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PubMed2004

Prevalence of serum IgE antibodies to the Staphylococcus aureus enterotoxins (SAE, SEB, SEC, SED, TSST-1) in patients with persistent allergic rhinitis.

BACKGROUND: Enterotoxins produced by Staphylococcus aureus and their specific IgE antibodies were thought to be important in worsening atopic dermatitis. However, few studies have documented an association between S. aureus or its exotoxins and exacerbations of upper airway/nasal disease. In the current study, we determined the prevalence of serum-specific IgE towards staphylococcal enterotoxin A, B, C, D (SEA, SEB, SEC, SED) and toxic shock syndrome toxin 1 (TSST-1) in patients suffering from rhinitis and/or asthma due to allergy. Therefore, we examined whether SEA, SEB, SEC, SED and TSST-1 were important in worsening the clinical status of patients allergic to house dust mites by means of assessing serum eosinophil cationic protein (ECP), which is thought to be a reliable marker of asthma and rhinitis severity. METHODS: 198 patients with persistent allergic rhinitis and/or asthma due to house dust mites were evaluated. Specific IgE towards SEA, SEB, SEC, SED, TSST-1, timothy grass and birch pollen recombinant allergens, and other aeroallergen extracts from common allergen sources were evaluated by the Pharmacia CAP System. Serum ECP was assessed, too. RESULTS: The percentages of sensitization to staphylococcal enterotoxins of 198 house dust mite-allergic patients were as follows: TSST-1-specific IgE 24.7% (n=49), SEC-specific IgE 22.2% (n=44), SEB-specific IgE 15.1% (n=30), SEA-specific IgE 9.1% (n=18), and SED-specific IgE 5.5% (n=11). Out of 198 individuals allergic to house dust mites 136 patients suffering from persistent rhinitis were subdivided into two subgroups: 53 patients with serum-specific IgE to at least one staphylococcal enterotoxin and 83 patients without specific IgE towards staphylococcal enterotoxins. Patients sensitive to staphylococcal enterotoxins had higher serum ECP levels than patients lacking specific IgE to SEA, SEB, SEC, SED and TSST-1(geometric mean 24.3 vs. 16.6 microg/100 ml; p=0.029), as well as total IgE levels (geometric mean 564 vs. 161 kU/l, p=0.00063) and specific IgE to Dermatophagoides pteronyssinus (geometric mean 16.7 vs. 6.6 kU/l; p=0.0235) and Dermatophagoides farinae (geometric mean 18.6 vs. 7.8 kU/l; p=0.0246). CONCLUSION: A status of sensitization to staphylococcal enterotoxins seems to be a factor increasing serum ECP, which is thought to be a reliable marker of clinical severity of allergic disease. Therefore, the evaluation of SEA, SEB, SEC, SED and TSST-1-specific IgE antibodies may have additional significance for the prognosis of persistent allergic diseases of the upper airway.

Adolescent↗

PubMed1974

Effects of prostaglandins and cholera enterotoxin on intestinal mucosal cyclic AMP accumulation. Evidence against an essential role for prostaglandins in the action of toxin.

Both cholera enterotoxin and certain prostaglandins have been shown to stimulate intestinal fluid secretion in vivo, to cause ion flux changes in vitro similar to those caused by addition of cyclic 3',5'-adenosine monophosphate (cyclic AMP), and to activate intestinal mucosal adenyl cyclase. It has been suggested that the effects of the enterotoxin on intestinal cyclic AMP metabolism may be indirect, and that locally synthesized prostaglandins may serve as required intermediates for the effects of the enterotoxin in activating intestinal mucosal adenyl cyclase. In order to clarify certain aspects of the mechanisms by which these two agents alter intestinal mucosal cyclic AMP metabolism and ion transport, their effects on cyclic AMP accumulation in rabbit ileal mucosa were examined in vitro. Addition of 5 mug per ml (75 mug per 150 mg mucosa) of purified cholera enterotoxin produced a peak increase in cyclic AMP level in 3 h but there was a time delay of at least 30 min before any effect was observed. Inhibition of cyclic nucleotide phosphodiesterase with theophylline failed to reduce this time delay. In contrast, addition of prostaglandin E(1) (PGE(1)) increased the cyclic AMP level rapidly, a peak effect being observed in 2 min. The time of the peak prostaglandin-induced changes in cyclic AMP level and short-circuit current correlated closely. A maximal increment in cyclic AMP level was achieved with 5 x 10(-5) M PGE(1). When 10(-4) M PGE(1) was added to mucosa already maximally stimulated with cholera toxin, the resulting cyclic AMP level was equal to the sum of the levels reached when each agent was added alone. Furthermore, the effects of the enterotoxin on mucosal cyclic AMP levels were not influenced by indomethacin under conditions where mucosal prostaglandins synthesis was inhibited. The results suggest that endogenous prostaglandins do not provide an essential link in the activation of intestinal mucosal adenyl cyclase by cholera enterotoxin. The present study also indicates that the effect of cholera enterotoxin on intestinal mucosal cyclic AMP metabolism involves a definite time delay which is not due to cyclic nucleotide phosphodiesterase activity.

