Effects of weaning on diarrhea caused by enterotoxigenic Escherichia coli in three-week-old pigs

We attempted to determine whether weaning is required for induction of diarrhea in pigs with postweaning enterotoxigenic Escherichia coli infection. Three-week-old newly weaned pigs and their suckling littermates were inoculated with the K88+ enterotoxigenic E coli strain M1823B. Fourteen of 21 weaned and 12 of 20 suckling pigs were genetically resistant to intestinal adhesion by the K88+ strain of E coli; they remained healthy, and gained weight at similar rates. Both groups of K88-resistant pigs gained weight faster, and shed fewer bacteria of strain M1823B in their feces, than did their K88-susceptible counterparts. Diarrhea developed in K88-susceptible pigs in the weaned (6 of 7 pigs) and suckling (4 of 8 pigs) groups, and 1 of the 4 affected suckling pigs died from complications resulting from diarrhea. The incidences of diarrhea, weight gain rates, and the numbers of strain M1823B shed in feces of susceptible weaned and suckling pigs were not significantly (P greater than 0.05) different. Diarrhea scores of susceptible weaned pigs were significantly (P less than 0.02) higher than those of susceptible suckling pigs on the second day after inoculation. In this experimental model, it was concluded that weaning is not required for induction of diarrhea, but may modestly increase its severity.     

Effects of preweaning exposure to a starter diet on enterotoxigenic Escherichia coli-induced postweaning diarrhea in swine

Experiments were conducted to evaluate the effect of restricted feeding of a starter diet to suckling pigs (creep feeding) in a model of postweaning colibacillosis. The hypothesis that restricted creep feeding primes an intestinal allergic reaction to starter diet ingested after weaning was tested. Twenty-eight suckling pigs were fed a starter diet for 3 h/d on days 7, 8, and 9 after birth (creep-fed). Twenty-six suckling pigs were not fed the diet until 3 weeks of age (not creep-fed), when all pigs were weaned and given the starter diet. One day after weaning, 24 creep-fed and 22 not creep-fed pigs were inoculated with K88+ enterotoxigenic Escherichia coli, and 4 pigs in each group were kept as noninoculated controls. Among inoculated pigs (principals), 10 creep-fed and 12 not creep-fed pigs were found to be genetically resistant to K88+ E coli and remained healthy during the 6-day postinoculation period, as did the noninoculated controls. Eighteen (10 creep-fed and 8 not creep-fed) of the 24 genetically susceptible principals developed diarrhea after inoculation. There were no significant differences in the incidence and severity of diarrhea, amount of body weight loss, and mortality between creep-fed and not creep-fed susceptible principal pigs. Histologic examination of intestine from control pigs and principals that survived for 6 days after infection did not reveal any substantial morphologic difference between creep-fed and not creep-fed groups. In conclusion, creep feeding was not required for the production of diarrhea in this model. Creep feeding did not induce morphologic changes characteristic of an allergic reaction in the small intestine.     

Effect of Streptococcus faecium C-68 in control of Escherichia coli-induced diarrhea in gnotobiotic pigs

Streptococcus faecium was fed to prevent colibacillosis in gnotobiotic pigs. Three strains of Escherichia coli were used. With strain O:K103, 987P:NM in pigs fed S faecium before the E coli challenge exposure, the pigs exhibited less severe diarrhea, recovered earlier, and produced better weight gains than did pigs given E coli only. Escherichia coli strains O157:K88ac:H19 and O8:K87, K88ab:H19 were more virulent. Pigs fed S faecium and challenge exposed with these 2 strains of E coli developed mild diarrhea; however, none of the pigs died, and they continued to eat well and gained weight. Pigs given E coli only developed severe diarrhea and lost weight, and 5 of 8 infected pigs died. Bacterial counts of E coli and S faecium from 3 areas of the small intestine and the cecum were all comparable among experimental groups. Histopathologic examinations demonstrated abundant colonization of the intestinal tract with S faecium. Seemingly, S faecium reduced the toxic effects of E coli and prevented generalized infection and death.     

