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209 Cards in this Set
- Front
- Back
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Name the 3 canine Parvovirus types
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-2a
-2b -2c |
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What is the name for the feline Parvo virus
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- Panleukopenia virus
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Parvo virus general info:
DNA or RNA single or double stranded enveloped or non-enveloped |
- DNA
- single stranded - non-enveloped |
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are Parvo viruses susceptible to detergents and inactivation?
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- no
- most likely due to non envelope |
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what part of the Parvo virus is most susceptible to mutation?
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- the capsid
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do parvo viruses replicate faster or slower than RNA viruses?
what about the rate as compared to other DNA viruses? |
- 10 fold slower than RNA viruses
- but much faster than other DNA viruses since it is ssDNA |
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what type of cell do parvo viruses show an affinity for during replication?
name 4 types of tissue |
- replicate in cells with HIGH MITOTIC RATES
- fetal tissues during development - enteric epithelium - hematopoietic cells - lymphoid tissues |
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Parvo: Phase 1 of infection
How does infection occur, what tissues are infected? Duration? |
- oronasal exposure
- infect tonsils, Peyers patches, GI lymphatics - 1-2 day duration |
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Parvo: Phase 2 of infection
what happens? Where does infection spread to? Duration? |
- virus is disseminated systemically via VIREMIA
- infection moves to CRYPT CELLS - also moves secondary lymphatics and bone marrow - 5-9 day duration |
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enterocyte information
location function are they proliferative? |
- located in the villus
- function in digestive and absorptive activities - they are NON-PROLIFERATIVE |
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Crypt cell info
function are they proliferative? |
- secretion
- they are the progenitor of the villous enterocytes |
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do parvoviruses target enterocytes or crypt cells? And what other tissues would be targeted?
How do they gain access to these cells? |
- parvo targets crypt cells
- also target primary and secondary lymphoid tissues - accesses crypts via lymphatics and vasculature |
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what would be a CS in parvo infection
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- hemorrhagic enteritis with electrolyte imbalance
- neutropenia - lymphopenia - pyrexia - vomiting - hyperproteinemia |
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how soon after CS does death occur in parvo?
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- 1-3 days
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what happens to depress a Parvo infection?
when should this be done? what is the result for the virus? |
- serum neutralizing Ab
- if present from day 5-9 - viremia will be terminated and animal will recover |
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what do neutralizing Abs attach on Parvo?
what does this prevent the virus from doing? |
- Capsid VP-2 proteins
- interferes with attachment ability of the virus |
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What animals are most prone to Parvo infections?
Predisposing factors for these groups |
- puppies (6 wks - 6 mo)
- lack of protective immunity - intestinal parasites - poor sanitation - STRESSERS - adults - most are subclinical - breed disposition (Rotts, Dobers, Labs, Pits) |
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what is the significance of Parvo infecting primary and secondary lymhoid tissues?
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- causes immunosuppresion
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what happens to immune system of puppies infected in utero or as neonates with Parvo
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- causes immunosuppression
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name some tests used to diagnose Parvo
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- feces lateral flow ELISA
- blood lateral flow ELISA - electron microscopy - serology: hemagglutination inhibition - PCR |
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what does a hemagglutination inhibition test measure?
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- tests for the presene of serum neutralizing Abs to the virus
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what does PCR test for in Parvo?
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- nucleic acid [DNA] in feces, blood, tissues
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is virus isolation used to diagnose Parvo?
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- NO
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vaccination for canine parvovirus
killed or MLV why? |
- killed vaccine for canine parvo
- if puppy is not- immunocompromised it should produce neutralizing Abs and clear the virus |
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what can interfere with immunization for parvo?
