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Epidemiology > Calcivirus > Flashcards

Calcivirus Flashcards

1
Q

Vesicular Exanthema of Swine

Species affected

A
  • Sea lions and other aquatic animals (whales, dolphins, seals, fish) are the natural hosts
  • Swine are the accidental hosts
  • Currently eradicated in swine!
  • Fox, Mink, Monkeys and Humans (zoonotic) are also susceptible to get the virus from the vesicles
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2
Q

Vesicular Exanthema of Swine

Most susceptible

A

Seals

All age groups

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3
Q

Vesicular Exanthema of Swine

Occurrence

A

1950s: swine cases in USA
Nowadays: present in seals in the Pacific costal region of America

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4
Q

Vesicular Exanthema of Swine

Spread

A

Spread by ingestion of raw meat of sea mammals and fish or by excretions of infected animals (saliva, vesicles
Less contagious than FMD

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5
Q

Vesicular Exanthema of Swine

Pathogenesis

A

Swine: PO infection —> mouth, snouts, limbs

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6
Q

Vesicular Exanthema of Swine

Primary replication

A

Swine: 1-4 days incubation period

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7
Q

Vesicular Exanthema of Swine

Clinical signs

A 
Swine:
• Fever, Anorexia, Depression
• Vesicles on mouth, snouts and limbs —> lameness
• Lesions heal rapidly
• Low mortality in piglets
Seals:
• Skin lesions
• Abortion
• Perinatal mortality
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8
Q

Vesicular Exanthema of Swine

Diagnosis

A

Clinical signs —> suspicion of disease but further testing required since it is a notifiable disease
Detection of virus: PCR
Virus isolation
Detection of antibodies: ELISA

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9
Q

Vesicular Exanthema of Swine

Treatment

A

No effective treatment

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10
Q

Vesicular Exanthema of Swine

Prevention and immunity

A

Outbreak: Restriction zones
and eradication zones
Prevention: Heat treatment of seafood and fish meals before fed to pigs

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11
Q

Feline Calicivirus Infection

Species affected

A
  • Domestic cat and other felids (ex cheetah), Marine mammals

* Rarely dogs

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12
Q

Feline Calicivirus Infection

Most susceptible

A

All age groups

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13
Q

Feline Calicivirus Infection

Occurrence

A

Worldwide

Frequently in shelters and breeding catteries

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14
Q

Feline Calicivirus Infection

Spread

A

*Spreading by direct contact
with infected animals or excretions
*Indirect transmission occurs but is less frequent —> aerogenous way is the most common indirect transmission

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15
Q

Feline Calicivirus Infection

Pathogenesis

A

Oronasal Infection —> pharynx —> Viraemia —> Other organs:
• Lungs —> alveolitis, exudative pneumonia, proliferative interstitial pneumonia
• Mouth, throat, nose/paw pads—> blisters, epithelial necrosis—> erosions, neutrophil infiltration
• Joints —> acute synovitis, thickened synovial membrane, liquid accumulation
• Very virulent strains are systemic and propagate in visceral organs too
*Virus is shed by the faeces and urine. Virus is also airborne.
*Persisting infections in the tonsils and nasopharyngeal mucosa
*Some virus strains: long term carrier and continuous shedder cats
• A least for 30 days after overcoming the infection
• 50% of cats are carriers on day 75 after overcoming infection
• Some cats are life-long carriers and shedders (20 30% of cats)
*FIV, FeLV facilitate shedding Shedders can be low, intermediate or high titre

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16
Q

Feline Calicivirus Infection

Primary replication

A
  • Upper Respiratory Tract —> Pharynx

* Incubation period of 3-4 days

17
Q

Feline Calicivirus Infection

Target organs

A

Lungs, mouth, throat, joints, visceral organs

18
Q

Feline Calicivirus Infection

Clinical signs

A

*After viraemia —> fever, mild depression —> secondary fever can be caused by lesions and signs
*Differences in virulence and tissue-tropism —> different clinical manifestations:
• Oral signs:
• Erosions in the oral cavity
• Mainly on the margin of tongue, lips, nose
• Also on nose/paw pads
• Rarely on skin
• Healing within 2-3 weeks
• Respiratory signs:
• Mild respiratory and conjunctival signs —> sneezing, clear lacrimation, nasal discharge,
• Rarely pneumonia, dyspnoea, salivation, wet fur
• Limping Syndrome:
• Lameness and fever
• Can be independent from oral and respiratory signs
• May be immunocomplex mediated
• Associated with depression and pneumonia
• Usually complete recovery within 24-48 hours
• Has been observed after immunisation with life attenuated vaccine
• Severe Systemic Syndrome:
• Virulent FCV strains
• Vasculitis, face and nose/paw pad lesions, fever, respiratory signs, icterus, nose and intestinal bleeding
• Up to 60% lethality
• More severe in adults, occurs in vaccinated cats too
• Chronic Stomatitis: Lymphoplasmic Gingivitis Stomatitis Complex (LPSG):
• Most of the patients are FCV shedders but other factors (such as FIV) may contribute

19
Q

Feline Calicivirus Infection

Pathology/Histopathology

A

*Erosions in the oral cavity, at the margin of the tongue
*Very virulent strains:
• Vasculitis
• Enlarged lived
• Pneumonia
• Pancreatitis
• Pericarditis

