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RNA Viruses
encode their own RNA dependent RNA polymerase - Coggle…
RNA Viruses
- encode their own RNA dependent RNA polymerase
PicoRNAviridae
- replicates in cytoplasm
- non-enveloped
- icosahedral
Foot and Mouth Disease
- tends to affect animals with hooves (cows, pigs, buffalo, sheep, goats)
- in humans, causes flu like symptoms
- HIGHLY CONTAGIOUS (non-enveloped) -> stays on farm for a while
- infection occurs from ingestion/inhalation of virtually any body fluid, aerosols/airbone, direct or indirect contact (droplets, contaminated semen), vectors (vehicles, clothing, equipment)
- extremely high morbidity, rare to see mortality unless young animals
- clinical signs: oral vesicles, teat lesions, foot lesions, reduced production (due to inability to eat/chew food), secondary infections with other viruses/bacteria
- 7 distinct serotypes and many are not cross protective = makes vaccination difficult
Caliciviridae
- non-enveloped
- replicates in cytoplasm
Feline Calicivirus
- very similar clinical signs as feline herpesvirus
- clinical signs: oral and upper respiratory infection (conjunctivitis, rhinitis, increased salivation, tracheitis, pneumonia), lingual ulcers
- transmission through air droplets and transfer of contaminated objects (clothes that have contaminated discharge to another cat)
- treatment is dependent on what clinical signs they're exhibiting
- high morbidity in unvaccinated cats, low mortality
- infection induced immunity is not life long and does not protect against all strains
- vaccines available
Vesicular exanthema of swine
- similar clinical signs as foot and mouth disease (lesions on mouth and hooves)
Flaviviridae
- replicates in cytoplasm
- icosahedral symmetry
- enveloped
Bovine Viral Diarrhea Virus - remember it causes ulcer in mouth area and nasal/ocular discharge too
- BVD is a complex disease that is caused by many different strains that differ in antigenicity, cytopathogenicity, virulence
- susceptible species: cows, buffalo, camelids
- horizontal (direct contact via tears, saliva, contaminated food, water, litter) and vertical transmission (transplacental)
- 2 biotypes: non-cytopathic and cytopathic (mutant)
- non-cytopathic = does not cause cytopathic changes in culture, causes persistent infections, predominant version that infects animals
- cytopathic (mutant) = causes cytopathic changes in culture, is rare
- 2 distinct genotypes - Type 1 BVDV-1 and Type 2 BVDV 2
- BVDV 1 - classic BVD virus
- BVDV 2 - recently described, highly pathogenic
- each genotype has isolates of non-cytopathic and cytopathic
- BVDV disease pattern varies between and within herds based on herd immunity and presence/absence of persistently infected animals
- clinical manifestation varies based on age and pregnancy status
- cows of all ages are susceptible but those who are 3-8 months are the most susceptible
- pathogenesis: initial replication in nasal mucosa and tonsils -> regional lymph nodes -> lymphoid tissue and intestine -> erosive/ulcerative lesions in GI tract
- clinical signs: diarrhea, nasal/ocular discharge, ulcers in lips, muzzle and oral cavity, distal limb sores, poor doing calves (PI)
- some strains induce profound thrombocytopenia because the virus replicates in lymph nodes (hematopoietic cells) and this affects platelet development -> extensive hemorrhage in the entire GI tract
- outcome depends on age (immunologic maturity) of the fetus and strain of virus
- infection when mom is less than 40 days pregnant = embryonic death
- infection when mom is mid pregnancy = mom is immune and fetus becomes tolerant but does not make antibodies. fetus is persistently infected and immunotolerant
- infection late pregnancy = fetus develops neutralizing antibodies and eliminates the virus
- mucosal disease occurs when persistently infected calves (those who's mom was infected mid pregnancy) become infected with a cytopathic (mutated) strain... it can mutate in the calf from non-cytopathic to cytopathic or they can get a strain from another cow. mucosal disease has very severe, acute BVDV signs
- identifying and culling persistently infected animals is key to getting rid of infection -> they are constantly spreading it
- diagnosis: RT-PCR, immunohistochemistry don't do serology virus neutralization bc animals who have been vaccinated will show a positive result and persistently infected animals don't produce antibodies, so they will appear to be negative
- to distinguish acutely infected from persistently infected: do RT-PCR and then do it again 3 weeks later. those who are acutely infected will be negative by then and PI will still be positive
