Dec 23

Certain aspects of the development of Ehrlichia canis, causative agent of canine ehrlichiosis (tropical canine pancytopenia) in Rhipicephalus sanguineus ticks were studied. It was found that partial feeding of nymphs infected as larvae with E canis was a desirable, if not necessary, preliminary treatment for successful infection of dogs with ground-up ticks. It remains unclear whether feeding increased the number or altered the virulence of ehrlichiae within tick tissues. Ehrlichia canis organisms were detected by immunofluorescent microscopy in the midgut and hemocytes and by electron microscopy in the midgut and salivary glands of partially engorged adult ticks which had been infected as larvae and nymphs. Organisms were not observed in the ovary. Intracytoplasmic inclusions contained 1 to 80 elementary bodies, each provided with 2 distinct membranes. Infection of the midgut and salivary gland was confirmed by injecting homogenates of these tissues into susceptible dogs. Staining of gut smears of partially engorged adult ticks by fluorescein-conjugated anti-E canis antibody was found to be a reliable indicator of the infection.
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PMID:Development of Ehrlichia canis, causative agent of canine ehrlichiosis, in the tick Rhipicephalus sanguineus and its differentiation from a symbiotic Rickettsia. 94

Gnotobiotic lambs were protected against rotavirus infection by the presence in the gut at the time of infection of colostrum or serum containing antibodies to rotavirus. This protection was observed even when passively-acquired antibody was not present in the serum of the infected lamb. Infection under these conditions may have conferred immunity to subsequent challenge.
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PMID:Rotavirus infection in lambs: studies on passive protection. 99 20

Based on a long-term study of many years, a report is given on the behaviour of Coxiella burneti in the argasid tick, Ornithodoros moubata. Recent observations were made on ticks infected on mice and subsequently maintained separately. Particular emphasis was placed upon the localization of the ricksettsiae in certain organs of the ticks, its excretion -also with regard to routes of transmission - and transovarial passage. C. burneti invade primarily the gut epithelial cells of the tick and these cells remain infested with the causative agent throughout the entire life of the vector. After a certain infection period, other organs of the tick may become also infected. Thus, infection of the coxal organ, of salivary glands, rectal ampullae and ovaries has been confirmed through the presence of the rickettsiae in the coxal fluid, saliva and excreta or through transovarial passage of the agent with the saliva during feeding transmission to a new host takes place. Infection of the various organs of the tick and excretion or passage of the agent is not necessarily the rule, but may be even considered as an exception. This is especially the case for transovarial passage. On the other side, the multiplication of rickettsiae in the tick can be so intensive that the haemolymph and all internal organs become flooded with the organisms. These observations have been made in moribund and dead ticks. One of the most remarkable results was that the behaviour of C. burneti in its tick host varied considerably not only within the same series of experiments but more frequently in one and the same individual tick as well. Thus, e.g. excretion of the agent - with the saliva or coxal fluid - could be interrupted and resumed again later on. Evidently, these variations indicate a shift in the host-parasite interrelationship in which the multiplication of the rickettsiae is greatly enhanced by a decrease in the host's immune response, whereas an increase in its defence reaction will cause suppression of multiplication. It is not known, however, if the relevant impulse is primarily given by the tick or the rickettsial organism. The behaviour of C. burneti in O. moubata which does not follow a definite pattern coincides well with the high adaptability and variability characterizing this microorganism in other aspects as well.
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PMID:[Observations on the behaviour of coxiella burneti in the argasid tick ornithodoros moubata (author's transl)]. 117 9

An analysis was undertaken, for the first time, of the total picture of the medical disorders of adults on a small Caribbean island. At present non-infectious diseases, especially diabetes and hypertension, are of major improtance. Parasitic infestation of the gut occurred in 50-60% of the hospital population. The pattern of diseases indicates that the island is in a transitional stage of its medical development, and that resources need not be directed to the curative as well as to public health programmes. The impact of peculiarities of local geography and customs are discussed as contributing to some of the more unusual diseases of the Caribbean.
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PMID:Medical disorders in a small Caribbean island. An analysis of the disease of adults in Dominica in 1972 and 1973. 126 3

