Block 4 Midterm Viruses

Front 1

Characterize a Coronavirus.

Back 1

+RNA; shperical env. virions

3' nested set replication
+ strand makes RdRP, then makes negative strand; each strand has same promoter but each gets smaller in lenght.

Coronaviruses change periodically due to POINT MUTATIONS.

Front 2

What is the general epidemiology of a Coronavirus?

Back 2

Replicate in epithelial cells of the gut and resp. tract, make many copies of themselves, then go to the next animal through secretions of various kinds (resp./diarrhea)

Coronavirions are quite labile ; thus the virus is only infectious when taken in with large amounts of milk to neutralize the acidity of the stomach (which would normally kill this virus).

Front 3

Infectious Bronchitis Virus

Back 3

CORONAVIRUS (+RNA; Env)

CHICKENS- Resp. Dz; major risk is sec. bacterial infection

PATHOGENESIS- Virus decreases mucociliary clearance; causes mucosal thickening w/ serous or catarrhal exudates in air sacs, nasal pasages, trachea, & bronchi

CLINICAL SIGNS- YOUNG BIRDS- gasping, coughing, rales, nasal exudates, resp. distress, lethargy, inapp, sudden death.

DIAGNOSIS: Indirect Immunoflouresence of tracheal epithelium w/ antibodies specific for IBV.

VENTILATION!!!!!!!!

Front 4

Transmissable Gastroenteritis of SWINE

Back 4

CORONAVIRUS (+RNA; Env)

PATHOGENISIS: fecal/oral trans, virus attacks mature cells of gut and tips of villi, killing them. No ability of the gut to absorb fluid and DIARRHEA is result.

CLINICAL SIGNS:
EPIZOOTIC Dz- virus intro. to nonimmune herd. Rapid spread and severity is inversly correlated w/ age.
ENZOOTIC Dz- virus persists w/in an immmune or semiimmune herd. Diarrhea in young piglets; mortality is low.

DIAGNOSIS: Fluorescent antibody of jejunum; paired acute or convelescent serum to measure antibodies by serum neutralization.

Front 5

Porcine Hemagglutinating Encephalomyelitis

Back 5

CORONAVIRUS (+RNA; Env)

PIGS< 2wks old

PATHOGENESIS: Virus invades resp. and/or gut epithelium and migrates up the axons to sensory ganglia of the trigeminal and vagus nerves with spread to brain stem, cerebrum and cerebellum, causing cell death.

CLINICAL SIGNS- vomiting (due to neuro stim. of vomiting center); anorexia, depressed
CNS signs also--> paddline, hyperesthesia, tremors--> emaciation and death.

Disease resistance increases with age

Front 6

Bovine Coronavirus

Back 6

CORONAVIRUS (+RNA; Env)

CALVES< 2wks of age & is VERY COMMON; common cause of calf scours, second only to rotavirus

PATHOGENESIS: Dz manifestation dependent on maternal antibody within milk waning at a time of large amounts of virus getting ingested via oral/fecal route with large amounts of milk that protects the virus from digestion. REPLICATION IN VILLI kill the TIPS.

CLINICAL SIGNS: diarrhea 4-5 days, can lead to dehydration and shock (unusal)

Front 7

Winter Dysentery

Back 7

CORONAVIRUS (+RNA; Env)

Dz of ADULT DAIRY CATTLE; sporadic epidemic type Dz that causes BLOODY DIARRHEA with low mortality.

OTHER CLINICAL SIGNS: dec. milk prod.

Front 8

Canine Coronavirus

Back 8

CORONAVIRUS (+RNA; Env)

Dz mostly in PUPS, often in conj. w/ K9 Parvo.

PATHOGENESIS: Replication in tips of villi, can make PARVO worse

CLINICAL SIGNS: watery, short-lived diarrhea of little consequence

Front 9

Feline Infectious Peritonitis Virus

Back 9

CORONAVIRUS (+RNA; Env)

Manifestation of FIP requires 1. must arise w/in pop of FECV (feline enteric coronavirus) and 2. cat must repsond with a too vigorous TH2 response.
More common in catteries

PATHENOGENESIS: ABs to FIP can promote antigen/antibody complex entry into macrophages via the macrophage Fc receptor, increasing the likliehood that macrophages will become infecgted. (ANTIBODY-MEDIATED ENHANCEMENT) of infection.

PATHOLOGY- pyogranulomas histologically; cell-free fluid in peritoneum (Very viscous, yellow w/ high conc. of protein.)

