Block 7 Flashcards
what is ANELLOVIRIDAE
GENUS: GYROVIRUS?
+/-?
A negative virus
characterisics and example of
ANELLOVIRIDAE
GENUS: GYROVIRUS
- CIRCULAR, SINGLE-STRANDED NEGATIVE
SENSE DNA - CHICKEN INFECTIOUS ANEMIA VIRUS HAS 12 TRUMPET-LIKE STRUCTURES
CHICKEN INFECTIOUS ANEMIA
host?
transmittion?
**HOST: **YOUNG CHICKENS (2-4 WEEKS). OLDER CHICKENS ARE MORE RESISTANT
* TRANSMISSION:
* VIA FECES AND FEATHER DANDER
* HORIZONTAL TRANSMISSION VIA
INHALATION/ORAL EXPOSURE
* VERTICALLY VIA EGG
CHICKEN INFECTIOUS ANEMIA
what is the environmental stability?
Pathogenisis?
- ENVIRONMENTALLY **STABLE **AND CAN REMAIN INCONTAMINATED FOMITES FOR A LONG PERIOD OF TIME
* PATHOGENESIS: -
REPLICATES VIA HEMOCYTOBLASTS IN THE BONE
MARROW, T-CELLS OF THE THYMUS AND DIVIDING CD4 AND CD8 CELLS IN THE SPLEEN - INDUCES APOPTOSIS VIA THE APOPTIN PROTEIN
- IMMUNOSUPPRESSION AND APLASTIC ANEMIA
- VULNERABLE TO SECONDARY BACTERIAL AND
FUNGAL INFECTIONS - REPLICATION MAY BE REGULATED BY ESTROGEN
CHICKEN
INFECTIOUS
ANEMIA
- CLINICAL SIGNS AND LESIONS?
- ANORECTIC, LETHARGIC,
DEPRESSED, WEIGHT LOSS,
PALE - THIN BLOOD WITH SLOW
CLOTTING - PCV IS LOW
- SUBQ AND SKELETAL
HEMORRHAGES (PALE
MUSCLES)
CHICKEN INFECTIOUS ANEMIA
- DIAGNOSIS? (7)
- CLINICAL SIGNS
- BLOODWORK
- NECROPSY
- HISTOPATHOLOGY
- SEROLOGY: ELISA, NEUTRALIZATION TEST,
FAT TEST - VIRUS ISOLATION
- PCR/RT-PCR
CHICKEN INFECTIOUS ANEMIA
VACCINATION?
who?
how?
VACCINATE THE HENS TO PROTECT THE
OFFSPRING THROUGH MATERNALLY
DERIVED ANTIBODIES
FAMILY: HERPESVIRIDAE
MORPHOLOGY?
MORPHOLOGY: ENVELOPES, SPHERICAL TO PLEOMORPHIC.
* THE CAPSID IS SURROUNDED BY A LAYER OF GLOBULAR MATERIAL CALLED THE TEGUMENT.
* VIRAL GENOME IS A DOUBLE STRANDED DNA GENOME
FAMILY: HERPESVIRIDAE
REPLICATION?
where?
how?
- DNA REPLICATION AND ENCAPSULATION OCCURS IN THE NUCLEUS.
- THE VIRAL ENVELOPE IS ACQUIRED BY BUDDING THROUGH THE INNER LAYER OF THE NUCLEAR ENVELOPE.
- MATURE VIRIONS ACCUMULATE WITHIN VACUOLES IN THE CYTOPLASM AND ARE RELEASED VIA EXOCYTOSIS OR CYTOLYSIS
FAMILY: HERPESVIRIDAE
GENERAL CHARACTERISTICS:
location for survival?
environmental conditions?
who serves as a reservoir?
Oncogenic?
what is a type A cowdry?
what does it form?
GENERAL CHARACTERISTICS:
* UNABLE **TO SURVIVE WELL OUTSIDE THE HOST
* NEED MOIST AND COOL ENVIRONMENTAL
CONDITIONS TO PROMOTE SURVIVAL.
** LATENTLY INFECTED ANIMALS **SERVE AS RESERVOIR FOR
TRANSMISSION.
* REACTIVATION IS USUALLY DUE TO STRESS AS A RESULT
OF INTERCURRENT INFECTIONS, SHIPPING, COLD, CROWDING, OR GLUCOCORTICOID DRUGS
** SOME **MAY BE ONCOGENETIC
* HAVE AN EOSINOPHILIC NUCLEAR INCLUSION BODIES
CALLED TYPE A COWDRY BODIES.
* FORMS A SYNCYTIUM
HERPESVIRIDAE
SUBFAMILY:
ALPHAHERPESVIRINAE
BOVINE HERPESVIRUS 1
Vaccine + Abortion?
Vaccine Abortion
HERPESVIRIDAE
SUBFAMILY:
ALPHAHERPESVIRINAE
BOVINE HERPESVIRUS 2
Vaccine + Abortion?
?
SUBFAMILY:
ALPHAHERPESVIRINAE
EQUINE HERPESVIRUS 1
vaccine abortion
SUBFAMILY:
ALPHAHERPESVIRINAE
what are the 8/9?
