Bacterial infection of the small intestines (bacterial enteritis) of foals can be caused by a variety of different bacteria, and the severity of the disease can range from mild self-limiting disease, to acute onset severe illness, to insidious onset protracted disease.
Bacterial enteritis in foals predominantly occurs in two subsets of foals, defined by age:
- Acute onset of infection in neonatal foals – when the neonatal immune system is immature, and especially when the immune system is incompletely primed by the failure to ingest colostrum.
- Chronic infection of the intestinal tract of older foals (4-10 months) – by intracellular bacteria.
Pathophysiology & Presentation of Bacterial Enteritis in Foals
In Neonatal Foals
The newborn foal is particularly at risk of bacterial enteritis during the first 24-hour period when the foal is learning how to nurse from the mare. The initial clumsy attempts can involve sucking on the flank or belly of the mare, or even on objects in the environment. Pathogenic bacteria present in the environment may be ingested, and if the foal has not yet ingested the protective colostrum, these pathogenic bacteria can quickly wreak havoc on the intestinal mucosa.
Strains of bacteria that are frequently implicated in the development of neonatal enteritis include Escherichia coli, Salmonella sp., Clostridium perfringens and Clostridium difficile. Other possible harmful bacteria include Bacteroides fragilis, and species of Campylobacter, Enterococcus and Aeromonas.
Each of these bacteria have different strategies and different toxins that work on the intestinal mucosa to cause one or more of the following effects:
- Hypersecretion
- Inflammation
- Destruction of the absorptive microvilli (brush border)
- Invasion of the mucosa
- Mechanical disturbances to smooth muscle function
- Disintegration of mucosal tight junctions
- Breakdown of the cytoskeleton
- Formation of pores that leak electrolytes and fluids
- Increased permeability of blood vessels
For some of these bacteria, the toxins and their effect have been identified (Table 1), however this is an area of ongoing research for almost all of the bacteria. For example, NetF has recently been identified as the primary virulence factor of foal necrotizing enteritis (Gohari, 2016); this research also suggests that the current typing system for C. perfringens is inadequate.
In some foals, more than one bacteria is involved in the development of enteritis, or another infectious agent such as Coronavirus, Rotavirus or Cryptosporidia is also present, and these agents can either be the initial instigators of mucosal trauma or they can exacerbate the problem.
The clinical signs shown by the foal will be influenced by the severity and extent of the inflammation and damage within the small intestine. The infection may also extend into the large intestine, resulting in enterocolitis.
Table 1: Some known bacterial toxins and their actions on the small intestinal mucosa
| Bacteria | Known Toxin | Effect of Toxin |
|---|---|---|
| Escherichia coli | Enterotoxin Other toxins, i.e. Shiga toxin | Hypersecretion Mucosal invasion and inflammation Destruction of microvilli |
| Salmonella sp. | A variety of virulence factors, still being researched | Hypersecretion Invasion of mucosa Inflammation Destruction of absorptive surface |
| Clostridium perfringens | Net F toxin Alpha, beta, epsilon, iota and cpe toxin, plus others | Pore-forming Variety of effects including inflammation, disruption of intracellular processes, destruction of mucosal cells |
| Clostridium difficile | Toxin B Toxin A, acting synergistically with B | Electromechanical disturbances to small intestinal smooth muscle Invasion of mucosa and disruption of intracellular enzymatic processes |
| Bacteroides fragilis | BFT (Bacteroides Fragilis Toxin) | Hypersecretion Alteration of cellular morphology |
| Campylobacter | CdtA,B,C | Cell cycle control and induction of host cell apoptosis |
| Bacteria | Known Toxin | Effect of Toxin |
|---|---|---|
| Escherichia coli | Enterotoxin Other toxins, i.e. Shiga toxin | Hypersecretion Mucosal invasion and inflammation Destruction of microvilli |
| Salmonella sp. | A variety of virulence factors, still being researched | Hypersecretion Invasion of mucosa Inflammation Destruction of absorptive surface |
| Clostridium perfringens | Net F toxin Alpha, beta, epsilon, iota and cpe toxin, plus others | Pore-forming Variety of effects including inflammation, disruption of intracellular processes, destruction of mucosal cells |
| Clostridium difficile | Toxin B Toxin A, acting synergistically with B | Electromechanical disturbances to small intestinal smooth muscle Invasion of mucosa and disruption of intracellular enzymatic processes |
| Bacteroides fragilis | BFT (Bacteroides Fragilis Toxin) | Hypersecretion Alteration of cellular morphology |
| Campylobacter | CdtA,B,C | Cell cycle control and induction of host cell apoptosis |
Older Foals
The same bacteria that affect the neonates can also affect older foals, especially if a particularly virulent strain of bacteria is ingested, or if a concurrent virus or cryptosporidial infection has weakened the mucosal defenses, or if stress, helminth infestation or other disease weakens the foal’s immune system.