Adenylyl Cyclases↗

PubMed1991

Enterotoxin-producing bacteria isolated from Swedish travellers with diarrhoea.

The isolation rate of bacterial enteropathogens of different species, particularly enterotoxin-producing Gram-negative bacteria, was determined in stool specimens from Swedish travellers with diarrhoea. Overall, bacterial enteropathogens were identified in 101 (47%) of the 217 travellers on their return home. The most common isolates were enterotoxin-producing bacteria (20%), Salmonellae (18%) and Campylobacter (8%), whereas Shigellae (3%) and Yersinia (0.5%) were rarely identified. Mixed infections were only found in 8 (4%) of the stool specimens. Enterotoxigenic bacteria of Escherichia coli (ETEC), Klebsiella, Morganella, Citrobacter, Pseudomonas and EF-group 10 species were identified. ETEC accounted for 37/43 (86%) enterotoxin-producing strains, and among them 54% produced heat-stable enterotoxin (ST) alone, 16% heat-labile enterotoxin (LT) alone and 30% both LT and ST. Four of the enterotoxin-producing non-E. coli strains produced ST and 2 produced LT alone. The isolation rate of enterotoxin-producing bacteria was somewhat higher in travellers visiting Africa, Asia and Latin America (24%) than in those travelling to Southern Europe (14%). Salmonellae, on the other hand, were identified in stools significantly more often after travel to Southern Europe (26%) than to various subtropical and tropical areas (12.5%).

Adult↗

PubMed2005

Prevalence of enterotoxigenic Bacillus cereus and its enterotoxins in milk and milk products in and around Nairobi.

OBJECTIVES: To determine the prevalence of enterotoxigenic Bacillus cereus (B. cereus) and enterotoxins in milk and milk products. DESIGN: A random sampling of milk products was carried out. SETTING: Market milk and milk products were collected from retail shops in Nairobi and analysed for contamination with enterotoxigenic B. cereus and its enterotoxins using reverse passive latex agglutination and TECRA ELISA immunoassay tests. SUBJECTS: Ninety six milk samples including 36 raw milk, 42 pasteurised milk, 10 yogurt and eight fermented milk samples. Forty seven Bacillus cereus isolated from milk and milk products. MAIN OUTCOME MEASURES: Isolation of enterotoxigenic B. cereus from milk and milk products and detection of B. cereus hemolytic (hemolysin BL) and non-hemolytic enterotoxins in milk. RESULTS: Fifty seven percent of the samples were contaminated with B. cereus. Eighty one percent (38 out of 47) of the isolates produced non-hemolytic enterotoxins, while 25 (53.2%) of the isolates produced hemolysin BL. Eighteen (38.3%) of the isolates produced both hemolysin BL and non-hemolytic enterotoxins. About fourteen percent (14.3%) of the pasteurised milk samples tested positive for non-hemolytic enterotoxin. CONCLUSION: Enterotoxigenic B. cereus and enterotoxins occur in market milk and their presence poses a potential risk of causing food poisoning. The risk can be reduced if milk products undergo thorough quality control checks and are always kept at below 4 degrees C till consumption. Post pastuerisation contamination which is commonly blamed for spoilage of milk products by B. cereus is not necessarily the most important source of this organism.

Animals↗

PubMed1982

Experimental production of staphylococcal enterotoxins A, B, and C on rice flour gel medium.