- BOVINE HERPESVIRUS 1
- BOVINE HERPESVIRUS 2
- EQUINE HERPESVIRUS 1
- EQUINE HERPESVIRUS 4
- PORCINE HERPESVIRUS 1
- FELINE HERPESVIRUS 1
- CANINE HERPESVIRUS 1
- GALLID HERPES VIRUS 1 AND 2
SUBFAMILY:
ALPHAHERPESVIRINAE
EQUINE HERPESVIRUS 4
vaccine
SUBFAMILY:
ALPHAHERPESVIRINAE
PORCINE HERPESVIRUS 1
vaccine (for prgs) Abortion
SUBFAMILY:
ALPHAHERPESVIRINAE
FELINE HERPESVIRUS 1
vaccine
abortion
SUBFAMILY:
ALPHAHERPESVIRINAE
CANINE HERPESVIRUS 1
abortion
SUBFAMILY:
ALPHAHERPESVIRINAE
GALLID HERPES VIRUS 1 AND 2
vaccine
SUBFAMILY BETAHERPESVIRINAE
what is it?
PORCINE HERPESVIRUS 2
abortion
inclusion body rhinitis
SUBFAMILY: GAMMAHERPESVIRINAE
what is it?
Rep in lymphoid cells
MALIGNANT CATARRHAL FEVER
AVH-1(wildabeast MCF)
AVHV-2 (sheep mcf)
SUBFAMILY: ALPHAHERPESVIRINAE
PROPERTIES
culture?
replication cycle?
host specificity?
lesions?
infections/organs/what kind of animals?
what about pregnant animals?
- HIGHLY CYTOPATHIC IN CULTURE
- RELATIVELY SHORT REPLICATION CYCLE
- MOST ARE VERY HOST SPECIFIC EXCEPT PSEUDORABIES VIRUS WHICH HAS A BROAD HOST
RANGE. - PRODUCE LOCALIZED LESIONS USUALLY IN THE SKIN OR THE MUCOSA OF THE RESPIRATORY
AND GENITAL TRACTS - IN GENERALIZED INFECTIONS THERE IS A FOCI OF NECROSIS IN ALMOST EVERY ORGAN OR
TISSUE OF VERY YOUNG OR IMMUNOCOMPROMISED ANIMALS. - IN PREGNANT ANIMALS, THE VIRUS WILL CROSS THE PLACENTA LEADING TO ABORTION. THE
FETUS WILL ALSO HAVE MULTIFOCAL AREAS OF NECROSIS IN THE ORGANS.
BOVINE HERPESVIRUS 1
causes?
CAUSES: INFECTIOUS BOVINE RHINOTRACHEITIS (IBR), INFECTIOUS PUSTULAR
VULVOVAGINITIS, OCULAR FORM OF IBR, ABORTION, SYSTEMIC DISEASE OF
NEWBORN CALVES
BOVINE HERPESVIRUS 1
3 SUBTYPES: (ONLY TWO ARE IMPORTANT)
- BHV-1.1 (RESPIRATORY)
- BHV-1.2 (GENITAL)
BOVINE HERPESVIRUS 1
TRANSMISSION:
- RESPIRATORY DISEASE AND CONJUNCTIVITIS DUE TO DROPLET
TRANSMISSION (BHV-1) - GENITAL DISEASE FROM COITUS OR AI WITH INFECTIVE SEMEN (BHV-2)
BOVINE HERPESVIRUS 1
* PATHOGENESIS:
lesions?
typical herpesvirus inclusions?
inflammatory response?
who are potential carriers?
latent infections? reactivation causes?
site of latency?
PATHOGENESIS:
* LESIONS ARE FOCAL AREAS OF EPITHELIAL CELL NECROSIS RESULTING IN
BALLOONING OF EPITHELIAL CELLS.
* TYPICAL HERPESVIRUS INCLUSIONS MAY BE PRESENT IN THE NUCLEI AT THE
PERIPHERY OF NECROTIC FOCI.
* INTENSE INFLAMMATORY RESPONSE WITHIN THE NECROTIC MUCOSA OFTEN
WITH ACCUMULATION OF FIBRIN AND CELLULAR DEBRIS (PSEUDOMEMBRANE)
* ALL SEROPOSITIVE ANIMALS ARE CONSIDERED POTENTIAL CARRIERS
* LIFE-LONG LATENT INFECTION WITH PERIODIC SHEDDING OCCURS AFTER
BHV-1
* CAN BE REACTIVATED FROM LATENCY VIA CORTICOSTEROIDS OR
STRESS
* SITES OF LATENCY
* TRIMGEMINAL NERVE: RESPIRATORY
Sciatic Nerve: genital disease
BOVINE HERPESVIRUS 1
CLINICAL SIGNS
what is it?
where is it?
why does it look this way?
recovery?
complications?
potential for death?
RESPIRATORY FORM (RED NOSE, NECROTIC RHINITIS, DUST
PNEUMONIA)
* RHINITIS (FIBRINONECROTIC RHINITIS), LARYNGITIS AND
TRACHEITIS
* INFLAMED NARES GIVE THE APPEARANCE OF “RED NOSE” DUE
TO HYPEREMIA. WILL ALSO HAVE GRAYISH NECROTIC FOCI ON
THE MUCOUS. THE NASAL D/C WILL BECOME MORE PROFUSE
AND MUCOPURULENT
* UNCOMPLICATED CASES WILL RECOVER IN 10-14 DAYS
* COMPLICATIONS CAN ARISE FROM MANNHEIMIA HEMOLYTICA
AND PASTEURELLA MULTICOIDA (SHIPPING FEVER)
* DEATH TENDS TO OCCUR DUE TO SECONDARY
BRONCHOPNEUMONIA.
what is this?
