Dossier H5N8: Wind-Borne Spread of Highly Pathogenic Avian Influenza Virus between Farms

The current outbreaks of H5N8 and H5N2 in Europe, North America and Asia it is important to implement high level bio security measures at farms to prevent production animals becoming infected. Once a farm is infected, culling entire flock is the only option to prevent further spreading with devastating consequences for the industry.

During the 2003 outbreaks of H7N7 in Holland the preferred culling technique was whole house gassing, also known as stable gassing.
Practical experience has shown that, in whole house gassing, the birds start to die after approximately 35 minutes and the entire operation ends after 2 to 3 hours. Killing by whole house gassing is most suited to large flocks in floor management systems. Under certain circumstances, it is possible to use whole house gassing in cage or aviary housing.
From the 1.100 farms that have been eradicated, stable gassing has been the technique of choice on 568 farms (51,6% of all farms), culling in total 21.740.000 birds (74,3% of all poultry). On 55 farms (10,7%), Carbon Monoxide (CO) has been used; on 513 farms (90,3%), Carbon Dioxide (CO2) was used.

Before the technique can be applied, the house must be well sealed. The screens and shuttering in an open house mean that it is also possible to make these houses gas-tight in order to carry out whole house gassing. The ventilation is switched off immediately before gassing.

The principle of stable gassing using CO2 is Hypoxia: displacement of atmospheric air by at least 70% , CO2 by volume. The gas is pumped into the house at high pressure and slowly fills the space. Stable gassing is a complicated technique to apply because it is difficult to measure whether the minimum concentration is achieved the animals can be stunned and killed and it is difficult to measure the concentration accurately. Therefore the total amount of gas that is pumped in resembles at least 2 to 3 time the volume of the house.
In order to fill the house with gas, the air in the house has to be replaced, exiting through any channel it can find. Most of the time, that is through ventilation at the top of the building or through cracks in the walls and the roof. The displaced air also causes (possibly) contaminated farm-dust particles and feathers deposited into the open air.

After the poultry is culled and before the dead birds can be collected safely, the house must be ventilated for approximately three hours to ensure rapid and complete removal of the gas from the house air. This ventilation also causes contaminated farm-dust particles from inside the house to deposit to the open air.
To understand the risks of spreading contaminated materials caused by stable gassing, a quantitative understanding of the spread of contaminated farm dust between locations is a prerequisite for obtaining much-needed insight into one of the possible mechanisms of disease spread between farms.

The researchers Amos Ssematimba, Thomas J. Hagenaars, Mart C. M. de Jong of the Dutch Department of Epidemiology, Crisis Organization and Diagnostics, Central Veterinary Institute (CVI) part of Wageningen University and Research Centre, Lelystad, The Netherlands, and Quantitative Veterinary Epidemiology, Department of Animal Sciences, Wageningen University, Wageningen, The Netherland developed a model to calculate the quantity of contaminated farm-dust particles deposited at various locations downwind of a source farm and apply the model to assess the possible contribution of the wind-borne route to the transmission of Highly Pathogenic Avian Influenza virus (HPAI) during the 2003 epidemic in the Netherlands.

The model is obtained from a Gaussian Plume Model by incorporating the dust deposition process, pathogen decay, and a model for the infection process on exposed farms. Using poultry- and avian influenza-specific parameter values we calculate the distance-dependent probability of between-farm transmission by this route. A comparison between the transmission risk pattern predicted by the model and the pattern observed during the 2003 epidemic reveals that the wind-borne route alone is insufficient to explain the observations although it could contribute substantially to the spread over short distance ranges, for example, explaining 24% of the transmission over distances up to 25 km.


Dossier H5N8: Fujian H5N8 Accelerated Spread In Germany

On December 20, 2014, dr. G. Koch, leading virologist at Central Veterinary Institute (part of Wageningen UR) in Holland commented on LinkedIn where he explained the connections between the current outbreaks of Avian Influenza. He referred to publications on the website of Reconbinomics.

Dr. Koch commented: “Remarkably the HPAI H5N2 causing the outbreaks in Brittish Columbia Canada is a reassortant virus existing of 5 genes of the HPAI H5N8 that is detected in Republic of Korea in the from the beginning of 2014 onward and Pb1, NP and NA form LPAI viruses present in wild birds in North America. The H5 gene relates to clade viruses detected in Asia This suggests a role for wild birds in the spread of this H5 virus”.

In a recent report, the Friedrich-Loeffler Institute(FLI) have signaled the spread and acceleration of H5N8 confirmed cases in Germany. The institute released sequences, A/turkey/Germany-NI/R3372/2014, from a turkey from Cloppenburg in Lower Saxony (see map) at GISAID from a December 15 collection. A partial (742 BP) H5 sequence was released, which was followed by a full N8 sequences, which was followed by a much larger H5 sequence (1342 BP). FLI is to be commended for the rapid release of these sequences.

The H5 was most closely related (1338/1342 matches) to A/duck/England/36254/14 and A/Chicken/Netherlands/14015526/2014, while the N8 was most closely related (1373/1377) to A/eurasian wigeon/Netherlands/emc-1/2014, A/eurasian wigeon/Netherlands/emc-2/2014, A/Chicken/Netherlands/14015526/2014, and A/turkey/Germany-MV/R2472/2014. The closest relationships were with isolates from The Netherlands which was expected because of the geographic proximity.

