Protection against neonatal Escherichia coli diarrhoea in pigs by vaccination of sows with a new vaccine that contains purified enterotoxic E. coli virulence factors F4ac, F4ab, F5 and F6 fimbrial antigens and heat-labile E. coli enterotoxin (LT) toxoid.

The efficacy of a new vaccine against neonatal Escherichia coli diarrhoea in piglets containing purified F4ab, F4ac, F5 and F6 fimbriae and detoxified heat-labile toxin (LT) was tested in challenge experiments by the method described by the European Pharmacopoeia (3rd edn, EDQM, Council of Europe, Strasbourg, France). A group of 11 young sows from a herd without E. coli problems was vaccinated 6-8 and 2-4 weeks prior to expected farrowing and another group of nine young sows were non-vaccinated controls. Escherichia coli antibody titres were determined in serum samples taken from the sows before first vaccination and before farrowing and in colostrum samples. The newborn piglets were allowed to suckle colostrum from their mother immediately after birth. The piglets were marked with individually numbered ear tags. Approximately 12 h after birth, 118 piglets from vaccinated sows and 79 piglets from non-vaccinated control sows were challenged by oral instillation of 5 ml of a freshly prepared culture of one of the challenge strains [O8:K87:F4ab (LT+) or O149:K91:F4ac (LT+) or O9:K30:F5 or O9:K103:F6 respectively]. The challenge cultures contained as a mean 6.8x10(9) CFU/ml. After challenge the piglets were observed for 7 days and mortality and morbidity were recorded. Vaccinated sows developed significant levels of antibody titres in colostrum and serum. Control sows stayed at a low/seronegative level. The protective efficacy was excellent because 66.7-87.5% of the piglets from vaccinated sows remained without clinical signs after challenge. Only 0.0-28.0% of the piglets from non-vaccinated sows remained healthy and more than 47.1% of the piglets in this group died after challenge. It is concluded that the new vaccine is very effective in protection of piglets against neonatal E. coli diarrhoea.

Protection of vaccinated pigs against experimental infections with homologous and heterologous Haemophilus parasuis.

The efficacy of a new Haemophilus parasuis vaccine for pigs was investigated. The vaccine contains H parasuis serotype 5 cells and is adjuvanted with Diluvac Forte (Intervet). Groups of pigs were vaccinated at five and seven weeks with 2 ml and their littermates served as unvaccinated controls. The vaccinated pigs were protected against a challenge with another strain of Hparasuis serotype 5 at two, eight and 17 weeks after the second vaccination, whereas the controls became very ill. The susceptibility of the pigs to the infection decreased with increasing age. After a heterologous challenge with H parasuis serotypes 1, 12, 13 and 14, two weeks after the second vaccination, the vaccine also gave clear protection. The severity of the illness among the control pigs differed with the different serotypes.

Bacterial colonization and invasion in pigs experimentally exposed to Streptococcus suis serotype 2 in aerosol.

A recently developed porcine model for aerogenous infection with Streptococcus suis serotype 2 was applied in a study of the phases of bacterial colonization and initial invasion. Eighteen pigs were exposed to aerosolized S. suis serotype 2 after pre-exposure to mild acetic acid in aerosol. The animals were killed consecutively within the first six days after challenge. After death, all animals were necropsied and examined by bacteriology, histopathology, and immunohistochemistry. Systemic infection was established in four out of 18 animals exposed to S. suis serotype 2. All systemically infected animals developed clinical signs and lesions typical of the infection. In four additional animals, subclinical infection was demonstrated by re-isolation of S. suis from the palatine tonsil. However, in all 18 challenged animals, immunohistochemistry demonstrated S. suis serotype 2 antigen in the palatine and/or nasopharyngeal tonsils. In all four systemically infected animals, S. suis serotype 2 antigen was also found in the mandibular lymph node. These observations point towards the tonsils as possible portals of entry for S. suis serotype 2 with subsequent lymphogenous spread. Thus, the present findings parallel the proposed pathogenesis for S. suis serotype 1 infection in pigs.

Protection of piglets against atrophic rhinitis by vaccinating the sow with a vaccine against Pasteurella multocida and Bordetella bronchiseptica.