BOVINE HERPESVIRUS 1
BOVINE HERPESVIRUS 1
CLINICAL SIGNS
Ocular Form if IBR:
Conjunctivitis is a common
finding in typical “red
nose”
* **DO NOT misdiagnose
as pink-eye: **IBR lesions
are confined to the
conjunctiva and no
lesions on cornea except
with diffuse edema.
BOVINE HERPESVIRUS 1
CLINICAL SIGNS
Abortion:
how common?
why occur?
when is the highest incidence?
what often precedes?
- Common sequel to
natural infection - Result of some modified-
live virus (MLV) vaccines
given to pregnant
animals in contact with
IBR-susceptible animals.
* Highest incidence in
second half of gestation
but early embryonic
death is possible
* Often preceded by
pustular vulvovaginitis
BOVINE HERPESVIRUS 1
Systemic disease of
newborn calves:
what result?
why?
- Severe in calves less than
10 days of age. Often
fatal. - Infected in-utero or right
after birth
BOVINE HERPESVIRUS 1
Genital Disease:
Infectious Pustular
Vaginitis
when does it occur?
cow behavior?
appearance?
- Occurs after coitus
- Causes frequent
urination, tail is usually
elevated with excessive
tail switching - Vagina mucosa, red and
swollen with mild d/c - Vulva will be swollen with
red spots and discrete
pustules can be seen - IN MALES: will get
Balanoposthitis
(inflammation and
pustules in the mucosa of
the penis and prepuce
BOVINE HERPESVIRUS 1
CONTROL
what?
for who?
cautions?
- MODIFIED LIVE VACCINES, SUBUNIT
VACCINE, INACTIVATED VACCINE ARE
AVAILABLE - PARENTERAL AND INTRANASAL VACCINES
- BOTH STIMULATE HUMORAL AB
PRODUCTION
* INTRANASAL IS SAFE FOR
PREGNANT COWS WHILE THE
PARENTERAL VACCINE MAY CAUSE
ABORTION
CONTROL
BOVINE HERPESVIRUS 2
what does the 2 mean?
2 diseases
* BOVINE ULCERATIVE MAMMILITIS
* PSEUDO-LUMPY SKIN DISEASE
BOVINE HERPESVIRUS 2
BOVINE ULCERATIVE MAMMILITIS
host?
transmission?
clinical signs?
- **HOST: **CATTLE, HEIFERS, USUALLY WITHIN 2 WEEKS
OF CALVING AND IS A PERSISTENT DISEASE - **TRANSMISSION: **DIRECT CONTACT AND FOMITE-
MEDIATED THROUGH THE SKIN OR MECHANICAL
TRANSMISSION VIA STABLE FLIES AND OTHER
ARTHROPODS. -
CLINICAL SIGNS: IN SEVERE CASES, TEATS BECOME
SWOLLEN AND PAINFUL, SKIN IS BLUISH, EXUDES
SERUM AND FORMS RAW ULCERS WITH A HIGH
INCIDENCE OF MASTITIS!
BOVINE HERPESVIRUS 2
PSEUDO-LUMPY SKIN DISEASE:
host?
transmission?
clinical signs?
- HOST: CATTLE MAINLY IN SOUTHERN AFRICA
- TRANSMISSION: MECHANICAL VIA ARTHROPODS
- CLINICAL SIGNS: MILD FEVER, SUDDEN ONSET OF SKIN NODULES ON THE FACE, NECK, BACK AND PERINEUM.
PORCINE HERPESVIRUS 1/SUID HERPESVIRUS 1
PSEUDORABIES (AUJESKY DISEASE, MAD ITCH)
what is unique about this and hosts?
only one with lots of secondary hosts
PORCINE HERPESVIRUS 1/SUID HERPESVIRUS 1
PSEUDORABIES (AUJESKY DISEASE, MAD ITCH)
host?
HOST: PRIMARILY A DISEASE IN SWINE. WIDE VARIETY OF SECONDARY: HORSES, CATTLE, SHEEP,
GOATS, DOGS, CATS AND OTHER FERAL SPECIES. HUMANS ARE RESISTANT TO INFECTION.
PORCINE HERPESVIRUS 1/SUID HERPESVIRUS 1
PSEUDORABIES (AUJESKY DISEASE, MAD ITCH)
TRANSMISSION IN PRIMARY HOST?
- RECOVERED PIGS ACT AS PRIMARY RESERVOIRS AND ARE LATENT CARRIERS FOR LIFE
- RODENTS ARE ALSO RESERVOIRS AND TRANSMIT FARM TO FARM
- SPREAD THROUGH SALIVA, NASAL DISCHARGES AND MILK OF INFECTED PIGS.
- NOT SHED IN URINE OR FECES
- CAN BE SPREAD VIA LICKING, BITING, AEROSOL, INGESTION, WATER AND FEED.
PORCINE HERPESVIRUS 1/SUID HERPESVIRUS 1
PSEUDORABIES (AUJESKY DISEASE, MAD ITCH)
TRANSMISSION IN SECONDARY HOST?
- **DOGS AND CATS: INGESTION OF INFECTED MEAT (PIG OR RODENTS)
- CATTLE: DIRECT CONTACT WITH PIGS, ORAL AND NASAL ROUTES**
PSEUDORABIES IN PIGS
PATHOGENESIS?
PATHOGENESIS: PRIMARY SITE OF VIRAL REPLICATION IS UPPER
RESPIRATORY TRACT.
PSEUDORABIES IN PIGS
SPREAD:
REPLICATES IN TONSILS AND NASOPHARYNX AND SPREADS
VIA THE LYMPHATICS TO REGIONAL LYMPH NODES. BRIEF VIREMIA IS
ASSOCIATED WITH VIRULENT STRAINS WITH LOCALIZATION OF THE
VIRUS IN DIFFERENT ORGANS.