Pathogenicity of porcine enterotoxigenic Escherichia coli that do not express K88, K99, F41, or 987P adhesins.

Three-week-old weaned and colostrum-deprived neonatal (less than 1 day old) pigs were inoculated to determine the pathogenicity of 2 enterotoxigenic Escherichia coli isolates that do not express K88, K99, F41, or 987P adhesins (strains 2134 and 2171). Strains 2134 and 2171 were isolated from pigs that had diarrhea after weaning attributable to enterotoxigenic E coli infection. We found that both strains of E coli adhered in the ileum and caused diarrhea in pigs of both age groups. In control experiments, adherent bacteria were not seen in the ileum of pigs less than 1 day old or 3 weeks old that were noninoculated or inoculated with a nonpathogenic strain of E coli. These control pigs did not develop diarrhea. Antisera raised against strains 2134 and 2171 and absorbed with the autologous strain, grown at 18 C, were used for bacterial-agglutination and colony-immunoblot assays. Both absorbed antisera reacted with strains 2134 and 2171, but not with strains that express K99, F41, or 987P adhesins. A cross-reaction was observed with 2 wild-type K88 strains, but not with a K12 strain that expresses K88 pili. Indirect immunofluorescence with these absorbed antisera revealed adherent bacteria in frozen sections of ileum from pigs infected with either strain. We concluded that these strains are pathogenic and express a common surface antigen that may be a novel adhesin in E coli strains that cause diarrhea in weaned pigs.     

Comparison of conventional and long-acting oxytetracyclines in prevention of induced Actinobacillus (Haemophilus) pleuropneumoniae infection of growing swine.

These experiments tested the hypothesis that long-acting oxytetracycline (oxytetracycline-LA) was more effective than regular oxytetracycline in preventing porcine pleuropneumonia when administered either 24 or 48 h prior to experimental challenge with virulent strains of Actinobacillus pleuropneumoniae. Two experiments (1 and 2) were conducted using growing pigs (average weight 12-15 kg). Antibiotic treatments were administered once intramuscularly at 20 mg/kg body weight; controls received an equivalent volume of saline. Clinical signs were recorded over seven days, and mortality rates and pathological lesions were analyzed using analysis of variance. Serum oxytetracycline levels were compared 48 and 72 h postinjection. All pigs developed clinical disease following experimental infection. Actinobacillus pleuropneumoniae was recovered from 42% of experiment 1 pigs and all of experiment 2 pigs. The data showed that both oxytetracycline and oxytetracycline-LA given at the same dose protected pigs against experimental infection when given 24 h prior to challenge, and there was no difference between the efficacy of the two drugs in this experiment. When administered 48 h prior to challenge, only oxytetracycline-LA reduced the clinical signs and pathological changes following A. pleuropneumoniae challenge. Between 48 and 72 h postinjection, oxytetracycline-LA blood levels were significantly greater compared to oxytetracycline-treated pigs.     

Experimental models of porcine post-weaning colibacillosis and their relationship to post-weaning diarrhoea and digestive disorders as encountered in the field

The aim of this study was to develop a reliable model system of porcine post-weaning colibacillosis, and in doing so to assess the primary relationship of enterotoxigenic Escherichia coli to post-weaning diarrhoea and digestive disorders as encountered in the field. Six sequential experiments were carried out using 168 SPF piglets weaned into an optimal controlled environment at 28 days of age. The piglets were allocated to 23 treatment groups, 17 of which were inoculated either orally or intragastrically with enterotoxigenic strains of E. coli (LT+, STI+, STII+) possessing adhesive factors including K88 (F4). The piglets were challenged either once (Day 4 post-weaning) or on several days post-weaning, with the challenge load for each inoculation varying from 10(8) to 10(12) CFU.Overall 14.5% of inoculated pigs developed severe illness and died: these had lesions in their digestive tracts typical of colibacillosis. Diarrhoea occurred on at least 1 day in 50% of inoculated pigs, but was transient (1.7 days on average), appeared very soon after challenge (sometimes within half a day), and was accompanied by signs of depression and low weight gain. Generally a prompt recovery then occurred. In the second 2 weeks post-inoculation daily weight gain reached the same level in most inoculated groups of pigs as in the uninoculated controls. Only a small number of pigs developed a chronic enteritis lasting several days, as is typically observed in field cases. Diarrhoea was more common in the piglets that were tested adhesive positive to the K88 fimbriae receptor, but the disorders were no more severe in these animals. The response of all pigs depended primarily on the inoculum used, and especially on the challenge load. Although enterotoxigenic E. coli are clearly important in the aetiology of post-weaning diarrhoea, other factors are also required for the production of the chronic post-weaning digestive disorders and ill-thrift that are commonly encountered in commercial piggeries.     

