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DOG, Derm > Dermatology > Flashcards

Dermatology Flashcards

1
Q

What are 3 skin diseases caused by Staphylococcus?

A
  1. Pyoderma (S. pseudintermedius in dog/ S. aureus in cats & horses)
  2. Greasy Pig (S. hyicus)
  3. Bumblefoot (S. aureus-most common)
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2
Q

What are 3 microbial agents that present as pruritus?

A
  1. Malessezia pachydermis
  2. Pseudomonas
  3. Staphylococcus
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3
Q

What test do you use to differentiate between pathogenic species of staph and poorer pathogenic staph?

A

Coagulase (clumping factor) tests (biochemical) determine coagulase +ve (pathogenic spp. s. aureus and s. pseudintermedius)
and poor pathogens (coagulase -ve) e.g. s. epidermidis, s. saprophyticus

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4
Q

What are the major virulence factors that pathogenic Staphylococcus have?

A
  1. Intracellular survival * KEY PRINCIPLE (evade immune system; evad antibiotics)
  2. Capsule and pseudo-capsule - (anti-phagocytic properties)
  3. Exotoxins - cytotoxins
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5
Q

Which Pseudomonas spp. is of major veterinary importance?

A

Pseudomonas aeroginosa

any other spp. isolated is not significant.

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6
Q

What is the major clinical sign of a Staphylococcus infection?

A

KEY PRINCIPLE:
Underlying disease process is usually one of suppuration & abscess formation which is typical of PYOGENIC bacteria (i.e. Staph, Strep & Corynebacterium)

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7
Q

How does pus form?

A

Pyogenic bacteria invade tissues, cause vasodilation,
marked exudation of neutrophils from blood vessels,
Neutrophils then move toward bacteria (chemotaxis), However, pathogenic bacteria are anti-phagocytic and produce toxins that kill cells (incl. phagocytic cells).
Enzymes liberated from dead neutrophils bring about additional tissue destruction..
Results in partial liquefaction of dead tissue and phagocytic cells –> becomes visible as thick, yellow pus.
Pus is viscous due to large amounts of DNA from the nuclei of dead cells.

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8
Q

How may Staphylococcus present clinically?

A
  • small pustules or

- Big walled-off abscesses

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9
Q

T/F: Staph are part of normal flora

A

TRUE, they are very common contaminants.

Therefore in order to place significance on an isolation on staph:

  • sample must be collected appropes
  • evidence of inflammation
  • staph isolated with the inflammation (e.g. intracellular bact)
  • Pathogenic staph are isolated (and preferable coagulase +ve)
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10
Q

What are the principles of Tx for Staph infections?

A
  1. DRAINAGE - ABs penetrate poorly into abscess
  2. Prolonged ABs in systemic diseases - Intracellular survival
  3. If simple, localised infections, topical Tx usually effective –> AVOID CONCURRENT ABs and GLUCOCORTICOIDS
  4. Increasing levels of AB resistance -> C&S testig for complicated infections
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11
Q

What are the 4(-5) microbial causes of ulceration, crusting & alopecia?

A
  1. Pseudomonas aeruginosa
  2. Dermatophylis congolensis
  3. Feline herpes/calicivirus
  4. Ovine scabby mouth (known as Orf or parapoxvirus)
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12
Q

What is ulceration of the skin?

A

break in the continuity of the epidermis
(erosion = partial thickness defect)
(ulcer = full thickness defect)

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13
Q

What is crusting of the skin?

A

liquid debris (exudates. serum, blood, pus) that has dried on the surface of the skin (often covers erosions/ulcers)

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14
Q

What is an infection caused by Dermatophylis congolensis (Dermatophilosis) commonly known as in horses?

A

‘Rain scald’,

also, rain rot, greasy heel

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15
Q

What is an infection caused by Dermatophylis congolensis (Dermatophylosis) commonly known as in sheep?