PSEUDORABIES IN PIGS
VIRUS IN THE CNS:
VIA AXONS OF CRANIAL NERVES WITH A
PREFERENCE OF SPREAD TO NEURONS OF THE PONS AND MEDULLA.
* LESIONS: GANGLIONEURITIS, NONSUPPURATIVE
MENINGOENCEPHALITIS, PERIVASCULAR CUFFING
PSEUDORABIES IN PIGS
CLINICAL SIGNS IN PIGS
Piglets?
pregnangt sows?
older piglets?
necropsy findings?
- NON-IMMUNE PIGLETS:
- 100% MORTALITY
- NON-IMMUNE PREGNANT SOWS:
- 50% ABORTION
- INFECTION BEFORE DAY 30 OF GESTATION RESULTS IN DEATH AND REABSORPTION OF THE EMBRYO
- IN LATE PREGNANCY: MUMMIFIED, MACERATED, STILLBORN, WEAK OR NORMAL SWINE
- UP TO 20% OF SOWS ABORTING END UP INFERTILE FOR THE NEXT BREEDING BUT WILL CONCEIVE AGAIN.
- PIGLETS BORN WILL BE MOST SUSCEPTIBLE. SIGNS OF CNS ARE COMMONLY SEEN: INCOORDINATION OF
HINDLIMBS, FITTING, TREMORS AND PADDLING - OLDER PIGLETS, GROWERS AND ADULT PIGS:
- MILD DISEASE WITH LESS THAN 2% MORTALITY
- CNS SIGNS REDUCED WITH MORE RESPIRATORY SIGNS
- **NECROPSY FINDINGS: **GROSS LESIONS ARE OFTEN ABSENT OR MINIMAL, SEROUS TO FIBRINOUS RHINITIS IS
COMMON WITH A NECROTIC TONSILLITIS
**no pruritis in pigs
PORCINE HERPESVIRUS 1/SUID HERPESVIRUS 1
PSEUDORABIES (AUJESKY DISEASE, MAD ITCH)
PSEUDORABIES IN SECONDARY HOSTS
cattle?
dogs?
cats?
what result?
what result vaccination?
- CATTLE:
- INTENSE PRURITIS, MAY BECOME FRENZIED, PROGRESSES INTO CNS, STAGE OF PARALYSIS AND
ATAXIA, DEATH FROM RESPIRATORY FAILURE - DOGS:
- FRENZIED FROM PRURITIS AND SELF MUTILATION, PARALYSIS OF THE JAWS, PHARYNX (DROOLING OF
SALIVA), PLAINTIVE HOWLING - CATS:
- DISEASE IS SO VERY RAPID PRURITIS IS OFTEN NOT SEEN
- SECONDARY HOSTS HAVE HYPERACUTE, RAPID PROGRESSION AND HIGH MORTALITY!!
- **VACCINATION: **CAN REDUCE LOSSES BUT DOES NOT PREVENT INFECTION OR LATENT INFECTION BUT CAN
ALLEVIATE CS IN PIGS. RECOMBINANT DNA, DELETE MUTANT, LIVE ATTENUATED AND INAVTIVATED VACCINES
ARE AVAILABLE
EQUINE HERPES VIRUS 1(EHV-1)
DISTRIBUTION?
TRANSMISSION?
DISTRIBUTION: ENDEMIC IN HORSES AROUND THE WORLD
TRANSMISSION: AEROSOLS, DIRECT OR INDIRECT CONTACT
WITH NASAL D/C, ABORTED FETUSES, PLACENTA OR
PLACENTAL FLUIDS
*no vicerative mammalitis
EQUINE HERPES VIRUS 1 (EHV-1)
* LATENCY?
LATENCY: CAN RESIDE IN TISSUES OF THE CNS AND LYMPH
SYSTEM WITHOUT CAUSING CLINICAL SIGNS OF DISEASE.
* WHEN THE HOST IS IMMUNOSUPPRESSED, THE VIRUS IS
REACTIVATED CAUSING DISEASE OR SHEDDING THE VIRUS.
EQUINE HERPES VIRUS 1 (EHV-1)
PATHOGENESIS?
- MAINLY VIA THE RESPIRATORY TRACT
-
INFECTS EPITHELIAL CELLS, THEN THE ENDOTHELIAL CELLS IN
THE LAMINA PROPRIA - VIRUS-INFECTED MONONUCLEAR CELLS AND T CELLS
APPEAR IN LYMPH NODE DRAINAGE LEADING TO VIREMIA
EQUINE HERPES VIRUS 1 (EHV-1)
PATHOGENESIS CONTINUES?
PATHOGENESIS CONTINUES:
* INFECTION OF RESPIRATORY EPITHELIUM OCCURS AND THEN ESTABLISHES LATENT INFECTIONS IN CIRCULATING T
CELLS AND TRIGEMINAL GANGLION
* REACTIVATION RESULTS IN SHEDDING FROM NASAL EPITHELIUM AND UTERINE INFECTIONS
* CENTRAL LESIONS CAN CAUSE RESPIRATORY, REPRODUCTIVE
AND CNS CONDITIONS CAUSE INFECTION OF ENDOTHELIAL CELLS LEADING TO VASCULAR NECROSIS, THROMBUS
FORMATION, AND ISCHEMIA
* CELLS ASSOCIATED WITH VIREMIA CAN PROTECT THE HOST’S IMMUNE SYSTEM ALLOWING FOR THE SPREAD OF
THE VIRUS.
