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year 2 Semester 1
what is the result of enteric viruses
diarrhea
what 2 enteric viruses cause systemic infection
parvovirus
FIP (feline infectious peritonitis virus)
enteric viruses
enveoloped or naked
transmission type
infections
incubation period
when does it cause severe disease
enveloped (except coronavirus)
feccal- oral
localized transient (mostly small intestine)
short
young animals, intestinal immunity not fully formed
2 sources of transmission of enteric viruses
transient infected animals
environment
factors of enteric disease severity
dose
host health/nutrition/stress
underlying/ concurrent infections
maternal AB/ vaccination
genetics of virus and of host
what anatomical parts do enteric viruses more often infect
small intestine
crypt: germinal differentiating epithelial cells responsible for secretion of electrolytes
villus: differentiated cells used for digestion and absorption
what does diarrhea lead to
dehydration and acidosis
what 3 mechanisms do enteric viruses use to cause diarrhea
villous blunting: decrease absorption = osmotic diarrhea
inflammation: vasodialation causing leaky vessesl
viral enterotoxin: rotavirus NSP4
Effects of Rotavirus NSP4
enterotoxin: disrupt Ca homeostasis, increase Ca intracellularly, activate Cl channels, secrete CL into lumen and Na and H2O follow: secretory diarrhea
cellular distribution: impair ting junctions = increased permeability
signalling effects: stimulate nervous system to increase motility and fluid excretion
distribution in intestine:
rotavirus
coronavirus
small intestine
small intestine and maybe some colon (more severe)
note: can be segmented or uneven distribution
rotavirus
enveloped or non enveloped
genome formation
common host- when is it most severe
incubation
mortality/ morbidity
distribution
non enveloped
segmented ds RNA
young, host specific (severe in neonates <2 weeks)
short (days)
high morbidity, low mortality
localized
likely virus: acute, watery, yellow diarrhea, non bloody
rotavirus
what is the main cause of death with rotavirus:
dehydration
Lab diagnostics for rotavirus
PCR
Ag detection assays
serology (limited)
too young to produce Ab
Maternal Ab change results
3 main mechanisms of diarrhea from rotaviruses
villous atrophy = malabsorptive diarrhea → infecting enterocytes on vilious tips
NSP4 = secretory diarrhea → ca homeostasis, Cl secretion
roatvirus treatment
self limiting
supportive treatment: fluids, electrolytes
how to avoid rotavirus
you cannot, it is ubiquitious
preventing rotavirus
decrease exposure
adequate colostrum
rotavirus vaccines
inactivated: for dam to protect calf
MLV: IM to dam for Ab in colostrum or oral to newborn calf for mucosal immunity
differnece in vaccine route for rotavirus
IM
oral
humoral immunity, Ag present in systemic lymphoid tissue. Circulating IgG
Ag present in GALT, increase IgA locally
coronaviruses
common type of disease
genome
enveloped or naked
enteric mostly, some systemic or respiratory
+ ssRNA
enveloped
pathogenesis of coronaviruses 3 characteristics
infect mature vilous enterocytes → atrophy with marked decrease in absorptive capacity
infect small and large intestine
extensive damage in neonates
3 major clinical syndromes of bovine coronaviruses
(neonatal) dalf dehydration
winter dysentery (adult diarrhea)
dairy cattle, blood diarrhea, high morbidity, low mortality, decreased production
bovine respiratory disease (calves and feedlot cattle)
lower and upper respiratory infection
part of bovine respiratory disease complex
control of coronavirus
vaccinate:
MLV or inactivated to dam with second dose <30 days before calving
oral MLV to calf (before colostrum)
feline enteric coronavirus
common?
