Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Virology RUSVM > Block 7 > Flashcards

Block 7 Flashcards

1
Q

what is ANELLOVIRIDAE
GENUS: GYROVIRUS?
+/-?

A

A negative virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

characterisics and example of
ANELLOVIRIDAE
GENUS: GYROVIRUS

A
  • CIRCULAR, SINGLE-STRANDED NEGATIVE
    SENSE DNA
  • CHICKEN INFECTIOUS ANEMIA VIRUS HAS 12 TRUMPET-LIKE STRUCTURES
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

CHICKEN INFECTIOUS ANEMIA

host?
transmittion?

A

**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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

CHICKEN INFECTIOUS ANEMIA

what is the environmental stability?
Pathogenisis?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

CHICKEN

INFECTIOUS
ANEMIA

  • CLINICAL SIGNS AND LESIONS?
A
  • ANORECTIC, LETHARGIC,
    DEPRESSED, WEIGHT LOSS,
    PALE
  • THIN BLOOD WITH SLOW
    CLOTTING
  • PCV IS LOW
  • SUBQ AND SKELETAL
    HEMORRHAGES (PALE
    MUSCLES)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

CHICKEN INFECTIOUS ANEMIA

  • DIAGNOSIS? (7)
A
  • CLINICAL SIGNS
  • BLOODWORK
  • NECROPSY
  • HISTOPATHOLOGY
  • SEROLOGY: ELISA, NEUTRALIZATION TEST,
    FAT TEST
  • VIRUS ISOLATION
  • PCR/RT-PCR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

CHICKEN INFECTIOUS ANEMIA

VACCINATION?
who?
how?

A

VACCINATE THE HENS TO PROTECT THE
OFFSPRING THROUGH MATERNALLY
DERIVED ANTIBODIES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

FAMILY: HERPESVIRIDAE

MORPHOLOGY?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

FAMILY: HERPESVIRIDAE

REPLICATION?
where?
how?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

HERPESVIRIDAE

SUBFAMILY:
ALPHAHERPESVIRINAE
BOVINE HERPESVIRUS 1

Vaccine + Abortion?

A

Vaccine Abortion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

HERPESVIRIDAE

SUBFAMILY:
ALPHAHERPESVIRINAE
BOVINE HERPESVIRUS 2

Vaccine + Abortion?

A

?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

SUBFAMILY:
ALPHAHERPESVIRINAE
EQUINE HERPESVIRUS 1

A

vaccine abortion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

SUBFAMILY:
ALPHAHERPESVIRINAE

what are the 8/9?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

SUBFAMILY:
ALPHAHERPESVIRINAE
EQUINE HERPESVIRUS 4

A

vaccine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

SUBFAMILY:
ALPHAHERPESVIRINAE
PORCINE HERPESVIRUS 1

A

vaccine (for prgs) Abortion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

SUBFAMILY:
ALPHAHERPESVIRINAE
FELINE HERPESVIRUS 1

A

vaccine
abortion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

SUBFAMILY:
ALPHAHERPESVIRINAE
CANINE HERPESVIRUS 1

A

abortion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

SUBFAMILY:
ALPHAHERPESVIRINAE
GALLID HERPES VIRUS 1 AND 2

A

vaccine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

SUBFAMILY BETAHERPESVIRINAE
what is it?

A

PORCINE HERPESVIRUS 2
abortion
inclusion body rhinitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

SUBFAMILY: GAMMAHERPESVIRINAE
what is it?

A

Rep in lymphoid cells
MALIGNANT CATARRHAL FEVER
AVH-1(wildabeast MCF)
AVHV-2 (sheep mcf)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

SUBFAMILY: ALPHAHERPESVIRINAE
PROPERTIES

culture?
replication cycle?
host specificity?
lesions?
infections/organs/what kind of animals?
what about pregnant animals?

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

BOVINE HERPESVIRUS 1

causes?

A

CAUSES: INFECTIOUS BOVINE RHINOTRACHEITIS (IBR), INFECTIOUS PUSTULAR
VULVOVAGINITIS, OCULAR FORM OF IBR, ABORTION, SYSTEMIC DISEASE OF
NEWBORN CALVES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

BOVINE HERPESVIRUS 1
3 SUBTYPES: (ONLY TWO ARE IMPORTANT)

A
  • BHV-1.1 (RESPIRATORY)
  • BHV-1.2 (GENITAL)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

BOVINE HERPESVIRUS 1
TRANSMISSION:

A
  • RESPIRATORY DISEASE AND CONJUNCTIVITIS DUE TO DROPLET
    TRANSMISSION (BHV-1)
  • GENITAL DISEASE FROM COITUS OR AI WITH INFECTIVE SEMEN (BHV-2)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

BOVINE HERPESVIRUS 1
* PATHOGENESIS:

lesions?
typical herpesvirus inclusions?
inflammatory response?
who are potential carriers?
latent infections? reactivation causes?
site of latency?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

BOVINE HERPESVIRUS 1
CLINICAL SIGNS

what is it?
where is it?
why does it look this way?
recovery?
complications?
potential for death?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is this?

