Avian Influenza

Recent Highly Pathogenic Avian Influenza outbreaks in Asia, Europe, and Canada highlight the need for preparedness in the Caribbean region.

In late November, the Canadian Food Inspection Agency (CFIA) of Ottawa in Canada reported 2 outbreaks of Highly Pathogenic Avian Influenza (H5) in the province of British Columbia based on preliminary testing and clinical signs. On Dec. 9th, the OIE confirmed reports of 3 additional outbreaks in the same province and identified the virus as an H5N2 based on RT-PCR, viral isolation and sequencing, and the IVPI test. Read more »

Monograph

definition: 

Highly contagious generalised viral disease affecting both wild and domestic birds. Various benign or sub-acute syndromes originate from "Avian influenza". It can be extremely serious and induce a death rate of up to 100%.

Situation in America: 

Type A, low-pathogenic or apathogenic flu virus strains, found in wild aquatic birds, are present throughout the world. Highly pathogenic strains may emerge through mutation or genetic reassortment and cause outbreaks of the disease.

Currently the Americas are not affected by the highly pathogenic avian influenza virus of sub-type H5N1, which is raging and diffusing to the rest of the world from sources which intially appeared in South-East Asia in 2004.

Susceptible species: 

All domestic bird species are presumed to be sensitive to the infection: chickens, ducks, geese, turkeys, quails, pheasants, etc. However outbreaks of the disease mainly occur in chickens and turkeys.

Ducks and other wild aquatic birds are also sensitive but the infection is generally subclinical (asymptomatic carriers).

Humans, horses, pigs and cats may also be affected.

Etiological agent: 

A segmented RNA virus from the family Orthomyxoviridae, type A influenzavirus.

The combination of haemaglutinin (H) and neuraminidase (N) determines the viral sub-type. To date all highly pathogenic virus strains are of the H5 or H7 sub-type.

Infections by the highly pathogenic virus are uncommon and must not be confused with low-pathogenic virus infections which may also belong to the H5 and H7 sub-types.

Resistance - Sensitivity

Virus inactivated by heat, acid pH, formol and iode compounds, oxidative agents, etc.

It may however persist for long periods in cold water, tissue and faeces.

Methods of transmission
Source: 

Virus sources are mainly ill and infected animals: asymptomatic carriers or those in the incubation stage, post-infectious chronic carriers, vaccinated animals.

Virulent matter: faecal matter, respiratory secretions.

Reservoirs: Clinically healthy freshwater and sea birds may transmit the virus to poultry farms and thus encourage spatial distribution of sources especially via migrating birds.

Receptivity and sensitivity factors

Species: high clinical sensitivity of chickens and turkeys, weak clinical expression in ducks.

Transmission: 

Vertical: Infected eggs are not viable (embryonic death), if the eggs are broken or cracked chicks in incubation may become infected.

Horizontal:

- Direct: through contact with secretions and faecal matter from infected birds.

- Indirect: through water, feed, equipment and contaminated clothing.

Method of contamination: 

Oral and respiratory route.

Symptoms: 

Incubation period: from 3 to 7 days.

Symptoms vary according to the species infected, to individual resistance to the virus, but also according to the virulence of the infecting strain and to tissue tropism.

Sub-acute form: septicaemia and death occur in 1 to 2 days and affects up to 100% of the population.

 

Acute form: Death rate between 50% and 100%.

- Invasive phase:

• severe depression

• egg drop syndrome

• anorexia

• ruffling of feathers

Followed by cephalic oedema with tumefaction and cyanosis of the crest and the caruncle.

- Status phase: Visible signs in one animal or in several different animals:

• Intestinal disorders: greenish, bloody, profuse diarrhoea, dehydration and thirst.

• Nervous disorders: signs of encephalitis up to the end of disease progression with convulsions, clonic paralysis, loss of balance, falls. Paralysis of the neck, wings and legs.

• Respiratory disorders: abundant tracheal mucous, discharge from the eyes and nose, respiratory difficulties(polypnea, rales, sneezing, scabs on the nostrils).

- Terminal phase: most often aggravation and death, otherwise clinical improvement with persisting nervous system damage and laying abnormalities. 

 

Chronic, subacute form: respiratory and laying disorders

 

Asymptomatic form: frequent, especially in wild acquatic birds, detectable by virological examination.

Lesions
Macroscopic lesions: 

• Sub-cutaneous oedema of the head and neck

• Discharge from the beak and nose

• Abundant mucous exudate in the trachea or severe haemorrhagic tracheitis

• Congestion: liver, kidneys, spleen, muscles, ocular conjunctiva

• Haemorrhage: of the digestive tract (glandular stomach lining and crop, intestinal lining lymphoid tissue) and of the ovaries which are subjected to degeneration.

• Petechia: serous membranes, adipose tissue, general cavity

Microscopic lesions: 

• Acute inflammation and necrosis of the intestinal lining with cytoplasmic viral inclusion.

• Diffuse encephalitis lesions: gliosis, vascular proliferation, neuronal degeneration

Diagnostics
Clinical diagnosis: 

Difficult to establish given the variety of lesions. Virus isolation is essential for confirming the clinically suspected diagnosis.

Differential diagnosis: 

May be confused with the acute form of avian influenza:

• Acute form of avian cholera

• Velogenous strain Newcastle disease

• Infectious laryngo-tracheitis


NB: Avian influenza and Newcastle disease are clinically indistinguishable

Virological diagnosis: 

Samples


- From living birds: tracheal and cloacal swabs or stool sample

- From dead birds: from organs (head, lungs, spleen) and grouped faeces

Tests

• Inoculation of embryonated hen eggs for 9 to 11 days.

Followed by:

• Haemagglutination demonstration

• A-type confirmation by immunodiffusion

• Determination of the sub-type (H, N) using monospecific antiserums

• Evaluation of strain virulence: determination of the pathogenicity index by intraveinous route in chickens of 4 - 8 weeks

Serological diagnosis: 

Samples: coagulated blood or serum.

Tests:

• Haemagglutination and haemagglutination inhibition

• Agar immunodiffusion

Treatment: 

No treatment exists to date.

Prophylaxis: 

Sanitary prophylaxis  

Defensive measures:

• Avoid all contact with poultry and wild birds, especially wild acquatic birds

• Do not introduce any animals of unknown sanitary status

• Limit the circulation of people on the farm

• Ensure effective cleaning and disinfection of equipment and premises

• Ensure (if possible) that only one age group per farm is present


Offensive measures:

Where an outbreak occurs,

• Killing of all birds

• Elimination of carcasses and products

• Cleaning and disinfection

• 21 day depopulation before introducing any new animals 

 

Medical prophylaxis

Very difficult to implement due to the variability in viral sub-types and the absence of cross-protection bewteen the different sub-types.

Vaccines: 

Inactive oil-adjuvant vaccines have proved effective in prevention of the disease and/or in reducing the death rate among chicken and turkey stocks.

However vaccination does not guarantee the absence of infection (asymptomatic) in certain vaccinated animals. They may therefore carry and excrete the virus, but in a lesser quantity than if they were not vaccinated.

No cross-protection exists between the various Influenza A virus sub-types. It is therefore essential to recognise the circulating viral strain in order to adopt the relevant vaccine. For the currently circulating H5N1 strain, a vaccine has recently been developped for animals.

A human vaccine against H5N1 is currently undergoing research.

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