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Order Manual

Diarrhea disease table

Intestinal hemorrhage table


Salmonellosis is the disease caused by any of more than 2000 Salmonella serotypes. In swine, only a few serotypes cause disease, usually manifested as septicemia and/or enterocolitis, sometimes by tissue localization of infection at various sites. Salmonella infections in asymptomatic swine may serve as a source of Salmonella infection to humans via contamination of pork products.


Infection of swine with a broad range of serotypes is common. Disease as a result of infection is relatively less common but occurs throughout the year in all major swine-raising countries. All age groups are susceptible but the disease usually occurs in weaned or growing/finishing pigs. Many other species, including people, are susceptible to salmonellosis caused by some of the Salmonella serotypes that affect swine. Contaminated pork products are not a primary source of food-borne salmonellosis outbreaks in people but efforts to reduce salmonellae in the pork food chain are a high priority for the swine industry.

Historical information

In 1886 the organism now known as Salmonella serotype choleraesuis was erroneously reported to cause hog cholera. After the viral etiology for hog cholera was identified, salmonellae were thought of as secondary pathogens. However Salmonella serotypes frequently do act as primary pathogens causing septicemia and/or enterocolitis in swine.

It has been shown that some outbreaks of salmonellosis in people are food-borne and that food products of animal origin, including pork, are sometimes are implicated as the source of these outbreaks. Species-adapted Salmonella serotypes are relatively infrequent; most serotypes are capable of infecting (though not necessarily causing disease in) multiple mammalian hosts. Both animal and human health could be improved if salmonellosis could be effectively controlled across animal production and food processing systems. Salmonella reduction programs at farm level constitute a logical step in minimizing the occurrence of outbreaks in humans. Swine industry-led national Salmonella control programs in North America and Europe are being implemented in an effort to understand what management strategies are most likely to minimize the impact of the organism on both human and animal health.


Salmonella is now recognized as a genus with about 2000 serotypes that can be serologically clustered in groups (see serogroup examples in Table 1). Pathogenic serotypes for swine are relatively few, with most outbreaks caused by Salmonella choleraesuis or Salmonella serotype typhimurium. Serotypes that are the most common cause of disease in both people and swine include Salmonella serotypes typhimurium, enteritidis, agona and heidelberg. Salmonella choleraesuis and Salmonella serotype typhisuis are host-adapted to swine and are rarely isolated from sources other than infected swine.

Salmonellae are small, hardy, ubiquitous, Gram-negative bacilli. All contain endotoxin and are capable of elaborating a variety of other toxins. They can readily survive in many swine environments but can be inactivated by chlorine, iodine and phenol-based disinfectants.

 Table 1: Common serotypes of Salmonella enterica serogroups B, C1, C2, D and E isolated from US pigs
 Group B  Group C1  Group C2  Group D  Group E
 Abortus-equi  Choleraesuis  Hadar  Dublin  Anatum
 Agona  Infantis  Kentucky  Enteritidis  Meleagridis
 Brandenburg  Lille  Litchfield  Miami  Muenster
 Bredeney  Mbandaka  Manhattan    New Brunswick
 California  Montevideo  Muenchen    Orien
 Derby  Tennessee  Newport    Riefild
 Heidelberg  Thompson      Senftenberg
 Saint Paul        Uganda
 San Diego        



Asymptomatic, clinically normal swine may harbor inapparent Salmonella infections that persist in their tonsils, intestine, lymph nodes, or gall bladder. Those carrier swine regularly or occasionally shed salmonellae in their feces and present a major source of exposure to susceptible swine. Mingling of healthy pigs with sick or inapparent carriers often precipitates an outbreak of salmonellosis. Once introduced, salmonellae are spread by the fecal-oral route, in contaminated feed and water, or sometimes by aerosol. Exposed pigs may either develop clinical signs of salmonellosis or resist infection and remain healthy. Any pig exposed to salmonellae should subsequently be considered as a possible carrier of the organism.