often presentation
typical life cycle
mutations
cells it infects
shedding
prognosis
lesion
common
subclinical, self limiting diarrhea in kittens
repeated cycles of infection and re infection - maintained in cat groups
persistance increases risk for FIP mutation
mature enterocytes
high fecal shedding
excellent
villous atrophy
What is FIP and what is the pathogenesis
systemic disease mutated from FeCov
allow infection of macrophages and monocytes
infected macrophages disseminate virus = systemic inflammation
how is FIP transmitted between cats
it is not, FeCov can be transmitted
FIP
common patient
predisposition?
notable clinical signs
2 types
young < 2, male often with many cats
genetic
unknown origin fever, pear shaped body
effusive/ wet, non effusive/ dry
wet FIP
common?
pathogenesis
content of effusion
common
vasculitis and increased permiability from inflammation from Macs cause leaking into the body cavity
peritoneal = distension
pleural: respiratory distress
high protein, low cellularity, yellow, viscous
what tests should be done on a young cat with a fever
FIV/FeLV
what test should be done on a young cat with uveitis
FECV serology
RT-PCR (blood)
dry FIP
key characteristic appearance
common locations
clinical signs
pyogranulomatous inflammation around blood vessels and tissues (white spots)
kidney, liver, LN, CNS, eyes (small blood vessels)
depend on organs, non specific
how to diagnose FIP
presumptive: signs, history, blood work, imagins, effusion
confirmatory: FCoV does not mean FIP
serology: test for Ab against FeCoV, not distinguish from FIP
RT-PCR: detect FeCoV RNA, does not mean FIP
Histopath (difinitive diagnosis) - postmortum
best locations for RT-PCR for FIP
effusion (best), if positive with this, likely FIP
FNA affected tissue
CSF: for neurologic signs
Aq humor (ocular dz)
whole blood (less useful)
FIP vaccination
nor recommended
low protection for FIP (could reduce severity)
modified live → could revert
many cats = already have FeCoV exposure
FIP prognosis
grave
parvo
enveloped or naked
genome
requirement
2 types
naked
ssDNA
rapidly dividing cells - replicate in nucleus
CPV 1 (minute virus), CPV 2 (canine parvovirus)
CPV 1: minute virus of canines - describe
origional, cause muld to subclinical signs
Puppies: myocarditis
adults: reprodtive loss
CPV 2: canine parvovirus
origin
effects
mutant of feline panleuk virus
severe enteritis in puppies
CPV 2 impact on young dogs and cats - what cells
intestinal crypt cells: villous atrophy → hemorrhage
bone marrow prevursor cells: leukopenia / immune supression
proliferating lymphoid cells: lymphoid depletion = immunosupression
what does CPV 2 do uniquely in young puppies
attach developing cardiomyocytes= myocarditis
what doe CPV 2 attack uniquely in neonate/fetal kittens
developing CB cells = CB hypoplasia
CPV 2 lab findings
luekopenia
anemia
hypoprotenemia
hypoglycemia
coagulation abnormalities
most common CPV 2 patient
puppy 6 wks - 6 months (when maternal Ab wanes)
source of CPV 2
environment, transient infected animals
CPV 2 vaccination
inactivated and MLV = effective (in DAPP)
can still have fecal shedding from vaccinated dogs = immunize other dogs
not vaccinate puppies or pregnant
dosing for CPV 2 vaccine
3 doses 6-16 weeks, 2-4 weeks apart because you do not know the level of the maternal Ab
what is the window of susceptability
maternal AB wane to unprotective but before the vaccine induced immunity is fully developed
= greatest risk of infection C
CPV 2 treatment
agressive supportive care
antimicrobial (secondary bacterial infection)
blood/plasma transfusion
diagnosis of CPV 2
ELISA SNAp - detect Ag in feces
PCR = sensitive, feces
IHC (post mortem)
what does it mean if CPV IFA is positive for IgM and negative for IgG
acute, primary infection, unvaccinated
why is there hypoprotenemia and hypoglycemia with CPV
intestinal crypt necrosis
feline panleukopenia
common patient
common lesion
main lab characteristic
neonatal/utero infection
young, unvaccinated, when maternal Ab decreases
intestinal crypt destruction
panleukopenia, damaged bone marrow and lymphoid tissue
CB disease (target rapid dividing cells of CB = hypoplasia)
how to diagnose feline panleuk
clical suspicion
lab tests
CBC : severe paleukopenia
Ag detection in SNAP of feces
PCR (Sen and SP)
serology: FPLV IFA- detect Ab
Histopath: crypt necrosis, villous collapse, lymphoid depletion
Canine Adenovirus (CAV 1)
naked or enveloped
genome
location of replication
disease name
common?