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- maternal Abs
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which is more stable:
canine parvovirus or feline panleukopenia virus |
- feline paneleukopenia virus seems to have undergone less mutation over the years
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pathogenesis for feline panleukopenia virus
Phase 1 duration |
- oronasal exposure
- infecting tonsil, Peyers Patches, GI lymphatics - 1-2 day duration |
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pathogenesis for feline panleukopenia virus
Phase 2 duration |
- virus disseminated systemically via VIREMIA
- infect crypt cells, primary and secondary lymphatics, bone marrow - 5-9 day duration |
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when is viremia of feline panleukopenia virus resolved?
why does this occur? |
- viremia resolved in 5-9 days
- because of serum neutralizing Ab formation |
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feline panleukopenia virus
mild or severe infection? duration? name 4 CS |
- infections generally mild
- last 4-7 days - transient diarrhea - pyrexia - short period of anorexia - depression |
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do most feline panleukopenia virus infections show CS?
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- no
- most are unrecognized and subclinical |
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what occurs in feline panleukopenia infections near term or in neonatal infections?
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- cerebellar hypoplasia
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3 things the cerebellum is important for
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- balance
- posture - cordination of movement |
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do other parvo viruses show cerebellar hypoplasia like FPLV?
what CS is similar? |
- no
- cause similar GI infections |
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diagnostics for FPLV
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- history and CS
- feces - lateral flow canine ELISA |
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what is the most important event in a FPLV infection?
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- brief period of immunosuppression
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prevention of FPLV
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- killed vaccine
- given annually (especially in multi-cat households) - good hygiene (1:10 chlorine bleach) |
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are adenoviruses species specific?
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- very species specific
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adenovirus genome
what does this tell us? |
- ds DNA
- fairly stable |
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are adenoviruses enveloped or non-enveloped?
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- non-enveloped
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canine adenovirus type 1
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- infectious canine hepatitis
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canine adenovirus type 2
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- infectious canine laryngotracheitis
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how is the pathogenesis similar for both type 1 and type 2 canine adenovirus?
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- oronasal introduction
- infects lymphatics in tonsils and pharynx - tonsillitis |
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pathogenesis canine adenovirus 1 following tonsillitis
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- 1 week post infection
- disseminated to endothelial cells (liver) by viremia - vasculitis |
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CS of infectious canine hepatitis (ICH)
duration of CS? |
- fever
- depression - diarrhea - vomiting - several weeks |
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CS of severe cases of ICH in puppies
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- pain on abdominal palpation
- edema of head and neck - possibly jaundice |
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most consistent findings with ICH (lesions)
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- petechial hemorrhages
- hepatic necrosis - edematous gall bladder |
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what do petechial hemorrhages and hepatic necrosis lesions hint at in ICH?
how did this happen? |
- exhaustion of blood clotting factors
- due to: -- consumption -- damaged endothelium -- hepatitis |
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other finding with ICH?
what is it? nickname? |
- corneal edema
- type III hypersensitivity (immune complex) - ICH induced "blue eye" |
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prevention for ICH
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- vaccination
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canine adenovirus II
aka? |
infectious canine laryngotracheitis
kennel cough |
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CS of kennel cough
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- nasal dishcarge
- coughing |
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clinical findings of canine adenovirus laryngotracheitis
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- rhinitis
- tracheobronchitis - exudative pneumonia |
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pathogenesis of canine adenovirus II
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- oronasal introduction
- lymphatics in tonsil and pharynx infected - tonsillitis |
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kennel cough associated viruses
name 7 |
- canine adenovirus I
- canine adenovirus II - paramyxovirus - canine herpes virus - canine distemper virus - mycoplasma - Bordatella bronchiseptica |
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what viruses are included in the DA2PP vaccine?
there are 4 |
- Distemper virus
- canine Adenovirus II - Parvo - parainfluenza virus |
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canine herpes virus (CHV)
type of herpes virus genome enveloped: yes or no |
- alpha herpes virus
- dsDNA - enveloped |
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what does CHV do in puppies?
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- inability to regulate body temperature until 2-3 weeks of age
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what does poikilothermia mean?
