Otitis Externa Flashcards

1
Q

Define otitis

A

Inflammation of the pinnae and/or ear canals, may or may not be associated with infection

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2
Q

Define ear infection

A

A clinically significant microbial overgrowth or infection, most cases representing a dysbiosis of local otic microbiome rather than true acquired infection

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3
Q

Define recurrent as it relates to otitis

A

Clinically significant ear inflammation/infection within 3 months

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4
Q

Define acute otitis

A

otitis without acquired proliferative changes in the ear canals

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5
Q

Define chronic otitis

A

otitis with the presence of acquired proliferative changes in the ear canals

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6
Q

What are the 2 distinct clinical presentations of otitis externa

A
  1. erythroceruminous otitis
  2. suppurative otitis
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7
Q

Describe erythroceruminous otitis

A

erythema with a ceruminous to seborrheic discharge, may be simply inflamed but most associated with Malassezia or staph overgrowths, pruritus; chronic inflammation may have gram- bacteria, stenosis, pain

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8
Q

Describe suppurative otitis

A

erythema, ulceration, and a purulent discharge often with a biofilm, most have neutrophils and Pseudomonas app with other gram- and gram+ less common, Malassezia rare but show a distinct phenotype that may be associated with IgE-associated Malassezia sensitivity and immune-mediated diseases that affect the ear canal, often very painful

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9
Q

Describe suppurative otitis

A
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10
Q

Are recurrent ear infections primary or secondary?

A

All recurrent ear infections are secondary, does not mean the treatment failed but the underlying triggers were not managed

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11
Q

What are the 3-4 factors that contribute to chronic otitis?

A

Primary factors
Predisposing factors
Perpetuating factors
Secondary infections
(PPP or PSPP/PPPS)

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12
Q

Name common primary triggers for otitis externa

A

Hypersensitivity (atopic dermatitis/food-induced atopic dermatitis)
Parasitic (Otodectes cyanotis, less common Demodex spp)
Space-occupying lesions (ceruminous gland adenoma/adenocarcinoma, plasmacytoma, others; inflammatory polyp), common in older dogs
Miscellaneous (foreign body eg grass awn)

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13
Q

Name UNcommon primary triggers for otitis externa

A

Hypersensitivity (cutaneous adverse food reactions, allergic or irritant contact reactions)
Parasitic (Demodex app with generalized disease)
Endocrinopathies (HAC, hypot4, hyperestrogenism/Sertoli cell tumors)
Immunosuppression (Iatrogenic eg. glucocorticoid, chemotherapy)
Miscellaneous (acquired scar tissue and stenosis)

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14
Q

Name rare primary triggers for otitis

A

Primary immunodeficiency
Congenital ear canal narrowing or atresi

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15
Q

Do predisposing factors trigger otitis externa by themselves?

A

Rarely, make otitis more likely to occur or more likely to progress in an animal with a primary condition

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16
Q

Name a breed example of a predisposing factor for otitis externa

A

Cocker Spaniels have a greater density of ceruminous glands than other breeds, predisposing them to ceruminous gland hyperplasia, ectasia, and cyst formation
Chinese shar peis have a tightly opposed rostrally facing pinna that is partly the outcome of a twist in the vertical canal in some dogs resulting in stenosis

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17
Q

List anatomy and conformational predisposing factors for otitis externa

A

Hairy pinnae and/or ear canals
Pendulous pinnae
Increased density and altered physiology of ceruminous glands
Narrow ear canals or atresia

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18
Q

List lifestyle and management predisposing factors for otitis externa

A

Swimming
Overcleaning (wetting, maceration, impaction of material deeper in the ear canals, iatrogenic damage)
Routine plucking of hairs
Hot and humid enviroments

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19
Q

What causes the “cobblestone” appearance of chronic otitis?

A

Nodular epidermal and and glandular hyperplasia

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20
Q

What are perpetuating changes in otitis externa?

A

Chronic acquired pathological changes in the ear canals that prevent resolution

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21
Q

Name early perpetuating changes in otitis externa

A

nodular epidermal and glandular hyperplasia (“cobblestone” appearance)

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22
Q

Name late changes perpetuating otitis externa

A

further epidermal and dermal hyperplasia and thickening, ear canal stenosis and occlusion, fibrosis, and mineralization, can result in tympanic membrane rupture, otitis media, and cholestoma formation

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23
Q

Why is it important that early chronic acquired pathological changes are recognized and treated?

A

best chance at good long-term outcome, more severe changes become progressively harder to treat increasing the complexity, complications, and cost

24
Q

Compare the healthy ear with chronic pathological changes

A

Healthy: thin cartilage tubes lines by skin, freely mobile, pliable, and free from discharge, pruritus, and pain; thin smooth, and pale lining with scant ceruminous discharge and a translucent, taut, and slightly concave tympanic membrane
Chronic: progressively immobile, firm, painful; roughened (cobblestone-like) appearance, ceruminous hyperplasia, cysts and polyps, thickening and stenosis, increased discharge, and tympanic membrane thickening and inflammation (myringitis), opacity, distortion, and/or rupture

25
Q

What information does CT give for otitis?

