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

EPI MT 2 DECK 2 Flashcards

1
Q

Disease caused by Hepatitis E virus?

A
  • Hepeviridae, Orthohepevirus Genus

- Chicken and Big Liver Spleen Disease

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2
Q

Aetiology of Hepatitis E?

A

• +ssRNA, ~40nm, icosahedral, non-enveloped
–>Very viable virus, frequent mutations
• Resistance: good (pH resistant, 70oC 5 min)
• Biological properties: stenoxen (zoonotic), good antigenicity

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3
Q

Hepatitis E Epidemiology?

A
  • Poor sanitary conditions–> Human, contaminated water transmits
  • Developed countries: zoonotic genotypes
  • Animal: contact with faeces
  • Spread Animal-Human: Direct contact with animal, contaminated meat products.
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4
Q

Hepatitis E Pathogenesis?

A
  • ANIMALS: Infection PO–> Virus replication in the liver–>Shedding with faeces. Viraemia–>Meat(slaughter)–>Extrahepatic replication. No gross lesions, clinical signs.
  • HUMANS: Symtoms similar to Hepatitis A, fatal outcome(Acute) or extrahepatic symptoms in Chronic cases such as neurological signs. Pregnant women at risk in the 3rd trimester.
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5
Q

Chicken Big Liver Disease?

A
  • Orthohepesvirus

- Hepatitis and Splenomegaly Syndrome

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6
Q

Chicken Big Liver Disease Epi, Patho, Clinical signs?

A
  • Chickens (broilers parents over 24weeks of age)
  • Infection: PO( faecal contamination of drinking water) primer virus replication: intestinal mucosa epithelial lymphatic tissue–> Viraemia–>Replication in Liver and Spleen–> Shed by faeces.
  • Clinical signs: Chronic under egg production, anaemia, premature moulting
  • PATHO: Enlarged Liver with subcapsular haemorrhage and enlarge spleen.
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7
Q

Astroviridae Family characteristics?

A
  • Mamastrovirus Genus: Human, swine, cattle, cat.
  • Avastrovirus Genus:
  • ->Chicken Astrovirus: Avian Nephritis 1 and 2
  • ->Duck and Turkey Astrovirus
  • Non-enveloped, +ssRNA
  • Resists PH 3, or 60 degrees for 5 minutes.
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8
Q

Avian Nephritis Epidemiology, Pathogenesis?

A
  • EPIDEMIOLOGY: Spreads with faeces, replicates in ducks, only chickens susceptible and any age group.
  • PATHOHENESIS: Per os–>Gut Epithelium–>Viraemia. Proximal Tubules of the Kidney.
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9
Q

Avian Nephritis Clinical Signs, Pathology?

A

• CLINICAL SIGNS: first 4 weeks of life. Day old chicken : Diarrhea, decreased weight, kidney lesions.
- Chronic: Visceral Urate deposits.
• PATHOLOGY: Enteritis, Nephrosis, Interstitial Nephritis, Chronic: Urate Depostion.

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10
Q

Duck Hepatitis?

A
  • 2 Astrovirus Serotypes.

- Like Duck Hepatitis caused by Picornaviruses

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11
Q

Astrovirus in Turkeys?

A
  • 2 Serotypes
  • Like Avian Nephritis
  • Clinical signs: Diarrhea in 1-5week old animals.
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12
Q

Togaviridae?

A
  • Family: Togaviridae
    1. ) Genus: Alphavirus
  • ->: Eastern,Western and Venezualan Equine Encephalitis Virus, Getah virus, Chikungunya virus.
    2. ) Genus: Rubivirus
  • ->Rubella virus
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13
Q

Eastern, Western and Venezuelan Equine Encephalomyelitis cause?

A
  • Acute neurological disease of Horses present on the American continent.
  • Rarely virus detected in rodents/birds in other continents.
  • +ssRNA, Enveloped–>Resistance to environment is Weak
  • Can’t survive 37+ degrees and low PH, sensitive to detergents(lipid bilayer)
  • Arboviruses: mosquito body protects virus.
  • Mosquitoes are biological vectors: Vertical transmission of virus to next generation of mosquitoes. When they lay eggs at the beginning of mosquito season with a mild winter Virus starts early next spring.
  • Euryxen: Human, rodents, birds, horses. Rabbits and Birds= RESEVOIR.
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14
Q

Eastern Equine Encephalomyelitis?