The efficacy of a new vaccine against atrophic rhinitis in pigs was tested in the Netherlands and Denmark. The vaccine contained protein dO (a truncated Pasteurella multocida toxin which is immunogenic and non-toxic), inactivated Bordetella bronchiseptica whole cells, and an adjuvant. The sows were either vaccinated intramuscularly with 2 ml of the vaccine at six to eight and two to four weeks before expected farrowing or left unvaccinated as controls. All the piglets were challenged intranasally with B bronchiseptica when three to seven days old and with P multocida three to four days later. Pigs born to the vaccinated sows performed significantly better than pigs born to the control sows when judged on growth, average daily weight gain and snout scores. The challenge organisms were reisolated more frequently from the control pigs than from the pigs in the vaccinated group. The vaccinated sows and their progeny developed high titres of antibodies against B bronchiseptica and P multocida toxin.

Actinobacillus pleuropneumoniae osteomyelitis in pigs demonstrated by fluorescent in situ hybridization.

Necrotizing osteomyelitis and fibrinopurulent arthritis with isolation of Actinobacillus pleuropneumoniae serotype 2 is reported in two pigs from a herd with lameness and mild coughing problems among 8 to 12-week-old pigs. Application of fluorescent in situ hybridization targeting 16S ribosomal RNA of A. pleuropneumoniae in formalin-fixed tissue was performed to verify the association of A. pleuropneumoniae with the bone and joint lesions. By in situ hybridization A. pleuropneumoniae was demonstrated as multiple microcolonies or single cells dispersed in focal fibrinonecrotizing pleuropneumonia, in joints with arthritis, and in bone necroses including lysis of growth plate and suppurative inflammation in the adjacent trabecular metaphysis, thus demonstrating that well-known infections manifest new, unusual lesions.

Characterization of Micrococcaceae isolated from post mortem examined pigs.

The investigation comprised 170 cases of infections due to Micrococcaceae among post mortem examined pigs that died during the preweaning period. The incidence was 3.1 promille of the live-born pigs. The infection was most frequent among pigs less than 4 weeks of age (Table I). ACute and subacute generalized infections occurred in 43.5% of the cases (Table II), and exudative epidermitis was the cause of death in 23.5%. In the remaining 32.9% of the cases, the post mortem findings included a variety of debilitating conditions, such as undersize, malformation, starvation or traumata. In all 248 strains of Micrococcaceae were isolated. A preliminary differentiation revealed 41.5% of the strains as Staphylococcus aureus and 34.5% as S. epidermidis and 22.6% as Micrococcus (Table III). A further characterization on 43 of the strains was performed (Table IV and V). Totally 19 different fermentation pattern were observed. In Table IV the strains are grouped into six groups. Fourteen strains were identified as S. aureus and 15 strains as S. epidermidis biotype 2, s. S. hyicus (Table VI). The distribution of the non-haemolytic strains according to biotypes is shown (Table VII). By this grouping, the 15 S. hyicus strains were designated type III B. It is concluded that various staphylococci may be isolated in pure culture from different pathological lesions in preweaned pigs. Biochemical characterization of the strains showed that part of the strains could not be classified by the previously described grouping systems.

Studies of the pathogenesis of enteric E. coli infections in weaned pigs: bacteriological and immunofluorescent studies.

Qualitative and quantitative, bacteriological studies were performed on spontaneous cases of post weaning E. coli diarrhoea (PWD). The pigs derived from a herd, D, in which the disease had persisted for a period of almost 2 years. Orally vaccinated healthy pigs from herd D and from herds A and M without the disease were also examined. The results showed that haemolytic E. coli were frequently isolated from faecal samples which had been collected 5--7 days after weaning but seldom from samples from the same pigs collected before weaning. Haemolytic E. coli dominated the aerobic intestinal flora at 3--5 days after weaning in pigs from herd D with PWD. Oral vaccination using a formalinized vaccine delayed and suppressed the occurrence of haemolytic E. coli in pigs from herd D (Table I). Intestinal counts of the bacteria showed that the number of haemolytic E. coli present in the anterior portion of the jejunum was 10(-3)--10(-5) times higher in pigs which suffered from PWD than in weaned pigs of the same age which did not show symptoms of the disease (Table II). The lowest bacterial counts in various portions of the intestine were consistently observed in the sections obtained from the orally vaccinated healthy pigs. Pure cultures of K88-negative enteropathogenic E. coli serotype O149:K91 were consistently isolated from all the diseased pigs. Fluorescent antibody studies showed that the specific strain of bacteria adhered to the villous epithelium of the jejunum in a layer which covered the villi from the tip to the base and sometimes continued down into the crypts (Figure 1). The bacterial adhesion coincided with an intensive colonization of the jejunum with the homologous E. coli serotype and was nerve observed in apparently healthy pigs which did not have symptoms of PWD. It was concluded that characteristic intestinal colonization by adhesion may occur with enteropathogenic strains of E. coli O149:K91 which lack the K88 antigen (Figure 2).