A

BOVINE HERPESVIRUS 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

BOVINE HERPESVIRUS 1
CLINICAL SIGNS
Ocular Form if IBR:

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

BOVINE HERPESVIRUS 1
CLINICAL SIGNS
Abortion:

how common?
why occur?
when is the highest incidence?
what often precedes?

A
  • 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

BOVINE HERPESVIRUS 1
Systemic disease of
newborn calves:

what result?
why?

A
  • Severe in calves less than
    10 days of age. Often
    fatal.
  • Infected in-utero or right
    after birth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

BOVINE HERPESVIRUS 1
Genital Disease:
Infectious Pustular
Vaginitis

when does it occur?
cow behavior?
appearance?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

BOVINE HERPESVIRUS 1
CONTROL

what?
for who?
cautions?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

BOVINE HERPESVIRUS 2

what does the 2 mean?

A

2 diseases
* BOVINE ULCERATIVE MAMMILITIS
* PSEUDO-LUMPY SKIN DISEASE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

BOVINE HERPESVIRUS 2
BOVINE ULCERATIVE MAMMILITIS

host?
transmission?
clinical signs?

A
  • **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!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

BOVINE HERPESVIRUS 2
PSEUDO-LUMPY SKIN DISEASE:

host?
transmission?
clinical signs?

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

PORCINE HERPESVIRUS 1/SUID HERPESVIRUS 1
PSEUDORABIES (AUJESKY DISEASE, MAD ITCH)

what is unique about this and hosts?

A

only one with lots of secondary hosts

38
Q

PORCINE HERPESVIRUS 1/SUID HERPESVIRUS 1
PSEUDORABIES (AUJESKY DISEASE, MAD ITCH)

host?

A

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.

39
Q

PORCINE HERPESVIRUS 1/SUID HERPESVIRUS 1
PSEUDORABIES (AUJESKY DISEASE, MAD ITCH)

TRANSMISSION IN PRIMARY HOST?

A
  • 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.
40
Q

PORCINE HERPESVIRUS 1/SUID HERPESVIRUS 1
PSEUDORABIES (AUJESKY DISEASE, MAD ITCH)
TRANSMISSION IN SECONDARY HOST?

A
  • **DOGS AND CATS: INGESTION OF INFECTED MEAT (PIG OR RODENTS)
  • CATTLE: DIRECT CONTACT WITH PIGS, ORAL AND NASAL ROUTES**
41
Q

PSEUDORABIES IN PIGS
PATHOGENESIS?

A

PATHOGENESIS: PRIMARY SITE OF VIRAL REPLICATION IS UPPER
RESPIRATORY TRACT.

42
Q

PSEUDORABIES IN PIGS
SPREAD:

A

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.

43
Q

PSEUDORABIES IN PIGS
VIRUS IN THE CNS:

A

VIA AXONS OF CRANIAL NERVES WITH A
PREFERENCE OF SPREAD TO NEURONS OF THE PONS AND MEDULLA.
* LESIONS: GANGLIONEURITIS, NONSUPPURATIVE
MENINGOENCEPHALITIS, PERIVASCULAR CUFFING

44
Q

PSEUDORABIES IN PIGS
CLINICAL SIGNS IN PIGS

Piglets?
pregnangt sows?
older piglets?
necropsy findings?

A
  • 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

45
Q

PORCINE HERPESVIRUS 1/SUID HERPESVIRUS 1
PSEUDORABIES (AUJESKY DISEASE, MAD ITCH)

PSEUDORABIES IN SECONDARY HOSTS

cattle?
dogs?
cats?

what result?
what result vaccination?

A
  • 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
46
Q

EQUINE HERPES VIRUS 1(EHV-1)

DISTRIBUTION?
TRANSMISSION?

A

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

47
Q

EQUINE HERPES VIRUS 1 (EHV-1)
* LATENCY?

A

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.

48
Q

EQUINE HERPES VIRUS 1 (EHV-1)

PATHOGENESIS?

A
  • 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
49
Q

EQUINE HERPES VIRUS 1 (EHV-1)
PATHOGENESIS CONTINUES?

A

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

50
Q

EQUINE HERPES VIRUS 1

what 3 forms?
who affected?

A
  • 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.

51
Q

EQUINE HERPESVIRUS 4

More or less severe than EHV1?

A

EHV1 is #1
EHV4 is less severe

52
Q

EQUINE HERPESVIRUS 4

causes?
transmission?

