Equine dermatology, diarrhoea, parasites Flashcards
What is the most common secondary infection of wounds and other skin damage in horses? Signs?
Streptococcal dermatitis: Strep equi var zooepidemicus: - opportunistic pathogen - folliculitis, furunculosis, cellulitis Strep equi var equi: - obligate pathogen - abscesses (bastard strangles) Strep equisimilis
Signs, diagnosis and treatment of streptococcal dermatitis?
Signs: - mild-moderate painful skin infections and abscesses Diagnosis: - clinical features and culture Treatment: - sensitive to penicillin - drain abscesses - topical antimicrobial washed in superficial infections
Staphylococcal dermatitis in horses: Most common species? Signs?
Treatment?
Staph aureus and intermedius Signs: - pain - localised exudative dermatitis - focal lesions also occur (abscesses or pyogranulomas) Treatment: - problematic! - clip hair and antiseptic washes with warm water - drain abscesses - systemic antibiotics based on C and S
What are the 5 clinical syndromes of Staphylococcal dermatitis in horses?
- Pyoderma: secondary to trauma, large painful exudative areas
- Saddle rash: associated with harness areas and saddle cloths
- Pastern folliculitis
- Wound infections
- Abscesses
What causes rain scald in horses? Clinical presentation and signs? Diagnosis?
Dermatophilus congolensis: gram positive, facultative anaerobe
Very common
Contagious
Signs/presentation:
- affects areas that are commonly or persistently soaked: back, head, neck
- initially small lesions, easier felt than seen (common presentation in summer)
- more severe disease in winter: moist matted hair, adherent crusts with purulent base
- pain usually mild
Diagnosis:
- easily recognised clinically
- direct smears: cytology
- culture
Treatment:
- remove to dry environment
- remove matted hair and crusts
- antimicrobial washes (dilute chlorhexidine)
- systemic antibiotics if severe
Ringworm in horses: Cause? Incubation period? Immunity? Signs? Diagnosis? Treatment?
= Dermatophytosis
Trichophyton equinum var equinum
Trichophyton verrucosum
Microsporum gyspeum
Microsporum equine
Highly contagious
Incubation period 2-3 weeks
Very common in young and immunocompromised
Some immunity with age - older horses can be re-infected but with smaller, quicker resolving lesions
Signs:
- small circular patches of hair sticking up
- accumulation of keratinised squames ("cigarette ash")
- weakening of hair -> bald patches
- poss secondary bacterial infections
- healing centrifugally from centre of lesion
Diagnosis:
- skin scrapes
- hair pluck
- culture (takes long time)
Treatment:
- isolate
- most are self limiting in 5-10 weeks
- topical natamycin, enilconazole, miconazole
- systemic treatment?
- environmental and tack disinfectionWhat causes grass warts in horses? Which horses? Signs? Diagnosis? Treatment?
= viral papilloma Host specific Papovavirus Affects mainly younger horses (6mo-4y) or immunocompromised Moderately contagious Multiple pink or grey lesions on muzzle, lips, face, limbs and genital areas No discomfort or pruritus Diagnosis: - straightforward - biopsy? virus isolation? Treatment: - spontaneous resolution in most cases - surgical excision? topical antivirals? - autogenous vaccination?
What causes pinnal acanthosis/aural plaques in horses? Signs? Diagnosis? Treatment?
Very common
Papillomavirus transmitted by black flies (Simulium spp)
Range from small raised depigmented areas to large clusters of white masses
Diagnose on signs (don’t biopsy)
Treatment:
- not necessary
- do not treat
Coital exanthema in horses: Cause? Transmission? Incubation period? Immunity? Signs? Diagnosis? Treatment?
Contagious, venereal disease caused by EHV-3
Transmission also by indirect contact and by inhalation of virus-laden droplets
Incubation period 5-7 days
Only significant in breeding animals
Solid immunity: most horses only infected once
Signs:
- Rapidly developing papule (1-5mm) on penis, vulva and perineum
- Lesions can be mildly pruritic but not painful
- Healing of lesions may leave permanently depigmented spots on skin
Diagnosis:
- Clinical signs
- Virus isolation difficult
Treatment:
- Stop breeding until >3 weeks after the lesions have healed
- Topical antimicrobials/antiseptics
- Local anaesthetic creams
Horse pox: Forms? Signs? Treatment?
Very rare
Buccal form and cutaneous form
Mild systemic signs: fever and depression
No treatment: spontaneous regression
Papular dermatosis in horses: Cause? Signs? Treatment?
Very rare
Unspecified Pox virus
Annular papular lesions - non pruritic or painful
Most cases resolve in 4-6 weeks: no need for specific treatment
Sarcoids: What are they? Associations? Types?
Most common skin tumour in horses Fibroblasts Potential association with bovine papillomavirus 1 and 2 Genetic predisposition Flies 6 Types: - Occult: flat - Verrucose: bumpy flat - Nodular - Fibroblastic: angry red nodular - Mixed: made up of multiple types - Malignant: nasty, lots
Diagnosis of sarcoids? Treatment?