Contaminated buildings and pens remain infectious for weeks and pigs moved into them are likely to become infected. Historically, feed was a major source of new infections and remains so for many serotypes. Salmonella choleraesuis, a host-adapted and frequent cause of disease in swine, has never been reported as a feed contaminant. Most serotypes are capable of infecting a broad host range. For example, S. typhimurium frequently infects many other kinds of animals, including livestock, poultry and mice, is readily transmitted between species, and occasionally is found in feedstuffs. Rodents and wild birds are believed to be important disseminators of Salmonella organisms.

Salmonellosis often appears during or following stressful events, e.g. prolonged transport, drought, overcrowding, change of rations, parturition, prolonged treatment with drugs or antibiotics, or another disease in the herd. Unusual stress lowers resistance and/or increases magnitude of shedding, hence dose, and can precipitate outbreaks. A balance of virulence, dose, and resistance exists between swine and the salmonellae they carry or with which they become infected.


Following ingestion or inhalation of S. choleraesuis, the organisms invade tonsil and/or intestinal mucosa and soon spread to regional lymph nodes, usually with septicemia. Other Salmonella serotypes usually remain confined to the intestine and, perhaps, adjacent lymph nodes producing only a transient septicemia. Host-adapted S. choleraesuis, and occasionally other serotypes, sometimes are phagocytized and survive within macrophages and neutrophils that transport them to other sites where they localize and cause lesions. Sites include lungs, liver, brain, meninges, joints and lymph nodes.

In enteric salmonellosis as typified by infection with S. typhimurium, mucosal damage and necrosis are the result of mucosal ischemia caused by vasculitis and microvascular thrombosis. Vasculitis is present in all forms of salmonellosis. Diarrhea is attributed to tissue fluids leaking from damaged mucosa and compromise of mucosal absorption. An enterotoxin similar to that produced by enterotoxigenic E. coli (causing cyclic AMP-mediated hypersecretion of fluids and salts from enterocytes) has been described for Salmonella  heidelberg.

Clinical signs

Septicemic salmonellosis usually is caused by host adapted Salmonella choleraesuis. It usually is seen in pigs from weaning to about 180 pounds but can occur in all ages of swine. Lactogenic immunity is usually protective. Acute onset of an outbreak may be signaled by acute death loss in a group of apparently thrifty pigs. Within a few days the disease spreads among other pigs in the group. Morbidity usually is low to moderate but mortality is high among those that become ill.

Clinical signs include inappetence, depression, huddling, weakness, temperatures up to 107° F (41.6° C), and red to purple discoloration of skin of the extremities (cyanosis). Diarrhea is not present initially but occurs after a few days of illness. The length of course is variable, both in individual animals and in the herd and may be influenced by treatment.

The enterocolitic form of salmonellosis usually is caused by Salmonella typhimurium and less often by S. choleraesuis or other serotypes. This form tends to involve pigs from weaning to about 180 pounds. Initial signs include moderate anorexia and diarrhea that may be watery to yellow and intermittent. Animals are moderately febrile initially but temperatures usually regress as diarrhea continues. As the disease progresses, there may be mucus, fibrin, and blood in the feces but blood is not a prominent feature. Over time, morbidity is high and mortality is moderate. Surviving animals often become emaciated or gain weight slowly.

Localization of salmonellae sometimes occurs in the lungs, brain, meninges and lymph nodes. Less common sites include gall bladder, joints and synovium. Localization in the lungs can lead to cough or dyspnea, or in the brain to central nervous system (CNS) signs.


In septicemic salmonellosis, gross lesions include red to purplish discoloration of the extremities, marked enlargement of the spleen, moderate swelling of the liver, swollen and wet lymph nodes and reddening of the fundic part of the stomach. Frequently there will be petechial hemorrhages in skin, larynx, lungs, heart, bladder and kidneys. The liver may or may not contain small, white to yellow foci of necrosis (paratyphoid nodules). In animals with localization of infection in the lungs, there is pulmonary congestion and edema and patchy consolidation; in the brain or meninges, congestion and, perhaps, hemorrhages; in joints, villous proliferation.

