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Bacteriology and mycology > Block 5 > Flashcards

Block 5 Flashcards

1
Q

Fungi overview

Is fungi widely distributed?
is fungi unicellular or multicellular?
is fungi eukaryatic?
sexual or a sexual reproducation?

A

Yes
both
yes
both

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2
Q

Fungi overview

what is eukaryotic?

A

organism that has a nucleus and produces spores

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3
Q

Fungi overview

Fungi is Hererotropic, what does that mean?

A

ingest or absorb organic carbon

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4
Q

Fungi overview

fungi is non-photosynthetic, what does that mean?

A

usually awrobic growth with an optimal tem of 25-37C
tolerable to a high osmotic pressure and asidic environment–they can surviv in salty or sour foods.

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5
Q

Fungi overview

Are all fungi saprophyes?

A

marjority of fungus is saprophytes (decayers) but can also be mutualistic symionts or parasites
typically opportunistic pathogens

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6
Q

Fungi overview

what is a fungal structure?

A

rigid cell wall (mannon, chitin, come cellulose, chitosan), nucleus, mitochondria, ribosomes, microtubules.

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7
Q

Fungi overview

what is chitin

A

provide rigidity, structural supposr and some protection

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8
Q

Fungi overview

what is ergosterol

A

is the dominand sterol (versus cholesterol in animals)

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9
Q

Fungi overview

do fungi cause disease in healthy animals?
what are predisposing factors?

A

rarely
immunosuppression (2nd fungal infections), prolonged antibiotic treatment, young or old, malnutrition, being in a place/are with a lot of fungal spores, damage tissue, persisitent moisture of skin, some nopplastic conditions

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10
Q

Fungi overview

classification?

A
  • superficial or cutaneous mycoses: effects epidermis, keratinized areas like hair and nails, mucous membranes
  • * subcutaneous mycosis: effects dermis, bone, muscle, fascia
  • systemic mycoses: mainly respiratory and GI track, but can spread and effect other organs
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11
Q

Fungi overview

multicellular filaments with branching hyphae, can see Mycelium on
culture (filamentous mass of hyphae making the cloudy/fluffy like structures)

what is it?

A

mold

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12
Q

Fungi overview

4 kinds of molds?

A

* Vegetative mycelium: grows INSIDE the agar/substrate, provides support and absorbs
nutrients
* Reproductive mycelium: aerial hyphae differentiate to support fruiting bodies
* Aerial hyphae: vertical growing hyphae
* Septate hyphae:** dived a cell into compartments** with a septa (does NOT divide whole
cells)

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13
Q

Fungi overview

unicellular spheres, use a selective media for fungi when culturing,
reproduce by budding or budding/spore formation
what are they?

A

Yeasts

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14
Q

Fungi overview

changes between mold and yeast based on temperature, CO2,
concentration, and pH

what is it?

A

Dimorphic fungi

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15
Q

Fungi overview

Dimorphic fungi
what relevance is temperature?

A
  • Mycelial form at room temp and yeast at 37oC (or in tissue of animals)
  • A lot of pathogenic fungi are dimorphic
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16
Q

Fungi overview

what is mycosis?
what is mycotoxicosis?

A

tissue invasion
toxin production
*both make spores
*hypersensitivity is key

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17
Q

Fungi overview

mostly see this type reproduction as it is very
effective, can happen a few different ways

what is it?

A

Asexual reproduction

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18
Q

Fungi overview

Asexual reproduction: what 4 ways?

A

* Fission: somatic cell division of nuclei by mitosis
* Budding: cell wall bulges out, daughter nucleus migrates into the bud, the
bud will then separate off
* Fragmentation of hyphae: each hyphae that separates will become a
new organism
* Sporulation: followed by germination of spores

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19
Q

Fungi overview

Asexual reproduction Sporulation:
when are spores produces and what are the 2 main types?

A
  • Spores are produced my mitosis and there are 2 main types
    * Sporangiospores: formed within a sac-like structure called a sporangium
    *** Conidia: **formed on conidiophores
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20
Q

Fungi overview

rare, pos. versus neg., fusion(key word) of 2 haploid nuclei
followed by meiotic division of the diploid nucleus
what is it?

A

Sexual reproduction:

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21
Q

Fungi overview

what benefit is sexual reproduction?

A
  • Benefit: enrichment of fused together genetic material
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22
Q

Fungi overview

What is this

A

Arthrospores
chlamydospores
sporangiospores
conidiospores
blastospores

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23
Q

what is this

A

phialospores

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24
Q

what is this

A

arthrospores

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25
Q

what is this?

A

no idea slide doesn’t say

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26
Q

what is this

A

no idea slide doesn’t say

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27
Q

what is this?

A

microconidia

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28
Q

what is this?

A

macroconidia

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29
Q

what is this?

A

a and b-Macrodium -the one with lots of little sausage links
top of a and bottom of c- microconidium- the one with one little bulge

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30
Q

what is this

A

microsporum spp
*macroconidia
**ring worm

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31
Q

what is this

A

trichohyton

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32
Q

Dermatophytoses overview

Cutaneous mycoses

classification? (3)

A

* Superficial or cutaneous mycoses: effects epidermis, keratinized areas like hair and nails, mucous membranes
* Subcutaneous mycoses: effects deep layers such as dermis, bone, muscle, fascia
* **Systemic mycoses: **mainly respiratory and GI tract, but can spread and effect other organs

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33
Q

Dermatophytoses overview

Cutaneous mycoses

not to be confused with dermatophilus, what is: An infection of keratinized tissues (hair, feathers, outside layers of skin, nails, claws, horns) caused by a
dermatophyte, the infectious form is arthrospores, zoonotic

A

Dermatophytoses

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34
Q

Dermatophytoses overview

Cutaneous mycoses

what is geophilic dermatophyte:

A

live and replicate in soil, especially where there is decomposing keratinous material

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35
Q

Dermatophytoses overview

Cutaneous mycoses
what is Zoophilic dermatophyte:

A

obligate animal pathogens and host specific

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36
Q

Dermatophytoses overview

what is invade hair and skin, thick-walled multiseptated macroconidia that are stalked and arranged singly along hypae

who gets it?

A

Microsporum: invade hair and skin, thick-walled multiseptated macroconidia that are stalked and arranged singly along the hyphae
* M. canis, M. gypseum, M. nanum, M. gallinae
* M. canis: the most common dermatophyte of domestic animals (what we typically see in clinics)

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37
Q

Dermatophytoses overview

what is: target keratinized tissue (hair, skin, nails, horns, claws), thin-walled macroconidia that are
cylindrical or cigar shaped, produced in small numbers
* M. mentagrophytes, T. equinum, T. verrucosum

A

Trichophyton

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38
Q

Dermatophytoses overview

what is Epidermophyton

A

no idea slide doesn’t say

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39
Q

Dermatophytoses

How transmitted?

