- Email: [email protected]
Escherichia coli Bacterins
242
CHARLES
A.
HJERPE
20. Myers LL, Snodgrass DR: Colostral and milk antibody titers in cows vaccinated with a modified live rotavirus-coronavirus vaccine. I Am Vet Med Assoc 181:486-488, 1982 21. Hudson 0: Rota-coronavirus vaccination of pregnant cows. Mod Vet Pract 62:626628, 1981 22. Snodgrass DR, Ojeh CK, Campbell I, et al: Bovine rotavirus serotypes and their significance for immunization. I Clin Microbiol 20:342 - 346, 1984 23. Fremont PY: Vaccinations antirotavirus et anticoronavirus chez les bovins: Elements pratiques du choix entre les vaccinations de la vache ou du veau. Rec Med Vet 159:345-349, 1983 24. Eichhorn W, Bachman PA, Baljer G, et al: Vaccination of pregnant cows with a combined rotavirusfE. coli K99 vaccine for preventing diarrhea of newborn calves. Tierarztl Umsch 37:599-600, 602-604, 1982 25. Navetat H: Methodologie de vaccination contre les gastroenteritis a colibacille (et) a rotavirus du veau. The Netherlands, Proc 12th Wrld Congr Dis Cattle, 1982, pp 366-373 26. Van Opdenbosch E, Wellemans G: Perspectives in the prevention of viral neonatal calf diarrhea. The Netherlands, Proc 12th Wrld Congr Dis Cattle, 1982, pp 374-379 27. SaifLI, Smith L, Landmeier BI, et al: Immune response of pregnant cows to bovine rotavirus immunization. Am I Vet Res 45:49-58, 1984 28. Rodak L, Babiuk LA, Acres SO: Detection by radioimmunoassay and enzyme-linked immunosorbent assay of coronavirus antibodies in bovine serum and lacteal secretions. I Clin MicrobioI16:34-40, 1982 29. Woode GN, Kelso NE, Simpson TF, et al: Antigenic relationships among some bovine rotaviruses: Serum neutralization and cross-protection in gnotobiotic calves. I Clin Microbiol 18:358-364, 1983 30. Ihara T, Samejima T, Kuwahara H, et al: Isolation of new serotypes of bovine rotavirus. Arch Virol 78:145-150, 1983 31. Murakami Y, Nishioka N, Watanabe T, et al: Prolonged excretion and failure of cross-protection between distinct serotypes of bovine rotatirus. Vet Microbiol 12:7-14,1986 32. Paul PS: Personal communications. Veterinary Medical Research Institute, Iowa State University, 1989 . 33. Radostits OM: Neonatal diarrhea in ruminants (calves, lambs, and kids). In Howard JL (ed): Current Veterinary Therapy-Food Animal Practice 2. Philadelphia, WB Saunders, 1986, pp 105 -113 34. Lopez JW, Allen SO, Mitchell I: Rotavirus shedding in dairy calf feces and its relationship to colostrum immune transfer. I Dairy Sci 71:1288-1294, 1988 35. Snodgrass DR, Nagy LK, Sherwood 0, et al: Passive immunity in calf diarrhea: Vaccination with K99 antigen of enterotoxigenic Escherichia coli and rotavirus. Infect Immun 37:586-591, 1982
Escherichia coli Bacterins Enterotoxigenic strains of E. coli cause severe diarrheal disease in neonatal calves by colonizing the small intestinal villi, replicating to extremely large numbers (10 9 to 10 10 E. coli per gram of intestinal contents), and producing a heat-stable enterotoxin. 1 E. coli enterotoxin causes a net increase in secretion of fluid by small intestinal secretory (crypt) cells, which is the basis for the diarrhea, hypovolemia, dehydration, weakness, shock, hyponatremia, hypochloremia, and acidosis/hyperkalemia that can result. I - 3 General Considerations Most E. coli bacterins currently marketed in the United States are formulated so as to ensure a high content of K99 pilus (fimbria for
BOVINE VACCINES AND HERD VACCINATION PROGRAMS
243
attachment) antigen. Cows are vaccinated in late gestation so as to ensure high concentrations of anti-K99 colostral antibodies. When colostrum from vaccinated cows is fed to newborn calves, these antibodies are believed to act within the small intestine of the calf to coat the binding sites on bacterial pili, thus inhibiting the binding of pili to specific receptor sites on the brush border of small intestinal villus enterocytes. 1 ,4 E. coli bacteria, thus prevented from attaching to the jejunal and ileal villi, are carried into the large bowel by peristalsis. As a result, colonization of villi and production of enterotoxin are avoided. Passive circulating humoral antibodies, absorbed into the blood stream from the gut of the calf, are thought to play little or no role in immunity to neonatal enteric disease caused by E. coli. 1 Anti-K99 antibodies are not involved in naturally occurring resistance to enterotoxigenic colibacillosis, and less than 3 to 4% of unvaccinated cows possess such antibodies. I During the first 24 hours of life, because of (1) low production of hydrochloric acid by the abomasum, (2) sluggish gastrointestinal motility, and (3) absence of a competing gut microHora, the calf is highly susceptible to infection and small intestinal colonization by enteropathogenic strains of E. coli. 1 By the time they are 48 to 96 hours