Avirulent K88 (F4)+ Escherichia coli strains constructed to express modified enterotoxins protect young piglets from challenge with a virulent enterotoxigenic Escherichia coli strain that expresses the same adhesion and enterotoxins

Virulence of enterotoxigenic Escherichia coli (ETEC) is associated with fimbrial adhesins and enterotoxins such as heat-labile (LT) and/or heat-stable (ST) enterotoxins. Previous studies using a cell culture model suggest that exclusion of ETEC from attachment to epithelial cells requires expression of both an adhesin such as K88 (F4) fimbriae, and LT. To test the ability of non-pathogenic E. coli constructs to exclude virulent ETEC sufficiently to prevent clinical disease, we utilized a piglet ETEC challenge model. Thirty-nine 5-day-old piglets were inoculated with a placebo (control), or with either of the three K88(+)E. coli strains isogenic with regard to modified LT expression: 8017 (pBR322 plasmid vector control), non-toxigenic mutant 8221 (LT(R192G)) in pBR322, or 8488, with the LT gene fused to the STb gene in pBR322 (LT(R192G)-STb). Piglets were challenged with virulent ETEC Strain 3030-2 (K88(+)/LT/STb) 24h post-inoculation. K88ac receptor-positive piglets in the control group developed diarrhea and became dehydrated 12-24h post-challenge. Piglets inoculated with 8221 or 8488 did not exhibit clinical signs of ETEC disease; most piglets inoculated with 8017 showed diarrhea. Control pigs exhibited significant weight loss, increased blood total protein, and higher numbers of colony-forming units of 3030-2 E. coli in washed ileum and jejunum than treated pigs. This study shows for the first time that pre-inoculation with an avirulent strain expressing adhesive fimbriae and a non-toxic form of LT provides significant short term protection from challenge with a virulent ETEC strain that expresses the same fimbrial adhesion and enterotoxin.     

Prevention and control of coccidiosis in goats with decoquinate

Decoquinate was evaluated as a coccidiostat in domestic goats. Fifty goats less than 4 months of age were assigned to 5 groups (pens) of 10 goats each and were treated for 87 days with 0 (control), 0.3, 0.5, 1.0, or 4.0 mg of decoquinate in feed/kg of body weight. Goats were inoculated orally weight. Goats were inoculated orally with 30,000 oocysts, mainly Eimeria christenseni (74%) and E ninakohlyakimovae (20%) on day 19. Nontreated goats developed profuse watery diarrhea and tenesmus and gained weight poorly; 2 died. Treated goats did not develop clinical coccidiosis and gained significantly more weight (P less than 0.05), regardless of the dose used. Treated goats also had significantly fewer (P less than 0.05) oocysts in feces than did nontreated controls. Oocyst numbers were inversely related to dose; a more rapid decrease in oocyst numbers occurred as the dose was increased. At the doses used, decoquinate was safe in goats and was an effective drug for the prevention of clinical coccidiosis.     

