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red nose, bovine herpesvirus (BHV-1.1)
What is Infectious bovine rhinotracheitis commonly called? What causes it?
high morbidity, low mortality
what is the morbidity and mortality typically in IBR?
fever, nasal discharge, cough, ocular discharge, hyperemic muzzle
What are some clinical signs of IBR?
fibrin deposition, necrotic mucosa, diptheritic membrane
In IBR, secondary bacterial infection leads to _________ over _____________. something we call a ____________
congestion, necrosis of epithelium, inflammatory cells, intranuclear inclusion bodies
What is seen with IBR on histopath?
neutrophils, macrophages, lymphocytes, plasma cells
What are the inflammatory cells seen on histopath in IBR?
asphyxiation
Animals who do die of IBR, can get large fibrin build up in the nasal passage... what do they usually die of?
secondary bacterial pneumonia
typically IBR is mild and self-limiting, but immunosuppression leads to _________________
Mannheimia hemolytica
BHV-1 increases number of adhesion sites for
atrophic rhinitis
What is the historically significant rhinitis disease in swine?
hypoplasia or atrophy of nasal turbinate bones, +/- facial distortion, epistaxis
What are the distinct lesions in atrophic rhinitis?
More susceptible to resp disease (can't filter as well)
If the nasal turbinates degeenrate, what does this do to an animal long term?
toxigenic Bordetella bronchiseptica
What is the cause of NON-PROGRESSIVE atrophic rhinitis?
toxigenic Pasteurella multocida
What causes the PROGRESSIVE atrophic rhinitis?
from sows to piglets, carriers keep reinfecting
How does atrophic rhinitis transfer through a swine herd?
PRRS, pseudorabies, inclusion body rhinitis, influenza, poor ventilation (dust and ammonia)
What are some predisposing agents for atrophic rhinitis?
sneezing in young pigs, cilia damaged in mucosa, mild turbinate atrophy, little effect on growth
What happens in non-progressive atrophic rhinitis?
nasal mucosa, dermonecrotoxin, turbinate atrophy, osteoblasts, fibrosis
In progressive atrophic rhinitis, P. multocida colonizes _______ and produces _________ which causes _________ by damaging ________. This results in replacement by ______
4-12 weeks, epistaxis, deformed nose and septum, tear stained facial skin,
Clinical signs in progressive atrophic rhinitis appeat typically between ____________ of age. What are some signs that go along with it and are not typically seen in the non-progressive form?
Fever, rhinitis, conjunctivitis and cough.
What are some symptoms of equine upper respiratory disease complex?
EHV-4, EHV-1, Eq adenovirus, Equine rhinovirus, equine influenza, strangles
What viruses make up the equine upper respiratory respiratory disease complex?
suppress cell mediated immunity, predispose secondary bacterial pneumonia
spontaneous recovery from equine upper respiratory diseases complex is common and there is very low mortality... BUT what does it do to the host?
IgA
Secretory ______ neutralizes and immobilizes viruses preventing infection on mucosal surfaces.
IgM, IgG
______ and ________ (systemic antibodies) are present in the lung and can enhance phagocytosis of the viral particles by neutrophils and macrophages.
Equine herpesvirus 1 and 4
What causes equine viral rhinopneumonitis (EVR)
young foals, mild respiratory issues and fever (snotty nose)
Who does equine herpesvirus affect? and What are the symptoms?
It is associated with abortion
Why is equine herpesvirus considered one of the most important upper respiratory diseases?
latant, stress
After the initial infection, EVR becomes ________ in nerve cells, often for the horse's lifetime.
But can be reactivated by _________, causing shedding and clinical signs.
Streptococcus equi ssp. equi
What causes strangles?
direct contact or fomites,
How is equine strangles spread?
true
true/false: equine strangles is highly contagious and fomites can survive for months in the environment
nope
is streptococcus equi part of normal flora?
tonsillar crypts, soft palate, retropharyngeal, mandibular lymph nodes, gutteral pouch
S. equi attaches to cells of _______ and ventral surface of _____________.
It then moves to the ________ or _________, and usually _________, too.
purulent inflammatory, phagocytosis, hyaluronic acid capsule, anti-phagocytic protein
After multiplying in lymph nodes, S. equi induced a ____________ response (neutrophils).
