What Is Avian Nephropathogenic Infectious Bronchitis?
Nephropathogenic infectious bronchitis is a pathological manifestation of avian infectious bronchitis caused by coronavirus. In recent years, especially since last winter and this spring, the incidence of nephropathogenic IB in Shandong Province, China, particularly in the Qingdao area, has risen significantly, causing considerable economic losses to the @#@230@#@ industry, especially the broiler industry, and thus attracting widespread attention.
Nephropathogenic IB is not an independent disease caused by an independent virus; it is a special phenotype of IB virus strains in the urinary organs of chickens; or rather, it is a prominent manifestation in the kidneys during the systemic infection of chickens by certain nephrotropic IB viruses under specific environmental conditions.
Research shows that the sum of all nephropathogenic IB virus strains worldwide does not indicate that they constitute an independent IB serotype. In fact, it can be said that IB viruses of any serotype may, under certain conditions, exhibit kidney-damaging effects. For example, nephropathogenic IB is very common in Australia; apart from the well-known "T strain," almost all IB viruses isolated in Australia can cause kidney lesions to a greater or lesser extent. Serum neutralization tests on the nephropathogenic IB virus strain C90/66 isolated from Thailand in 1990 showed that it does not belong to the T strain and has no relationship with the UK IBV4/91 strain, but is closely related to the Mass-type H120 strain. The variation of IB virus is extremely complex. Humanity has not yet fully understood and grasped all its secrets. Perhaps we can now say that nephropathogenic IB viruses (strains) are, under certain conditions, some variants of common respiratory-type IB viruses at the level of biological characteristics and serotypes.
This disease infects only chickens, with broilers being particularly susceptible; other poultry are not infected. It occurs more frequently during the rainy season and cold season. It is characterized by regional sporadic occurrence. The susceptible age is between 15 and 50 days of age, with a peak incidence at 3 to 6 weeks of age, which is almost identical to infectious bursal disease.
The typical course of nephropathogenic IB can be divided into two stages: The first stage (around 3 weeks of age) has mild respiratory symptoms, which are often overlooked and disappear after 2 to 4 days; the second stage occurs 7 to 10 days after onset (i.e., around 4 weeks of age), when a mortality peak appears, the flock's systemic symptoms suddenly worsen, with depression, anorexia, discharge of grayish-white loose stool or white pasty feces, sometimes watery diarrhea, severe dehydration, and dry and withered feet and claws (commonly known as "dry leg" or "dry claw disease"). The entire course lasts 21 to 25 days, with a mortality rate of 10% to 30%. Generally after 6 weeks of age, the condition tends to ease, and the mortality rate drops below 1%, but growth is markedly slowed and the feed conversion ratio declines.
The pathological changes of nephropathogenic IB are mainly concentrated in the kidneys, manifesting as bilateral kidney enlargement and pallor, with the renal tubules causing the kidneys to appear areca-nut-like mottled due to accumulated urates. Both ureters become noticeably distended due to deposited urates, thickened and whitish. In chronic cases, the kidneys are discolored, and the renal parenchyma is filled with millet-sized yellowish-white urate nodules, sometimes reaching the size of soybean to broad bean (kidney stones). In some cases, one or both ureters are completely blocked by white urates, forming ureteral stones and urinary retention. Sometimes urates also accumulate on the pericardium and liver surface, like a layer of white frost; this is visceral gout. The cloaca is filled with white lime-paste-like urate excrement.
The severity of kidney lesions depends on 6 main factors: (1) strain characteristics; (2) maternal antibody levels; (3) sex (mortality in males is higher than in females); (4) nutritional status (mortality in chickens on high-protein feed is lower than in those on low-protein feed, which is related to uremia levels); (5) breed line, with broiler chicks having the highest incidence; (6) age at infection (the younger the age at onset, the higher the mortality). In addition, it is also related to the immune system status of the affected chickens. Preliminary statistics show that broilers vaccinated with high-virulence infectious bursal disease vaccine have a higher proportion of nephropathogenic IB incidence.
