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This article was published in 1962
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INSTITUTE OF INSPECTORS OF STOCK OF N.S.W. YEAR BOOK.
Salmonellosis of Pigs
G. E. CHARLES, B.V.Sc., Veterinary Inspector, Forbes
Salmonella cholerae suis was isolated and described in detail by Salmon and Smith in the U.S.A. in 1885 - 1886, and in fact the bacteriological history of the Salmonella group in general did not commence until about this time.
Buxton (1958) states that some 350 serotypes of Salmonella have been recognised and the majority of these have been associated with animal infections. Pigs are known to be common carriers of Salmonella and many serotypes have been isolated from these animals, but the majority of clinical infections are confined to S. cholerae suis and S. typhi-murium. In fact, of 1056 cases listed by Bruner & Moran (1949), 810 were due to the former and 79 to the latter.
DEVELOPMENT OF INFECTION
There may be a significant effect by nutrition on the susceptibility of pigs to Salmonella infections but the exact nature of this relationship is not clear. However, the resistance of chickens to infection with S. gallinarum was increased by high level of protein and vitamins in the diet, and there appears to be some connection between the levels of nicotinic acid and the susceptibility of pigs to Salmonella infection.
While infection is often associated with poor sanitation, faulty nutrition and other stress factors, Hayston (1946) states that the disease has appeared in self-contained piggeries providing good housing and grazing and that bad conditions are not essential for the demonstration of Salmonella pathogenicity. Hayston (1946) also states that mortality usually follows purchase of pigs in saleyards. This, of course, produces a stress factor. Virus diseases may increase the susceptibility of animals to Salmonella infections and the relationship between Swine Fever virus and S. cholerae suis has been known for many years.
The source of infection is the infected animal or clinically normal "carrier" but in view of the nature of various mortalities, involving one or two pigs only, seen in recent months it would appear that the organism may be a symbiont while the animal's environment remains on an even plane, but becomes an immediate pathogen when any stress factor occurs.
The usual portal of entry is through the intestinal lymphatics and the constant involvement of the mesenteric lymph nodes confirms this. A brief bacteraemia occurs and is ended rapidly by the removal of the organisms from the bloodstream by the cells of the reticulo-endothelial systems, especially of the liver and spleen. In these organs the organisms multiply and escape to give rise to a secondary bacteraemic phase with wide distribution of the organisms throughout the body, particularly to the lungs, skin and a secondary invasion of the intestine.
SYMPTOMS
Pigs of all ages are affected but the highest mortality is in the 24 month age group. The duration of illness prior to death is variable and ranges from 24 hours to 16 days, but pigs are often found dead without having exhibited any symptoms at all. The morbidity ranges from the odd pig to 50% or more of a herd and the same applies to the mortality rate. This has been noticeable in recent investigations, when very often only one or two pigs have died and no other pigs have been affected. Affected pigs which do not die make a slow recovery and usually remain stunted.
Sick pigs are dejected, lose condition rapidly, show inappetence and pyrexia (up to 107 deg. F.), and exhibit a marked disinclination to move. Skin discolouration, a reddish-purple, may appear as blotches along the undersurface of the body. Pulmonary involvement may occur with rapid and heavy respiration and a cough may be heard. In the febrile stages affected pigs may exhibit rapid and shallow respiration with no macroscopic lung lesions. Nasal and ocular discharges occur but these may be due, in some cases to a concomitant Inclusion Body Rhinitis. Towards the end of the illness, pigs may develop a yellowish, watery scour, accompanied by a sudden disappearance of the fever. The faeces have a putrid smell and may contain shreds of necrotic mucosa. Marked thirst is evident and pregnant sows usually abort at this stage. A chronic enteric form may develop if death does not occur at this stage and this is characterised by a persistent diarrhoea, severe emaciation and intermittent fever. At intervals the faeces contain blood, mucus, and sometimes firm intestinal casts.
There is a tendency for each individual outbreak to conform to one particular syndrome rather than to run the gamut of all types. POSTMORTEM FINDINGS
In peracute septicaemic cases there may be no gross lesions but usually submucosal and subserous petechiation are present.
In acute enteric cases the mucosa of the gastric fundus may be bright red and covered with a thin film of tenacious mucus. Intestinal contents are watery and foul smelling, containing traces of blood or whole blood. Enteritis is present and ranges from muco-enteritis to haemorrhagic enteritis. Mesenteric lymph nodes are enlarged, oedematous and haemorrhagic. The wall of the gall bladder is thickened and there may be fatty degeneration of the liver. The serous cavities may contain blood-stained fluid. Subserous petechiation is present, but a number of cases have been seen recently where there were no petechiations on the kidneys, although S. cholerne suis was recovered on culture. Lung congestion is common and pneumonia may be present. In the chronic form lesions are most commonly confined to the caecum and colon. The wall is thickened with a yellow-grey necrotic material which reveals a red granular surface when stripped off. Button ulcers occur in the caecum around the ileo-caecal valve but there is a divergence of opinion as to their cause, Blood & Henderson (1960) state that they may be due to invasion by Salmonella when not associated with Swine Fever or by Swine Fever virus. Biester (1968), on the other hand, implicates Spherophorus necrophorus in the deeper necroses which occur, and states: "The so-called button ulcers of swine present an arrangement which must be interpreted as a progressive process caused by S. necrophorus in the deeper tissues as a secondary invader in a suitable field for growth prepared by a primary agent."
