Monoclonal Antibody for the Protection of Neonatal Pigs and Calves from Toxic Diarrhea

Sadowski, Peter L.; Acres, S. D.; Sherman, David M.

doi:10.1007/978-1-4684-4460-5_7

Cited by 6 publications

(3 citation statements)

References 13 publications

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“…In contrast, the same F41+ vaccines conferred no demonstrable protection against challenge with strains that expressed both F41 and K99 pilus antigens. This differs from results indicating that K99-specific vaccines can protect against challenge with K99+ F41+ ETEC strains (1, 17,27,29).…”

Section: Discussioncontrasting

confidence: 98%

F41 pili as protective antigens of enterotoxigenic Escherichia coli that produce F41, K99, or both pilus antigens

Runnels¹,

Moseley²,

Moon³

1987

Infect Immun

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Pigs suckling dams that have been vaccinated with pilus antigen are protected against challenge with enterotoxigenic Escherichia coli (ETEC) strains that express the same pilus antigen. However, some ETEC strains express more than one pilus antigen. Pregnant swine were vaccinated either with E. coli HB101 that harbored a recombinant plasmid coding for F41 expression (F41+) or with the HB101 parent strain that carries the pHC79 vector (F41-). Suckling pigs born to vaccinated dams were challenged with ETEC that expressed either K99, F41, or both pilus antigens. Production of F41 in vivo was demonstrated by immunofluorescence assay of sections of ileum and by seroconversion against F41 antigen by pigs challenged with F41+ and K99+ F41+ ETEC strains. The F41+ vaccine protected against challenge with an F41+ ETEC strain. In contrast, F41+ vaccination did not protect against challenge with K99+ or K99+ F41+ ETEC strains. The F41vaccine did not protect against challenge with any strain used. The results indicate that K99Q F41+ ETEC strains produce F41 antigen in the small intestine during disease and that F41+ vaccination can be a protective antigen if the challenge strain expresses only F41 antigen, but that F41+ vaccination may not protect against strains that produce both K99 and F41 antigens. Enterotoxigenic Escherichia coli (ETEC) strains colonize the small intestine, secrete enterotoxins, and cause diarrhea. Colonization is facilitated by pili (fimbriae). Pili facilitate adherence of ETEC to intestinal mucosa (13). Pilus adhesins that are known to be important in ETEC infections of neonatal animals are K88, K99, 987P, FY, and F41 (3, 15, 19, 21, 23, 25, 30). The K88, K99, and 987P pili are also designated F4, F5, and F6, respectively (24). The F41 pilus was originally referred to as anionic K99 (18). Pilus adhesins known to be important in humans are colonization factor antigens (CFA) I and 11 (10). Some ETEC strains produce more than one of these adhesins. For example, many strains that produce K99 also produce F41 (19, 20); some strains that produce K88 also produce 987P (28); and the CFA II of human ETEC is a complex of three different pili designated CS1, CS2, and CS3 (10). Purified pilus vaccines protect against challenge with ETEC strains that produce the same pilus antigen (1, 9, 17). There are two lines of evidence that K99+ vaccines protect against challenge with ETEC strains that produce both K99 and F41 (K99+ F41+). First, a purified K99 pilus vaccine protects pigs and calves from challenge with K99+ ETEC strains 431 and B44, respectively (1, 17). Both of these strains were subsequently shown to be K99+ F41+ (19, 20). The purified K99 pilus (7) vaccine that was used (1, 17) did not contain F41, since it was prepared from a K-12 transconjugant that produces K99 but not F41 (8, 19). It was the absence of F41 (anionic K99) from these purified K99 pilus preparations that resulted in the controversy (7, 8, 18-20), leading to recognition that F41 is distinct from K99 (4, 8, 19, 31). Second, monoclonal antibod...

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Section: Discussioncontrasting

confidence: 98%

F41 pili as protective antigens of enterotoxigenic Escherichia coli that produce F41, K99, or both pilus antigens

Runnels¹,

Moseley²,

Moon³

1987

Infect Immun

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“…MAb. The K99 MAb was prepared from hybridoma K992 BD4E4 as reported previously (20,21). The K88 MAb was prepared from hybridoma 21BA13G4.…”