- VACCINES AVAILABLE
Togaviridae
- enveloped
- replicate in cytiplasm
- all 3 are arboviruses and zoonotic
Eastern Equine Encephalitis Virus (EEEV)
- pathogenesis: mosquito bite -> replication in regional lymph nodes -> viremia -> replication in more lymph nodes and muscle -> secondary viremia -> invasion into brain (cortex) -> neuronal necrosis
- clinical signs: neurological, fever, recumbency, paralysis, death
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Arteriviridae
- enveloped
- virus replication in macrophages and endothelial cells
Porcine Respiratory and Reproductive Syndrome (PRRS)
- most economically significant swine disease
- type 1 found in Europe and type 2 in North America. Type 2 = more virulent
- virus survives well in low temps (over winter)
- horizontal transmission through aerosol, semen and direct contact
- clinical signs: cyanosis of ears "blue ears", anorexia, fever, lethargy, depression, respiratory distress (pneumonia), SMEDI
- virus destroys alveolar macrophages bc it replicates in them
- virus is maintained in a population indefinitely by asymptomatic pigs who shed the virus for up to 3-5 months
- diagnosis: PCR, immunohistochemistry, virus neutralization
- secondary bacterial infections common: mycoplasma hyopneumonia, streptococcus suis, hemophilus parasuis
- control: intentional exposure before breeding, vaccines (questionably efficacy)
Coronaviridae
- enveloped with helical nucleocapsid
- high genetic variability
- presenting symptoms of coronaviruses = diarrhea, enteritis, respiratory infections, immune mediated disease (FIP)
Enteric Coronaviruses = TGEV (Transmissible Gastroenteritis Virus), PEDV (Porcine Epidemic Diarrhea Virus), PDCoV (Porcine Deltacoronavirus)
- CLINICALLY INDISTINGUISHABLE but antigenically different, so no cross protection
Clinical signs = profuse watery diarrhea, vomiting, rapid dehydration, emaciation
- transmission = fecal oral, aerosol, direct contact, fomites
- pathogenesis: virus enters body -> viral replication takes place in the villus epithelium of the small intestine -> intestinal columnar epithelial cells are destroyed by the virus = villar atrophy -> profuse diarrhea and malabsorption
- diagnosis: PCR and sequencing to differentiate the strains, serology for antibodies, histopathology to detect villar atrophy
- vaccines available
- treat with fluids, antibiotics for secondary infection
Feline Infectious Peritonitis (FIP)
- Starts with FeCF (feline coronavirus) and this invades intestinal epithelial cells -> diarrhea
- FIP occurs when virus mutates and then FIP replicates in macrophages
- How a cat gets FIP after FeCF = stressed or immunocompromised -> viral mutation of FeCF -> profuse replication in macrophages -> vascular injury (vasculitis) and leakage -> peritonitis
- 2 forms: WET FORM AND DRY FORM
- Wet form = thick, viscous and clear peritoneal exudate with extensive fibrin plaques and grey-white nodules (aggregates of macrophages and other inflammatory cells)
- Dry form = non-effusive but characteristic foci of pyogranuloma
- wet form clinical signs: abdominal distension, pleural effusion, dyspnea, pericardial effusion
- definitive diagnosis is done by IMMUNOHISTOCHEMISTRY where you can visualize the virus inside macrophages
- control is hard -> its easily spread and there are no vaccines. some antivirals have been proven to work
Reoviridae
- non enveloped
- many serotypes and strains of each virus species (genetic reassortment and mutation rate (genetic drift) is high
- replicates in cytoplasm
Rotavirus
- infects a ton of species (including humans)
- DIARRHEA -> often seen in intensively reared young farm animals
- Horizontal transmission (fecal oral) -> very stable in environment
- it's very infective bc proteolytic enzymes can cleave outer capsid and this increases infectivity
- 8 groups of rotaviruses that infect a bunch of species and clinical signs are all the same
- pathogenesis: fecal oral route -> attacks enterocytes which line the tips of the villi in the small intestine -> malabsorption -> diarrhea
- diagnosis: ELISA for viral antigen, PCR for viral nucleic acid, immunohistochemistry, histopathology to look for villar atrophy
- treatment: fluids and antibiotics
- vaccines available
Bluetongue Virus
- affects sheep, goats, cows and deer
- 24 different serotypes
- transmitted through insects (arthropod borne)
- mostly a tropical disease (Canada currently free of the disease)
- pathogenesis: virus infects endothelial cells (vasculature) and macrophages -> vascular injury occurs -> thrombosis, infarction of tissues, ulceration of tissues, cyanosis of lips, tongue and coronary band
