Exam 2 Flashcards
Indicate whether most enteric viruses are enveloped or not, and describe why this is important.
- Most are not enveloped
- Helps stability in environment
Be able to outline the common pathogenesis for enteric viral infections as it relates to the intestinal mucosa architecture, segment of gut affected and clinical signs.
- Villous blunting (atrophy) = malabsorption & osmotic D
- Cl- secretion = water drawn to lumen = secretory D
- Inflammation = vascular permeability = loose tight junctions = exudative D
List the common features of enteric viruses with regards to transmission, incubation period, age of most susceptibility, host specificity.
- Fecal-oral transmission
- Short incubation period
- Severe disease in young animals
- Most are host species specific
- Most cause localized, transient infections
Describe which factors influence the severity of disease for enteric viral infections
- Dose of virus
- Host nutrition / health
- Underlying / concurrent infections
- Maternal Ab or vaccination
- Genetics of virus & host
Explain why it is important to provide non-oral fluid replacement in cases of rotavirus/coronavirus enteritis.
These viruses cause villus atrophy/blunting which results in decreased ability to absorb water and nutrients. If you give oral fluids, those fluids will not be absorbed in the intestine or at all.
Rotavirus: who does is affect? diagnosis? Pathogenesis? Treatment? Prevention?
- Species specific for cows, pigs, goats, horses, dogs, & humans
- non-enveloped & stable
- Results in acute white/yellow mucoid D (no blood) in baby animals (scours)
- Lasts 8-10 days
- Diagnosis: PCR/ELISA
- Pathogenesis: infects mature epithelial cells at villous tips in small intestine -> enterocyte damage = malabsorptive D & NSP4 enterotoxin -> secrete Cl- = secretory D
- Treatment: self-limiting, provide fluids & limit food
- Prevention: Vx dam prior to birthing, manage quality of housing, stress, nutrition
Coronavirus: enveloped or not? Pathogenesis?
- Enveloped but relatively stable
- Pathogenesis: infects mature epithelial cells at villous tips in small intestine -> enterocyte damage = malabsorptive D & enterotoxin -> secrete Cl- = secretory D
- Can also go to colon
2 Coronaviruses in Pigs
Transmissible Gastroenteritis (TGE) in pigs
- Highly contagious, localized enteric infection
- Incubation period 18-72 hrs - Naïve herds (never exposed to virus)
- All ages affected, mortality in young
- profuse diarrhea and some vomiting
- starts when maternal Abs waning
- Pathogenesis: same as any coronavirus
Porcine epidemic diarrhea virus (PED)
- Pathogenesis: same as any coronavirus
- New to US
Bovine Coronavirus 3 clinical presentations
- Calf diarrhea (similar to endemic TGE)
- Winter dysentery of adult dairy cattle: Sporadic acute enteric disease, diarrhea with blood, low mortality
- Respiratory disease
Equine Coronavirus; who does it affect? shedding? clinical signs? diagnostics? pathogenesis? treatment?
- usually affects adult horses
- Incubation period 48-72 hrs with peak viral shedding 3-4 days AFTER clinical signs
- Shedding is usually for 3-25 days, but up to 99 days
- Clinical signs: anorexia, lethargy, fever, mild colic, maybe Ds, neuro symptoms
- Diagnostics: CBC/Chem shows leukopenia & hypoalbuminemia
- Pathogenesis: Overgrowth of urease-producing bacteria or increase in ammonia absorption through disrupted small intestinal mucosa = hyperammonemia & associated encephalopathy
- Death unusual
- Treatment: fluid therapy and NSAIDS
Feline Enteric Corona Virus
- Common
- Subclinical or mild D
- Can mutate to feline infectious peritonitis (FIP)
Feline infectious Peritonitis (FIP) clinical signs, prevention, wet form, dry form
- Mutation from FECV or FIPV
- Usually < 1yo from multi-cat household
Clinical signs:
- fever, weight loss, anorexia
Prevention
- FIP vx is not effective
Effusive or wet form of FIP
- 75% of cases
- Inflammation of the serosal surfaces of the abdomen and/or thorax
- Accumulation of proteinaceous fluid in the body cavities
- Often leads to apparent abdominal distention, respiratory distress (due to pleural effusion)
Non effusive or dry FIP
- Pyogranulomatous inflammation following vessels of parenchymal organs
- kidneys, lymph nodes, liver, pancreas, CNS, uveal tract of the eye
- Effusion absent or minimal
Describe the importance in an individual cat’s immune response (humeral and CMI) in the development of disease with FIP infection.
- FIPV infection -> strong CMI (cell mediated) -> no disease
- FIPV infection -> strong Ab & weak CMI -> wet FIP
- FIPV infection -> weak Ab & moderate CMI -> dry FIP
Indicate the pathological cause for body cavity effusion in feline infectious peritonitis virus infection.