old, however, most calves are highly resistant to infection. I ,5 There is evidence that this resistance develops because the villus epithelial cells present at birth are rapidly replaced by a new population of cells that lack K99 receptors l ,6; consequently, the feeding of colostrum containing high concentrations of antibodies against K99 antigen, even though restricted to the first day of life, is often sufficient to prevent the disease. When enterotoxigenic colibacillosis occurs in calves older than 4 days, mixed infections with rotavirus or other viral enteropathogens are usually present. In these cases, large numbers of E. coli are attached to the virus-infected small intestinal mucosa, and it is thought that either the viral infection has prolonged the life of K99-sensitive enterocytes or that E. coli is attaching by some other mechanism. 1 Because anti-K99 antibody titers in milk of vaccinated cows decline rapidly after calving and are negligible by 5 days postpartum, 1 vaccination is of little value for preventing this kind of E. coli infection. Nearly all strains of enterotoxigenic E. coli that have been"isolated from neonatal calves have been found to possess K99 pili. 1 •3 •7 In addition, these strains may also possess other fimbriae types, including F 41, F(Y), F92b, Att25, F210, and Type 1. 1 Most strains possess both K99 and Type 1 pili,7 and many possess both K99 and F41 pili.l The in vivo importance of most of these latter pilus types is, at present, unknown. I However, the existence of an enterotoxigenic strain of E. coli possessing only Type 1 pili has been reported. 7 The same group also reported isolation of enterotoxigenic strains of E. coli possessing K88 and 987P pilus types from calves. 7 This finding should be accepted subject to confirmation by others, however, in view of the failure of previous investigators to demonstrate similar results. I It is believed that production of capsular (K) antigens assists enteropathogenic strains of E. coli in attaching to villus enterocytes, by reinforcing fibrial attachments and by encasing and cementing micro-
244
CHARLES
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HJERPE
colonies of E. coli to the mucosal surface, thus protecting them from removal by fluid movement and phagocytosis.I,3 There are approximately 90 known E. coli K groups3; however, only 11 of these have been commonly identified on enterotoxigenic calf isolates, and most of these were of the (A) type. I Currently, there are at least three wholecell E. coli bacterins marketed in the United States (Coligen, Fort Dodge Laboratories, Fort Dodge, IA 50501; Coli-4, Franklin Laboratories, Fort Dodge, IA 50501; Piliguard E. Coli-I, Schering Animal Health) that contain either three or four capsular (K) antigens (K28, K30, K35, and K85) selected because they are among the most common on enterotoxigenic E. coli isolated from calves in North America. I,7,s There is, at present, no conclusive evidence from research in cattle that colostral anticapsular antibodies are protective or that bacterins containing both capsular and fimbrial antigens are more efficient than those containing only purified fimbrial antigen. I There is a study in swine, however, in which protection was conferred by vaccination with a strain of E. coli that shared only the capsular antigen with the challenge strain. 9 Villus attachment and colonization by strains of enterotoxigenic E. coli possessing multiple fimbriae types appear to be effectively prevented by vaccination with bacterins that have only a single pilus antigen in common with challenge strains. For example, vaccination of cows with Coli-4 (Franklin Laboratories), which stimulated production of F41 (pilus) and K30 (capsular) but not K99 (pilus) antibodies, protected calves from challenge with a strain of E. coli that possessed K30, K99, and F41 antigens. 1 Similarly, vaccination of cows with either purified K99 antigen or purified F 41 antigen protected calves from challenge with the same strain (B44).1 All commercial E. coli bacterins do not contain the same complement of pilus antigens: For example, Coli-4 (Franklin Laboratories) contains only F 41 antigen, I Vicogen (Langford, Inc, Guelph, Ontario, Canada NIK lE4) contains both K99 and F41 antigens, I and Piliguard E. Coli-l (Schering Animal Health, Union, NJ 07083) contains K99, F 41, and Type 1 antigens. 7 There is, presently, no evidence that bacterins containing multiple pilus antigen types are more effective than those containing only one pilus type, so long as the vaccine and the challenge strains share a common pilus antigen. However, the Schering vaccine7 could prove to be more effective than alternative products in dealing with outbreaks of enterotoxigenic colibacillosis involving K99negative, Type 1- positive strains.
