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EPI MT 2 DECK 1 > EPI MT 2 DECK 1 > Flashcards

EPI MT 2 DECK 1 Flashcards

1
Q

African Swine Fever virus family?

A

Asfarviridae, Asfivirus

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2
Q

Vectors of ASF?

A

Biological vectors, can replicate in all stages of life. Present in Ornithodorus

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3
Q

ASF resistance?

A

HIGH. Can survive in the environment for 100-200 days. Years long in freezer. 3-7 months in the soil.

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4
Q

Pathogenesis of African Swine Fever?

A
  • Infection Per os or tick bite.
  • Shedding in saliva , nasal discharge 48hrs before clinical symptoms.
  • Primary replication in tonsils, lymph nodes.
  • Viraemia for months
  • Replication in monocytes, macrophages, hepatocytes, tubular epithelial, granulocytes.
  • NOT lymphocytes
  • Virus releases proteins causing immunosuppression.
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5
Q

Clinical Signs of African Swine Fever?

A
  • Fever, transient anorexia, abortion on ALL variants.

- Haemorrhages on the skin with necrotic areas and nasal discharges.

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6
Q

Pathology of African Swine Fever?

A
  • Acute: Petechial Haemorrhages, Pulmonary Oedema
  • Chronic: Spleen, Lymphoid Hyperplasia, Fibrin fluid rich. Chronic in wild boar.
  • LOW virulence: Multifocal skin necrosis, swelling of carpal and tarsal joints.
  • Blood and Haemorrhages everywhere. Black, bloody lymph nodes.
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7
Q

Teschovirus Encephalomyelitis Virus genera?

A

Picornaviridae

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8
Q

Properties of Teschovirus Encephalomyelitis?

A
  • Non-enveloped, +ssRNA
  • PH 3-9
  • 13 different serotypes
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9
Q

African Swine Fever properties?

A
  • Linear dsDNA
  • 1 Serotype, Many Genotypes
  • Virulence variants High.
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10
Q

Teschovirus Epidemiology?

A
  • Only Pigs are susceptible
  • Teschen: all group ages
  • Talfan: Below 4 months of age
  • Spreading with faeces for 7-8 weeks
  • Resistant in for 3 weeks
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11
Q

Teschovirus Pathogenesis?

A
  • Infection PO, nose, olfactory nerves–> CNS
    1. ) Enteral Phase: GI epithelium –> Primary replication in lymphoid tissue. Asymptomatic infection frequent.
    2. )Viraemia: Depression, anorexia
    3. ) Neural Phase: Secondary replication. Encephalomyelitis.
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12
Q

Teschen clincal signs?

A
  • Incubation 1-3weeks.
  • Mild fever, anorexia
  • Piglet, grower phase–> Vomiting, ataxia, convulsions, flaccid paralysis, respiratory, paralysis, Hyperaesthesia.
  • Flaccid Paralysis of HL.
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13
Q

Talfan clinical signs?

A
  • Piglets below 4 months of age.
  • Ataxia, paralysis of HL
  • Recover, ataxia can remain
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14
Q

Swine Vesicular Disease Properties?

A
  • Enterovirus
  • One Serotype
  • Good resistance ( faeces, meat)
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15
Q

Swine Vesicular Disease Epidemiolgy?

A
  • Spreading: direct contact( discharges, faeces)
  • Shedding the virus: lasts for 4 months.
  • Asymptomatic carriers also shed.
  • Indirect infection- Human can transmit.
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16
Q

Swine Vesicular Disease Pathogenesis?

A
  • Infection PO–> Throat, gut. Epitheliotrop.
  • Viraemia : Epithelial cells of mouth, snouts, teats, legs: vesicles.
  • CNS: Rare or Asymptomatic.
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17
Q

SVD Clinical signs?

A 
o Incubation time: 2-7 days
o Fever: 1-2 days (41oC)
o Vesicles: nose (snout), oral MM, legs
(damaged horn production), vesicles will
be ruptured w/in 1-2 days
o Lack of appetite, limping
o Fast recovery
o Frequently asymptomatic
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18
Q

SVD caused by Senecavirus?

A
  • Clinical signs: Suckling piglets general Fever, depression, Diarrhea. Growers, fatteners: Vesicles on the legs.
  • PATHO: Piglet Inflammation of the oral mucosa, interstitial pneumonia, encephalitis. Adults do not die.
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19
Q

Vesicular Exanthema of Swine cause?

A

Caliciviridae, Vesivirus

20
Q

Vesicular Exanthema Patho n Clinical signs?

A
  • EPI: primary infection–> raw meat of sea mammals.
  • Shedding: with saliva and excretions
  • Survives for at least 2 weeks in the environment. Good resistance.
  • Less contagious than FMD, doesn’t replicate as fast.
  • CLINICAL SIGNS: 1-4 days of incubation. Skin lesions, anorexia, fever, depression, vesicles, lameness due to vesicles on the feet
21
Q

Avian Encephalomyelitis Virus? Properties?