Biopsy: - histologically distinctive - danger of exacerbation so must treat if positive diagnosis (ie don't take sample if wouldn't be prepared to treat) Treatment: - surgery/cryo/laser - immune therapy: BCG injections, vaccines - cytotoxics (topical and injections) - antimitotics (topical) - photodynamic therapy - radiation - homeopathy/natural medicine
Prognosis rules for sarcoids?
Rule 1: the more they have, the more they get
Rule 2: the fewer they have, the fewer they get
Rule 3: multiply over summer, grow over winter
Rule 4: a single sarcoid implies (genetic) susceptibility
Differentials for acute colitis?
Idiopathic - most common Salmonella Clostridium perfringens and dificile Drug induced - antibiotics, NSAIDs Larval cyathostomosis Carbohydrate overload
Rotavirus - acute enterocolitis in foals
Ehrlichia risticii - Potomac Horse Fever (acute colitis)
Acute necrotic colitis and dysentery (Colitis X)
When should a horse be put in isolation for possible infectious colitis?
Any 2 of the following:
- Acute diarrhoea
- Fever (temperature >38.5)
Low white blood cell count (<4x10^9 cells/L)
Salmonella enterocolitis: Which species? Features of the bacterium?
Salmonella enterica
6 subspecies, especially subs enterica
>2000 serovars, especially Typhimurium
Host specific forms cause more systemic disease
Gram -ve motile bacillus
Modified flagella and pilli used for plasmid exchange
Facultative anaerobe
Facultatively intracellular - the most pathogenic strains are best at this
Wide range of antibiotic resistance
Survives in damp soil for up to 9 months
Contagious
Water and feed contaminated with faecal material
Recovered animals may shed for weeks or months (source of infection is asymptomatic shedders or diseased horses)
Mostly seen in hospitalised patients
Virulence factors of Salmonella enterica?
3 types of adhesion molecules
Invasion genes - encode proteins that cause ruffles in enterocyte membrane and Salmonellae become interiorised
Salmonella virulence plasmids - allow intracellular growth, serum resistance and cellular invasion
3 exotoxins that result in diarrhoea - cAMP, Cytotoxin, Phospholipase A activity
What host factors predispose to Salmonella enterica infection (and acute colitis in general)?
Antibiotic treatment GA Transport Competition Hospitalisation Surgery Feed changes Anthelmintic treatment Immunosuppression ANY STRESS
Pathogenesis of Salmonella enterica?
Opportunistic
LPS (endotoxin) triggers massive neutrophil dominated inflammatory cascade
Facultatively intracellular in macrophages
Inflammation and tissue necrosis -> leakage of protein and fluid -> diarrhoea
Exotoxins exacerbate inflammation and necrosis and promote more diarrhoea:
- Cytotoxin: morphological damage and increases penetration of mucosa
- Enterotoxins: increases sodium and water secretion
Diarrhoea and endotoxaemia -> severe shock and cardio-circulatory collapse
Variable mortality (related to virulence) - if hydration can be maintained, diarrhoea and inflammatory response eliminates infection and the mucosa heals
When can a horse in isolation with Salmonella be taken out of isolation?
5 faecal cultures q12-24h all negative
Or when goes home
Differentials for acute colitis?
Clostridium per
Clostridium perfringens and dificile colitis: Features of bacterium??
Saprophytic and part of normal intestinal flora
Large gram +ve endospore forming bacilli
Obligate anaerobes and haemolytic in culture
C perfringens:
- non motile
- type A most common in horses: enterotoxin (cytotoxic), alpha toxin (lecithinase: phospholipase activity), B2-toxin (toxigenic strain)
C dificile
- motile
- Toxin A: pro-inflammatory (IL-1 and TNF) = toxic to macrophages
Requires host ‘stress’ or intestinal flora change (e.g. grain overload, rapid diet change)
High mortality rates
Spore forming
Resistant to heat, cold and many disinfectants
Predisposing stress factors for Clostridial colitis in horses?
Intercurrent infections Extreme temperature Water deprivation Overcrowding Sudden change in diet Transportation Antibiotic therapy GA
Diagnosis of Clostridium perfringens and dificile colitis in horses?
Culture not reliable as part of normal flora and not all isolates toxigenic
Identification of C perfringens enterotoxin by ELISA or B2 toxin by ELISA or PCR
Identification of C dificile toxin A by ELISA or PCR
Rotavirus: Features?
Reoviridae genus
Strains appear predominately host speciesspecific
Coat protein VP4 is the haemagglutinin that dictates species susceptibility
VP4 protein - target Ag of neutralising Ab response
Contagious
Water and feed contaminated with faecal material
Survive in environment up to 9mo
Resistant to bleach disinfectant - ethanol, phenols and formalin can inactivate the virus
Pathogenesis of Rotavirus?
