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BVETMED2 > Skin > Flashcards

Skin Flashcards

1
Q

What are the layers of the epidermis

A
  • Stratum basale - Tranasient amplyfying cells ( go through few cycles ofcycle division before differentiation). Attached to keratinocytes via desmosomes & to basement membrane by Hemi-desmosomes
  • Stratum spinosum - Cells are commited to terminal differentiation. Makes up bulk of living epidermis
  • Stratum granulosum - Keratohyaline granules bind keratin filaments together. secrete lamellar bodies, giving skin its hydrophobic property
  • Stratum corneum - Desquamation. Dead remnants of keratinocytes. Attached by Corneo-desmosomes. 40 cell layers thick. Turnover can be increased
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2
Q

What is parakeratosis

A

Abnormal cornification. Causes the replacement of annular squames with nucleated cells. Occurs during chronic inflammation and metabolic diseases. Causes flakes of dry skin

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3
Q

What do motor and sensor innervate in the skin

A

Motor

  • Blood vessels
  • Sweat galnds
  • Pilomotor apparatus

Sensory

  • Plexus of nerve fibres, both superficial and dep
  • Pain and itch - Many free nerve endings in skin
  • Touch and vibration - Merkel cells
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4
Q

What causes the sensation to itch and what are 3 drugs used to treat

A

Mediators:

  • Histamine
  • Bradykadin
  • Opiate peptides
  • IL-31 produced by t-cells has receptors on macrophages, eisoniphils. Acts via JAK STAT receptor

Try to treat original cause I.e Ectoparasiticide, Anti-microbial or allergen avoidances.

  1. Glucocorticoids - Binds to promoter region, inhibiting molecules of inflammation (e.g cytokines). Also upregulate anti-inflams
  2. Ciclosporin - Blocks transcription of cytokine genes in T-cells. highly specific inhibitor of T-cell activation
  3. Oclactinib - Blocks janus kinase enzyme. Blocks IL-2, IL-4, IL-6, IL-31
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5
Q

What are the two types of sweat gland

A
  1. Atrichial - Discharges onto the skiin surface E.g footpads
  2. Epitrachial - Discharge into hair follicle
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6
Q

What are the stages of hair growth

A
  1. Telogen - No growth, Hair sits loosely in outer sheath
  2. Anagen - Period of active hair growth. Inferior portion of hair follicle only present at this stage. Dermal papillae (mesenchymal cells) determine hair growth
  3. Catagen - short transition period between Anagen and telogen
  4. Exogen - Active shedding of hair
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7
Q

What are the areas of the hair follicle and what is a compund follicle

A

Infundibulum - Top of the hair shaft

Isthmus - From the sebaceous gland to the arrector pili muscle

Inferior - Only present during anagen

Compound follicle - Several hairs emerging from one ostium

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8
Q

What pathological processes can occur in the hair follicle

A
  • Inflammation - Infestation into hair shaft causing infalmmation. E.g dermatophytosis (ringworm) or demodicosis (over population of dermodex canis)
  • Follicle disease - Matrix/melanocyte abnormalities. pigment is clumped causing washed out or dilute colours (colour dilution alopecia)
  • Atrophic disease - Hyperadrenocortism causes cycle arrest of follicular growth
  • Dysplastic disease - Saddle back curley coat retriever
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9
Q

Describe species differences in epidermis in fish, reptiles and birds

A
  • Fish - Epidermis lacks a layer of dead, fully keratinised cells
  • Reptiles - Epidermis has high degree of cornification. Almost no glands
  • Birds - Epidermis only has two layers (has feathers) No sweat or sebaceous glands
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10
Q

What are the most common commensual bacteria on skin?

