The horse!

Note: urticaria is not a diagnosis but rather a reaction pattern.

Mast cell degranulation followed by the liberation of chemical mediator of inflammation leading to the development of dermal edema. 

Immunologic (drug eruption, insect allergy, food allergy, atopy, contact (type 1 = rare, likely type IV)

VS

Non-immunologic (cold urticaria, pressure urticaria aka dermatographism and excercise induced)

A wheal (flat topped papule or nodule with steep walled sides) that exhibits pitting edema and may have a depressed center

Conventional = wheals of varying sizes; from 2-3mm to 3-5cm 

Papular = all the wheals are small; 3-6 mm; likely due to insect hypersensitivity 

Giant = single or mutiple huge wheals; 20-40cm in diameter

Gyrate or polycyclic patterns of urticaria are often associated with drug eruptions

Corticosteroids and Antihistamines

Prednisone or prednisolone at the lowest possible dose on alternate days

Hydroxyzine hydrochloride = anithistamine of choice

600 mg/horse TID then after 3-4 days reduce dose to BID and then to minimum effective 

*teratogenic: do not use in pregnant mares!

2-4 years of age, no sex prediliction 

virtually undiagnosed in horses < 1yr

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Name this insect and describe characteristics.

Culicoides spp. (biting midges, no-see-ums)

Winged insects that are gnerally 2mm or smaller in length which breed in standing water and have a flight range of 1-2km. 

Only the female sex feeds, usually in the early morning or early evening hours

Culicoides are most active during hot, humid and still environmental conditions 

Similium spp

Stable flies

Mosquitoes  

Initially the disease is seasonal and often first appears in the spring, worsens in the summer and then regresses in the fall.

Which each successive year the clinical signs tend to become more severe and prolonged 

In temperate climates, more severe cases can present with year round clinical signs.  

1. Dorsal pattern that primarily affects the mane and tail regions (base of tail, rump, back, withers, poll, crest and ears)

2. Ventral pattern (entire ventral midline)

Different species of Culicoides spp are responsible for each pattern 

Pruritus and self trauma

The primary lesions are small papules but in ost cases these are obliterated as the result of intense pruritus and self trauma

Initially only partial alopecia is observed but this can progress to widespread alopecia, licheification (rugae may develop on the withers, neck and tail base) and excoriation 

Classic = 

**A young seasonally pruritic horse with tail involvement and NO depigmentation**

Eosinophillic and lymphocytic perivascular dermatitis and fibrosis with chronicity

+/- Eosinophillic vasculitis, focal areas of epidermal necrosis/spongiosis/exocytosis 

**Histopath is only supportive of a diagnosis of CHS**

Insect control in the early evening and morning hours (this is when the females feed).

Stable affected animals from dusk to mid-morning

Very fine mesh screens should cover all openings to the stable

The use of fans as Culicoides are weak flyers 

Topical insecticides and repellents

Horse blankets and fly covers 

Pyrethrins with synergists and synthetic pyrethroids 

2% permethrin applied in the late afternoon can be an effective repellent 

Corticosteroids

Antihistamines are not effective

Immunotherapy can also be of use

1. Drugs (environmental chemicals)

2.  Infections (viral - especially herpes, fungal, bacterial

3. Neoplasia (especially lymphoreticular neoplasms)

Often this disease can only be classified as idiopathic...

Acute onset and potentially recurrent with mild to severe lesions that tend to be symmetrical

Primary lesions = macules, bulla or vesicles (which often present as multifocal ulcerations, erosions and crusts)

Mucous membrane involvement can be common (erosions and ulcerations)

Epidermal: keratinocyte apoptosis that span all layers of the epidermis (+/- adnexal epithelium), lymphocyte exocytosis and satillitosis, vaculoization of the basal cell layer and sometimes the BM, marked parakeratosis scale and crust 

Dermal: superficial edema, free RBCs, superficial perivascular lymphocytic infiltrate

Trick question!

There is no specific therapy...mild cases will resolve spontaneously over weeks to months and severe cases may need corticosteroids for symptomatic relief

Antibiotics (especially penicillin and the sulfonamides)

Phenothiazine-based tranquilizers

NSAIDS

Diuretics

Local anesthetic agents

Anticonvulsants 

Urticaria and/or angioedema

Erythroderma

Bilateral symmetry 

Papular eruptions

Intense puritus 

Sharply demarcated erosions and ulcerations 

Vesicular and bullous lesions

Photosensitization 

Non-inflammatory acquired alopecia 

Lack of response to corticosteroids 

An abnormal host response to some antigen or antigens.

Hairy vetch has been potentially implicated

The most common form manifests as crusting and scaling with varying degrees of alopecia which may be focal, multifocal or generalized 

There is a rare nodular form which presents with large tumor-like masses

Both types can coexist 

SGD is a syndromic disease and nearly all cases have internal organ involvement with lung (exercise intolerance, increased RR and mild dypsnea) , LN (hitologically) and liver/GI (icterus and diarrhea) being common targets 

Skin and LN samples

Most likely to show granulomatous changes 

This is a diagnosis of exclusion :) 

The majority of cases occur in mature horses (5yrs +) but a small number occur in horses less then 1 yr old. 

