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Veterinary Bacteriology & Mycology > Subcutaneous Mycoses > Flashcards

Subcutaneous Mycoses Flashcards

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1
Q

What are subcutaneous mycoses? What are the 3 most common genera causing this?

A

dimorphic fungi and fungus-like microorganisms affecting the skin and subcutaneous tissue

  1. Sporothrix schenkii - sporotrichosis most commonly in humans, horses, dogs, and cats
  2. Histoplasma capsulatum var. farciminosum - epizootic lymphangitis in equids
  3. Oomycosis (Aphanomyces, Lagenidium, Pythium, Saprolegnia) - chromoblastomycosis, phaehyphomycosis, and mycetoma in fish and mammals
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2
Q

What is Sporothrix schenkii? How does it present in immune-competent people and horses/dogs?

A

saprophytic, dimorphic fungi

  • PEOPLE: chronic ulcerative lymphangitis of skin and subcutaneous tissue
  • HORSES/DOGS: limited to cutaneous/cutaneolymphatic forms with sparse presence in lesions
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3
Q

How are cats affected by Sporothrix schenkii?

A

develop cutaneoulymphatic or disseminated disease regardless of immune status at the time of infection

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4
Q

What are the 2 possible structural forms of Sporothrix schenkii?

A
  1. MOLD - room temperature (25 degrees C on Sabourand’s agar)
  2. BUDDING, PLEOMORPHIC YEAST - at 35-37 degrees C in tissue or rich media, like blood agar; “cigar bodies”
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5
Q

Which form of Sporothrix schenkii is easily stained? What 3 stains work best?

A

yeast phase

  1. Gram stain
  2. phase accepts Romanowsky-type stain (Wright-Giemsa)
  3. phase accepts fungal stains (periodic acid Schiff, Grocott methenamine silver, Gridley)
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6
Q

What are the 5 major cell wall components of Sporothrix schenkii?

A
  1. adhesins - affinity for extracellular matrix proteins
  2. lipid - inhibits phagocytosis by monocytes and macrophages
  3. melanin - protects from ROS within phagolysosomes
  4. peptide-rhamnomannan - immunosuppressive by suppressing the liberation of proinflammatory cytokines
  5. sialic acid - inhibits uptake by phagocytic cells and directs complement proteins toward the degrative pathway
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7
Q

What secreted enzymes are thought to contribute to Sporothrix schenkii virulence?

A

proteinases - may hydrolyze stratum corneum

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8
Q

Where is Sporothrix schenkii commonly found? In which animals is disease most common? What is disease most commonly associated with in humans?

A

soil rich in decaying organic matter, live plants

cats, dogs, horses

rose gardening - rose gardener’s disease

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9
Q

What are the 5 steps to Sporothrix schenkii transmission/pathogenesis?

A
  1. infection
  2. contaminated cutaneous infection
  3. underlying tissue - suppurative inflammation, ulceration, necrosis of skin, granuloma
  4. invades tissue and lymphatics
  5. regional LN - lymphadenitis, granuloma
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10
Q

What does the inflammatory reaction to Sporothric schenkii result in? What is the most common inflammatory reaction?

A

draining wounds (abscesses) that can become ulcerated cutaneous nodules

pyogranulomatous with purulent center surrounded by epithelioid and multinucleated macrophages, lymphocytes, and plasma cells

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11
Q

What happens in immunocompetent patients in response to Sporothrix schenkii infection?

A

usually limited to cutaneous or cutaneoulymphatic forms
- EXCEPT CATS

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12
Q

What is significantly related to Sporothrix schenkii resistance? How is this organism identified?

A

cell-mediated immunity

  • oval to cigar-shaped yeast forms in exudates/biopdies
  • immunofluorescence
  • latex agglutination
  • agar gel diffusion
  • PCR (chitin synthase 1)
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13
Q

What 5 treatments is Sporothrix sckenkii susceptible to?