A
  • Staphylococci pseudintermedias is the most common coagulase +ve
  • Staphylococci simulans is the most common coagulase -ve

S.pseudointermedius is the one concerned with pathogenesis. But as animals are becoming more frequently in a immunocopromised state, S.simulans is a problem

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11
Q

What is Malassezia pachydermatis

A

A canine cutaneous fungal flora

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12
Q

What mite is aquired from the mother at birth and in what conditions can it be pathogenic

A

Demodex mites aquired from mother after birth. A functional demodex specific T-lymphocyte defect or immunodefiency allows disease

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13
Q

What is biofilm

A

A slime of DNA, proteins and polysacchrides that attach to abiotic/biotic surfaces. Microbial cells in biofilm are physiologically distinct from planktonic cells. Theres a change in phenotype for better resistance to the environment, chemical stress, antimicrobials & stress

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14
Q

What role do keratinocytes play in immune response?

A
  • Animicrobial response - defensins, reactive 02 intermediates
  • Inflammatory response - Cytokines, chemokines, eicosanoids
  • Influence adaptive immune response - activates T-cells
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15
Q

What is 1st and 2nd intension healing

A
  • 1st intension healing - Clean wound is sutured together. No granulation tissue formation
  • 2nd intention healing - Filling the wound with granulation tissue. Important to consider blood supply & how long wounds have been contaminated
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16
Q

Describe the stages of wound healing

A
  1. Inflammatory phase - Immediate wound retraction. haemorrhage causes influx of platelets and fibrinogen, then formation of haemostatic plug => scab. Platelets induce vasodilation (permeability) and chemotaxis (influx of WBC’s to remove bacteria).
  2. Proliferative stage - Myofibroblastic mesenchymal cells are activated by low 02, cytokines and ECM causing fibroblast migration. Fibroblasts lay down elastin, Type III collagen, proteoglycans and glycoproteins. Lateral edges contract bringing skin closer. Decrease in 02 tension causes increase in lactic acid the release of VEGF => angiogenesis. fibroplasia + angiogenesis = granulation tissue
  3. Epitheliasation - Epidermal and dermal cells seperate and become mobile. Epidermal cells proliferate and migrate over granulation tissue. Contact inhibition prevents furthur migration once all tissue is covered. Basememnt membrane accumulation. Affected by oxygen tension, adequate protection, absence of infection and moist environment
  4. Maturation - Can continue for years. Epithelium stratifies and collagen matures. Wound becomes less defined
17
Q

What are the advantages of granulation tissue

A
  • Resistant to local infection
  • Barrier to systemic infection
  • Surface for epithelial cell migration
  • Wound contraction
  • Source of myofibroblasts
  • Provides blood supply
18
Q

What are the factors affecting wound healing

A

1) Patient & physical factors

  • Age
  • Species
  • Temperature
  • Nutritional status
  • 02

2) Disease factors

  • Hypovalaemia
  • Aaemia
  • D.Melitus
  • Neoplasm
  • Liver disease
  • Hyperadrenocortism

3) Exogenous factors

  • Vitamins Corticosteroids
  • GF’s
  • Cytotoxic drugs

4) Wound factors

  • Bacteria
  • Necrotic tissue
  • Oxygen tension
  • Location
  • Moist
  • Blood supply
19
Q

What is dermatophytosis, what causes it what can cause secondary infection

A

Dermatophytosis is ringworm, caused by dermatophytes (fungi). Fungi usually accumulates on Stratum corneum or can invade hair shaft. Arthrospores can be seen on plucked hair and can remain for 14 months. A secondary infection can occur with S.aureus or S.intermedius and will cause pustules (pus under epidermis)

20
Q

What are Ctenocephalides, whats their life cycle and how are they treated/controlled

A

Flea’s

  • Can cause flea allergy dermatitis
  • Intermediate host for tapeworms, feline parvovirus & myxomatosis
  • Can be classified by pronatal (back of head) and gonal (under chin) combs

Life cycle

  • Adult flea produces dirt after blood meal
  • Lays eggs which are not sticky so easily deposited in environment
  • Larvae hatch withing 1-6 days and feed on flea dirt
  • undergo pupatation, adult flea emerges in 6-7 days
  • Pupal window - Once in cocoon, can remain unhatched for some time (140 days)

Seeks out host by seeking CO2, then seeks out warmth to detect most superficial capillaries. Adults live for 10 days. Once Insect juvenile hormone falls below critical adult flea emerges.