* IMMUNOSUPPRESSION IS NECESSARY
EQUINE HERPES VIRUS 1
what 3 forms?
who affected?
-
RESPIRATORY DISEASE: AFFECTS MOSTLY YOUNGER
HORSES. CAUSES RHINOPNEUMONITIS -
ENCEPHALOMYELOPATHY (EHM): MAY AFFECT HORSES OF
ANY AGE OR BREED. -
REPRODUCTIVE FORM: EFFICIENCY IS NOT COMPROMISED-
ABORTION MAY HAPPEN EARLY, MOST ABORTIONS OCCUR
IN THE LAST TRIMESTER (8-10M). CAUSES ARE SPORADIC AND
CAN CAUSE ABORTION STORMS IF THERE IS A LARGE
NUMBER OF MARES ARE EXPOSED TO ABORTED FETUSES.
TYPICALLY EVERY 3 YEARS YOU WILL SEE THE STORM SINCE
NATURAL IMMUNITY CAN LAST 2-3 YEARS.
EQUINE HERPESVIRUS 4
More or less severe than EHV1?
EHV1 is #1
EHV4 is less severe
EQUINE HERPESVIRUS 4
causes?
transmission?
- CAUSES EQUINE VIRAL RHINOPNEUMONITIS
- IS ANTIGENICALLY RELATED TO EHV-1
- TRANSMISSION:
- MOST INFECTIONS ARE SPORADIC AND
OCCUR IN HORSES UNDER 2YRS OLD - OFTEN CAUSES LIFELONG LATENT INFECTIONS
WHICH CAN BE REACTIVATED - DROPLET INFECTION FROM INFECTED HORSES
AND OLDER HORSES THAT ARE SHEDDING
EQUINE HERPESVIRUS 4
* PATHOGENESIS?
* CLINICAL SIGNS?
- PATHOGENESIS:
- EHV CAUSES LESS SEVERE TISSUE
DESTRUCTION, RARELY CAUSES ABORTION
AND VIREMIA. DEATH IS RARE. - CLINICAL SIGNS:
- UPPER RESPIRATORY TRACT DISEASE-
RHINOPHARYNGITIS AND
TRACHEOBRONCHITIS)
VACCINATION OF EHV-1 AND
EHV-4
-
LIVE-ATTENUATED AND INACTIVATED COMMERCIAL EHV-1
VACCINES AS WELL AS COMBINES PRODUCTS THAT
INCLUDE BOTH EHV-1 AND EHV-4 - IMMUNITY IS SHORT-LIVED
- IDEALLY, THE VACCINE SHOULD PREVENT EARLY
INFECTIONS IN SUCKLING FOALS AS WELL AS LATENCY
OF INFECTION IN PREGNANT MARES
CANINE HERPESVIRUS 1 (CHV-1)
HEMORRHAGIC DISEASE OF PUPPIES
Hosts?
transmission? neonates/older dogs
- HOST: DOGS, WILD CANIDAE.
- HIGHLY FATAL GENERALIZED HEMORRHAGIC DISEASE
OD PUPPIES (FADING PUPPY SYNDROME) - TRANSMISSION:
-
NEONATES: CONTACT WITH INFECTED ORAL, NASAL
OR VAGINAL SECRETIONS FROM THE MOTHER, IN-
UTERO, PASSAGE FROM THE BIRTH CANAL, SECRETIONS
OF LITTERMATES, RARELY INFECTED FOMITES. -
OLDER DOGS: VENEREAL, CONTACT WITH SALIVA,
NASAL D/C OR URINE FROM INFECTED DOGS OR
PUPPIES. **basically body secretions
CANINE HERPESVIRUS 1 (CHV-1)
HEMORRHAGIC DISEASE OF PUPPIES
PATHOGENESIS
what 3 types of infection?
IN-UTERO INFECTION
CNS INFECTION
SYSTEMIC NEONATAL INFECTION
CANINE HERPESVIRUS 1 (CHV-1)
HEMORRHAGIC DISEASE OF PUPPIES
PATHOGENESIS:
IN-UTERO INFECTION
result?
IN-UTERO INFECTION
* ABORTION, STILLBIRTH, INFERTILITY
* IF PUPPY SURVIVES, WILL DEVELOP SYSTEMIC
DISEASE INFECTIONS WITHIN 9DAYS OF BIRTH
CANINE HERPESVIRUS 1 (CHV-1)
HEMORRHAGIC DISEASE OF PUPPIES
PATHOGENESIS: CNS INFECTION
what is it? what result?
CNS INFECTION
- MENINGOENCEPHALITIS HAPPENS WITH ORO-
NASAL INFECTIONS IN NEONATAL PUPS - TRAVEL UP NERVE AXONS TO CNS
- PUPPIES TYPICALLY DIE FROM SYSTEMIC INFECTION
BEFORE CNS SIGNS ARE EVIDENT
CANINE HERPESVIRUS 1 (CHV-1)
HEMORRHAGIC DISEASE OF PUPPIES
PATHOGENESIS: SYSTEMIC NEONATAL INFECTION
who gets it?
how does it occur?
what result?
