19 Mar 2024
Zoë Gratwick considers the causes behind this pronounced change and how to effectively identify them.
Image © encierro / Adobe Stock
A number of common causes of weight loss exist in horses in the UK – particularly parasitism, equine gastric ulcer syndrome (EGUS), liver disease and pituitary pars intermedia dysfunction (PPID).
However, to ensure that all contributing factors are identified, thinking broadly about the possibilities is recommended – especially at the history taking and clinical examination stages.
The following factors can lead to weight loss:
Factors affecting access to nutrition can include:
Factors physically affecting nutritional intake can include:
Factors affecting digestion or absorption can include:
Factors increasing nutritional demands can include:
With cachexia, skeletal muscle loss occurs, which might be accompanied by fat loss. Metabolism is abnormal and appetite is reduced. Multiple mechanisms exist.
Weight loss cannot be fully corrected by adequate nutritional provision. Cachexia is most often seen due to neoplasia, chronic renal failure or cardiac failure.
Primary muscle loss occurs due to:
In most cases, the initial route of investigation will be guided by the signalment, clinical history, examination findings and consideration of the previously described factors.
Collection of a comprehensive clinical history will enable the most efficient investigation. This increases the likelihood of a quick and cost-effective diagnosis. Questions investigating the possibilities raised in this article can be informative.
A number of factors that could be seen during clinical examination can point towards the reason for weight loss.
In addition to assessment of vital parameters and cardiopulmonary auscultation, consideration of the following factors could also be useful.
Watching the horse eat both its usual roughage and any concentrates it receives will provide information about the ability to prehend, masticate and swallow. Particularly if any of these appear abnormal, then oral examination would be advisable.
A faecal egg count will often offer insight regarding ascarid and strongyle infections.
Although faecal egg counts are not a reliable method for the detection of ascarids, a better laboratory-based alternative does not exist. Encysted cyathostomins should not be excluded by a low faecal egg count. If moxidectin therapy has been given in the past six months, and a low faecal egg count is observed, a relevant cyathostomin burden is unlikely (although, not impossible). Cyathostomin serology can be useful in some cases with a low faecal egg count.
The antibodies measured are to both luminal and encysted stages. The test is highly sensitive for the detection of large burdens; therefore, a low result makes a large burden unlikely. However, it must be considered that ELISAs rely on antibody formation, and this may be reduced in animals affected by certain conditions. Immunoglobulin G loss may occur in animals with severe protein-losing processes (this is also applicable to tapeworm serology). Use of the test is not recommended within four months of anthelmintic treatment, as antibody levels take a while to reduce following successful treatment.
Furthermore, not all animals with high scores will develop disease, and a high serological score does not guarantee that cyathostomins are the cause of disease.
Faecal flotation has a low sensitivity for the detection of tapeworm infections, although it is actually good for the detection of heavy burdens. If a relevant anthelmintic has not been given in the past four months, then an ELISA may offer further insight about the likelihood of a significant burden.
Serum biochemistry may offer guiding insight. Hypoalbuminaemia is most often associated with a protein-losing enteropathy, although renal or third-space losses are also possibilities.
A concurrent increase in alkaline phosphatase (ALP) would add further support for intestinal disease – especially if in the context of loose faeces or colic signs.
Increases in glutamate dehydrogenase, gamma-glutamyl transferase, ALP or aspartate aminotransferase (AST) may be hepatic in origin. If hepatic function is compromised, serum bile acids and occasionally serum bilirubin concentration may also be increased.
Increases in creatine kinase (CK) and AST can be of skeletal muscle origin, although, in some conditions – such as polysaccharide storage myopathy type 1 and polysaccharide storage myopathy type 2 – CK and AST levels are not always increased.
Minor, incidental increases in CK concentration are common, but quickly resolve and do not typically exceed 1,000U/L. Mild increases are often seen secondary to muscle mobilisation during weight loss. Persistent or recurrent increases, even if mild, can be indicators of muscle disease.
If azotaemia is observed then further investigation for renal disease is always advisable. However, serum biochemistry is a poorly sensitive test for the identification of renal disease. If any reason exists to suspect this, then urinalysis is advised.
Horses with PPID are not always geriatric. PPID can be a consideration in horses from seven years of age onwards.
Signs can include lethargy, decreased muscle mass, fat redistribution, hypertrichosis, abnormal sweating, recurrent infections, delayed healing, and increased thirst and urination. Often – especially in younger animals – not all such signs will be present.