Colicin resistance in relation to pathogenicity factors in strains of Escherichia coli isolated from the intestinal tract of piglets

Three hundred and fifteen E. coli strains isolated from the intestine of piglets were examined for K-antigens 88 and 99, enterotoxin production and colicin resistance. Of these strains 308 belonged to one of 3 following different groups: Group 1: 0149, K88, producing heat-labile (LT) and heat-stable (ST) enterotoxins, group 2: 064, K99, producing ST, and group 3: variable O-antigens, no K-antigens or enterotoxin production.Almost 100 % of the E. coli strains were found to be resistant to colicins E₁, E₃, Ia, H and D+X. Resistance to colicins E₂, B+M, V and K+X were found in 91.7 %, 43.8 %, 49.8 % and 62.2 % respectively.E. coli strains in group 1 were always (resistant to colicin E₂, while about 87 % of the other strains were resistant to this colicin. E. coli strains in group 2 were more often resistant to colicin B+M, V and K+X (65 %, 94 %, 83 %) than strains in group 1 (37 %, 24 %, 64 %) and strains in group 3 (37 %, 52 %, 46 %).E. coli strains in group 2 showed a high degree of multiresistance, 45.1 % of the strains being resistant to all of the 9 colicins. About 10 % of the other strains were resistant to all of the 9 colicins.E. coli strains harbouring the enteropathogenicity factors K99 antigen and ST production, showed a higher degree of colicin resistance than both the E. coli strains with K88 antigen and ST and LT production, and the E. coli strains lacking enteropathogenicity factors.     

Effect of acupuncture on young pigs with induced enteropathogenic Escherichia coli diarrhea

Thirty-four preweaning pigs with induced enteropathogenic Escherichia coli diarrhea were treated with electroacupuncture, traditional acupuncture, or neomycin. In the group treated with electroacupuncture, points GV-1, bilateral ST-36, and Bai-hui were stimulated electrically. In the group treated with traditional acupuncture, points GV-1, bilateral ST-36, BL-20, bulb points, bilateral ear tip, and Shan-gen were used. Acupuncture points CV-12 and bilateral ST-25 also were treated with moxibustion (applying heat generated by a burning herb, Artemisia argyi). Hemoacupuncture also was applied to Shan-gen, bilateral ear tip, and bulb points. Pigs in the third group were given neomycin orally. Five pigs were inoculated with E coli, but were not treated and served as nontreated controls. At postinoculation day 5, 60% of control pigs and greater than 80% of pigs in treated groups recovered from diarrhea. However, at postinoculation day 3, recovery rates for pigs in the control and group treated with electroacupuncture were only 20 and 27.3%, respectively; whereas pigs treated with acupuncture or neomycin attained 81.8 and 71.4% of recovery rates, respectively. Seemingly, traditional acupuncture, but not electroacupuncture, was effective in controlling induced E coli diarrhea in pigs at its early stage.     

Bacterial colonization and morphology of the intestine in porcine Escherichia coli enterotoxemia (edema disease)

Twenty-one pigs were divided into three groups. Pigs in one group were inoculated with the intestinal contents which included bacteria from a pig with edema disease. Pigs in another group were inoculated with a culture of Escherichia coli serogroup O 139:K12(B):H1 isolated from the aforementioned contents, and pigs in a third group served as uninoculated controls. The infection was similar following both inocula. Enterotoxemia developed in 11 of the 14 pigs allowed to survive for more than two days. The onset varied from two to seven days after inoculation. There were maximal viable counts of E. coli in the intestine from the second day post-inoculation and thereafter. In frozen and paraffin sections, as well as by scanning electron microscopy, the organisms were seen on the surface of the small intestinal epithelium where they formed either isolated colonies or continuous layers. They colonized the lower small intestine more intensely than the upper section. The intestinal epithelium and the villi of infected pigs were indistinguishable morphologically from the tissues of three uninoculated control pigs. The diarrhea which was observed in controls and inoculated pigs before inoculation and the villus atrophy in controls and inoculated pigs indicated a preexisting infection with at least one other agent.     