Kidneys and other organs are affected by pyogranulomatous vasculitis -> increases intravascular pressure -> leakage of high protein fluid
Describe the utilities of serology and PCR as diagnostic tests for feline infectious peritonitis virus infection and indicate the gold-standard for FIP diagnosis. Explain why it is difficult to diagnose FIP in a living patient, and what findings support a diagnosis.
- no single antemortem test available to diagnose FIP so combine serolgy & symptoms to presume diagnosis
definitive diagnosis:
- combine biopsy of grnauloma & immunohistochemistry
Parvovirus Pathogenesis & Clinical Findings
Pathogenesis
- Oronasal exposure -> entry & replication in GI lymph tissue -> moves to systemic lymph tissue -> systemic viremia -> Replication and necrosis of intestinal crypt epithelium, bone marrow, lymphoid tissue
Clinical Findings
- Fever, bloody osmotic D, & loss of immune cells
Explain how incorrect timing/frequency of parvovirus vaccination can lead to a lack of protection.
- If given too early, maternal Ab block pup from making own Abs
- If given too late, no maternal Ab and no own Ab = high exposure
- Should vaccinate multiple times while young to hopefully land in perfect window
Explain how mitotically active cells are important in the viral lifecycle and clinical pathogenesis of parvoviral enteritis
- Small DNA virus that does not carry DNA polymerase genes
- Uses cellular DNA polymerase
- Needs mitotically active cells to have plenty polymerase
- Crypt epithelium, lymph tissue, cerebellum (cat), heart (dog)
Parvovirus Treatment, Diagnosis, Prevention
Treatment
- Aggressive supportive care to counteract diarrhea & immunosuppression
- Antibiotics for secondary bacterial infections
Diagnosis
- Rapid antigen ELISA detects virus in feces (retest if negative because intermittent shedding)
- If fatal histologic lesions and intranuclear inclusions are diagnostic
Prevention
- Inactivated and attenuated (modified live) vaccines are available and effective
- Fecal shedding from vaccinated (MLVs) dogs can immunize other dogs
- DO NOT vaccinate pregnant or very young animals with MLV - potential for myocardial infections and cerebellar disease
Parvoviral Myocardial Disease in Dogs
- Was common when disease first emerged
- pups born w/out maternal Ab and susceptible to infection at a very early age
- Pups infected while myocardium still developing and susceptible to infection = acute heart failure and sudden death
- now pups usually not susceptible at young age or infected when older and myocardium no longer in active development
Parvoviral Cerebellar Disease in Cats
- Infection during late gestation/early neonatal period
- Virus has tropism for cells in the cerebellum
- cerebellar hypoplasia most commonly
- Ataxia, incoordination, tremors, broad-based stance with hypermetric movements
Canine Adenovirus
- Non-enveloped, stable DNA virus
- Seldom seen anymore due to highly effective vaccination
- <1yrs or unvaccinated dogs
- Clinically-asymptomatic to fatal
- Highly contagious virus that can cause clinical disease in bears, fox, coyotes, wolves, raccoons, skunk, mink and ferrets
- Makes intranuclear occluisons in hepatocytes & endothelial cells -> fatal hepatitis, hepatic necrosis and hemorrhagic disease
- Use canine adenovirus 2 to avoid “blue eye”
Identify the major source of parvovirus for susceptible animals and major ways to control transmission.
Transiently infected animals & environment (survives well outside of host)
2 clinical outcomes of alpha herpesvirus & transmission
Clinical outcomes
i. Active replication
ii. Latency/reactivation
Transmission
i. Close contact, Short-distance aerosol
ii. Between moist epithelial surfaces
iii. Closely confined populations
Explain the differences in pathogenesis and associated clinical signs between EHV-1 and EHV-4. Explain how EHV-1 can causes systemic disease, how neurologic disease can develop in EHV-1, and which cells are infected
EHV – 1
i. Starts in resp. epithelium -> infection of lymphocytes -> affects other organs systems thru infection of endothelium
EHV – 4
i. Localized upper respiratory infection
ii. Regional lymphadenopathy, nasal discharge, coughing
iii. Subclinical or mild to moderate,
iv. self-limiting = full recovery
v. low resp. infection rare
Explain how herpesviruses are maintained in the population.
a. Life-long infection (carriers)
b. Viral replication and shedding occurs w/ or w/out clinical Dz
Equine Herpes Virus Persistence
a. Both EHV-1 and 4 target neuronal cells in sensory ganglia innervating nasopharyngeal mucosa
b. EHV-1 is lymphotrophic (latency in T cells)
c. Reactivation with lytic infection occurs in adult horses with or without clinical signs
d. seen with “stress” – e.g. pregnancy, shipping, racing, training, etc.