Other bacteria that can specifically affect older foals include the intracellular specialists Lawsonia intracellularis and Rhodococcus equi.
In Australia, Iran and Japan, the spirochete Brachyspira has also been linked to an enterocolitis syndrome in young horses, however there have only been rare reports of this disease, and the link is not yet clear.
Lawsonia intracellularis is a bacteria that most frequently causes disease in foals between the age of 4-7 months. This intracellular bacteria will preferentially invade the ileum where it causes proliferation of an abnormal population of enterocytes. This proliferation alters the architecture of the intestinal mucosa and results in malabsorption of nutrients. This syndrome is called Equine Proliferative Enteropathy (Slovis, 2014).
Rhodococcus equi is another intracellular bacteria that can cause infection of the intestinal tract of older foals, although less commonly than L. intracellularis. Infection with R.equi is more frequently associated with the formation of lung abscesses in older foals, however occasionally it may also cause multifocal ulcerative enterocolitis and granulomatous inflammation of abdominal lymph nodes (Magdesian, 2008).
Clinical Signs of Bacterial Enteritis in Foals
The symptoms of enteritis in neonatal foals can vary greatly and may include:
- Behavioral signs: lethargy, depressed behavior, not nursing well
- +/- Diarrhea: mild to severe; watery to bloody
- Fever
- Colic symptoms that range from mild to severe and may include abdominal bloating caused by fluid and/or gas accumulation
- Gastric reflux
- Dehydration and electrolyte derangements
- Potentially rapid deterioration to septicemia and multiple organ dysfunction
- Weight loss, with prolonged disease
The symptoms of enteritis in older foals may include many of the above, but the more insidious nature of L. intracllularis and R.equi more commonly lead to clinical signs such as:
- Weight loss
- Ill-thrift: rough hair coat, failure to thrive
- Weakness
- Intermittent fever
- Peripheral edema
Diagnosis of Bacterial Enteritis in Foals
Diagnostics tests include:
- Faecal analysis
- Worm egg count +/- larval culture
- Bacterial culture and virus isolation
- PCR analysis for the presence of bacteria and bacterial toxins, viruses and cryptosporidium
- Detect the presence of blood (albumin) and protein (SUCCEED Equine Fecal Blood Test)
- Blood tests – to look for signs of protein loss, blood loss and systemic infection and disease.
- Abdominal Ultrasound – L. intracellularis infections tend to show a distinct thickening of the wall of the small intestine. For other bacteria the changes can be more variable, but ultrasound may reveal thickened or edematous intestinal wall, hypo- or hypermobility, gas or fluid distention and possibly an increased amount of peritoneal fluid.
- Thoracic ultrasound and radiographs – if R.equi is suspected.
Fecal culture, toxin analysis and PCR analysis can help identify some of the causes of enteritis, although these tests need to be interpreted with the knowledge that many of the bacteria that are capable of inducing enteritis in foals are also bacteria commonly found in the environment, especially E. coli and the Clostridial organisms. The presence of pathogenic toxins may indicate whether the bacteria are the source of the problem or not.
If Salmonella is identified, it is generally presumed to be pathogenic in foals.
