Equine gastro parasites Flashcards
what are the shape, site and clinical signs of small strongles (cyathostomins)?
small and red or white
large instestine
- ill thrift
- colic
- D+++ (ealry L3)
what are the shape, site and clinical signs of large strongles?
a bit bigger but still quite small, red or white
large intestine
- ill thrift
- blood vessle wall damamge, haemorrhage and infarction - S. vulgaris (adn others but to lesser extent)
what are the shape, site and clinical signs of parascaris equorum (round worms)?
large (up to 10cm), fat and white
small intestine
- ill thrift
- colic in large numbers due to physical small intestine obstruction
- cough ++
what are the shape, site and clinical signs of oxyuris equi (pinworm)?
up to 5cm, white, pointy tail like a bean sprout
rectum
- itchy bottom
what are the shape, site and clinical signs of anaplocephala magnum and perfolata (tapeworm)?
small flat white
ileocaecal area (perfoliata), small intestine (magna)
- ill thrift
- colic ++
what species of worm is the stomach worm in horses?
how are they transmited?
what are the clinical signs?
how can they be diagnosed?
what is the prevention?
Habronema spp. - stomach worms, after flies deposit the larvae around the mouth and nose of horse
Habronemiasis:
Mainly associated with skin sores (‘Summer sores’) and occasionally conjunctivitis - adult worms live and reproduce in the stomach
Those deposited in conjunctiva or in wounds can’t migrate so cause disease locally
Seen in all age of horses during June to September
Some horses prone to re-infection
- Adults in stomach - Mostly no disease
- Occasionally horses mount a response against the worms causing nodules of granulation tissue which also contain eosinophils
- Often hard to diagnose on faecal analysis as eggs are very fragile and rupture
- Identify gastric lesions using gastroscopy
Prevention of habronemiasis
* Good fly control and muck heap management
* Frequent replacement of bedding
* Collection/removal of droppings in paddocks
* Cover wounds and treat ocular diseases causing ocular discharge
* Will be killed in horse with worming for other parasites (Avermectins/Benzimidazoles to lesser extent)
what worm causes disease in horses less than 2 years old, why is this?
what is the life cycle?
what is the reservoir?
what are the clinical signs?
what is the treatment?
parascaris equorum (ascarids) - immune response more developed in older animals - equine specific
* Largest worm of horses – up to 10cm in length, cream and round
* Regarded as the up and coming parasite and one to watch due to emerging resistance
- Life cycle involves migration through the liver, vena cava, alveoli, bronchi, trachea so eggs are coughed up and swallowed
- Reservoirs – adult horses – small numbers but shed enough eggs to infect foals/young stock
- Foals NOT infected in utero or via milk
clinical signs and diagnosis:
* Coughing and nasal discharge – often ‘mini-outbreaks’ on farms – when parasites in the lungs – some of this is hypersensivity to worm
* Poor coat and weight gain, dull, anorexic
* Occ colicking incl bowel obstruction
* Disorders of bone and tendons as the parasites consume lots of Ca, P, Zn, Cu
* Diagnosis can be difficult – very distinct eggs when present
treatment:
* Multi-Drug Resistance – Avermectins
* Can see colic if treat lots of adult worms with paralytic drugs – (avermectins and pyrantel)
* PYRANTEL is effective
what are the clinical signs of anoplocephala perfoliata infection in horeses?
what is the intermendiate host, and when are horses typically infecte?
how can it be diagnosed?
what is the treatemnt?
- Disease seen frequently in horses associated with this – usually young horses, but can be any age
Colic
* Ileal impaction – often very painful
* Intussusceptions
* Caecal impactions and motility disorders
* Spasmodic (gas) colic
* (Diarrhoea)
* Functional and physical blockages
- The eggs released are infective to ORIBATID MITES, (IH).
- Mites live on the ground eating plant debris and lichens - overwinter in the soil
- Overwinters to extent in horses, but overwintering Oribatid mites play equal or more important role
- Horses infected in Spring (grass) -ingest mites
- PPP – 6-10 weeks –can then shed large numbers of eggs
- Disease most common Oct/Nov
diagnosis:
- egg shedding is irregular - cant use FWEC
* use the Immune response to test for presence - looks for antibodies
* Blood test
* Saliva test
- Currently < 25% of horses tested require treatment - most horses do not have a level of tapeworm infestation that requires treatment
Treatment and prevention:
* Two drugs – high dose pyrantel (double the dose required for other worms) and praziquantel – treat in Autumn/Winter
* Prevention – stable horses for 48 hours after worming to prevent increased pasture contamination. Can’t kill the mites…nature’s dustman
what are the three species of large strongles in horses?