A

‘Lumpy wool’, ‘mycotic dermatitis’ and ‘strawberry foot’

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16
Q

List some features of Dermatophylis congolensis:

A
  • Branching; Gram +ve; filamentous rods
  • facultatively anaerobic
  • looks like railroad/tram tracks
  • interesting lifecycle
  • in order to cause disease -> need host compromise
  • Obligate parasite of the skin (may exist saprophytically only transitory, it cannot multiply in soil)
  • Reservoir for the bacteria are infected animals (mostly cattle, goats, sheep & horses)
  • worldwide dist.
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17
Q

Outline the lifecycle of dermatophylis:

A
  1. Reproductive unit = zoospore
  2. Zoospore germinates forming germ tube
  3. Germ tube elongates & thickens, divides both longitudinally and transversely and forms a strand several layers thick
  4. strand is enclosed within gelatinous sheath & constituent cells become cocoid as they differentiate into multi-flagellated zoospores
  5. The zoospores are then liberated as the strand disintegrates, completing the lifecycle.
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18
Q

What is the rule of 3’s for Dermatophytes?

A
  1. 3 genera of fungi (Microsporum spp.; Trichophyton spp. & Epidermophyton spp.)
  2. 3 ecological niches (Geophilic, zoophilic, anthropophilic)
  3. 3 spp. associated with cats & dogs (Microsporum canis; Microsporum gypseum; Trichophyton mentagrophytes)
  4. 3 main ways to diagnose Dermatophyte infections (Trichogram; Wood’s lamp; & fungal culture)
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19
Q

What are the main differential diagnoses for pruritic skin diseases in dogs?

A

Ecto: fleas, scabies, demodicosis, mites

Microbial skin infections; staphyloccocal pyoderma, malessezia pachydermatis; Pseudomonas

Allergies: FAD, Atopic dermatitis, Insect bite hypersensitiviity, contact dermatitis

Neoplastic skin disease; cutaneous lymphoma

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20
Q

What are the microbial suspects of cutaneous skin masses?

A
  1. Viruses: papilloma viruses & poxviruses

2. Fungi: Cryptococcus

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21
Q

What are the microbial suspects of suppurative/ pyogranulomatous/ granulomatous Inflammation?

A
  1. Restless residents: Staph, Actinomyces, oral flora & Corynebacterium
  2. Soil Saprophytes: Nocardia, Rhodococcus & rapidly growing Mycobacterium
22
Q

Staphyloccocus causes a range of skin disease:

A
  1. Pruritus (associated with inflammation, due to Staph products and host’s immune response (type III and type IV hypersensitivity rxns)
  2. Alopecia (due to self trauma)
  3. Ulceration/crusting (typical lesion = epidermal collarette > burst pustules)
  4. Nodules (Typical staph lesion = suppurative inflammation; small lesions = pustule; Big lesions = abscess)
23
Q

What type of bacteria are Actinomyces spp?

A
  • Gram +ve, branching rods
  • Facultatively anaerobic
  • Normal flora of oral MM and tooth surfaces of mammals so most infections are ENDOGENOUS
  • diseases come about from the introduction of normal flora to susceptible tissues of the host
  • NOT contagious (communicable only via bites); commonly seen in dogs with stick injuries.
24
Q

Name the differences and similarities of Dermatophilus and Actinomyces.

A

Both are gram +ve branching rods.

Dermatophilus produces zoospores; lives in skin crusts; is not part of normal flora; causes rain scald; mostly large animals; causes crusty skin disease.

Actinomyces does NOT produce zoospores; part of normal oral flora; causes boney or subcutaneous inflammation, especially around the head; found in ALL mammals

25
Q

What diseases fo Actinomyces spp.?

A
  1. Lumpy jaw -
    Osteomyelitis of mandible
  2. Soft tissue pyogranulomatous abscesses (many spp. of animals; commonly secondary to bite or scratch wounds or migrating grass awns)
26
Q

What are common bacteria associated with cat fight abscess?

A

Peptococcus; Peptostreptococcus; Pasteurella & Anaerobes

27
Q

What are the principles of treating subcutaneous abscesses?

A
  1. Drain - remove infectious agents, foreiggn material and by-products of the inflammatory response
  2. Debride - remove devitalised tissue and areas of potential “media” or ecological niches for bacteria. Allow access for further drainage over the following few days
  3. Lavage -flush with lots of sterile saline
  4. Antimicrobials (if cat is systemically unwell) - could be azotemic, bacteria spread haematogenously.
28
Q

What are common soil saprophytes?