E.
COLI VACCINATION PROGRAMS
General recommendations for use of E. coli bacterins are summarized (see Table 8). Oil-adjuvant E. coli bacterins are adIl1:inistered by intramuscular injection in a single dose, 2 weeks to 6 months prior to calving, repeated annually.lo Localized fibrosis at the site of injection may be an objectionable feature of oil-adjuvant vaccines, when used in registered stock or show cattle. Non-oil-adjuvant E. coli bacterins are
BOVINE VACCINES AND HERD VACCINATION PROGRAMS
245
recommended for intramuscular or subcutaneous injection in two doses, administered at a 2- to 4-week interval, with the second dose to be given 2 to 3 weeks before calving. In subsequent years, a single booster dose should be administered, 2 to 3 weeks prior to calving. As with the rotavirus-coronavirus vaccines, which are also administered to pregnant cows, E. coli bacterins will not protect calves that do not ingest sufficient amounts of colostrum soon enough after birth. For maximum protection, calves should ingest, within the first 24 hours of life, an amount of colostrum from a vaccinated dam that is equal to 10% of birth weight. l At least half of this should be consumed within the first 2 hours}·ll
REFERENCES 1. Acres SD: Enterotoxigenic Escherichia coli infections in newborn calves: A review. J Dairy Sci 68:229-256, 1985 2. Moon HW: Mechanisms in the pathogenesis of diarrhea: A review. J Am Vet Med Assoc 172:443-448, 1978 3. Haggard DL: Bovine enteric colibacillosis. Vet Clin North Am [Food Anim Pract] 1:495-508, 1985 4. Morris JA, Wray AC, Sojka WJ: Passive protection oflambs against enteropathogenic E. coli: Role of antibodies in serum and colostrum of dams vaccinated with K99 antigen. J Med MicrobioI13:265-271, 1980 5. Smith HW, Halls S: Observations on the ligated intestinal segment and oral inoculation methods on E. coli infections in pigs, calves, lambs, and rabbits. J Pathol Bacteriol 93:499-529, 1967 6. Runnells PL, Moon HW, Schneider RA: Development of resistance with host age to adhesion of K99 + Escherichia coli to isolated epithelial cells. Infect Immun 28:298 - 300, 1980 7. Jayappa HG, Strayer JG, Goodnow RA: Controlling colibacillosis in neonatal calves: 1. Evaluation of multiple-pilus, multiple-capsule phase-cloned Escherichia coli bacterin. 2. Virulence and prevalence of Escherichia coli bearing Type 1 pili among isolates from neonatal calf diarrhea. Vet Med/Small Anim Clin 78:388393, 1984 8. Myers LL, Guinee PAM: Occurrence and characteristics of enterotoxigenic Escherichia coli isolated from calves with diarrhea. Infect Immun 13:1117 -1119,1976 9. Moon HW, Runnells PL: Trials with somatic (0) and capsular (K) polysaccharide antigens of enterotoxigenic Escherichia coli as protective antigens in vaccines for swine. Proc 4th Int Symp Neonatal Diarrhea, VIDO, University of Saskatchewan 1984, pp 553 10. Collins NF, Halbur T, Schwenk WH, et al: Duration of immunity and efficacy of an oil emulsion Escherichia coli bacterin in cattle. Am J Vet Res 49:674-677, 1988 11. Lopez JW, Allen SD, Mitchell J, et al: Rotavirus and Cryptosporidium shedding in dairy calf feces and its relationship to colostrum immune transfer. J Dairy Sci 71:1288-1294,1988
Salmonella Vaccines· Salmonella spp can cause neonatal diarrhea and septicemia, pneumonia and septicemia in calves, diarrhea and/or septicemia in adult *By Bradford P. Smith, DVM, Department of Medicine, School of Veterinary Medicine, University of California, Davis, Davis, CA; with permission.
