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
Why is it important to understand drug [] when looking at a C&S report?
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
26
What are the mechanisms of *Pseudomonas* that contribute to its intrinsic resistance?
Genetic mechanisms: lack of porins, efflux pumps, lack of target proteins, chemical alternation of the Ab
27
What drugs should theoretically never work with *Pseudomonas*?
Cephalosporins, B-lactams, Tetracyclines, TMS, Macrolides, Lincosamides, Chloramphenicol
28
What commercial products may be suitable/effective?
Enrofloxacin/SSD, Plymyxin B sulfates (Surolan), gentamicin (Mometamax), orbafloxacin (Posatex)
29
What is the most common compounded medication that is used topically?
amikacin
30
What is the 2nd most common compounded medication that is used topically?
Ceftazidime
31
What are common antiseptics used?
Silver (SSD, micronized), N-acetylcysteine, chlorhexidine, Tris-EDTA, acetic acid
32
What has SSD been used for historically?
burn management
33
SSD is a _____ \_\_\_\_\_ antibacterial and antifungal agent.
broad spectrum
34
How many mcg/ml is a 1% SSD cream?
10,000 mcg/ml (10 mg/ml)
35
What are possible adverse effects of SSD?
Adverse drug eruptions, EM, TEN
36
What is the most common treatment currently by dermatologists for *P**seudomonas*?
SSD
37
What antiseptic can SSD be combined with to lower the MIC?
Tris-EDTA
38
What is the other silver antiseptic we can use but that has little clinical data available?
Micronized silver
39
What is N-acetylcysteine and what does it do?
Mucolytic agent with antibacterial properties that decreases biofilm production, reduces, production of EPS, and disrupts mature biofilm
40
What happens to MIC when NAC is combined with a FQ or aminoglycoside?
It increases
41
What formulation of NAC is preferred?
Topical - has inherent antimicrobial actions
42
How can NAC be used and what is it compounded with?
Used as a rinse to break down biofilm; Compounded with tris-EDTA and antibiotic (enrofloxacin)
43
What is chlorhexidine usually combined with in ear cleansers?
Other active agents or potentiating compounds
44
What are the actions of tris-EDTA?
Alters cell envelope of bacteria and chelates Ca++
45
Tris-EDTA is an excellent adjunctive therapy with \_\_\_\_\_, \_\_\_\_\_, and \_\_\_\_\_.
FQs, aminoglycosides, and SSD
46
What effect on bacteria does Tris-EDTA have when used alone?
Bacteriostatic
47
To what treatments does Tris-EDTA add value?
Antibiotics (FQs and aminoglycosides), SSD, antiseptics (chlorhex)
48
What bacteria is acetic acid effective on?
*Pseudomonas* and *S. aureus*
49
With what products is acetic acid synergistic?
Tobramycin, colistin, ciprofloxacin
50
What is best for controlling pain associated with *Pseudomonas* otitis?
glucocorticoids
51
What is the best practice for using GCs in *Pseudomonas* otitis?
Use it aggressively initially, then back off ASAP
52
What does systemic antimicrobial therapy depend on?
C&S results, history of previous drug exposure, historical knowledge of the organism
53
What type of systemic therapy is recommended?
Aggressive - use high end of dosage range
54
T/F: Systemic antibiotic therapy is generally NOT necessary to manage *Pseudomonas* otitis externa (or interna).
True
55
How long past negative cytology/culture should we treat for *Pseudomonas* otitis?
2 weeks
56
What is best for checking for clearance of infection?
culture
57
What often appears as a perpetuating factor after the *Pseudomonas* has been cleared?
*Malassezia*
58
What is done for possible *Malassezia* infections after treating for *Pseudomonas*?
We start preventative anti-yeast meds as soon as the bacteria appears to be under control (azole or terbinafine)
59
What types of chronic infection and inflammation are represented with hyperplastic changes?
Folliculitis, furunculosis, fibrosis, calcification, cystic changes
60
What diagnostics can be done with hyperplastic otitis?
Palpation of ear canals and bullae, otoscopic exam, imaging
61
Why do we palpate the ear canals and bullae in hyperplastic otitis?
To check for calcification or fibrosis, pain (bullae involvement), open mouth (pain?)
62
Why do we do an otoscopic exam on hyperplastic ears?
To check if the hyperplasia is the entire length of the canal
63
What length of treatment is indicated for hyperplastic otitis?
Long term (Weeks to months)
64
What is the first thing to try with hyperplastic ears therapy wise?
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
What topical glucocorticoids can be used on hyperplasia?
Flucinolone or mometasone
66
What therapy can be used for **severe** hyperplasia?
Cyclosporine or Triamcinolone
67
How is Triamcinolone administered?
Through the operating head otoscope while under GA, injected through a 23g spinal needle in a corkscrew pattern
68
What are indications for laser ablation?
Early lesions, polypoid otitis, apocrine cysts