A
  • Tremovirus
  • High Resistance
  • One Serotype
  • Good Antigen, Widespread seropositivity–> Clinical signs rare.
22
Q

Avian Encephalomyelitis Epidemiology?

A
  • Chicken and Pheasant are susceptible.
  • All age groups are susceptible.
  • Maternal protection 3-6weeks.
  • Clinical signs: 1-2weeks up to 4-5weeks old.
  • Spread: germinative–>infected eggs for 3weeks, faeces.
  • Morbidity: 50-60%, Lethality high.
23
Q

Avian Encephalomyelitis Pathogenesis?

A
  • Per os, mucous membrane of the gut.
  • Viraemia–> Pancreas, Liver, kidney, ovarium( does not kill embryo).
  • CNS: inflammation, necrosis.
  • Good immunity, maternal protection
24
Q

Avian Encephalomyelitis Clinical Signs?

A
  • Incubation 1-11 days
  • Nervous signs: ataxia, tremor, paralysis
  • Older animals: subclinical
  • Egg production drops
25
Q

Duck Viral Hepatitis Virus? Properties?

A
  • DVH Type 1: Duck Hepatitis A Virus Type 1
  • Genus: Avihepatovirus
  • 3 Genotypes: Genotype 1–>Highly pathogenic. Genotype 2+3–>Less Pathogenic( now astrovirus).
  • Duck Hepatitis B virus: Hepadnavirus circular dsDNA, enveloped.
  • Highly resistant: survives in bedding for 10 weeks.
26
Q

Duck Viral Hepatitis Epidemiology?

A
  • Shed in faeces for several weeks.
  • Infection: Per os, Tracheal discharge, no germinative infection.
  • Fast spreading within the flock.
  • Day-old duckling–>Explosive, 90% mortality.
  • Clinical signs in young ducklings (0-4weeks)
  • Mycotoxins, complications can make more severe.
27
Q

Duck Viral Hepatitis Pathogenesis?

A
  • Replication in mucous membrane of GI tract.
  • Viraemia: Liver, spleen, kidney: replication.
  • Liver Dystrophy, Necrosis, Yolk immunity (3-6weeks)
  • Kidney Nephrosis
  • Secondary Bacteria infection can happen (salmonellosis)
28
Q

Duck Viral Hepatitis Clinical Signs?

A
  • Incubation 2-3days
  • In young Duckling (0-4weeks)
  • Peracute: Large scale death.
  • Acute: Ataxia, spasmodical paddling (opisthonus)
29
Q

Duck Viral Hepatitis Prevention?

A
  • Strict Isolation in the first 4 weeks of age.
  • VACCINE: inactivated vaccination of layers
  • Attenuated: Layer + Day old ducklings
  • Attenuated + Inactivated 7-12 weeks ( attenuated), 18 weeks: Inactivated
30
Q

Avian Encephalomyelitis Prevention?

A

o Vaccination with live vaccine in drinking water (retained virulence, isolation of animals!) – vaccinate
4-5 weeks before the laying period
o Layers have to be vaccinated 1 month before laying

31
Q

Foot and Mouth Disease Cause? Properties?

A
  • Picornaviridae, Aphtovirus
  • +ssRNA: Short replication time(9hours after infection, infected animal sheds the virus in high concentration). Physically look like mRNA(messenger). Infection starts with decapsidation introducting virus into the cell.
  • Non- enveloped. Resistency: Good (56 degrees, PH 6.5(sensitive))
  • Survive in frozen meat, milk powder for months!
  • 7 Serotypes: 0( 1st) , A(2nd), C(3rd). C: rare. O,A: worldwide. Many mutations because RNA virus.
  • Several subtypes, no cross protection! Important for vaccines, in endemic areas they should include the serotypes present in that specific area.
32
Q

FMD Epidemiology?

A
  • Main Hosts: cattle and buffalo(resevoirs).Cattle can shed the virus for months without recovery Buffalo resistant to clinical signs. Guinea pigs, hedgehogs, and dogs susceptible. In dogs causes a heart problem not a vesicular disease
  • Swine: carry virus for short time but shedding virus 1000-3000x more concentrated compared to ruminants.
  • Spread: Live animals through direct contact All body fluids cant transmit infection
  • Shedding: usually 1-2 weeks after the infection
  • Long-term carrier: tonsils and lymphatic tissue
33
Q

FMD Pathogenesis, Clinical Signs, Pathology?

A
  • Infection: Per os, air.
  • Primary replication in the laryngeal and pharyngeal mucosa.
  • Viraemia: spreads within the body
  • Onset of clinical signs 2-7 days after infection.
  • Fever, sudden drop of milk production, salivation v characteristic–> too painful to swallow saliva due to vesicles, erosions..
  • Vesicles break and become erosions leading to secondary bacterial infections.
  • Lameness: in case swine infection of the feet so severe the pigs can loose their hoof.
  • PATHOLOGY: In young animals Myocarditis. Pale stripes , tiger heart. Erosions from break up vesicles. Erosions on the mucosa and hoof.
34
Q

FMD Vaccines?