Production of staphylococcal enterotoxins A, B, and C was studied on the rice flour gel plate consisting of rice flour and distilled water devised by the authors simulating cooked rice that has commonly been incriminated for staphylococcal food poisoning in Japan. Enterotoxin produced on the rice flour gel plate was determined quantitatively by reversed passive hemagglutination. The rice flour plate supported production of fairly large quantities of enterotoxins A, B, and C. The rice flour concentration of the plate and the quantity of the surface water largely affected the enterotoxin production. The largest amount of enterotoxin, 0.2-0.4 mg/25-ml plate, was produced in 3 days at 37 C on 16% rice flour gel plates overlaid with 4 to 8 ml of saline. It appeared that the production of enterotoxin A was more rapid than that of enterotoxin B or C.

Culture Media↗

PubMed1999

Identification of serotype by use of serologic assay and detection of the enterotoxin gene of Escherichia coli by means of a polymerase chain reaction assay for isolates from pigs, chickens, and cows.

OBJECTIVE: To serotype an enterotoxin gene from Escherichia coli isolated from cows, pigs, and chickens in Korea. SAMPLE POPULATION: Isolates from 37 cows with mastitis, 51 diarrheic pigs, and 5 diarrheic chickens. PROCEDURE: Serogroups and serotypes were identified by slide agglutination testing, using pathogenic E coli sera. Detection of E coli enterotoxins by use of reversed passive latex agglutination and ELISA was compared by proving existence of the gene by polymerase chain reaction (PCR) analysis. RESULTS AND CONCLUSIONS: Detection of E. coli enterotoxin by either method was positive for 1 strain (O20:H10; heat-labile enterotoxin [LT+], heat-stable enterotoxin [STa+]; isolation rate, 2%) and 3 other strains (O111:H10, O119:H9, and O125:H6, STa+; isolation rate, 5.9%) isolated from fecal specimens obtained from diarrheic pigs. The E coli enterotoxin genes were identified by use of PCR analysis in 1 strain containing the 417- and 163-base pair (bp) genes (LT+, Sta+; O20:H10) and in 3 strains containing only the 163-bp gene (STa+; O111:H10, O119:H9, and O125:H6). CLINICAL RELEVANCE: Serotyping of E coli enterotoxin may be used to analyze patterns of transmission among species of domestic animals.

Animals↗

PubMed1999

Prevalence of Clostridium perfringens enterotoxin and Clostridium difficile toxin A in feces of horses with diarrhea and colic.

OBJECTIVE: To determine prevalence of clostridial enterotoxins in feces of horses with diarrhea and colic, and to determine whether an association exists between detection of clostridial enterotoxins in feces and development of diarrhea as a complication of colic. DESIGN: Prospective case series and case-control study. ANIMALS: 174 horses with diarrhea, colic, or problems not related to the gastrointestinal tract. PROCEDURE: Horses were assigned to 1 of 4 groups: colic with diarrhea (group 1; n = 30); colic without diarrhea (group 2; 30); diarrhea without colic (group 3; 57); and control (group 4; 57). Feces were evaluated by use of ELISA to detect Clostridium perfringens enterotoxin (CPE) and C difficile toxin A (TOXA). Frequency of detection of CPE or TOXA in groups 1 and 3 was compared with that in groups 2 and 4, respectively. RESULTS: Prevalence of enteric clostridiosis in horses in group 3 was 25%. Clostridium perfringens enterotoxin was detected in 9 of 57 (16%), TOXA in 8 of 57 (14%), and both toxins in 3 of 57 (5%) fecal samples collected from these horses. Neither toxin was detected in feces of the age-matched horses in group 4. Clostridial enterotoxins were detected in feces of 7 of 60 (12%) horses with colic (groups 1 and 2), however, a significant association was not found between detection of enterotoxins in feces and development of diarrhea as a complication of colic. CONCLUSIONS AND CLINICAL RELEVANCE: Clostridia are important etiologic agents of diarrhea in horses. Additionally, changes in intestinal flora of horses with colic may allow for proliferation of clostridia and elaboration of enterotoxins regardless of whether diarrhea develops.

Animals↗

PubMedDate not supplied

Enzyme immunoassay of staphylococcal enterotoxins in dairy products with cleanup and concentration by immunoaffinity column.

