What we need to know to beat African Swine Fever

Date posted: January 9, 2020

Twelve years ago, African swine fever (ASF) outside of Africa was a so-called exotic disease with minor impact. That has changed drastically. ASF is one of the most important threats to the global pig-farming sector with no drugs or vaccines are available to cure or prevent the disease.

To prevent, control and eradicate ASF is a big job Klaus Depner of the Friedrich-Loeffler-Institute, told the 2020 Banff Pork Seminar. If we are going to beat this disease the world need to look beyond just biological and include social science, he says.

"Knowledge about disease biology, epidemiology and the human-host interactions is needed. But humans are recognized as the main cause of both long-distance transmission and virus introduction into domestic pig farms," says Depner.

"By considering only the biological particularities of the disease, contagiosity, tenacity and case fatality rate, but ignoring the human aspects, the epidemic will not be controlled. It is crucial to include social science when planning prevention, control, or eradication measures."

Tracking ASF origins

The ASF epidemic started in Georgia in 2007 and subsequently spread throughout the Caucasus and the Russian Federation. In 2014, ASF reached the European Union (EU) and four years later the first outbreaks were reported in Asia. In several European countries the disease has become endemic in the wild boar populations, while it could still be managed in domestic pigs.

When ASF reached the EU, it was expected to either spread rapidly within the wild boar population or fade out due to high case fatality rate and the absence of long-term carriers. The current situation, where the disease has become endemic in several countries, shows that none of these predictions held true. The infection survived locally in the wild boar population independently from outbreaks in domestic pigs.

In addition to local transmission in wild boars, long distance jumps into disease-free areas occurred. Human activities have been identified as main drivers of disease transmission in the domestic pig epidemiological cycle.

The disease and the ASF virus

The ASFV strain in the current epidemic is highly virulent. While the disease is asymptomatic in warthogs, domestic pigs and wild boar mostly develop a severe haemorrhagic disease and die within a couple of days. If naïve pigs come into contact with the diseased animal or its secretions, some will become infected, and meet the same destiny.

However, the case fatality rate (proportion of infected individuals that succumb to the disease within a certain time period) is high, often reaching 90-100 percent. So far, there is no evidence that the few survivors may become carriers playing a significant role in the ASF epidemiology.

ASF virus has been shown to be relatively stable in the environment (high tenacity). It survives the process of putrefaction, and carcasses of infected animals may remain infectious for weeks. In frozen meat, the virus may survive for several years, in dry meat and fat almost one year, in blood, salted meat and offal more than three months, in faeces over one week.

Given this tenacity data, it is easy to understand why and how contaminated meat and meat products have played a crucial role in ASF transmission and epidemiology.

ASF contagiosity

One important aspect for understanding ASF is contagiosity. That is the percentage of animals that get infected after contact with the ASF virus; or the probability that an animal picks up an infection after contact with the virus.

However, the ancient sylvatic cycle in Africa, involving warthogs and Ornithodoros ticks, is the non-contagious form of the infection. The asymptomatic wild suids and ticks allow a transmission cycle, which can be maintained indefinitely in Africa. Tick bites are transmitting the disease within the warthog population without clinical manifestation.

The balance between natural hosts and ASF was altered by the introduction of domestic pigs by colonists from Europe into Africa. In contrast to infected warthogs, domestic pigs and European wild boar develop severe clinical disease. In absence of ticks or iatrogenic transmission by parenteral injection, the virus is transmitted orally by direct contact with infected pigs or contaminated fomites.

This oral transmission route is less efficient than the parenteral pathway. The probability that an animal picks up an infection after virus contact depends on several factors: e.g. virus dose, infectious material, animal behaviour, management, contamination of environment, etc.

In the past ASF was often described as a highly contagious disease with high mortality affecting a large number of pigs within an epidemiological unit.

However, analyses of the domestic pig outbreaks in the current epizootic revealed that the contagiosity is rather low. The initial mortality within an epidemiological unit is rather low regardless of the high case fatality rate.

The low contagiosity is complicating early disease detection as the initially low mortality rates can easily get unnoticed in larger farms. For wild boar however, in combination with the environmental stability of the virus and high population densities, the low contagiosity represents a major challenge for effective disease control.

High risk period

The high risk period (HRP) is defined as the time that elapses from virus introduction until disease confirmation. Due to the low contagiosity, which might be due to a low dose exposure and/or oral transmission route, the speed of virus spread within an epidemiological unit is slow.

Therefore, at the beginning of an outbreak usually only few pigs are affected and die.

In a small farm the death of few pigs would be noticed immediately, e.g. if three out of 10 pigs would die (30 pertcent mortality). However, if only three pigs die in a stable with 1,000 pigs (0.3 percent mortality) ASF is likely to remain unsuspected from the start.

In large farms with thousands of animals, the initial low mortality might lead to a prolonged HRP and it in can last several weeks until the mortality increases and exceeds a given threshold (e.g. 3 percent) before ASF is suspected.

The initial low mortality might lead to a prolonged HRP, particularly in farms with thousands of animals. In large farms it can take several weeks until the mortality increases and exceeds a given threshold (e.g. 3 percent) before ASF is suspected.

For keeping the HRP as short as possible, passive surveillance, which means targeted testing of sick and dead animals, has to be enhanced in ASF restricted and risk areas, says Depner. For example in breeding farms all dead gilts, sows and boars should be compulsory tested for ASF even if farm mortality is below the usual threshold.

Random sampling of healthy animals for spotting ASF would not lead to early disease detection, since the probability of ASF detection in clinically healthy animals is close to null. Besides that, the negative results would lead to a false sense of security.

When infected animals are detected early (short HRP), it can be assumed that large parts of the farm are not yet affected by ASF. Under the preconditions of slow virus spread, attempts to prevent further infections and avoid culling of pigs in non-affected farm units can be undertaken.

Persistency triangle

In wild boar populations, the ability of the virus to remain infective after putrefaction is of particular importance for wild boar carcasses that remain in the environment until total decomposition. In this regard, the low contagiousity of ASFV is contrasted by the high tenacity.

Contaminated wild boar carcasses might facilitate virus persistence for months within a region, significantly influencing the course of an ASF epidemic. Even if the probability of infection for each contact is low, the long-lasting persistence will allow maintenance of virus circulation.

The qualities of the three epidemiological traits contagiosity, tenacity, and case fatality rate make ASF virun efficient in both persistence and transmission. The interaction of these three parameters maximizes both local persistence and geographical spread of the virus making its eradication a challenge.

Depner calls it "The persistency triangle". Low contagiosity prevents fast and complete depletion of the host population. High case fatality makes the virus largely available in the form of carcasses. High tenacity ensures long term virus persistence in the environment.

The interaction of these three parameters maximizes local persistence and limits fast geographical spread.

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