Avian Mycology Flashcards
Thrush in avian species is caused by what fungus?
How is it diagnosed?
How is it treated?
How is it transmitted?
Can humans be affected?
- Candidiasis
- Candida albicans
- Oral cavity/nasal cavity
- Dx cytology, endoscopic bx, histo, culture
- Tx nystatin, fluconazole
Candidiasis
- Etiology: Candida albicans
- Synonyms: Moniliasis, thrush, sour crop
- Susceptible Species: Few in free ranging birds. Poultry. Wild birds in pet bird industry.
- Geography: Worldwide.
- Seasonality: None.
- Clinical Signs - Poultry: retarded growth, listless, ruffled feathers.
- Transmission: Feco-oral; usually environmental contamination
- Pathology: Mouth, esophagus, crop have gray-white loosely attached plaques. Circular raised ulcers in crop. Pseudomembra
- Control: None really–it occurs infrequently. Vaccination was apparently useful in the venereal disease in geese
- Other: Normal inhabitant of GI
- Human Issues: Can be affected. Oral thrush; skin//nails affected.
What is the etiologic agent of avian gastric yeast?
Where is it typically located?
What species is overrepresented?
What are the clinical signs?
How is it treated?
What are some other differentials to consider for regurgitation?
- Avian gastric yeast
- Macrorhabdus ornithogaster
- Anamorphic ascomycetes yeast (formerly megabacteria)
- Isthmus
- Budgies
- Regurgitation, diarrhea, weight loss
- Tx oral amphotericin B
- Absence on fecal does not rule it out if clinical, but usually shedding
- Other causes of regurgitation in birds – obstruction, avian bornavirus, lead toxicity, neoplasia, behavioral
- Macrorhabdus ornithogaster
What are the two cryptococcus species that affect birds?
Where do they commonly infect?
- Cryptococcus gattii
- Compare and contrast
- Neoformans – worldwide, pigeon droppings, opportunistic, immunocompromised, disseminated
- Gattii – restricted to warmer climates, assoc with euacalyptus trees, localized usually, primary pathogen of immunocompetent hosts.
- Commonly infect the keratin of the beak and spread on the face from there
- Compare and contrast
Aspergillosis is a common problem in avian species.
What factors contribute to disease?
What anatomic and physiologic characteristics of teh avian respiraotry system make birds more susceptible?
- Aspergillosis
- Infectious, non-contagious, ubiquitous, opportunistic saphrophytic fungus
- Forms spores – can survive harsh conditions
- What factors contribute to disease?
- Immunosuppression, chronic debilitation, prolonged antibiotic use, number of spores inhaled.
- Wild birds require fewer spores? No studies.
- Stress – trauma, smoke inhalation, corticosteroids, malnutrition, hypovitmainosis A
- Species – falcons, penguins, RTHA
- Immunosuppression, chronic debilitation, prolonged antibiotic use, number of spores inhaled.
- What anatomic and physiologic charracteristics of the avian resp system make birds more susceptible?
- No epiglottis or diaphragm
- Limited ciliated epithelium in resp tract
- Greater respiratory tract surface area
- Thinner air-blood capillary barrier
- Air sacs
- Unidirectional flow thorugh lungs, bidirectional through air sacs
- Hinders elimination of inhaled particles
- Less free respiratory macrophages
- Infectious, non-contagious, ubiquitous, opportunistic saphrophytic fungus
How common is this aspergillus in penguins in rehabilitation settings?
How do environmental fungal loads compare between indoor and outdoor settings for African penguins?
Aspergillosis
- Indicence, density, proportionate mortality, and risk factors of asper in magellanic penguins in a rehab center from brazil.
- 66/327 penguins developed asper and died during rehab
- All except one had A. fumigate
- 75% positive cases transported from other centers
- 22% of juveniles vs 6% adults
- 11% of oiled pengiuins vs 25% non oiled birds
- BW on admission NOT considered a risk factor
- Were using compounded itraconazole… which may explain the suboptimal effectiveness of this drug.
- Significantly LOWER in animals that developed asper
- 66/327 penguins developed asper and died during rehab
- Environmental fungal loads in an indoor-outdoor African penguin (spheniscus demersus) exhibit
- Environmental and air sampling for fungi
- Asper spp assessed for antifungal drug susceptibility
- Compressed paper cat litter pellets used in the nest boxes were evaluated for fungal contamination and growth
- Overall outdoor areas had higher fungal counts than indoor microenvironments during warmest months
- A. flavus more susceptible to itra and terbinafine vs A. fumigatus samples, less susceptible to voriconazole.
- A. niger most susceptible to terbinafine, but was least susceptible to itraconazole and voriconazole.
- Nest boxes – chrysonilia sitophila isolated from paper pellets cultured directly from unopened bags from vendor
- No clinical dz attributed to chrysonilia spp in penguins
- No aspergillus spp recovered from any of the nest samples
What is the most common species of aspergillosis that affects birds?
Why?
Where does infection commonly occur?
How does the disease spread?