Treatment

  • Long acting adulticide - Kills adults flea, preventing furthur reproduction
  • Insect growth hormone regulators - Prevents flea reaching maturity
  • Hygiene - Vacuum carpets, especially hotspots !
21
Q

What are lice, whats their life cycle, clinical signs, how are they transmitted and how are they controled

A

Lice are perminent parasites that are highly host specific. They are dorso-ventrally flattened to avoid being groomed off easily and are transmitted by direct contact. Heavy infestations are known as pediculosis. There are 2 types:

  1. Blood sucking - Head is narrow and have large legs/claws. Feed on blood
  2. Chewing - Broad head (broader than thorax) with small legs. Feed on epithelial scales and scabs

Life cycle:

  • Adult louse lays eggs cemented onto hair follicles
  • Nymph emerges which moults into adult

Clinical signs include restlessness, self inflicted injurys and hair loss.

Treated with 2 treatments 2 weeks apart, this is to ensure any new nymphs emerging are killed

22
Q

What are warble flies, what is their life cycle, whats their pathogenic significance and how are they controlled

A

Warble flies (Hypoderma) are OBLIGATORY parasites. Currently have been eradicated from the uk and affect ruminants and horses. Similiar appearance to bumble bees with only one pair of wings.

Life cycle

  • Adults emerge in summer (june-august) laying eggs in belly/legs
  • H.lineatum approach stealthly and can lay a row of eggs whereas H.bovis is loud and causes gadding, therefore only lays one egg. Female survives 3 weeks, laying hundreds of eggs
  • Larvae hatch in a few days and migrate to winter resting sites withing 3 months
  • H.bovis resides in epidural fat of near SC & H.lineatum in wall of oesophagus
  • Remain here untill march, moult into L2 and migrate to subcutus in the midline of the back
  • Larvae burrow hole in skin to breath, moult to L3. These warbles are palpable
  • Larvae emerge in 4-10 weeks, fall to ground and pupate
  • Adult emerges in a month. One gen per year

Pathogenic significance

  • Downgrade hides with holes
  • Gadding => decreases milk yield
  • Trimmed meat losses due to green jelly around larvae
  • Larvae death of H.lineatum can cause bloat (oesaphageal obstruction, stopping erructation) and H.bovis causes neurological symptoms due to compression

Control

  • _Systemic organophosphorus insecti_cides - Dont use while larvae are over wintering, can cause paraplegia (paralysis of legs) or bloat
  • Avermectins can be used any time as larval antigen released slowly
23
Q

What are blow flies, whats their life cycle, what are thei categories, predesposing factors, pathogenesis and control methods

A

Lucilia sericata (greenbottle) is a FACULTATIVE parasite. affects 80% of uk sheep farms. Spiracles of larvae are used for identification. rabbits with blowstrike have a 45% of death

Life cycle

  • Attracted by odour of soiled faeces, urine or dead animals. lays cluster of eggs which hatch withing 24 hours
  • Feed on skin, moult twice within 1-2 weeks into adult maggots
  • They fall to ground to pupate. Adults emerges in less than a week in summer
  • Female becomes sexual mature after protein meal. adults survive a month

Categories

  • Primary flies - initiate strike. Larvae penetrate skin (Lucilia sericata)
  • Secondary flies - Cant initiate attack. Larvae attack areas already damaged and extend area of damage
  • Tertiary flies - Found when lesion becomes dry

Predesposing factors

  • Temperature - Early summer causes hatching of overwintering pupae
  • Rainful
  • Host susceptibility - Putrefactive odour due to soiling ( Oestertagia?)