A
  • Birds involved in cycle with mosquitoes. ( Bird- Mosquito)
  • Human: dead end host source always birds.
  • Can be transmitted long distance with migration of birds.
  • Seasonal Epidemics See clinical signs during wet, warm summers where mosquitoes can replicate.
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15
Q

WESTERN EQUINE ENCEPHALOMYELITIS?

A
  • Bird, mosquitoes, rodents maintain virus.
  • Depending on host preference of mosquitoes (Birds vs mammals).
  • Horse, Human: Dead-end hosts = during viraemia virus titre not high enough to transmit.
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16
Q

Venezuelan Equine Encephalomyelitis?

A
  • Enzootic: Rodent-Mosquito-Human. Low virulence, rare clinical signs.
  • Epizootic: Horse-Mosquito-Horse cycle. More virulent. Death as outcome freq.
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17
Q

Equine Encephalomyelitis Pathogenesis?

A

• RULES OF ARBOVIRUSES:

  • Virus transmitted by bite–>lands in blood–>Damage of vessels, rash, haemorrhages.
  • Damages of placenta vessels= Abortion ( No O2 supply)
  • Encephalitis: if cross BBB
  • Cross Placenta: embryo congenital problems.
  • Mosquito Bite–> regional Lymph node–>1st Viraemia–>Visceral organs–>2nd viraemia (2-5days)
  • Brain and spinal cord affected by the virus.
  • Course of infection depends on age and viral dose.
  • Abortive infection: animal immunocompetence
  • Unapparent infection: no fever, low titres
  • MORTALITY: Eastern–>80% Western–>10%, Venezuelan–>32-86%
  • Lifelong immunity for animals who survive
  • Lifelong problems from damages to CNS.
18
Q

Equine Encephalomyelitis Clinical Signs?

A
  • Incubation time: 1-3 weeks
  • Peracute: fever, shock, death
  • Acute: Biphasic fever, excitement, increased sensitivity, signs of encephalitis(convulsions) and myelitis( lameness, paralysis)
  • Colic can be seen in Venezuelan.
19
Q

Equine Encephalomyelitis Pathology?

A
  • Encephaltis and Myelitis.
  • Both grey and white matter affected.
  • Blood vessel damage, thrombosis.
  • Chronic: degenerative and reparative processes.
  • Lymphatic, Neutrophil granulocytes.
20
Q

Flaviviridae Properties?

A

– enveloped, icosahedral symmetry, +ssRNA viruses
– Flavivirus, Pestivirus, Hepacivirus genus
– Flavivirus
• tick-transmitted / mosquito-transmitted / non-arbovirus groups
– biological vectors
– possible non-vectorial transmission (air-borne, p.o.)
• weak resistance (65ºC - 30’, detergents, disinfectants)
• euryxen, many zoonotic
• fever and rash, encephalitis/meningitis, haemorrhage.
• antigenicity
– strong antigens
– serological cross-reactions!
– sometimes cross-protection

21
Q

Flaviviridae Diseases?

A
  • Tick Borne Encephalitis
  • Louping Ill
  • West Nile Virus
  • Zika Virus
  • Yellow Fever Virus
22
Q

Tick-Borne Encephalitis Epidemiology?

A
  • • A human febrile illness with meningio-encepahlomyelitis In certain cases.
  • Principle vector: Ixodes ricinus (Siberia: Ixodes persulcatus)
  • Susceptibility: human, domesticated & wild mammals, birds
  • Natural cycle: rodents, small mammals, (birds) – ticks
  • Infection of humans, domesticated animals–>Tick bite – seasonal(Spring/ Autumn) ▪ Consumption of raw milk (goat!) because goats are asymptomatically infected.
  • Pathogenesis: infection – local multiplication – viraemia – visceral organs (CNS).
23
Q

Tick-Borne Clinical Signs?

A
  • In animals usually, in humans frequently subclinical infections.
  • 1-2 weeks incubation
  • 1st fever + influenza-like disease
  • 7-10 days after: 2nd fever, CNS signs
  • Headache, restlessness, neck stiffness, weak limbs, paralysis
  • Usually complete recovery, but permanent lesions may also remain
  • Rarely in foals, dogs, goats clinical signs occur: depression, ataxia, convulsions, tremor
24
Q

Louping Ill Epidemiology?

A
  • Febrile illness with meningo-encephalomyelitis in sheep & rarely in other animals.
  • Principle vector: Ixodes ricinus → seasonal outbreaks
  • Susceptibility: sheep, domesticated & wild mammals, humans
25
Q

Louping Ill Clinical signs and Pathology?

