Investigation and Management of Weight Loss in Horses

By Zoë Gratwick


EBVS® European Specialist and RCVS Recognised Specialist in Equine Internal Medicine

Causes of weight loss

There are a number of common causes of weight loss in horses, particularly parasitism, equine gastric ulcer syndrome (EGUS), liver disease and pituitary pars intermedia dysfunction PPID. However, in order to ensure that all contributing factors are efficiently identified, broader consideration and thinking about each case in a systematic way is recommended. The following should be considered:

  1. Factors affecting access to nutrition

  2. Factors physically affecting intake or absorption of nutrition

  3. Factors increasing nutritional demands

  4. Factors leading to altered metabolism causing cachexia

Primary muscle loss

1) Factors affecting access to nutrition can include:

  • Inadequate feed provision

  • Unpalatable food being declined (e.g. poor quality, mouldy or contaminated)

  • Appetite being affected by pain, pyrexia or fear

  • Difficulty accessing food e.g. hayrack space, bullying, lameness or neck pain

2a) Factors physically affecting nutritional intake can include:

Decreased prehension due to:

  • Reduced lip function

  • Neurological

  • Local lesions

Decreased mastication due to:

  • Dental pathology

  • Oral soft tissue lesions

  • Masseter muscle disease

  • Temporomandibular joint disease

Decreased swallowing ability due to:

  • Lesions of the tongue, pharynx or oesophagus

  • Neurological dysfunction

2b) Factors affecting digestion and absorption can include:

  • Diseases causing reduced gastric function

  • Diseases affecting hepatic and pancreatic function

  • Diseases affecting intestinal mucosal health and transit

3) Factors increasing nutritional demands can include:


  • Exercise

  • Late gestation

  • Early lactation

Pathologic for example:

  • Severe respiratory disease e.g. severe equine asthma (involves a significant amount of physical work of breathing)

  • Sepsis

  • Some neoplastic diseases

4) Factors leading to altered metabolism causing cachexia

With cachexia skeletal muscle loss occurs, which might be accompanied by fat loss. Metabolism is abnormal and appetite is reduced. There are multiple mechanisms. Activity of catabolic inflammatory cytokines, physiologic stress or pain can lead to catecholamine and cortisol production, which leads to catabolism. Weight loss cannot be fully corrected by adequate nutritional provision. Cachexia is most often seen due to neoplasia, chronic renal failure or cardiac failure.

5) Primary muscle loss This can be seen due to:

  • Disuse

  • Neurogenic wasting e.g. equine motor neurone disease

  • Primary muscle disease e.g. polysaccharide storage myopathy

  • PPID

Causes of liver disease in horses can include:

  • Toxic plants

  • Mycotoxins

  • Bacteria

  • Viruses

  • Fasciola hepatica

  • Metabolic disease (leading to hepatic lipidosis)

  • Neoplasia

  • Infiltrative disease (e.g. Multisystemic eosinophilic epitheliotropic disease (MEED)

Heavy metals Cause of chronic protein losing intestinal disease can include:

  • Encysted cyathostomins

  • Salmonella spp

  • Idiopathic inflammatory bowel disease

  • Gluten sensitivity

  • Neoplasia

  • Sand

  • Non-steroidal anti-inflammatory drug (NSAID) toxicosis

  • Mercury toxicosis (rare)

  • Aluminium (rare)

  • Mycobacterial infection (rare)

Investigating weight loss

In most cases the initial route of investigation will be guided by the signalment, clinical history, examination findings and consideration of the above factors. Information about some of the diagnostics which might be useful is provided below.

Parasite-associated diagnostics

A faecal egg count will often offer insights regarding ascarid and strongyle infections. However, encysted cyathostomin burdens should not be excluded by a low faecal egg count. If moxidectin therapy has been given in the last six months and a low faecal egg count is observed, a relevant burden would be considered unlikely (although not impossible). Cyathostomin serology can be useful in some cases with a low faecal egg count.