Virus ingested and infects absorptive epithelium of the apices of the villi
Mostly SI involved (occasionally colon)
Damage and loss of cells in villi leads to villus atrophy, resulting in poor nutrient absorption and osmotic diarrhoea
Virulent strains cause more necrosis and haemorrhage
Humoral response by host neutralises virus
Incubation period 18-24h
Disease course usually 5-7d (self limiting)
Recovered foals shed for 2 weeks
Low mortality but can be high morbidity (highly infectious - oubreaks)
Predisposing factors for Rotavirus diarrhoea?
Age <2mo (naive immune status) Intercurrent infections Extreme temperatures Poor food and water sanitation Overcrowding Transportation High levels of infection on property in previous year Stressed adult horses may intermittently shed
Diagnosis of Rotavirus? Treatment?
Clinical signs and identification of virus in faeces Electronmicroscopy (gold standard) ELISA Rule out concurrent disease Treatment: - vaccination - supportive therapy
Rotavirus vaccine?
Mare in months 8, 9 and 10 of each pregnancy
Relies on good passive transfer and protects for approx 60 days
What types of skin diseases cause pruritus in horses?
Parasitic skin disease
Hypersensitivities (allergies)
Which lice affect horses? Where on the body do they affect? Morphology? When seen? Signs? Diagnosis? Treatment?
Haematopinus asini: - sucking louse (feeds on blood) - mane, tail, fetlock and pastern Werneckiela: - biting louse (feeds on epidermal debri) - dorsolateral trunk
Permanent - die within days if off host
1 month life time - lays 200-300 eggs
Hemimetabolous
Morphology: small, wingless insects (0.5-8mm), flattened, stout legs, claws
More common in winter
Asymptomatic (naturally well tolerated in healthy animals) -> restless, poor appetite, poor coat, irritation -> severe debilitation
Diagnosis: demonstration of adults or eggs on hair
Treatment: pyrethrins, pyrethroids, permethrin, fipronil
Which mite causes intense pruritus with stamping of feet in horses? Other signs? Which horse breeds affected? When more common?
Morphology? Life cycle?
Chorioptes equi Chewing mite Host adapted strain of C bovis Affects lower limbs, especially if feathered fetlocks Other signs: - papules - crusty lesions - hair loss Draft breeds More common in winter Morphology: - rounded head - thumb print - unjointed pedicels which end in cup-shaped sucker Life cycle: - 6 legged larva hatches from egg, feeds and moults to 8 legged protonymph, tritonymph and adult - 3 week life cycle
Sarcoptes scabiei: where on body do they affect in horses?
Burrowing mange mite
Head, neck, ears -> entire body
Difficult to see on skin scrapings
Psoroptes equi: Where on body of horses does it affect? Morphology?
Rare Host specific Forelock, main and tail -> trunk Ears: head shaking Morphology: - 3 jointed pedicel - trumpet shaped suckers
How are mites diagnosed and treated in horses?
Diagnosis: skin brushings
Treatment:
- systemic avermectins (not licensed, e.g. doramectin in dectomax)
- topical lime sulphur, lindane, coumaphos, diazinon, malathion
(dog/cat frontline sprays)
(head and shoulders..)
Treat at 2 week intervals
Trombicula: What is seen? Where on body of horses?
Larvae of free living adult mites
Papules with small orange or red larvae in centre
Face, distal limbs, ventral thorax and abdomen
Dermanyssus gallinae: Where affected on horses?
Poultry mite
Head and legs
Same treatment as other mites and remove birds
Demodex: When seen in horses? Where?
Rare - check for immunosuppression
D equi: body
D caballi: eyelids and muzzle
Treatment for ticks on horses?
Topical pyrethrin, pyrethroid, fipronil, ivermectin
Onchocerca cervicalis: Where does it live in horses? What does it cause? Treatment?
Adult lives in nuchal ligament Microfilarie migrate to skin -> hypersensitivity Worse in spring and summer Face, neck, ventral chest and abdomen Ocular lesions Ivermectin (+ pred?)
Habronemiasis: What do they cause in horses? Treatment?
Flies -> larvae in skin or wounds
Ulcerative nodules in spring and summer
Exuberant granulation tissue with yellow granules
Ivermectin and corticosteroids
Oxyuris equi: What does it cause? Features of adults and eggs? Diagnosis? Treatment? Life cycle? PPP?
= Pinworm 'Anal rust' Adults: translucent yellowish-white, pointed tails, 1-10cm' Eggs: 80um, mucoid plug Perianal pruritus Diagnosis: clinical signs and cellophane tape Anthelmintics - challenge as lack of efficacy Life cycle: - direct - females lay eggs on peri-anal skin - eggs fall to ground - develop to L3 in the egg - ingested - larvae develop in mucosal crypts in LI - adults in lumen of LI PPP 5 months
What hypersensitivities are seen in the horse?
- Insect hypersensitivity
- Food allergy
- Contact allergy
- Atopy
- Urticaria
What causes insect hypersensitivity? How does it present? Risks? Treatment?
Culicoides spp
Dorsal surface of horse: mane, back, tail
Seasonal
Risks: standing water, dawn and dusk, no wind
Treatment: avoid contact, reduce hypersensitivity
Food allergies: how common in horses? Signs? Diagnosis?