Streptoccal infections in pigs. 2. Serological and biochemical examinations.

A total of 2,275 strains of haemolytic streptococci (HS) from 1,338 post mortem examined sucking pigs were studied. The serological examination revealed that 43.9 per cent of the strains belonged to group-C and 33.7 per cent belonged to group-L (Table I). Other serogroups amounted to 8.0 per cent and 13.8 per cent of the strains were non-typable. The distribution of serogroups in relation to different organs is presented in Table II. The fermentation pattern of 115 group-C strains against trehalose, sorbitol and lactose was determined (Table III). All but one of the strains appeared to be S. equisimilis. The ability of 127 group-L strains to ferment lactose, hippurate, sorbitol and glycerol is shown in Table IV. Eleven different fermentation patterns were encountered. An antimicrobial resistance pattern was determined for 69 strains (Table V). All the strains, except one, were sensitive to penicillin and chloramphenicol. Only two strains were sensitive to streptomycin. None of the isolated serogroups or biochemical types could be related to a particular pathological lesion or to a particular herd or group of sows within the herd. By comparing the fermentation patterns of the group-L strains isolated from pigs dead with HS infection with those of previously group-L strains from healthy swine, different predominant patterns were found. Possibilities of using these differences in biochemical reactions in separating pathogenic and saprophytic strains are discussed.

Streptococcal infections in sucking pigs. 1. Epidemiological investigations.

The investigation comprises 5,811 litters and 55,641 liveborn pigs. Among the pigs which died before weaning, infection with haemolytic streptococci (HS) was determined in 1,338. This corresponds to 2.4 per cent of the liveborn pigs (Table I). In the examined herds the incidence of fatal cases with HS infections ranged from 1.2 to 3.8 per cent. The highest incidence was observed in litters born by gilts (Table II) and in litters with more tha 11 pigs (Table III). HS infections were identified in 17.5 per cent of the examined litters, and in most of the litters only one pig was lost (Table IV). A marked seasonal variation was observed, with a predominance of HS during the winter period (Table V). Analyses of the influence of some possible determinative factors revealed the highest incidence among the progeny of sows which were housed separately during pregnancy (Table VI), whereas herd size and the hygiene level did not exert any influence on the frequency of HS. The incidence of fatal HS infections was higher in herds where tail docking and clipping of the canine teeth were performed than in herds where these procedures were omitted (Table VII). Most of the death with HS infections (53.8 per cent) occurred among pigs less than 14 days of age (Table VIII). The main diagnoses of the pigs with streptococcal infections are presented in Table IX. A survey of the isolation frequency of HS from various organs is given in Table X. The most frequently isolated serogroups were group-C (40.2 per cent) and group-L (31.3 per cent) (Table XI). Preliminary investigations on the source of infection and the pathogenesis are reported (Tables XII and XIII). In two herds, 8 of 10 sows carried HS on mucosal surfaces at the time of farrowing, and in 6 of 10 examined litters, HS bacteraemias were observed in pigs during the first days of life. Furthermore, an analysis showed that part of the sowa (109) lost pigs with HS infections in several (2-6) subsequent litters (Tables XIV) and XV).

Causes of culling and death in sows.

Over a 4-year period, the annual number of culled sows in 9 Danish herds averaged 54.8 per cent of the year-sows and the number of culled sows in per cent of total number of farrowings averaged 25.8 (Table I). -- The culling rate varied considerably from herd to herd within the same year and from year to year (Tables I and II); however, the average annual culling rate for all the herds only presented small variations (Table II). The average number of litters reared per sow before culling was 3.6. The culling rate was higher in pedigree herds than in commercial herds, and it was highest in the small pedigree herds (Table III). The hygiene level in the herds and the introduction of new female breeding stock did not influence the culling rate (Table IV). A proportionally lower percentage of the sows was culled in herds where the dry and pregnant sows were housed in stalls and/or were tethered, as compared to herds where these sows were housed in pens (Table V). -- The culling rate in the age groups of sows with less than 8 farrowings remained at approximately the same level (Table VI). The main reason for culling was infertility problems, which were recorded in 41.4 per cent of the culled sows, while 16.7 per cent of the sows were culled because their litters were poor and/or small (Table VII). The mortality rate among the culled sows was 11.9 (Table VII), and the main causes of death were chronic pyogenic infections, which occurred in 25.5 per cent of the fatal cases (Table VIII). Certain aspects concerning the recording and calculation of culling rates in the different herds are discussed and it is emphasized that the culling rate per se may not have any direct relationship to the productivity in the herd.