CLINICAL SIGNS- persistent fever--> death; dyspnea from thoracic effusion; abdominal fluid wave; retinal pyogranulomas;

Front 10

Feline Enteric Coronavirus

Back 10

CORONAVIRUS (+RNA; Env)

Relatively common (40%)

PATHOGENESIS: causes mild diarrhea in kittens; can replicate in lymph nodes as well as in gut; epitheliotropic

Front 11

Name the 7 viruses in the CORONAVIRUS family

Back 11

Infectious Bronchitis Virus (RESP; CHICKENS)

Transmissable Gastroenteritis of Swine (ALIMENTARY; SWINE)

Porcine Hemagglutinating Encephalomyelitis (ALIMENTARY & NS; SWINE)

Bovine Coronavirus (ALIMENTARY; BOVINE (calves))

Winter Dysentery (ALIMENTARY; BOVINE)

Canine Coronavirus (ALIMENTARY; PUPS)

Feline Coronavirus (FIP; FECV) (ALIMENTARY; CATS)

Front 12

Name the 7 viruses in the PICORNAVIRUS family

Back 12

Foot and Mouth Disease (FMD) genus: aphthovirus (SYSTEMIC; SKIN LESIONS; CATTLE, PIGS, SHEEP)

Equine Rhinovirus (rhinitis) virus- genus: aphthovirus (RESP; Horses)

Swine Vesicular Disease- genus: enterovirus (SYSEMIC; LESIONS; PIGS)

Enterovirus encephalomyelitis of pigs- genus: enterovirus (NS; PIGS)

Avian Encephalomyelitis- genus: hepatovirus (NS; CHICKENS & TURKEYS)

Duck Hepatitis- genus: hepatovirus (NS; Aliementary; DUCKS)

Encephalomyocarditis virus infection (EMCV)- genus: Cardiovirus (NS; PIGS)

Front 13

Name the 4 viruses in the CALICIVIRUS family

Back 13

Vesicular Exanthema of Swine (VESV)- genus: vesivirus (NS; Alimentary; Lesions; PIGS)

San Miguel sea lion virus (SMSV)- genus: vesivirus (ABORTIONS; LESIONS; SEA LIONS)

Feline Calicivirus- genus: vesivirus (RESP; CATS)

Rabbit hemorrhagic disease= Rabbit Calicivirus disease- genus: Lagovirus (SYSTEMIC; NS; RABBITS)

Front 14

Name the 6 viruses in the FLAVIVIRIDAE family of the genera FLAVIVIRUS

Back 14

St. Louise Encephalitis Virus (NS; BIRDS; ZOONOTIC)

Wesselbron Disease (SYSTEMIC; ABORTIONS; SHEEP; ZOONOTIC)

West Nile Virus (NS; HORSES; ZOONOTIC)

Yellow Fever (NS; HUMANS & PRIMATES)

Tick Borne Encephalitis (NS; HORSES & Sm. Mammals)

Louping Ill (NS; Sheep)

Front 15

Name the 3 viruses in the FLAVIVIRIDAE family of the genera PESTIVIRUS

Back 15

Bovine viral Diarrhea (BVD & Mucosal Dz) (NS; ALIMENTARY; CATTLE)

Border Disease (NS; SHEEP & GOATS)

Hog Cholera (ALIMENTARY; NS; SYSTEMIC; PIGS)

Front 16

Name the disease in the TOGAVIRUS family

Back 16

WEE, VEE, EEE (NS; HORSES)

Front 17

Name the 4 RETROVIRUSES (not including lentiviruses)

Back 17

Avian Leukosis and Sarcoma: genus: alpharetrovirus (SYSTEMIC; LYMPHOID TUMORS; CHICKENS)

Ovine pulmonary adenomatosis-genus: betaretrovirus (RESP; SHEEP & GOATS)

Feline Leukemia and Sarcoma Virus- genus: gammaretrovirus (RESP; NS; LYMPHOID TUMORS; Cats)

Bovine Leukemia Virus- genus: deltaretrovirus (LYMPHOCYTIC LYMPHOCYTOSIS; BOVINE)

Front 18

Name the 5 LENTIVIRUSES of the FAMILY RETROVIRIDAE.

Back 18

Visna Maedi or Ovine Progressive Pneumonia (RESP; SHEEP)

Caprine Arthritis-Encephalomyelitis (NS; GOATS)

Equine Infectious Anemia (SYTEMIC; EQUINE)

Feline Immunodeficiency Virus (RESP; NS; CATS)

Bovine Immunodeficiency Virus (Sytemic; BOVINE)

Front 19

Foot and Mouth Disease Virus

Back 19

PICORNAVIRUS: genus- aphthovirus
(+RNA; non-Env)

Spreads rapidly by aerosol; highly contagious for all cloven-hoofed animals.

PATHOGENESIS- virus enters thru damaged oral epithelium or the tonsils--> spreads to regional lymph nodes--> bloodstream--> resulting viremia seeds secondary sites of replication in cornified epithelia of the skin, tongue and mouth. Vesicles develop and large amounts of virus are shed in the vesicular fluid when the vesicles rupture.

CATTLE- dec. milk prod.--> secondary mastitis; oral & hoof lesions are common

PIGS- lameness (severe hoof lesions); oral lesions are rare; death due to myocarditis can approach 100% and can precede any other signs

SHEEP & GOATS- (MAINTENANCE HOST); mild clinical signs; sudden-onset lameness may occur in a large proportion of the flock.

DIAGNOSIS- Clinical signs; virus isolation; serology; antigen detection; and serotype determination using ELISA.

VACCINES- use ring vax to reduce spread of virus; produced by growing the virus in BHK cells, and then inactivating it.

