Unit 2: Difficult Problems in Otitis Flashcards

1
Q

Most difficult cases are NOT the result of _____ (3 things).

A
  1. Resistant organisms (MDR)
  2. Strange conformational problems
  3. Infections with rare organisms
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2
Q

What are difficult cases created by?

A

Inadequate treatment, chronic changes/biofilm production, failure to ID and control the primary factor, and lack of client commitment

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3
Q

What are some difficult problems you may encounter in practice?

A

“Allergic” ears, Malassezia infections, Pseudomonas infections, ceruminous otitis externa, hyperplastic ear changes

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4
Q

What are the 7 best practices in the management of otitis?

A
  1. Use appropriate diagnostics
  2. Prepare the canal for treatment
  3. Choose treatment wisely
  4. Meds must be administered properly
  5. Use quality control to evaluate treatment
  6. Consider long-term maintenance therapy
  7. ID and control primary factor(s)
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5
Q

Pseudomonas infections are suspected with unusually _____ ears.

A

painful

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6
Q

What is seen on cytology with a Pseudomonas infection?

A

Single population of Gram(-) rods

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7
Q

What is the etiology behind Pseudomonas infections?

A

Same primary factors as all otitis cases (atopy, masses, endocrinopathy, AI disease);

It is almost always a secondary bacterial invader after previous antibiotic therapies

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8
Q

What do you see at the opening of the canal with Pseudomonas infections?

A

Mucopurulent, sticky material

Swollen, sore, painful

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9
Q

What is the relationship between biofilm and MIC?

A

MIC of drugs like polymyxin B, enrofloxacin, and gentamicin is significantly higher for biofilm producers

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10
Q

What is biofilm?

A

Matrix of proteins in a sticky, gel-like substance containing sugary strands (EC polymeric substances)

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11
Q

What are the EC polymeric substances?

A

Polysaccharides, proteins, EC DNA

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12
Q

Where do bacteria live in biofilm?

A

In clusters separated by channels

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13
Q

Why is biofilm a good defense mechanism?

A

Provides protection from abx, antibodies, and phagocytes

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14
Q

What % of human infections are associated with biofilm?

A

80%

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15
Q

What are the mechanisms of antimicrobial intolerance?

A
  1. Antimicrobial depletion (agent doesn’t reach biofilm)
  2. Slow penetration (gives cells a chance to initiate stress response)
  3. Stress response (cells change activity in response to challenge)
  4. Altered microenvironment (metabolically inactive - alive)
  5. Persister cells (spore-like cells that can survive an antimicrobial challenge)
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16
Q

What are some advantages that bacteria have?

A

Structural stability, firm adherence to biotic/abiotic surfaces, increased virulence, resistance to antimicrobial therapy, resistance to host immune response

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17
Q

How may cells be dispersed in biofilm?

A

Shedding of daughter cells, detachment as result of nutritional levels or quorum sensing, shearing of biofilm aggregates

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18
Q

T/F: We should never assume that Pseudomonas and Staph otitis form biofilm.

A

False - we should assume that they all produce biofilm

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19
Q

What is the most important aspect of management of Pseudomonas otitis?

A

cleaning the ears

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20
Q

Why is cleaning the ears important?

A

Removes barriers to topical administration (wax, debris, biofilm), decreases bacterial burden, removes material (pus) that may inactivate meds

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21
Q

What does deep cleaning under anesthesia allow for?

A

Evaluation of the tympanic membrane and allows use of topical antiseptic

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22
Q

What is a good way to do a deep ear cleaning for Pseudomonas infections?

A

Flush with body temp saline

Ensure the ear drum is intact

Put in betadine (toxic to middle ear)

Allow to sit then flush out

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23
Q

Some cleansers show _____ activity vs. Pseudomonas.

A

antimicrobial

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24
Q

How can you maximize the value of your treatment?

A

Use cultures appropriately, understand the impact of biofilm, and use materials that lower MICs (i.e. Tris-EDTA, N-acetylcysteine/acetic acid)

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25
Q

Why is it important to understand drug [] when looking at a C&S report?

A

Many dogs will respond to certain therapies even though the report says the organism is resistant; at high enough [] you can get over the bacterial defense mechanisms

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26
Q

What are the mechanisms of Pseudomonas that contribute to its intrinsic resistance?

A

Genetic mechanisms: lack of porins, efflux pumps, lack of target proteins, chemical alternation of the Ab

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27
Q

What drugs should theoretically never work with Pseudomonas?

A

Cephalosporins, B-lactams, Tetracyclines, TMS, Macrolides, Lincosamides, Chloramphenicol

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28
Q

What commercial products may be suitable/effective?

A

Enrofloxacin/SSD, Plymyxin B sulfates (Surolan), gentamicin (Mometamax), orbafloxacin (Posatex)

29
Q

What is the most common compounded medication that is used topically?