A

bone and soft-tissue windows with contrast enhancement give highly detailed information about ear canal inflammation and chronic changes (including thickening, ceruminous hyperplasia, stenosis, and mineralization), polyps and tumors, discharge, tympanic membrane integrity, otitis media, and otitis interna

26
Q

What are the phases of treatment of recurrent otitis externa?

A

Induction and Remission
it is a progressive chronic inflammatory process
1. Phase 1 reactive therapy: the treatment of existing acute and/or chronic lesions and/or infection to clinical remission
2. Phase 2 proactive therapy: long-term regular therapy to maintain remission and prevent flares

27
Q

What are the most common pathogens in ear infections?

A

Malassezia yeasts
Staph pseudointermedius
Pseudomonas aeruginosa

28
Q

Describe the ear canal microbiome

A

mix of bacterial and fungal microbiotas
diversity reflects richness (total number of microbial species present) and evenness (relative abundance of each species in the microbial community) of the microbial population
Proteobacteria, Actinobacteria, Firmstes, Fusobacteria, and Baceteroidetes
Malassezia spp dominate, M globosa and M restricta on healthy skin

29
Q

What are some organisms found in ears?

A

Malassezia pachydermatis
Staphylococcus pseudointermedius
Staphylococcus schleiferi
more unusual anaerobes: Finegolda magna, Peptostreptococcus canis, and Porphyromonas cangingivalis
Ralstonia spp
E. coli and some Porphyromonas (including cangingivalis) are abundant in healthy ears
GSD study: few differences between allergic and non-allergic, Actinobacteria macrococcus in nonallergic and Proteobacteria sphingomonas in allergic

30
Q

What is the sequelae of loss of diversity of the otic microbiome?

A

staphylococcal, Malassezia, and Pseudomonas spp dominated populations
likely mutual interaction between skin barrier function, cutaneous immunity, and the microbiome
contribute to ongoing inflammation and epidermal changes through the exclusion of less pathogenic organisms, expression of pro-inflammatory mediators, and (in some atopic individuals) sensitization and specific IgE production

31
Q

What topicals preserve fungal and bacterial microbiota diversity?

A

2% chlorhexidine/2% miconazole on the skin
topical mometasone in ears
systemic glucocorticoid and ciclosporin

32
Q

Are cultures and antimicrobial susceptibility tests of benefit in otitis externa?

A

Limited.
Cannot be used to reliably select antimicrobials, results poorly predictive of response to topical treatment
Sensitive result does not guarantee treatment success due to local factors that affect efficacy (ongoing inflammation, discharge, biofilm, ear canal stenosis, and other primary, predisposing, and perpetuating factors)

33
Q

What is a situation where a culture may be helpful for otitis externa?

A

Organisms with unusual morphology (coryneforms, cocco-bacilli, filaments, yeasts, hyphae, etc) are seen on cytology raising suspicion of rare infections (unusual bacteria, Candida yeasts, Aspergillus hyphae, etc)
Culture can also be used to differentiate rods when considering leave-in products containing florfenicol (effective against E. coli, Klebsiella, Proteus spp, etc. but not Pseudomonas spp.)

34
Q

What are risk factors for Aspergillus otitis externa?

A

Immunosuppression
Otic foreign bodies
Prior antibiotic use

35
Q

What are risk factors for Aspergillus otitis externa?

A

Immunosuppression
Otic foreign bodies
Prior antibiotic use

36
Q

What rod bacteria are susceptible to florfenicol?

A

NOT Pseudomonas spp.
E. coli
Klebsiella
Proteus spp.

37
Q

Why are Pseudomonas spp ear infections challenging?

A

They show widespread inherent resistance, mutate and develop acquired resistance rapidly, and readily form biofilms

38
Q

What is a common source infection?

A

Associated with exposure of susceptible individuals to a fomite/vehicle or vector contaminated by an infectious organism
eg. Pseudomonas

39
Q

Where are Pseudomonas common and widespread?

A

Any wet environment: wet outdoor habitats as well as indoor sources such as washing facilities, drains, water, and food bowls
Veterinary sources: improperly cleaned and dried equipment, shampoos/ear cleaners, disinfectants, multi dose vials, and other solutions
Some dogs carry their own Pseudomonas bacterial population where conformation and other factors provide a suitable moist and protected habitat (lip folds, facial or body folds, and perivulvar folds)

40
Q

Pseudomonas otitis externa risk factors

A

uncommon and opportunistic, infections are secondary to specific risk factors
- atopic diseases
- masses
- endocrinopathies
- autoimmune diseases
*Pseudomonas-associated otitis develops more quickly with masses or autoimmune disease compared with atopic disease and endocrinopathies