REPORTABLE DISEASE

Front 20

Equine Rhinovirus (rhinitis) virus infection

Back 20

PICORNAVIRUS- genus: aphthovirus
(+RNA; non-Env)

HORSES- mild upper respiratory tract infection (little clinical significance)

Front 21

Swine Vesicular Disease

Back 21

PICORNAVIRUS: genus- enterovirus
(+RNA; non-Env)

(Looks like FMD)
SWINE- fever, lameness w/ vesicles on coronary band; lesions may be found on snout, lips and tongue

DIAGNOSIS: main goal is to distinguish from FMD; RT-PCR, ELISA for antigens, immunofluorescent staining, and virus isolation in tissue-cultured cells

Front 22

Enterovirus Encephalomyelitis of Pigs

Back 22

PICORNAVIRUS: genus- enterovirus
(+RNA; non-Env)

PIGS- Neuro Dz; TESCHEN Dz (REPORTABLE DZ); FAD, ataxia--> total paralysis, tremors, painful skin hypersensitivity, convulsions, coma, and death 3-4 days after signs appear. High mortality and morbidity.

DIAGNOSIS: Histo Diagnosis- typical lesions in CNS are inflammatory with perivascular lymphocyte infiltration in the gray matter.; Virus neutralization and other serologic tests can be used to identify serotypes. RT-PCR.

Front 23

Avian Encephalomyelitis (Epidemic Tremor)

Back 23

PICORNAVIRUS: genus- hepatovirus
(+RNA; non-Env)

CHICKENS & TURKEYS- (young birds 1-21 days) Infected adult birds may show drop in egg prod.; chicks show proggressive ataxia; falls to the side--> paralysis and death

DIAGNOSIS: Clinical signs; immunofluorescence detection of virus; virus can be isolated in cell culture or following innoculation into chick embryos. (important differential is Newcastle Dz)

Front 24

Duck Hepatitis

Back 24

PICORNAVIRUS: genus- hepatovirus
(+RNA; non-Env)

DUCKS- similar to avian encephalomyelitis; can cause acute dz in ducks less than 21 days of age; high mortality; ataxia, spasmodic paddling of feet, and sometimes diarrhea

POST-MORTEM- liver is enlarged, edematous, and evidence of hemmorhage

Histologically: hepatic necrosis, inflammatory cell infiltration and proliferation of bile duct epithelium and encephalitis

Front 25

Encephalomyocarditis virus infection (EMCV)

Back 25

PICORNAVIRUS: genus- cardiovirus

Natural hosts are rodents (high levels of virus where there are high levels of rodent infestation)

PIGS- acute onset with sudden deaths due to myocardial failure in pre-weaning pigs. Less dramatic signs--> anorexia, listlessness, trembling, staggering, paralysis, dyspnea. Younger pigs are more susceptible and mortalitiy can reach 100% in unweaned animals. PWpigs usually sub-clinical. Infected preg. sows may have near-term abortions and low farrowing rates.

Oral transmission through rodent feces.

Front 26

Calicivirus Characteristics?

Back 26

+RNA, non-Env, 2 genera (Vesivirus & Lagovirus)

icosahedral virion; relatively resistant to heat and detergents, but sensitive to pH below 4.

In general calicivirus tend to be environmentally stable, highly variable genetically and antigenically, and highly contagious.

Front 27

Vesicular Exanthema of Swine

Back 27

CALICIVIRUS: genus- vesivirus
(+RNA; non-Env)

ERADICATED FROM US; originated from san miguel sea lion virus

PIGS- acute febrile illness w/ vesicular lesions on snout, tongue, teats, and feet (b/w claws, and in coronary band); also may cause encephalitis, myocarditis, fever, diarrhea, and pregnant sows may abort. High morbidity, low mortalitiy.

(NOT TO BE CONFUSED with FMD)

Front 28

San Miguel Sea Lion Virus

Back 28

CALICIVIRUS: genus- vesisvirus
(+RNA; non-Env)

SEALS, SEA LIONS, WALRUSES- SEA LIONS- abortions and vesicles on flippers

Front 29

Feline Calicivirus

Back 29

CALICIVIRUS: genus- vesivirus
(+RNA, non-Env)

CATS- RESPIRATORY DISEASE w/ conjunctivitis, vesiculation, and ulceration of the oral epithelium; (rarely- interstitial pneumonia, chronic stomatitis and a "limping" or polyarthritis syndrome.
FCV can cause severe VIRULENT SYSTEMIC DISEASE (VSD)- high fever, facial and limb edema, ulceration, and focal hair loss around face and mouth, ulceration and sloughing of footpads and jaundice.

PATHOGENESIS: natural trans by aerosol and fomites; highly contagious and readily spread on clothing. OrAL ULCERATIONS MOST COMMON

DIAGNOSIS: primarily clinical signs; virus is readily isolated in cell culture and identified by immunofluorescence.

VAX, QUARANTINE, HYGIENE!

Front 30

Rabbit Hemorrhagic Disease

Back 30

CALICIVIRUS: genus- lagovirus
(+RNA; non-Env)
NOTIFIABLE DISEASE!