naked
ds DNA
nucleus (intranuclear inclusions)
canine infectious hepatitis
uncommon (in vaccinated)
canine adenovirus pathogenesis
systemic infection with viremia
and
infect hepatocytes and endothelial cells → wide spread activation of clotting = microthrombi and organ damage = DIC
canine adenovirus major cell targets
hepatocytes
vascular endothelial cells
renal tubular epithelium
common unique symptom of canine adenovirus
“blue eye” / corneal edema
type 3 hypersensitivity = immune complex disposition
can occur in recovery
transient, self limiting
inflammatory
CAV 1 vaccination
use CAV 2 vaccine (DAPP)
CAV 1 vaccine can cause blue eye and excretions in urine
family of herpes viruses
orthohperesviridae
herpesvirus
naked or enveloped
transmission
genome
replication location
durration of infection
enveloped
close contact
ds DNA
nucleus
for life, latency
for hepresviruses, does replication require clinical disease
no
hepresvirus treatment
antivirals
alphaherpesvirinae
replication
site of replication
site of latency
disease
primary cite of infection
fast with necrosis
epithelial cells
PNS neurones
causes Dz and cell lysis
epithelium
3 main organ systems target by alphahrpesvirinae
respiratory (usualy location of start)
reproduction
CNS
Equine alphaherpes virus: 2 types
EHV 1: respiratory disease, abortion, perinatal mortality, CNS
respiratory epithelium, sensory neurons (PNS), lymphocytes, endothelium
EHV 4: respiratory disease
respiratory epithelium, sensory neurons
differ in cell tropism
describe EHV 1 and 4 latency
in neurons of sensory ganglia innervating nasopharyngeal mucosa
reactivate in adult horse ± clinical signs
what is the most important agent of acute respiratory disease in horses
EHV 4
EHV respiratory infections
localised upper respiratory infection
non specific signs, nasal discharge, regional lymphadenopathy, subclinical and self limiting
lower respiratory infection: rare
in immune deficient individuals
extrarespiratory pathogeneisis with EHV
endothelial cell infection leading to vasculitis and ischemia
EHV abortion
what type
how
what can it lead to
EHV 1 mostly
-
uterine vasculitis (enough alone)
can cross placenta to infect fetus (not always)- causing disseminated disease in fetus
abortion storms- whole group aborts, less now with vaccination and management
what is seen in EHV necropsy of fetus
could be uninfected or
disseminated disease and wide spread petechial hemorrhage
EHV -1 Perinatal mortalitiy
common?