A
  • 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
53
Q

EQUINE HERPESVIRUS 4
* PATHOGENESIS?
* CLINICAL SIGNS?

A
  • PATHOGENESIS:
  • EHV CAUSES LESS SEVERE TISSUE
    DESTRUCTION, RARELY CAUSES ABORTION
    AND VIREMIA. DEATH IS RARE.
  • CLINICAL SIGNS:
  • UPPER RESPIRATORY TRACT DISEASE-
    RHINOPHARYNGITIS AND
    TRACHEOBRONCHITIS)
54
Q

VACCINATION OF EHV-1 AND
EHV-4

A
  • 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
55
Q

CANINE HERPESVIRUS 1 (CHV-1)
HEMORRHAGIC DISEASE OF PUPPIES

Hosts?
transmission? neonates/older dogs

A
  • 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
56
Q

CANINE HERPESVIRUS 1 (CHV-1)
HEMORRHAGIC DISEASE OF PUPPIES

PATHOGENESIS
what 3 types of infection?

A

IN-UTERO INFECTION
CNS INFECTION
SYSTEMIC NEONATAL INFECTION

57
Q

CANINE HERPESVIRUS 1 (CHV-1)
HEMORRHAGIC DISEASE OF PUPPIES

PATHOGENESIS:
IN-UTERO INFECTION

result?

A

IN-UTERO INFECTION
* ABORTION, STILLBIRTH, INFERTILITY
* IF PUPPY SURVIVES, WILL DEVELOP SYSTEMIC
DISEASE INFECTIONS WITHIN 9DAYS OF BIRTH

58
Q

CANINE HERPESVIRUS 1 (CHV-1)
HEMORRHAGIC DISEASE OF PUPPIES

PATHOGENESIS: CNS INFECTION

what is it? what result?

A

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
59
Q

CANINE HERPESVIRUS 1 (CHV-1)
HEMORRHAGIC DISEASE OF PUPPIES

PATHOGENESIS: SYSTEMIC NEONATAL INFECTION

who gets it?
how does it occur?
what result?

A

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

60
Q

CANINE HERPESVIRUS 1 (CHV-1)
HEMORRHAGIC DISEASE OF PUPPIES

FACTORS GOVERNING SYSTEMIC NEONATAL INFECTION:

name 2
how do they occur?

A

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.

61
Q

CANINE HERPESVIRUS 1 (CHV-1)
HEMORRHAGIC DISEASE OF PUPPIES

CLINICAL SIGNS OF CHV-1

puppies?
adults?

A
  • 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
62
Q

CONTROL OF CHV-1

treatment of pups?
vaccines?

A

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!

63
Q

FELINE HERPESVIRUS 1
FELINE RHINOTRACHEITIS

is it common?

A

ONE OF THE MOST COMMON ETIOLOGIES OF RESPIRATORY DISEASE WITH THE OTHER BEING FELINE
CALICIVIRUS (FCV)

64
Q

FELINE HERPESVIRUS 1
FELINE RHINOTRACHEITIS
TRANSMISSION?

A

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

65
Q

FELINE HERPESVIRUS 1
FELINE RHINOTRACHEITIS

PATHOGENESIS

A
  • 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
66
Q

CLINICAL SIGNS OF FHV-1

kittens?
cats over 6mo?
pregnant?

A
  • 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

67
Q

how would you tell feline herpes virus from calicivirus?

A

oral ulcers

68
Q

VACCINATION OF
FELINE
RHINOTRACHEITIS

A

*** MODIFIED LIVE VIRUS-INJECTABLE OR
INTRANASALLY

  • INACTIVATED VACCINE INJECTABLE
69
Q

GALLID HERPESVIRUS 1
(INFECTIOUS
LARYNGOTRACHEITIS
**know both names

host?
transmission?

A
  • 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.
70
Q

GALLID HERPESVIRUS 1
(INFECTIOUS
LARYNGOTRACHEITIS

PATHOGENESIS?

A

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

71
Q

CLINICAL SIGNS OF ILT

  • SEVERE FORM:

symptoms?
common?

A
  • 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

72
Q

GALLID HERPESVIRUS 1
(INFECTIOUS
LARYNGOTRACHEITIS

diagnosis

A

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.

73
Q

GALLID HERPESVIRUS 1
(INFECTIOUS
LARYNGOTRACHEITIS

control?
vaccines?

A

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
74
Q

GALLID HERPESVIRUS
2
MAREKS DISEASE

importance?
host?
transmission?