CHARLES
A.
HJERPE
20. Myers LL, Snodgrass DR: Colostral and milk antibody titers in cows vaccinated with a modified live rotavirus-coronavirus vaccine. I Am Vet Med Assoc 181:486-488, 1982 21. Hudson 0: Rota-coronavirus vaccination of pregnant cows. Mod Vet Pract 62:626628, 1981 22. Snodgrass DR, Ojeh CK, Campbell I, et al: Bovine rotavirus serotypes and their significance for immunization. I Clin Microbiol 20:342 - 346, 1984 23. Fremont PY: Vaccinations antirotavirus et anticoronavirus chez les bovins: Elements pratiques du choix entre les vaccinations de la vache ou du veau. Rec Med Vet 159:345-349, 1983 24. Eichhorn W, Bachman PA, Baljer G, et al: Vaccination of pregnant cows with a combined rotavirusfE. coli K99 vaccine for preventing diarrhea of newborn calves. Tierarztl Umsch 37:599-600, 602-604, 1982 25. Navetat H: Methodologie de vaccination contre les gastroenteritis a colibacille (et) a rotavirus du veau. The Netherlands, Proc 12th Wrld Congr Dis Cattle, 1982, pp 366-373 26. Van Opdenbosch E, Wellemans G: Perspectives in the prevention of viral neonatal calf diarrhea. The Netherlands, Proc 12th Wrld Congr Dis Cattle, 1982, pp 374-379 27. SaifLI, Smith L, Landmeier BI, et al: Immune response of pregnant cows to bovine rotavirus immunization. Am I Vet Res 45:49-58, 1984 28. Rodak L, Babiuk LA, Acres SO: Detection by radioimmunoassay and enzyme-linked immunosorbent assay of coronavirus antibodies in bovine serum and lacteal secretions. I Clin MicrobioI16:34-40, 1982 29. Woode GN, Kelso NE, Simpson TF, et al: Antigenic relationships among some bovine rotaviruses: Serum neutralization and cross-protection in gnotobiotic calves. I Clin Microbiol 18:358-364, 1983 30. Ihara T, Samejima T, Kuwahara H, et al: Isolation of new serotypes of bovine rotavirus. Arch Virol 78:145-150, 1983 31. Murakami Y, Nishioka N, Watanabe T, et al: Prolonged excretion and failure of cross-protection between distinct serotypes of bovine rotatirus. Vet Microbiol 12:7-14,1986 32. Paul PS: Personal communications. Veterinary Medical Research Institute, Iowa State University, 1989 . 33. Radostits OM: Neonatal diarrhea in ruminants (calves, lambs, and kids). In Howard JL (ed): Current Veterinary Therapy-Food Animal Practice 2. Philadelphia, WB Saunders, 1986, pp 105 -113 34. Lopez JW, Allen SO, Mitchell I: Rotavirus shedding in dairy calf feces and its relationship to colostrum immune transfer. I Dairy Sci 71:1288-1294, 1988 35. Snodgrass DR, Nagy LK, Sherwood 0, et al: Passive immunity in calf diarrhea: Vaccination with K99 antigen of enterotoxigenic Escherichia coli and rotavirus. Infect Immun 37:586-591, 1982
Escherichia coli Bacterins Enterotoxigenic strains of E. coli cause severe diarrheal disease in neonatal calves by colonizing the small intestinal villi, replicating to extremely large numbers (10 9 to 10 10 E. coli per gram of intestinal contents), and producing a heat-stable enterotoxin. 1 E. coli enterotoxin causes a net increase in secretion of fluid by small intestinal secretory (crypt) cells, which is the basis for the diarrhea, hypovolemia, dehydration, weakness, shock, hyponatremia, hypochloremia, and acidosis/hyperkalemia that can result. I - 3 General Considerations Most E. coli bacterins currently marketed in the United States are formulated so as to ensure a high content of K99 pilus (fimbria for
BOVINE VACCINES AND HERD VACCINATION PROGRAMS
243
attachment) antigen. Cows are vaccinated in late gestation so as to ensure high concentrations of anti-K99 colostral antibodies. When colostrum from vaccinated cows is fed to newborn calves, these antibodies are believed to act within the small intestine of the calf to coat the binding sites on bacterial pili, thus inhibiting the binding of pili to specific receptor sites on the brush border of small intestinal villus enterocytes. 1 ,4 E. coli bacteria, thus prevented from attaching to the jejunal and ileal villi, are carried into the large bowel by peristalsis. As a result, colonization of villi and production of enterotoxin are avoided. Passive circulating humoral antibodies, absorbed into the blood stream from the gut of the calf, are thought to play little or no role in immunity to neonatal enteric disease caused by E. coli. 1 Anti-K99 antibodies are not involved in naturally occurring resistance to enterotoxigenic colibacillosis, and less than 3 to 4% of unvaccinated cows possess such antibodies. I During the first 24 hours of life, because of (1) low production of hydrochloric acid by the abomasum, (2) sluggish gastrointestinal motility, and (3) absence of a competing gut microHora, the calf is highly susceptible to infection and small intestinal colonization by enteropathogenic strains of E. coli. 1 By the time they are 48 to 96 hours