Pathogenic significance

  • Sever skin damage
  • Secondary bacterial infection causes production losses
  • Sheep become anorexic
  • Stand away from rest of flock

Control

  • Prophylactic insecticide - Kill larvae and persist in fleece
  • Insect growth regulators (IGR) - 2-4 months of protection
  • Effective worm control (avoid diarrhoea)
  • Removing excess wool
24
Q

What are thew morphological differences between hard and soft ticks

A

Hard ticks

  • Have a scutum, a hard chitinous plate covering the dorsal surface of the body. Females have smalled scutum to allow for expansion during feeding and eggs
  • Festoons - Apple pie like notches around posterior margin of body
  • Mouth parts are visible

Soft ticks

  • Scutum is absent
  • Mouth parts are not visible
  • Dont swell as much, feed little and often
25
Q

How do ticks feed and what does their salavia contain

A

Ticks use their Chelicerae to puncture the skin, the hypostome then inserts deep into skin. Contains backwards facing spines to lock into place. Tick then feed continously

Saliva contains:

  • Histamine blockers (decrease inflammation)
  • Cytolysins - Enlarge lesion created by Chelicerae
  • Vasoactive mediators - Vascular permeability
  • Anti coagulants
26
Q

Whats the difference between trans-stadial transmission and trans-ovarian transmission

A
  • Trans-stadial - Disease contracted as a larvae, and is retained through life ( nymph and adult stages) but not passed to offspring (eggs)
  • Trans-ovarian - Infection passed onto eggs (E.g babesia)
27
Q

Whats the most relevant tick in the uk, whats its life cycle, what diseases does it transmit and epidemiology.

A

Ixodes ricinus (hard tick)

  • Life cycle - Egg => Larvae (6legs) => Nymph => adult
  • Mechanical vestor for Lyme disease (humans) and Babesia, louping ill and tick borne fever
  • Its a three host tick, with the whole life cycle lasting 3 years. Most of their time is spent on the ground. Require high humidity to contine development, found in mated vegetation. Increase in activity coincides with temperature
28
Q

What is Integrated parasite control and how are tick numbers controlled

A

Integrated parasitic control is when several approaches are used to control parasite not just drug treatment

Control

Kill ticks on the ground

  • Alter microclimate (drainage)
  • Remove live stock from pastures for an appropriate amount of time to starve ticks
  • Burn pasture

Seperate host from infection

  • Remove stock from pasture
  • Fence off infested pasture

Acaricides

Stock hybridisation

Vaccination - against hidden antigen, located in the gut. Apon blood meal, Ig’s in blood kill tick

29
Q

Describe Sarcoptes, Its life cycle, Pathogenic significane and how it diagnosed and treated

A

S.scabiei is a small round burrowing mite. It has short legs.

Life cycle: 3 weeks

  • Female creates tunnel in upper layer of epidermis, lays eggs and feeds on oozing from damaged tissues
  • Eggs hatch within a week
  • Larvae burrow into epidermis, forming moulting pockets where they moult
  • Nymphs moult twice before coming adults

Pathogenic significance:

  • Papule formation & erythema
  • Crust formation & alopecia
  • Wrinkling and thickening of skin
  • Self inflicted trauma

Notifiable disease in horses and sheep

Diagnosed by taking skin scraping until capillary blood appear. Add KOH and warm slide

Treat with acaricide or avermectins

30
Q

What is Knemidocoptes, whats its life cycle, pathogenic significance and hows it treated

A

Knemidocoptes is a burrowing mite with short legs and a U shaped chitinous bar.