Section: Methodsmentioning

confidence: 99%

In vivo emergence of enterotoxigenic Escherichia coli variants lacking genes for K99 fimbriae and heat-stable enterotoxin

et al. 1987

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Neonatal pigs were inoculated with porcine enterotoxigenic Escherichia coli 431, which carries genes for K99 fimbriae and STaP enterotoxin. Colonies of strain 431 were recovered from feces of pigs for up to 17 days after inoculation and tested for hybridization with gene probes for K9 and STaP. Variants of strain 431 that did not hybridize with the probes were considered to have lost the genes. Variants were recovered from 10 of 13 suckling pigs that survived the infection. Only 0.4% of the isolates recovered during the first 2 days after inoculation were variants. Of the isolates recovered 3 to 5 days after inoculation, 20 to 36% were variants. Variant colonies were detected more frequently among pigs in some litters than in others. The litter with the highest number of variant-shedding pigs had the dam with the highest titer of K9 antibody in her colostrum. Variants also occurred in colostrum-deprived, artificially reared pigs. However, the number of variants detected was lower and they occurred later in the course of the infection in colostrum-deprived pigs than in suckling pigs. More variants were detected and they were detected earlier in colostrum-deprived pigs fed anti-K99 monoclonal antibody than in controls fed anti-K88 monoclonal antibody. Loss of STaP appeared to be secondary to loss of K99 in that some variants lacked only K99 (K99-STaP+) and some lacked both genes (K99-STaP-), but none was of the K99+ STaP-type. Our results confirmed reports of gene loss from enterotoxigenic E. coli during infection. They are consistent with the hypothesis that variants emerge under in vivo selection pressure of K99 antibody and with the speculation that gene loss may be an important component of protection in vaccinated populations. However, the emergence of variants did not appear to play a major role in the recovery of individual pigs from clinical disease. Fimbriae (pili) and enterotoxins are virulence factors of enterotoxigenic Escherichia coli (ETEC) (1,15). Fimbriae mediate adherence of E. coli to host intestinal epithelium, and enterotoxins stimulate intestinal secretion of water and electrolytes, resulting in diarrhea. Some ETEC strains of the K88 (F4) and K99 (F5) fimbrial antigen types lose these antigens (and, apparently, the plasmids carrying the genes encoding them) during experimental infections in mice (5). Loss of K88 antigen also occurs during infections in pigs, which are natural hosts for K88+ ETEC (17,18). A human ETEC strain (6) and an enteropathogenic E. coli strain (7) have been shown to lose genes encoding heat-labile enterotoxin and an adherence factor, respectively, during infection in humans.Loss of K88 in pigs is thought to be caused by antibody, because it was detected in immunized pigs but not in control pigs (18) and because it can be induced in vitro by growth in immune colostrum (8,17,18). It has been suggested that the antibodies involved in loss of K88 are not K88 specific but rather are directed against a novel antigen(s) and act by a novel mechanism which also impedes the spread ...

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“…The application of specific antibodies represents another possible way to control infectious diarrhea. The antibodies are extracted from either serum, colostrum, or milk (Snodgrass et al, 1977;Sadowski et al, 1983;Murakami et al, 1985;Yolken et al, 1990). Specific antibodies are also produced from chicken eggs, and are used for diagnostics as well as for treatment (Bartz et al, 1980;Jensenius et al, 1981;LGsch et al, 1986).…”

Section: Introductionmentioning

confidence: 99%

Dose-dependent effects of specific egg-yolk antibodies on diarrhea of newborn calves

Özpınar¹,

Erhard

Aytuğ

et al. 1996

Preventive Veterinary Medicine

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In a field trial on a farm in Turkey, we tested whether specific egg-yolk antibodies had a prophylactic effect on neonatal diarrhea. Owing to its antibody spectrum, this egg powder was very suitable for this farm since mainly rotavirus was identified. Regardless of the dosage (2 g, 4 g, or 8 g egg powder), the calves (n = 164) which received specific egg-yolk antibodies via the whole egg during the first 14 days of life showed significant improvements in risk and duration of diarrhea and in body weight gain compared with calves of the control group (n = 80) which had not received any egg powder. These significant differences in body weight still persisted after 3 months of life. The mortality risk in the control group amounted to 8.8%, while in all egg powder groups (n = 164) only one calf died as a result of diarrhea. Breed-dependent differences in the parameters were not observed.

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Monoclonal Antibody for the Protection of Neonatal Pigs and Calves from Toxic Diarrhea

Cited by 6 publications

References 13 publications

F41 pili as protective antigens of enterotoxigenic Escherichia coli that produce F41, K99, or both pilus antigens

F41 pili as protective antigens of enterotoxigenic Escherichia coli that produce F41, K99, or both pilus antigens

In vivo emergence of enterotoxigenic Escherichia coli variants lacking genes for K99 fimbriae and heat-stable enterotoxin

Dose-dependent effects of specific egg-yolk antibodies on diarrhea of newborn calves

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