RABBITS- peracute, causes hepatitis, intestinal and lymphoid necrosis that leads to DIC and death.

TRANSMISSION- highly contagious, direct contact w/ infected rabbits and fomites such as cages, feeders and clothing. Rabbits are infected orally, nasally, or conjunctivally

PATHOGENESIS: (only in rabbits older than 40-50 days of age); damages liver, intestines, and lymphatic tissue and causes terminal massive blood clots; virus has a tropism for hepatocytes, where it replicates in the cytoplasm.

DIAGNOSIS: clinical finding, peracute nature of disease, and post-mortem findings. Hemagglutination tests, PCR and negative stain EM can be done on virus recovered from the liver, blood and spleen of infected animals. Antibodies can be detected in convalescing rabbits using hemagglutination-inhibition assays or ELISA.

Front 31

Flaviviridae Family Characteristics?

Back 31

2 Genera of Veterinary Importance: Flavivirus and Pestivirus

+RNA; ENV; Spherical virion;

Virus not stable in environment, can survive in meat allowing the spread of virus in products from infected animals.

Many members of the flavivirus genera replicate in INSECTS as well as their vertebrate hosts.

Front 32

St. Louis Encephalitis

Back 32

FLAVIRIDAE- genus: flavivirus
+RNA; ENV

PASSERINE BIRDS- mosquito-bird-mosquito cycle; may emerge in epidemics and cause significant HUMAN Dz

ZOONOTIC

Front 33

Wesselbron Disease

Back 33

FLAVIVIRIDAE- genus: Flavivirus

SHEEP- subsaharan african; Fever, Jaundice, Sub-cutaneous edema; Abortions

ZOONOTIC- febrile disease w/ mylagia and arthralgia

Front 34

West Nile Virus

Back 34

FLAVIVIRIDAE: genus- flavivirus

HORSES- Mosquito transmitted, maintained in birds. Nervous System signs and Death.

DIAGNOSIS: FA in infected tissues; serology (paired samples or IgM detection), virus isolation, or CSF; RT-PCR, FA, and immunohistochemistry are also standard methods for detecting the infection.

Front 35

Tick Borne Encephalitits

Back 35

FLAVIVIRIDAE: genus- flavivirus
(+RNA; ENV)

Small mammals- maintain virus and replicate in ticks

ZOONOTIC

Front 36

Louping Ill

Back 36

FLAVIVIRIDAE: genus- flavivirus
(+RNA; ENV)

SHEEP- tick-borne dz in sheep; encephalomyelitis in UK & Spain & Portugal; prolonged viremia and biphasic febrile response, 2nd stage assoc. w/ cerebellar ataxia, tremors, hyperexcitability, and paralysis

ZOONOTIC

Front 37

Bovine Viral Diarrhea

Back 37

FLAVIVIRIDAE- genus: Pestivirus
(+RNA, ENV)

2 Dz forms:
-milder acute dz in older animals
- severe disease (MUCOSAL Dz) resulting after fetal infection when there is a breakdown of TOLERANCE. Due to postnatal infection in nonpregnant cattle and fetal infection in pregnant cattle leading to chronic persistent infection in calves leading to mucosal disease.

POSTNATAL INFECTION IN NONPREGNANT CATTLE- fever, leukopenia, some animals develop diarrhea, nasal or ocular discharge and erosive stomatitis, dec. in milk prod.

INFECTION IN PREGNANT CATTLE- fetal death or low birth weight; congenital defects in the eye and CNS (cerebellar hypoplasia or cavitation of the cerebellum)

MUCOSAL Dz- Fever, anorexia, profuse watery diarrhea, nasal discharge, erosive or ulcerative stomatitis, dehydration; emaciation and death.

PATHOGENESIS: normally- ulcers in mouth--> esophagus, forestomachs, abomasums, and intestine (hyperemia & hemmorhage may occur)

DIAGNOSIS: clinical hx; herd hx, pathological lesions (oral); viral isolation; FA; RT-PCR.

Front 38

Border Dz

Back 38

FLAVIVIRIDAE- genus: pestivirus
(+RNA; ENV)

SHEEP and GOATS- congenital dz in lambs, with low birth weight, and poor viability; hairy coat and tremors "HAIRY SHAKERS"

PATHOGENESIS: Adults- sub-clinical; pregnant ewes- dead, deformed or mummified lambs. Neuro signs due to defective myelination of nerve fibers in CNS.

Front 39

Hog Cholera (Classical Swine Fever)

Back 39

FLAVIVIRIDAE; genus- pestivirus
(+RNA, ENV)

Eradicated in USA, CANADA etc.

SWINE- acute infection with high fever, anorexia, conjunctivitis, followed by vomiting, diarrhea, bacterial pneumonia, and NS dysfunction--> paresis, paralysis, lethargy, tremors; young pigs may die peracutely

PATHOGENESIS: Oronasal route; replication in tonsils, secondary replication in other lymphoid organs and endothelial cells. Hemorrhages, leukopenia, and thrombocytopenia. DIC/ Encephalitis.

