ear Flashcards
portals of entry to the ear
Extension from the
external environment** most common
Hematogenous spread
Extension from the middle ear
defense mechanisms of the external ear
Defense Mechanisms:
Integumentary defenses
Epithelial migration
Cerumen barrier and acidity
Commensal organisms
Structural defenses
middle ear portals of entry
Extension through TM
(perforation)**
Ascending (auditory tube)
Extension (temporohyoid joint degeneration)
Extension (TB erosion)
Migration – vascular/neural path
defense mechanisms of the middle ear
Defense Mechanisms:
Mucociliary apparatus
Surfactant
Auditory tube lymphoid tissue
Commensal organisms
internal ear portals of entry and defense mechanisms
Main anatomical features:
Petrous bone and cochlea
Portals of entry:
Extension from the middle ear
Hematogenous spread
Migration along vascular or neural pathways
Defense Mechanisms:
Structural defense (bone)
aural hematoma
Dogs and Pigs»_space; Cats
sporadic occurrence
Secondary to HEAD SHAKING
Shearing forces damage auricular cartilage in the middle and rupture small vessels within the pinna leads to pooling of blood.
ear necrosis (vascular injury)
Circulatory or Trauma
Usually INFARCTION:
Vascular injuries
Thrombosis
Bacterial septicemia
- Salmonelosis
- Erysipelas
Frostbite
Toxins: Ergot and fescue
Biting injury: Other Trauma
frost bite in ears (vascular injruy)
Young animals most susceptible outdoors
Ischemia to keep blood warm in core body
Leads to infarction and necrosis: Dry gangrene
ERGOT vasoconstriction similar in appearance
blue ear disease in pigs
Ears are dark red to purple-
black
caused from PRRS virus vasculitis (arteriovirus)
-ear tip necrosis due to vasculitis from immunesuppression
DDX: Salmonellosis:
- Thrombosis due to endotoxin
released by bacterium.
May also include the tail and
sloughing of ear/tail
otitis externa
-prevelant in dogs
- Chronic and repeated:
-Permanent changes to structure and function with no chance of return to
normal.
ODOR and COLOR of discharge can be indicative of pathogen present.
different exudate in otitis externa and what they cause?
ear mites: dry, dark and grangular (otodectes cynotis) usually in cats
bacteria: moist, yellow, odiferous
yeast: reddish brown, waxy (malassezia otis externa)
ceruminous or sebaceous: yellow, waxy to oily
otitis media (most common)
Usually Suppurative +
bacteria
Extension of Otitis Externa
Dogs may be up to 80% of cases of OM
Perforations reported >40%
Large animals:
Nasopharyngeal ascent of
bacteria through the auditory
tubes.
otitis media in pics bacterial causes
Pasteurella multocida,
Trueperella pyogenes, and
Mycoplasma hyorhinis are most
commonly isolated from
suppurative otitis media.
otitis media in cattle bacterial causes
Histophilus somni, Pasteurella
multocida, Trueperella pyogenes
(Arcanobacterium pyogenes),
and Mycoplasma bovis
pasturellosis in rabitts
- May start as ‘snuffles’ (rhinitis
caused by Pasteurella multocida) - Presented as torticollis (head tilt from in inner ear)
hearing loss
Congenital or Acquired
Conduction loss or
Neurosensory loss
Genetic:
Heterochromia
Blue eyes (NOT 100% linked)
Age related
Ototoxicity:
Noise trauma
Aminoglycosides
Asprins
pinnal alopecia
Herefords (polled): congenital
disease**
Ears and muzzle in newborns
Epidermal maturation and
keratinization defects
Acquired disease in Dogs and
Cats
Dachshunds
(Chihuahuas, Boston terriers, Whippets and
Italian greyhounds)
Progressive over time
Anagen follicles are smaller in diameter and shorter
than normal areas
Siamese Cats
non congenital causes of pinnal alopecia
Atopy
Food allergy
Canine hypothyroidism
Hyperadrenocorticism
Demodicosis
Dermatophytosis
neoplasia of the skin and pinnae
Melanoma
Squamous cell Carcinoma (actinic dermatitis)
Dentigerous cysts
nasopharyngeal polyps in cats
Non-neoplastic, inflammatory
masses affecting cats often under 2 years of age
They may be confined to the
middle ear
protrude through the auditory tube
into the nasopharynx
penetrate through a ruptured
tympanic membrane
Symptoms may be Otitis externa
or media, or Respiratory Stridor
feline ceruminous cytomatosis
Cause unknown
Hyperplasia of ceruminous
glands
Symptoms may be Otitis
externa or media
otitis externa predisposing factors
- Conformation or obstructive ear diseases
- Auricular phenotype or Breed (Chinese Shar Pei)
- External ear moisture (swimmer’s ear)**
- Excessive cerumen production**
- Systemic diseases (immune suppression, etc.)