EHV Systemic Dz
a. Spread outside of resp. associated w/ lymphocyte tropism
b. Virus accesses lymphocytes -> Replication in regional lymph nodes -> Cell-associated viremia -> Virus disseminates to endothelium in target tissues
-> causes abortion in uterus & neuro dz in CNS
Abortion due to EHV-1
a. Frequently occurs without respiratory or CNS disease
b. Uterine vasculitis necessary and sufficient for abortion
c. Fetus can be virus (-) but usually also crosses the placenta and infects the fetus, causing disseminated disease in the fetus
Equine Herpes Myeloencephalitis: clinical signs, key lesions, diagnosis
Clinical signs:
i. mild ataxia to paresis
ii. incoordination, gait abnormalities
iii. inability to rise from the sitting position
iv. may have paralysis and recumbency
Key lesions
i. vasculitis and ischemia
ii. neurons are not infected
Diagnosis
i. History and clinical signs very important!
ii. EHV-1 Serology (acute and convalescent)
iii. EHV-1 PCR
(Blood PBMCs or nasal swab)
Vaccine for Equine Herpes
i. Widely used
ii. EHV-1 and EHV-4 are cross-protective
iii. reduce severity of respiratory and abortive disease and/or prevent outbreaks of disease
iv. Frequent revaccination is needed
v. Maternal antibodies interfere with protection of young horses
vi. Vaccines not protective against neurologic disease
Bovine Alpha herpesvirus
Infectious Bovine Rhinotracheitis (IBR)
BHV-1
- major cause of resp dz and abortion
- does not infect endothelium
- abortion due to actual infection of the fetus in all cases
BHV-5
i. CNS disease affects brain, infects neurons
Feline alpha herpes virus 1; basics, how long is shedding, symptoms
o most important pathogen of upper respiratory disease in cats
o localized in upper respiratory tract
o Secondary bacterial infections
o Active shedding usually lags behind stressful event – can transmit virus for 3 weeks post event
o Viremia – very rare; occurs in hypothermic kittens
Symptoms
• conjunctivitis, ulcerative keratitis/dermatitis/ stomatitis, rhinitis, sometime abortion
Feline Calcivirus; basics, symptoms, hypervirulent strain
o Upper respiratory
o Small, non-enveloped, RNA virus
o Shed in ocular, nasal, oral secretions (think Calici if oral issues)
o Common persistent infections
o Virus persists in tonsils and other oropharyngeal tissues
Symptoms
• fever, sneezing, coughing, nasal and ocular discharge
• may have disease in lungs or joints
Hypervirulent strain
• infects endothelial cells = hemorrhagic disease
Canine Alphaherpesvirus
o In utero infection = abortion/fetal loss
o Neonatal infection = fatal multisystemic hemorrhage and necrosis
o Adult infection = typically not pathogenic but can cause mild respiratory disease (rhinotracheitis)
Macacine Herpesvirus
o Macaques
o Oral and gingival ulcers
o High seroprevalence in captive and wild cohorts
Fatal cross-species transmission
• humans can get fatal encephalitis
Betaherpes virus Family Basics
o Slow replication and “cytomegaly”
o Latency - established primarily in secretory epithelium
o Ubiquitous - frequently encountered when searching for causative agents
o generally NOT true cause of disease
o Disease, if any, is generally limited to immunocompromised hosts
o Example of disease causing: Elephantid herpesvirus 1
Elephantid herpesvirus 1
- Betaherpes virus
- Targets endothelial cells -> lethal hemorrhagic disease
- Seen in young Asian elephants
- Responds to antiviral therapy if administered rapidly
Gammaherpes virus Family basics
o Lymphotropic herpesviruses
o Often non-productive, non-lytic infections
o express various viral genes that activate cells, interfere with cell cycle, modulate the host immune response
o most are non-pathogenic in immunocompetent natural hosts
o if disease = lymphoid neoplasia and/or lymphoproliferative disease
o Example of disease caused: Malignant Catarrhal fever
Malignant Catarrhal fever: basics, clinical signs
- Gammaherpesvirus
- Infection of non-adapted host
- Caused in cows by Ovine Herpesvirus 2
- Fatal systemic dz
- Cannot pass from cow to cow (dead end hosts)
Clinical signs
• Epithelial erosion of upper respiratory and intestinal tracts,
eyes, lymph nodes
Malignant Catarrhal fever: pathogenesis
Pathogenesis
• OHV-2 infects sheep respiratory tract ->
• viremia ->
• infection of lymphocytes ->
• difficult to detect virus replication ->
• no clinical disease ->
• passed to cattle thru nasal secretions ->
• Proliferation of perivascular lymphocytes ->
• Necrotizing vasculitis systemically ->
• Ischemic necrosis
• Mucosal erosion & ulceration
Malignant Catarrhal fever: Diagnosis, Transmission, & Control
Diagnosis
• Clinical signs, exposure to carriers, vasculitis on histopathology, PCR detection of virus (lymphoid tissues)
• Serology - limited value since some animals may be subclinically infected
• Important differentials includes exotic diseases
Transmission
• Close Distance
• Cool moist environment
• Sheep shed OVH-2 most intensely at 6-8 months old
Control
• There is no vaccine available
• Management practices - separate sheep from cattle, bison, deer