- What is the most common species of asper in birds
- Aspergillus fumigatus
- Why? Smaller spores
- Spores inhaled, lodge in caudal air sacs, lung parenchyma (parabronchus)
- Tracheal bifurcation
- Resp macrophages early in immune defense against infection (birds don’t have many to begin with)
- How does systemic infection?
- Overwhelming infection of spores or innate immunity suppressed
- If conidia overwhelms the immune system, start germination, multicellular hyphae.
- Hyphae are tissue invasive
- Aspergillus fumigatus
How is aspergillosis in birds diagnosed?
What is the gold standard? Are there any downsides to this?
What might you see on hematology?
What changes would be present on a protein electrophoretogram?
What are teh major acute phase proteins in birds?
What antigen is commonly tested for?
What is the use of 3 hydroxybutyrate and gliotoxin in these cases?
- Endoscopy is the gold standard!
- Visualization, biopsy, culture, tx
- White-yellow plaques, sometimes pigmented
- Contraindications – ascites, disease on one side, proventricular dilatation
- Other dx hematology, chemistry
- Severe leukocytosis
- Leukemia, mycobacterium, aspergillosis, chlamydia
- Protein electrophoresis
- Decreased A:G ration, albumin
- Increased beta and gamma globulins
- Nonspecific test!
- Species specific reference ranges.
- What protein methodology is not accurate in birds?
- Bromethyl green test (Abaxis) for albumin
- Acute phase protein
- Major APP – haptoglobin
- Major APP – serum amyloid A
- Variable results from multiple studies
- Serology
- Not appropriate as solo test for asper
- Negative results to not rule out this dz
- Antigen detection – galactomannan
- Antigen from cell wall of the asper
- Cross reactivity – Histoplasma, penicillium, beta lactams
- Application of 3 hydroxybutyrate measurement and plasma protein electrophoresis in the dx of asper in African penguins
- 3-hydroxybutyrate, lipids, and fatty acids are increased in falcons with asper vs healthy birds
- Severe leukocytosis
What are some of the difficulties with nebulization for the treatment of aspergillosis.
What is the mechanism of amphotericin b? What is a common adverse effect?
What is the mechanism of terbinafine? Why is that not a great choice for asper?
- Treatment
- Nebulization – traditional human nebulizers do not create aerosol drops small enough to reach the avian lungs and air sacs
- Polyenes
- Ampho B
- Binds to ergosterols in fungal membranes, pokes holes
- Poor GI absorption
- Nephrotoxic
- Ampho B
- Allylamine
- Terbinafine
- Inhibits ergosterol synthesis (inhibits squalene monooxygnase and squalene epoxidase)
- Accumulation of toxic squalene in fungal cells
- Highly lipophilic and keratinophilic
- Unaffected by feeding
- Poor efficacy vs asper
- Terbinafine
What is the mechanism of action for the azole antifungals? How are they excreted?
What compound enhances absorption of itraconazole?
How is itraconazole excreted?
What species are sensitive to itraconazole?
What species is particularly sensitive to fluconazole?
What are some adverse effects of voriconazole in panguins?
Why are penguins more sensitive?
- Azoles
- Inhibits ergosterol formation
- Metabolized by hepatic P450
- Itraconazole
- Fungistatic
- Mex tissue concentrations ~14 days after starting therapy
- Extensive protein binding
- Dependent of renal function
- Resistance esp in falcons
- Variable affects of feeding and fasting
- Affected by GI acidity
- Compounded products not recommended
- Sporonox contains cyclodextrin which improves absorption of name brand – compounded itra is not useful.
- African greys are sensitive – death
- Anorexia in raptors
- Fluconazole
- Some CNS penetration
- Use with caution in renal dz
- Some effects against asper
- More toxic to budgies
- Voriconazole
- Fungicidal in molds, fungistatic in yeasts
- Time dependent rather than concentration dependent
- Optimal doses should have largest AUC and MIC rather than peak exposure (CMAX)
- Nonlinear pharmacokinetics
- Autoinduction of own metabolism – extrapolation of doses across spp BAD
- Build ups in concentration
- Variable effects depending on species
- Voriconazole toxicity in multiple penguin spp
- Case series – 18 probable and 6 suspect cases of vori toxicity in 6 penguin species treated for prophylaxis and tx for asper
- CS
- Seizure, ataxia, paresis, severe neuro signs
- 6 birds died
- Hypothesis for why penguins more sensitive:
- Polymorphisms in P450 enzymes similar to people
- Lack of autoinduction
- Drug-drug interactions
- Caution with concurrent administration of:
- Enrofloxacin, dlindamycin, chloroquine
- Idiosyncratic
- Liver does NOT appear to be primary target in penguins
What is the dermatophyte of birds?
What clinical signs does it produce?
How is it transmitted?
How is it treated?
How long is it stable in the environment?
Trichophyton gallinae.
Produces a focal facial dermatitis that is highly contagious.
Direct contact
Griseofulvin is the treatment.
Viable for a year in the environment.
