There are three Strongylus species that infect horses, Strongylus vulgaris, Strongylus edentatus and Strongylus equinus. Of these only S. vulgaris is considered to be of clinical importance. It is known as the equine ‘bloodworm’ and is one of the most pathogenic parasites in domestic animals. S. edentatus is also known as the ‘flank worm’.
The worms sensitivity to a range of anthelmintics, particularly the macrocyclic lactones, saw a dramatic reduction in these parasites after the release of ivermectin 40 years ago. However, the parasites are not extinct, and have made a reappearance in response to regulated (prescription-only) anthelmintic use in some European countries, where horses may go without any treatment. Ironically, the controlled use of anthelmintics was introduced to prevent parasite resistance.
Life cycles
The life cycles of all three parasites involve amazing migratory phases within the host.
Strongylus vulgaris
Horses ingest infective stage 3 larvae (L3) which burrow into the intestinal walls of the ileum, caecum and large colon. They moult to stage 4 larvae (L4) and then gain access into the small arteriole blood vessel walls. From here they migrate up the arterial system in the intimal layer of the vessel walls to the origins of the cranial mesenteric and celiac arteries. The process of migration from the intestine to the cranial mesenteric artery takes around 14 days.
The larvae stay around the root of cranial mesenteric artery for 4 months. During this time they further moult to stage 5 larvae (L5), around 3 months after ingestion of infective larvae. The L5 larvae are viewed as small adult worms, and move with arterial flow back to the intestine where they form small pea-sized nodules (<1 cm diameter) in the walls of the caecum and ventral large colons. These will eventually rupture into the lumen of the intestine, releasing adults. The adult worms are 1.5 – 2.5 cm long.
The life cycle (prepatent period) takes approximately 6 months (5.5 – 7 months), with most of it spent in the mesenteric arteries (4 months). There may be a seasonal basis to the life cycle with infections occurring in the autumn, migration over winter and peak egg shedding in spring.
Strongylus edentatus
Similar to S. vulgaris horses ingest infective stage 3 larvae (L3), after which they invade the intestinal wall and migrate via the portal blood system to the liver. Within the liver they moult to 4th stage larvae (L4). After migration through liver tissue they parasites exit via the hepatorenal ligament on the right side of the abdomen, and then beneath peritoneal lining to the ventral and lateral abdominal wall muscles (mostly on the right side of the horse) and peri-renal fat. They form parasite nodules, This is why they are referred to as ‘flank’ worms. The young adults then migrate back to the ventral colon, and again similar to S. vulgaris, form nodules which eventually rupture into the lumen release adults. The adults are 2.5 – 4.5 cm in length. This amazing migration results in prepatent period of around 12 months.
Strongylus equinus
After ingestion of infective L3 larvae the parasites invade the wall of the caecum and large colon and moult to 4th stage larvae. There migration path is through the abdominal cavity to the pancreas and finally to the liver. L4 larvae will then spend several weeks moving throughout the liver parenchyma. They then move back to the large intestine, again via the pancreas, and the peritoneal cavity. It is possible to found both L4 and L5 S. equinus larvae free in the peritoneal cavity. They also form nodules in the large intestinal wall which eventually rupture releasing the adults into the lumen. The adults are 2.5 – 4.5 cm in length. The prepatent period of S. equinus is 8-9 months.
Signs of infection
The principle clinical disease is associated with Strongylus vulgaris larvae. As adults in the caecum and large colon all of the large strongyles are capable of causing an inflammatory response and small focal areas of ulceration. In the process they can consume cells, blood and plasma. The loss of nutrients to the animal is minimal as the number of worms are rarely great enough to impact any of the red blood cell or protein indices.
It is the presence of large L5 S. vulgaris larvae at the root of the cranial mesenteric (and other) artery that provides the greatest opportunity for severe disease. The larvae cause a local exudative arteritis, hypertrophy and fibrosis of the artery wall, and thrombi formation within the artery lumen. The enlargement of the cranial mesenteric artery root is known as a verminous aneurysm. It is also possible for L4 migration into other organs such as the kidney or the brain or spinal cord. Verminous meningoencephalomyelitis due to S. vulgaris larvae has also diminished in incidence because of anthelmintic use. A role for S.vulgaris larvae has been postulated in some cases of aortic-iliac thrombosis in horses.
The primary lesions is an infarct or ischemic necrosis to the intestine. The mechanisms responsible for these lesions remains controversial, although the prevailing thought was that bits of thrombi break free, travel down the arterial system and occlude the vasculature supplying the gut. Alternatively, the L5 larvae may occlude vessels when they leave the mesenteric artery. It has also been postulated that vasoconstrictive mediators, such as thromboxane, could be released from the arteritis lesion.
Signs of infection and diagnosis
The result is an acute, non-strangulating colic. The signs can be variable dependent on the area of intestine that is infarcted. Most show signs of acute, persistent abdominal pain (colic) but the intensity can be highly variable. Signs of toxaemia become apparent, including elevated pulse rate, congested mucous membranes with a prolonged CRT, gastrointestinal stasis, and possible increase in rectal temperature. An increase volume of peritoneal fluid is noted on ultrasound, and potentially there may be thickening of bowel if the region of gut affected is imaged. Peritonitis is expected due to leakage across the devitalized serosal surface.
The diagnosis of mesenteric arteritis remains problematic in asymptomatic horses or donkeys. When the disease was common it was possible to palpate a thickened cranial mesenteric artery in some asymptomatic and symptomatic horses on rectal palpation. If the artery was squeezed some horses would buckle, as if experiencing a sharp pain.
Faecal egg counts aren’t reliable as the disease can obviously occur in the absence of egg-producing adults. In addition, the differentiation between large and small strongyle eggs cant be made on a standard faecal flotation.
Treatment and Prevention
Treatment of ischemic bowel disease almost always leads to surgery, euthanasia or spontaneous death.
There have treatments recommended for horses with suspected mesenteric arteritis in the absence of ischemia. In the 1970s the successful treatment of arteritis was declared using low molecular weight dextran, at a dose and frequency of 2.5 ml/kg of 6% dextran 70 in 5% dextrose daily for 3 days, then 500 ml every 4 days until 9 treatments had been administered. The treatment remains unchallenged because of the ‘disappearance’ of the disease.
Based on the Scandinavian experience it is clear that the use an anthelmintic effective against large strongyles once yearly is recommended. This most likely would be a macrocyclic lactone, such as ivermectin, abamectin, or moxidectin.
Tags: Parasites; Gastrointestinal diseases