Two different immunoaffinity columns (IACs) were prepared for detection of staphylococcal enterotoxins (SETs) from dairy products. First, a specific IAC for staphylococcal enterotoxin A (SEA), IAC-1, was prepared by coupling monoclonal antibody (mAb) directed against SEA; second, a polyspecific IAC for SEA, staphylococcal enterotoxin B (SEB), staphylococcal enterotoxin C (SECs), and staphylococcal enterotoxin D (SED), IAC-2, was prepared by coupling a mixture of mAbs against SEA, SECs, and SED, and rabbit IgG against SEB. These columns were applied for detection of SETs in dairy products, after extraction, immunoaffinity chromatography, and enzyme immunosorbent assay (EIA). Overall recoveries from dairy products spiked with 1 ng SEA/25 g averaged 81.2% (range, 76-85%) on IAC-1. The repeated use of IAC-1 was then determined with good efficiency of 91.5%, in more than 10 runs. On the other hand, a recovery yield of 77% of SETs (SEA, SEB, SEC, and SED) from dairy products spiked with 2.5 ng of each enterotoxin per 25 g, was obtained with IAC-2. IAC-2 was also successfully subjected to the chromatography of naturally contaminated foods implicated in staphylococcal food poisoning outbreaks. This new extraction-concentration-immunoaffinity-chromatography method (ECIC) is very useful for improving staphylococcal enterotoxin detection and eliminating matrix effect in EIA of dairy products.

Antibodies↗

PubMed1991

Enterotoxins, colonization factors and serotypes of enterotoxigenic Escherichia coli from humans and animals.

Enterotoxigenic Escherichia coli (ETEC) strains may synthesize both thermolabile (LT-I and LT-II) and thermostable (STa and STb) enterotoxins. Whereas thermolabile enterotoxins are high molecular weight proteins (85,000 d-90,000 d) composed by a single enzymatic A subunit combined with five B subunits which enable toxin for the receptor recognition, thermostable enterotoxins are small peptide chains with molecular weight between 1,900 d and 5,000 d. In addition to the synthesis of enterotoxins, the ability of ETEC strains to cause diarrhoea is also conditioned by the possession of colonization factors which enable bacteria adhere-to and colonize the luminal surface of small bowel. Colonization factors in ETEC strains were located in rigid fimbriae and flexible fibrils constituted by protein subunits ranging in size from 14,500 d to 31,000 d and usually responsible for mannose-resistant haemagglutination with determined erythrocyte species. Both enterotoxins and colonization factors are controlled by plasmids. There exist plasmids which may code separately enterotoxins and colonization factors, and besides there also exist recombinant plasmids coding together these two virulence factors. Human ETEC strains may synthesize LT-I and/or STa enterotoxins, they may possess the colonization factors named CFA/I, CFA/II, CFA/III or CFA/IV, and they belong mainly to serogroups O6, O8, O15, O20, O25, O27, O63, O77, O78, O114, O115, O126, O128, O139, O148, O153, O159 and O167. ETEC strains from porcine origin synthesize LT-I, STa and/or STb, they possess the colonization factors K88, P987, K99 or F41, and they usually belong to serogroups O8, O9, O20, O45, O64, O101, O115, O138, O141, O147, O149 and O157. Bovine and ovine ETEC strains are usually STa producers harbouring on the bacterial surface K99 or F41 colonization factors and they belong to serogroups O8, O9 and O101. Nevertheless, some particular bovine ETEC strains synthesizing LT-II have been described. Thus, a high specificity level between ETEC strains causing diarrhoea in humans and domestic animals can be observed. This is mainly due to the specific recognition between bacterial colonization factors and the epithelial receptors during host-parasite interaction.

Adhesins, Escherichia coli↗

PubMed1989

Calcium calmodulin in altered NaCl transport by heat-labile enterotoxin of Escherichia coli.