A
  1. sodium/potassium iodides
  2. itraconazole
  3. ketoconazole
  4. amphotericin B
  5. flucystosine
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14
Q

Sporothrix schenkii:

A
  • yeast cells = cigar-shaped
  • lymphatic involvement
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15
Q

Sporothrix schenkii, feline:

A
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16
Q

Sporothrix schenkii, canine:

A
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17
Q

What 2 forms can Histoplasma capsulatum take?

A
  1. MOLD: 25-30 degrees C, saprophytic
  2. YEAST: 37 degrees C, parasitic
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18
Q

What are the 3 varieties of Histoplasma capsulatum?

A
  1. var. capsulatum - histoplasmosis
  2. var. duboisii - histoplasmosis
  3. var. farciminosum - epizootic lymphangitis (pseudoglangers), a chronic pyogranulomatous disease involving the skin and lymphatics in horses, donkeys, and mules, but also reported in camels, cattle, and dogs
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19
Q

How does Histoplasma capsulatum var. farciminosum grow in tissue? Culture?

A

TISSUE = budding yeasts

CULTURE = sterile hyphae in its myecelial form when grown at 25 degrees C or room temperature on SDA

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20
Q

How is the yeast phase of Histoplasma capsulatum var. farciminosum best demonstrated?

A
  • Romanowski-type stains - Wright or Giemsa
  • fungal stain - periodic Schiff, Grocott methenamine silver, Gridley
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21
Q

How can mold growth of Histoplasma capsulatum var. farciminosum be converted into yeast?

A

grow in blood-containing agar with incubation at 37 degrees C under 15-20% CO2

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22
Q

Histoplasma capsulatum var. farciminosum is quite resistant in the environment. What is it able to survive? Where is it typically found?

Study These Flashcards
A
  • physical and chemical agents
  • ambient temperatures
  • refrigerator temperatures
  • dessication

found in soil in its mycelial form—> can survive weeks in corrals and stables

23
Q

What is the primary reservoir of Histoplasma species? How is it transmitted?

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A

nitrogen-rich soil

  • through skin wounds from other lesions or nasal/ocular exudate
  • soil
  • fomites: grooming and harness equipment
  • arthropod vectors
24
Q

What are the 6 steps to Histoplasma capsulatum var. farciminosum pathogenesis?

