Flu in pigeons, flu in humans...

The labor market and the influence of flu

For some time now, the labour market has been under severe pressure.
For every 100 people leaving, only 85 people are entering. Only 80% of those entering the labour market want to work. The labour shortage remains structural. Unfortunately, only an announced economic contraction can relieve the pressure in the near future.

There are no vacancies for pharmacists either. We are looking in vain for another colleague to join us for a whole career. Our duties are becoming more extensive and, for example, we recently had to deal with corona vaccinations and, later this year, combined influenza vaccinations. The government wants to increase the crucial vaccination rate by lowering the threshold.

Influenza in humans, is still a serious disease, causing significant economic damage each year and one million deaths worldwide. At the end of last year, two months earlier than usual, the flu virus became active. This is being watched with suspicion as the season’s peak is still to come.

Traditionally, the influenza virus is monitored in Southeast Asia (northern hemisphere) to find out which variants (AB and HN strains) are circulating there. This helps us to have the appropriate vaccines available in the autumn. Predicting is always good but never perfect. This is why the effectiveness of the flu vaccine is a little lower (+/- 60%) than that of the Corona vaccine (+/- 90%). However, there has been an increase in effectiveness against influenza due to recent vaccines with 4 different strains. Their effectiveness is, therefore more than sufficient for epidemic control if vaccination coverage is high enough (80% or more).

So the global recommendation is increasingly explicit and generic:
"Get vaccinated" is also for those who do not belong to a risk group (a healthy middle-aged person has a one in three chance of developing complications due to a risk factor such as smoking or drinking alcohol). This is why pharmacists are involved. They can help keep the threshold low and thus increase vaccination rates.

The origin of the flu 

The reservoir of this influenza virus is waterfowl, to which it is highly contagious and dangerous. It then spreads to all birds, for which it can also be highly contagious and fatal.

Reassortment = the exchange of genetic material from one species to another.

Sometimes the virus is transmitted to pigs, which (depending on the variant) may or may not easily infect each other. Exceptionally, it can be transmitted from pigs to humans and, depending on the variant, from human to human…

There are several components to this influenza virus.

Influenza A has two key features on its surface: Haemagglutinin (H) and neuraminidase (N) provide the adhesion to the cell, which allows the virus to enter the cell.

If we can block this with antibodies , it is harder for the virus to attach. The neutralised virus in the blood can be eaten by special cells (phagocytosis).

Sixteen H traits and nine N traits provide all possible combinations with their familiar names (H 1 N1 or H3 N1...). 

Due to constant mutation (viruses have been doing the same thing for 200 million years), there exist:

  • Antigenic drift: these are minor changes = "facelifts" to the traits (tacks). They require slight changes to the vaccine every year to protect us from an annual epidemic.
  • Sometimes, antigen shift occurs. This is a significant change = "completely new model". Big, complex parts of the virus are changing by reassortment of genetic material (between pigs and humans, for example), for which no background immunity exists, so a whole new vaccine is needed, but before that, a global pandemic, because it takes a long time to develop a whole new vaccine.

A "perfect viral storm" could be on the horizon if influenza and corona both surprise us with mutations to which we have no immunity(*).
The flu virus undergoes such a shift about four times every century.

In 1918 Spanish flu (H1N1): caused more casualties than WWI.

In 1957 Asian flu (H2N2).

In 1968 HongKong flu (H3N2).

Influenza in animals

The daily “De Tijd” wrote last week: "Avian flu is hitting harder than ever”.

Source: https://www.tijd.be/ondernemen/voeding-drank/vogelgriep-grijpt-harder-om-zich-heen-dan-ooit/10436028

Fortunately, our pigeons are not at high risk in this chain of infection. (**)
They can be infected with the avian influenza virus but do not usually become ill (**).

Source: https://pubmed.ncbi.nlm.nih.gov/26443061/

In addition, they do not usually spread the virus to others.

Source: https://www.kbdb.be/vogelgriep/ 

Our National Pigeon Fanciers' Association is closely monitoring the situation where the measures have only caught the pigeons in the restricted zones (blast zone, e.g. 3 to 10 km around a hotspot).

Otherwise, no measures apply outside the restricted areas.
We may yet
• participate in competitions;
• transport your pigeons;
• release your pigeons outside the loft.

👉🏻 Racing pigeons are hardened due to the rigour selection of the sport, where only those with robust immune systems survive, despite the use of antibiotics, which tend to weaken them.

This touches on the basis of the Comed method and is all the more reason to focus on antibiotic-free care, which only increases their resistance to bird flu and similar diseases. Our desire is to continue our sport in spite of all the virus circulations and, of course, to perform more purely with pigeons as sharp as possible.

There were fears of an H1N1 pandemic in the United States in 2009. There were fears of a global tsunami with major socio-economic consequences.
The virus was a unique combination of influenza A virus genes never before identified in animals or humans. This combination of viruses and genes was closely related to the North American H1N1 pig lineage and to the H1N1 influenza viruses of the Eurasian pig strain. For this reason, initial reports suggested that it was a swine flu virus. However, no exposure to pigs was found when the first human cases were investigated. It soon became clear that this new virus was circulating in humans and not in the pig herds of the USA. Worldwide, the death toll is estimated at between 150,000 and 600,000.

We experimentally infected three different pigeon species (meat, city and race) with two different doses of H7N9 avian influenza virus  A/Chicken/China/2013 by intranasal and intraocular inoculation (IN + IO) or intravenous injection (IV) to determine the susceptibility of pigeons to the newly emerged avian influenza virus subtype H7N9. In addition, the potential for transmission of H7N9 to pigeons by direct close contact with experimentally infected pigeons and chickens was evaluated. The results showed that none of the experimentally infected pigeons showed clinical signs, irrespective of the route and dose of infection. Of the 12 racing pigeons that were randomly selected and had necropsy, none of them had coarse lesions. Consistent with this finding, the virus was not isolated from all pigeons. No detectable levels of H7-specific antibodies were found in any of the pigeons. In contrast, conjunctivitis was present in 11 out of 31 chickens infected with H7N9 by inoculation with IN + IO or by contact with chickens infected with IN + IO. The virus was isolated from all of the 31 chickens, and antibodies specific to H7 were detected in these chickens. However, no clinical signs were observed in any of the IV-infected chickens or chickens in direct contact with IV-infected chickens. There has been no isolation of virus from these chickens and no detection of H7-specific antibodies. Overall, our conclusion is that at the doses used, pigeons have little or no susceptibility to the H7N9 virus and are unlikely to be a reservoir for the virus.
However, the virus is a cause of conjunctivitis in chickens and can be transmitted to susceptible hosts by direct contact.
Source: https://pubmed.ncbi.nlm.nih.gov/26443061/

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