Rare Pruritus \+/- Diarrhoea \+/- Respiratory signs Diagnosis: diet elimination
Contact allergies: how common in horses? What allergens? Diagnosis? Treatment?
Rare
Plants, chemicals, tack etc
Diagnosis: provocative exposure
Treatment: avoid contact
What is Atopy in horses? Diagnosis? Treatment?
Skin or respiratory condition Sensitivity to multiple allergens Diagnosis: intradermal skin testing Treatment: - avoid allergens - hyposensitisation - corticosteroids - antihistamines
How does urticaria look on horses? Cause? Treatment?
Wheals, oedema and often pruritus
Cause difficult to determine
Rule out food and insect allergy
Treatment: corticosteroids, antihistamines
Define scale, crust, erosion and ulcer?
Scale: dry, grey
Crust: yellow/red/brown, wet/damp
Erosion: superficial
Ulceration: deeper
Causes of crusting, scaling, erosion and/or ulceration in horses?
Viral papillomatosis (grass warts, aural plaques) Dermatophilosis Bacterial folliculitis Dermatopytosis Photosensitisation Leukocytoclastic vasculitis Pastern dermatitis Pemphigus foliaceous
What are the 2 causes of photosensitisation in horses? Where affected? Diagnosis? Treatment?
- Hepatogenous
- Ingestion or application of photodynamic agent
Lesions most common in white areas
Diagnosis: signs, blood tests
Treatment: treat liver disease, remove agent
Leukocytoclastic vasculitis in horses: How common? Where affected? Diagnosis? Treatment?
Common
Affects non pigmented areas on distal limb
Painful
Diagnosis: skin biopsy
Treatment: avoid exposure to light, corticosteroids
Pastern folliculitis/dermatitis in horses: Colloquial name? How common? Requisite? When more common? Diagnosis and treatment?
"Greasy heel" syndrome Very common Requisite: chronic wetting of skin on distal limb More common in winter and in white limbs Difficult diagnosis and treatment
Pemphigus foliaceous: What is it? Signs? Diagnosis? Treatment?
Rare, autoimmune disease Severe crusting Diagnosis: skin biopsy Treatment: immunosuppressive drugs Prognosis: guarded
Causes of cutaneous swellings/nodules/tumours in horses?
- Warbles
- Genetic/developmental: dentigerous cyst, atheroma, dermoid cyst, vascular hamartoma
- Eusinophilic granuloma
- Tumours: sarcoid, melanoma, SCC, mast cell tumour, lymphoma
Warbles: what is it? Where seen? Signs? Treatment?
Larval stages of Hypoderma bovid and lineatum
Neck and trunk
Nodules with central pore, often painful
Treatment: enlargement of pore to remove central grub, surgical removal
What is a eosinophilic granuloma in horses? Signs? Diagnosis? Treatment?
Collagen necrosis Very frequent Insect bites? Trauma? 0.5-10cm Non painful, non pruritic Diagnosis: skin biopsy Treatment: surgical removal?
Melanomas in horses: How common? How do they present? Diagnosis? Treatment?
Very common - 80% of grey horses >15yo
Most benign but some can be malignant
Lesions solitary or multiple
Most commonly: perineum, tail head, parotid region
Diagnosis: clinical signs, biopsy
Treatment: surgical excision, immunotherapy
Squamous cell carcinomas in horse: Which horses? Where? Diagnosis? Treatment?
Common
Most common in poorly pigmented animals
Most common: external genitalia, eye (e.g. non pigmented third eyelid)
Diagnosis: clinical signs, biopsy
Treatment: surgical excision, cryotherapy, chemotherapy
Mast cell tumours in horses: how common? which horses?
uncommon
Head
Solitary
Males > females
How to take a skin biopsy in horses?
Do not clip and scrub skin
Place small amount of local anaesthetic subcutaneously
Rotate biopsy punch in just one direction
Handle biopsy carefully
Take 12-15
Leave to heal by second intention
Blood tests for skin disease in horses?
Haematology
Serum biochemistry
Endocrine testing
Serum IgE levels
How much water goes into the proximal GIT every day in a normal 500kg horse? How much is then absorbed by the large colon? Normal production of faeces?
125L/day secreted and reabsorbed
Faeces: 8-10 times/day, 10-15kg/day, 75% water
Mechanisms of diarrhoea?
- Malabsorption:
- loss of absorptive cells/tight junctions
- often inflammation - Increased secretion:
- active/passive
- intracellular cAMP/Ca
- bacterial exotoxins
- inflammation - Osmotic overload:
- feeds/additives
- maldigestion
- e.g. Mg sulphate - Abnormal motility:
- inadequate mixing/time for absorption
- primary: gut-brain axis - stress related diarrhoea?
- secondary: to other mechanisms - Extravasation of fluid (oedema):
- hydrostatic
- colloid osmotic
- capillary permeability
- reduced lymph drainage
Which part of the intestine is affected with diarrhoea in horses?