Prevalence of K88, K99, and 987P pili of Escherichia coli in neonatal pigs with enteric colibacillosis

One hundred nineteen live neonatal pigs with diarrhea less than or equal to 2 weeks old were euthanatized, and frozen sections of their ilea were submitted to an indirect fluorescent antibody technique to identify K88, K99, and 987P pili (also referred to as F-4, F-5, and F-6 pili, respectively) in Escherichia coli. Ten-centimeter ileal sections were used to determine numbers of lactose-fermenting bacteria. Of 52 pigs in which E coli pili were found, 14 had K88 (27%), 23 had K99 (44%), 13 had 987P (25%), and 2 had K88 and K99 simultaneously (4%). Numbers of lactose-fermenting bacteria were significantly (P less than or equal to 0.05) higher in pigs with piliated E coli than in pigs without piliated E coli. Results of this study indicated that piliated E coli are a major cause of enteric disease in neonatal swine in Michigan, and that in pigs less than or equal to 2 weeks of age, K99 was the most frequently encountered pilus antigen.     

Evaluation of lasalocid as a coccidiostat in calves: titration, efficacy, and comparison with monensin and decoquinate

Two experiments were conducted to evaluate lasalocid as a coccidiostat in Holstein calves and to compare lasalocid with monensin and decoquinate. In experiment 1, calves in 3 groups (6 calves/group) were each inoculated with 500,000 sporulated oocysts, 88% of which were Eimeria bovis and 12% were E zuernii. Calves in each group were given lasalocid-medicated feed at 0.50 (group 3), 0.75 (group 4), or 1 mg/kg (group 5) of body weight/day for 45 days. Two control groups (6 calves/group) were also evaluated; calves in control group 2 were inoculated and nontreated, and calves in control group 1 were noninoculated and nontreated. At 0.50, 0.75, or 1 mg/kg/day, lasalocid was equally effective in preventing induced coccidiosis (E bovis and E zuernii) in calves. Compared with inoculated nontreated controls, treated calves had significantly (P less than 0.05) fewer oocysts in feces and had fewer clinical signs of coccidiosis from days 16 to 30 after inoculation. Experiment 2 was conducted to compare the effectiveness of monensin, lasalocid, and decoquinate for the prevention of experimentally induced coccidiosis. Calves (n = 48) were allotted into 4 groups (12 calves/group); each was inoculated orally with 275,000 sporulated oocysts, predominantly E bovis and E zuernii, and each was given nonmedicated feed (group 6) or feed medicated with 33 mg of lasalocid (group 7), decoquinate (group 8), or monensin (group 9)/kg of feed for 46 days. Calves given medicated rations had significantly (P less than 0.05) fewer oocysts in their feces and fewer clinical signs of coccidiosis than did calves given nonmedicated rations.(ABSTRACT TRUNCATED AT 250 WORDS)     

Susceptibility of Chinese Meishan and European large white pigs to enterotoxigenic Escherichia coli strains bearing colonization factor K88, 987P, K99, or F41

Conventionally raised Chinese Meishan and European Large White pigs were intragastrically challenge exposed with 2.1 x 10(10) enterotoxigenic Escherichia coli strains bearing colonization factor K88, 987P, F41, or F41 plus K99. In response to challenge exposure with the K88-positive (K88+) organisms, 96% of Large White pigs died within 48 hours, whereas none of the Meishan pigs died. Both breeds of pigs had similar susceptibility to strains bearing 987P or F41. Lastly, Meishan pigs were found to be more susceptible than Large White pigs to a strain expressing K99 and F41. In pigs with diarrhea, challenge-exposure strains intensively colonized the jejunum (10(8) to 10(10) bacteria/g of tissue) and, to less extent, the duodenum (except K88+ strain, which comprised 10(8)/g). In most cases, jejunal concentrations of the challenge-exposure strains were substantially lower in pigs that did not have diarrhea. Half the resistant Meishan pigs eliminated the K88+ strain from the intestines. Colostral antibody titer that agglutinated challenge-exposure strains did not differ between Meishan and Large White gilts. Results indicate that resistance of pigs to the K88+ strain did not extend to enterotoxigenic strains bearing other well-known factors. They indicate, in addition, that genetic resistance to K88+ strains described in pigs in Europe may exist in pigs in China.     