Use of the test is not recommended within four months of anthelmintic treatment as antibody levels take a while to reduce following successful treatment. The antibodies measured are not only to encysted stages. The test is highly sensitive (>90%) for high burdens, therefore a low result makes a high burden unlikely. However, it must be considered that ELISAs rely on antibody formation and this may be reduced in animals affected by certain conditions. IgG loss may occur in animals with severe protein losing processes (this is also applicable to tapeworm serology). 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. The manufacturers advise that the primary role of the tests is for animals with low management risks and low faecal egg counts, to give confidence to abstain from routine anthelmintic therapy (as was previously customary in the autumn in the UK).

Ascarid egg counts in particular are thought to be poorly correlated with the level of burden. Faecal flotation has a low sensitivity for the detection of tapeworm infections, although it is actually relatively good for the detection of heavy burdens. If relevant anthelmintics have not been given in the last five months, then an ELISA may offer further insight about the likelihood of a significant burden.

Faecal Salmonella testing

Chronic salmonellosis can cause significant weight loss. This is typically accompanied by diarrhoea. Ideally= 3-5 separate faecal cultures are recommended when attempting to confirm or refute infection with a Salmonella sp. 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.

Serum biochemistry

Serum biochemistry may offer guiding insights. Hypoalbuminaemia is most often associated with a protein losing enteropathy, although malabsorption, or renal or third space losses are also possibilities. A concurrent increase in ALP would add further support for intestinal disease, especially if in the context of loose faeces or colic signs. Increases in GLDH, GGT, ALP or 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 CK and AST can be of skeletal muscle origin, although in some conditions such as polysaccharide storage myopathy type 1 (PSSM-1) and polysaccharide storage myopathy type 2 (PSSM-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 1000 U/L. 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 weak test for renal disease. If there is any reason to suspect this, then urinalysis is advised.

Assessment for PPID

Measurement of chilled plasma ACTH will enable detection of PPID in approximately 75% of cases. 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 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 ACTH concentrations. However, in some cases a TRH stimulation test may be worth consideration, as 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 <250kg 0.5mg TRH may be used.


In many cases affected by weight loss gastroscopy is advisable. 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 ulceration is often present in horses with inflammatory intestinal diseases. In addition to EGUS, other gastric pathology such as neoplasia, foreign body or impaction might be detected by gastroscopy.

Abdominal ultrasonography

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 e.g. the liver or intestine, in other instances it 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.

Assessment of liver disease

In the investigation of hepatic disease ultrasonography can help to identify whether biliary obstruction or a focal lesion are 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 often not this case. In such scenarios it may still be useful, as it can offer insights about prognosis. Biopsy tissue culture sometimes offers additional useful information. Feed can be tested for mycotoxins. Both serology and faecal sedimentation technique can help to confirm exposure/ the presence of F. hepatica, however both can be negative in some affected animals.

Assessment for sand enteropathy

When present in the intestine, 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. The presence of sand in the faeces doesn’t guarantee that it is playing a role in the clinical signs. Further insights can be gained from the amount of sand seen radiographically and the presence of serum biochemistry findings that support intestinal disease.

Management of weight loss

The management of weight loss will depend upon the underlying cause. When possible, specific management of the underlying disease process is usually indicated. Furthermore, management changes and additional supportive care may be required. It is important that nutritional support is not excessive, as additional secondary complications could result.


Management by lifelong pergolide therapy is typically effective. In some instances, clinical signs may be inadequately controlled by pergolide, and in such cases, twice daily dosing (off license) can sometimes be beneficial. The addition of cyproheptadine therapy can also be helpful in refractory cases. Although, sedation can occur, which can affect safety to ride. Cabergoline injections can sometimes be an alternative solution in refractory cases. Concurrent disease is common in animals with PPID. This should always be considered, enabling management of any current issues.


When managing liver disease, if a particular cause is evident then specific management strategies or therapies may be able to be adopted. Triclabendazole therapy is often effective for F. hepatica infection. Hepatic lipid deposition is primarily managed through obesity management and supportive care. Bacterial cholangiohepatitis is rare in adult horses. When it occurs, it is usually secondary and management of the primary condition as well as targeted protracted antimicrobial therapy are usually required. In cases where toxic exposure is identified the removal of the source is paramount. Although there is anecdotal support, published evidence for most hepatic support supplements is lacking. In cases with chronic active (often idiopathic) hepatitis corticosteroids might be beneficial. These are contraindicated in animals with hepatic lipidosis.