Adults: colon very effective at absorbing water so LI always affected if diarrhoea
(disease of only the SI will not cause diarrhoea)
Foals: diarrhoea can occur with just SI disease (fluid overloads LI absorptive capacity, e.g. Rotavirus/Lawsonia intracellularis)
Chronic diarrhoea: How serious is this? Appearance?
Rarely immediately life threatening
Ranges from soft ‘cow-pat’ faeces to ‘projectile fluid’
Occasionally normal pellets but some extra fluid
Diarrhoea will only occur if there is extensive colonic pathology (but colonic pathology doesn’t always cause diarrhoea)
Differential diagnoses for chronic diarrhoea in the adult horse?
(Any of the diseases that cause acute diarrhoea can progress to chronic diarrhoea)
Dietary causes - abnormal fermentation
Dental disease
Parasites e.g. strongylosis (cyathostomosis usually more acute)
Sand ingestion
Antimicrobial associated diarrhoea
NSAID toxicity (right dorsal colitis)
Non-gastrointestinal causes (kidneys, liver, heart)
Infiltrative disorders (chronic inflammatory bowel disease)
Neoplasia (e.g. lymphosarcoma)
(Chronic salmonellosis)
Presenting clinical signs that may accompany chronic diarrhoea in horses?
No/mild dehydration Bright/eating well (not SIRS) \+/- Weight loss \+/- Polydipsia \+/- Oedema
How to investigate chronic diarrhoea?
History and clinical exam 5 faecal samples for Salmonella culture Haematology and biochemistry to check for inflammation Check plasma protein concentration Peritoneal fluid US Rectal biopsy Absorption tests Diagnosis <50% of time
Treatment for chronic diarrhoea?
Treat underlying disase
Tincture of time
Lavicidal deworm - fenbendazole 10mg/kg daily for 5 days or ivermectin, followed in 1 week by moxidectin
Yeast/probiotic
Access to normal manure
Anti-diarrhoea medications usually ineffective in long term
Clinical signs of acute colitis and SIRS?
Depression Fever Tachycardia >80bpm Tachypnoea Congested to purple mms Slow CRT Anorexia Dehydration Reduced GI sounds Colic Diarrhoea (endotoxaemia can precede diarrhoea)
Pathophysiology of acute colitis?
Fluid loss
Mucosal inflammation, ischaemia and repercussion injury
Breakdown of GI mucosal barrier - absorption of endorphins/exotoxins
What is the pathophysiology of endotoxaemia/SIRS?
- Compromise of intestinal barrier allows large quantities of bacterial and other toxins to enter the portal circulation
- Hepatic clearance mechanisms are overwhelmed
- Toxins enter systemic circulation
- Gram negative bacteria release endotoxins
- Initiates cascade of inflammatory mediators ->
- fever, obtundation
- neutrophil margination and activation -> neutropenia, endothelial activation, permeability and injury -> interstitial oedema
- coagulation activated -> impaired fibrinolysis -> DIC -> micro thrombi/haemorrhage -> tissue hypo perfusion and hypoxia -> lactate
- myocardial depression -> hypotension -> tissue hypo perfusion etc
- vasodilation -> hypotension etc
= multi organ failure
Laminitis due to damage to extraceullar matrix of laminae
Antibiotic-induced diarrhoea: which antibiotics? which horses? Why happens? Management?
Any antibiotic
Mares with foals receiving erythromycin - probably ingestion of drug from foal’s faeces
Allows overgrowth of pathogens or poorly understood dysbiosis in colon
Management:
- withdraw antibiotics
- supportive
- faecal transfaunation?
Diagnostic approach to acute diarrhoea?
Determine hypovolaemia/dehydration for requirement of fluid therapy:
- HR
- mentation
- urination
- PCV/lactate
Assess electrolyte, albumin, acid-base status
Infectious disease? Isolation if possibility?
Determine underlying cause - idiopathic most commonly
Fluid therapy for acute colitis?
Boluses of isotonic crystalloids: - 10-20ml/kg over 20-30 mins - reassess and repeat if no improvement - give maximum of 4 boluses If severe hypovolaemia: - give 2-4ml/kg hypertonic saline rapidly - or 10ml/kg colloids if hypoalbuminaemic - follow up with isotonic crystalloids
Treatment for acute colitis?
Treat SIRS: - NSAIDs: flunixin - Polymixin B IV - Ice feet against laminitis - misoprostol??? Antibiotics: - questionable role - metronidazole esp if Clostridial diarrhoea suspected/confirmed Oral protectants: - bismuth subsalicylate - activated charcoal - smectite (biosponge)
Cyathostomins: Life cycle? Infective stage? Appearance of different stages?