old, however, most calves are highly resistant to infection. I ,5 There is evidence that this resistance develops because the villus epithelial cells present at birth are rapidly replaced by a new population of cells that lack K99 receptors l ,6; consequently, the feeding of colostrum containing high concentrations of antibodies against K99 antigen, even though restricted to the first day of life, is often sufficient to prevent the disease. When enterotoxigenic colibacillosis occurs in calves older than 4 days, mixed infections with rotavirus or other viral enteropathogens are usually present. In these cases, large numbers of E. coli are attached to the virus-infected small intestinal mucosa, and it is thought that either the viral infection has prolonged the life of K99-sensitive enterocytes or that E. coli is attaching by some other mechanism. 1 Because anti-K99 antibody titers in milk of vaccinated cows decline rapidly after calving and are negligible by 5 days postpartum, 1 vaccination is of little value for preventing this kind of E. coli infection. Nearly all strains of enterotoxigenic E. coli that have been"isolated from neonatal calves have been found to possess K99 pili. 1 •3 •7 In addition, these strains may also possess other fimbriae types, including F 41, F(Y), F92b, Att25, F210, and Type 1. 1 Most strains possess both K99 and Type 1 pili,7 and many possess both K99 and F41 pili.l The in vivo importance of most of these latter pilus types is, at present, unknown. I However, the existence of an enterotoxigenic strain of E. coli possessing only Type 1 pili has been reported. 7 The same group also reported isolation of enterotoxigenic strains of E. coli possessing K88 and 987P pilus types from calves. 7 This finding should be accepted subject to confirmation by others, however, in view of the failure of previous investigators to demonstrate similar results. I It is believed that production of capsular (K) antigens assists enteropathogenic strains of E. coli in attaching to villus enterocytes, by reinforcing fibrial attachments and by encasing and cementing micro-
244
CHARLES
A.
HJERPE
colonies of E. coli to the mucosal surface, thus protecting them from removal by fluid movement and phagocytosis.I,3 There are approximately 90 known E. coli K groups3; however, only 11 of these have been commonly identified on enterotoxigenic calf isolates, and most of these were of the (A) type. I Currently, there are at least three wholecell E. coli bacterins marketed in the United States (Coligen, Fort Dodge Laboratories, Fort Dodge, IA 50501; Coli-4, Franklin Laboratories, Fort Dodge, IA 50501; Piliguard E. Coli-I, Schering Animal Health) that contain either three or four capsular (K) antigens (K28, K30, K35, and K85) selected because they are among the most common on enterotoxigenic E. coli isolated from calves in North America. I,7,s There is, at present, no conclusive evidence from research in cattle that colostral anticapsular antibodies are protective or that bacterins containing both capsular and fimbrial antigens are more efficient than those containing only purified fimbrial antigen. I There is a study in swine, however, in which protection was conferred by vaccination with a strain of E. coli that shared only the capsular antigen with the challenge strain. 9 Villus attachment and colonization by strains of enterotoxigenic E. coli possessing multiple fimbriae types appear to be effectively prevented by vaccination with bacterins that have only a single pilus antigen in common with challenge strains. For example, vaccination of cows with Coli-4 (Franklin Laboratories), which stimulated production of F41 (pilus) and K30 (capsular) but not K99 (pilus) antibodies, protected calves from challenge with a strain of E. coli that possessed K30, K99, and F41 antigens. 1 Similarly, vaccination of cows with either purified K99 antigen or purified F 41 antigen protected calves from challenge with the same strain (B44).1 All commercial E. coli bacterins do not contain the same complement of pilus antigens: For example, Coli-4 (Franklin Laboratories) contains only F 41 antigen, I Vicogen (Langford, Inc, Guelph, Ontario, Canada NIK lE4) contains both K99 and F41 antigens, I and Piliguard E. Coli-l (Schering Animal Health, Union, NJ 07083) contains K99, F 41, and Type 1 antigens. 7 There is, presently, no evidence that bacterins containing multiple pilus antigen types are more effective than those containing only one pilus type, so long as the vaccine and the challenge strains share a common pilus antigen. However, the Schering vaccine7 could prove to be more effective than alternative products in dealing with outbreaks of enterotoxigenic colibacillosis involving K99negative, Type 1- positive strains.