A

Transmission: direct contact with an infected animal, by exposure of
arthrospores from the environment or fomites

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40
Q

Dermatophytoses overview

what are arthrospores

A

Arthrospores: shed by infected animals, they can remain viable in the environment for
years

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41
Q

Dermatophytoses

Pathogenesis?

A

Pathogenesis: dermatophyte spores invade skin abrasions and enter into the
stratum corneum (top layer of skin), release keratinase, protease, and elastase
to break down keratin proteins which results in an inflammatory reaction
(redness, swelling, heat, alopecia)
* Once the inflammatory reaction has occurred, fungal growth will stop and move
away from the site of infection and on to the next hair follicle which results in the
classical ring shaped lesion

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42
Q

Dermatophytoses

CS?

A

alopecia, erythema, scaling, crusting, annular-ringed lesions, vesicle or
papules
* Due to inflammation, Trichophyton infections are more severe than Microsporum
infections

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43
Q

Dermatophytosis infections

Cutaneous mycoses

Canine ringworm
T or M which is more virulent?
is it zoonotic?
M. gypseum is associated with?
T. erinaceid is associated with?
T. mentagrophytes is associated with?
what is kerion?
what about lesions?

A
  • Remember: T is more virulent than M
  • M. canis: most commonly seen in small animal
    clinics, zoonotic
  • M. gypseum: associated with digging
  • T. erinaceid: contact with hedgehogs
  • T. mentagrophytes: catching rats
  • Kerion: intense inflammation with swelling, ulceration
    and purulent exudate
  • Lesions: brittle hair, dry/scaly skin, crust, scabs
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44
Q

Dermatophytosis infections

Feline ringworm
cats re teh primary reservoir of ?
what is feline otitis?
most common in what kind of cats?
what is the CS?
is this a problem?
what about lesions?

A
  • Cats are the primary reservoir of M. canis
  • Feline otitis: expressed as a persistent waxy
    discharge
  • Most common to appear on kittens (immature
    immune system) or adults with immune deficiency
  • CS: usually asymptomatic
  • Public health risk!
  • Lesions: circular areas of stubbed hair, alopecia,
    mild scaling, folliculitis
  • Usually seen on the head/face
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45
Q

Dermatophytosis infections

Bovine ringworm
what is the name?
what is the optimal temp?
who gets it?
when do they get it?
what about lesions?
what about recovery?
prevention?
is it zoonitic?

A

Bovine ringworm
* Trichophyton verrucosum
* Optimal temp is **37oC **for growth
* Calves are more susceptible
* Higher incidence in the winter due to cattle being
housed in close contact
* Lesions: circular, scattered, skin scaling, alopecia,
large plaques of thick scabs/crust may develop
* Severe inflammation and puritis
* Usually seen around the eyes first
* Spontaneous recovery will occur
* Prevention: vaccinate!!!
* Zoonotic!

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46
Q

Dermatophytosis infections

Porcine ringworm
what is the primarily seen infection?
who gets it?
predisposing factors?
what about lesions?

A
  • Primarily see infection by M. nanum, but can also
    get infections from M. gypseum, M. canis, T.
    mentagrophytes
  • Common disease affecting market pigs
  • Predisposing factors: crowding or high density,
    humidity, poor sanitation and management
  • Lesions: circular and rough, mildly inflamed
  • Can be seen anywhere on the body
  • **Economic loss
    **
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47
Q

Dermatophytosis infections

Equine ringworm
name?
what about lesions?
cause?

A
  • T. equinum or M. gypseum
  • Lesions: multiple, dry and scaly raised lesions,
    matted hair due to inflammation and exudates
    that can clump together and appear moth eaten
  • Lesions can be all over the body
  • Infections often become chronic or subclinical,
    and reoccur under stress
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48
Q

Dermatophytosis infections

Avian ringworm
aka?
what about lesions?

A
  • AKA: Favus or White comb
  • M. gallinae
  • Lesions: white patches on the combs of male
    birds, sometimes the infection will extend into the
    feathers
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49
Q

Dermatophytoses Dx, Tx, control

what 4 ways can you Dx?

A
  1. Woods lamp
  2. Microscopic examination
  3. Culturing
  4. Physiological tests
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50
Q

Dermatophytoses Dx, Tx, control

With a Woods lamp how accurate is it? what happens?

A

Woods lamp: will fluoresce green when fungi is present (50-60%), shine light over lesions to make the best choice when selecting an area to sample from
* Remember: no illumination does not necessarily mean there is no infection!!!

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51
Q

Dermatophytoses Dx, Tx, control

Microscopic examination: what is the process?

A

Microscopic examination: look for hyaline septate hyphae on scale and hair shafts, or arthroconidia on hair

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52
Q

Dermatophytoses Dx, Tx, control

Culturing:
what is the process?
what is Dermatophytes test medium (DTM)?
How does it work?

A

Culturing: cleanse lesion with alcohol to reduce bacterial contamination, clip hair if needed, scrape skin and pluck hair from the PERIPHERY of the lesion
* Dermatophytes test medium (DTM): Sabouraud’s dextrose sugar with peptones, antibiotics, cyclohexamine and phenol red pH indicator,
incubated at 25o-35oC (unless T. verrucosum then optimal temp is 37oC)
* If red BEFORE 10 days: dermatophyte
* If yellow, and then red AFTER 10 days: non-dermatophyte
* M. canis culture: spreads across the agar plate, **white **cottony surface growth with a golden-yellow reverse pigment

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53
Q

Dermatophytoses Dx, Tx, control

Physiological tests:
what is the process?

A

Physiological tests: temp. tolerance, urease production, in vitro hair perforation test for Trichophyton spp. (develop few microconidia)

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54
Q

Dermatophytoses Dx, Tx, control

Tx
what 2 ways and how long do you treat?

A

1-Removal and/or killing: clipping, shampoos, dips, sprays, topicals
2-Systemic: Griseofulvin, Azole-Ketoconazole, Terbinafine
* Treat until there are 3 negative cultures

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55
Q

Dermatophytoses Dx, Tx, control

Prevention & control:
How?