Life cycle:
- direct and non migratory
- females pass large numbers of eggs into gut lumen -> eggs in faeces -> develop to L1 within 24h if optimal conditions -> moults to L2 in faecal pat -> moults to L3 (egg-L3 in 7-10 days with optimal conditions) -> L3 wrapped around grass -> L3 ingested -> sheds outer sheath in SI -> goes into mucosa in LI and develops to L4 -> L4 pushes way out of lumen and develops to L5 (6-8 week ppp)
EL3 = early L3 - just after penetrated mucosa
LL3 = late L3 - close to becoming L4
DL4 = developing L4
Infective stage: iL3
Appearance of adults:
- 0.5-1cm
- very small buccal cavity
- females: no bursa
- males: obvious bursa with dorsal lobe elongated on one side
- stacked gut cells
Appearance of eggs: same as Trichostrongyle eggs (80 microns length)
Appearance of iL3:
- outer L3 sheath and inner retained L2 sheath (so resilient and can persist over winter)
- long tail (can propel across water)
- triangular gut cells
EL3 (mucosal L3):
- curved shape
- sheath has been stripped away
- may be main parasitic burden but difficult to detect (can have negative FEC)
Hypobiosis:
- mostly as EL3
- trickle emerge after hypobiosis
- may constitute >70% worm burden in autumn/winter
Define hypobiosis
Arrested stage of development of nematode larvae within host due to external trigger of drop in temperature
When is disease seen with cyathostomins? Why? Clinical signs?
With heavy mucosal burden
Get L4 emergence on mass after hypobiosis
Causes protein losing enteropathy and disease
= Larval cyathostomosis (severe enteritis)
Higher incidence in young horses (<3yo) - often fatal
Clinical signs:
- acute diarrhoea, weight loss, oedema
- collapse
- colic
What horse Strongyles are there?
Small strongyles: Cyathostomins Large strongyles: - Strongylus spp (edentatus, equinus, vulgaris) - Triodontophorus spp - Oesophagodontus - Craterostomum
Strongylus spp. sizes and morphology? PPP? Where do they migrate to?
S. edentatus - 2.5-5cm - no teeth in buccal cavity (just a thickening of cuticle called dorsal gutter) - ppp 10 months - Flanks and hepatic ligaments S equinus: - 2.5-5cm - 3 teeth - ppp 8 months - liver then pancreas S. vulgaris: - 1.5-2.5cm - 2 rounded teeth (mickey mouse ears) - ppp 6 months - cranial mesenteric arteries All have well developed buccal capsule and bursa in males
How is the life cycle of large strongyles in horses? Infective stage?
Direct and migratory
Infective stage: iL3
When do Strongylus spp cause disease in horses?
Large numbers: unthriftiness and anaemia
Adults cause damage to LI due to their feeding habits
Larvae clinically most relevant
S vulgaris: non strangulating infarction secondary to larvae in cranial mesenteric arteries
Which Strongyles have anthelmintic resistance in horses?
Cyathostomins
Not Strongylus spp.
Triodontophorus spp?
Non migratory
Contribute to the damage caused by the adult worms of other spp.
Rarely pathogenic on their own
Feed in groups
Eggs twice the size of other strongyle eggs
Conditions required for the development of pre-parasitic stages and survival of L3 of Strongyles?
Pre-parasitic: - >10C - Humidity - Dispersion from faecal pat (rainfall) L3: - ensheathed - low temperature (tolerates cold) - moisture (desiccation is lethal) - warmer, wetter conditions allow development to L3 through winter
Host factors affecting epidemiology of Strongyles?
Age and immune status:
- don’t develop strong immunity
- all ages carry infections and contaminate pasture throughout their lives
What is over dispersion?
Small proportion of the host population carries the majority of the parasite population
80% burden in 20% horses
Allows targeted treatment - treat those with moderate-high FECs to reduce pasture contamination
What is usually happening with Strongyles in horses in April-May?
Overwintered L3 on pasture
Once ingested, L3 mature
Eggs produced onto pasture
Continuous excretion of eggs
Hypobiotic larvae mature to adults and eggs passed onto pasture
Ambient temperature gradually start to increase so eggs start to develop more rapidly
What is usually happening with Strongyles in horses in August-September?
Egg and L1-L3 development is temperature dependent
Highest egg shedding August
Peak of L3 on pasture in late summer
If only do one FEC, do in August
What is usually happening with Strongyles in horses in late Autumn?
L3 on pasture exposed to drop in temperatures
Cyathostomins:
- L3 ingested undergo hypobiosis
- accumulation of hypobiosed EL3/L4 in large intestinal mucosa
What is usually happening with Strongyles in horses in late Winter-Spring?
Cyathostomins:
- larval development resumes
- simultaneous emergence of EL3/L4
- cyathostominosis - severe clinical disease, high mortality
Options for endoparasite control in horses?
Pasture management: - poo picking - pasture rotation - mixed species grazing - 'clean pasture' at turnout - harrowing Anthelmintics: - targeted (animals with higher FECs), strategic (use at key times of year e.g. August) or interval dosing - moxidectin only drug that kills hypobiosed small strongyles
Anthelmintic resistance against Strongyles in horses?
BZs ineffective on all yards
PYR effective on 50% of studs
IVM effective on all studs but reduced ERPs
MOX effective on all studs but reduced ERPs
Limitations of FECs?