By the time disease is advanced enough for an overall impression of weight loss to be evident, most cases will have increased adrenocorticotropic hormone (ACTH) concentrations. However, in some cases, a thyrotropin-releasing hormone (TRH) stimulation test may be worth consideration, as this is a more sensitive test than basal ACTH.
This involves the administration of 1mg TRH intravenously, followed by measurement of chilled plasma ACTH 10 minutes later.
For animals weighing less than 250kg, 0.5mg TRH may be used.
Gastroscopy is advisable in many cases affected by weight loss. Even if EGUS is not the primary disease process, secondary ulceration can be significant. It is advised that EGUS is not excluded by the horse’s signalment.
Anecdotally, such lesions can be missed by being thought unlikely; for example, in a riding school pony versus a racing Thoroughbred.
Gastric disease is often present in horses with inflammatory intestinal diseases. Occasionally, other gastric pathology, such as neoplasia or foreign bodies, might be detected during gastroscopy.
Abdominal ultrasonography can be useful in a variety of cases affected by weight loss. In some instances, serum biochemistry may prompt further assessment of a specific area (for example, the liver or intestine).
In other instances, ultrasonography may be used to look for the presence of abnormalities when the reason for weight loss is unknown. Rectal palpation may also enable identification of abnormalities.
Ultrasonography can help to identify when biliary obstruction or a focal lesion is present. It may also demonstrate an end stage appearance (small hyperechoic liver). Biopsy histology may enable a definitive diagnosis, facilitating the best prognosis. However, this is not always the case. In such scenarios, it may still be useful, as it can offer insight about prognosis. Biopsy tissue culture sometimes offers additional useful information. Feed can be tested for mycotoxins. Both serology and faecal sedimentation testing can help to confirm exposure to, or the presence of, Fasciola hepatica.
However, results of both can be negative in some affected animals. When the animal lives with other horses, assessment of hepatic enzyme concentrations in these other animals can be useful.
This is not only to guide their management, but if enzyme concentrations are increased in some or all animals, this can help to narrow down the differential diagnosis list. When only some animals are affected, identifying the management factors in common can be helpful.
Causes of liver disease that could lead to weight loss include:
To optimise the likelihood of sustained clinical improvement, identifying the underlying reason for intestinal disease is important. Protein-losing intestinal disease – also known as protein-losing enteropathy – is not synonymous with idiopathic inflammatory bowel disease (idiopathic IBD).
Idiopathic IBD is not well defined in horses, but tends to be used to describe inflammation of the intestine of unknown origin, which is associated with recurrent or chronic colic, diarrhoea or weight loss. This can only be presumed when the more specific reasons for these signs have been excluded.
It is thought that idiopathic IBD is due to an abnormal immune response to unidentified antigens, leading to intestinal inflammation. One case of equine gluten-associated enteropathy has been reported. Testing for this is not commonplace, and it seems likely that IBD secondary to gluten or other dietary antigens is underdiagnosed.
Please see “Parasite-associated diagnostics” for information regarding cyathostomins. Chronic salmonellosis can cause significant weight loss. This is typically accompanied by diarrhoea. Ideally, three to five faecal cultures are recommended when attempting to confirm or refute infection with a Salmonella species.
Enriched faecal PCR may be considered as an alternative. The exact number to recommend is unclear, but exclusion based on a single result is not advised.
When present in the intestine, sand can lead to a variety of presentations. These include weight loss, colic (can be recurrent), and either acute or chronic diarrhoea. It can also be present without causing clinical signs. In these cases, sand is sometimes detectable in the faeces by faecal sand sedimentation testing, although its presence in the faeces can be intermittent. Sand may also be audible when auscultating the ventral abdomen, caudal to the sternum. It can often also be visualised ultrasonographically.
Further insights about the relevance of any sand detected can be gained from the amount of sand seen radiographically.
Lymphoma is by far the most prevalent form of equine intestinal neoplasia. A variety of primary tumours can also occur. Findings may include: weight loss, acute or recurrent colic, inappetence, lethargy, pyrexia and paraneoplastic syndromes. All age groups can be affected.
Diagnosis can be challenging. In some cases, cytological examination of needle aspirates obtained from enlarged lymph nodes, or abnormalities (for example, in the spleen), will offer a diagnosis. Peritoneal fluid cytology can occasionally also be useful.
Definitive diagnosis is frequently only achievable by tissue histology of biopsy samples obtained via laparoscopy or laparotomy. Occasionally, this may be achievable by rectal mucosal biopsy sampling, or biopsy via a gastroscope.
Cause of chronic protein-losing intestinal disease can include:
1. When investigating weight loss, consider the following possibilities:
2. If intestinal disease is present, investigate the cause when possible.