Final Exam - Orthomyxoviridae Flashcards Preview

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Flashcards in Final Exam - Orthomyxoviridae Deck (36):


High Pathogenicity Avian Influenza Virus (HPAI)



Low Pathogenicity Avian Influenza Virus (LPAI)


Reservoirs for LPAI A Viruses

Aquatic birds; they replicate in intestinal epithelium of these birds with no over disease and are excreted with fences


Genus: Influenza A

contains human, equine, swine and domestic poultry viruses


Genus: Influenza B

contains human viruses


Genus: Influenza C

contains human and swine viruses that rarely cause disease


Genus: Thogotovirus

Contains tick borne viruses which infect livestock and humans in Africa, Europe, and Asia.



Has only one member, infectious salmon anemia virus. Also has hemagglutinin esterase and F protein


Classification of Orthromyxoviruses

There are 16 hemagglutinin (H) and 9 Neuraminidase (N) types


Two types of glycoprotien spikes for Influenza A and B

Homotrimer HA and homotetramer NA


Influenza C lack neuraminidase

have only 1 type of glycoprotein spikes - the hemagglutinin is multifunctional - esterase molecule


Surface HA structure, performs 3 functions:

1. receptor binding
2. membrane fusion
3. receptor cleavage


Structure of the Influenza A Virus

Lipid envelope derived from the host cell. Envelope harbors hemagglutinin (HA), the neuraminidase (NA) and M2 protein. M1 - matrix protein lies beneath the lipid layer.



In aquatic birds the virus is shed in feces - fecal oral transmission is common. In poultry - ingestion and inhalation. In mammals - aerosols, droplets and fomites.


Thogotoviruses - Tranmission

Are transmitted by ticks and replicate in both in the ticks and mammals


Isavirus - Transmission

Transmitted in water - gill being the important route


Antigenic change in orthomyxoviruses

1. Genetic shift - changes in antigenic setup due to reassortment of gene segments
2. Genetic drift - changes in antigenic setup due to point mutations (nucleotide substitution, deletion, insertions).


Equine Influenza Viruses

Respiratory Disease. Affects horses, donkeys, and mules world wide. It is the most important viral respiratory disease or horses.


Equine Influenza Virus - Pathogenesis

Virus replicates in the epithelial cells of the upper and lower respiratory tracts. Ciliated epithelial lining is destroyed by virus replication leading to inflammation and exudate formation including nasal discharge.


Equine Influenza Virus - Clinical signs

Morbidity is high - symptoms visible within 24-48 hours after infection. Fever, inappetence and depression, reddening of the nasal mucosal, conjunctivitis, serous nasal discharge with dry paroxysmal cough, mucopurulent nasal discharges.


Animals at Risk of Infection

Race horses, breeding stock, show jumper, horses sent to sales are at high risk of infection with equine influenza virus. Equids are the only source of equine influenza viruses.


Equine Influenza Virus - Diagnosis

Acute disease is very characteristic and straight forward. RT-PCR is a diagnostic test of choice - highly specific. Nasal and pharyngeal swabs collected early in infections are samples of choice. Virus isolation - swabs should be protected from desiccation (transportation medium).


Equine Influenza Virus - 10 day old chicken embryos

Can be used to detect virus in allantoic and amniotic fluids of infected chicken embryos using standard hemagglutination test.


Equine Influenza Virus - Prevention and Control

Isolation, cleaning, vaccination (inactivated vaccines or live vectored vaccines), retrospective serology.


Swine Influenza Viruses

Pigs are considered as a "mixing vessel" for influenza viruses because of their ability to become co-infected with both human and avian strains of influenza viruses.


Swine Influenza Viruses - Pathogenesis

Highly contagious virus. Replication in the upper respiratory tract. Airway plugging, peribronchial and perivascular mononuclear cell infiltration.


Swine Influenza Viruses - Symptoms

Appears in many animals at the same time. Fever > 42C. Nasal discharge at later stages of disease. Not fatal if animals are kept warm and stress free. Some animals may develop severe pneumonia and die.


Swine Influenza Virus - Diagnosis

Virus identification. Deep nasal swabs. Embryonated chicken eggs can be inoculated. Hemagglutination inhibition (HI) test for detection. ELISA. RT-PCR.

A four fold or greater increase in titre between the first and second sample is suggestive of a recent infection.


Swine Influenza Virus - Control

No feasible therapeutic options. Commercial vaccines (whole virus, inactivated and are adjuvanted). They do NOT consistently confer crossprotection against new subtypes. Swine influenza viruses are economically important due to losses arising from the requirement to cull infected pigs.


Avian Influenza Virus

Most devastating infection in chicken referred to as "fowl plague". Are economically important due to losses arising from the requirement to cull infected birds. A REPORTABLE DISEASE!


Notifiable Avian Influenza (NAI)

An infection of poultry caused by any influenza A virus of the H5 or H7 subtype any AI virus that causes at least 75% mortality. Divided as HPNAI or LPNAI.


Avian Influenza Pathogenesis

Influenza virus replicates int he intestinal and respiratory tracts. Viremia leads to multifocal lymphoid and visceral organ necrosis. Pancreatitis, myocarditis, myositis, encephalitis, and hemorrhage.


HPAI - Clinical Features

A highly virulent strains of AI can cause sudden death without symptoms. Cessation of egg production, diarrhea, edema of the face, head and neck, cyanosis of combs or wattles, torticollis


LPAI - Clinical Features

May cause considerable losses due to decreased egg production


Avian Influenza Virus - Diagnosis

RT-PCR to detect matrix protein (M) gene, H5 and H7 genes. Virus isolation, agar gel immunodiffusion, ELISA, Hemagglutination inhibition assay


Avian Influenza Virus - Control

Surveillance, biosecurity, and depopulation. Segregate poultry from wild birds. Vaccination has not been used to control HPAI.