The diagnosis of nephropathogenic IB is generally not difficult. From the age at onset, white loose stool, severe dehydration, plus the severe kidney swelling and urate-deposited mottled kidneys found during necropsy, a preliminary diagnosis can be made. Nephropathogenic IB lacks hemorrhages in the pectoral and leg muscles, and also lacks a lightning-fast course and peak-type mortality, so it is generally not confused with infectious bursal disease. Although some IB strains can also cause edema and a certain degree of hemorrhage in the bursa of Fabricius, an agar gel diffusion test using bursal tissue suspension and infectious bursal disease positive serum can distinguish the true from the false.
For the prevention of nephropathogenic IB, in addition to good biosecurity control, isolation, and disinfection on the chicken farm, vaccination is mainly relied upon. For broilers and broiler breeders, if nephropathogenic IB epidemic disease or the threat of epidemic disease exists locally, then in addition to immunization with ordinary-type IB vaccines (such as H120, Ma5, etc.), high-quality nephropathogenic IB vaccines should also be selected for immunization (such as H120+28/86 nephropathogenic IB). On some broiler farms in the Qingdao area, after using ND-VH+H120+28/86 at 1 day of age (eye drop or nasal drop), generally speaking, nephropathogenic IB is extremely rare. Conversely, if only H120 or Ma5 vaccine is inoculated, then nephropathogenic IB is relatively more common. However, since last winter and this spring, cases of nephropathogenic IB have gradually increased on some broiler farms that had been immunized with H120+28/86 vaccine. Through laboratory testing, IB virus causing dwarf embryos can indeed be isolated. After excluding the effects of immunization procedures and vaccine quality, the reason may be related to variation of nephropathogenic IB (including virulence variation and molecular variation), invasion of new-type IB viruses, and the immune status of the chickens. Since most of the newly emerging nephropathogenic IB cases occur after using high-virulence infectious bursal disease (IBD) live vaccines, in order to reduce damage and pressure on the immune center. This is not only beneficial for the prevention of nephropathogenic IB, but also of great significance for the prevention of other infectious diseases, especially Newcastle disease, avian influenza, and colibacillosis.
If nephropathogenic IB still occurs after vaccination with the 28/86 strain nephropathogenic IB vaccine, consideration can be given to trying Gallivac IBn nephropathogenic IB vaccine (a product of Merial) at 7 days of age. This is a new-type live nephropathogenic IB vaccine developed from a nephropathogenic IB virus strain (C90/66) isolated from Thailand in 1990 after attenuation through 65 passages in SPF chicken embryos. It is reported that after a single immunization at 7 days of age, it can provide 100% protection against nephropathogenic IB in Thailand, Taiwan, China, and Malaysia, with a protection period lasting about 6 weeks, making it very suitable for broiler use. If Newcastle disease live vaccine inoculation is scheduled at 7 days of age, it can be administered separately from Gallivac IBn vaccine by eye drop (one drop on each side); doing so will not have a significant impact on Newcastle disease immunization.
It is worth noting that a vaccine with good protective efficacy against nephropathogenic IB in one region may have no protective effect against nephropathogenic IB in another region. If nephropathogenic IB vaccines from other regions are blindly introduced, they may have a protective effect against local nephropathogenic IB, or they may provide no protection at all and instead introduce new viruses to the local area. Everything should be based on practice as the criterion.
If various commercially available IB vaccines cannot well protect the local chicken flock against IB or nephropathogenic IB, the best approach is to use virus strains isolated from affected chickens on the farm and ask a qualified research institute or laboratory to produce an oil-emulsion autogenous inactivated vaccine, and immunize in combination with classical-type live IB vaccine at the same time; this can better solve the problems of serotypes and variant strains.
When nephropathogenic IB is complicated by mycoplasmosis, colibacillosis, and especially viral diseases such as Newcastle disease and avian influenza, the mortality rate will increase substantially. At this time, strengthening veterinary hygiene and feeding management becomes even more important.
In terms of treatment, there is currently no specific drug. Symptomatic medication is mainly for diuresis and detoxification. Rehydration salts, or high-quality electrolytes + vitamins, can be added to drinking water. Certain traditional Chinese medicines for kidney swelling and detoxification may be somewhat helpful for uremia.