Study These Flashcards
A
  1. painless, freely movable skin nodule enlarges, becomes abscessed, and bursts, resulting in ulceration
  2. adjacent lymphatics develop nodules along their course
  3. regional LN develop abscesses that drain by sinus tracts to the outisde
  4. hematogenous spread and visceral involvement
  5. evolved from suppurative to granulomatous with yeast cells present extracellularly and intracellularly, especially in macrophages
  6. skin lesions - head, neck, limbs
25
What suggests the involvement of an arthropod vector in Histoplasma capsulatum var. farciminosum transmission? What species are most affected?
seasonal peaks equids; young horses most susceptible - also cattle, camelids, dogs
26
What is the key host defense against Histoplasma capsulatum var. farciminosum?
cell-mediated immunity
27
In what 3 ways if Histoplasma capsulatum var. farciminosum infection diagnosed?
1. antigens demonstrated by agar gel diffusion or by serum agglutination 2. direct examination of stained exudate (Wright, Giemsa) or biopsy material (fungal stains) may reveal yeasts within macrophages or extracellularly 3. growth on SDA
28
What 4 treatments for for Histoplasma capsulatum var. farciminosum?
1. griseofulvin* 2. amphotericin B 3. itraconazole 4. flucoconazole
29
Histoplasma capsulatum var. farciminosum, horse:
30
What causes phytiosis? What are other names for this syndrome?
aquatic oomycete, Phythium insidiosum, with wide, sparsely septate hyphae - swamp cancer - Florida horse leeches
31
How does Phythium insidiosium cause? Where is infection most common?
pyogranulomatous conditions (phythiosis) of dogs (swamp cancer), horses (Florida horse leeches), cattle, cats, and people - ulcerative fibrogranulomatous or pyogranulomatous and eosinphilic (sub)cutaneous lesions Gulf Coast - mostly dogs and horses
32
In what 3 ways do horses with phytiosis typically present?
1. large, exudative swellings on extremities, ventral trunk, or head 2. nasal mucosa may be involved 3. hyphae demonstrated within granulomatous coagula (kunkers, leechers) with necrotic macrophages and eosinophils
33
Why is culturing not a typical way to diagnose phytiosis? What are the 2 treatments?
Phythium insidiosus requires cultural techniques that are tedious and time-consuming, requiring the growth of the mold-like organism on SDA for 24-48 hours at 30 degrees C 1. amphotericine B 2. immunotherapy utilizing killed whole organisms
34
Phytiosis, kunkers:
horse, Phythium insidiosus
35
What are the 4 major steps to using immunotherapy to treat phytiosis?
1. purified P. insidiosum antigens 2. Th2 response 3. Th1 response 4. activated macrophages and cytotoxic T cells release IFN and IL-2 90% success in equines; 71% in canines, 100% in bovines
36
Phytiosis immunotherapy:
37
Phytiosis:
P. insidiosum
38
What typically causes phaeohyphomycosis in dogs and cats? What is frequently seen with this disease?
Cladophialophora bantiana CNS localization
39
What typically causes chromoblastomycosis and phaeohyphomycosis? In which animals are these seen?
dark-pigmented (dematiaceous) fungi - C = rare in nonhuman mammals, but occurs in frogs and toads - P = sporadically seen in cats, dogs, horses, cattle, and goats (typically systemic)
40
What is the pathogenesis of chromoblastomycosis and phaeohyphomycosis?
- soil and plant-associated saprophytes (Cladophialophora bantiana) enters through skin - multiplies subcutaneously, causing pyogranulomatous reactions - nodular or larger swellings develop, which may ulcerate and discharge pus
41
How is chromoblastomycosis and phaeohyphomycosis diagnosed? What is characteristically seen?
biopsy and culture sclerotic bodies (chromoblastomycosis) and hyphae (phaeomycosis) are seen in stained biopsy sections - H&E, peiodic acid Schiff, Gorcott methenamine silver
42
What are the 4 treatments to chromoblastomycosis and phaeohyphomycosis?
1. flucytosine 2. itraconazole 3. amphotericine B 4. ketoconazole - mixed results
43
Chromoblastomycosis and phaeohyphomycosis:
44
Chromoblastomycosis and phaeohyphomycosis, feline:
Cladophialophora bantiana
45
What 3 fungi are associated with eumycotic mycetoma?
1. Pseudallescheria boydii 2. Cochliobolus spiciferus 3. Curvularia geniculata - all are saprophytes and enter through a wound
46
What is characteristic of mycetoma? What 2 bacteria are also associated?
swelling, granule formation, and draining sinus tracts ACTINOMYCETES 1. Nocardia 2. Actinomyces
47
How do fungal colonies appear in mycetoma lesions? How is this treated?
surrounded by suppuration bordered by granulomatous reactions with sinus tracts that carry pus and granules to the surface - excision - azoles - amphotericin B
48
Myecytoma:
49
What causes rhinosporidosis? How does this present?
Rhinosporidium seeberi chronic granulomatous type of infection a mucocutaenous junctions in horses, cattle, mules, dogs, goats, and wild waterfowl (rare in humans)
50
What is characteristic of Rhinosporidium seeberi infection? Where is this disease most commonly a problem?
formation of cauliflower-like growths (polyps) tropical and subtropical countries - sporadic cases in US
51
What is diagnosis of Rhinosporidiosis based on? Is treatment effect?
- gross lesions - microscopic examination of tissue sections or polyp discharge NO - surgical excision is practiced, but many lesions recur
52
What is definitive of Rhinosporidiosis on tissue sections and cytologic preparations?
TISSUE: large sporangia filled with endospores CYTOLOGY: sporangia rarely seen; numerous endoscpres are present
53
Rhinosporidiosis:

Veterinary Bacteriology & Mycology (47 decks)

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