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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
What diseases fo Actinomyces spp.?
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
What are common bacteria associated with cat fight abscess?
Peptococcus; Peptostreptococcus; Pasteurella & Anaerobes
27
What are the principles of treating subcutaneous abscesses?
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
What are common soil saprophytes?
Nocardia, Rhodococcus and rapidly growing Mycobacterium.
29
What are some features of Coryneform bacteria?
- 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
What is Caseous lymphadenitis and what bacteria is it caused by?
- 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
Describe some features of Nocardia.
- 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
What are 3 different types of Gram +ve branching rods?
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
What are the mycobacteria that are not rapidly growing?
Lepromatous Mycobacteria
34
What is pharmacodynamics?
What the drug does to the body . - Drug receptor interaction - Effect - Clinical outcome
35
What is pharmacokinetics?
What the body does to the drug. - Concentration of drug in blood (Absorption; Distribution; Metabolism & Excretion)
36
What compounds can penetrate the skin?
Lipophilic compounds such as organophosphates (organophosphates are clinically important poisons e.g. insecticides; bind to ACh esterase >> 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
What is the primary barrier to penetration of foreign compounds in the skin?
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
What additional defences does the s. corneum have?
- 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
The "bricks and mortar" model describes what?
Potential routes of xenobiotic penetration via s. corneum Keratinocytes = bricks, proteins = mortar
40
What is the role of the dermis in drug absorption?
- 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
What metabolic pathways are associated with skin metabolism of xenobiotics?
- 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
What are the major species differences of skin?
The major known determinants of species differences are: - skin thickness - hair/fur density - lipid composition - cutaneous blood flow
43
What effects does rubbing, scratching and licking have on drug absorption?
- 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
What are the types of dermal formulations?
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
What type of dermal formulation are 'spot-on pesticides'
'transdermal' delivery >> target systemic circulation (absorption is important) compared with 'dips' for treatment of surface parasites
46
What are the therapeutic families that treat pruritic animals?
1. Anti-inflammatories (Glucocorticosteroids; T-lymphocyte inhibitors - cyclosporine; Anti-histamines; Janus kinase inhibitors) 2. Antiparasiticides 3. Antibacterials 4. Antifungals
47
What are the 'First-line' families used to inhibit inflammation?
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
How do Glucocorticosteroids work?
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
How do glucocorticosteroids carry out their anti-inflammatory effect and what are common formulations seen in vet practice?
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
When would you use GCS?
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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