41
Q

Describe cytology of Pseudomonas bacterial otitis

A

severe suppurative otitis with rod bacteria and neutrophils, biofilm formation is common

42
Q

What is the treatment for Pseudomonas infection

A

Topical more effective, systemic may not adequately penetrate the inflamed ear canals and lumen but systemic may be necessary when topical is not feasible (select antibiotic based on culture as AST using highest safe doses possible to minimize the risk of treatment failure, especially in chronic otitis and/or with biofilms)
Concurrent glucocorticoid therapy
Pain control

43
Q

Epidermal migration

A

Results in the outward movement of desquamated cells, cerumen, and debris from the tympanic membrane to the pinnae
Breaks down in otitis allowing desquamated cells, cerumen, and debris to build up

44
Q

Importance of ear cleaning

A

improved clinical and cytological scores, decreased debris, and altered lipid profiles which may promoted a more diverse microbiome (topical “prebiotic”)

45
Q

What ingredients are most effective in ear cleaners?

A

isopropyl alcohol, parachlrometaxylenol, chlorhexidine, hypocholorous acid, and low pH; Tris-EDTA at 50mg/ml can show additive activity with chlorhexidine, ahminoglycosides, and fluoroquinolones, inclusion of mono- and polysaccharides can reduce microbial adherence to keratinocytes
(alcohols and acids may irritate inflamed or ulcerated ear canals)

46
Q

Biofilm description

A

Complex and dynamic populations of microorganisms that adhere to each other and to a substrate (including the skin and hairs in and around the pinnae and ear canals)
Microbial cells are embedded within a slimy extracellular matrix composed of a complex array of polysaccharides, proteins, lipids, and DNA

47
Q

How do biofilms persist?

A
  • differentiate to specialize in motility
  • matrix production
  • nutrient sharing
  • sporulation
    almost all microbes can form biofilms, they are most common with Pseudomonas spp in otitis but also Staph spp, other bacteria, and Malassezia yeasts
48
Q

Cytology of biofilms

A

modified Wright-Giemsa form a pink-cerise veil or net-like material embedding the neutrophils and organisms
periodic acid Schiff more specific stain

49
Q

What do biofilms do?

A

enable bacteria to persistently colonize tissues, medical equipment (including otoscopes), and environments
they are sheltered from environmental factors, cleaning, disinfection, antimicrobials, and innate and adaptive immunity

50
Q

How do biofilm-associated infections rapidly recrudesce following treatment?

A

Exposure to sublethal antimicrobial concentrations within biofilms selects for antimicrobial and disinfectant resistance, which can then spread within and between populations
Some organisms within biofilms may also have altered physiological susceptibility to antimicrobials (ie persister cells that show reversible antimicrobial tolerance)
All biofilm must be removed from the ear canals, pinnae, hairs, and other body sites (eg lip folds and body folds) at the start of treatment

51
Q

What can damage biofilms?

A
  • N-acetyl cysteine (NAC), can damage, lower the MIC, and enhance the efficacy of systemic antibiotics
  • Tris EDTA-NAC may facilitate removal and treatment of biofilms in ear canals, leave time between this treatment and topical antibiotics
  • potential anti-biofilm and antimicrobial activity: chlorhexidine, polihexanide, hypochlorous acid, and Tris-EDTA
52
Q

How do you reverse chronic pathologic changes?

A

broad spectrum anti-inflammatory (topical or systemic glucocorticoids, given to remission before tapering (2-3 weeks)
Cyclosporine does not appear to be effective at reversing inflammatory changes but may be helpful for long term maintenance
Semi-broad (eg oclacitinib) or narrow (eg lokivetmab and antihistamines) spectrum agents have limited efficacy in otitis

53
Q

How long do the topicals florfenicol/terbinafine/mometasone or florfenicol/terbinafine/betamethasone maintain therapeutic efficacy in the ear canal?

A

up to 35 days

54
Q

What are potential complications of leave in florfenicol/terbinafine/mometasone or florfenicol/terbinafine/betamethasone?

A

potentially ototoxic
can trigger inflammation in the conjunctiva
have been associated with neurogenic keratoconjunctivitis sic
florfenicol is not effective against Pseudomonas spp so not appropriate for suppurative otitis

55
Q

What are some examples of future treatment options for otitis externa?

A
  • photobiomodulation and cold plasma
  • bacteriophages, specific anti-pseudomonas phages cleared MDR ear infections in 10 dogs
  • various essential plant oils and extracts, Manuka honey, antimicrobial peptides, lactoferricin, and Tris-EDTA/monensin
56
Q

What are the short term and long term treatments for otitis externa?

A
  1. induction to get the ears in remission: may involve cleaning the ear with an appropriate technique/product, antimicrobial therapy, and topical or systemic glucocorticoids
  2. long term maintenance to prevent relapses: may involve regular ear cleaning and topical glucocorticoids alongside therapy appropriate to primary and predisposing problems