SYSTEMIC NEONATAL INFECTION
* LESS THAN 1 WEEK OLD ARE MOST SUSCEPTIBLE TO
FATAL GENERALIZED INFECTION
* INITIAL REPLICATION IN NASAL EPITHELIUM, TONSILS,
PHARYNX
* MUCOSAL INVASION IS FOLLOWED BY LEUKOCYTE
(MACROPHAGE)–ASSOCIATED VIREMIA
* REPLICATES IN ENDOTHELIUM
* DIFFUSE NECROTIZING VASCULITIS, MULTIPLE
HEMORRHAGIC NECROSIS IN SEVERAL ORGANS
* THROMBOCYTOPENIA, DIC
CANINE HERPESVIRUS 1 (CHV-1)
HEMORRHAGIC DISEASE OF PUPPIES
FACTORS GOVERNING SYSTEMIC NEONATAL INFECTION:
name 2
how do they occur?
FACTORS GOVERNING SYSTEMIC NEONATAL INFECTION:
* BODY TEMP IS CRITICAL
* CHV-1 REPLICATES OPTIMALLY AT 330C (THE TEMP OF
OUTER GENITAL AND UPPER RESP TRACTS)
* THERMOREGULATION DOESN’T FULLY OPERATE UNTIL 2-3
WEEKS OF AGE
* THE MORE SEVERE THE HYPOTHERMIA IS THE MORE
SEVERE AND RAPID THE DISEASE.
* MATERNAL IMMUNITY:
* MATERNAL ANTIBODIES PROVIDE PROTECTION, PUPPIES
BORN FROM SERONEGATIVE BITCHES ARE HIGHLY
VULNERABLE TO THE SEVERE FORM OF DISEASE.
CANINE HERPESVIRUS 1 (CHV-1)
HEMORRHAGIC DISEASE OF PUPPIES
CLINICAL SIGNS OF CHV-1
puppies?
adults?
- PUPPIES:
- PAINFUL CRYING, ABDOMINAL PAIN, ANOREXIA, DYSPNEA, PASSING SOFT,
ODORLESS, GREENISH STOOL AND NO ELEVATION OF BODY TEMP. - PUPPIES THAT SURVIVE DEVELOP NEURO SIGNS SUCH AS BLINDNESS AND ATAXIA.
- ADULT GENITAL INFECTION:
- BITCHES: GENERALLY ASYMPTOMATIC OR LIMITED TO VAGINAL HYPEREMIA,
VESICULAR VAGINITIS WITH D/C AND VESICULAR LESIONS. IN UTERO INFECTION
MAY RESULT IN ABORTION, STILLBIRTH, MUMMIFIED FETUS AND/OR INFERTILITY - MALE: BALANOPOSTHITIS
- ADULT RESPIRATORY INFECTION:
- MILD RESPIRATORY INFECTION (RHINITIS AND PHARYNGITIS)
- OCULAR INFECTION: CONJUNCTIVITIS
CONTROL OF CHV-1
treatment of pups?
vaccines?
REDUCE HYPOTHERMIA VIA HEATED WHELPING BOXES OR PLACING PUPS
UNDER INFRARED LAMPS
* BODY TEMPERATURE IS VITAL
* LOW PREVALENCE OF SEVERE ILLNESS IN PUPS AND SCARCITY OF CLINICAL
SIGNS IN ADULT ANIMALS HAS RESULTED IN LACK OF AVAILABILITY OF
VACCINES
* NO VACCINE!
FELINE HERPESVIRUS 1
FELINE RHINOTRACHEITIS
is it common?
ONE OF THE MOST COMMON ETIOLOGIES OF RESPIRATORY DISEASE WITH THE OTHER BEING FELINE
CALICIVIRUS (FCV)
FELINE HERPESVIRUS 1
FELINE RHINOTRACHEITIS
TRANSMISSION?
TRANSMISSION:
* SHED IN NATURAL ROUTES OF OCULAR, NASAL, ORAL SECRETIONS. REACTIVATION MAY CAUSE
SHEDDING
* DIRECT CONTACT WITH AN INFECTED ROUTE
* AEROSOL IS NOT IMPORTANT
* ALL RECOVERED CATS BECOME LATENT CARRIERS
FELINE HERPESVIRUS 1
FELINE RHINOTRACHEITIS
PATHOGENESIS
- REPLICATES IN MUCOSA OF NASAL SEPTUM, TURBINATES (bony structures inside nosem covered by soft tissue/mucosa), NASOPHARYNX, AND TONSILS
- VIREMIA IS RARE DUE TO REPLICATION BEING RESTRICTED TO AREAS OF LOW TEMPERATURES
- INFECTION CAUSES AREAS OF MULTIFOCAL EPITHELIAL NECROSIS, INFLAMMATION, AND
FIBRINOUS EXUDATION - SECONDARY BACTERIAL INFECTIONS CAUSE COMPLICATIONS
CLINICAL SIGNS OF FHV-1
kittens?
cats over 6mo?
pregnant?
- KITTENS-UP TO 4 WEEKS:
- SEVERE UPPER RESPIRATORY DISEASE
- EXTENSIVE RHINOTRACHEITIS
- FATAL BRONCHOPNEUMONIA MAY DEVELOP DUE TO SECONDARY BACTERIAL INFECTION
-
CONJUNCTIVITIS AND ULCERATIVE KERATITIS
**Ddx: calicivirus UR: symptoms, crusty eyes
CATS MORE THAN 6M: - MILD OR SUBCLINICAL DISEASE IN OLDER KITTENS
PREGNANT QUEEN:
* ABORTION AROUND 6TH WEEK OF PREGNANCY
* MAY BE DUE TO SEVERE SYSTEMIC EFFECTS OF ILLNESS AND NOT A DIRECT EFFECT OF THE VIRUS
ORAL ULCERS ARE RARE IN CATS WITH FHV-1 BUT COMMON IN FELINE CALICIVIRUS **ural ulcers
how would you tell feline herpes virus from calicivirus?
oral ulcers
VACCINATION OF
FELINE
RHINOTRACHEITIS
*** MODIFIED LIVE VIRUS-INJECTABLE OR
INTRANASALLY
- INACTIVATED VACCINE INJECTABLE
GALLID HERPESVIRUS 1
(INFECTIOUS
LARYNGOTRACHEITIS
**know both names
host?
transmission?
