by: Dr. Milad Ibrahim Aribi – Iraq

Many veterinarians have questions about adenovirus, and I will address some of the most common inquiries regarding this topic, even if simply, so that everyone can understand what adenovirus is from my perspective.

How does adenovirus spread?
Adenovirus can be transmitted through eggs to the embryo, and antibodies (Ab) can also be transferred. The virus remains in a latent state in chicks (broilers) until the maternal antibodies are cleared from the body. The virus will then activate under certain conditions, such as toxin exposure or immunosuppressive diseases.

It is important to note that adenovirus infection cannot be diagnosed through an ELISA test alone, as the presence of antibodies does not confirm whether they resulted from infection or vaccination. Therefore, when diagnosing adenovirus in chicks, both ELISA and PCR should be used. ELISA helps determine the antibody levels and the duration they remain in the bird, while PCR is used to detect the presence of the virus itself and determine its viral load (CT value). The CT value can also indicate the strength of the virus in the chicks.

Summary:

When diagnosing adenovirus in chicks, regardless of whether the maternal vaccination history is known, we must:

1. Use ELISA to measure the level of antibodies (Ab) transferred from the mother, and develop a vaccination program for the chicks.
2. Use PCR to measure the CT value for the virus (virus load), which helps confirm whether the virus is present in the chicks.

Can adenovirus spread from ducks to chickens?

It has been confirmed that adenovirus can spread from pigeons and sparrows to chickens, so it is possible for adenovirus to be transmitted from pigeons to chickens in poultry houses with poor biosecurity. As a result, egg and hatchery owners might unjustly be blamed for spreading the disease, even though they are not responsible for the outbreak.

Furthermore, wild birds may serve as carriers of the virus without being infected themselves, as they may consume poultry waste used by farmers as fertilizer for agricultural fields after being discarded from poultry houses.

The antibodies transferred from the mother to the embryo will not protect the embryo from other types of adenovirus. For example, if the mother was vaccinated against serotype FAdv8, the antibodies would not protect against serotype FAdv4 infection. This applies to all types of adenovirus. The infection will result in antibodies against the specific serotype that affected the mother during her breeding period.

From my field observations, I have noticed some adenovirus infections in chicks older than 24 days. The infection tends to be typical in broiler chickens but is minimal and does not significantly affect the birds. For example, in a poultry house with 6,000 birds, the daily infection rate might be around 6 birds, with very low mortality. Upon investigating the source of the breeder hens, it was found that the breeders were infected with adenovirus, and the antibody levels transferred to the chicks, as measured by ELISA, were above 8,000 titers. As a result, the immune system of the chicks was strong, and the adenovirus was in a latent state, unable to overcome the antibodies. However, if the flock becomes infected with immunosuppressive diseases, feed toxins, or is exposed to stress, the antibody titers will decrease, and the infection will be much more severe.

Adenovirus can also be transmitted through the eggshell if infected birds lay in the same nest, or through droppings or contaminated feathers. After hatching, the virus can spread via contact, ingestion, or inhalation. This horizontal transmission requires proper egg disinfection before entering the incubators.

The virus can be isolated on the first day of infection, but shedding peaks around the third week. When maternal-derived antibodies (MDA) decrease, the peak shedding occurs between the fourth and sixth week and may continue for up to 14 weeks after infection.

I have read many reputable studies on adenovirus infection, and I found that most cases are subclinical, primarily due to the presence of maternal antibodies and the low virulence of some serotypes. These two factors explain the presence of the virus without clinical symptoms. Therefore, scientists generally agree that most examined chicks carry the adenovirus.

In normal poultry house conditions, there are no significant issues with FAdv infection when MDA levels are high. However, as the titers decrease, the adenovirus will shift from latency to an active state and begin primary replication. Adenovirus has a unique feature of cell-free viremia, meaning the virus can spread to all parts of the body during replication and development, except in two areas: the central nervous system (CNS) and the testes.

However, researchers have concluded that adenovirus can also be found in semen. The main replication sites for the virus are the intestines and liver. Recent studies, based on samples I frequently send for PCR testing, showed a higher viral load (CT) in the liver, cecal tonsils, and bursa. The CT value in these organs can drop to below 12.

The severity and virulence of adenovirus increase at the peak of egg production, especially when the hens' age is between 31 and 39 weeks. The increased levels of steroid hormones and stress during this time can trigger the virus to shift from latency to activation, resulting in the transmission of the virus from the hens to the embryos.

Finally, it is important to note that detecting adenovirus through PCR does not necessarily mean that there is a clinical disease in the poultry house. This is because the virus can be present in healthy birds that are not showing symptoms, as the virus is naturally found in the poultry environment. This is a critical point for laboratory owners to consider when testing.