Salmonellosis
Introduction
There are many different serotypes of Salmonella. All can produce disease, but only a few commonly produce illness in UK. Salmonella poses a serious risk to man and is hence a zoonosis and a public health issue. Disease in man is mostly contracted from poultry or cattle. Reptiles are also healthy carriers of Salmonella and these may also infect humans that are in frequent contact with these animals.
Salmonella enteritidis and Salmonella typhimurium are widespread in most species. Salmonella dublin is a cause of disease in cattle and Salmonella cholerae suis is prevalent in pigs and is usually septicaemic, although is now quite rare. Salmonella montevideo causes disease in humans and animals from contaminated imported meat and bone meal.
Salmonellosis is NOT very common in the dog and cat, however, the horse is often a carrier. Stress may precipitate the disease, meaning Salmonellosis is seen often in veterinary hospitals.
Salmonella strains are often named after where they were first isolated. All strains can occur epizootically, enzootically and sporadically. The strains can all produce similar clinical signs. Infection is via the faecal- oral route and organisms penetrate enterocytes before crossing the mucosa and entering macrophages. After entering macrophages, organins may then either remain localised to the gut, or are carried round the body to cause disease. There are 2 main types of disease; septicaemic and enteric. Each outbreak causes only one type of disease. The type of disease is linked to serotype- some serotypes produce septicaemia, whereas others remain localised in the gut.
Septicaemic disease
Septicaemic salmonellosis is very dramatic and produces death quite suddenly and diarrhoea is often not seen before death. This form of the disease is unusual in the very young and usually occurs post-weaning. This is around 6 to 9 months in calves and around 6 to 10 weeks in pigs.
The organism colonises bowel epithelium, where it affects the Peyers patches. It then invades macrophages, which enable it to invade across the epithelium to the submucosa. It may then either remain localised to submucosa, or spread to the lymph nodes and enter the circulation to become septicaemic. Animals may die at this stage (30%), but this depends on such factors as the infecting dose and strain. Is similar to septicaemic E. Coli.
Clinical Signs
Animals suffer from pyrexia, and occasionally a little bit of diarrhoea. The skin is reddened diffusely and bruise-like dark purplish-red blotches may be seen. The intestines may show mild catarrhal enteritis, becoming fibrinous lower down. The bowel is generally flaccid, reddened and filled with fluid. Ecchymotic and petechial haemorrhages are often seen on the serosa and mucosa. There may also be enlarged, haemorrhagic mesenteric lymph nodes and excessive blood-tinged peritoneal fluid. The lungs are collapsed and frothy and the heart is often dilated with ecchymotic haemorrhages. The liver and kidneys are also flabby and may have subcapsular haemorrhages and may contain small white foci of necrosis known as paratyphoid granulomas.
Diagnosis
Diagnosis is by culture of blood and from mesenteric lymph nodes (which are oedematous and red).
Enteric Salmonellosis
Enteric Salmonellosis shows differences in clinical presentation between species: Horse - acute fatal colitis. Cows - lingering febrile diarrhoea with passage of pseudomembranes. Calves - acute diarrhoea like colibacillosis. Dogs - acute bouts of diarrhoea. Cats - febrile enterocolitis. Pigs - septicemia or enterocolitis.
Clinical Signs
Affected animals produce acute diarrhoea, which causes many deaths by dehydration. The diarrhoea may appear watery and yellow and may be blood- tinged. In some outbreaks, particularly in pigs, chronic low-grade diarrhoea only is seen. Calves usually die in the acute stage of the disease, but may also recover.
Pathologically enteritis is seen throughout the gut, but is more severe proximally. Inflammation is catarrhal in the duodenum. By the ileocaecal junction enteritis is often fibrinous, sometimes with formation of diptheric membranes on the mucosal surface. The necrotic and fibrinous changes particularly affect the Peyers patches and the caecal and colonic lymphoid nodules. These may lead to "button ulcers" in the terminal ileum and colon, but these ulcers rupture very rarely. Focal necrosis may also be seen, particularly in the liver, but also in the spleen. Histologically, foci show a central zone of necrosis, surrounded by macrophages and lymphocytes- paratyphoid granulomas. Although this indicates the animal has had a systemic incfection, paratyphoid granulomas may be present without showing signs of septicaemia. Enteric cases of salmonella infection nearly always show some evidence of systemic spread. The septicaemic form may relocalise in the gut, resulting in enteric disease.
Animals can remain carriers for months/years following recovery from the acute diarrhoea phase. Bacteria is shed from the bile duct and mesenteric lymph nodes, which is a source of infection for other animals and people. The pathogen is shed particularly in times of stress.
Diagnosis
Diagnosis is by culture of blood or faeces.
Hepatitis
Salmonella dublin can cause hepatitis in calves.
Clinical signs will include pyrexia, dehydration and diarrhoea.
Treatment and Control
Treatment is mainly supportive with fluids and electrolytes being most important at preventing death by dehydration. Antimicrobial drugs can be given however, the use of antibiotics for salmonella enteritis without septicemia (bacteremia) is controversial as the population of normal intestinal bacterial microflora may be altered as well as the possible development of antibiotic resistance by salmonella organisms. NSAIDs should also be given in order to control pyrexia and for pain relief.
Prevention should involve decreasing the chances of exposure to the organism and increasing resistance in cattle.
Ways of decreasing exposure are to have the herd serotested and cull carrier cows or to quarantine and serotest replacement stock. Isolation of sick cows is vital as is general hygiene and disinection of calf pens and maternity areas. Rodent and bird control is also important in the spread of the disease. Do not allow rendering trucks access to feed or animal areas. Do not use front-end loaders for manure or to haul dead animals and then haul feed with them.
Increasing resistance in the young calf can be accomplished in two ways. One method is to vaccinate pregnant cows in late gestation with a salmonella bacterin vaccine. The pregnant cow will respond by producing increased antibodies to salmonella that will be passed on to the calf through the colostrum. Salmonella bacterins are also helpful in building immunity when salmonellosis is a problem in adult beef and dairy cows. The second method to increase resistance is to supplement the antibodies by administering an antibody solution containing additional antibodies to salmonella.
References
Andrews, A.H, Blowey, R.W, Boyd, H and Eddy, R.G. (2004) Bovine Medicine (Second edition), Blackwell Publishing.
Blood, D.C. and Studdert, V. P. (1999) Saunders Comprehensive Veterinary Dictionary (2nd Edition), Elsevier Science.
Divers, T.J. and Peek, S.F. (2008) Rebhun's diseases of dairy cattle Elsevier Health Scieneces.
Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial.
Nelson, R.W. and Couto, C.G. (2009) Small Animal Internal Medicine (Fourth Edition), Mosby Elsevier.
Quinn, P.J., Markey, B.K., Carter, M.E., Donnelly, W.J., Leonard, F.C. (2007) Veterinary Microbiology and Microbial Disease, Blackwell Publishing.
Radostits, O.M, Arundel, J.H, and Gay, C.C. (2000) Veterinary Medicine: a textbook of the diseases of cattle, sheep, pigs, goats and horses, Elsevier Health Sciences.