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- dependent on their surroundings for warmth
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signalment for CHV
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- crying pups
- painful palpations - rhinitis |
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pathognomonic lesion of CHV
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- mottling of kidneys
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prevention of CHV
is there a vaccine? management factor? |
- no vaccine available
- maintain temp > 35 degrees Celsius |
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canine distemper virus
genus genome type enveloped/non-enveloped |
- morbillivirus
- ssRNA - enveloped |
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route of infection for canine distemper
location of primary replication secondary locations for replication timeline for the infection |
- inhaled
- primary replication in macrophages and bronchial lymph nodes - virus replication spreads through lymphatic system (spleen, marrow, thymus, lymphatics) - replication phase takes about 1 week |
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canine distemper virus results in 3 things as a result of viral replication in lymphatic tissue
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- immune suppression
- fever and VIREMIA |
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canine distemper causes depletion of these vascular cells
primary one and a secondary one |
-depletion of CD3 T cells
- depletion of CD21 B cells |
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experimental infections with canine distemper resulted in what... and what is the big result
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- necrosis and depletion of the cortical lymph node
- IMMUNE SUPPRESSION |
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cell mediated and humoral immune responses are necessary for protection against canine distemper.
What must happen in order for clearance of the virus? |
- production of serum neutralizing Ab
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canine distemper virus is pantropic, what does this mean?
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- affinity for many tissues
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mucosal phase of canine distemper virus (CDV) includes infection of what epithelium?
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- alimentary
- urogenital - respiratory - skin - endocrine - CNS |
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common lesions found with CDV infection
name 3 |
- conjunctivitis/rhinitis
- pneumonia - diarrhea |
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neurological effecs of CDV acute phase
name 1 when would signs begin? |
- convulsions/seizures
- 1-5 wks after systemic infection |
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CDV caused "acute encephalitis" is a result of what CS and replication of what area in the brain?
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- convulsions/seizures
- infection of the cerebral/cortical region |
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acute CDV infection in the brain
target and result |
- neurons are primary target
- cause neuronal degeneration and inflammation - grey matter disease |
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CDV subacute encephalitis involves what areas of the brain and what are the CS with each?
name 2 |
- ataxia: cerebellar/vestibular dysfunction
- posterior paralysis: spinal cord |
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subacute encephalitis with CDV infects what cells in the brain?
3 (1 most important) result/pathogenesis? |
- astrocytes and microglia
- oligodendrocytes have most damage - white matter disease --degeneration of white matter develops into a non-suppurative inflammation with macrophages and neutralizing Abs |
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CDV diagnosis via CSF
what is found in: recovering dogs acute infection subacute infection |
- no interferon or Ab
- interferon - Ab and interferon |
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diagnosis of CDV infections
general |
- CS
- hyperkeratosis -inclusion bodies |
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PCR for CDV infection is done on what sample?
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whole blood
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what other type of animal has been infected with CDV
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large cats
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the genus Henipavirus includes what 2 viruses
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- Hendra virus
- Nipah virus |
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hendra virus causes what condition in horses and cats?
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fatal pneumonia
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ROI with Hendra virus in horses?
replication occurs where? pathologic lesions found where? |
- oronasal infection
- replication in macrophages and bronchial lymph nodes - lesions found in the lungs but there is widespread vasculitis |
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is air transmission important for hendra virus?
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no
- oral ingestion or injection of virus are the only infectious routes |
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feline rhinotracheitis is caused by what type of virus?
genome type what is special about this type of virus? |
- feline herpes virus Type 1 (FHV-1)
- ds DNA - herpes viruses become latent viral infections |
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what area of the resp tract does FHV-1 infect?
timeline? lesions? CS? |
- infects the upper respiratory epithelium
-2-5 post infection focal necrosis of the upper resp tract - fever, anorexia, sneezing, conjunctivitis, nasal discharge |
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what animals are predisposed for infection with FHV-1?
what normally happens with cat after they are infected? |
- young cats
- 80% of infected cats will be chronic shedders |
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importance of arginine with herpes viruses
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- herpes viruses produce arginine rich proteins
--- reducing arginine reduces replication, but dont use in cats as arginine suppresses conversion of ammonia to urea |
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what AA other than arginine is important for reducing herpes virus replication? how?