E.
COLI VACCINATION PROGRAMS
General recommendations for use of E. coli bacterins are summarized (see Table 8). Oil-adjuvant E. coli bacterins are adIl1:inistered by intramuscular injection in a single dose, 2 weeks to 6 months prior to calving, repeated annually.lo Localized fibrosis at the site of injection may be an objectionable feature of oil-adjuvant vaccines, when used in registered stock or show cattle. Non-oil-adjuvant E. coli bacterins are
BOVINE VACCINES AND HERD VACCINATION PROGRAMS
245
recommended for intramuscular or subcutaneous injection in two doses, administered at a 2- to 4-week interval, with the second dose to be given 2 to 3 weeks before calving. In subsequent years, a single booster dose should be administered, 2 to 3 weeks prior to calving. As with the rotavirus-coronavirus vaccines, which are also administered to pregnant cows, E. coli bacterins will not protect calves that do not ingest sufficient amounts of colostrum soon enough after birth. For maximum protection, calves should ingest, within the first 24 hours of life, an amount of colostrum from a vaccinated dam that is equal to 10% of birth weight. l At least half of this should be consumed within the first 2 hours}·ll
REFERENCES 1. Acres SD: Enterotoxigenic Escherichia coli infections in newborn calves: A review. J Dairy Sci 68:229-256, 1985 2. Moon HW: Mechanisms in the pathogenesis of diarrhea: A review. J Am Vet Med Assoc 172:443-448, 1978 3. Haggard DL: Bovine enteric colibacillosis. Vet Clin North Am [Food Anim Pract] 1:495-508, 1985 4. Morris JA, Wray AC, Sojka WJ: Passive protection oflambs against enteropathogenic E. coli: Role of antibodies in serum and colostrum of dams vaccinated with K99 antigen. J Med MicrobioI13:265-271, 1980 5. Smith HW, Halls S: Observations on the ligated intestinal segment and oral inoculation methods on E. coli infections in pigs, calves, lambs, and rabbits. J Pathol Bacteriol 93:499-529, 1967 6. Runnells PL, Moon HW, Schneider RA: Development of resistance with host age to adhesion of K99 + Escherichia coli to isolated epithelial cells. Infect Immun 28:298 - 300, 1980 7. Jayappa HG, Strayer JG, Goodnow RA: Controlling colibacillosis in neonatal calves: 1. Evaluation of multiple-pilus, multiple-capsule phase-cloned Escherichia coli bacterin. 2. Virulence and prevalence of Escherichia coli bearing Type 1 pili among isolates from neonatal calf diarrhea. Vet Med/Small Anim Clin 78:388393, 1984 8. Myers LL, Guinee PAM: Occurrence and characteristics of enterotoxigenic Escherichia coli isolated from calves with diarrhea. Infect Immun 13:1117 -1119,1976 9. Moon HW, Runnells PL: Trials with somatic (0) and capsular (K) polysaccharide antigens of enterotoxigenic Escherichia coli as protective antigens in vaccines for swine. Proc 4th Int Symp Neonatal Diarrhea, VIDO, University of Saskatchewan 1984, pp 553 10. Collins NF, Halbur T, Schwenk WH, et al: Duration of immunity and efficacy of an oil emulsion Escherichia coli bacterin in cattle. Am J Vet Res 49:674-677, 1988 11. Lopez JW, Allen SD, Mitchell J, et al: Rotavirus and Cryptosporidium shedding in dairy calf feces and its relationship to colostrum immune transfer. J Dairy Sci 71:1288-1294,1988
Salmonella Vaccines· Salmonella spp can cause neonatal diarrhea and septicemia, pneumonia and septicemia in calves, diarrhea and/or septicemia in adult *By Bradford P. Smith, DVM, Department of Medicine, School of Veterinary Medicine, University of California, Davis, Davis, CA; with permission.