Transmission and pathogenicity of canine H3N2 influenza virus in dog and guinea pig models

Abstract

Background: Influenza A virus causes respiratory disease in many animal species as well as in humans. Due to the high human-animal interface, the monitoring of canine influenza in dogs and the study of the transmission and pathogenicity of canine influenza in animals are important.

Methods: Eight-week-old beagle dogs (Canis lupus familaris) (n = 13) were used for the intraspecies transmission model. The dogs were inoculated intranasally with 1 ml of 10⁶ EID₅₀ per ml of canine H3N2 influenza virus (A/canine/Thailand/CU-DC5299/2012) (CIV-H3N2). In addition, 4-week-old guinea pigs (Cavia porcellus) (n = 20) were used for the interspecies transmission model. The guinea pigs were inoculated intranasally with 300 µl of 10⁶ EID₅₀ per ml of CIV-H3N2.

Results: For the Thai CIV-H3N2 challenged in the dog model, the incoculated and direct contact dogs developed respiratory signs at 2 dpi. The dogs shed the virus in the respiratory tract at 1 dpi and developed an H3-specific antibody against the virus at 10 dpi. Lung congestion and histopathological changes in the lung were observed. For the Thai CIV-H3N2 challenge in the guinea pig model, the incoculated, direct contact and aerosol-exposed guinea pigs developed fever at 1-2 dpi. The guinea pigs shed virus in the respiratory tract at 2 dpi and developed an H3-specific antibody against the virus at 7 dpi. Mild histopathological changes in the lung were observed.

Conclusion: The result of this study demonstrated evidence of intraspecies and interspecies transmission of CIV-H3N2 in a mammalian model.

Keywords: Canine influenza; Dog; Guinea pigs; H3N2; Pathogenicity; Transmission.

Fig. 1

Study design of the transmission and pathogenicity of CIV-H3N2 in dog and guinea pig models

Fig. 2

Clinical presentations and body temperature of CIV-H3N2-challenged dogs in the inoculated group, direct contact group and control group

Fig. 3

Viral shedding of CIV-H3N2-challenged dogs in the inoculated, direct contact and control groups. Viral shedding was presented as log10 of the geometric mean (copies per microliter). Bars represent the standard deviation of the mean viral titer

Fig. 4

Antibody response (HI test) of CIV-H3N2-challenged dogs in the inoculated, direct contact and control groups. The antibody titer was presented as the HI titer. Bars represent the standard deviation of the mean HI titer

Fig. 5

Histopathological changes in CIV-H3N2-challenged dogs, (a) interstitial pneumonia (4x), (b) bronchiolitis obliterans lesion (40x), (c) inflammatory cell infiltration with shortened tracheal epithelium (10x), (d) centrilobular fatty change degeneration (40X)

Fig. 6

Clinical presentation and body temperature of CIV-H3N2-challenged guinea pigs in the inoculated group, direct contact group, aerosol-exposed group and control group

Fig. 7

Viral shedding of CIV-H3N2-challenged guinea pigs in the inoculated group, direct contact group, aerosol-exposed group and control group. Viral shedding was presented as log10 of the geometric mean (copies per microliter). Bars represent the standard deviation of the mean viral titer

Fig. 8

Antibody response (HI test) of CIV-H3N2-challenged guinea pigs in the inoculated group, direct contact group, aerosol-exposed group and control group. The antibody titer was presented as the HI titer. Bars represent the standard deviation of the mean HI titer

Fig. 9

Histopathological changes in CIV-H3N2-challenged guinea pigs, (a) bronchointerstitial pneumonia, BALT hyperplasia and hemorrhage 40x; (b) bronchointerstitial pneumonia, BALT hyperplasia and hemorrhage 40x; (c) bronchointerstitial pneumonia and BALT hyperplasia 10x; (d) interstitial pneumonia and type II pneumocyte hyperplasia 40x