The mucosal-to-serosal and serosal-to-mucosal fluxes of Na+ and Cl- were carried out in control and experimental groups treated with different doses of heat-labile enterotoxin in the presence or absence of Ca2+-ionophore, Ca2+ channel blocker and calmodulin inhibitor. There was net secretion of Na+ and Cl- in 16 and 32 units of heat-labile enterotoxin treated groups in comparison to net absorption in control group, however, in animals treated with 8 units of heat-labile enterotoxin, no change in Na+ and Cl- fluxes was found when compared to control. Ca2+- ionophore increased net secretion of Na+ and Cl- in 16 and 32 units of heat-labile enterotoxin treated groups and also caused secretion in control group instead of net absorption. Ca2+ channel blocker and calmodulin inhibitor partially reversed the effect of heat-labile enterotoxin. The effect of Ca2+-ionophore was more pronounced in the control group while that of Ca2+ channel blocker and calmodulin inhibitor was more pronounced in 16 and 32 units of heat-labile enterotoxin treated groups. The findings suggest the involvement of Ca2+ and calmodulin in the action of heat-labile enterotoxin of Escherichia coli in mice.

Animals↗

PubMed1986

[Enterotoxin-like factor(s) produced by Vibrio parahaemolyticus].

Culture filtrates obtained from several isolates of Vibrio parahaemolyticus were tested for their enterotoxin-like activities. Also their antigenic relationship with cholera enterotoxin and Kanagawa hemolysin were tested. In the Chinese Hamster Ovary (CHO) cells assay which are usually employed for detecting cholera toxin or heat labile enterotoxin produced by enterotoxigenic Escherichia coli, crude culture filtrates obtained from both Kanagawa positive and negative strains isolated from patients showed positive reaction whereas most of the Kanagawa negative strains isolated from environmental sources did not. After concentration, however, both the culture filtrates of Kanagawa positive and negative strains of Vibrio parahaemolyticus showed positive reactions in CHO cell assay and rabbit skin permeability assay but not in rabbit ileal loop test. Antisera against concentrated culture filtrates obtained from both Kanagawa positive and negative strains neutralized neutralized the activities of concentrated culture filtrates in CHO cell assay and Rabbit permeability assay but not of cholera toxin and Kanagawa hemolysin. Immunodiffusion test was also carried out using the antisera and the concentrated culture filtrates obtained from both of Kanagawa positive and negative strains of Vibrio parahaemolyticus. The antisera cross-reacted with all concentrated culture filtrates obtained from both Kanagawa positive and negative strains but not reacted with cholera toxin and Kanagawa hemolysin. These results indicated that both of Kanagawa positive and negative strains of Vibrio parahaemolyticus can produce the enterotoxin-like factor(s) such as cholera enterotoxin or heat labile enterotoxin produced by enterotoxigenic Escherichia coli, but this factor(s) dose not show cross-antigenicity with cholera enterotoxin and the Kanagawa hemolysin produced by Kanagawa positive Vibrio parahaemolyticus.

Bacterial Proteins↗

PubMed1986

Comparative prevalence of four enterotoxin genes among Escherichia coli isolated from swine.

Presence of Escherichia coli enterotoxin genes LT (heat-labile enterotoxin), STaP (heat-stable enterotoxin a, porcine genotype), STaH (heat-stable enterotoxin a, human genotype), and STb (heat-stable enterotoxin b) among 874 swine isolates of E coli was determined, using DNA probes and the DNA colony hybridization technique. Of the 874 isolates evaluated, 45% hybridized with at least one of the enterotoxin gene probes and were designated as enterotoxigenic E coli (ETEC). Eighty-five percent of the ETEC were from pigs with enteric colibacillosis. The remaining 15% were from pigs with edema disease or various other diseases, and from healthy swine. Seventy-four percent of the ETEC hybridized with the STb probe, 52% with STaP, and 31% with LT; ETEC did not hybridize with the STaH probe. Most of the ETEC hybridized with more than one enterotoxin gene probe. Isolates that hybridized with the LT probe also hybridized with STb. The most prevalent gene combination was LT-STb. However, 35% of the ETEC from neonatal (less than or equal to 1 week old) swine with enteric colibacillosis were of the STaP-only genotype, and 33% of the ETEC from older swine with enteric colibacillosis were of the STb-only genotype.

Animals↗

PubMed1985

[Production of enterotoxins A, B and C in staphylococcal strains isolated from animal food products and other sources].