20
Q

Feline Calicivirus Infection

Diagnosis

A
  • Clinical signs may cause suspicion of disease but not always
  • Oral, pharyngeal, tonsil swab for ELISA, IF, RT-PCR and virus isolation
  • Serology is not useful as calciciviruses are wide spread and almost all cats are seropositive
21
Q

Feline Calicivirus Infection

Treatment

A

*Supportive treatment, enteral nutrient, parenteral fluid, antibiotics, hyperimmune sera
• NSAIDs
• Antibiotics for prevention of secondary bacterial infection
• Hyperimmune sera used only in early stage of disease as if used later in infection the diesel can get worse due to immunocomplex formation

22
Q

Feline Calicivirus Infection

Prevention and immunity

A

*Maternal antibodies protect for a few weeks, may persist for 10-14 weeks
*Hygiene and management: closed farming, identification of shedders
*Vaccine:
• Attenuated and inactivated vaccines, usually bivalent (FCV and FHV)
• Residual virulence, shedding of attenuated strain
• The strains of calicivirus are all different meaning that vaccination will only protect against the strains vaccinated for and not the others
• Commercial vaccines have a relatively broad spectrum of protection (225 strains)
• Primary vaccination at 9, 12 and 16 weeks of age and then yearly
• Vaccination may protect from clinical signs but not from infection and becoming a carrier

23
Q

Rabbit Hemorrhagic Disease

Species affected

A

RHDV-1: Rabbit only (Oryctolagus cuniculus)

RHDV-2: Rabbit and Hare (Lepus eurupaeus)

24
Q

Rabbit Hemorrhagic Disease

Most susceptible

A

RHDV-1: Rabbits over 2 months of age

RHDV-2: Younger rabbits also susceptible, mostly in pet rabbits, in autumn

25
Q

Rabbit Hemorrhagic Disease

Occurrence

A

Worldwide: Asia, Europe, America, North-Africa, Australia
RHDV-2 outbreak in France in 2010 —> spread within Europe and Australia with high virulence causing high
mortality

26
Q

Rabbit Hemorrhagic Disease

Spread

A

Very contagious!

Spread by contact with infected animals and faeces, contaminated food and water sources, fomites and people

27
Q

Rabbit Hemorrhagic Disease

Pathogenesis

A

*PO/Airborne Infection >
Viraemia —> Propagation in Liver—> Vasculitis, Liver Dystrophy, Thromboembolism in airways and visceral organs —> Haemorrhages
*Virus is shed via faeces, excretes

28
Q

Rabbit Hemorrhagic Disease

Primary replication

A

Incubation period of 1-4 days

29
Q

Rabbit Hemorrhagic Disease

Target organs

A

Liver

30
Q

Rabbit Hemorrhagic Disease

Clinical sign

A 
*Hyperacute cases:
• No specific clinical signs are seen due to rapid course of infection
• Depression and fever
• Death within a few hours
*Acute cases:
• Depression and fever
• Foamy and/or bloody nasal discharge
• Heavy breathing, incoordination, shaking, terminal opisthotonus, hindlimb paralysis, convulsions
*Mortality up to 100%
31
Q

Rabbit Hemorrhagic Disease

Pathology/histopathology

A
  • Haemorrhages everywhere especially in lung and respiratory tract
  • Trachea is filled with foamy contents because of severe pulmonary oedema
  • Lungs: mottled and non-collapsed, oedema, emphysema
  • Kidney: haemorrhages, infarcts, petechiae, congested medulla
  • Liver: swollen, hepatitis, necrotic cells —> necrosis starting from the portal area
  • Catarrhal enteritis
32
Q

Rabbit Hemorrhagic Disease

Diagnosis

A

*Clinical signs with high mortality, PM lesions and histopathology —> liver dystrophy and necrosis
Virus detection: RT-PCR, HA
Serology: HAI, ELISA
Disease is notifiable!

33
Q

Rabbit Hemorrhagic Disease

Treatment

A

No effective treatment

34
Q

Rabbit Hemorrhagic Disease

Prevention and immunity

A

*Sanitary prophylaxis:
• Movement restriction, humane slaughter and disposal of sick and in contact animals
• Healthy animals in the same farm may be immunised
*Medical prophylaxis for RHDV:
• Inactivated vaccine from rabbit liver
• Recombinant, myxomatosis virus vectored live vaccine
• Vaccination at 4-5 weeks of age and then yearly
• Recently, RHDV-2 inactivated vaccine was launched

35
Q

European Brown Hare Syndrome

Species affected

A

Rabbit and Hare

36
Q

European Brown Hare Syndrome

Most susceptible

A

Over 2 months of age

37
Q

European Brown Hare Syndrome

Occurrence

A

Europe since 1980s

38
Q

European Brown Hare Syndrome

Spread, Pathogenesis, primary replication, target organs, clinical signs, pathology/histopathology, Diagnosis, treatment, prevention and immunity

A

same as rabbit haemorrhagic disease

39
Q

General characteristics of Calicivirus

A
  • +ssRNA virus with an icosahedral capsid (cup shaped capsomeres) which has no envelope
  • Highly resistant in the environment, survives for weeks
  • Relatively stenoxen viruses
  • Good antigens —> good immunity
  • Distinct serotypes, serological cross reactions

Epidemiology (16 decks)

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