A

• VACCINES: inactivated vaccine every 6-12 months. Difference between bovine and swine is that in bovine they use aluminium gel as adjuvant and in swine they use oil. Vaccination used in ONLY endemic areas. Problem with vaccination is that you can’t diff between vaccinated animals and infected from the environment animals.

35
Q

Feline Calicivirus Infection Properties?

A
  • Feline Calicivirus (FCV) Vesivirus
  • Susceptible: domestic cats and other felids, marine animals
  • Survive in environment for several weeks. Good resistance.
  • Several strains: may differ in their virulence.
  • One serotype, Antigenic variants.
36
Q

Feline Calicivirus Epidemiology?

A
  • World-wide present, more frequent in shelters.
  • Shedding with excretes, Direct contact transmission.
  • Long term carrier and continuous shedder cats despite vaccination sometimes. Separate animals and observe quarantine if new cat.
  • Persistent infection in the tonsils and nasopharyngeal mucosa mostly shed by head discharges.
  • Long term carrying can be up to 75 days.
  • Those cats infected with FIV shed virus for longer time with increased titre.
  • 20-30% of cats are carriers.
37
Q

Feline Calicivirus Pathogenesis?

A
  • Oronasal infection–>Pharynx–>Viraemia–>Lungs, mouth, throat, Joint synovial membrane pads, visceral organs(very virulent strains).
  • Oral mucosa, pads: blisters, epithelial necrosis Erosions, neutrophil infiltration
  • Lungs: Exudative Pneumonia, Alveolitis
  • Joints: Acute synovitis, thickened synovial membrane.
38
Q

Feline Calicivirus Clinical Signs?

A
  • Difference in virulence and tissue tropism
  • Fever and depression of cats
  • Erosions on the oral cavity especially the tongue.
  • Respiratory and conjunctival signs: Lacrimation, salivation, nasal discharge.
  • Lameness from very virulent strains because of position of immune complexes.
  • Low mortality but secondary bacterial infections can cause death.
  • If infected with virulent systemic strains can observe vasculilits, oedema on pads and intestinal bleeding even in vaccinated cats can be seen.
  • Chronic Stomastitis can be observed if infections going on in the background.
39
Q

Rabbit Haemorrhagic Disease Virus 1 (RHDV-1)?

A
  • Lagovirus
  • Only rabbits susceptible. Resistant in the environment.
  • Cannot be propagated in cell cultures. Have to test vaccine in live animals.
40
Q

Rabbit Haemorrhagic Disease Virus 1 2 (RHDV-2)?

A
  • Rabbit and Hare( Lepus Europaeus) are susceptible.
  • Longer incubation period
  • Younger rabbits are more susceptible
41
Q

Caliciviridae Family?

A
  • Vesivirus genus: Vesicular exanthema of swine virus (VESV), feline calicivirus
  • Lagoviruse genus: Rabbit haemorrhagic disease virus (RHDV), European brown hare syndrome virus (EBHSV)
  • Norovirus genus: Norwalk virus, (porcine calicivirus)
  • Sapovirus genus: Sapporo virus
  • Nebovirus genus: Newbury-1 virus
42
Q

Caliciviruses Properties?

A
  • 30-40nm diameter, icosahedral capsid (cup shaped capsomers, VP60), no envelope, +ssRNA genome
  • Resistant in the environment (no envelope, can pass the stomach pH)
  • Relatively stenoxen viruses
  • Good antigens – if wanting to use for vaccination
43
Q

European Hare Syndrome Virus?

A

▪ Hare & rabbit are susceptible
▪ Serologically distinct from RHDV
▪ Known in Europe since the early 1980s
▪ The disease in hares is very similar to RHD

44
Q

RDHV + EHSV Epidemiolgy, Pathogenesis?

A

o Rabbits susceptible over 1 (2) months of age
o Shedding via faeces, excretes – very contagious
o Direct & indirect transmission (fomites, people etc.) – flies can spread the virus
o PO, air-borne infections – viremia, propagation in liver, vasculitis
o Liver dystrophy, thrombo-embolia in airways & visceral organs – haemorrhages
o Mortality up to 100%

45
Q

RDHV + EHSV Clinical Signs?

A

o Incubation 1-4 days
o Hyperacute: no specific clinical signs, depression & fever, death w/in few hours
o Acute: depression, fever, foamy &/or bloody nasal discharge, heavy breathing, incoordination,
shaking, terminal opisthotonus.

46
Q

RDHV + EHSV Pathology?

A

o Haemorrhage: lung, resp tract, everywhere
o Lungs: oedema, emphysema
o Kidney: haemorrhages, infarcts
o Catarrhal enteritis
o Liver: swollen, necrotic cells; necrosis starting from portal area

EPI MT 2 DECK 1 (3 decks)

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