- Strongylus vulgaris
- Strongylus equinus
- Strongylus edentatus
what is the most clinically important large strongyle, why?
what is the epidemiology of this worm?
how is it diagnosed?
what disease does it cause?
what is the treamtment and prevention?
Strongylus vugaris- causes ‘verminous arteritis’
◦ immune response in the walls of vessels
◦ Was very important cause of surgical colic that was frequently fatal – mainly the larvae that cause disease
epidemiology:
* Get some immunity but never complete to stop re-infection
* Disease often most severe in those young/unexposed animals
* See in all ages – worse in weanlings and yearlings
* Reservoirs-asymptomatic horses that shed large numbers of eggs
Diagnosis:
* Difficult as this is a pre-patent disease – disease caused by larval stage
* May be able to feel thrombi when perform rectal examination
* Faecal analysis –not always useful and can’t tell from other Strongyle eggs (large vs small strongyles)
◦ No correlations with Strongyle egg counts and luminal worm counts!
Disease:
* Due to high numbers on pasture in Spring/Summer, often in arteries in Autumn/Winter - when see disease
* Adults – protein-losing enteropathy and anaemia
* Colic, diarrhoea, anorexia
* Ischaemic, dying gut = sick, colicking, dying horse – need surgery for resection if possible
* Can form thrombi at aorto-iliac junction – can lead to lameness and poor performance
* Occasionally migrate aberrantly and end up in the brain, kidneys, lungs, liver and can form granulomas
Treatment:
Drugs:
* benzimidazoles and avermectins – larvae and adults
* Pyrantel – adults only
- Avoid overgrazing (eggs often on ground)
- PICK UP FAECES REGULARLY
what is the key lifecycle difference with S. edentatus and equinus vs S. vugaris?
what disease do they cause?
S. edentatus - hepatoperitoneal strongyle
* goes through liver and peritoneal cavity
◦ PPP=11 months
S. equinus - hepatopancreatic strongyle
* goes through liver and pancreas
* THEY DO NOT ENTER BLOOD VESSELS LIKE THE OTHER TWO STRONGYLES DISCUSSED
◦ much less likely to cause infarction and mesenteric disease.
* PPP=9 months
disease
* S. edentatus – colic due to liver disease or peritonitis
* S. equinus – mild colic. Some association with pancreatic disease and primary diabetes mellitus– both of these conditions EXTREMELY rare in horses
what are the two disease processes caused by cyathostomins?
First syndrome – seen in SPRING
* ACUTE LARVAL CYATHOSTOMINOSIS
* Due to mucosal damage caused by emergence of the late L3
◦ Colic
◦ Weight loss
◦ Diarrhoea – acute and chronic
◦ Wasting and death either acutely or chronically
Autumn syndrome – when L3 larvae entering intestinal wall – less common than that seen in the Spring - tends to be milder disease
* Colic
* Diarrhoea due to inflammation
Due to the current change in climate if a horse presents with D+ outside of spring or autumn does not exclude cyathostomins
what are the main clinical facts for cyathostomins?
- Encysted (wall of large colon and caecum), hypobiotic larvae largely unaffected by any anthelmintic
- Hypobiotic population makes up 50% of the larval population, which is 90% of the total population (10% adults)
- two syndromes of disease:
◦ Larvae emerge in Spring, often many many at once - causes disease due to physical damage to the intestinal mucosa
◦ lavea entering the intestinal wall in autum - PPP-6-14 weeks if no hypobiosis
- Most larvae on the pasture in Autumn
- Do see immunity to cyathostominosis, but takes a long time and never complete
◦ Younger horses more likely to have higher burdens
how is Cyathostominosis diagnosed?
- Very difficult as PPP disease
- History and clinical signs – young animals, poor worming history or change
- May see larvae in faeces or on glove after rectal examination in animals with acute larval cyathostominosis
what is the parasite of stabled horses?
what are the clinical signs?
how is this worm diagnosed?
what is the treatment and prevention?
Oxyuris equi - equine pin worm
* Affect any age
eggs don’t survive well outdoor
* Reservoirs – other infected horses and immediate environment
clinical signs:
* Anal pruritus and skin excoriation and/or myiasis
* Eggs in the perianal region on examination
Diagnosis:
* Sellotape test – put on slide and examine under the microscope
Treatment and prevention:
* All anthelmintics should be effective – some resistance
* Anal application as a paste
- Can use topical or systemic anti-inflammatories to decrease pruritus and keep area clean with disposable material
- Good stable hygiene – water troughs, mangers etc