DIAGNOSIS: FA staining or immunohistochemistry; RT-PCR. Serologic methods to detect virus infection- SNT, ELISA.

Front 40

Togavirus Family Characteristics?

Back 40

+RNA; ENV; Spherical virion

WEE, VEE, EEE

Replicateds in mammalian cells causing cytopathic effects, and also in insect cells where they cause little cytopathic effects.

Front 41

Western, Venezualan, Eastern Equine Encephalitis Viruses

Back 41

TOGAVIRUS- genus: alphavirus
(+RNA; ENV)

HORSES: infections may be subclinical or present with FAD--> Neurological signs- wide stance, hanging head, flaccid lips, irregular gait and encephalitis (impaired vision, photophobia, inability to swallow, circling)--> paralysis and convulsions in terminal stages.

PATHOGENESIS: Mosquito bite gives virus replication to local lymphoid tissues, and then spread to more distant tissues. Replication is in muscle, connective tissue, and reticuloendothelial cells. Widespread neuronal necrosis, mononuclear cell infiltration and interstitial edema.

DIAGNOSIS: Serology- IgM capture ELISA detects recent infections; virus isolation into suckling mice, also tissue culture, RT-PCR, FA or immunohistochemistry.

ZOONOTIC

Front 42

Briefly characterize Retroviruses.

Back 42

ssRNA; ENV;
2 types of Retrovirus genomes:
-SIMPLE (gag, pol and env)
-COMPLEX (gag, pol, env, and "accessory genes")

REPLICATION- use viral integrase and reverse transcriptase that transforms the genome into dsDNA from 2 RNA strands

**Retroviruses are often ONCOGENIC**
1. integration of provirus upstream of an oncogene; viral long terminal repeat or LTR causes upregulation of oncogene
2. defective retroviruses arise that cannot replicate but have picked up an oncogene from the host cell
3. retroviral genomes integrate in, or carry a viral gene that interferes with, cellular genes that control host cell transcription

Front 43

Avian Leukosis and Sarcoma

Back 43

SIMPLE RETROVIRUS
ENV; ssRNA

CHICKENS- lymphoid tumors; anemias or leukemias

PATHOGENESIS: have to get infected w/ exogenous virus after 5-6 days of birth, only rarely develop leukemia, still produce neutralizing antibody though; some become latent or tolerant to virus SHEDDING HORIZONTALLY TO THE FLOCK.

Front 44

Ovine Pulmonary Adenomatosis

Back 44

SIMPLE RETROVIRUS
ENV; ssRNA

SHEEP- onset slow and insidious; can't keep up with the flock; bouts of coughing, production of large amounts of viscous fluid from resp tract; fluids leads to blockage of airways, anoxia and bacterial pneumonia.

PATHOGENESIS: virus shed in saliva & resp secretions (INCUBATION IS 1-3 YEARS!)

Front 45

Feline Leukemia Virus

Back 45

SIMPLE RETROVIRUS
ENV; ssRNA

CATS- 1. immunosuppressive- ginivitis, chronic stomatitis, stunting, failure to thrive, recurrent infections including subcutaneous abcesses, nonhealing skin lesions, and high susceptibility to FIP.
2. Immunopathologic- high levels of viremia and nonneutralizing antibody combine to form immune complexes in the blood which lead to glomerulonephritis.
3. FELINE LYMPHOSARCOMAS- MOST COMMON NATURALLY OCCURING LYMPHOSARCOMA IN ANY MAMMAL
4. Feline myeloproliferative diseases and anemia- tumors of granulocyte and erythrocyte precursors, and fibroblasts--> anemia and immunosuppression

RESP. DISTRESS

TRANSMISSION- FIGHTING, mutual grooming

PATHOGENESIS- viral replication in oral-associated lymphoid tissue and epithelium (during this time animal with test positive on ELISA, but negative on the HARDY TEST, an indirect immunofluorescence antibody test designed to detect viral GAG-encoded antigen in lymphocytes w/in blood smears.) Approx. 2/3rds of cats will then self-cure & plasma becomes antigen negative; lifelong protection after that.

IF HARDY TEST is POSITIVE--> viremic--> contain viral antigen in lymphoid precursors in the bone marrow; EVENTUALLY WILL DIE of their persistent infection, either through immunosuppresive effects or tumors induced by the virus

Front 46

Bovine Leukemia Virus

Back 46

SIMPLE RETROVIRUS
ENV; ssRNA

CATTLE- mostly assymptomatic; usually ONLY SIGN is persistent B lymphocytic lymphocytosis; animals that develop other signs (4-8 yrs.)--> lymphoid tumors in lymph nodes, spleen, abomasums, heart, uterus, kidneys, meninges, brains.

TRANSMISSION- blood to blood; usually iatrogenic (rectals/ injections)

Front 47

Characterize Lentiviruses.