A
  • 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)
75
Q

PATHOTYPES OF GALLID
HERPESVIRUS 2

Name 4

A

MILD [MMDV]:
VIRULENT [VMDV]:
VERY VIRULENT [VVMDV]:
VERY VIRULENT PLUS [VV+MDV]:

76
Q

PATHOTYPES OF GALLID
HERPESVIRUS 2

MILD [MMDV]: describe

A

MILD [MMDV]:
* MOSTLY ASSOCIATED WITH NEURAL MD, PREVENTABLE WITH HVT (TURKEY
HERPESVIRUS VACCINE)
**give HVT and they will survive

77
Q

PATHOTYPES OF GALLID
HERPESVIRUS 2
VIRULENT [VMDV]: describe

A
  • HIGH INCIDENCE OF NEURAL AND VISCERAL LYMPHOMAS. PREVENTABLE
    WITH HVT.
    **give HVT and they will survive
78
Q

PATHOTYPES OF GALLID
HERPESVIRUS 2

VERY VIRULENT [VVMDV]: describe

A

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

79
Q

PATHOTYPES OF GALLID
HERPESVIRUS 2

VERY VIRULENT PLUS [VV+MDV]: describe

A

HIGH INCIDENCE OF NUERAL AND VISCERAL LYMPHOMAS. ARE ONCOGENIC
IN CHICKENS VACCINATED WITH BIVALENT VACCINES

**give bivalent vaccines and they will die

80
Q

GALLID
HERPESVIRUS 2
PATHOGENESIS
what are the 4 types of infection in order?

A
  1. PRODUCTIVE-RESTRICTIVE INFECTION
  2. NON-PRODUCTIVE INFECTION
  3. NON-PRODUCTIVE NEOPLASTIC
    TRANSFORMATION
  4. FULLY PRODUCTIVE INFECTION
81
Q

GALLID
HERPESVIRUS 2
PATHOGENESIS

PRODUCTIVE-RESTRICTIVE INFECTION

DESCRIBE

A
  • PRODUCTION OF NAKED VIRIONS (NON-
    INFECTIOUS) AND VIRAL ANTIGENS
  • CELL DEATH VIA LYSIS
  • IN B CELLS AND ACTIVATED T CELLS (CD4+)
  • IMMUNOSUPPRESSION
82
Q

GALLID
HERPESVIRUS 2
PATHOGENESIS

NON-PRODUCTIVE INFECTION

DESCRIBE

A
  • VIRAL GENOME PERSISTS IN CD4+
  • NO ANTIGENS ARE EXPRESSED
83
Q

GALLID
HERPESVIRUS 2
PATHOGENESIS

NON-PRODUCTIVE NEOPLASTIC
TRANSFORMATION

DESCRIBE

A
  • SOME LATENTLY INFECTED T CELLS UNDERGO
    NEOPLASTIC TRANSFORMATION
  • MATSA (MAREK’S DISEASE ASSOCIATED TUMOR
    SPECIFIC ANTIGEN) APPEARS IN TRANSFORMED T-cells
    **oncogenic
84
Q

GALLID
HERPESVIRUS 2
PATHOGENESIS

FULLY PRODUCTIVE INFECTION

A
  • 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

85
Q

GALLID
HERPESVIRUS 2
PATHOGENESIS

CHARACTERISTICS OF VIRUS?
LESIONS?

A
  • 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
86
Q

GALLID
HERPESVIRUS 2

WHAT 4 CLINICAL SIGNS?

A
  1. NEUROLYMPHOMATOSIS
  2. VISCERAL LYMPHAMATOSIS
  3. Ocular lymphomatosis
  4. Cutaneous lymphomatosis
87
Q

GALLID
HERPESVIRUS 2

NEUROLYMPHOMATOSIS: EXPLAIN

A

NEUROLYMPHOMATOSIS:
* ENLARGEMENT OF NERVE TRUNKS, LOSES
STRIATIONS, EDEMATOUS, GREY OR YELLOWISH
APPEARANCE
* LAMENESS, DROOPY WINGS, PARTIAL PARALYSIS OF
LEGS, LIMBERNECK, TORTICOLLIS, INCOORDINATION

88
Q

GALLID
HERPESVIRUS 2
VISCERAL LYMPHAMATOSIS: EXPLAIN

A
  • 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
89
Q

GALLID
HERPESVIRUS 2
Ocular lymphomatosis:
EXPLAIN

A
  • Graying of the iris of one or both eyes
  • Interference with normal pupilar
    constriction/dilation
  • Partial or total blindness
90
Q

GALLID
HERPESVIRUS 2
Cutaneous lymphomatosis: EXPLAIN

A
  • Plucking of feathers to reveal nodular
    lesions
  • Enlarged feather follicles
91
Q

VACCINATION OF MAREK’S
DISEASE

WHAT IS THE MOST WIDELY USED?
WHAT IS BIVALENT VACCINES?
WHAT IS THE MOST PROTECTIVE?

A
  • 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

Virology RUSVM (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions