JPC SYSTEMIC PATHOLOGY
INTEGUMENTARY SYSTEM
November 2022
I-P06
Signalment (JPC# 21474-15): A young dog
HISTORY: This dog presented with a generalized alopecic and pruritic skin condition.
HISTOPATHOLOGIC DESCRIPTION: Haired skin: Diffusely, the epidermis is hyperplastic, thickened up to 0.5 mm with acanthosis, prominent rete ridges, spongiosis, and multifocal orthokeratotic and parakeratotic hyperkeratosis, with embedded adult arthropods and eggs. Within the stratum corneum, occasionally within tunnels, adult arthropods are characterized by an ovoid, 200-300 x 100-150m body with a 3µm chitinous exoskeleton, dorsal spines, jointed appendages, striated muscle, body cavity (hemocoel), and intestinal and reproductive structures. Eggs are oval, thin-shelled, and 70 x 40µm. There are multifocal intracorneal pustules composed of degenerate neutrophils, necrotic cellular debris, and proteinaceous fluid. Diffusely the superficial dermis is expanded by clear space (edema) with ectactic lymphatics and infiltrated by few lymphocytes, plasma cells, neutrophils, and eosinophils. There are few ectatic hair follicles.
MORPHOLOGIC DIAGNOSIS: Haired skin: Epidermal hyperplasia and hyperkeratosis, diffuse, marked, with mild eosinophilic dermatitis and numerous intracorneal mites, breed unspecified, canine.
ETIOLOGIC DIAGNOSIS: Sarcoptic dermatitis
CAUSE: Sarcoptes scabiei var. canis
CONDITION: Sarcoptic mange
CONDITION SYNONYM: Canine scabies
GENERAL DISCUSSION:
- Species is divided into numerous host-adapted varieties with essentially identical features that rarely cross species
- Common in dogs, pigs, goats (common per one reference, uncommon per another reference), wild canids, and other exotic species; uncommon in cattle (psoroptic mange is more important); rare in horses, sheep, and cats
- Highly contagious, intensely pruritic, nonseasonal skin disease that is relatively host specific but can cause transient disease in other species, including humans
- Reportable disease of food animals in some countries
PATHOGENESIS:
- Transmission is by direct contact or via fomites; highly contagious
- In the natural host, the parasite completes its life cycle in tunnels burrowed into and under the stratum corneum
- Burrowing female mites directly damage the epidermis > mite secretions and excreta incite local irritation > the host becomes sensitized to the mite or mite products > allergic reaction (most important) > intense pruritus > self‑trauma, secondary infection
- The proteins released by the mites create an immediate (type I) and delayed (type IV) hypersensitivity
- Both a humoral and cell‑mediated hypersensitivity reaction occur, with formation of circulating immune complexes
- Cell mediated immunity limits spread in normal animals
- Poorly-nourished or immunosuppressed animals develop massive mite infestations
LIFE CYCLE:
- Entire life cycle (2-3wks) is spent on the host; poor viability in external environment
- Mating occurs near surface in a “molting pocket” à female mite burrows through superficial keratin and feeds on lymph/cells in stratum granulosum and stratum spinosum > deposits 1-4 eggs per day for 6 weeks before dying > eggs > larva > (six-legged) > nymphs (eight-legged) > reach maturity in 10-15 days
TYPICAL CLINICAL FINDINGS:
- Severe pruritus and alopecia
- 50-100% of affected dogs with pinnal lesions have a positive pinnal-pedal reflex
- Self‑trauma; secondary bacterial infections; generalized lymphadenopathy
- Immunosuppressed (e.g. long-term corticosteroid therapy in dogs) often have more widespread (and more hyperkeratotic) lesions and higher mite populations
- Multiple animals typically affected; asymptomatic carriers can exist with minimal pruritus
TYPICAL GROSS FINDINGS:
- Lesions often concentrated in sparsely haired regions of body; especially ears (lateral margins of the pinna), lateral elbows, hocks, ventral thorax and abdomen
- Most often the dorsum is spared
- Primary parasite-related lesions: Erythematous maculopapular eruptions, crusting (crusts are often thick and yellowish white) and alopecia
- Secondary lesions: Bleeding, hemorrhagic crusts, self‑induced traumatic excoriations, and lesions due to secondary bacterial infections