Escherichia coli diarrhoea in pigs with or without the K88 receptor.

There was a high incidence of neonatal scours in 38 litters of pigs born at Compton in a four month period during 1978. The most important cause of the disease was an enteropathogenic Escherichia coli strain which possessed the K88 antigen. The Compton herd has been bred to produce pigs of three genotypes with respect to the presence or absence of the intestinal receptor for the K88 antigen. These are homozygous dominants (SS) and heterozygotes (Ss) susceptible to infection by virulent K88-positive E coli, and homozygous recessives (ss) resistant to the disease. The highest incidence of diarrhoea was in the susceptible progeny of resistant dams and susceptible sires. There was no K88 associated diarrhoea in resistant progeny or in susceptible progeny of susceptible dams.     

Postweaning diarrhea in swine: experimental model of enterotoxigenic Escherichia coli infection

A reproducible model of postweaning colibacillosis was obtained by controlling management and environmental variables to simulate conditions often seen at weaning. Suckling pigs were exposed briefly to starter diet at 1 week of age, weaned at 3 weeks of age, held at an ambient temperature of 20 +/- 2 C, and again given the starter diet. One day after weaning, each pig was given 10(10) colony-forming units of enterotoxigenic Escherichia coli strain M1823B (O157:K88ac:H43-LT+ STb+) in broth containing 1.2% sodium bicarbonate via stomach tube. In vitro adhesion by strain M1823B to isolated intestinal branch borders was used to test pigs for susceptibility to K88. In this model, 3 syndromes were induced in susceptible pigs: (1) peracute fatal diarrhea; (2) moderate diarrhea, weight loss, and fecal shedding of the inoculum strain; and (3) no diarrhea, weight loss, and fecal shedding of the inoculum strain. Rotavirus particles were not found in fecal specimens of pigs with diarrhea. The K88-susceptible, noninoculated control pigs remained clinically normal. It was concluded that susceptibility to adhesion by K88+ enterotoxigenic Escherichia coli was a requirement for the production of disease in this model; inoculation with rotavirus was not necessary.     

Preliminary characterization of Escherichia coli isolated from pigs with diarrhoea in Venezuela

The aetiology of neonatal porcine diarrhoea was studied in 15 different herds located in the north-western region of Venezuela. Of 56 strains of Escherichia coli analyzed, 16 (28.6%) were shown to produce heat-stable (STa) enterotoxin, as detected by infant mouse assay. Only four of these STa+ isolates also possessed the K88 pilus antigen, two were 987P+ and none possessed the K99 antigen, leaving 10 STa+ samples in which no pilus antigen was identified. Among the 40 STa negative samples were six K88+ specimens, one K99+, four 987P+, one which reacted as K88+ + K99+ and one K88+ + 987P+. Considering as pathogenic any strain showing at least one of the characters studied, pathogenic E. coli were detected with an overall frequency of 42.9%, being more prevalent during the second week of life. An electrophoretic analysis of the plasmid content of the field isolates of E. coli, revealed the presence of numerous species of extrachromosomal DNA, although no direction association could be made between a particular plasmid and any of the pathogenic characteristics identified. Results of Southern blot analysis indicate that the STa enterotoxin was preferentially encoded within an endemic plasmid of 4.9 Md. Other plasmids present in the E. coli isolates could be related to antibiotic resistance. With the exception of one strain, all E. coli isolates were resistant to more than one of the nine drugs tested; multiresistant E. coli were frequently isolated, including four strains which were resistant to seven antibiotics.     

Evaluation of a live avirulent Escherichia coli vaccine for K88+, LT+ enterotoxigenic colibacillosis in weaned pigs.