A

amikacin

30
Q

What is the 2nd most common compounded medication that is used topically?

A

Ceftazidime

31
Q

What are common antiseptics used?

A

Silver (SSD, micronized), N-acetylcysteine, chlorhexidine, Tris-EDTA, acetic acid

32
Q

What has SSD been used for historically?

A

burn management

33
Q

SSD is a _____ _____ antibacterial and antifungal agent.

A

broad spectrum

34
Q

How many mcg/ml is a 1% SSD cream?

A

10,000 mcg/ml (10 mg/ml)

35
Q

What are possible adverse effects of SSD?

A

Adverse drug eruptions, EM, TEN

36
Q

What is the most common treatment currently by dermatologists for P**seudomonas?

A

SSD

37
Q

What antiseptic can SSD be combined with to lower the MIC?

A

Tris-EDTA

38
Q

What is the other silver antiseptic we can use but that has little clinical data available?

A

Micronized silver

39
Q

What is N-acetylcysteine and what does it do?

A

Mucolytic agent with antibacterial properties that decreases biofilm production, reduces, production of EPS, and disrupts mature biofilm

40
Q

What happens to MIC when NAC is combined with a FQ or aminoglycoside?

A

It increases

41
Q

What formulation of NAC is preferred?

A

Topical - has inherent antimicrobial actions

42
Q

How can NAC be used and what is it compounded with?

A

Used as a rinse to break down biofilm;

Compounded with tris-EDTA and antibiotic (enrofloxacin)

43
Q

What is chlorhexidine usually combined with in ear cleansers?

A

Other active agents or potentiating compounds

44
Q

What are the actions of tris-EDTA?

A

Alters cell envelope of bacteria and chelates Ca++

45
Q

Tris-EDTA is an excellent adjunctive therapy with _____, _____, and _____.

A

FQs, aminoglycosides, and SSD

46
Q

What effect on bacteria does Tris-EDTA have when used alone?

A

Bacteriostatic

47
Q

To what treatments does Tris-EDTA add value?

A

Antibiotics (FQs and aminoglycosides), SSD, antiseptics (chlorhex)

48
Q

What bacteria is acetic acid effective on?

A

Pseudomonas and S. aureus

49
Q

With what products is acetic acid synergistic?

A

Tobramycin, colistin, ciprofloxacin

50
Q

What is best for controlling pain associated with Pseudomonas otitis?

A

glucocorticoids

51
Q

What is the best practice for using GCs in Pseudomonas otitis?

A

Use it aggressively initially, then back off ASAP

52
Q

What does systemic antimicrobial therapy depend on?

A

C&S results, history of previous drug exposure, historical knowledge of the organism

53
Q

What type of systemic therapy is recommended?

A

Aggressive - use high end of dosage range

54
Q

T/F: Systemic antibiotic therapy is generally NOT necessary to manage Pseudomonas otitis externa (or interna).

A

True

55
Q

How long past negative cytology/culture should we treat for Pseudomonas otitis?

A

2 weeks

56
Q

What is best for checking for clearance of infection?

A

culture

57
Q

What often appears as a perpetuating factor after the Pseudomonas has been cleared?

A

Malassezia

58
Q

What is done for possible Malassezia infections after treating for Pseudomonas?

A

We start preventative anti-yeast meds as soon as the bacteria appears to be under control (azole or terbinafine)

59
Q

What types of chronic infection and inflammation are represented with hyperplastic changes?

A

Folliculitis, furunculosis, fibrosis, calcification, cystic changes

60
Q

What diagnostics can be done with hyperplastic otitis?

A

Palpation of ear canals and bullae, otoscopic exam, imaging

61
Q

Why do we palpate the ear canals and bullae in hyperplastic otitis?

A

To check for calcification or fibrosis, pain (bullae involvement), open mouth (pain?)

62
Q

Why do we do an otoscopic exam on hyperplastic ears?

A

To check if the hyperplasia is the entire length of the canal

63
Q

What length of treatment is indicated for hyperplastic otitis?

A

Long term (Weeks to months)

64
Q

What is the first thing to try with hyperplastic ears therapy wise?

A

Glucocorticoids;

This should open up the ears if hyperplasia is due to inflammation and edema; if it doesn’t work, the pet needs surgery

65
Q

What topical glucocorticoids can be used on hyperplasia?

A

Flucinolone or mometasone

66
Q

What therapy can be used for severe hyperplasia?

A

Cyclosporine or Triamcinolone

67
Q

How is Triamcinolone administered?

A

Through the operating head otoscope while under GA, injected through a 23g spinal needle in a corkscrew pattern

68
Q

What are indications for laser ablation?

A

Early lesions, polypoid otitis, apocrine cysts