L_ife cycle (same as sarcoptes)_

  • Female tunnels into epidermis, lays eggs and feeds on oozing damaged tissues
  • 6 legged larvae emerge and burrow into epidermis creating moulting pockets
  • Moult various times until adult stage reached

Pathogenic significance:

  • Scaly leg (K.mutans) - Burrow beneath scales of legs in poultry causing lameness
  • Depluming itch (K.gallinae) - Burrow into feather shafts causing irritation and pain
  • Scaly beak (K.pilae) - Attacks beak. Scaliness at base of beak

Treated with acaricides or avermectins

31
Q

What are demodex mites, whats their life cycle, their possible pathogenic significance, predisposing factors to disease and how you would diagnose the disease

A

Demodex mites are cigar shaped burrowing mites with stumpy legs.

Life cycle - Live as commensuals. Spend life in hair follicles or sebasceous glands. life cycle is 3 weeks. Transmitted from bitch to pup during suckling

Pathogenesis

  • Squamous demodecosis - Alopecia and thickening of skin
  • Pustular demodecosis - Skin invasion of staphylococci. Skin is wrinkled, containing pustules with ooze serum, blood or pus

Predisposing factors include family susceptibility, immunosuppression or immunosuppressants.

Can be diagnosed by applying drop of liquid paraffin on skin then take a skin scraping. A large number or larvae or nymphs will be active in an infection

32
Q

What is Psoroptes, what is its epidemiology, pathogenesis, diagnosis and treatment

A

Psoroptes is a non burrowing mite responsible for sheep scab. has a funnel shaped sucker mounted on segmented pedicles

Life cycle is restricted to the surface of the skin, where they suck serous exudate.

Epidemiology:

  • Seen in winter in long humid fleece
  • Population numbers decline after shearing
  • Spread by direct transfer and indirectly by fomite

Pathogenesis - Antigenic material in faeces causes hypersensitivity and inflammation/scale formation. followed by self inflicted injury

Diagnosed by skin scraping + 10% KOH and warm slide

Treatment includes plunge dipping sheep for 1 min with there head emerced atleast once and avermectins (injected)

33
Q

What is chorioptes, what is it similiar to and what is there pathogenesis

A

Chorioptes is a non burrowing mite, very similiar to Psortoptes, but has unsegmented pedicles with suckers. Alot less pathogenic than Psoroptes. Feeds on surface skin cells causing chorioptic mange. Affects rough legged horses inducing crusty lesions

34
Q

What is otodectes, what is its pathogenesis and how is it treated

A

Otodectes is a non burrowing mite with one species, O.cynotis. Most common mite in cats and dogs. Most cats harbour O.cynotis with no clinical signs. However in dogs is the most common cause of otitis externa.

Causes a brown waxy exudate which is suceptible to secondary bacterial infection. mites live under exudate/crust. frequent head shaking and scatching of ears seen

Treatment with ear drops which contain acaricide, fungicide, antibiotics and steroids. Repeat after 10-14 days to kill hatchlings

35
Q

What is cheyletiella

A

Cheyletiella is a Non burrowing mite with long legs and a waisted body.

Lives in fur, visiting the skin to feed. Highly contagious as its lives in the hair. easily transmitted by direct contact. Excessive dandruff/scaly dermatitis can be seen.

Scraping of flakey skin, it may be possible to see mites moving the dandruff. Treated with acaricide

36
Q

What is dermanyssus, whats its life cycle, pathogenesis and treatment

A

Dermanyssus is a spider like non burrowing mite that becomes red after meal.

Most of life cycle spent off host, only visiting to feed at night. Commonly lay eggs in crevices in poultry houses. Can survive months with no feed

Causes Irritation and restlessness. Can also cause anaemia if present in large numbers. Can also be a vector for bacteria (salmonella)

Treated with acaricide and treating building

37
Q

What is Neotrombicula, whats its life cycle and pathogenesis

A

Non burrowing mite found in soil. Bright orange.

Eggs are laid in soil, and larvae emerge to seek host to feed on. Only larvae are pathogenic. Increase in numbers in summer.

Larvae insert mouth parts and release cytolytic enymes, feeding on partly digested tissue causing irritation and can lead to hypersensititvity

BVETMED2 (10 decks)

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