- HOST: HIGHLY CONTAGIOUS INFECTION OF CHICKENS
- TRANSMISSION:
- MOSTLY VIA INHALATION, BUT CAN BE DROPLETS TO
CONJUNCTIVA, SOMETIMES INGESTION, FOMITES (LITTER/FARM
WORKERS), MECHANICAL TRANSMISSION (SCAVENGERS).
RECOVERED AND VACCINATED CHICKENS CAN ALSO BE CARRIERS
AND SHED DURING STRESS.
GALLID HERPESVIRUS 1
(INFECTIOUS
LARYNGOTRACHEITIS
PATHOGENESIS?
PATHOGENESIS:
* SEVERE LARYNGOTRACHEITIS
* EXTENSIVE DIPHTHERITIC (an infection caused by corynbacterium diphtheriac) MEMBRANE FORMATION CAN FORM
CAUSING BLOCKAGE OF THE TRACHEA RESULTING IN ASPHYXIA (similar to fowl pox)
* CAN PERSIST IN INFECTED BIRDS. THE TRIGEMINAL GANGLION IS
THE TARGET FOR VIRAL LATENCY
CLINICAL SIGNS OF ILT
- SEVERE FORM:
symptoms?
common?
- SEVERE RESPIRATORY DISTRESS
- HEAD SHAKING WITH COUGHING IS VERY CHARACTERISTIC
- NECK RAISED AND HEAD EXTENDED DURING INSPIRATION (PUMP
HANDLE RESPIRATION) - COUGH UP BLOODY MUCUS WHICH MAY STAIN BEAK, NECK, FEATHERS
- STRAINS OF LOW VIRULENCE ARE ASSOCIATED WITH CONJUNCTIVITIS,
OCULAR D/C, SWOLLEN INFRAORBITAL AND NASAL SINUSES AS WELL
AS DECREASED EGG PRODUCTION. - SEVERE EPIZOOTIC FORM IS UNCOMMON WHILE MILD ENZOOTIC
FORM IS MOST COMMON
**epidemic is more uncommon and always severe
GALLID HERPESVIRUS 1
(INFECTIOUS
LARYNGOTRACHEITIS
diagnosis
DIAGNOSIS
* MAINLY VIA HISTORY AND CS
* NECROPSY: TRACHEAL PLUG
* HISTO: DETECTION OF INTRANUCLEAR INCLUSIONS IN
THE RESPIRATORY TISSUES
* ISOLATION: NASAL MUCOSA
* GROWS WELL IN CAM OF EMBRYONATED EGGS
* FARM BIOSECURITY:
* IMPLEMENTATION OF FARM BIOSECURITY MEASURES.
GALLID HERPESVIRUS 1
(INFECTIOUS
LARYNGOTRACHEITIS
control?
vaccines?
CONTROL
* IF THERE IS AN OUTBREAK CULL ALL BIRDS AND
DISINFECT.
- VACCINES:
- **CHICK EMBRYO ORIGIN (CEO)-REVERTING TO
VIRULENCE AND CAUSING FULL-BLOWN ILT SIGNS
(INDUCES BETTER IMMUNITY -
TISSUE CULTURE ORIGIN (TCO)-ONLY GIVEN VIA EYE-
DROP AND DOES NOT SPREAD/REVERT TO VIRULENCE,
IMMUNITY IS LIMITED. THIS IS **THE BETTER CHOICE** - POX-VECTORED RECOMBINANT VACCINE
GALLID HERPESVIRUS
2
MAREKS DISEASE
importance?
host?
transmission?
- VERY IMPORTANT DISEASE IN POULTRY!!!!!
- HOST: CHICKENS, BUT ALSO CAN BE
TURKEYS, QUAILS, AND PHEASANTS - TRANSMISSION:
- HIGHLY CONTAGIOUS
-
INHALATION OF FEATHER DEBRIS
(HIGHLY INFECTIOUS BUT LABILE),
DANDER OR DUST (LESS INFECTIOUS
BUT CAN SURVIVE IN DUST OR
LITTER FOR MONTHS)
PATHOTYPES OF GALLID
HERPESVIRUS 2
Name 4
MILD [MMDV]:
VIRULENT [VMDV]:
VERY VIRULENT [VVMDV]:
VERY VIRULENT PLUS [VV+MDV]:
PATHOTYPES OF GALLID
HERPESVIRUS 2
MILD [MMDV]: describe
MILD [MMDV]:
* MOSTLY ASSOCIATED WITH NEURAL MD, PREVENTABLE WITH HVT (TURKEY
HERPESVIRUS VACCINE)
**give HVT and they will survive
PATHOTYPES OF GALLID
HERPESVIRUS 2
VIRULENT [VMDV]: describe
- HIGH INCIDENCE OF NEURAL AND VISCERAL LYMPHOMAS. PREVENTABLE
WITH HVT.