A
  • 1-3 weeks incubation – biphasic fever
  • Depression, salivation, trembling, convulsions, tic
  • Ataxia (louping ill), coma, death
  • Frequent permanent lesions after recovery
  • HISTOPATH: Lymphocytic encephalitis, neuron necrosis, glia-proliferation.
26
Q

West Nile Fever Epidemiology?

A

• Mosquito transmitted disease with febrile, general signs, rash & meningio-encephalomyelitis.
• Natural hosts: birds
–>Detected in several bird sp. , 20-100 days viraemia.
–>Differences in the level of viraemia –>ability of transmission.
–>Migratory birds play a role in the long-distance spread.
• Arthropod vectors: mosquitoes (ticks)
• Detected in more than 60 mosquito sp.
• Principle: Culex pipiens
• Biological vector, vertical transmission.
• • Incidental, dead-end hosts: human, horse, small mammals, amphibians, reptiles.
• Non-vectorial transmission: rare, mainly human.
• Seasonal Disease: Spring/ Autumn
• Suspicious if CNS signs

27
Q

West Nile Virus Clinical Signs?

A
  • 80-90% of the infections are subclinical.
  • General, febrile signs.
  • CNS signs.
  • Sometimes Liver, Heart problems and other CNS problems like Guillain-Barre.
28
Q

West Nile Virus Pathogenesis?

A
  • Local multiplication → viraemia
  • Neuroinvasiveness: tumour necrosis factor-alpha, toll-like receptors
  • Neuron apoptosis
  • Abs emerge on 7-11 days post infection
  • Persisting infections are rare
29
Q

Flaviviridae Family, Pestivirus Genus?

A
  • Pestivirus A = BVDV-1
  • Pestivirus B = BVDV-2
  • Pestivirus C = CSF
  • Pestivirus D = Border Disease
30
Q

BVD CAUSE? Properties?

A
  • Pestivirus very resistant to the environment, doesn’t need a vector.
  • Is a febrile illness of cattle with general signs, diarrhea, rarely with erosions in the mucosal surfaces of the digestive tract. Immunosuppression also.
  • Bovine Viral Diarrhea Virus
  • Susceptibility: cattle, zebu, buffalo, wild Ru, sheep (can cause border disease-like symptoms), goat, swine (subclinical).
  • Moderate resistance ▪ 60oC – few minutes; sensitive to disinfectants. Better compared to flavivirus other members.
  • In faeces, mucous survives for few weeks. Much better resistance in bodily fluids, faeces.
31
Q

BVD antigenicity?

A

4 structural proteins, 3 enveloped with glycoprotein. There is an antigen which the AB can react, neutralizing antibodies produced against gp53 gene. One Serotype with antigenic difference between the strains so antibodies may not provide 100% protection. Lower Antibody titre produced if not the same strain that produced that antibodies.

32
Q

BVD Epidemiology between farms?

A

Transmission between farms:
• Causes cell assocaiated viraemia, BVD linked to lymphocytes–>can transmit with the same injection needle.
• Persistently infected, carrier cattle (+/- without signs)
• Semen of persistently infected bull.
• Faeces, contaminated vehicles.

33
Q

BVD Epidemiology within the farm?

A

Transmission in the farm:
• Sick or persistently infected shedders (faeces, milk, discharges, semen, aborted foetus)
• Infection: PO, airborne, mating/AI
• Persistently infected animals – long term (lifelong) carrier, continuous, or intermittent shedder.
• Semen may contain the virus even if it is not detected in the white blood cells.
• Relatively slow “invisible” spread.
• In enzootic herds calves are protected by maternal Abs until the age of 3-4 months.
• Signs are usually seen in 4-18 month old calves/heifers. Calves may not show clinical signs up until 6 months.
• Mucosal disease is sporadic. Most severe and Rare.
• Immunosuppressive virus: increased other viral & bacterial diseases, typically respiratory disease.
• Ovary follicles are not infected – not transmitted with sufficient embryo transfer.

34
Q

BVD Pathogenesis?

A
  • PO infection – primary virus multiplication in the enteric mucosa & in the lymphatic tissue
  • Viraemia in 1-4 days: serum, lymphocytes → visceral organs (digestive tract, lung, spleen, lymphatic tissue, salivary gland…).
  • BVs endothel damage – haemorrhages.
  • Mucosal epithel damage – erosions.
  • Lymphatic tissue damage – immunosuppression
35
Q

BVB Pathogenesis of Pregnant?