R.equi is especially difficult to identify as the causative agent, as it does not have toxins that can be identified, and it is frequently passed in manure. If a foal has a history of exposure to R.equi, is showing signs of disease and perhaps evidence of concurrent lung infection, and if the intestines look thickened on ultrasound, the R.equi can be considered a potential cause.
If L. intracellularis is identified in feces, it should generally be suspected as the cause of the problem, especially in a foal with weight loss, hypoproteinemia and thickened small intestines on ultrasound.
The SUCCEED Equine Fecal Blood Test may help to determine the severity of the bacterial infection. If blood and protein (albumin) are present in the feces, then the foal will have significant damage to the intestinal wall and should be monitored closely, as prolonged antimicrobial coverage and supplemental nutrition may be required.
Treatment for Bacterial Enteritis in Foals
Treatment of bacterial enteritis will depend on the bacteria identified, or at least suspected to be the causative agent. In general, treatment will involve some or all of the following:
- Antibiotics:
- In neonatal foals, broad-spectrum antibiotics are usually indicated, both to treat the intestinal infection and also to treat any opportunistic bacteria that may access the systemic circulation through the inflamed intestinal wall.
- R.equi is treated with a combination of a macrolide and rifampin.
- L. intracellularis infections usually respond to doxycycline, oxytetracycline or chloramphenicol.
- Fluid therapy for dehydration and electrolyte replacement.
- Plasma or hyperimmune plasma – to help replace protein loss, and to provide immunologic assistance. In some areas, plasma is available that has concentrated antibodies against certain bacteria such as E. coli, Salmonella, and R.equi.
- Gastrointestinal support
- Some neonates may require Lactase administration to assist with milk digestion, especially if the brush border has been damaged or destroyed.
- Foals that have been inappetent should be considered at risk of gastric ulceration, and treated appropriately.
- Nutritional support – some foals may require administration of total or partial parenteral nutrition. Older foals that are partially or completely weaned may require supplementation with an easily digestible diet (i.e. pelleted feed) while their intestinal tract is recuperating.
Prevention of Bacterial Enteritis in Foals
In neonatal foals, prevention of disease includes the following:
- Ensure the environment is clean, with minimal contamination from potential infectious sources such as manure and stagnant water.
- Ensure the mare is as clean as possible while the foal is learning to nurse.
- Ensure that the foal receives adequate colostrum, and if not, supplement the foal with hyperimmune plasma, and seriously consider prophylactic administration of antibiotics.
- Prevent exposure of the foal to other sick animals.
In older foals:
- Minimize the amount of stress they experience (i.e. during weaning).
- Ensure they are fed good quality diets, especially during the stressful weaning period.
- If R. equi or L. intracellularis are known problems in the region, then be vigilant for early clinic signs of disease, and consider monitoring the foals for the presence of disease through fecal analysis, blood tests, serology and abdominal ultrasound.
References:
- Arroyo, L.G., et al. (2006) Potential role of Clostridium difficile as a cause of duodenitis-proximal jejunitis in horses. J Medical Microbiology, 55:605-608.
- Barton, M. (2001) Endotoxemia: The Movie. Dorothy R. Havemeyer Foundation Neonatal Septicemia Workshop. http://www.havemeyerfoundation.org/nsw/III-02-Barton.htm
- Gohari, I.M., et al. (2016) Plasmid Characterization and Chromosome Analysis of Two netF+ Clostridium perfringens Isolates Associated with Foal and Canine Necrotizing Enteritis. PloS one
Knottenbelt, D. et al. (2004) Equine Neonatology, Medicine and Surgery. Elsevier Health Sciences pp. 232. - Magdesian, G. (2008) Inflammatory Bowel Disease in Foals. In: Current Therapy in Equine Medicine 6, chapter 188 ed: AT Blikslager; book ed: N.E. Robinson. Saunders, St Louis Missouri pp. 872-873
- Slovis, N.A. (2014) Lawsonia intracellularis Proliferative Enteropathy in Foals. AAEP Focus on the First Year of Life Proceedings. http://www.aaep.org
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