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- lysine
- competes against arginine |
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feline calicivirus
genome type enveloped? |
- ss RNA
- non-enveloped |
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ROI for feline calicivirus
lesions? |
- oronasal transmission
- infects oral epithelium -- causes oral vesiculation and ulceration |
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CS of feline calicivirus infection
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- transient fever
- vesicles and ulcerations - transient limping and stiffness |
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what can an oral feline calicivirus infection progress to?
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- interstitial pneumonia with secondary bacterial infections
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what type of immunity is produced with feline calicivirus vaccination?
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- induce only relative, not absolute protection
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coronaviruses
genome type enveloped? |
- ss RNA
- (+) sense - enveloped |
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feline enteric coronaviruses (FeCoV) infect what type of cell?
what is the result? |
- enterocytes in the intestinal villa
- BLUNTING of the villi - alters digestive and absorptive abilities - mild/self limiting diarrhea |
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ROI of FeCoV?
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- fecal oral route
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what is the major dz associated with FeCoV?
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- feline infectious peritonitis
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2 forms of FIP
when does death occur in each? |
- wet, effusive form
-- death w/in wks to months - dry, non-effusive form -- death greater than several months |
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effusive FIP is a more "acute" form of FIP.
what exudates can be present and what CS would accompany each? |
- pleural: dyspnea
- pericardial - peritoneal: vomiting, diarrhea, abdominal extension |
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what is the most common presentation of effusive FIP?
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hydroperitoneum
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what would commonly be found with dry FIP?
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- more chronic condition
- perivascular granulomas |
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do you see neurologic signs with the wet or dry FIP?
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dry
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name three ocular lesions found with FIP
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- bilateral anterior uveitis
- retinal hemorrhage - retinal detachment |
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what has to occur for FeCoV to cause the disease FIP?
3 things |
- FeCoV mutates
- FeCoV can then infect macrophages/monocytes outside of the GI tract - Viremia |
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what is the normal immune responses to FeCoV?
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- CMI response
- Humoral response |
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with wet FIP, what is the major immune response?
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- humoral
- B cells stimulated to produce neutralizing antibodies - not controlled by T cells |
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what is the "hallmark" of acute inflammation with wet FIP?
what causes this? |
- edema
- FeCoV induced immune complexes damage small vessels (Type 3 hypersensitivity rxn) - leakage of plasma proteins into extra-vascular spaces |
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immune response to dry FIP
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- humoral response
- ineffective, only partially protective CMI response - type IV hypersensitivity |
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hallmark of dry FIP
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- granulomatous inflammation
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how is the definitive diagnosis of FIP made?
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- post mortem exams
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presentation of cats with wet FIP
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- non painful progressive abdominal distention
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what clin path findings would be present with FIP?
name 3 |
- lymphopenia
- hyperglobulinemia - hypoalbuminemia |
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2 test used to diagnose FIP
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- IFA
- ELISA |
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is FeCoV vaccine considered a core vaccine?
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- no
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can FeCoV be treated?
prevention methods? |
- cant be treated, FIP is fatal
- prevention important -- sanitation, maintain good immune status --segregate cats by age |
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rabies virus
genome type and shape genus and family |
- negative stranded bullet shaped
- genus: Lyssavirus - family: Rhabdoviridae |
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where does the rabies virus get its RNA polymerase?
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- RdRp in the virion
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neutralizing Abs against rabies are formed against what viral protein?
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G protein
- this is the glycoprotein |
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what rabies viral protein is important for binding to host cell receptors and allowing endocytosis to occur?