A

Prevention & control: clean up environment (vacuum, wash bedding, disinfect collars/leashes/tack/brushes/clippers)
* Use 10% bleach solution
*wear gloves

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56
Q

Dermatomytoses Infections

what is a member of the normal skin microbiota and an opportunistic yeast pathogen
* M. fufur, M. pachydermatis, M. sympodialis, M. globose, M. obtuse, M. resticta, M. dermatis, M. nana, M. sloofiae

A

Malassezia

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57
Q

Dermatomytoses Infections

what are the predisposing factors?

A

Predisposing factors: humidity, waxy ears, hairy/pendulous ears, neoplasm, allergies, change in sebum,
recent antibiotic or steroid therapy, trauma

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58
Q

Dermatomytoses Infections

Otitis externa- M. pachydermatis:
CS?
Dx?
Tx?

A
  • CS: head shaking, puritis, odorous, pain
  • Dx: not very zoonotic
  • Otoscope exam of the ear canal
  • Cytological exam for bacteria/yeast/mites
  • Tx: M. pachydermatis infection is always
    secondary    , so treat the underlying cause!
  • Topicals antifungals, systemic antimicrobials
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59
Q

Dermatomytoses Infections

Seborrheic dermatitis- M. pachydermatis

what is it?
who gets it?
predisposing factors?
CS?
Dx?
Tx?

A
  • Superficial deramitits
    * Breed disposition: poodles, cocker spaniels, chihuahuas, German
    shepherds, boxers, bassets
  • Predisposing factors: allergies, seborrhea
  • CS: face rubbing, foot licking, erythematous and scaly skin, alopecia,
    hyperpigmentation, lichenification (leathery skin)
  • Dx: history of poor AB response, looks for yeast cells on skin scaping
  • **Tx: **remove predisposing factors, shampoo, creams/dips, topical or
    oral ketoconazole
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60
Q

Dermatomytoses Infections

Trichosporon spp.
what is it?
who gets it?
how do you treat it?

A
  • Nasal mass in cats
  • Can occlude the nares and will need surgically
    removed
  • Follow up treatment with parenteral administration
    of ketoconazole
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61
Q

Dermatomytoses Infections

Geotrichum candidum
what is it?
where is it found?
who gets it and what happens?
what relevance is Geotrichosis? hint what type of animal and when they get it what does it look like?

A
  • Saprophyte: found in the soil or decaying matter
  • Can be isolated from the feces of a normal
    healthy animal
  • Can cause diarrhea in dogs and apes on
    occasion
  • **Geotrichosis: retiles and amphibians
    **
  • Cutaneous lesions, nodular, circumscribed, dermo-
    epidermal masses
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62
Q

Subcutaneous mycoses

Classification: what are the 3 classifications?

A
  1. Superficial or cutaneous mycoses
  2. Systemic mycoses
  3. Systemic mycoses
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63
Q

Subcutaneous mycoses

Classification:
what type effects epidermis, keratinized areas like hair and nails, mucous membranes

A

Superficial or cutaneous mycoses

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64
Q

Subcutaneous mycoses

Classification:
what type effects deep layers such as dermis, bone, muscle, fascia

A

Subcutaneous mycoses

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65
Q

Subcutaneous mycoses

Classification:
what type mainly respiratory and GI tract, but can spread and effect other organs

A

Systemic mycoses

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66
Q

Subcutaneous mycoses

This group is composed of what 2 things?
where are they found?
what do they look like?

A

This group is composed of dematiaceous or hyaline molds and dimorphic fungi, and they are found in soil
or decaying vegetation
* Dematiaceous: brown pigment
* Hyaline: colorless

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67
Q

Subcutaneous mycoses

Infections are typically associated with what?
how do they present?
how do they contract and spread?
How does this affect the time to develop and severity?

A

Infections are typically associated with **injuries or traumatized tissues **and are chronic and insidious
* Organisms establish on the skin/wound, cause a localized infection and spread to the LN’s
* AKA they take more time to develop and they are more severe

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68
Q

Subcutaneous mycoses

what are they often confused with?
how can you distinguish?

A

Can easily be confused with bacterial infections based on the skin lesions, BUT
* Bacteria should respond to antibiotic treatment and the fungi will not

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69
Q

Sporotrichosis

what is a dimorphic (changes shape with temp), dematiaceous (brown) fungus that is
found world wide, but most common in tropical and sub-tropical areas

A

Sporothrix schenckii

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70
Q

Sporotrichosis

how do you distinguish between molds and yeasts?

A
  • Yeast: animal, 37oC, cigar shaped, pleomorphic budding yeast cells
  • Mold: **environment, 25oC, **thin septate hyphae with tapering conidiophores bearing conidia in rosette like clusters
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71
Q

Sporotrichosis

where does it come from and what animals are affected?

A

S. Shenckii can be isolated from soil, vegetation, peat moss and wood and susceptible species include
dogs, cats, horses, humans, etc.

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72
Q

Sporotrichosis

What are the Virulence factors?

A

Virulence factors: thermotolerant, acid phosphatase, proteinase I and II, adhesion (T.A.P.P.A)

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73
Q

Sporotrichosis

How is it transmitted?
is it painful?
is it pruritic?
can it travel through the body?

A

Transmission: conidia are introduced into the skin by bite or puncture wound from thorns
* The lesions start where the fungus has entered the skin causing subcutaneous nodules that ulcerate and heal
* The lesions are NOT painful and they are NOT pruritic
* Lesions can can travel the course of the lymphatics and involve the LN’s

74
Q

Sporotrichosis

How are spores produced?
what are the 2 types?
is it sexual or asexual reproduction?

A

produced by mitosis
asexual
1. sporangiospores: formed within a saclike structure called the sporangium
2. conidia: formed on conidiophores

75
Q

Sporotrichosis

Pathogenesis?

A

molds and conidiophores are in the environment, conidia/mycelia are produced and
enter the animal through broken skin, TEMP CHANGE from the environment to the animal cause change
to the yeast/parasitic form, we will see nodules at the site of injury (lymphocutaneous manifestation) and
then spread of nodules along the lymphatics

76
Q

Sporotrichosis

CS in Dogs?
cats?

A

CS in dogs:
* Cutaneous: localized with nodules, multicentric
** Lymphocutaneous**: *most common presentation, nodules along the lymphatics
* Disseminated: rare and potentially fatal
* Cats usually have yeast form

77
Q

Sporotrichosis

Dx: wha t3 ways?
how do you dertmine fungi is dimorphic?
how are cat lesions different?