- Poorly-nourished or immunosuppressed animals: Chronic infection with lichenification, marked alopecia, hyperpigmentation, and fissuring
TYPICAL LIGHT MICROSCOPIC FINDINGS:
- Typical allergic form lacks mites and lesions are indistinguishable from other allergic dermatoses; diagnosis depends on history of extreme pruritis and nature of cutaneous lesions; definitive diagnosis requires demonstration of parasite
- Epidermis: Moderate to severe acanthosis; variable spongiosis and leukocytic exocytosis; hyperkeratosis and multifocal parakeratosis or serocellular crust +/- intraepidermal eosinophilic pustules
- Mites and ova are rarely present in microscopic sections
- Numerous mites may be present in chronic form with poorly developed hypersensitivity reactions
- Adult female is 200-400µm in diameter, oval, with a spiny chitinous exoskeleton, 8 legs, jointed appendages, skeletal muscle, and a terminal anus; 2 anterior sets of legs are short with long unjointed stalks and suckers, two posterior pairs of legs are poorly developed but have long bristles
- Dermis: Edema; superficial, perivascular to interstitial dermatitis of eosinophils, lymphocytes and macrophages; +/- neutrophils and plasma cells in traumatized lesions
- Immunosuppressed animals: Numerous mites in epidermal burrows; marked parakeratosis
ADDITIONAL DIAGNOSTIC TESTS:
- Definitive diagnosis requires demonstration of the parasite
- Response to appropriate therapy: the most useful diagnostic procedure
- Multiple, superficial skin scrapings (ear margin, lateral elbow); up to 80% skin scrapes of affected dogs are negative
- IHC: Recent study (Doukas et al; J Comp Pathol. 2021) found all layers of affected stratum spinosum are immunoreactive for cytokeratins MNF116, K5/6, and K14 compared to only the 2-3 deepest cell layers in healthy animals
DIFFERENTIAL DIAGNOSIS:
- Gross:
- Food hypersensitivity: Pruritic; face, feet and ears commonly affected with erythematous or crusted papules
- Flea allergy dermatitis: Flea debris or fleas observed; crusted papules; alopecia along dorsal midline and sacrum
- Cheyletiellosis: Mites do not burrow; live on epidermal surface; prominent hyperkeratosis not uncommon
- Microscopic:
- Cutaneous dirofilariasis: Often form nodular perivascular aggregates; segments of microfilaria within vessels or within extravascular inflammatory foci
- Zinc-responsive dermatosis: Primarily a diffuse parakeratotic hyperkeratosis; no organisms evident
- Hookworm dermatitis: Distal extremities and footpads; linear accumulations of neutrophils and eosinophils form “tracks” that extend into the dermis
- Food allergy dermatitis: Superficial perivascular infiltrates composed of lymphocytes, macrophages, eosinophils, and mast cells; eosinophils may extend to surround deep dermal vessels (highly suggestive of food allergy)
- Flea allergy dermatitis: Mild chronic epidermal lesions; dermal changes very similar to food allergy dermatitis and may be indistinguishable
COMPARATIVE PATHOLOGY:
- Pigs (S. scabiei var suis): Most important ectoparasite of swine; both domestic and wild swine affected; most common site for primary lesions/mites is inner surface of pinna; papular lesions associated with allergic reactions; lesions secondary to self-trauma occur on rump, flank, and abdomen; 2 distinct clinical forms exist:
- Hypersensitivity form: Most common; intense pruritus; papules and crusts in/on the ears becoming widespread (dorsum spared); young growing pigs
- Hyperkeratotic mange: Affects multiparous sows and debilitated animals; moderate to severe pruritis; chronic infestation with thick, asbestos-like crusts on the pinnae, head, neck, and legs
- Cat: S. scabiei is rare, often nonpruritic in cats; has been likened to "Norwegian-type scabies" (a crusted scabies that occurs in immunosuppressed humans)
- Agent of “feline scabies” is Notoedres cati (I-P08)
- Goats: S. scabiei var caprae; lesions on face, pinna, neck, and legs; may become generalized
- Cattle: S. scabiei var bovis; predilection for head (“head mange”), neck; may become generalized; reportable disease in United States