Don’t accurately reflect adult worm burden
Don’t detect immature or larval stages e.g. encysted cyathostomins
Tapeworm eggs often not detected
Anoplocephala perfoliata: What is it? Morphology? Where found in horses? Life cycle? PPP? When are peak levels of infection?
Tapeworm
Adults found at ileo-caecal junction
Made of short, broad segments
Lappets behind each of 4 suckers
Life cycle:
- adults at ileo-caecal junction
-> proglottids passed in faeces, disintegrate and eggs released
-> eggs ingested by free living orbited mites (intermediate host) found in soil, shavings, hay and develop to cysticercoid
-> infected mite ingested by horse
PPP 2 months
Peak levels of infection in autumn/winter but infection possible all year round
What do Anoplocephala perfoliata eggs look like?
Irregularly spherical (D shaped)
50-80um
Onchosphere supported by pyriform apparatus
What disease can Anoplocephala perfoliata cause? Clinical signs?
Spasmodic colic Intussusception Ileal impaction, rupture Clinical signs: - ulceration and pathological changes in intestine - unthriftiness - enteritis - colic
Diagnosis of Anoplocephala perfoliata? Treatment?
Eggs in faeces - FEC 60% sensitivity
ELISA for circulating Ag (68% se, 95% sp)
EquiSal saliva test
Treatment/control: double dose pyrantel, or praziquantel
Parascaris equorum: morphology? General features? Infective stage? Cause of disease?
Large, white Adults in SI Eggs: round, brown, 80-90um, rough shell Females lay huge numbers of eggs Eggs are highly resistant L2 larvae develop in the egg L2 in egg is infective stage Direct life cycle Hepato-tracheal migration Migrating larvae stimulate profound inflammatory response Adults browse on intestinal contents, compete for nutrients Adults can cause mechanical blockage due to size No damage to mucosa
Parascaris equorum life cycle? PPP?
Eggs passed in faeces
Develop on the ground - temp dependent (~4wks)
Egg (containing L2) eaten by horse
L2 migrates to liver -> lung (L2-L3)
Coughed up, swallowed, L4-L5 (adult) in SI
PPP 12 weeks
What disease does Parascaris equorum cause? Which horses?
Typically affects foals Transient cough Poor weight gain, unthrifty No diarrhoea Poss obstruction in heavily infected individuals Foal-foal infection Adults immune
Control of Parascaris equorum?
Anthelmintics Ivermectin resistance reported Pasture rotation (but eggs resistant and long lived)
What are Anoplura and Mallophaga lice?
Anoplura: sucking lice
Mallophaga: biting/chewing lice
Permethrins for horse flies and lice: How do they work? How often to apply? Toxicity?
Neuro-poison - acts on axons of the PNS and CNS by interaction with Na channels
Single application usually controls Werneckiela for 3 months but re-treatment recommended after 14 days to kill eggs unaffected by first treatment
Extremely low mammalian toxicity
Dangerous to fish and crustaceans
Toxic for cats
Clinical syndromes of Salmonellosis?
Severe disease
Marked neutropenia and dehydration
Septicaemia
Fluids for horse with diarrhoea?
Boluses of isotonic crystalloids: - 10-20ml/kg over 20-30 mins - reassess and repeat if no improvement - max 4 boluses Severe hypovolaemia: - hypertonic saline 2-4ml/kg rapidly - colloids up to 10ml/kg (esp. if hypoalbuminaemia) - follow with isotonic crystalloids Monitor: - HR - urination - improved mentation - extremity temp - blood lactate/PCV/TPP - CRT/arterial BP - electrolyte concentrations
Diagnosis of endoparasites in horses: Cyathostomins, large Strongyles, Parascaris equorum, Anoplocephala perfoliata and Oxyuris equi?
Cyathostomins: - FEC (adult stages) Large strongyles: - FEC (indistinguishable from Cyathostomins) - larval culture time consuming and needs skill - diagnostics not routinely performed - PCR? Parascaris equorum: - FEC (spherical thick shelled eggs) Anoplocephala perfoliata: - FEC and centrifugation flotation - ELISA - EquiSal saliva test Oxyuris equi: - adults in faeces - eggs in perianal region
Which types of flies are important in horses?
Muscidae = ‘nuisance flies’, feed on secretions or suck blood
- Biting: Stomoxys calcitrans (stable fly)
- Non biting: Hydrotaea irritans (headfly), Musca autumnalis (facefly), Musca domestica (housefly)
Myiasis flies = larvae invade and feed on living or necrotic tissue
Stomoxys calcitrans: what is it? Life cycle? Signs? What do they transmit?
Stablefly Lives inside (stables, barns etc) Feeds on blood Horses and cattle mainly Eggs in dung mixed with straw and urine, damp compost heaps etc Populations build up in summer Rest and mate on warm, sun exposed surfaces e.g. posts Prefers to feed on lower parts of animal, especially legs and flanks Signs: - stamping feet - shivering the skin - rapid head turn to try to dislodge flies from flank - tail swishing Transmit: - EIA - Certain trypanosomes (not UK)
Hydrotaea irritans: What is it? Life cycle? Morphology? Signs?