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- G protein
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rabies virus is enveloped, meaning what?
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easily disinfected
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rabies virus is neurotropic, meaning high concentrations can be found where?
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- brain
- saliva/salivary glands |
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rabies infection of the brain drives the behavior we see:
4 things |
- aggression
- changes in activity - vocalization - loss of normal protective aversion (self-mutilation) |
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section of the brain used to identify rabies in a sample?
be specific |
- cross section of cerebellum and brain stem
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gold standard test for diagnosing rabies in a brain sample
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- direct fluorescent antibody test
- dFA |
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ante mortem diagnosis samples for rabies
name 4 |
- saliva
- skin biopsy - serum - CSF |
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what is the most natural and successful route for transmission of rabies
what are 4 other modes of transmission, even though risk is much smaller in these modes |
- bite is #1
- exposing fresh, open bleeding wounds - oral exposure - inhalation - ocular |
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what happens after an animal is bitten by a rabies positive animal?
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- virus moves up the peripheral nerves into the spinal cord and brain
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incubation period for rabies is highly variable, name the time frame
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- 10 days to 6 months, or possibly more
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human rabies post-exposure prophylaxis should be based on the result of what 2 things following a bite from a dog, cat, or ferret?
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- 10 day observation period
- laboratory result |
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what are the outcomes for potentially exposed animal that is naive or outdated on its vaccination, or no licensed vaccine is available for the species?
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- euthanasia
- 6 month quarantine |
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what are the 3 steps to the human post exposure prophylaxis?
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- wound cleansing
- human rabies IgG - five doses of vaccine (0, 3, 7, 14, 28) |
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how often should vaccinated people check their titer?
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- every 2 years
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tumor of epithelial origin is called what?
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- carcinoma
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tumor of mesenchymal origin is called what?
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- sarcoma
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cell growth is controlled by 4 different types of proteins
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- growth factors
- growth factor receptors - intracellular transducers - intranuclear transcription factors |
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what are oncogenes
name the 2 types |
genes that have the ability to cause neoplasia
proto oncogenes: cell origin viral oncogenes: viral origin |
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retroviruses are RNA viruses capable of doing what?
|
transforming infected cells
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8 steps of FeLV infection
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- oronasal contact with virus
- replication in tonsil and local lymphoid tissue - mononuclear leukocyte associated viremia - systemic lymphoid replication - replication in bone marrow/crypt epithelium - marrow origin viremia w/in PMNs and platelets - infection of glandular and mucosal epithelium - leukemogenesis or aplasia |
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name the two types of FeLV infections
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- progressive and regressive
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progressive FeLV infection characteristics
|
- persistent FeLV replication
--lymphoid, hematopoietic, mucosal/glandular epi - ineffective response of host to anti-virals |
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regressive FeLV infection characteristics
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- early curtailment of replication
- viremia terminated or undetectable - virus present with minimal incidence of dz |
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proliferative FeLV causes 2 types of diseases in cats
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- blastopenic: degenerative
- neoplastic: proliferative |
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neoplastic FeLV disease characteristics
|
- lymphosarcoma
- leukemias or myeloproliferation |
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blastopenic FeLV disease characteristics
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- change in immune function
- decreased B and T cells - autoimmune dz, impaired phagocytosis |
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thymic lymphosarcoma of FeLV
age affected lesions cell type most common |
- cats < 3 yrs old
- thymus displaced heart caudodorsally - thoracic effusion - dyspnea and cyanosis - usually T cell malignancies |
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multicentric lymphosarcoma of FeLV
age affected signs and lesions cell type most common |
- any age
- CS related to lymph nodes involved -- lympadenitis, neoplastic cell infiltrate - malaise, anemia, anorexia - T cells |
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alimentary FeLV lymphosarcoma
age lesions cell type |
- older cats
- CS related to renal or intestinal dysfunction -- uremia, GI blockage, malabsorption - B or T cells |
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common sequela of degenerative form of FeLV
|
- secondary infections due to depressed immune function
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which is more common, neoplastic or blastopenic FeLV infection in single cat homes
|
blastopenic: 80%
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FeLV infections in multiple cat homes
|
30% progressive infections
40% regressive infections |
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3 subgroups of FeLV
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- subgroup A
- subgroup B - subgroup C |
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FeLV subgroup A
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- all naturally infected cats
- long incubation period - only subgroup found in cell-free fluids |
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subgroup B FeLV
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- not transmitted naturally b/w cats
- result of recombination with A and endogenous retrovirus sequences - 50% of all naturally infected cats - cats with A and B most likely to be persistently infected - exclusively cell-associated |
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FeLV subgroup C
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- recombinant of type A with proto oncogenes
- 1% of cases - rapidly fatal |
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Feline Sarcoma Virus (FeSV) is a mutant of what virus that contains proto oncogenes?