Back 47

COMPLEX RETROVIRUSES
Accessory genes include: tat- encoding a TRANSACTIVATOR works to prevent (ANTI) premature TERMINATION of transcription by cellular RNA polymerase
vif-involved in INITIATION of INFECTION
rev- allows cytoplasmic export of viral RNAs that are not completely spliced (such RNAs encoding the structural proteins in gag and env.)
vpu- promotes viral budding
nef- mediates phosphorylation of CD4, causing its endocytosis and degradation

VIRUS TRANSMISSION is EXCEEDINGLY INEFFICIENT but when an animal is infected they are INFECTED FOR LIFE. In any single animal, various genomes arise from mutation and are propagated giving rise to QUASISPECIES (or closely related strains). In this virus population some individuals are more fit than others to infect different cell types and to escape from the immune system.

Front 48

Visna Maedi or Ovine Progressive Pneumonia

Back 48

LENTIVIRUS- COMPLEX RETROVIRUS
ENV; ssRNA
Visna- wasting
Maedi- dyspnea

SHEEP- slow onset (2-8 yrs); disease is rare in sheep less than 3 yrs. of age; exercise intolerance; animal lag behind the flock (like pulmonary adenomatosis) eventually showing dyspnea, which is progressive over 3-8 months and can be severe, with animals lying down to breath before death ensues. Animals die quicker if PREGNANT or if coinfected with Pasteurella multocida or M. haemolytica, or STRESSED by bad weather, shipping or poor nutrition.

PATHOGENESIS- virus establishes a cell-associated viremia; disease progresses despite robust production of neutralizing antibodies, cell mediated immunity and interferon production

PATHOLOGY: marked consolidation of lungs; bronchial and mediastinal lymph nodes are greatly enlarged; hyperplasia of alveolar septae and mononuclear inflammatory cell infiltrate; major feature is demyelinating leukocephalomyelitis which is at least partially responsive to immunosuppresive therapy

Front 49

Caprine Arthritis- Encephalomyelitis

Back 49

LENTIVIRUS- COMPLEX RETROVIRUS
ENV; ssRNA

GOATS- 2 syndomes:
1. CNS w/ onset in young goats (2-4 mos); starts w/ clumsiness--> asc. paralysis; animals remain bright and alert, then paddling, paralysis and death.
2. ARTHRITIC (more common)- in goats over 1 year of age- lameness.. usually slowly progressive over months to years exacerbated by cold weather; joints are swollen and painful, esp. the carpi; tendon sheaths and joint capsules become thickened and spaces become distended w/ fluid--> proliferative synovitis and synovial cell hyperplasia w/ monocytic inflamm. infiltrate including lymphocytes, plasma cells and macrophages.

Front 50

Equine Infectious Anemia

Back 50

LENTIVIRUS- COMPLEX RETROVIRUS
ENV; ssRNA

HORSES- Fever, weakness, severe anemia, jaundice, blood stained feces, tachypnea, and petechial hemorrhage of the mucosae; many cases FATAL; some can get bouts of RECURRENT EPISODES OF Dz (anemia/fever)

TRANSMISSION: Blood to blood (biting arthropods/ iatrogenic)

PATHOGENESIS: All horses, whether or not they show clinical signs of disease, have a LIFELONG cell-associated viremia w/ peripheral blood mononuclear cells. Bulk of virus production seems to come from persistently infected mature macrophages in the spleen, lymph nodes, liver, kidney, lung, and adrenal gland; RECURRENT disease and CHRONIC disease are assoc. with constantly changing strains w/ different antigenic profiles (LTR changes which is the promoter of the virus)

DIAGNOSIS: COGGINS TEST (cornell)- agar gel immunodiffusion test- detects antibody to the virus.

Front 51

Feline Immunodeficiency Virus

Back 51

LENTIVIRUS- COMPLEX RETROVIRUS
ENV; ssRNA

CATS- gingivitis, poor coat condition, slow progressive weight loss, persistent fever, anemia, chronic skin infections/ URI's. Some queens will abort. 5% suffere from CNS dz including encephalitis (mental deterioration) and seizures.

PATHOGENESIS: INFECTION THRU BITES, Acutely infected queens will shed virus in milk and kittens can get it that way. Following infection virus infects CD4+Tcells in regional lymph nodes--> T cell associated viremia and results in generalized enlargement of lymph nodes; cell associated viremia in CD4+ T cells persists for YEARS, and eventually signs of immunodeficiency develop. (NO CLEARING OF VIRUS)

DIAGNOSIS: ELISA (Ab snap tests)-very high false positive fate; WESTERN BLOT more specific & accurate; also problem of kittens testing positive for antibody because of maternal antibodies, it should be taken into account that antibodies are detectable only 8-12 weeks after infection, so any tests done in the interim may be negative in an infected animal.

Front 52

Bovine Immunodeficiency Virus

Back 52

LENTIVIRUS- COMPLEX RETROVIRUS
ENV; ssRNA

CATTLE- no clinical signs; brief lymphopenia

Front 53

Jembrana Disease

Back 53

LENTIVIRUS- COMPLEX RETROVIRUS
ENV; ssRNA

CATTLE (BALI)- FAST INFECTING!!! High morbidity and high mortality: fever, lethargy, panleukopenia, and lymphadenopathy occur w/in 5-12 days after infection; 17% of cattle die acutely

POSTMORTEM- widespread hemorrhage, lymphadenopathy and splenomegaly

Front 54

Characterize Pox viruses.