Intestinal lesions vary in severity, largely related to duration of illness. At onset there may be only congestion with superficial fibrinous inflammation of small or large areas of the cecum, colon and terminal end of the small intestine. In long standing cases the intestinal lesions resemble those of the enterocolitic form of salmonellosis.

In the enterocolitic form of salmonellosis, the large intestine and the lower small intestine are heavy, edematous and the wall is thickened. There may be excessive peritoneal fluid and strands of fibrin on the serosa. Ileocolic and mesenteric lymph nodes usually are markedly enlarged, congested and edematous. There is a marked enterocolitis with focal or diffuse areas of mucosal necrosis with fibrinonecrotic exudates in small intestine, cecum, colon and/or rectum. In chronic cases there may be raised, circular lesions in the colon (“button ulcers”). Rectal stricture with accompanying megacolon has been described as a sequelae to Salmonella infection. Dry gangrene may occur on the ears or tail of survivors.


The history, clinical signs and typical gross lesions may be adequate for a tentative diagnosis. Diagnosis should be confirmed by laboratory culture and identification of Salmonella, especially if the disease is new on the premises. Serogrouping is readily available and can aid in determining potential serotypes involved (see Table 1); serotyping is available upon request and is sometimes useful to define epidemiology and expected clinical outcome. A few typical, untreated animals, preferably alive, should be submitted for culture and histopathologic study. Diagnosticians often culture multiple organs including liver, spleen, lung, mesenteric lymph nodes and colon. Microscopic examination of tissues will help identify typical lesions and differentiate them from those of other enteric and septicemic diseases. Salmonella choleraesuis typically causes rather unique paratyphoid nodules in the liver.

Septicemic salmonellosis must be differentiated carefully from classical swine fever, erysipelas and other septicemias as well as other causes of interstitial pneumonia. The enterocolitic form must be differentiated from coliform enteritis, porcine proliferative enteritis, trichuriasis, and swine dysentery. The latter two diseases tend to be restricted to the large intestine.


Breeding stock should be acquired only from suppliers with no recent history of salmonellosis. If feasible, all breeding stock should be from a single source. Essential additions to the herd should be made only after a quarantine period of 30-60 days.

Ideally, only pigs from a single source and of similar age should be raised together in a closed, all in/all out system. Buildings should be cleaned and disinfected carefully between batches. All possible carriers, including rodents, birds, pets and wildlife, should be eradicated or excluded. Unusual stresses should be avoided insofar as possible. Perhaps the most important approach to control of salmonellosis involves comfortable dry housing, proper animal density, good ventilation and a high standard of sanitation. Early weaning and removal of piglets to a separate, clean site has been successful in avoiding transmission of S. choleraesuis from breeding populations known to include carriers.

For control of Salmonella choleraesuis, and perhaps S. typhimurium, avirulent live vaccines are available and quite effective. Killed Salmonella bacterins and a mutant-derived endotoxin vaccine are available but thought to be less effective. All vaccination programs should be coupled with proper sanitation, husbandry and pig flow.

Numerous antibiotics and chemotherapeutic agents have been used for prevention and/or treatment. Some reduce mortality as well as the duration and severity of salmonellosis. Frequently used products include carbadox, gentamycin, neomycin, tiamulin, ceftiofur, and others. Systemically absorbed or injectable antimicrobials are preferred for septicemic salmonellosis. Because salmonellae have developed resistance to many therapeutic agents, isolation and antimicrobial sensitivity are usually warranted. It has not been confirmed that treatment of infected pigs with antimicrobials induces a Salmonella carrier status as has been suggested in humans.

Successful reduction of salmonella infections in swine herds has been reported in Europe and the US. The programs are based largely on serologic testing of breeding stock, culture of samples taken at slaughter, establishment of measures that reduce contamination of carcasses at slaughter, and controlling risks that are likely to result in introduction of Salmonella through feed or drinking water. The hazard analysis critical control point (HACCP) programs instituted by United States abattoirs have adopted many of these measures.

See the table: Diseases Associated with Hemorrhage in Intestine