A

Nocardia, Rhodococcus and rapidly growing Mycobacterium.

29
Q

What are some features of Coryneform bacteria?

A
  • Club-shaped
  • Pleiomorphic (different sized)
  • Gram +ve coccobacilli/short rods - structure as ‘chinese letters’ or ‘pallisades’
  • 2 coryneform bacteria that cause skin inflammation:
    1. Corynebacterium genus
    2. Rhodococcus equi species
30
Q

What is Caseous lymphadenitis and what bacteria is it caused by?

A
  • C. pseudotuberculosis
  • Major disease of sheep + goats
  • Is a commensal of oral cavity & GIT
  • can survive in soil
  • Causes abscessation
  • Infection of superficial lymph nodes
  • AKA ‘cheesy gland’.
  • Source of infection is discharge from rupture lesions (which contaminates soil)
  • Usually gains access via break in skin (macerated; shearing, castrating, dipping; marking, docking and mulesing; headbutting; discharging abscess
  • May disseminate thin ewe syndrome
  • Increased incidence with age (risk of exposure)
31
Q

Describe some features of Nocardia.

A
  • Gram +ve, branching rods (may also appear as short, club shaped rods
  • May be beaded due to uneven staining
  • some are partially acid fast (ZN stain)
  • strict aerobes
  • Variable mycolic content in cell wall > spp. may vary in their ability fr intracellular survival and staining properties
  • Saprophytes - found in soil, decaying vegetation, fresh & salt water & on plants
32
Q

What are 3 different types of Gram +ve branching rods?

A
  1. Dermatophilus: zoospores form parallel packets/tram tracks within the rod
  2. Nocardia: mycolic acid in cell wall may cause patchy gram staining
  3. Actinomyces: looks like Nocardia, culture often require to differentiate. More common in large animals
33
Q

What are the mycobacteria that are not rapidly growing?

A

Lepromatous Mycobacteria

34
Q

What is pharmacodynamics?

A

What the drug does to the body .

  • Drug receptor interaction
  • Effect
  • Clinical outcome
35
Q

What is pharmacokinetics?

A

What the body does to the drug.
- Concentration of drug in blood
(Absorption; Distribution; Metabolism & Excretion)

36
Q

What compounds can penetrate the skin?

A

Lipophilic compounds such as organophosphates

(organophosphates are clinically important poisons e.g. insecticides; bind to ACh esterase&raquo_space; ACh not being broken down and have prolonged effect at Neurotransmitter at peripheral NS Parasymp organs - prolonged stimulation» See SLUD signs (Salivation; lacrimation; Urination; Dehydration; Diarrhea)

37
Q

What is the primary barrier to penetration of foreign compounds in the skin?

A

S. corneum (most outer layer, consists of 8-16 layers of flattened stratified, highly keratinised cells embedded in a lipid matrix composed primarily of sterols, other neutral lipids and ceramides; Although highly water retarding, the dead keratinized cells are highly water absorbent - keeps skin supple & soft)

38
Q

What additional defences does the s. corneum have?

A
  • Apertures protected by lysozyme
  • Antimicrobial proteins (AMP) such as cathelicidins and defensins (induced by infection/injury; AB activity; Recruit WBCs)
  • Presence of normal flora
  • Acidic skin pH
  • Keratinocyte shedding
  • Sebum envelopment & movement from dermis to epidermis
39
Q

The “bricks and mortar” model describes what?

A

Potential routes of xenobiotic penetration via s. corneum

Keratinocytes = bricks, proteins = mortar

40
Q

What is the role of the dermis in drug absorption?