A
  • Most frequently in the first pregnancy.
  • The virus infects the embryo/foetus.
  • Consequences depend on the age of the foetus & on the virulence of the virus strain.
  • CP strain: foetal damages, abortion, developmental disorders. First half of pregnancy= ABORTION. Second half of pregnancy foetal damages, CNS signs.
  • NCP strain: infertility, immunotolerance, immune response (seropositivity). And in the case on NCP: no clinical signs in cows. Day 0-40: abortion. Day 40-120: Immunotolerance. After 120 day the the immune system already developed and we can detect seropositivity in detected calves.
36
Q

Pathogenesis Mucosal Disease?

A
  • Immunotolerant cattle, which is persistently infected with NCP strain is superinfected with a CP strain .
  • Or the NCP stain mutates to CP in the animal.
  • Severe, haemorrhagic enteritis, fibrin precipitation & erosions on the mucosal surfaces – lethal.
37
Q

BVD Clinical Signs?

A
  • 7-9 days incubation
  • In calves: Cp strain –>Fever, salivation, diarrhea, respiratory disease, Central cataract. Recovery within 1-2 weeks.
  • Ncp strain–>Subclinical (seroconversion), Milder immunosuppression.
  • Mucosal disease (rare): High fever, haemorrhagic diarrhea, Erosions on the mucosal surfaces: oral cavity, eyelids, hooves, legs , Weakness, exsiccosis, high mortality.
  • In cows: infertility, weaker fertilization index. Cp strain: abortions, weak, underdeveloped calves born.
  • Aborted foetus/infected newborn calf (cp strain): –>Brachignatia, hydrocephalus, Cerebellar hypoplasia – ataxia, ankyloses, Eyesight disorders.
  • In swine–>Subclinical, sometimes permanent carrier & shedder – seropositive. In pregnant sow foetal damages, delivery of weak piglets is possible.
38
Q

BVD Pathology?

A

• MUCOSAL DISEASE:
- Sharp-edged, usually round/oval ulcers.
- Gums, palate, tongue, cheek, lips
- Hydroptic dystrophy, necoris (str. sp.) → erosion, ulceration –>Inflamed enteric mucosa–>Inflammation of the Peyer-patches, haemorrhagic ulceration–>Croupous or diphteroid pseudomembranes.
-Haemorrhages under the serosal surfaces & on the kidney cortex.
• Intrauterine infections – cerebellar hypoplasia, hydrocephalus, mictrophtalmia.
• Histopath: degenerated villi, submucosal inflammatory cell infiltration.

39
Q

Bleeding Calf Syndrome?

A
  • Bovine neonatal pancytopenia, idiopathic haemorrhagic diathesis of calves, Blood sweating disease, Thrombocytopenic syndrome of newborn calves.
  • In calves until the age of 3-4 weeks: Fever, skin haemorrhages, haematomas, blood faeces.
  • Low 3-5% morbidity, high mortality .
  • BM aplasia, thrombocytopenia, leukocytopenia.
  • Idiopathic: Immunopathologic process, Mycotoxicosis, other poisoning, Infectious (i.e, circovirus).
  • Effect of a vaccine or adjuvant: The cattle were immunized against BVDV → suspected connections with the Vaccine produced on bovine cells – anti-bovine MHC I Antibodies in the cow might damage the calf.
40
Q

Border Disease of Sheep cause and epidemiology?

A

• “Foetopathogen infection of pregnant ewes characterised by retarded development & CNS damages of the lambs”.
• Border disease virus (BDV)
• Closely related to the BVDV.
• BVDV strains can also cause disease in sheep similar to the border disease.
• Rarely infects goat too.
EPIDEMIOLOGY:
• Persistently infected animals (sheep, cattle, wild Ru) are reservoirs.
• Horizontal & vertical spread.

41
Q

Border Disease Pathogenesis?

A
  • Similar to BVD.
  • Manly abortions in the 1st half of the pregnancy.
  • Mainly foetopathy (epithelial, nervous tissue) in the second half of the pregnancy
  • Immuntolerance, later immune response.
42
Q

Border Disease Clinical Signs?

A
  • Weak lambs, hair-like, pigmented wool, usually on the neck & back.
  • Ataxia, trembling (hairy shaker).
  • Cranial developmental problems.
  • Retarded growth, high lethality.
  • Ewes show no signs, post-partum infections are subclinical.

EPI MT 2 DECK 1 (3 decks)

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