otitis externa primary causes
-Parasites (Otodectes cynotis “ear mites” and skin parasites)
- Hypersensitivity reactions (ATOPY, food and contact hypersensitivity)**
- Keratinization disorders (ENDOCRINE DISEASE)**
- Foreign bodies
cattle lactation
dairy Around 23,000 lbs or 2674 gal per
305 days of lactation
Beef:
IgG receptors are present for about 1
week before parturition and disappear
during lactation
-glands and ducts with fibrovascular stroma
failure of passive transfer lesions
-not enough colostrum in first 24 hours.
-mild fibrinous polyserositis, polyarthritis, meningitis,
-all from endothelial damage and leakage of fibrinogen
-diffuse pulmonary edema and congestion: from vasodialation, endothelial leakage and cardio compromise.
-skin: generalized petechiation from endo damage-> DIC
-spleenomegaly MEATY spleen and lymphomegaly from activation of macrophages.
mammary anatomy
Epithelial remodeling can lead
to unchecked hyperplasia and
cell transformation
The normal check for this is the
stimulus of chronic and solid
stress
hyperplasia within the lumen
should trigger removal of these
cells
If not – the pre-neoplastic ductal
mass may invade surrounding
tissue and migrate further
portals of entry to mammary
Ascending infections**: can be forced
up ducts by an automated milker
(DAIRY).
-Bacteria, fungi, parasites
- Teat lesions
Direct penetration: Penetrating injury
Systemic infection and localization
-Systemic fungi, viruses, mycoplasmas,
mycobacteria
defense mechanisms of the mammary glands
Drainage of secretions
NORMAL CONFORMATION of
ducts and sphincter
Neutrophils/ macriophages
Lactoferrin: Increases with MASTITIS and involution, Withholds iron from bacteria
Lysozyme: Cell wall Lysis
Complement
Cytokines
Microbial recognition molecules
clinical manifestations of mastitis (types)
- Severe mastitis (± necrosis)
Severe with necrosis = gangrenous
mastitis - Suppurative mastitis
- Subclinical mastitis
- Granulomatous mastitis
etiology of mastitis
Contagious:
Streptococcus agalactiae**
Staphylococcus aureus**
Mycoplasma bovis
Skin or environmental
contaminants:
Escherichia coli
Klebsiella pneumonia
streptococcus agalatactia
Suppurative to Severe (±Necrotizing) mastitis due to endotoxin release
NOT FATAL
Milk quality is altered, and strands or clumps of debris or pus are present in the milk
Associations:
Older cattle, inadequate hygiene and antibacterial treatments
-large $$ loss
pathogenesis of strep. agalactiae
Pathogenesis:
Edema + neutrophils -> brief epithelial hyperplasia -> Macrophages and fibrosis in lumen of alveoli -> spreads
outward to adjacent alveoli -> INVOLUTION and periductal fibrosis and granulation** -> squamous metaplasia with
regeneration of the ducts
staphylococcus aureus pracute form
PERACUTE form: most severe, necrosis and
infarction (gangrenous)**
Occurs shortly after parturition.