Back 54

dsDNA; only DNA that replicates in CYTOPLASM

2 types of infectious VIRIONS:
1. virion that lacks an external envelope but contains a surface membrane and exits when cells blow apart
2. enveloped version that buds out of cells (this version plays the more important role in spread through lesions in the animal, and infection in general seems to be more efficient with THIS TYPE!

LARGE VIRAL GENOMES

IMMUNE EVASION: have extra coding capacity of their genomes to encode a number of proteins that modulate the host response and thereby contribute to viral survival (inhibit inflammation by blocking complement), and toll like receptor analogs that cannot signal properly.

USE AS RECOMBINANT VACCINES- used as vectors to deliver other vaccines to animals; a gene of another pathogen shown to provide protective immunity is inserted by direct recombination into the poxvirus genome. (FeLV)

Front 55

Vaccinia virus infection of CATTLE.

Back 55

ORTHOPOXVIRUS of POXVIRIDAE family
dsDNA, nonenv?, replicate in CYTOPLASM

CATTLE- papular lesions--> vesicles, break and then scab over; somewhat painful; problem when on teats making them difficult to milk

Spread by contamination of milking machines, personnel or other fomites.

Front 56

Cowpox

Back 56

ORTHOPOXVIRUS of family POXVIRIDAE
dsDNA; nonenv?; replicates in CYTOPLASM

Natural pathogen of rodents but caused outbreaks of wildlife in zoo, large felids, elephants, okapis, anteaters and rhinos

CATS- single lesion, then general rash; the erythematous macules develop into vesicles that ulcerate and scab over.

CHEETAHS rarely survive and virtually always die of pneumonia.

Front 57

Capripoxvirus (Lumpy Skin Dz)

Back 57

ORTHOPOXVIRUS of family POXVIRIdAE
dsDNA; nonenv?; replicates in CYTOPLASM

CATTLE- lumps throughout skin; limbs are edematous and usually lymphadenopathy and lymphadenitis

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Ovine Range Fever (ORF)

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PARAPOXVIRUS of the family POXVIRIDAE
dsDNA; nonenv?; replicates in the CYTOPLASM

SHEEP- virus present WW; does not enter skin but enters exposed living layers of the skin that have been made available by friction or microtrauma. Virus contaminates feed bunks, and feed and fomites of all kinds, including wheat and stubble. Virus infects living layers of the skin and replicates, causing cell death and local inflammation. Lesions progress from papules to pustules--> break and scab over; scabs falling off animals contain large amounts of infectious virus as do secretions from the lesions.
Dz not dangerous unless the pain induced by the lesion interferes with feeding.
NEVER VAX an ORF-free herd.

ZOONOTIC- MOST COMMON ANIMAL Dz infecting Animal handlers.

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Bovine papular stomatitis

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PARAPOXVIRUS of the family POXVIRIDAE
dsDNA; nonenv?; replicates in the CYTOPLASM

CATTLE (less than 2 yrs): Lesions margin of lips, muzzle, and buccal mucosa and consist of erosions that heal in a couple weeks

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Swine Pox

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SUIPOXVIRUS of the family POXVIRIDAE

Trans- louse Haematopinus suis and fomites; After inoculation by the bite of a louse or contact through other fomites, lesions develop and progress like ORF lesions, vesicles more common in pigs because the stratum corneum is THICKER. Lesions most common on lower abdomen.
SWINE

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Myxomatosis

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SYSTEMIC POXVIRUS
dsDNA; env; replicates in CYTOPLASM

RABBITS- trans by bites of insects that transmit the virus mechanically; severe local infection, leading to primary viremia; virus in lymphocytes--> circulates to regional lymph nodes and replicates there. Then 2nd viremia which seeds most of the lymph organs of the rabbit incl. spleen, all LNs and thymus. ANOGENITAL EDEMA, SEVERE CONJUNCTIVITIS and SRS (sick rabbit syndrom) ensue. Rabbit dies in 4-14 days, depending on the strain.

NATURAL HOSTS- Sylvagus rabbits of N & S americas; 2 strains:
1. brazilian strain--> natural host S. basiliensis, the tropical forest rabbit
2. Californian strain--> natrual host S. bachmani, California bush rabbit
These strains produce long lasting fibromas in their natural hosts; virus is maintained in their pop by insect bites of the lesions and mech. trans.

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Ectromelia

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SYSTEMIC POXVIRUS
dsDNA; env; replicates in CYTOPLASM

MICE- high mortalitiy
WW. due to shipment of infected lab mice; virus causes primary lesion in skin (prolly introduced by direct contact by infected material, handlers or animals); virus then becomes viremic and enters the liver and spleen where it replicates to a high titer. There is extensive necrosis of the liver and spleen;

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GOATPOX

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SYSTEMIC POXVIRUS; genus- capripoxvirus
dsDNA; env; replicates in CYTOPLASM

PATHOGENESIS: spread thru resp. droplets, mechanical trans by stable flies and fomites. Shed scabs contain high titers of infectious virus which maintain the virus in the environment.