Studies were carried out on the production of enterotoxins A, B, and C by a total of 654 strains of Staphylococcus aureus. Of these, 326 were isolated from food products of animal origin (and had no connection with intoxications); 190 were isolated from personnel working in the food industry; and 138 were isolated from milk animals, containers, and equipment at productional enterprises. Thirty strains of S. epidermidis, isolated from food products and workers were likewise tested for the production of the same enterotoxins. The enterotoxins were obtained by the modified method of Hallander, and their demonstration was performed by a variant technique of the double gel diffusion test after Ouchterlony. It was found that the Staphylococcus aureus strains isolated from food products produced enterotoxins in 12.3 per cent of the cases; was found in 6.1% of the strains, C--in 3.1%, and B--in 2.5%. Types A and C were found simultaneously in 0.6% of the strains. Enterotoxins were found in 16.6% of the strains isolated from workers and in 1.7% of those isolated from the udder of cows. The incidence of toxin production and the relative share of the three types of enterotoxins depended on the origin of staphylococci and their capacity to produce them in amounts that could be demonstrated by the methods employed. Under optimal conditions the amounts varied: for strains that produced type A they ranged from 1 to 20 micrograms/cm3; for those that produced type B they were from 1 up to 100 micrograms/cm3; and for those that produced type C they were from 1 to 40 micrograms/cm3. No production of enterotoxins A, B, and C was established with S. epidermidis strains.

Animals↗

PubMed1985

[Determination of staphylococcal enterotoxins A, B and C in foods using ELISA with labeled antigen].

The competitive ELISA (polystyrene balls) with labeled antigen according to Stiffler-Rosenberg and Fey (1978) was applied to the analysis of Staphylococcal enterotoxins (SE) A, B and C in food to see if the enterotoxin concentration corresponding to maximum limit for SEA and SEB (1 ng/g food and 10 ng/g food respectively) could be measured. The effect of various food ingredients on the quantitative determination of SE in single-step and two-step variants of competitive ELISA was investigated. Generally, the effect of food was the lowest in extracts of cheeses and the highest in extracts of meats and pasta products. All enterotoxins were equally affected. However, within the same type of food significant differences in binding of both labeled and unlabeled antigen were found. The effect of food components often depended on the assay variant; the extracts of cheese gave better results in the two-step and the extracts of pasta better results in the single-step ELISA. In some weak-positive extracts, false positive results could not be excluded. In the samples of cheese which were involved in food poisoning exclusively the enterotoxin type A was found (up to 30 ng/g). The recovery of added SE (1-10 ng/g food) ranged from 50-70% in cheese and was about 70% in pasta foods. The assay sensitivity in buffer ranged from 0.2 ng/ml for enterotoxins A and B and 0.3 ng/ml for enterotoxin C (20 ml sample) to 0.5 ng/ml for A and B and 0.6 ng/ml for C (5 ml sample) to 1 ng/ml for A and B and 2 ng/ml for C (1 ml sample). In food, especially in meat and pasta the detection limit was often higher. With some exceptions the required sensitivity for enterotoxin A (1 ng/g) could only be reached in cheese.

Cheese↗

PubMed1985

[Determination of staphylococcal enterotoxins A, B, C and D in foods using sandwich ELISA with labeled antibody].

The noncompetitive Sandwich-ELISA (polystyrene balls) with labelled antibody for staphylococcal enterotoxins (SE) A, B, C, and D according to Fey et al. (1984), which have recently been introduced commercially, was applied to analysis of foods. The effect of various food ingredients on the quantitative determination and recovery of SE was investigated. The unspecific effect of food components which, in some cases, caused false-positive results in the competitive ELISA was less frequent. Nevertheless, the differences in binding of unlabeled antigen between buffer and food were still observed. Using ELISA microtiter plates the effect of food components was less pronounced. Enterotoxin type A or a mixture of A and D were dominant in foods which were involved in food poisoning (about 150 samples). In meat the recovery of SE added (1-10 ng/g) ranged from 30-60%. The assay sensitivity in buffer ranged from 0.1 ng/ml for enterotoxins A, B, C and D (5 ml sample) to 0.2 ng/ml for enterotoxins A-D (1 ml sample) using polystyrene balls and was 1 ng/ml for enterotoxins A-D using ELISA plates. In foods the detection limit was occasionally higher. The required sensitivity for enterotoxin A (maximum limit 1 ng/g) could mostly be reached. Because of the differences in antigen binding in buffer and in various food extracts the determination of the enterotoxin content in this range is laborious.