•S. equi is resistant to________ due to _________________ and production of an _________________ (SeM).
yes
does equine strangles have a vaccine available in the US?
Acute upper respiratory tract obstruction, Suppurative rhinitis and lymphadenitis, Lymph node abscesses often with rupture to the outside, dyspnea, open mouth breathing
What are some lesions or signs of equine strangles?
inspissated
thickened or dried out pus
guttural pouch, empyema
The inflammatory response can extend into what horse specific cavity? And causes ___________>
cranial nerves (glossopharyngeal, vagus, accessory, hypoglossal), stylohyoid apparatus, recurrent laryngeal
what are some important anatomical features that run through the guttural pouch?
dysphagia, horners syndrone, abscess of cervical or retropharyngeal lymph nodes
What are the outcomes of guttural pouch empyema?
horner's syndrome
_________: damage to the sympathetic nervous system controlling the facial muscles and eye.
Bastard strangles
Bacteria and inflammation can spread during strangles to the lungs, kidney, mesentary, liver, spleen, kidneys, brain, and internal lymph nodes... what is this called?
Yes
Is strangles a re-portable disease?
feline herpesvirus-1, feline calicivirus, bordetella bronchiseptica, chlamydophila felis,
What is included in the feline upper respiratory disease complex
common, common
Secondary bacterial infections are [common/rare] due to mucosal damage, by feline upper respiratory agents.
Chronic carriers are [common/rare] after acute infection.
oculonasal discharge, rhinitis, conjunctivitis
What are some common symptoms of feline upper respiratory disease complex?
spontanreous, secondary bacterial infection, short-lived, yes
Feline upper respiratory disease complex RECOVERY is usually _________ unless ___________________________.
Anti-viral immunity is ___________. So can animals be reinfected?
upper respiratory tract
Where does feline viral rhinotracheitis (herpes-1) replicate?
keratoconjunctivitis, upper resp tract disease, abortion, neonatal death
What are some clinical syndromes of feline viral rhinotracheitis?
marked nasal discharge, sneezing, ulcerated nares, conjunctivitis, ulcerative keratitis
What are some SYMPTOMS of feline viral rhinotracheitis?
fibrinous rhinotracheitis, acute viral pneumonia, secondary bacterial pneumonia
In cases of feline viral rhinotracheitis where patients die.... they have ___________ with ____________ or they have __________________
feline calicivirus
Which feline virus is a recently described and affects mostly adult cats in a manor similar to rabbit hemorrhagic disease
40-50
Feline calicivirus has a __________% mortality rate
facial and limb edema, icterus, pancreatitis, high fever, anorexia, oral ulceration, ocular and nasal discharge
what are some symptoms of feline calicivirus
fomite, ulcerative glossitis
Feline calicivirus uses _______ transmission, and ______________is a hallmark
oculonasal and oral disease syndrome, acute lameness and pyrexia syndrome, febrile and hemorrhagic syndrome
What are some disease SYNDROMES of feline calicivirus?
oral cavity, tongue, palate
feline calicivirus has a high affinity for the _________ resulting in ulcers of the ______ and ________
(and pneumonia like all the others also)
cryptococcus neoformans
Which organism is responsible for cryptococcosis?
monomorphic, yeast-like, wide capsule of mucopolysaccharide
Describe cryptococcus neoformans
cats, horses, dogs
Cryptococcosis is most commonly seen in ______ but also occurs occasionally in _______ and ________
Facial swelling, Gelatinous nasal exudate, numerous organisms on histo with scant granulomatous inflammation.
What are common lesions in cryptococcosis
distemper, adenovirus, parainfluenza, reovirus, herpesvirus
In DOGS viral rhinitis is part of a systemic viral infection like: __________________________
bordetella bronchiseptica, E. coli, P. multocida
What are the most common isolates in a bacterial rhinitis in dogs?
Aspergillus spp.
__________ is BY FAR the most common canine fungal rhinitis
true
true/false: Localized or generalized impaired immunity predisposes opportunistic fungal infection in dogs.
Lymphoplasmacytic to granulomatous, friable
What TYPE of rhinitis is associated with fungal invaders?
The exudate produced is ________
bone, turbinates, nasal septum
fungi from a fungal rhinitis may invade _______ and cause destruction of the _____________ and ________