At present, chicken-origin Riemerella anatipestifer has become the hottest topic in the poultry industry, a bona fide “star disease,” and the trend appears to be worsening. But is the emergence of chicken-origin Riemerella anatipestifer really what has caused such enormous losses to the industry? I personally believe this issue should be analyzed comprehensively rather than focusing solely on Riemerella anatipestifer in chicken flocks.
I. About the pathogen
Riemerella anatipestifer is a Gram-negative bacterium. To date, 25 serotypes of Riemerella anatipestifer have been reported. This is a highly prevalent infectious disease that can spread among waterfowl such as ducks and geese, as well as chickens and wild birds. As of the middle of this month, the strains isolated by the laboratory from chicken embryos and commercial broilers have mainly been serotype 1 and YB1, with serotype 1 accounting for more than 90% of these two serotypes. The strains isolated from caseous material in the oviduct were mainly serotype 10, while serotypes 5, 1, and 7 were also detected to varying degrees. However, in terms of pathogenicity, strains originating from chicken embryos are relatively low in virulence. This comes with an important caveat: their virulence is low when they cause disease alone, not when they are co-infected with Escherichia coli, or when there is concurrent infection with pullorum disease, variant-strain bursal disease, H9, infectious bronchitis, or stimulation from vaccination. In clinical practice, the likelihood of chickens being infected with chicken-origin Riemerella anatipestifer alone is almost nonexistent. This point must be made clear.
II. Infected breeds
Among the breeds currently affected, white-feather broiler breeders, commercial white-feather broilers, and layer chickens have relatively high detection rates. It has also been detected in Chinese native chickens, but the detection rate in the latter is much lower than in the former.
III. Age at infection
Disease can occur within the first seven days after infection, with pathological changes involving three types of inflammation. The first peak occurs after the first vaccination. If, after the first vaccination, only respiratory signs worsen and no obvious anatomical changes appear, then, if respiratory disease is not managed properly, around 15 days of age becomes the second peak. If the flock’s condition has not clearly improved through husbandry management and medication before 20 days of age, then any age after 20 days may become the third peak. This may be related to the level of husbandry management and whether the medication regimen is appropriate, resulting in differences in disease severity and age at onset. However, it should be noted that these outbreaks all occur as co-infections, not as outbreaks caused by Riemerella anatipestifer alone. In my view, based on the virulence of the isolated serotype strains, they are not sufficiently virulent to cause severe disease on their own.
IV. Mixed infections
1. Among bacterial diseases, mixed infection with Escherichia coli is the most common, occurring in almost 100%. In every case in which Riemerella anatipestifer of chicken origin was detected, Escherichia coli was also detected, without exception.
2. Viral co-infections: the rate is highest with variant infectious bursal disease virus (80%), followed by infectious bronchitis, H9, chicken infectious anemia, and Newcastle disease, which has a relatively lower co-infection rate.
V. Clinical symptoms
1. In the early stage, respiratory problems are the main issue, primarily presenting as coughing, including a wet cough, and mild rattling. Treatment is not notably effective, and the condition does not resolve despite prolonged treatment.
2. Head swelling may occur, but at a much lower rate than with influenza.
3. Lethargy, weight loss, dry feet, closed eyes and a tucked-in neck, ruffled feathers, and paralysis are prominent signs, with birds lying prone and motionless.
4. Mortality in most flocks continues for a prolonged period, sometimes until they are ready for market, and medication is not very effective. An unusual pattern is also seen in which the flock appears generally healthy, yet daily mortality and culling remain high.
5. If environmental stress is also present before disease onset, it can significantly accelerate disease progression and increase mortality. This may also be closely related to the activation of other pathogens.
6. The hock joints are swollen, and the contents range from pus-like to caseous.
Five. Pathological changes
1. The main findings are pericarditis, airsacculitis, peritonitis, and perihepatitis. Pericarditis and peritonitis are the most severe and occur earliest. When obvious perihepatitis is present, the peritoneum of dead birds examined at necropsy has often already developed extremely dry, sheet-like yellow caseous material. This suggests that, early in the disease, infection may primarily affect the heart and peritoneum. At this stage, anti-inflammatory drugs and other medications with an advantage against abdominal cavity infections may be more effective.
2. Another finding is the state of the exudate: it may be yellow fibrin or slightly gelatinous (particularly evident around the liver). The time required for infectious ascites to develop is substantially shorter, and its likelihood is also greatly increased. One point bears emphasis: these pathological changes are not caused by chicken-origin Riemerella anatipestifer alone; other bacteria and viruses are also involved.
3. In white-feather broiler flocks, necropsy may reveal incomplete regression of the oviduct due to pathogen infection, with caseous material obstructing it, but this occurs relatively infrequently.
Six. Summary
1. The 100% concurrent infection rate with large rods indicates that simultaneous infection with chicken-origin Riemerella anatipestifer and other bacteria is a common and serious phenomenon. This may be a major factor contributing to severe inflammatory exudation in the thoracic and abdominal cavities.
2. The presence of variant-strain infectious bursal disease, chicken infectious anemia, infectious bronchitis, H9, and Newcastle disease in mixed infections indicates that immunosuppressive diseases and common viral diseases may be important factors contributing to disease caused by chicken-origin Riemerella anatipestifer.
Based on the two points above, immunosuppressive diseases interact and act synergistically with common viral diseases and frequently occurring bacterial diseases. Immunosuppressive diseases can significantly increase the virulence, pathogenicity, and reproductive capacity of common viral diseases and frequently occurring bacterial diseases, while common viral diseases and frequently occurring bacterial diseases can, in turn, significantly intensify the immunosuppressive effects of immunosuppressive pathogens. This creates a difficult problem: antibodies, antiviral drugs, or antibacterial drugs used relatively alone are unlikely to be effective.
Seven. Based on the above analysis, I personally believe effective approaches can start with these aspects
1. Address immunosuppression (chicken infectious anemia and variant-strain infectious bursal disease)
2. Address common viral diseases (infectious bronchitis, H9, and Newcastle disease)
3. Use antimicrobial susceptibility testing or clinical drug-efficacy trials to select drugs effective against chicken-origin Riemerella anatipestifer and “large bacilli”; initially, select drugs that are effective for intraperitoneal infection.
4. Select appropriate symptomatic drugs based on the clinical presentation of the chicken flock.
The purpose of this approach is to cut off, as much as possible, the synergistic relationships among immunosuppressive diseases, common viral diseases, and frequently occurring bacterial diseases. Even if chicken-origin Riemerella anatipestifer is highly drug-resistant, once this relationship is disrupted, treating it as a relatively isolated pathogen can still produce relatively satisfactory results.
Source: Poultry Disease Professional Network Forum, author: Persistent Shepherd (Liang Chengyu). Please indicate the source and author when reprinting!