CLINICAL SIGNS IN SHEEP AND GOATS- fever, arched back, mucous discharge from the nose, followed by generalized rash--> scaby lesions; Mortality can occur before or after the rash develops. Lesions may include marked lymph node enlargement, due to lymphoid cell hyperplasia, edema and congestion. May be lesions on the MM of the eyes, mouth, nose, pharynx, epiglottis, trachea, and on the rumenal and abomasal mucosae. Lung may contain pox lesions which are focal or uniformly distributed with assoc. edema, necrosis, and atelectasis.

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FOWLPOX

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SYSTEMIC POXVIRUS genus: avipoxvirus
dsDNA; env; replicates in the CYTOPLASM

Proliferative disesase of DOMESTIC AND WILD BIRDS- proliferative lesions on the featherless areas of the face (skin of the comb, wattle, corners of the eyes, nostrils, and in front of the beak); lesions often become necrotic and ulcerate, at which time they are called CANKERS.

In DIPHTHERIC form- cells in MM are infected and sloughed necrotic material forms a pseudo-membrane in the mouth and trachea. Can lead to RESP signs (open mouth breathing, gasping, coughing) and ASPHYXIATION. Anorexia and systemic sings (depression, sick bird syndrome) often precede MORTALITY

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Asfarviridae- AFRICAN SWINE FEVER VIRUS

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dsDNA; transcribes its own RNAs in the cytoplasm thru a virally encoded DNAdRNAp; however, it REQUIRES THE CELL NUCLEUS to replicate DNA; NON-ENV?

not in US

Virus spreads in 2 separate cycles:
Sylvatic--> virus produces a viremia in young warthogs and ticks become infected when they are feeding on them; viremia is more common in young animals and they are the major source of virus for spread; warthogs don't get sick (or spread virus)
DOMESTIC CYCLE- domestic pigs become infected by direct contact with infected material, virus present on fomites, coughed virus in droplets, or consumed in uncooked garbage fed to pigs

PATHOGENESIS: virus infects cells like lymphocytes and neutrophils which disseminate the virus throughout the body; virus can also attach to erythrocytes, leading to their destruction

CLINICAL SIGNS- many found dead; high fever, abortion, resp. signs (includ. dyspnea w/ hemmorhage from the nose), reddish dicoloration on the skin of the snout, ears, fetlocks and flanks, bloody feces, bloody diarrhea, weakness and incoordination. Closely resembles HOG CHOLERA. HIGH MORTALITY

REPORTABLE Dz in US

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ARTERIVIRIDAE

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+RNA; ENV; replication stragy like CORONAVIRUS (nested set replication; smaller virions and genomes)

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Equine Viral Arteritis

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ARTERIVIRUS (+RNA; ENV; nested set replication)

EQUINE- mainly on breeding farms, and seen as infections of fetuses and pregnant mares; Marked fever, leukopenia, depression, urticaria ('hives') of the head, neck and trunk, and edema particularly near the eyes and abdomen as well as the hind limbs often resulting in a stiff gait. Most horses recover, although death may result from interstitial pneumonia and intestinal necrosis; pregnant mares can abort 10-30 days after infection.

PATHOGENESIS: initially infects alveolar macrophages, then spreads to bronchial LNs. Spreads through the body, and is found in almost all tissues.
Vascular damage results in edema, congestion, and hemorrhage in many tisues. Terminal stage disease is characterized by infarctions in intestine, lung and spleen, and fluid accumulation in many body cavities. Aborted fetuses: mild edema, excess fluid in abdominal and pleural cavities, and petechial hemorrhages in peritoneal and pleural mucosal surfaces.
Acutely infected stallions shed virus continuously in semen and long term shedding is seen in some horses. Virus is found in ACCESSORY GLANDS AND VAS DEFERENS. Recovered horses are protected for LIFE against re-infection.

ABORTION STORMS!!
Trans via resp, sexual and transplacental routes

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Porcine Respiratory and Reproductive Syndrome virus (PRRSV)

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ARTERIVIRUS (+RNA; ENV; nested set replication)

PIGS- anorexia, fever, cyanosis of ears, snout, and abortion of piglets late in gestation; premature births, stillbirths and mummifications may all be observed

PATHOGENESIS: viremia can persist for several weeks and virus spreads widely w/in the pgis; virus replicates in mucosal and resp. tract macrophages, then spreads to local lymph nodes--> systemic viremia and infection of macrophages and monocytes in many tissues. There may be antibody-mediated enhancement of infection, where the initial immune response enhances the disease developed. After the immune response develops, pigs are protected from re-infection.

Some pigs may persistently shed the virus in the presence of neutralizing antibodies.

Spread--> contact, sexual and airborne; can be spread thru contaminated needles; virus can be shed in SEMEn for long periods in some boars.

DIAGNOSIS: serology (taking paired samples and looking for increased titers), RT-PCR, virus isolation, immunohistochemistry.