A

Dx: Keep in mind, you always want to grow at 2 temps to check that the fungi is dimorphic!
* Larger numbers of yeast can typically be found form a cat lesion- can shed fungi from lesion exudates and feces
1. * Direct microcopy: easiest but not always possible to see YEAST structures
2. * Culture for MOLD: growth on SDA in 2-7 days at 25oC, cream colored and wrinkled colonies that turn black/grey with age
due to melanin
3. * Culture for YEAST: growth on brain-heart infusion agar with CO2 in 3-5 days at 37oC, colonies are soft white/cream colored

78
Q

Sporotrichosis

  • Tx?
    is it slow or fast?
    what about cats?
A

can take a lot of time!
* Idodide and azole compound, except in cats (iodine sensitive) use itraconazole

79
Q

Sporotrichosis

what is occurs by cat scratch/bite (most common) or vegetation (rose bushes)

is it zoonotic?

what relevance is Lymphocutaneous sporotrichosis?

A

Zoonotic: Rose handlers disease- occurs by cat scratch/bite (most common) or vegetation (rose bushes)
* Lymphocutaneous sporotrichosis: nodules on skin and following lymphatic vessels

80
Q

Epizootic lymphangitis

what is a thermally
dimorphic fungus found in North Africa, Europe, India, and Rusia

A

Histoplasma capsulatum var. farcimunosum is a thermally
dimorphic fungus found in North Africa, Europe, India, and Rusia
* Yeast: 37oC, pear shaped, double contoured budding yeasts, found
inside macrophages or neutrophils
* Mold: 25oC, not good for diagnostics because it takes 8 weeks to
grow

81
Q

Epizootic lymphangitis

Where is it found?
who gets it?

A
  • Found in soil that is enriched with BIRD and/or BAT feces
  • Susceptible Species: equines such as horses, donkeys, and mules
82
Q

Epizootic lymphangitis

transmission?
CS?
Dx?

A
  • Transmission: wound infection or bloodsucking parasites
  • CS: granulomatous, nodular lesions that will likely ulcerate (skin,
    SQ tissue, along lymphatics)
  • Dx: rely on light microscopy from a first impression smear
83
Q

Dematiaceous fungi diseases

what is a rare but chronic fungal
infection that is typically seen in tropical areas

A
  • Chromoblastomycosis
84
Q

Chromoblastomycosis

who gets it
how are they infected?

A

Cats and humans are infected- traumatic implantation
of fungi in cutaneous and subcutaneous tissues
* AKA fungus grows down into the skin and acts like a
“second skin”
* People do NOT have to be immunocompromised to be
infected

85
Q

what is bodies: thick walled muriform cells formed by
dermatiaceous fungi

A

Sclerotic bodies

86
Q

Chromoblastomycosis
CS?

A

very firm and wart like, ulcerative nodules mostly on
the feet and legs
* Will appear dark brown when stained due to the melanin

87
Q

Dematiaceous fungi diseases

Eumycotic mycetoma what is it?

A

Eumycotic mycetoma is rare, but can be
seen in humans and animals but the
infection is limited to one area of the body

88
Q

Dematiaceous fungi diseases

what is Triad of CS:

A

Triad of CS: swelling, fistulas (draining
tract), grains/granules in exudate
(aggregates of mycelium)
* SQ swelling with draining tracts that can
resemble chronic non-healing abscesses

89
Q

Dematiaceous

what are Chronic mycetomas:

A

Chronic mycetomas: fistulas heal and
tissue fibrosis occurs resulting in hard tumor
like masses
* Can potentially cause osteomyelitis if the
periosteum is penetrated

90
Q

Dematiaceous fungi diseases

what is caused by a saprophytic
and pigmented fungi that has been reported in
dogs and cats

A

Phaeophyphomycosis

91
Q

Dematiaceous fungi diseases

what does it look like?

A

Dematiaceous lesions with septate hyphae
* CS: pustules, abscesses, granulomas, shallow
ulcers, open lesions

92
Q

Dematiaceous fungi diseases

what is Bovine nasal granuloma
is it observable?

A

Bovine nasal granuloma is a granulomatous
swelling in the nasal cavity and trachea of cattle
* Goes un-noticed until you see the CS

93
Q

Bovine nasal granuloma
CS?
Endoscopy?

A

CS: dyspnea, inspiratory stidor (harsh sound), nasal
discharge
* Endoscopy: pinkish white polyps inside nares,
collect sample of polyp for examination

94
Q

Bovine nasal granuloma
Dx: 2 ways?

A

Dx:
* Microscopy: direct exam of crushed polyp to look
for dematiaceous fungi
* Culture: white colonies that become floccose or
wooly looking, and can see olive green, brown, or
black pigment

95
Q

Systemic mycoses

  • Classification: what are the 3?
A
  • Superficial or cutaneous mycoses: effects epidermis, keratinized areas like hair and nails, mucous membranes
  • Subcutaneous mycoses: effects deep layers such as dermis, bone, muscle, fascia
    * Systemic mycoses: mainly respiratory and GI tract, but can spread and effect other organs
96
Q

Systemic mycoses

This group of fungi cause what?
why?
specific characteristics?

A

This group of fungi cause systemic infections and are very virulent due to their ability to evade host
defense mechanisms
* Thermally dimorphic or yeast only

97
Q

Systemic mycoses

what is the primary site of infection?

A

The primary side of infection is the lung so there is typically an asymptomatic respiratory infection that
resolves rapidly, but it some cases the infection can disseminate to other organs (unique to each fungi)

98
Q

Systemic mycoses

Each fungi are associated with a specific geographical region based on reservoir/soil types

Blastomycosis?

A

central-eastern
and all of africa

99
Q

Systemic mycoses

Each fungi are associated with a specific geographical region based on reservoir/soil types

Histoplasmosis:

A

southeast

100
Q

Systemic mycoses

Each fungi are associated with a specific geographical region based on reservoir/soil types

Coccidioidomycosis

A

southwest

101
Q

Systemic mycoses

is present worldwide, but is highly endemic in North America where it is one of the main systemic
mycoses
* Found in Eastern US: Ohio, Tennessee, Mississippi, and anywhere from US to Canada that borders the St. Lawrence River and Great
Lakes

A

Blastomycosis

102
Q

Blastomycosis

is it zoonotic?

A

Zoonotic transmission possible, but usually animals and humans get it from the environment (not each other)

103
Q

Blastomycosis

reservoir?

A

moist soil (acidic and rich in decay) especially along river beds

104
Q

Blastomycosis

Susceptible species?

A

humans (most common), dogs, cats, etc.

105
Q

Blastomycosis

Pathogenesis?

A

Pathogenesis: inhaled as mold, changes to yeast in the dog and spreads
* Aerosolized mycelial fragments/spores from the environment are inhaled and deposited into the alveoli of the host
* The mature yeast develops and grows into large budding yeasts (37oC)
* May spread from the lungs via lymphatics/blood to a variety of tissues like skin, eyes and bone

106
Q

Blastomycosis

Lesions? 3 kinds

A

*1-Lung lesions: a few to multiple, variable sized, irregular but firm nodules showing grey to yellow areas of pulmonary consolidation,
there will also be nodules on the thoracic LN’s
*2- Disseminated lesions: nodular lesions on various organs but especially the skin, eyes, and bone
*3- Cutaneous lesions: a few to multiple papules or chronic, draining nodular pyogranulomas

107
Q

Blastomycosis

explain the acute pulmonary phase

A

There is an acute pulmonary phase that can be subclinical/self-limiting, but the disease has the potential to progress and
cause pyogranulomatous inflammation in the lungs (lungs full of nodules) and other sites

108
Q

Blastomycosis

  • CS? name 3
    cats?
    dogs?
A

CS: there are several nodules alredy on the lung by the time CS will be present
* Coughing, dyspnea, dry/hard lung sounds, anorexia, depression, lameness, lymphadenopathy
* Skin: pronounced in cats, proliferative granulomas and SQ abscesses that ulcerate and drain a serosanguineous discharge (watery discharge with blood)
* Ocular: mostly seen in dogs with systemic infection, starts as a draining eye and you will see corneal opacity, uveitis, conjunctivitis
and potentially blindness

109
Q

Blastomycosis

Dx and sampling: name 5

A

Dx and sampling:
* CS and history
* Radiographs: snow storm pattern will be seen on lungs
* Sampling: look for YEAST, tissue, tracheal wash, LN aspirate or biopsy, cutaneous lesion exudates or biopsy
* Microscopy: look for LARGE BUDDING YEAST, spherical, thick-walled, large and broad
* Culture: usually not necessary and poses a** severe biohazard** risk, must use pathogen handling cabinet
* Yeast: 37oC, typical yeast cell, spherical, broad based, thick cell wall
* Mold: room temp, hyaline hyphae that develop spherical conidia that appear as balloons on short stalks

110
Q

Blastomycosis

Tx: name 2

A

**Itraconazole: **drug of choice in dogs, expensive, long term treatment, can see side effects if used for an extended amount of time
* Amphotericin B lipid complex: effective, treatment of choice in fulminating cases, potential to cause liver problems

111
Q

is a very virulent fungal pathogen found in SW US (Arizona, California, New Mexico, Texas,
Utah, Nevada), Mexico, Central and South America

A

Coccidioidomycosis (San Joaquin Valley Fever)

112
Q

Coccidioidomycosis (San Joaquin Valley Fever)

how transmitted?
zoonotic?
contagious?
reservoir?

A

Dust born infection and NOT considered zoonotic or contagious
* Reservoir: arid and dry regions, dust

113
Q

Coccidioidomycosis (San Joaquin Valley Fever)

Susceptible species:

A

Susceptible species: humans, dogs, horses, llamas, etc.
* High rates of infection seen in dogs- maybe due to their tendencies to sniff and dig in soil

114
Q

Coccidioidomycosis (San Joaquin Valley Fever)

primarily affects what? resulting in what?
important to remember what?

A

Primarily effects the lungs causing a chronic respiratory disease, but infections in dogs will disseminate to many
tissues, especially eyes, joints and bones
* Be aware of the potential of fungus to grow in the mycelial phase on bandages of draining lesions

115
Q

Coccidioidomycosis (San Joaquin Valley Fever)

Pathogenesis:

A

Pathogenesis: arthroconidia mature to mycelia in the environment, they will fragment into arthrospores which
will be inhaled by the host
* Mold transition to **spherules ** (type of fungi) in 1-7 hours inside the host at 37oC
* Spherules, in the lung, will mature and produce endospores that are released in vivo

116
Q

Coccidioidomycosis (San Joaquin Valley Fever)

where are the lesions?

A
  • Lesions can be localized to foci within the lung, extend to the LN’s, or disseminate to eyes, joints, and bones
117
Q

Coccidioidomycosis (San Joaquin Valley Fever)

CS:

A

primarily see respiratory disease/symptoms
* Anorexia, cough, weight loss, lameness, abscess, draining tracts,
lymphadenopathy, meningitis, intermittent diarrhea

118
Q

Coccidioidomycosis (San Joaquin Valley Fever)

Dx and sampling: name 3

A

1
CS and history (think about history and region the dog lives in/has been in
and outside activity)
* 2-Sampling: look for SPERULES (large, thick walled, contain round
endospores), exudate from draining lesions, biopsy, fine-needle aspirate
of infected tissue
* 3-Culture: reference lab only, mycelial form is extremely dangerous, difficult
to demonstrate dimorphism
* Mold: room temp and 37oC, hyaline hyphae that develop barrel-shaped
arthroconidia

119
Q

what are these?

A

SPERULES

120
Q

Coccidioidomycosis (San Joaquin Valley Fever)

Tx?

A

azoles long term (8-12 weeks) and eventually amphotericin B (but
can affect liver/kidneys)

121
Q

Systemic mycoses

is a dimorphic fungus found worldwide, but especially seen in
Tennessee, Mississippi, Ohio, Missouri, and St. Lawrence River basins

A

Histoplasma capsulatum var. capsulatum

122
Q

Histoplasmosis

describe
reservoir?

A

Chronic, NOT contagious, infection will cause a granulomatous disease that disseminates from lungs
Reservoir: humid environments with highly nitrogenous soils contaminated with BIRD and/or BAT droppings
(roosting areas, old chicken houses, and bat caves are high risk)

123
Q

Histoplasmosis

Susceptible species:

A

humans, but mainly dogs and cats, especially under the age of 4 and if they are mostly
outside

124
Q

Histoplasmosis

  • Pathogenesis?
A

Pathogenesis: microconidia or hyphal fragments from then environment are inhaled or ingested by the host
* Will change to the yeast phase in vivo and replication of the yeast will occur in monocytic cells
* Infection in the lungs can spread via lymphatics and/or blood to a variety of tissues including the spleen and bone
marrow

125
Q

Histoplasmosis

Lesions?

A

Lesions: granulomatous lesions are characteristic
* Lung lesions: yellow-white, variable sized nodules, and enlargement of the bronchial LN’s
* Secondary organs: enlargement of liver, spleen, mesenteric LN’s
* Ascites and foci of granulomatous inflammation on liver, myocardium, and small intestines

126
Q

Histoplasmosis

CS?
what is the predominating infection?
what about chronic infection?
dogs?

A

CS: the predominating infection is pulmonary, but dissemination is common
* Enlarged LN’s, exercise intolerance, lameness
* Chronic infection: inappetence, weight loss and muscle wasting, fever, poor response to antibiotic treatment
* Infection in DOGS: GI tract involvement and will likely result in death
* Anemia: due to GI blood loss and/or bone marrow involvement

127
Q

Histoplasmosis

Dx and sampling: name 3

A
  • CS and history
  • Sampling: look for small round YEAST cells within macrophages- will have basophilic center with clear halo, Buffy
    coat smear, LN aspirate, rectal scraping, biopsy, bone marrow aspirate
  • Culture: poses a severe biohazard risk, must use pathogen handling cabinet
  • Yeast: 37oC, small budding yeast cell
  • Mold: room temp, hyaline hyphae that develop microconidia and large, thick walled tuberculated macroconidia
128
Q

Systemic mycoses

what is this?

A

Histoplasmosis
Sampling: look for small round YEAST cells within macrophages-

129
Q

Histoplasmosis

Tx?

A

azoles long term (4-6 months) and potentially amphotericin B combined with azole for severe disease

130
Q

Systemic mycoses

Blastomyces dermatitidis
name the ecology
saprobic form
parasitic form

A
131
Q

Systemic mycoses

Coccidioides immitis
name the ecology
saprobic form
parasitic form

A
132
Q

Systemic mycoses

Histoplasma capsulatum var. capsulatum
name the ecology
saprobic form
parasitic form

A
133
Q

Systemic mycoses

a YEAST, comes from the environment and is NOT considered contagious
* Zoonotic potential is very low, but immunocompromised are at risk

what is it?

A

Cryptococcosis
Cryptococcus neoformans

134
Q

Systemic mycoses

Cryptococcosis
reservoir?
suseptible species?
pathogenesis?

A
  • Reservoir: soil with PIGEON excreta
  • Susceptible species: mostly seen in **cats, **can be seen in dogs, rare in large animals
  • Pathogenesis: un-encapsulated YEAST cells are inhaled from the environment, then capsulation occurs in vivo
  • Nasal mucosa is the primary site of infections and lesions range from gelatinous mass to granulomatous
135
Q

Cryptococcosis

CS?
cats?
dogs?

A

CS:
* Cats: sneezing, labored breathing, nasal discharge, hard nodular skin swellings over the nose bridge, skin lesions on the head, swollen LN’s, lethargy, loss of appetite
* Bone invasion results in distortion of the nasal cavity
* Not far from the nose to the brain, therefore, neurological abnormalities may be present (seizures, incoordination, behavioral changes)
* Eye disorders can occur such as chorioretinitis (due to yeast spreading from nasal cavity to the eyes)
* Dogs: more common to see the disseminated form and CNS signs

136
Q

Cryptococcosis

Dx?
Tx?

A
  • Dx: look for CS, impression smears of exudate or granulomatous tissue, biopsy/CSF/exudate are easily cultured- look for CAPSULATED YEAST
  • Tx: surgery, cryotherapy, antifungals (azole derivitives)
137
Q

is a normal inhabitant of the nasopharynx, GI tract and external genitalia of many animal
species, making it an OPPORTUNISTIC fungi causing localized mucocutaneous disease (mucous + skin layers)

A

Candida albicans

138
Q

Candida albicans

susceptible species?
predisposing factors?

A

Susceptible species: many species, but most commonly seen in birds
* pelicans
* Predisposing factors: disruption of mucosal integrity, catheters (indwelling, IV, urinary), antibiotics,
immunosuppression (drugs, disease)

139
Q

Candidiasis in birds
who is most susceptible?
crop lesions?

A

Candidiasis in birds: chickens and turkeys, young chicks/poults are the most susceptible
* Crop lesions: thickened mucosa (delays crop emptying), whitish, raised pseudomembranes

140
Q

Candidiasis in birds:

CS?
Dx?
Tx?
Prevention and control?

A

CS: listlessness, inappetence, anorexia, fluffed feathers, abnormal stance, beak abnormalities with a prolonged
infection, white plaques in the mouth
* Can sometimes see shallow ulcers and sloughing of necrotic epithelium
* Dx: culture from lesions and ID
* Tx: Nystatin and fluconazole
* Prevention & control: good sanitation, minimize antibiotic use

141
Q
  • Infrequent in dogs: exfoliative dermatitis on the muzzle, inguinal area, scrotum, and dorsal/lateral aspects of the feet
  • Rare in cats and Foxhounds get otitis externa

what is it?

A

Cutaneous candidiasis

142
Q

what is GI candidiasis:

A

can cause gastric ulceration in foals and calves
* Found in the stomach, thickened mucosa and white plaques, can become systemic

143
Q

Cutaneous and mucocutaneous candidiasis can be seen in what animal?

A

pigs

144
Q

Candidiasis

Diagnosis name 3

A

Microscopy: exam of scraping or biopsy from mucocutaneous lesion
* Ovoid, budding yeast cells with thin walls
* Pseudohyphae or true hyphae
* Pseudohyphae: blastospores remain attached after budding (incomplete budding)
* Germ tube test: differentiates C. albicans from other Candida spp.
* Several colonies are places in animal serum and incubated from 3 hours at 37oC, microscopic examination will show short
germ tubes if a C. albicans infection
* Biochemical tests and molecular tests

145
Q

are found worldwide and primarily causes a respiratory infections that
vary in predilection site based on species
* Susceptible species: domestic animals, birds, wild species

what is it?

A
  • Aspergillus spp. (A fumingatus, A. terrus)
146
Q

Aspergillosis
* Common forms?

A

Common forms: pulmonary infections in poultry/birds, mycotic abortion in cattle, guttural pouch mycosis in
horses, infection of the nasal/paranasal tissues, intervertebral sites and kidneys of dogs, pulmonary and
intestinal forms in cats

147
Q

Aspergillosis in birds
primarily where?
what occurs?
lesions?
CS?
what unique effect can spores have?

A

Primarily bronchopulmonary: dyspnea, gasping, polypnea
* Change in voice will occur if the syrinx is involved
* Lesions: yellow nodules of varying size/consistency or plaque lesions can be seen in the respiratory passages,
lungs, air sacs, or membranes of body cavities
* CS: respiratory symptoms occur first
* Flood flicking, somnolence, loss of appetite and anorexia, emaciation, torticollis, equilibrium disturbances (birds will start
sleeping for long periods of time), discharge if the nares are involved
* **Spores can kill embryos by penetrating fresh or incubating eggs
**

148
Q

Aspergillosis

Aspergillosis in ruminants:
what result?
what importance mycotic pneumonia?
CS?
what effect on lungs?
at what point is it too late to treat?

A

Aspergillosis in ruminants: asymptomatic, bronchopulmonary form, or will cause placentitis/abortion
* Mycotic pneumonia: subacute to chronic and the lungs will contain multiple discrete granulomas
* CS: pyrexia, rapid/shallow/noisy respiration, nasal discharge, moist cough
* Lungs: firm, heavy, mottled, and do not collapse
* Usually too late to treat once the animals has respiratory symptoms

149
Q

Aspergillosis

what is Bovine mycotic abortion?
describe uterine lesions
marernal caruncle lersions
cutaneous lestions of aborted fetus

A

dead fetus is aborted at 6-9 months gestation, fetal membranes are retained
* Uterine lesions: grossly thickened intercarunclular areas, leathery, dark red-tan, elevated or eroded foci covered by a yellow-grey adherent pseudomembrane
* Maternal caruncle lesions: dark red-brown, severely thickened cotyledons
* Cutaneous lesions of aborted fetus: foci that look like ringworm, red-grey, elevated plaques

150
Q

Aspergillosis

Aspergillosis in dogs:
what is it?
CS?
Dx?
Tx?

A
  • Mucosa of nasal/paranasal sinuses can be covered by a layer of grey-black necrotic material and fungal growth, can
    potentially see loss of bone definition
    *** CS: **lethargy, sneezing, nasal pain, ulceration of the nares (if a large growth), sanguinopurulent discharge (unilateral or bilateral), frontal sinus osteomyeltisis, epistaxis
  • Dx: CS, culture, biopsy for histology or cytology, radiographs, rhinoscopy to look for fungal plaques
  • Tx: administer itraconazole through** tube that is surgically inserted into the frontal sinus,** and systemic anitifungals
151
Q

Aspergillosis

Aspergillosis in horses: guttural pouch mycosis, “ticking time bomb”
explain
CS?
Dx?
Tx?

A
  • Mycotic plaques are usually located in the caudodorsal aspect of the medial guttural pouch, over the ICA
    (covering an artery is v. dangerous)
  • CS: based on which cranial nerves or arteries are effected, will see epistaxis and CNS signs
  • Can see hemorrhage, usually do to damage of the ICA, can result in fatal hemorrhage if repeated bouts of bleeding
  • Dx: endoscopic exam of the guttural pouch
  • Tx: sensitivity testing needed, topical and systemic antifungal therapy
  • Poor prognosis if the nerves involved in swallowing/respiration are effected, but the horse can recover if it’s a
    mild infection
152
Q

Aspergillosis in horses:
Diagnosis
Tx?
is it zoonotic?

A

* Microscopy: wet mount using KOH
* Hyaline, septate hyphae that have dividing branches with a 45o angle
* Characteristic conidial arrangement (can differentiate from other fungi just based on the structure)
Tx: topical azole given as 1 hour infusion (oral and systemic antifungal therapy can be toxic and $$$)
Zoonotic potential and immunosuppressed individuals are at a higher risk

153
Q

Pneumocystic pneumonia Pneumocytis jirovecii (P. carninii)

most common in what animal
CS?
Dx and sampling?
antibiotics?
explain a cytology exam
explain Gormori methanamine silver stain

A
  • Pneumocytis jirovecii (P. carninii) is most common in horses
  • CS: cough, dyspnea, exercise intolerance
  • **Dx and sampling:
  • History of poor response to antibiotics**
  • **Cytology exam **of fine needle aspirate of lung biopsy or BAL,
    and stain with Wright-Giemsa-type stain to look for trophozoites
    and intracystic bodies
  • Trophozoites: basophilic, dense, oval to irregular with lobed surface,
    foamy background
  • Intracystic bodies: groups of spherical to oval, dense basophilic
    structures, foamy background
  • Gomori methenamine silver stain: confirmatory diagnosis from
    alveolar exudates if ‘commas’ or ‘parentheses’ appear
154
Q

identify the
Intracystic bodies
Trophozoites

A

Intracystic bodies (on top)
Trophozoites (on bottom)
yellow arrow

155
Q

what is a fungal-like organism that LACKS chitin and ergosterol, and causes a granulomatous disease
* Mostly seen in Gulf coast states
* Susceptible species: mostly seen in horses and dogs

A

Pythium insidiosum

156
Q

Equine Pythiosis, Bursatti, Swamp cancer, leeches in horses

what is it?

A

Cutaneous and subcutaneous mycosis, causing chronic granulomatous and ulcerative lesions of the limbs and ventral
abdomen

157
Q

Equine Pythiosis, Bursatti, Swamp cancer, leeches in horses

Lesions:

A
  • Often self-traumatized, pruritic, discharge mucosanguineous exudate
  • “Kunkers” or “leaches” are irregular and yellowish concretions that form in sinus tracts– essentially masses of coral-like necrotic
    debris     that develop due to calcification
158
Q

Equine Pythiosis, Bursatti, Swamp cancer, leeches in horses
Dx?
Tx?

A

Dx: direct exam of kunker/lesion, histopathology, culture, PCR, ELISA
* Pythium insidiosum: appears as large, hyaline, non-septate hyphae
* Tx: response to therapy is not great, best option is radical excision, immunotherapy

159
Q

Canine Pythiosis:

what is it?
what does it cause?
treatment?

A

Canine Pythiosis: cutaneous, subcutaneous, and GI disease in dogs
* Mainly causes pyogranulomatous enteritis which causes anorexia and emaciation due to poor nutrient absorption (poor
prognosis), cutaneous lesions can also occur
* Surgical excision is the best chance for recovery

160
Q

Microsporidia: general characteristics

Phylum Microsporidia –> genera Encephalitozoon and Enterocytozoon

what are they?

A

-Unicellular, spore-forming eukaryotes
-Obligate intracellular parasites

161
Q

Microsporidia: general characteristics

In this Cellular Morphology

ldentify the
anchoring disk
spore wall
polaroplasts
nucleus
polar filament
posterior vacuole

A
162
Q

Microsporidian spores

what do they lack?
what is the cell wall made of?
describe the filament
resistent to what?