A
  • Skin is an amazing storage area for lipophilic drugs & small water soluble molecules.Dermis important with circulation/picking up molecules that way.
  • Dermis is highly vascular; Blood flow is affected by complex, interacting neural & local humoral influences
  • e.g. Local anaesthetic agents are complexed with Adrenaline which causes vasoconstriction (sympathetic on alpha1 receptos (ones on the arteries, NTR is NA) –» keeps it in a ‘local area’ via vasoconstriction so blood supply doesn’t take it away.
  • Sebaceous glands = SPREADING; excrete sebum, which may be a vehicle for lateral diffusion of topical substances on the surface of the skin (e.g. flea products such as fipronil or imidacloprid)
  • Orifice of both hair ducts & sweat glands may trap particulate drug formulations, which then function as extended - release depots to the surface of the skin

PK –» epidermis & dermis involved in all 4 PK processes

41
Q

What metabolic pathways are associated with skin metabolism of xenobiotics?

A
  • Phase I AND phase 2 metabolic pathways have been identified in the skin
  • Resident bacteria (normal flora) on surface of the skin may also metabolise topical drugs
42
Q

What are the major species differences of skin?

A

The major known determinants of species differences are:

  • skin thickness
  • hair/fur density
  • lipid composition
  • cutaneous blood flow
43
Q

What effects does rubbing, scratching and licking have on drug absorption?

A
  • Could either; INCREASE
    1. the absorbed dose by reducing the s. corneum layers
    2. Long-term mechanical stimulation could increase cellular thickness of s. corneum & REDUCE drug absorption
    3. Licking may increase absorption secondary to oral drug delivery
  • Mechanical trauma is the issue, not infection (as Enzymes in saliva counteract bacteria)
  • e.g. Lead poisoning from paint -> effects NTR, also vocalisation
44
Q

What are the types of dermal formulations?

A
  1. SKin surface protectants/barriers e.g. silica, sunscreen
  2. ‘dermatological’ to target the epidermis & dermis (penetration is important) - e.g. local anti-inflammatory creams, local anaesthetic creams ( alot of inflammatory cells in the skin that cause pruritus, some medication to dampen down some rxns)
  3. ‘Transdermal’ preparations target drugs to the systemic circulation (absorption is important)
45
Q

What type of dermal formulation are ‘spot-on pesticides’

A

‘transdermal’ delivery&raquo_space; target systemic circulation (absorption is important)

compared with ‘dips’ for treatment of surface parasites

46
Q

What are the therapeutic families that treat pruritic animals?

A
  1. Anti-inflammatories (Glucocorticosteroids; T-lymphocyte inhibitors - cyclosporine; Anti-histamines; Janus kinase inhibitors)
  2. Antiparasiticides
  3. Antibacterials
  4. Antifungals
47
Q

What are the ‘First-line’ families used to inhibit inflammation?

A
  1. NSAIDS - musculo-skeletal pain; analgesics; antipyretics
  2. Steroidal anti-inflammatories (a.k.a. Glucocorticosteroids) - pruritus; allergiesl higher doses used to treat immunosuppressive diseases
48
Q

How do Glucocorticosteroids work?

A

On liganf binding to GCS recepto, the complex undergoes conformational change that triggers its translocation to the nucleus, where it exerts its actions mainly through genomic transactivation or transrepression mechanisms

49
Q

How do glucocorticosteroids carry out their anti-inflammatory effect and what are common formulations seen in vet practice?

A

GCS have a role in ‘stabilising’ cell membranes.

Formulations:

  • Oral tabs (e.g. pred)
  • Injectable - IV, IM, or SC, intra-articular, intralesional
  • Topical formulations - skin creams, ear drops, eye ointment, inhalants
50
Q

When would you use GCS?

A
  1. To control clinical signs of allergies (acute allergic rxn)
    - Histamine or glucocorticosteroid
  2. To reduce acute inflammation or swelling
    - e.g. dog vaccination rxn
    - e.g. allergic sting, airway obstruction, swollen around larynx and pharynx, reaction may effect bronchoconstriction (give adrenalin + Antihistamine + quick-acting glucosteroid to get down swelling)
  3. Autoimmune diseases
    - control immune-mediated diseases e.g. myasthenia gravis
  4. WBC tumours (lymphoma & leukaemias)
  5. To delay healing in some circumstances - nly after infection control e.g. corneal ulcer

DOG, Derm (6 decks)

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