- Sheep: S. scabiei var ovis; predilection for non-wooled regions, lips, nostrils, external pinna, +/- legs
- Horses: S scabiei var equi; rare; lesions on head, pinna, neck
- Wild canids (red fox, kit fox, grey wolf, coyote): Highly susceptible to sarcoptic mange; associated with reduced hunting and reproductive success and can lead to emaciated and mortality; can be a conservation threat
- Two recognized forms: Hyperkeratotic and alopecic
- Hyperkeratotic form: more common in naïve or immunocompromised animals; thick fissured crusts with many intralesional mites, lymphoplasmacytic or lymphohistiocytic inflammation
- Alopecic form: the hypersensitivity form more common in animals able to mount strong type I and IV hypersensitivity reactions to the mites; alopecia with primarily eosinophilic inflammation and few intralesional mites
- Two recognized forms: Hyperkeratotic and alopecic
- Guinea pigs (Trixacarus caviae): Keratosis, crusting, alopecia over the neck, shoulders, inner thighs, and abdomen; mite burrows in stratum corneum
- Rabbits: One report of an outbreak of S. scabiei in Holland lop rabbits; Notoedres cati produces similar lesions in rabbits
- Psoroptes cuniculi (I-P10) is the agent of rabbit “psoroptic mange”
- Camelids: Both NW and OW affected
- Alpacas: S. scabiei var auchinae; weight loss and decreased fiber production; lesions begin on ventral abdomen and chest
- Wombats, wallabies and koalas: Most significant parasitic disease of common wombats; fissuring of parakeratotic crust and skin is pathognomonic for sarcoptic mange in these species
- Raccoons
- NHPs: Marked pruritus, anorexia, emaciation; alopecia with thickening and scaling of skin; cause of neonatal death
- S. scabei: OWM (cynomolgus monkeys and drills) and great apes (gorillas, chimpanzees, orangutans, gibbons, and simangs)
- Prosarcoptes pitheci: OWM (African green monkeys and baboons) and NWM in captivity (cebus)
- Dunnalges lambrechti and Rosalialges cruciformis: Sarcoptifrom species reported in NWM (marmosets and owl monkeys)
- Human: Infestations of animal origin have been reported; however, mites stay on skin surface and do not complete life cycle
REFERENCES:
- Agnew A. Camelidae. In: Terio KA, McAloose D, St. Leger J, eds. Pathology of Wildlife and Zoo Animals. Cambridge, MA: Elsevier; 2018: 201.
- Barthold SW, Griffey SM, Percy DH. Pathology of Laboratory Rodents and Rabbits, 4th ed. Ames, IA: Blackwell Publishing; 2016: 238, 303-4.
- Church ME, Terio KA, Keel MK. Procyonidae, Viverridae, Hyenidae, Herpestidae, Eupleridae, and Prionodontidae. In: Terio KA, McAloose D, St. Leger J, eds. Pathology of Wildlife and Zoo Animals. Cambridge, MA: Elsevier; 2018: 316.
- Doukas D, Liakou Z, Koukoulis GK, Tontis D. Immunohistochemical Expression of Keratins in Normal Ovine Skin and in Chronic Dermatitis due to Sarcoptes scabiei. J Comp Pathol. 2021;183:63-71.
- Higgins D, Rose K, Spratt D. Monotremes and marsupials. In: Terio KA, McAloose D, St. Leger J, eds. Pathology of Wildlife and Zoo Animals. Cambridge, MA: Elsevier; 2018: 475-6.
- Jimenez Martinez MA, Gasper DJ, Carmona Mucino MC, Terio KA. Suidae and Tayassuidae. In: Terio KA, McAloose D, St. Leger J, eds. Pathology of Wildlife and Zoo Animals. Cambridge, MA: Elsevier; 2018: 221-2.
- Keel MK, Terio KA, McAloose D. Canidae, Ursidae, and Ailuridae. In: Terio KA, McAloose D, St. Leger J, eds. Pathology of Wildlife and Zoo Animals. Cambridge, MA: Elsevier; 2018: 252-3.
- Lowenstine LJ, McManamon R, Terio KA. Apes. In: Terio KA, McAloose D, St. Leger J, eds. Pathology of Wildlife and Zoo Animals. Cambridge, MA: Elsevier; 2018: 402.
- Mauldin E, Peters-Kennedy J. Integumentary system. In: Maxie MG, ed. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals. Vol 1. 6th ed. Philadelphia, PA:Elsevier; 2016:673-680.
- Strait K, Else JG, Eberhard ML. Parasitic diseases of nonhuman primates. In: Abee CR, Mansfield K, Tardif S, et al. Nonhuman primates in biomedical research: Diseases. Vol 2. San Diego, CA: Academic Press; 2012: 266-8, 575.
- Welle MW, Linder, KE. The integument. In: McGavin MD, Zachary JF, eds. Pathologic Basis of Veterinary Disease. 7th ed. St. Louis, MO: Elsevier; 2022:1179,1181-2.