what is required in order for FeSV to develop? what usually develops? |
- FeLV
- needs simultaneous infection of replicating FeLV - multicentric fibrosarcomas |
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prognosis of FeLV cats in multiple cat households?
what is the only way to make a diagnosis/prognosis? |
- 83% with progressive FeLV have 3.5 yr life span
- defining a persistent (progressive) infection is key to making a diagnosis/prognosis - can only be determined by testing |
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detection of FeLV done how?
test used what does the test look for |
- IFA test
- detect gag protein in peripheral blood/tissues - ELISA test used to screen, IFA as confirmatory |
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how long after initial exposure will FeLV test be positive?
|
- 2-3 wks after initial exposure
- with regressive infections, may test negative 2-8 wks later |
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neutralizing Ab to FeLV interferes with what?
|
- viral attachment/uncoating
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the tests for FeLV detect what genomes?
|
- FeLV specific genomic RNA
- proviral DNA |
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do regressive FeLV infections usually progress to the marrow?
|
no
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infection rate of FeLV is directly related to what?
how do we attemp to avoid transmission? |
- cat population density
- testing |
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killed and MLV vaccines
immune response booster? |
- humoral in killed
- CMI and humoral in MLV - booster needed with killed, not with MLV |
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Feline immunodeficiency virus (FIV)
genus what type of disease is most common with this genus of virus? |
- lentivirus
- usually cause a blastopenic disease |
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how many different subtypes of FIV are there?
vaccine cross protection? |
- 5
- poor cross protection |
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FIV pathogenesis
|
- bite
- acute infection 2-6 wks later - asymptomatic carrier for years -- viremia in macrophages and lymphocytes -- titer is low and sporadic - Immune deficiency syndrome (IDS) |
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characteristics of IDS associated with FIV
|
- fever
- abscesses - lymphadenitis - weight loss - upper and lower resp infections |
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50% of cats infected with FIV progress to what
|
absolute lymphopenia or neutropenia
|
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FIV diagnosis done how
|
- ELISA: screening
- IFA or western blot: confirmatory |
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can tests differentiate b/w natural and vaccinated FIV infections?
|
no
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testing for FIV test for Ag or Ab
|
Ab
|
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vaccination for FIV is what type of vaccine?
what strains? |
- killed vaccine
- subtypes A and D |
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FIV prognosis
|
- can live normal lives
|
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equine infectious anemia (EIA) is usually transmitted how
|
- mechanical transmission via insect vectors
- mechanical transmission by vets with needles, teeth floating equipment, tatooing, etc |
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EIA infects what cell types
when could we see this in the tissue? |
- infects monocytes and macrophages
- can see in macrophages in tissue 5-14 days |
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how does EIA cause anemia?
