Enteric Salmonellosis

Introduction:  Salmonellae are Gram negative aerobic and facultative-anaerobic bacterial rods.  Salmonellae spp. are ubiquitous and widely variant.  Over 2200 serotypes have been identified, most being pathogenic for humans and animals.  Luckily, there are only 10 serotypes responsible for most of the disease associated with Salmonella in both humans and animals, making control of these diseases possible and even effective.  Unfortunately, morbidity and mortality are both high in salmonellosis.

Pathophysiology:  Salmonella organisms are very invasive and can be transmitted through fecal-oral, mammary secretions, nasal, and ocular routes.  Fecal-oral transmission is the most common route, and in strains capable of invasion of the gastrointestinal tract, this method leads to diarrhea.  

The mechanism of diarrhea associated with Salmonella spp. is complex and multifactorial.  There are three basic mechanisms of disease:  inflammation and necrosis and decreased absorption.   Increased fluid secretion is also proposed.  The mechanism of disease is determined by the particular strain of Salmonella the animal is infected with.

• Exudation due to inflammation and necrosis:  Salmonella organisms directly attack and invade enterocytes.  Destruction of these cells allows the bacteria to penetrate down to the lamina propria.  Macrophages respond to the invasion and may destroy or be destroyed by the organism.  Extensive infiltration of the lamina propria with polymorphonucleocytes leads to inflammatory edema and loss of fluid across the damaged intestinal mucosa (exudative diarrhea).

• Decreased absorption and/or maldigestion:  Destruction of the intestinal villi and interruption in the secretion of digestive enzymes further impedes digestion of nutrients.  Infiltration of lymphocytes and macrophages decreases both lymphatic and blood flow effectively decreasing absorption of nutrients.  Healing of the villi may result in fusion and decreased surface area, contributing to malabsorption.

• Increased fluid secretion:  Though the exact mechanism is unknown, Salmonella organisms are hypothesized to induce local production of prostaglandins which stimulate adenlylate cyclase in the enterocytes.  Activation of the adenlylate cyclase pump causes hypersecretion, which overwhelms the absorptive capacity of the mucosa leading to diarrhea.

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Signalment:  Salmonellosis occurs universally and in all species.  Pigs, cattle, horses, and exotic species have traditionally been most commonly affected, but it can affect any species.

Clinical Signs:  Clinical signs in food animals include depression, fever, decreased milk production, and severe diarrhea.  The animal's feces may be watery to soft and may contain fibrin, blood, and mucus (reflecting mucosal injury).  Pregnant animals may abort.  In horses, the signs of endotoxemia may predominate.

Gross Pathology:  

• Intestine:  The organism is invasive and can produce impressive mucosal destruction.  The intestinal mucosa may be reddened or necrotic with a fibrin coating.  Loose or watery fecces may be found in the lumen.  Depending on the lesion, the contents may also contain blood.  The "classic" lesion of acute enteric salmonellosis is acute, severe fibrinonecrotic enteritis or enterocolitis.

• Regional lymph nodes:  May be swollen and hemorrhagic.  

Copyright Cornell College of Veterinary Medicine	This image is the jejunum from a calf with intestinal salmonellosis.  The mucosa is granular and the wall is slightly thicker than normal.  The lumen is larger than normal.  An irregular cast of fibrin is present which was found in the lumen.   Click on the image to see a larger view.
Copyright Cornell College of Veterinary Medicine	This image is the colonic mucosa from a pony with acute Salmonellosis. Click on the image to see a larger view.
Copyright Cornell College of Veterinary Medicine	This image is a classic enteric salmonellosis lesion from a pig.  The large bowel has been cut open to reveal the mucosa.  Note the fibrinonecrotic pseudomembrane that is adherent to the mucosa (especially in the lower specimen).  If you were to scrap this pseudomembrane away, it would reveal a severely damaged (e.g. ulcerated) mucosa. Click on the image to see a larger view.

Histopathology:  Microscopic examination of affected intestine should show extensive mucosal damage characterized by necrosis, loss of enterocytes, inflammatory cells, and fibrin (acute enteritis).   To see the lesion, you'll need to click on the image for a larger view.

Clinical Pathology:  A CBC may show leukopenia due to a profound neutropenia, a left shift, toxic changes in neutrophils, and hemoconcentration.  These changes reflect the endotoxemia that typically is a part of acute salmonellosis.  Circulating endotoxin is a result of the invasive gram-negative bacteria as well as absorption of endotoxin from the GI normal flora following loss of the mucosal barrier.  Hyperfibrinogenemia  is noted on blood work 2-3 days post-infection, and is secondary to inflammatory changes in the bowel.

Diagnosis:  In order to diagnose a salmonella infection, the organism must be isolated from feces, blood, or other tissues.  The best tissues to culture include:  the distal small intestine, cecum, colon, Peyer's patches, regional lymph nodes, liver, gall bladder, and lung.  NOTE ON SENSITIVITY:  The organism can be difficult to isolate.  In horses, it is recommended that 3-5 fecal samples be submitted to enhance the chances of a positive culture.  A rule of thumb in horses is that the animal is not considered negative until there have been 5 consecutive negative cultures.   Equine Salmonellosis