A
  • Lack typical mitochondria
  • Tri-layered cell wall composed of chitin, (glycol)proteins
  • Coiled polar filament
  • Resistant to harsh environmental conditions and inside host organisms
163
Q

Microsporidia: life cycle

Simple and direct life cycle
explain?
How many cycles?

A

Spore germination: extrusion of the polar filament -> injecting
sporoplasm into host cells (e.g. epithelial cells, macrophages,
endothelial cells)
* Two proliferative cycles

164
Q

Microsporidia: life cycle

what animal groups infected?

A

Infect every major animal group (esp. arthropods and fish)

165
Q

Microsporidia: life cycle

Transmission:

A

ingestion or inhalation

166
Q

Microsporidia: life cycle

Primary site of infection:

A

respiratory tract, small intestine–>
kidneys, liver, brain,

167
Q

Microsporidia: life cycle

Shedding:

A

feces, urine, respiratory secretions

168
Q

Microsporidia: life cycle

Sources:

A

water, contaminated food, animal reservoirs

169
Q

Microsporidiosis: public and animal health

importance

what relevance redarding commercial importance?

A
  • Infect commercially important (cultured) species (e.g. bees, silkworm, many fish species)
  • Reduced host fitness, chronic infections
    §
  • Death
170
Q

Microsporidiosis: public and animal health

importance

what relevance as opportunistic pathogens?

A
  • Opportunistic pathogens creating new or emerging diseases with financial losses (e.g. shrimp industry)
  • Emerging opportunistic infections in humans: zoonotic microsporidia, food production chain
  • Resistant in environment à need to further determine risk factors, preventative strategies, life cycles in
    different hosts
171
Q

Encephalitozoonosis in rabbits

Encephalitozoon cuniculi
where found?
how transmitted?
what kind of infection?
how does it present?
treatment?
what is the zoonotic importance?

A
  • Global distribution in domestic rabbits
  • Transmission: ingestion of spores or transplacental
  • Asymptomatic infections
  • Some animals develop encephalitozoonosis (CNS, eyes, kidneys) ~ immune status
  • Head tilting (torticollis), circling, seizures, tremors, paralysis
  • Uveitis, hypersensitivity, cataract
  • Shedding of spores in urine
  • Treatment: 28d fenbendazole (no guaranteed cure; life-long) and/or
    euthanasia in case of recurrent clinical signs
  • Zoonotic importance: important reservoir for humans (ingestion of spores)
172
Q

Encephalitozoonosis in dogs

Encephalitozoon cuniculi
who gets it?
transmission?
what result?
diagnosis?
treatment?
prevention?
zoonotic importance?

A
  • Clinical infections mostly in young or immunocompromised dogs
  • Transmission: ingestion of spores or transplacental
  • Opthalmologic signs: blindness, uveitis
  • Neurological signs: convulsions, paralysis, aggressive behavior
  • Stunted growth, kidney failure
  • Sudden death
  • Diagnosis: CBC, serum biochemistry, urine and fecal analysis
  • Treatment: spontaneous resolution, supportive care, antifungal drugs
    ~ immune status and severity of clinical signs
  • Control: cleaning environment, bedding, … (use PPE!)
  • Zoonotic importance
173
Q

Encephalitozoonosis in dogs

what is this?

A

Intraluminal E. cuniculi spores (mod. trichrome blue stain)

174
Q

Enterocytozoonosis in animals

Enterocytozoon bieneusi
who gets it? when?
transmission?
clinical signs?

A
  • Many immunocompetent animals are passively infected and only clinical flare up during immunosuppression
  • Transmission: ingestion of spores from environment
  • Clinical signs (~ immunosuppression):
    § Malabsorption, dehydration
    § Chronic diarrhea, enteritis
    § Growth disorders
175
Q

Chytridiomycosis

Batrachochytrium dendrobatidis

who gets it, what result?
source?
transmission?
how does it grow?
clinical signs?

A
  • Highly infectious and lethal skin disease of amphibians à massive decline in frog and salamander biodiversity
  • Notifiable disease (OIE)
  • Source: soil or water (streams, soaks, ponds)
  • Transmission: skin contact with water
  • Grows solely in keratinized cells
    –>stratum corneum from 2-5 μm to 30 μm
    –> mouthparts of tadpoles
  • Clinical signs: skin shedding, redness of skin,
    apathy, death
176
Q

Chytridiomycosis

what is this?

A

Histopathology and SEM image of Batrachochytrium dendrobatidis
(Bd) within the epidermal layer of an infected frog. Note the fungal
tubes poking through the skin surface on the Scanning EM picture

177
Q

Chytridiomycosis

Batrachochytrium salamandrivorans
clinical signs?

A

Clinical signs: epidermal ulcers, sores, apathy, nervous signs, death

178
Q

Chytridiomycosis: control

captive populations?
what should you wear?
what regulations?
what should you avoid doing?
what should you do?

A
  • Captive populations: antifungal drugs, disinfection of contaminated enclosures
  • Use single-use vinyl gloves when handling frogs
  • Optimize housing, hygiene and handling protocols
  • Avoid moving amphibians between places
  • Don’t release captive individuals uncontrolled in the wild
  • Monitoring and surveillance of amphibian populations and disease
    outbreaks
  • Notifiable disease!
179
Q

Mycotoxins: general characteristics

Mycotoxins
what are they?
where do they grow?
what sort of molecular weight?
heat stable–>?
active at ?
are they antigenic?
what leads to human exposure?

A

Mycotoxins = fungal secondary metabolites produced when toxigenic strains of certain fungi grow under
defined conditions on crops, pasture or stored feed (e.g. aflatoxins, fumonisins, zearalenone, … )
* Low molecular weight metabolites
* Heat-stable à retain toxicity following temperatures used for pelleting
* Active at low dietary levels
* Non-antigenic
* Accumulation in tissues of food-producing animals or excretion in milk à human exposure

180
Q

Mycotoxins: general characteristics

Ecological roles?

A
  • Contribute to pathogenicity and virulence of fungi
  • Disrupt bacterial quorum sensing
  • Act as antimicrobials
181
Q

Mycotoxicoses ?

A

acute or chronic intoxication following ingestion of contaminated plant material

182
Q

Mycotoxicoses

what characteristics of outbreaks?
contagious?
what controls the severity of the clinical signs?
treatment?
who gets it?

A
  • Outbreaks usually seasonal and sporadic
  • No evidence of lateral spread to in-contact animals (non-contagious)
    Severity of clinical signs ~ amount and type of mycotoxin ingested, host-related factors, stage of production
  • Antimicrobial medication is ineffective
  • Pigs, poultry, ruminants

Bacteriology and mycology (6 decks)

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