Ciprofloxacin (200 mg) was infused to seven patients at the beginning of elective colorectal surgery. Thirty minutes after the end of infusion (i.e. 60 min after the start of the operation) ciprofloxacin reached concentrations of 1.60 mg/l in serum and of 3.42-6.07 mg/kg fresh weight in the ileum and colon. During the next 30 min (90 min after the start of operation) the concentration of ciprofloxacin in serum decreased to 86% of its initial level, but this decrease was less rapid than that observed in the ileal (to 56.8%) or colonic (to 74.8%) mucosa. Three metabolites could be identified (desethylen-, sulpho-, oxociprofloxacin). Initially, at 60 min the amount of these metabolites was about 15% of the total drug concentration in serum, but only 2-3% of that in the gut tissues. At 90 min the relative amount of metabolites was increased in serum as well as in the gut tissues. It is concluded that transintestinal elimination of ciprofloxacin is a general feature of the whole gut. Obviously, the elimination process is not due to degradation of ciprofloxacin within the gut wall.
Infection
PMID:Transintestinal elimination of ciprofloxacin in humans--concomitant assessment of its metabolites in serum, ileum and colon. 129 50

Rotavirus is the major cause of severe, dehydrating infantile gastroenteritis. Infection is limited to the gut, but the relative roles of serum and secretory copro-immunoglobulin A (IgA) in protection are unclear. Specific copro-IgA is predictive of duodenal antirotaviral IgA and correlates with virus-neutralizing coproantibody. Copro-IgA conversion is a more sensitive marker of rotavirus reinfection than seroconversion. We measured rotavirus reinfections by copro-IgA conversion prospectively in 35 children recruited at a time of severe rotavirus illness. The children were followed up longitudinally for 14 to 31 months to determine whether high coproantibody levels correlated with clinical protection against rotavirus disease. Ninety-four percent of the children experienced reinfection, and 38% developed persistent elevations in specific copro-IgA termed plateaus. Plateau children had a higher mean annual rate of rotavirus infection and a lower ratio of symptomatic to total number of rotavirus reinfections than did nonplateau children. The annual rates of rotavirus infection and disease were significantly higher outside the plateau than inside it in children experiencing antirotavirus copro-IgA plateaus. Frequent rotavirus infection of children appears to stimulate production of a specific copro-IgA plateau which correlates with protection against an excess of infection and symptomatic disease.
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PMID:Role of coproantibody in clinical protection of children during reinfection with rotavirus. 132 Nov 67

Infection of rabbits with Escherichia coli RDEC-1 is a useful model for diarrheal disease caused by mucosally attaching E. coli. Understanding of the protective immunity induced by RDEC-1 infection in rabbits should provide information useful in the design of vaccines for protection against this infection and other mucosally attaching organisms as well. Thus, to define the time course and location of specific immunoglobulin A secretion in relation to bacterial colonization during primary RDEC-1 infection, we infected rabbits with RDEC-1, which express AF/R1 adherence pili, and compared sites of anti-AF/R1 antibody-containing cells in the intestinal mucosa with the sites of luminal colonization and mucosal attachment of RDEC-1. Also, anti-AF/R1 antibodies in intestinal fluids and bile were measured by enzyme-linked immunosorbent assay, and attachment sites of RDEC-1 to the intestinal epithelium were determined by immunohistochemical examination. Anti-AF/R1 pilus antibody-containing cells were most numerous in the proximal intestine (duodenum and jejunum). In contrast, both luminal colonization and attachment of RDEC-1 to epithelial cells were densest in the distal intestine (cecum and colon). Anti-AF/R1 antibodies were present in approximately equal amounts in fluids collected from all levels of the gut after week 1 postinfection. Anti-AF/R1 antibody levels in undiluted bile exceeded those in gut flushes by at least 2 orders of magnitude. Loss of RDEC-1 attachment to epithelial cells preceded resolution of diarrheal illness despite the presence of large numbers of organisms in the intestinal lumen. Our studies indicate that during RDEC-1 infection (i) sites of greatest mucosal anti-AF/R1 antibody secretion are proximal to sites of maximal RDEC-1 luminal colonization and attachment, (ii) bile is a major source of specific antibodies in the intestinal lumen, and (iii) interference with RDEC-1 attachment to epithelial cells may permit resolution of disease.
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PMID:Mucosal immune response to RDEC-1 infection: study of lamina propria antibody-producing cells and biliary antibody. 134 8


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