According to FLI H5N8 confirmed ducks in Emsland, which is even closer to The Netherlands, as well as a dead mallard in Aken which is in Anhalt-Bitterfeld and 200 miles southwest of Emsland, signaling an increase in geographic spread and an acceleration of detection rates.
Germany had reported the first case of H5N8 in Europe, on November 4 in Heinrichswalde in northeast Germany which was followed by confirmation of H5N8 in a wild teal. The three recent confirmations identify continuing spread through wild birds as well as poultry infections in spite of enhanced biosecurity.

Similarly, H5N8 was confirmed on multiple farms and wild birds in the Netherlands and sequences have also been deposited at GISAID. More recently, H5N8 was confirmed in Italy and sequences were released, A/turkey/Italy/14VIR7898-10/2014.

All sequences are closely related to each other and November sequences from Japan (A/duck/Chiba/26-372-48/2014 and A/duck/Chiba/26-372-61/2014), signaling a dramatic geographic expansion.

The expansion increased with reports of H5N8 in four dead pet falcons in Lynden, Washington, who had eaten a widgeon caught near Wiser Lake, as well as a backyard holding in Winston, Oregon where there were 100 chickens and guinea fowl. Although sequences have not been released for the US infections, the H5 and N8 were closely related to Genbank sequences from South Korea, confirming the close relationship to the above sequences.

In addition to H5N8, the US and Canada have reported H5N2. The first US sequence was from a northern pintail, which was part of a massive die-off at Wiser Lake. H5N2 and aspergilliosis were identified in dead ducks (about 600), but additional confirmations of H5N2 are expected. These sequences will likely be closely related to sequences in British Columbia, where H5N2 has been confirmed in 11 farms, including a cluster located 7 miles north of Wiser Lake.

H5N8 has 3 gene segments from Fujian clade 2.3.4 H5 (H5, PA, MP) and the H5N2 has 5 gene segments from H5N8, including Fujian H5 as well as 3 wild bird North American segments, including N2. More H5N2 and H5N8 infections in Canada and the US are expected in the near term.


Dossier investigation: identification of the agent

Influenza in birds is caused by infection with viruses of the family Orthomyxoviridae placed in the genus influenzavirus A. Influenza A viruses are the only orthomyxoviruses known to naturally affect birds. Many species of birds have been shown to be susceptible to infection with influenza A viruses; aquatic birds form a major reservoir of these viruses, and the overwhelming majority of isolates have been of low pathogenicity (low virulence) for chickens and turkeys. Influenza A viruses have antigenically related nucleocapsid and matrix proteins, but are classified into subtypes on the basis of their haemagglutinin (H) and neuraminidase (N) antigens (World Health Organization Expert Committee, 1980). At present, 16 H subtypes (H1–H16) and 9 N subtypes (N1–N9) are recognised with proposed new subtypes (H17, H18) for influenza A viruses from bats in Guatemala (Swayne et al., 2013; Tong et al., 2012; 2013). To date, naturally occurring highly pathogenic influenza A viruses that produce acute clinical disease in chickens, turkeys and other birds of economic importance have been associated only with the H5 and H7 subtypes. Most viruses of the H5 and H7 subtype isolated from birds have been of low pathogenicity for poultry. As there is the risk of a H5 or H7 virus of low pathogenicity (H5/H7 low pathogenicity avian influenza [LPAI]) becoming highly pathogenic by mutation, all H5/H7 LPAI viruses from poultry are notifiable to OIE. In addition, all high pathogenicity viruses from poultry and other birds, including wild birds, are notifiable to the OIE.


Basic information about avian influenza

Avian influenza is usually an inapparent or nonclinical viral infection of wild birds that is caused by a group of viruses known as type A influenzas. These viruses are maintained in wild birds by fecal-oral routes of transmission. This virus changes rapidly in nature by mixing of its genetic components to form slightly different virus subtypes. Avian influenza is caused by this collection of slightly different viruses rather than by a single virus type. The virus subtypes are identified and classified on the basis of two broad types of antigens, hemagglutinan (H) and neuraminidase (N); 15 H and 9 N antigens have been identified among all of the known type A influenzas.


Dossier Avian Influenza: the next pandemic?

Kathleen Harriman PhD, MPH, RN published an interesting presenation on the relationship between outbreaks of high pathogen Avian Influenza and the risks of the next human pandemics. Kathy has worked in the healthcare and public health fields for the past 35 years as a pediatric emergency room nurse, a hospital infection control practitioner, and as an infectious disease epidemiologist.

For the last two years, Kathy has been Chief of the Vaccine Preventable Disease Epidemiology Section in the Immunization Branch of the California Department of Public Health. Prior to joining CDPH, she worked for 15 years at the Minnesota Department of Health in a number of public health areas, including HIV/AIDS and the Emerging Infections Program.

During her last five years there she supervised the Infection Control Unit where she worked on community-associated MRSA and a variety of infectious disease issues, including many community and healthcare-associated outbreaks. Kathy has an MPH from the University of Sydney (Australia) and a PhD from the University of Minnesota.