Allen E. Page
Screening Herds for Lawsonia
As a clinical entity, equine proliferative enteropathy (EPE) caused by Lawsonia intracellularis infection in horses has been recognized for more than 30 years; however, it is mostly within the past 10 to 15 years that this disease has received an increased level of attention. Primarily a disease of weanlings and young yearlings, EPE has been anecdotally reported as increasing in incidence with time. Unpublished data, however, show that the incidence has remained the same, suggesting that improved recognition of EPE has resulted in a perceived increase in the incidence. Given the increased notoriety of EPE, the nonspecific clinical signs typically seen with the disease (anorexia, depression or lethargy, dependent edema, weight loss, unthrifty appearance, fever, colic, and diarrhea), and the suggestion that previously affected horses sell for significantly less at public auction as yearlings, many horse farms have opted to screen weanlings and yearlings for exposure to L intracellularis or signs of EPE in an attempt to prevent or blunt the severity of clinical disease.
Abdominal Ultrasonography
A hallmark of the proliferative enteropathies caused by L intracellularis is mucosal hyperplasia, which is often confined to the ileum or terminal jejunum in horses. Abdominal ultrasonography can be a useful diagnostic test. In the author’s experience, routine ultrasonographic evaluation of the abdomen with a curved convex or microconvex probe should provide enough detail and depth to examine most of the abdominal cavity. A linear rectal probe can also be used, although it may be difficult to achieve enough detail and depth for adequate examination. Small intestine wall thickness in excess of 3 mm anywhere in the abdominal cavity of young horses should be considered suggestive of EPE even in the absence of clinical signs, and increased wall thickness can likely be considered diagnostic for EPE when accompanied by compatible clinical or clinicopathologic signs.
Care should be exercised when no small intestine wall thickening is observed sonographically, because clinical EPE has been reported in horses in which intestinal wall thickness was within normal limits. No work in horses has conclusively documented the relationship between the onset of detectable increases in small intestine wall thickness and clinical signs of EPE. Thus it is possible that clinical signs of EPE and increased intestinal wall thickness develop simultaneously, preventing ultrasonographic screening from providing any real benefit. Given the likely cost, as well as the lower sensitivity, of this procedure, it is recommended that abdominal ultrasonography be used more as a confirmatory diagnostic test and not a herd screening tool.
Clinicopathologic Changes
In horses, it is well reported that hypoalbuminemia and, by extension, hypoproteinemia, are nonspecific but highly suggestive changes of EPE. These changes likely reflect both protein loss and malabsorption in the affected small intestine. Total protein and albumin concentrations can decrease rapidly, over a span of 4 to 7 days. For total protein or albumin analysis to be a viable option with regard to EPE screening, the method requires screening one or both of the markers at least once per week, and preferably biweekly. This frequent screening can become cost prohibitive if screening is to involve a large number of horses over the course of several months. However, total protein can be readily measured by farm personnel using refractometry, which provides a rapid and inexpensive method for EPE screening. Although reference ranges will vary with the population, total protein concentrations below 5.5 mg/dL and albumin concentrations below 2.8 to 3.0 mg/dL should be considered hypoproteinemic and hypoalbuminemic, respectively. It is important to note that there are a number of conditions, including renal disease, colitis, salmonellosis, and intestinal parasites, that can cause decreases in albumin concentrations, so it is recommended that horses with low total protein or albumin be screened with additional diagnostic tests.
With regard to other clinicopathologic tests, including biochemistry panels, complete blood counts, and fibrinogen levels, none are typically considered useful for EPE screening. This is largely because routine clinical cases of EPE are devoid of a detectable inflammatory response and the L intracellularis infection is primarily localized to the intestinal enterocytes. Further, in uncomplicated cases of EPE, metabolic derangements are rare unless the horse has severe diarrhea, the infection is chronic, or there is concurrent disease.
Fecal Polymerase Chain Reaction Testing
Fecal polymerase chain reaction (PCR) testing for L intracellularis is probably the most specific test available in that it detects sequences of DNA unique to the bacterium. Unlike serologic tests (discussed later), L intracellularis PCR tests are not species specific. Issues arise, however, with L intracellularis PCR in that the bacterium appears to be intermittently shed by infected horses and there are a variety of PCR inhibitors in feces. Additionally, antimicrobial administration before the collection of feces further decreases the sensitivity of the assay.
Previous work with weanlings on an EPE-endemic farm revealed that bimonthly collection of feces for L intracellularis PCR was not sufficient, on its own, to screen the herd for EPE. Although a more frequent collection schedule might increase the chances of detecting the organism in feces, the cost of this would be prohibitive and the investment would be better spent on total protein or albumin screening, or on serology. As with abdominal ultrasonography, fecal PCR for L intracellularis is likely best performed as a confirmatory test while taking into account the possibility for false-negative results. For a horse found to be fecal PCR positive for the bacterium and yet free of clinical EPE, it is recommended that a standard course of antimicrobials be initiated to prevent the occurrence of clinical EPE and to combat the infection.