Polyserositis in pigs due to generalized Escherichia coli infection.

A fibrinous polyserositis syndrome due to generalized Escherichia coli infection in pigs was observed in 13 out of 17 systematically monitored herds. The mortality rate was approximately 0.1% among liveborn pigs. The occurrence was usually sporadic but a minor enzootic was observed in one herd. Most of the affected pigs succumbed during first or second week of life but cases were observed throughout the suckling period. The clinical signs included marked depression, anorexia, rough haircoat, laboured respiration and death in two to five days. Predominant gross pathological lesions were signs of septicaemia and a voluminous, gelatinous and fibrinous exudate in the pleural, the pericardial and the peritoneal cavities. Frequently also a firbinous polyarthritis and a fibrinous pneumonia were present. The majority of the isolated invasive E. coli strains were nonhaemolytic. Serologically 11 different E. coli O groups were encountered. O group most frequently represented was 020. None of the examined E. coli strains belonged to the serogroups which frequently are associated with enteropathogenicity in pigs.

Preweaning mortality in pigs. 5. acute septicaemias.

A 2-year study on preweaning mortality revealed that 2.1 per cent of the liveborn pigs succumbed to acute bacterial septicaemias. The most frequently encountered causative organisms were haemolytic streptococci and E. coli.

Occurrence of K88-negative escherichia coli serotypes in pigs with post weaning diarrhoea.

Faecal swabs from pigs with post weaning E. coli diarrhoea in 43 different herds were bacteriologically examined. A survey of the isolated haemolytic E. coli strains showed that only 1 of the examined strains possessed the K88 antigens and that E. coli strains belonging to serogroup O149:K91 were most frequently isolated. The results suggest that the K88 antigen is of minor significance in the development of post weaning diarrhoea associated with E. coli serotype O149:K91.

Preweaning mortality in pigs. 4 Diseases of the gastrointestinal tract in pigs.

The incidence of fatal gastroenteropathies in sucking pigs was studied during a 2-year period in 17 sow herds involving 2,936 litters. The results showed that 2.8 per cent of the liveborn pigs died with gastroenteropathies during the sucking and immediate post weaning period. The incidence was lowest in offspring from second-litter sows (Table I) and the progeny from large litters tended to have the highest incidence (Table II). Fatal gastrointestinal diseases were observed in a total of 17.6 per cent of the examined litters, and the average number of death per affected litter was 1.5 (Tables III and IV). The progeny of sows with post parturient diseases had significantly higher death losses than had the progeny from normal healthy sows (Table V). Climate had no apparent influence on death losses, but they were lowest during the warmer period of the year (April-September) (Tables VIII and VI.) The incidence varied considerably from herd to herd, but was not influenced by herd size (Table III). However, the level of hygiene exerted a pronounced influence on the incidence (Table VII), and self-contained herds had significantly lower death losses than had herds where female breeding stock was occasionally brought in (Table IX). Approximately 65 per cent of the pigs which succumbed due to gastrointestinal diseases died during the first week of life, which means that 1.8 per cent of the pigs at risk died during this period (Table X). The material was grouped according to the results of the post mortem and bacteriological examinations (Table XI). Approximately 50 per cent of the fatal cases were associated with an intestinal bacterial infection, which in most instances was caused by pathogenic strains of E. coli (Tables XII and XIII), while approximately 14 per cent had distinct gross pathological lesions which alone were indication of a diagnosis. In the remaining one third of the fatal cases the aetiology and pathogenesis remained by and large unexplained; however, nutritional and dietetic disorders played a role in many of these cases. Aetiological, epidemiological and pathological aspects of the fatal gastrointestinal diseases are discussed, and it is concluded that a high level of hygiene, the prevention and treatment of post parturient diseases, "closed" management systems, and the avoidance of unsuitable or damaged sow feed would be instrumental in keeping the level of fatal gastrointestinal diseases low among sucking pigs.