- clinical signs: blue tongue/coronary band, fever, reluctance to move, edema in mouth/face, ulcers in mouth, abortion
- diagnosis: ELISA
Orthomyxoviridae
- RNA virus organized into segments
- enveloped
- RNA virus that replicates in nucleus
- classified into subtypes based on surface antigens
- Hemagglutinin (H) is responsible for attachment and fusion and Neuraminidase (N) is responsible for release of virus from host cell after replication
- H1N1 example -> new combinations occur due to antigenic drift and shift (drift = point mutations over time and shift = re-assortment of viral RNA)
- drift responsible for seasonal outbreaks and shift responsible for pandemics, epidemics
Avian Influenza Virus
- pathogenecity of the virus depends on hemagglutinin being cleaved post-translationally -> if it does get cleaved, then it can fuse with cell membrane of host cell, travel to nucleus and replicate
- low pathogenic avian influenza = produced in a non-infectious form and cleavage of HA occurs extracellularly)
- highly pathogenic avian influenza = produced in a non infectious form BUT cleavage of HA occurs in the infected cell by proteases
Highly Pathogenic Avian Influenza Virus
- transmitted fecal oral route
- migrating birds keep infection going between summer and winter
- clinical signs = depression, anorexia, drop in egg production, conjunctivitis, respiratory signs, swollen and cyanotic combs and neurological signs
- diagnosis: PCR -> if positive then test for H5 and H7 genes -> sequence to determine properties of cleavage site (looking for H5 and H7). could also do virus isolation and serology
- if detected, improve biosecurity, surveillance and depopulation
Paramyxoviridae
- non-segmented
- enveloped
- causes respiratory or systemic illness
Newcastle Disease Virus
- 9 different serotype, but 1 is most important
- clinical signs: CNS, respiratory, circulatory, GI, edema in head and neck
- zoonotic! in humans it causes conjunctivitis
- main contributor to how virulent the disease is depends on cleavability of the fusion protein
- similar to avian influenza, avirulent strains are cleaved by extracellular proteases only and virulent strains are cleaved by proteases within the host cell
Rinderpest aka Cattle plague
- clinical signs similar to foot and mouth disease: oral and foot lesions, hemorrhagic diarrhea, fever, depression, anorexia, nasal/ocular discharge, necrosis and erosion of oral mucosa, lymphadenopathy
- virus attaches to receptors on immune cells and epithelial cells
Canine distemper virus
- infects other species (ferrets, raccoons, coyotes, skunks etc)
- young dogs main host (2-6 months)
- virus shed through nasal/ocular secretions, urine and feces
- disease of the immune system -> infects leukocytes = immunosuppression and this makes them more susceptible to other diseases
- most infections are subclinical
- mortality rate between 30-80%
- clinical signs: CNS, respiratory, enteritis, hyperkeratosis of foot pads and nose and tooth enamel hypoplasia
4 different forms: peracute, acute, subacute neurological, late form
- peracute = rare, but causes sudden death
- acute = fever, leukopenia, anorexia, conjunctivitis, depression, respiratory and GI signs. CNS signs might also develop.
- subacute neurological form = this may follow acute or subacute form and causes encephalitis with convulsions and seizures. Most surviving dogs will have permanent CNS sequelea like involuntary leg movements
- late forms = slow progressive loss of neurological functions and hyperkeratosis of footpads and nose can be seen
- treatment: fluids and antibiotics
Rhabdoviridae
- helical
- bullet shaped virus
Vesicular Stomatitis
- affects horses, cows, swine, camelids, humans zoonotic
- resembles foot and mouth disease -> fever and vesicles/sores on feet and mouth. in humans causes flu like symptoms
- transmitted through direct contact with infected animals or vectors (sandflies, blackflies)
Rabies
- fatal disease of CNS
- all mammals can get rabies
LONG INCUBATION: 2 weeks - 6 months (it travels along axons and it can take awhile)
- 2 phases: early and advanced
- early = behavioural changes
- advanced = furious form and paralytic stage
- **clinical signs: neurological (nervousness, aggression, difficulty swallowing due to salivation, convulsions, paralysis, incoordination, coma, death)
- transmission through saliva (bite)
- maintained in wildlife reservoirs (called sylvatic rabies)
- affects the limbic system (part of brain that controls behaviour and movements)
- Diagnosis: none while animal is alive, but post mortem do RT-PCR and look for negri bodies (eosinophilic inclusion bodies found in the cytoplasm of nerve cells infected with rabies) in the neurons (view histology)