Infectious canine hepatitis virus
Canine adenovirus belongs to the Adenoviridae family and the genus Mastadenovirus. It is divided into two types: CAV-1 and CAV-2. CAV-1 causes infectious canine hepatitis (ICH), while CAV-2 leads to infectious tracheobronchitis in dogs. Notably, the two types share a common complement-binding antigen. However, they differ in their biochemical characteristics and nucleic acid homology, allowing them to be distinguished using hemagglutination inhibition assays, neutralization tests, and molecular biology techniques. Infectious canine hepatitis is one of the major, highly contagious diseases affecting dogs, making it a mandatory test for both general-grade and SPF dogs in China.

Pathogenic characteristics
Canine adenovirus is a non-enveloped, linear, single-molecule double-stranded DNA virus approximately 80 nm in diameter, characterized by the presence of a capsid. CAV-1 measures around 80 nm in diameter and shares morphological features typical of other animal adenoviruses—specifically, a highly symmetrical icosahedral structure. Its protein capsid consists of 252 capsomeres, organized into key components such as hexon trimers, penton bases, and fiber proteins. Notably, the fibers extending from the penton base bear a globular structure on their surface, which contains hemagglutinin molecules. During viral infection, this globular structure facilitates binding to cellular receptors, enabling the virus to enter host cells effectively.

Popular Characteristics
Canine adenovirus is primarily transmitted through the digestive tract but can also spread via parasites. Infected dogs, as well as healthy dogs that have recovered from the disease and still carry the virus, excrete large amounts of adenovirus in their feces, urine, secretions, and blood. As a result, any environment—or even items like feed,饲养器具 (feeding equipment), and drinking water—that becomes contaminated with the virus can serve as a source of transmission. Dogs of all ages are susceptible to infection; however, adult dogs typically experience asymptomatic or mild infections, while puppies younger than one year old are particularly vulnerable. Once infected, these young pups often face a high mortality rate—typically dying within 2 to 10 days after onset, with mortality rates reaching as high as 30% to 40%. Additionally, artificial infection poses a significant risk, as medical personnel can inadvertently transmit the virus to dogs through routes such as intramuscular injection, subcutaneous injection, intravenous administration, or oral ingestion. Notably, canine adenovirus exhibits remarkable resistance to ether and chloroform. It can survive for up to 270 days at 4°C, remains viable for 70 to 91 days at room temperature, and persists for 29 days at 37°C. Even when exposed to 56°C for 30 minutes, the virus retains its infectivity. Meanwhile, the virus can endure for up to 3 days in the liver, serum, and urine of sick dogs stored at 20°C. Fortunately, canine adenovirus is highly sensitive to iodophors and sodium hydroxide, making these disinfectants effective for eliminating the pathogen.
CAV-1 can be excreted in urine within 6 to 9 months after infection. Dogs have an incubation period of 4 to 6 days after ingesting the infectious agent, and 6 to 9 days after direct contact with infected dogs.

Clinical symptoms and pathological changes
The hepatitis type primarily manifests clinically as mild symptoms such as loss of appetite lasting several days, sensitivity to cold, depression, increased thirst, and discharge from the eyes and nose—sometimes reaching up to 41°C. As the disease progresses, additional symptoms may emerge, including an elevated heart rate, rapid breathing, fatigue, vomiting, diarrhea, or even the passage of bloody stools. In acute cases of death, blood-like ascites is often observed in the abdominal cavity, accompanied by noticeable liver enlargement. Upon incision, the liver appears everted, with a dull yellowish-brown color and a notably brittle texture. The tissue structure at the cut surface lacks clarity, revealing numerous dark red spots. Meanwhile, the gallbladder walls exhibit edema, turning blackish-red in appearance. Regarding the pathogenesis of infection in dogs: After entering the body through the oropharynx, the virus initially infects the tonsils before spreading to local lymph nodes and lymphatic vessels, where it multiplies. From there, the virus enters the bloodstream via lymphatic ducts, triggering viremia in the dog. This viral spread subsequently leads to infections in other tissues, damaging endothelial cells throughout the body and impairing liver function, ultimately resulting in liver damage. The virus is eliminated from the body primarily through infected secretions. During the acute phase of the disease, the virus becomes widely distributed across all tissues of the infected dog. Occasionally, during the recovery phase, corneal opacity—a condition commonly known as "blue eye"—may appear.
The respiratory form primarily manifests clinically as elevated body temperature, rapid breathing, irregular pulse rhythm, along with symptoms such as coughing and purulent nasal discharge. In some cases, affected dogs may also experience vomiting and bloody stools. Post-mortem examination reveals incomplete lung expansion accompanied by congestion.

Dogs with ICH exhibit bilateral corneal haze.

The resulting impact
CAV-1 is a highly contagious, widespread infectious disease in dogs, characterized by high incidence and mortality rates. In addition to causing canine infectious hepatitis, CAV-1 can also lead to encephalitis in foxes and bears. This virus is found globally, posing significant threats to both canine and fur-bearing animal industries.

Laboratory testing
Electron microscopy revealed crystalline-arranged viral particles within the nuclei of the affected cells. Molecular biology techniques such as PCR and qPCR are employed for detection. Serological methods, including IFA, HI, and ELISA assays, are used for diagnosis. (The HI assay, established in 2019 by Meng Xing et al., involves the binding of serum antibodies to CAV-1, preventing the virus's hemagglutinin from attaching to receptors on red blood cell surfaces, thereby inhibiting hemagglutination and enabling the detection of CAV-1-specific antibodies in the serum.)
The blood routine test results showed that the dog's WBC (white blood cell count) and PLT (platelet count) were significantly lower than the lower limits of the normal range, while all other measured parameters remained within normal limits, suggesting that the infection may be caused by this virus. Meanwhile, the blood biochemistry tests revealed that the dog's alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and total bilirubin (TBIL) levels were markedly elevated—exceeding the upper limits of the normal range—indicating severe liver damage. Notably, both canine distemper virus (CDV) and canine parvovirus (CPV) antigen tests came back negative, whereas the adenovirus (CAV) test was positive. Based on these findings, it can be concluded that the dog is infected with adenovirus (CAV).

Effective prevention
Effective disinfection measures can fundamentally prevent the widespread transmission of viruses and promptly cut off routes of infection. For dogs aged one week or younger, regular vaccinations are recommended. Puppies should receive their first dose of attenuated infectious hepatitis vaccine 3 to 7 days after weaning, followed by a second injection 3 to 4 weeks later. Thereafter, boosters should be administered every 6 months. In addition, proactive treatment strategies are also crucial.
References
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