Equine gastric ulcer syndrome

Equine squamous gastric disease is typically well managed using oral omeprazole therapy alone, with around 75% cases resolving in 28 days. The optimal therapy for equine glandular gastric disease continues to be debated. Responses to oral omeprazole monotherapy are poor. Options include combination therapy using oral omeprazole with sucralfate, injectable omeprazole either alone, or with sucralfate or misoprostol. Corticosteroid therapy may be of benefit in cases thought to be associated with idiopathic inflammatory bowel disease (idiopathic IBD).

Pasture turnout is considered to reduce the risk of EGUS (although evidence supporting this belief is conflicting). Constant access to roughage is widely considered to reduce gastric ulceration risk. Feeding more than 2 g/kg of starch per day is associated with approximately twice the likelihood of equine squamous gastric disease grade ≥2/5. Furthermore, feeding less than 1 g/kg bodyweight of starch per meal is advised.

Inflammatory intestinal diseases

If the reason for disease can be identified, then specific treatment might be an option.

Sand enteropathy can be treated using 1g/kg psyllium and 1g/kg MgSO4 via nasogastric tube, once daily for 4 days, followed by subsequent in feed supplementation. A study looking at repeated doses of MgSO4 for the treatment of non-sand large colon impactions found that animals can develop signs of magnesium toxicity at the above dose, therefore 0.5g/kg might be preferable. Rare cases of gastric rupture have been reported following high doses of psyllium, therefore ideally at least four hours without access to feed is recommended beforehand. Horses can colic as the sand moves, so administration of analgesia can be considered at the time of intubation.

When it comes to the nutritional management of sand enteropathy it is very important to prevent further access to sand.

In cases with a cyathostomin burden moxidectin treatment is recommended, unless the animal has a BCS ≤ 1/5. In these cases, ivermectin therapy (won’t treat as many larval stages as moxidectin), or five days of fenbendazole therapy (widespread resistance) is recommended in the first instance. The following management changes could be worthwhile:

  • Poo picking at least twice weekly

  • Keeping the muck heap away from grazing areas

  • Ruminant co-grazing

  • High egg shedders being kept separately

  • Underlying health conditions being managed (also recommended form a welfare perspective)

In animals affected by NSAID toxicity NSAIDs should be discontinued. Misoprostol therapy might be beneficial. This must not be handled by pregnant women, or used in pregnant mares.

In animals suspected of having gluten sensitivity gluten should be removed from the diet.

Clear treatment recommendations for most equine inflammatory intestinal diseases are not available. Infectious or irritant causes should always be considered before presuming that inflammation is idiopathic. For idiopathic cases, corticosteroid therapy represents a mainstay, but its efficacy is variable. One study demonstrated a 65% survival rate at three years in cases that had received anthelmintic and corticosteroid therapy. In some cases, the T cell inhibitor azathioprine has been suggested to be a beneficial adjunct. Recently the “anti-metabolite” methotrexate has begun to be discussed for its use in immune meditated conditions. There may be a place for it in the management of some idiopathic IBD cases and it is not known to be associated with an increased risk of laminitis.

Adlib good quality, palatable roughage is usually recommended. Short, soft roughage may decrease the risk of risk of impactions in horses with concurrent recurrent colic signs. Provision of a vitamin and mineral balancer or concentrates is also recommended. If concentrates are given, then excess starch should be avoided and high protein and high fat feeds (slowly introduced) are recommended. Using stabilised rice bran as a component of a balanced diet can be a helpful source of moderately soluble fibre and fat.

Key points

1. Take a systematic approach to investigating weight loss:

  1. Reduced access to nutrition

  2. Reduced intake or absorption of nutrition

  3. Factors increasing nutritional demands

  4. Altered metabolism causing cachexia

  5. Primary muscle loss

2. If there’s intestinal disease, investigate the cause

3. Effective management often includes:

– Specific therapy

– Non-specific therapy

– Management changes/supportive care

Investigation and management of weight loss in horses

Watch Here