Cheese↗

PubMed1972

The significance of proliferation and enterotoxin production by Escherichia coli in the intestine of gnotobiotic pigs.

The significance of enterotoxin production and proliferative ability of Escherichia coli in the intestinal tract as related to porcine enteric colibacillosis was studied in 68 gnotobiotic pigs. The animals were monocontaminated at seven to ten days of age with eight selected strains of E. coli. The strains were two naturally occurring porcine enteropathogens - P155 (0149:K91;K88a,c:H10) and P307 (08:K87;K88a,b:H19), two nonenteropathogenic strains - P104 (0139:K82:H1) and F11 (018-ab:K?:H14), and four enterotoxigenic derivatives of the above strains - P104(P155), P104(P307), F11(P155) and F11(P307). The response of the animals was evaluated on the basis of clinical observations and necropsy lesions 22 hours after exposure to the organisms. E.coli counts were determined at seven different levels of the intestinal tract. Cell free extracts of the intestinal contents were examined for enterotoxic activity by the ligated pig intestine loop test. All of the strains possessing the enterotoxin plasmid produced enterotoxin in the pig's intestine and were capable of causing diarrhea. The nonenteropathogenic E. coli failed to do so. The strains possessing the P155 enterotoxin plasmid were more virulent than the corresponding derivatives with the P307 enterotoxin plasmid. Strains P155, P307 and P104(P155) proliferated in the upper small intestine at a greater rate and were more virulent than the other strains. The numbers attained in the upper small intestine by the other enterotoxigenic derivatives were comparable to those of their nonenteropathogenic parent strains. It was considered that enterotoxin produced by E. coli was the essential factor for causing a diarrheic response in gnotobiotic pigs. The virulence of each of the tested strains appeared to be governed by the degree of enterotoxicity associated with a particular enterotoxin plasmid, the numbers attained by these organisms in the upper small intestine, (but not in the lower small intestine or in the colon), and by other undetermined factors.

Animals↗

PubMed1980

Extraction and separation of staphylococcal enterotoxin in foods: collaborative study.

A study was performed by 15 collaborators on a method for the extraction and chromatographic separation of Staphylococcus aureus enterotoxins from foods. Enterotoxin types A--E were added to crabmeat, milk, ground beef, and potato. Evaluation of the method was based on solubility of food eluates after extraction and separation of the enterotoxin; efficiency of recovery of enterotoxins A--E from foods; and serological categorizing of foods, as determined by the presence or absence of enterotoxins in the 8 food samples studied. The collaborative results on sample solubility, detection and identification of enterotoxin in foods, and differentiation of toxic from nontoxic samples showed overall positive rates of 94.79, 72.69, and 99.23%, respectively. The method, which has been substantiated by statistical evaluation, appears to be effective for the separation of staphylococcal enterotoxins from foods. The Association has adopted the method as official first action and no adverse comments have been received.

Animals↗

PubMed1978

On the cross-reactivity of staphylococcal enterotoxins A, B, and C.

Strong cross-reactions were demonstrated for staphylococcal enterotoxins B (SEB) and C1 (SEC1) by antigen-binding capacity and by competitive binding ability. Both SEB and SEC1 combined completely with the heterologous antibody although requiring four times as much antiserum as the homologous enterotoxin and both displaced about one-third of the other enterotoxin from a heterologous antigen-antibody system. It is proposed that one of the three major antigenic determinants of these enterotoxins possesses a significant similarity but probably not an identity of structure. SEB and SEC1 did not combine with antiserum to enterotoxin A nor inhibit the reaction of SEA with anti-SEA. SEA had no intrinsic binding capacity for anti-SEB or anti SEC1 nor did it inhibit the binding of either enterotoxin to its own antibody. Affinity chromatography was employed to demonstrate that a small apparent binding of SEA to anti-SEB was due to antibody to SEA in the anti-SEB serum and that an almost complete displacement of SEC1 binding to anti-SEC1 was caused by contaminating SEC (about 0.01%) in preparations of enterotoxin A.

Antigen-Antibody Reactions↗