Disease in younger horses tends to be less severe than in older animals, responds better to treatment and may spontaneously regress.

The head and the lower limbs - the coronary bands maybe the only affected site

Severe cases may include the entire body surface

Mucous membrane involvement is extremely rare 

Fever, drepression and anorexia may be seen 

Pruritus is variable 

As in other affected species, the primary lesion is a vesicle or pustule but these are fragile and so crusted papules are more commonly seen (look on the nostrils, lids or lips)

Transient or persistent urticaria may occur weeks before crusting lesions are seen

Edema of the hind limbs and ventral abdomen  

Subcorneal and/or intraepidermal pustule formation with ancantholysis that may be present in waves

Neutrophils are the primary infiltrating cell with occasional eosinophils 

Corticosteroids! 

Dexamethasone = 1st choice @ 0.02-0.1 mg/kg as a loading dose and eventual maintenance @ 0.01-0.02 mg/kg q48-72 hours; reduce initial dose by 20% weekly

Some horses may respond better to Prednisone/prednisolone and this drug may be better for long term therapy (switch to this after they are controlled on dex)

Gold salts (aurothioglucose) might be a maintenance option (1 mg/kg weekly) IM injection

**PF in the young horse is worth treating but a serious convo needs to be had with owners of older horses that develop PF as the prognosis is less favorable and may require life-long expensive therapy**

1) Primary (ingestion of photosensitizing molecules present in plants or drugs)

2) Hepatogenous (liver disease interfering with the metabolism of phylloerythrin- porphyrin derived from chlorophyll)

3) Abnormal pigment production (Hereditary porphyria)

***Manifestations can include photoactivated vasculitis

• D.congolensis is likely a saprophyte in the soil
• It is spread by direct contact between animals and through contaminated environments or possibly via biting insects

• Certain equine leukocyte antigen (ELA) alleles are at increased risk
• A3 and W13 are strongly associated with an increase in Thoroughbreds and in Swiss, French, and Irish Warmbloods
• Lower incidence with certain ELA (W13 allele in Standardbred horses supports genetic resistance)

• Bovine papillomavirus is implicated and often isolated from sarcoids
• Both BPV-1 and BPV-2 have been recovered, may find both viruses in the same horse with different sarcoids
• BPV-transforming genes (E5, E6 and E7) have been found in a small number of sarcoids and increase viral gene expression

• Clinical appearance
• Histopathology should reveal a fibrosarcoma appearance with pseudoepitheliomatous hyperplasia
• In some case the epidermal changes are lacking creating misdiagnosis as fibrosarcomas, neurofibromas or schwannomas
• PCR used to check for BPV DNA can be also be a valuable additional diagnostic test

• Topical treatment
  • 5% imiquimod (Aldara cream)
  • Bloodroot extract (Sanguinaria canadensis; XXTERRA, Larson Labs)
  • European mistletoe extract (Viscum album; Ttriterpene, viscotoxins, alkaloids and lectin (ML-1))
• Treatment extremely variable
• surgical excision with adjunctive therapy is often associated with high recurrence rates
• laser ablation to remove or debulk tumors appears more successful than traditional therapy
  • likely due to ability to ablate wound bed and destroy remaining tumor cells
• Cryotherapy is used with success in 85% of cases
• Hyperthermia successful in small number of cases
• Radiotherapy good success rate but expensive and needs special housing to give it (Radon-222, gold-198, radium-226, cobalt-60, iridium-192)
• Immunostimulants (Mycobacterium cell wall extracts, Live whole cell bacillus, purified Bacillus Camette-Guerin (BCG), Proproionobacterial cell wall extracts (EqStim, Neogen)
  • stimulates cell mediated immune response and causes tumor destruction
  • need multiple injections and better success post-surgical debulking
• Intralesional cisplatin
• Intralesional (TNF) with xanthine derivatives
• Topical 5-fluorouracil (5-FU)
• Compounded creams containing heaving metals 5-FU and thiouracil
• Topical Aciclovir 5%
• Immunotherapy for equine sarcoid using chimeric virus like particles (CVLPs) of BPV 1 L1-E7
  • stimulate antibody response

• Equine sarcoids are the most common skin tumor in horses, donkeys and mules
• occur in horses less than 7 years of age, with a higher risk in Appaloosas, Arabians and quarter horses
• Donkeys (particularly male donkeys) and mules have a higher risk than horses
• can often isolate bovine papilloma virus (BPV) from sarcoids
• Both BPV-1 and BPV-2 have been recovered 
  • may find both viruses in the same horse with different sarcoids
• BPV-transforming genes (E5, E6, and E7) have been found in a small number of sarcoids and increase viral gene expression

• Seasonality seen in up to 80% of cases
• Allergies vs insects?
• Photoperiod-neurohormonal changes
• changes in temperature and humidity
• Treatment options:
  • allergy testing and immunotherapy
  • antimicrobials, glucocorticoids, antihistamines, gabapentin, fly control, acupuncture and cyproheptadine (0.3mg/mg BID) and others

• Perioral, periorbital, neck
• circular alopecia +/- scaling
• BPV 1 and 2 
• E5, E6, E7 genes- malignant transformation