Classic heat, redness, swelling, and pain (inflammation)
progresses to coldness, blue-black color and edema (necrosis)
Can be fatal
Pathogenesis:
Interalveolar edema -> epithelial swelling, vacuolation, and focal
erosion (ductal junctions) -> epithelial attachment of bacteria -> focal
damage, necrosis and neutrophils -> luminal pus accumulation
staph aureus acute form
ACUTE form: less severe form
Fever, anorexia, toxemia
May be fatal
staph aurues chronic form
Chronic is MOST COMMON
FORM
Decreased milk yield
watery with clots
Inflammation and abscessation
can lead to Botryomycosis: granular bacterial and necrotic debris surrounded by granuloma**
Pathogenesis: (<48h post infection)
CHRONIC: similar to S. agalactiae ±
lymphocytes
mycoplasma bovis
Sporadic individual cases and
outbreaks -> culling ($$$)
Infection by hematogeous and
ascending routes
Quarters are enlarged and firm with
nodular abscesses
Dramatic drop in milk production
Systemic disease limited
mycoplasmal arthritis or pneumonia
coliform mastitis
Milder forms in herds with good
control of contagious mastitis
Environmenatl Bacteria ->
ascending infection
Milk quality is altered,
strands or clumps of debris or pus***
Gram negative bacteria with
endotoxins (LPS) -> vascular
damage
Endotoxemia -> Death
septicemia ~1/3 of clinical cases
-in well maintanted healthy herd, enviro basteria: E.coli, klebsiella pneymoniae
coliform mastitis acute form
ACUTE form (Gram negative):
Older cattle, inadequate hygiene and
antibacterial treatments
Hyperemia, edema, hemorrhage, necrosis
and inflammation centered on the
lactiferous ducts
Sequestration:** necrotic mammary tissue
separates from the viable tissue (can be a
large portion of a quarter)
Suppurative mastitis causes
Suppurative mastitis:
* Trueperella pyogenes
* Mycoplasma bovis
* Streptococcus dysgalactia
mastitis of sheep
-blue bag:
There are two main bacterial
agents recovered from mastitis of
sheep:
Mannheimia haemolytica and
Staphylococcus aureus
ACUTE, unexpected death:
bacteria cause an acute
necrotizing/gangrenous mastitis
“blue bag”
Maedi-visna virus (multisystemic)
chronic inflammation
mammary glands = “hard udder”
mastitis of goats
Staphylococcal and streptococcal
mastitis in goats are similar to
cattle
Mycoplasma agalactiae:
Inflammation in mammary gland is
followed by progressive fibrosis and
glandular atrophy, hence dramatic
decrease in milk production (agalactia).
This disease is initially septicemic and
often fatal.
Caprine arthritis encephalitis virus: Chronic mastitis = hard udder
mastitis in dogs
Mastitis occurs early in lactation
or pseudopregnancy**
Staphylococcus sp., Streptococcus
sp., and Escherichia coli
May be superimposed on top of
mammary hyperplasia or
neoplasia
mammary tumors dogs and cats
Cat vs. Dog
Mammary tumors are most common in dogs and uncommon in cats
~80% are benign in dogs vs. ~80% are malignant in cats
-Epithelial and combined epithelial
and myoepithelial tumors
Fibrosarcoma and osteosarcoma are
particularly aggressive and metastatic
Ovariohysterectomy after the
second estrus** dramatically
increases the prevalence of this
disease.
A high-protein diet decreases
susceptibility
fibroadenomatous hyperplasia
Highly prevalent and is the most common
disease of the gland
It occurs in young, intact queens (<2y) and
most often in SPRING
The lesion is proliferation of mammary
ducts and adjacent stroma
Progesterone -> Overstimulation/dysregulation of tissue
growth
Hemorrhages, coagulative necrosis, and/or
ulceration can occur
Resolution is spontaneous or with
ovariohysterectom
feline mammary tumors
Most often carcinomas with
relatively wide range of post-
excisional survival
Metastasis common
Ovariohysterectomy before the
second estrus dramatically decreases
the prevalence of mammary tumors
in cats**
Cats with neoplasms that are greater
than 3 cm in diameter have shorter
survival
-**graded based on: invasion, mitotic rate,
and nuclear shape