DIAGNOSIS
This may be made on the symptoms present, but generally speaking laboratory identification is necessary. Postmortem findings are sometimes helpful, and Blood & Henderson (1960) consider "the most satisfactory method for immediate examination is a thick smear from the lining of the gall bladder."
Peracute Salmonellosis can resemble Swine Fever and also Pasteurellosis and requires laboratory differentiation. Acute Erysipelas, where the characteristic skin lesions have not appeared, is usually indicated postmortem by the larger, subserous ecchymoses. The lesions of Swine Dysentery are confined to the alimentary tract.
Enteritis may result from nutritional deficiencies, such as deficiency of nicotinic acid, niacin, pantothenic acid and possibly riboflavin. This type is seen sometimes in pigs fed solely on boiled offal and scraps at slaughter-yards, even under fair hygiene. Boiling over a lengthy period destroys the Vitamin B complex. Bloodstained scours occur, but no organisms can be recovered from specimens. Antibiotic treatment yields no result, but injections of Vitamin B complex quickly prove successful. Vibrionic enteritis is recorded in the U.S.A, and has a longer incubation period than S. cholerae suis.
Pigs fed tissue infected with Vibrio coli showed a temperature rise 4-6 days after feeding and the diarrhoea appeared on the sixth day. With S. cholerae suis tissue the temperature rise occurred 24 hours after feeding and the diarrhoea one to four days after feeding.
Laboratory identification is necessary. Coccidia may occur in pigs but do not produce necrosis or haemorrhagic changes, and do not involve the deeper tissues. Considerable mucus may be present in the droppings but no haemorrhage is attributable to coccidiosis.
TREATMENT
Sulphadimidine, the antibiotics, streptomycin and tetra-cyclines, neomycin, chloramphenicol and nitrofurazone all may be used successfully, although in many cases recovered animals continue to excrete the organisms and act as "carriers". If systemic reaction is present, both oral and parenteral routes of administration should be used. In general chloramphenicol, nitrofurazone and neomycin appear to be most effective, and in young animals high dose levels are necessary because of the rapid excretion.
For flock (sic) treatment use is made of medicated drinking water or medicated food, the former being better as sick animals often do not eat. If it is not possible to medicate the water supply. it may be necessary to treat each sick pig individually until the animals regain their appetite, when they can be put on medicated food. In the case of valuable pigs, demulcent and astringent preparations and fluids to replace lost electrolytes and body fluids will help animals to survive the period of acute dehydration and toxaemia. Rasmussen et al. (1944) recommend the administration of the Vitamin B complex as an aid to convalescence. Guthrie (1952) controlled the disease with nitrofurazone at the rate of 1 km. on the first day and 0.5 gm. on the second day.
CONTROL
In the event of any outbreak the infected animals and in-contacts, which latter may include carriers, should be isolated and treated.
Pigs should not have access to open waterholes or dams, as these are subject to gross faecal contamination and may remain contaminated for six months or more. Water supply should be by "waterers" of such a type as to preclude the entry of anything but the snout of the pig. Pens and feeders should be vigorously disinfected and "mucked out" regularly.
As young pigs are most commonly affected, the use of nitrofurazone in the feed has much to recommend it as a preventive measure, and the use of oxytetracycline as a feed supplement appears to be of some value.
Although Salmonellosis can and does occur in well managed piggeries with a high standard of hygiene, it reaches epizootic proportions only in those piggeries where hygiene, management and nutrition are individually or collectively deficient.
References:
- Biester, H. E. (1958) — Diseases of Swine. The lowa State University Press. Ames, Iowa, U.S.A.
- Blood. D. C. & Henderson, J. A. (1960) — Veterinary Medicine. Bailliere, Tindall & Cox. London
- Bruner, D. W. & Moran, A. B. (1949) — Cornell Vet., 39: 53
- Buxton, A. (1958) — Vet. Rec., 70: 1014
- Guthrie, J. E. (1952) — Vet. Med., 47: 307
- Hayston. J. T. (1946) — Aust. vet. J., 22: 132
- Rasmusen, R. A.. Stafseth, H. J. Freeman. V. A. & Miller. M. J.
- (1944) — Vet. Med., 39: 421
- Salmon, D. E. & Smith. T. (1886) — Amer. Monthly Microbiol. Jour. 7: 204