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F T Koster

Publications and source records attributed to F T Koster.

49 records · Page 3Linked to original sources
PubMed1981

Circulating immune complexes in bacillary and amebic dysentery.

In order to study the relationship between the presence of circulating immune complexes (CIC) and the severity and duration of acute dysentery, we studied 11 adults and 45 children in Bangladesh with bacillary and amebic dysentery, using the Raji cell and solid-phase C1q (C1q-SPA) assays. CIC were found in 70% of patients with shigellosis and in all eight cases of amebic dysentery. Mild shigellosis was associated with positive samples in the first week of clinical illness, whereas severe cases, including those with the hemolytic-uremic syndrome, had negative admission assays but positive convalescent assays. Samples positive in the first two weeks of illness were more likely positive by the Raji cell assay alone whereas samples in the third and fourth weeks of illness were positive more often by the C1q-SPA assay. Only one shigellosis sample was positive by both assays. In amebiasis 11 of 13 samples were positive by the Raji assay alone. In dysenteric disease circulating immune complexes probably represents the failure of the inflamed mucosa to exclude microbial and dietary antigens, and suggests that the presence of CIC in any intestinal disease must be interpreted with caution.

Anemia, Hemolytic↗
PubMed1980

Priming and suppression of the intestinal immune response to cholera toxoid/toxin by parenteral toxoid in rats.

Parenteral immunization of rats with cholera toxoid had both priming and suppressive effects upon the antitoxin response in jejunal lamina propria to locally applied toxoid/toxin. Priming was detected when parenteral toxoid was given i.p. but not i.v. or s.c., was enhanced by Freund's adjuvant, and appeared to reflect enhanced encounter of i.p. antigen with IgA-committed lymphocytes in extra-intestinal mucosa-associated lymphoid tissue. In contrast, suppression followed parenteral toxoid given i.p., i.v., or s.c.; suppression was antigen specific and lasted at least 16 weeks. Parenteral toxoid suppressed both primary and secondary types of mucosal antitoxin responses, ultimately preventing the generation of antitoxin-containing immunoblasts from Peyer's patches. Since suppression followed parenteral immunization by routes that did not provoke mucosal priming, it was, at least in those instances, not simply a regulatory consequence of mucosal priming. These results support the notion that priming and suppression of a specific mucosal immune response are independent effects of parenteral immunization that are probably determined by the distribution of antigen to mucosa-associated and systemic lymphoid tissue, respectively.

Animals↗
PubMed1979

Relationship between enterotoxin production and serotype in enterotoxigenic Escherichia coli.

We examined the relationship between serotype and enterotoxin production in 109 enterotoxigenic Escherichia coli strains isolated from 109 patients with severe cholera-like diarrhea in Dacca, Bangladesh. Of 69 strains producing both heat-labile and heat-stable toxins, 59 (86%) belonged to the one of four O serogroups, and 56 (81%) of these strains belonged to one of six O:K:H serotypes. In contrast, 34 strains producing only heat-stable toxin were distributed among 15 O serogroups, and six strains producing only heat-labile toxin were distributed among six O serogroups. Twelve strains producing heat-labile and heat-stable toxins and five strains producing heat-stable toxin were found which had the same serotype (O78:K-:H12) and biotype. It appears that at least in one geographic setting E. coli strains producing both heat-labile and heat-stable toxins are more restricted in their O groups and O:K:H serotypes than E. coli that produce only heat-stable toxin and that certain serobiotypes may commonly include strains which produce both toxin types.

Bacterial Toxins↗
PubMed1976

Nutritional status: a determinant of severity of diarrhea in patients with cholera.

The severity of diarrhea and nutritional status were measured in a prospective study of 97 patients hospitalized with cholera in Dacca, Bangladesh. Ninety-five percent of both adults and children were below their respective medians in weight as related to height; greater than 15% of each group showed second-degree protein-calorie malnutrition. Duration of diarrhea, but no volume of stool per hour, was prolonged by 30%-70% in those adults and children suffering from more severe malnutrition. The increased stool loss was unrelated to antibiotic usage, to presence of intestinal parasites, or to the refeeding diet given. It is suggested that the prolongation of diarrhea represents the continued effect of cholera toxin that is irreversibly bound to intestinal mucosal cells, the replacement of which would be retarded under conditions of poor nutrition.

Bangladesh↗
PubMed1971

The mediator of cellular immunity. 3. Lymphocyte traffic from the blood into the inflamed peritoneal cavity.

A substantial portion of the lymphocyte-like cells in induced peritoneal exudates derive from cells which enter the blood by way of the thoracic duct. The migrant cells have been identified as large and medium lymphocytes, but they may also include short-lived small lymphocytes derived from them. Small lymphocytes which have a potentially long circulating life-span are excluded from exudates, although cells of this type predominate in thoracic duct lymph. The results imply that many (perhaps all) of the small round cells in inflamed tissue are members of a line of rapidly proliferating lymphocytes. Specifically committed lymphocytes with precisely these properties are added to the blood of rats infected with Listeria monocytogenes. The localization of committed lymphocytes in inflammatory foci could be the crucial event which enables the host to focus his cellular defenses at sites of bacterial implantation.

Animals↗
PubMed1971

The mediator of cellular immunity. I. The life-span and circulation dynamics of the immunologically committed lymphocyte.

Thoracic duct cells from rats which have survived an infection with Listeria monocytogenes can confer a high level of antimicrobial resistance upon normal recipients. The cells which confer protection appear in the thoracic duct during the 1st wk of the immunizing infection, at a time when newly formed lymphocytes are being added to the lymph in substantially increased numbers. The protective cells differ in at least two respects from the majority of small lymphocytes in central lymph: they have a rapid turnover rate and a short life-span in the circulation. Evidence was also obtained that lymphopoiesis affecting the long-lived small lymphocyte, which belongs to the recirculating pool, is not increased during an acute Listeria infection.

Animals↗
PubMed1971

The mediator of cellular immunity. II. Migration of immunologically committed lymphocytes into inflammatory exudates.

Peritoneal exudates from rats which have survived an infection with L. monocytogenes can protect cyclophosphamide-treated recipients against a Listeria challenge. They are more effective in this respect than cells obtained from the spleen or thoracic duct lymph. Since exudate cells from normal rats and inocula prepared from the resident peritoneal cell populations of infected donors are unable to inhibit the challenge infection, the protective cells must belong to a class of lymphocytes that emerges from the blood in response to inflammation. It is significant therefore that thoracic duct lymphocytes formed during an acute Listeria infection can move into exudates induced by a variety of inflammatory stimuli. The affinity of newly formed lymphocytes for inflamed tissue points to a mechanism whereby the host marshalls its cellular defenses at sites of bacterial invasion. The tendency of short-lived lymphocytes to leave inflamed vessels might also explain their short-circulating life-span.

Animals↗
PubMedDate not supplied

Mortality among primary and secondary cases of measles in Bangladesh.

Data were reviewed from an intensive 1975-1976 survey in two Bangladeshi villages that experienced a high incidence of measles. Mortality among secondary cases (four of 50, 8.0%) was significantly higher than that among primary cases (six of 290, 2.1%). In every case in which there was a death in a household with more than one case, it was the youngest patient who died. All children with secondary cases who died had a pre-illness weight-for-height status above the population mean. Measles mortality in Bangladesh appears to be determined by three factors: age, superinfections, and having a secondary case. The last two factors may be due to increased intrafamilial exposure to both the measles virus and the superinfecting pathogens.

Age Factors↗