Review/Oorsig Volume 22, Issue 04 - Page 26

Oorsig/Review and affect many animal types and tissues, or very specific, and only affect certain species, tissues, or age of animal. The K99 attachment factor, which is in the common commercial vaccines, is a good example of this. It attaches to the same mechanism which allows the passage of large immunoglobulin molecules from the colostrum through the gut wall in ruminants. As you are well aware, colostrum is only useful for the first 3 days of life, and then the gut closes against it. This means, that pathogenic E. coli strains which carry the K99 attachment factor can only attach during the first few days of life, and make the calf or lamb sick during that time. K99 vaccines have little effect on E. coli strains which cause disease at other times during calfhood. Vaccines containing K99 also contain the viruses that commonly caused diarrhoea during the 1990’s, so they are still very important in calf raising enterprises. Please do not discourage your clients from using them. E. coli is easy to culture in the lab, and it is also a common contaminant. Isolating E. coli is not a diagnosis. Determining the virulence factors requires a molecular [PCR] test, and that does constitute a diagnosis. It does not help to prepare a vaccine from an isolate of a case of diarrhoea, as the E. coli may be an environmental [non- pathogenic] one. Once a pathogenic strain has been identified by determining the virulence factors, the isolate would be a suitable vaccine candidate. The disappointments around the poor performance of vaccines are therefore due to the incorrect selection of suitable candidate vaccine strains. The K99 containing vaccines are very effective for protecting calves and lambs during the first week of life, but do not work for diarrhoea in animals older than a year. Vaccines made from strains isolated as secondary invaders after initial Cryptosporidium damage to the intestinal wall, are also very unlikely to be effective, especially if a variety of antibiotics have been given before the sample is collected for culture. One cannot use the degree of antibiotic resistance as a marker to estimate whether an E. coli strain is a pathogen or not, as antibiotic resistance and virulence factors are passed down in totally different ways. AO - 27 Nov 2017 Could I ask why if resistance and virulence is not linked does the diarrhoea continue or worsen if antibiotics are given and I suspect resistant E coli is to blame. Does this resistant E coli strain contribute to the disease syndrome through other 26 mechanisms? How or does the virulence factor carrying strains survive the antibiotic treatment? MH - 28 Nov 2017 Bacteria [nearly all] possess a single chromosome, a single circle of double-stranded DNA. They also have genetic material in plasmids, which are far smaller circles of DNA. Bacteria can exchange their genetic material with other, similar species of bacteria. E. coli can exchange DNA with other E. coli, Salmonella, Klebsiella and also with other bacteria less closely related. It is much easier for bacteria to exchange genetic material from one of the plasmids, than from the large chromosome, but they can do both. The rate at which genetic material is exchanged thus depends on where the gene is. Virulence factors are mostly on the large chromosome, and antibiotic resistance genes are mostly on the plasmids. It is quick and easy for one bacterium to donate antibiotic resistance [on the small plasmid] to another bacterium. It takes a long time for a virulent bacterium to donate the genetic material coding for a virulence factor [on the large chromosome] to another one. A huge effect is that of selection pressure. There is nothing that pressurizes virulent bacteria to donate virulence genes to another isolate. However, when antibiotics are used, the bacteria susceptible to the antibiotic die out, and the ones with the antimicrobial resistance gene multiply massively to fill the vacuum. They are then in a prime position to be able to donate their genes to any other bacteria associated with them when antibiotic treatment ends. And as the resistance is on an easily transmissible plasmid, this happens frequently. Antibiotic resistance plasmids may be for only one antibiotic, e.g. only tetracycline, but they mostly carry resistance for many antibiotics. This explains things when an isolate is found to be resistant to antibiotics that have never been used on the farm. The animals were e.g. treated with potentiated sulphas, and the resistance factor that they acquired happened to have genetic material for potentiated sulphas and 5 other antibiotics as well. Regarding diarrhoea continuing or worsening when antibiotics are given: The primary cause of the problem was the Cryptosporidium, or a virulent strain of E. coli. Antibiotics are given, and if effective, the virulent strain of E. coli mostly dies, and other, resistant E. coli isolates multiply to fill the void. The damage to the intestine does not get a chance to heal, because the environmental E. coli strains irritate the damaged portions of the wall as a secondary invader. The antibiotics also probably killed off the normal flora, and normal