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African swine fever in wild boar
n Part 2 - Characteristics of ASFV circulating in Europe and Asia
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THE following is an ex- cerpt from ‘African swine fever in wild boar popula- tions – ecology and bio- security’ created by the Food and Agriculture Or- ganisation of the United Nations, World Organisa- tion for Animal Health and the European Com- mission.
Only virus isolation proves the viability of the virus and is a more sen- sitive diagnostic method than PCR testing – how- ever, virus isolation is dif- ficult to routinely perform and is therefore much less frequently used for diag- nostic purposes at present.
taminate the environment as carcasses.
show visible clinical signs of the disease.
ditions, wild boar show clinical signs for four to nine days before death – 90-95 percent of diseased animals die.
The extreme environ- mental resistance of the African swine fever virus is the key to understanding the epidemiology of ASF and developing adequate measures and interventions for its control, both in the pig production sector, and under natural conditions when it circulates in wild boar populations.
Second, any environment – such as the central Euro- pean continental platform – is composed of a number of ecosystems that contain a number of habitat, each subdivided into a number of microhabitats.
In any ASF-infected wild boar population, there are seven categories of ani- mals, each with a different epidemiological role in spreading the disease. Susceptible
The number of incu- bating animals is usually very small – usually less than 2 percent – and is dependent on the phase of virus invasion, the season and other factors.
Sick animals could be more prone to predation.
Two points deserve spe- cial consideration.
Any healthy individual that has never been in- fected by ASFV is thus susceptible to it.
However, during the in- cubation period, especially during the first days, no virus can be detected.
However, according to local sampling strategies or specific epidemiolog- ical situations, it could be higher – as an example, 13.7 percent in southern Estonia.
First, most of the litera- ture describing the tenacity of the ASFV is based on virus detection with a poly- merase chain reaction test.
Such animals normally comprise the largest part of the population.
Usually, the virus is de- tectable between the end of the incubation period and the beginning of the clinical phase, in the very early stage of which signs can still go unnoticed. Diseased
The true proportion of virus-positive animals in the population can be under-represented in the hunting bag, as sick ani- mals deviate from their predictable behaviour, changing their daily rou- tines, losing appetite and shifting to inaccessible parts of their territory, all of which prevent them from being easily hunted.
However, the detection of its genome does not nec- essarily mean that a live infectious virus is present in the animal.
The thousands of square kilometres of forests in central and northern Eu- rope consist of a wide range of different micro- habitats in which the virus can persist for a variety of periods, while infected live wild boar continue to spread the virus or con-
The number of suscep- tible animals changes sea- sonally due to reproduc- tion and mortality, with the latter largely due to hunting, though predation, limits on food resources and disease may also con- tribute.
A wild boar showing clinical signs of ASF or ap- pearing healthy but when tested is shown to be virus positive.
The virus genome can be detected even when the virus itself is not viable and thus no longer infectious.
Incubating
While abiotic factors – such as sunlight, radiation, temperature, humidity and air composition – are largely shared in the envi- ronment, each of the habi- tats and microhabitats is characterised by specific individualities such as pH, retained humidity and solar exposition.
The only way to deter- mine if a hunted wild boar is in the incubation phase is to collect samples and conduct laboratory testing – positive animals should be safely destroyed.
In the hunting bag, the average virus prevalence ranges from 0.5 percent to 2.5 percent.
Both environmental complexity and diver- sity – together with these infectious wild boar and contaminated carcasses – guarantee the continuous presence of the viable virus, and the consequent risk of repeated reinfec- tion, determining the wild boar habitat cycle.
Incubating animals could spread the virus for a number of days – usually one – before showing evi- dent signs of the disease.
Clinical signs are not pathognomonic, instead being represented by many possible abnormal behav- iours – such as lack of es- caping, trembling of hind legs and prostration – that simply indicate that the wild boar is sick.
Any individual that is infected but does not yet
In experimental con-
Only laboratory tests can verify if a wild boar is infected with ASF and, if positive, it must be de- stroyed.
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Any wild boar killed in a road accident in ASF- affected or at-risk areas should also be tested.
A wild boar infected with the Caucasian strain of genotype II has a limited probability of survival.
However, seropositive an- imals do occur in low num- bers where ASF is present in wild boar populations.
For the animals that sur- vive the infection, the sci- entific literature describes three distinct occasions when serological tests may turn positive, of which only the two latter are observed with genotype II. Chronically sick
Animals with a reduced lifespan that host the virus for the rest of their life.
These animals shed the virus when showing clin- ical signs and ASF lesions.
The animals show as positive according to both PCR and antibody tests.
There is no evidence that the ASF Caucasian geno- type II induces the chronic form of the disease. Convalescent
Animals that completely recover from the infection and will not show any clin- ical signs or lesions.
ASFV remains attached to the external membrane of the erythrocytes, the lifespan of which deter- mines the presence of the virus in the blood.
There is no evidence that these animals became long- term spreaders of the virus.
They become virus nega- tive at around 96 days after infection.
Often, convalescent ani- mals are wrongly regarded as ‘carriers’ – similarly to foot and mouth disease carrier individuals – but they are not capable of playing this specific epi- demiological role – see Figure 4.