|
- EIA binds to RBCs
- acts as opsonin and macrophages phagocytize |
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3 types of EIA infections
|
- acute
- re occuring episodes (chronic) - asymptomatic persistent carriers |
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acute EIA infection
characteristics |
- often only pyrexia of short duration
- high EIA titer - re occuring episodes of fever, thrombocytopenia, depression |
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re occuring EIA infections
characteristics |
- reoccuring episodes of fever, anemia, thrombocytopenia, petechial hemorrhage
- febrile episodes correlate with peak viremia - Ab+Ag complexes (type 3 HS rxns) |
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acute EIA infections are generally not b/c of insect vectors but what other mode?
|
- contaminated needles
|
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what happens to the EIA virus during periods b/w febrile episodes?
|
- virus is genetically changing
|
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testing for EIA
|
coggins test for Abs
|
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EIA is a retrovirus that results in life long infections, so what is the big risk associated with EIA
so how is prevention accomplished? |
infecting naive horses
eliminating inapparent carriers |
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equine arteritis virus (EAV)
genome type |
ss RNA
non-enveloped |
|
|
EAV mode of infection
patho |
- inhaled
- 48hrs - infects bronchial macrophages - 24hrs - spreads to regional lymphatics - after 3 days virus is sytemic, targeting endothelial cells leading to vasculitis |
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CS of EAV
6 |
fever
depression anorexia respiratory dependent edema potential of abortion |
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clinical features of EAV
2 most consistent |
- fever
- leukopenia |
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EAV aborted fetuses have what feature
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partially autolyzed
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EAV acute phase vasculitis occurs for about how long
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1 month
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EAV in males is thought to be influenced by what
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testosterone
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whats the difference b/w males and females infected with EAV
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- females free of virus after day 28
- males remain infected after day 28 and shed virus |
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EAV susceptibility
breeds ages/status |
- thoroughbred and standardbred
- young, old, immunosuppressed |
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EAV diagnosis during the acute phase can be done how
EAV diagnosis during late acute phase and early convalescent period |
- nasopharyngeal swab or unclotted blood
- serology |
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prevention of EAV
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prevent infection in breeding population by preventing exposure
- TEST |
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MLV vaccine for EAV should only be used in what animals
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- only for seronegative animals
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Equine encephalomyelitis virus (EEE)
nickname genome genus |
sleeping sickness
ss RNA arbovirus |
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EEE is found where in the US
what other countries |
- east of the mississippi
- philippines, south american ,caribbean |
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EEE, WEE, VEE zoonitic status and concern
which is different zoonotic-wise? |
- EEE, WEE enzootic in birds, VEE zoonotic in rodents
- public health concern as it is zoonotic - 50-75% fatality in humans for EEE - 3-7% fatality in humans for WEE - 10% fatality in humans for VEE |
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EEE patho
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- vasculitis leading to inflammatory response
- PMNs and mononuclear cells penetrate BBB - virus cell interaction is lytic to cells in gray matter of cerebral cortex |
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most prominent CS of EEE
2 others |
fever
depression neurologic involvement |
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EEE neurologic signs present when?
what are the signs? |
- 2-4 days after infection
- resltessness early, then remain static, then paralysis |
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horses are dead end hosts for EEE and WEE, how is this differnent than VEE?
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- horses are amplifiers for VEE
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VEE patho
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- VEE viremia leading to vasculitis and centripetal spread up olfactory and trigeminal nerves
- PMN and lymphocyte mediated focal necrosis with perivascular cuffing - direct cytopathic effect |
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control of the EE viruses
treat suspect EE cases how? |
vaccination with killed vaccine
treat as if they were as transmissable as VEE and as virulent as EEE -- cant tell the difference until testing |
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differentials for EE viruses
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sarcocystis neurona (EPM)
rabies |
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west nile virus
amplifier host? dead end hosts? |
- birds are amplifier
- humans and horses are dead end hosts |
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WNV patho
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- WNV viremia
- vasculitis - encephalitis (meningitis) associated with the spinal cord |
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WNV CS
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- ataxia
- knuckling over - head tilt - partial paralysis |