describe
cause
uncommon
foal born at term but dead or weak and die soon
due to sever lower respiratory infection and disseminated systemic infection
EHV 1 neurologic disease
name
key lesions
common signs
equine herpes myeloencephalitis
vasculitis and ischemia
inability to rise from sitting, paralysis, recumbency
EHV 1 hypervirulent strains - describe
cause outbreaks in high morbidity and mortality
increased replication rate
unknown why
EHV 1 differentials
respiratory disease (cannot clinically distinguish)
neurologic disease: rabies, west nile, etc
EHV testing
PCR for viral DNS from nasal secretions early one and blood with viremia
serology: compounded to see if infection or vaccine
histopathology: aborptions
significance in controling EHV
it is reportable in WA
there are vaccines
EHV vaccination
common
cross protect 1 and 4
not prevent infection or protect from neuro disease
prevent disease outbreaks
short protection: need revaccination
Bovine alphaherpes virus
name
major cause of what
difference from EHV -1
aborptions
CNS disease
bovine herpesvirus 1 (BHV -1)
bovine respiratory co plex and secondary bacterial pneumonia
not infect endothelium and rare meningoencephalitis
always due to fetal infection
BHV 5 infects neurons
components )viruses and bacteria) of bovine respiratory complex
viruses:
BHV-1,
bovine parainfluenza,
bovine respiratory synscitial virus
bacteria:
mannhemia haemolytica,
histophilus sommi,
pasteurella multocida
Feline Alphaherpisvirus
name
type of pathogen
common clinical signs
viremia
common sign in kittens
feline herpesvirus 1
upper respiraotry (part of feline respiratory disease complex)
conjuncitivitis, ulceration, abortions
rare
hypothermia
feline alphaherpesvirus vaccination
FVRCP
modified life/ inactivated
SQ or internasal
diagnosis of feline herpesvirus 1
PCR of nasal swab
treatment for feline herpesvirus 1
supportive care
antivirals
main differential for feline herpesvirus 1
feline calicivirus
feline calicivirus
naked or enveloped
genome
key lesion
location of persistence
localization
unique locations
naked
RNA
stomatitis with ulcers
tonsils and oropharynx
upper respiratory tract
some strains can cause disease in joints and lungs
hypervirulent strains of feline calicivirus
infect endothelial cells = hemorrhage
can be in fully vaccinated animals
canine alphaherpesvirus - young dog infection
neonatal: fata multisystematic hemorrhage and necrosis
cause hypothermia
in utero = abortion
turkey egg kidney is common necropsy find
caine alphaherpesvirus - in adult dogs
apathogenic or mild rhinotrachitis
not have much disease
non human primate alphaherpesvirus
name
species
common lesion
concerns
seroprevelence
macacine herpesvirus 1 (B virus)
macaques
oral and gingival ulcers
fatal zoonosis: encephalitis in people
high in captive and wild populations
do herpesviruses jump hosts?
not often, but when they do they are lethal
betaherpesvirinae
replication
location of latency
disease
location of exposure
slow, less damage
secretory epithelium (often salivary gland)
only in immmunecompromised hosts, no cell lysis
ubiquitous - but not likely the main cause od disease
elephantid herpesvirus 1
name
cell tropism
results
patient
treatment
type of virus
endotheliotrophic elephant herpesvirus
endothelial cells
highly fatal from hemorrhage disease
young asian elephants
antiviral therapy, rapid intervention
betaherpesvirus
non human primate betaherpesvirus
name
patient
disease
diagnose
Rheus Cytomegalovirus
endemic to macaques
in immunosupressed and recurrent (asymptomatic in immunocompetent)
not testable
gamaherpesvirinae
replication
site of latency
disease
results
location in the environment
slow
lymphocytes
no cell lysis, disease in non adapted hosts
lymphoid dysregulation, proliferation and neoplasia
ubiquitous in mammals though mostly non pathogenic
Equine herpesvirus 5
type of herpesvirus
appearance
other name
pathogenesis
cellular appearance
gamma
progressive, nodular fibrosis, with enlarged LN
equine multinodular pulmonary fibrosis
unknown
see inclusions
malignant catarrhal fever
causitive agent
2 types
who are they dangerous to
type of herpesvirus
genus macavirus
-
ovine herpesvirus 2: common in sheep, ubiquitous in domestic sheep
alcelaphine herpesvirus 1, wildebeasts
cattle
gamma
what virus do all sheep have
ovine herpesvirus 2 (gamma herpesvirus)
Malignant catarrhal Fever - describe transmission from natural host
no disease in natural host
replication in nasopharynx
shed in nasal secretions
close contract trasnmission
sheep shed at 6-9 months old most