Headfly
Non biting muscidae
Most notorious pest species of livestock
Only one generation of flies each summer
Deposits eggs on pasture soil
Doesn’t enter buidlings
Typically on wooded pasture
Most numerous on overcast, warm, humid days in August
Morphology:
- orange wing base and greenish abdomen
- rasping/sponging mouthparts
Pesters horses, cattle, sheep, humans etc
Rabbits and deer support large populations
Signs:
- rapid head turn to try to dislodge flies from flank
- tail swishing
- congregated around corners of eyes or around ends of udder teats in cows
Musca autumnalis: What is it? Life cycle? Morphology? Signs? Transmits?
Facefly Non biting muscidae No proboscis, sponging mouthparts Southern parts of England Found on eyes, muzzle and face Mainly horses and cattle Affects pastured animals outdoors Develops in dung on pasture Populations build up in late Autumn Do not enter animal accommodation Tranmits: - Moraxella bovis to cattle (IBK) - likely also problem in horses - vector of Thelazia (eye worms) and Habronemia But main significance in UK is nuisance
Tabanidae: What are they? Morphology? Where? Life cycle? Species? Vectors of?
Non muscidae biting flies Morphology: - large body and head - bulging iridescent eyes - antennae - stubby mouthparts - pool feeders Painful bite Females blood feed Efficient mechanical vectors Breed in wet pasture: marshy land, edges of ponds Tabanus: large with clear wings Haematopota: mottled wings Gadding (July/August) Active during sunny days Several small meals often taken Mechanical vectors of: - EIA - Bacillus anthracis - Trypanosomes - Bovine anaplasmosis
Culicoides: What are they? Morphology? Life cycle? Transmits?
Biting midges
Morphology:
- tiny 1-4mm
- brownish/black body and mottled/spotted wings
Life cycle:
- dig a hole and feed on free blood
- eggs laid in damp compost heaps, any decaying vegetation, marshy land etc
- eggs-to-adult in <3 weeks
- one or two generations/year in temperate regions
- life cycle can be as little as 3 weeks
Significance:
- feed in dull humid weather, very active at dawn
- cause sweet itch (seasonal recurrent allergic dermatitis) due to hypersensitivity to saliva
Tranmits:
- AHS
- Blue tongue
- Schmallenberg virus
Simulium: What are they? Morphology? Life cycle? Transmits?
Blackflies Morphology: - small 1-4mm - brownish/black (orange) stout body - humped thorax - clear wings Life cycle: - lay eggs on stones etc in running water - aquatic larvae and pupae - require flowing waters - adults active in mornings and evening - adults live up to 4 weeks and feed on horses and cattle Transmits: - Leucocytozoon to ducks and geese - non pathogenic Onchocerca to horses and cattle (river blindness in humans in Africa/America)
Fly control?
Insecticides:
- synthetic pyrethroids
- treat accommodation (resting surfaces e.g. walls)
Dung removal inside housing to reduce build up of M domestic and Stomoxys
Housing
Barriers - head masks, rugs
Gasterophilus spp: What are they? What do they do? Life cycle? Species? Significance? Diagnosis? Control?
Horse bot fly
Myiasis
Larvae feed on tissue exudates
Active late summer
G intestinalis (most important):
- eggs laid late summer on inner forelegs, hocks and shoulders
- burrow in tongue, moult and exit to pharynx
- moult to L2
- cluster in oesophageal portion of stomach
- moult to L3 and remain until spring
- passed in dung around June
G nasalis:
- eggs laid under jaw
- burrow in spaces around teeth
- moult to L2 and move to pyloric part of stomach
G haemorrhoidalis:
- eggs laid on lips
- migrate into mouth
- moult and migrate to stomach and duodenum
- moult
- attach to rectum
Single generations per year
Not very significant:
- occasional disease due to crater like ulcers and inflammation
- large ‘maggots’ in faeces cause alarm to owners
Diagnosis:
- larvae in faeces in spring: orange when fresh, barrel shaped double row of spines
- eggs on coat in summer
Control:
- remove eggs
- IVM/moxidectin
Common post op
Profuse watery diarrhoea
High PCV, low TP, neutropenia, toxic neutrophils
Salmonella
What type of colitis do NSAIDs cause?
Right dorsal colitis
Young Coughing Dyspnoea Diarrhoea Mixing with other horses and foals
Rhodococcus
Dull Intermittent pyrexia Cowpat faeces Poor body condition but normal appetite Ventral oedema Peripheral lymphadenopathy
Intestinal lymphosarcoma
1 month old
Sudden onset watery fetid diarrhoea
Depressed
Responded well to oral fluids and NSAIDs
Rotavirus
Profuse diarrhoea Depressed Pyrecia High HR and RR Red mm Being treated for skin lacerations
Clostridium difficile