Live, avirulent Escherichia coli vaccine strains were constructed and tested for efficacy in preventing colibacillosis in 4-week-old pigs. Either or both of 2 plasmids were inserted into avirulent E coli strain G58-1 (0101:NM). These plasmids were pPMC4, which encodes for LTb subunits of heat-labile enterotoxin, and pDHF1, which encodes for K88ac fimbriae. Litter- and weight-matched pigs were removed from sows when they were 10 days old and vaccinated orally with the constructed strains or with G58-1 (negative control vaccine) when they were 2 weeks old and 5 days later. All pigs were challenge-inoculated with virulent E coli strain 3030-2 (O157:K88, LT+, STb+) 2 weeks after the first vaccination. Only 1 pig vaccinated with G58-1/pPMC4/pDHF1 developed diarrhea and none died following challenge inoculation. Seventeen of 31 control pigs developed diarrhea and 11 died. Of 18 pigs vaccinated with G58-1/pDHF1 then challenge-inoculated with the virulent strain, 5 developed diarrhea and 2 died. Fifteen of 18 litter- and weight-matched controls developed diarrhea and 8 died. When compared with G58-1 (negative control), G58-1/pPMC4 afforded no protection to pigs challenge-inoculated with 3030-2.     

Effect of supplemental potassium in the receiving diet and form of antibiotic on feeder pig performance

In five separate trials 901 feeder pigs (769 purchased and 132 university-raised) were used to determine the effect of level of dietary K (.64 vs 1.00 vs 1.40%), form of neoterramycin (feed-grade vs water-soluble) and a long-lasting oxytetracycline injection on subsequent performance. Purchased pigs fed a 28-d receiving diet with 1.00% K gained faster (P less than .05) than the control pigs fed a .64% K diet (.64 vs .60 kg) during a 1980 summer trial. Feed efficiency was not affected by level of dietary K. Three additional trials conducted during January, July and October of 1981 failed to substantiate this beneficial effect on rate of gain. Feeder pig performance was not different (P greater than .05) when either feed-grade or water-soluble neoterramycin was used as a 14-d receiving treatment at preventative levels. However, in one trial nearly twice as many pigs on the medicated feed diet required additional treatment for sickness compared with pigs receiving water medication (14.5 vs 7.9%; P less than .1). Giving pigs an injection of a long-lasting oxytetracycline (LA-200) either at the market or upon arrival at the finishing facility had no effect on performance; however, the pigs were home-raised rather than purchased; consequently, their health was excellent.     

Effects of cyadox and olaquindox on intestinal mucosal immunity and on fecal shedding of Escherichia coli in piglets

A 2 x 3 factorial arrangement of treatments was used to determine the effects of olaquindox and cyadox on the intestinal mucosal immune response and on fecal shedding of Escherichia coli in Landrace x Large White barrows that had been orally given 10(10) cfu of E. coli (O139:K88). Factors included 1) E. coli inoculation or no inoculation, and 2) no antimicrobial, 100 mg of olaquindox/kg, and 100 mg of cyadox/kg in the basal diet, respectively. The effects of cyadox and olaquindox were assessed in terms of fecal shedding of E. coli, the number of intraepithelial lymphocytes (IEL), immunoglobulin A-positive cells (APC) in the intestinal lamina propria, and ADG. There was no difference in the fecal shedding of total E. coli or the inoculated E. coli between olaquindox-supplemented pigs and cyadox-supplemented pigs during the experiment. However, fecal shedding of the inoculated E. coli in olaquindox- or cyadox-supplemented pigs was less (P < 0.05) than that in nonsupplemented pigs. Escherichia coli inoculation increased IEL and APC in the jejunum and ileum, but olaquindox or cyadox decreased IEL and APC (P < 0.05). Jejunal APC in cyadox-supplemented pigs was less (P < 0.05) than that in olaquindox-supplemented pigs. Escherichia coli inoculation reduced (P < 0.05) ADG, whereas the supplementations improved ADG (P < 0.01) during the experiment. Average daily gain in cyadox-supplemented pigs was greater (P < 0.05) than that in olaquindox-supplemented pigs. The data indicated that olaquindox and cyadox reduced the number of intestinal E. coli and suppressed E. coli-induced immune activation, which might be responsible for the enhanced growth that was observed.