**give HVT and they will survive
PATHOTYPES OF GALLID
HERPESVIRUS 2
VERY VIRULENT [VVMDV]: describe
VERY VIRULENT [VVMDV]:
* HIGH INCIDENCE OF NEURAL AND VISCERAL LYMPHOMAS. **ONCOGENIC
WITH HVT **VACCINATED CHICKENS, PREVENTABLE WITH BIVALENT VACCINES.
**give hvt and they will die, but if you give bivalend vaccines they will survive
PATHOTYPES OF GALLID
HERPESVIRUS 2
VERY VIRULENT PLUS [VV+MDV]: describe
HIGH INCIDENCE OF NUERAL AND VISCERAL LYMPHOMAS. ARE ONCOGENIC
IN CHICKENS VACCINATED WITH BIVALENT VACCINES
**give bivalent vaccines and they will die
GALLID
HERPESVIRUS 2
PATHOGENESIS
what are the 4 types of infection in order?
- PRODUCTIVE-RESTRICTIVE INFECTION
- NON-PRODUCTIVE INFECTION
- NON-PRODUCTIVE NEOPLASTIC
TRANSFORMATION - FULLY PRODUCTIVE INFECTION
GALLID
HERPESVIRUS 2
PATHOGENESIS
PRODUCTIVE-RESTRICTIVE INFECTION
DESCRIBE
- PRODUCTION OF NAKED VIRIONS (NON-
INFECTIOUS) AND VIRAL ANTIGENS - CELL DEATH VIA LYSIS
- IN B CELLS AND ACTIVATED T CELLS (CD4+)
- IMMUNOSUPPRESSION
GALLID
HERPESVIRUS 2
PATHOGENESIS
NON-PRODUCTIVE INFECTION
DESCRIBE
- VIRAL GENOME PERSISTS IN CD4+
- NO ANTIGENS ARE EXPRESSED
GALLID
HERPESVIRUS 2
PATHOGENESIS
NON-PRODUCTIVE NEOPLASTIC
TRANSFORMATION
DESCRIBE
- SOME LATENTLY INFECTED T CELLS UNDERGO
NEOPLASTIC TRANSFORMATION - MATSA (MAREK’S DISEASE ASSOCIATED TUMOR
SPECIFIC ANTIGEN) APPEARS IN TRANSFORMED T-cells
**oncogenic
GALLID
HERPESVIRUS 2
PATHOGENESIS
FULLY PRODUCTIVE INFECTION
- PRODUCE ENVELOPED VIRIONS AND CELL DEATH
VIA LYSIS - OCCURS IN FEATHER FOLLICLE EPITHELIUM
-
INFECTED T CELLS= TROJAN HORSE FOR MDV TO
ENTER
**WHY INHALATION OF FEATHERS IS A THING
GALLID
HERPESVIRUS 2
PATHOGENESIS
CHARACTERISTICS OF VIRUS?
LESIONS?
- VIRUS IS SLOWLY CYTOPATHIC AND REMAIN
ASSOCIATED WITH CELLS (CELL-FREE ARE ALMOST
IMPOSSIBLE TO OBTAIN EXCEPT IN DANDER FROM
FEATHER FOLLICLES) - LESIONS RESULT FROM INFILTRATION AND IN SITU
PROLIFERATION OF TRANSFORMED T-CELLS
GALLID
HERPESVIRUS 2
WHAT 4 CLINICAL SIGNS?
- NEUROLYMPHOMATOSIS
- VISCERAL LYMPHAMATOSIS
- Ocular lymphomatosis
- Cutaneous lymphomatosis
GALLID
HERPESVIRUS 2
NEUROLYMPHOMATOSIS: EXPLAIN
NEUROLYMPHOMATOSIS:
* ENLARGEMENT OF NERVE TRUNKS, LOSES
STRIATIONS, EDEMATOUS, GREY OR YELLOWISH
APPEARANCE
* LAMENESS, DROOPY WINGS, PARTIAL PARALYSIS OF
LEGS, LIMBERNECK, TORTICOLLIS, INCOORDINATION
GALLID
HERPESVIRUS 2
VISCERAL LYMPHAMATOSIS: EXPLAIN
- DIFFUSE OR NODULAR LYMPHOID TUMORS IN
VARIOUS ORGANS BUT MAINLY THE LIVER, SPLEEN,
GONADS, HEART, LUNG, KIDNEY, MUSCLE AND
PROVENTRICULUS - BURSA IS ATROPHIC AND HELP DISTINGUISH THE
DISEASE FROM LYMPHOID LEUKOSIS
GALLID
HERPESVIRUS 2
Ocular lymphomatosis:
EXPLAIN
- Graying of the iris of one or both eyes
- Interference with normal pupilar
constriction/dilation - Partial or total blindness
GALLID
HERPESVIRUS 2
Cutaneous lymphomatosis: EXPLAIN
-
Plucking of feathers to reveal nodular
lesions - Enlarged feather follicles
VACCINATION OF MAREK’S
DISEASE
WHAT IS THE MOST WIDELY USED?
WHAT IS BIVALENT VACCINES?
WHAT IS THE MOST PROTECTIVE?
- TURKEY HERPESVIRUS (HVT) IS MOST WIDELY USED
- BIVALENT VACCINES CONSIST OF HVT AND EITHER SB-1
OR 301B/1 STRAINS OF GALLID HERPESVIRUS 3 - MOST PROTECTIVE COMMERCIAL VACCINE IS THE
CVI988/RISPENS: AN ATTENUATED MAREK’S DISEASE
VIRUS STRAIN THAT IS ALSO MIXED WITH HVT AT
VACCINATION
