An influenza A virus, A/mink/Sweden/84 (H10N4), was isolated from farmed mi
nk during an outbreak of respiratory disease, histopathologically character
ised by severe interstitial pneumonia. The virus was shown to be of recent
avian origin and closely related to concomitantly circulating avian influen
za virus. Serological investigations were used to link the isolated virus t
o the herds involved in the disease outbreak. Experimental infection of adu
lt mink with the virus isolate from the disease outbreak reproduced the dis
ease signs and pathological lesions observed in the field cases. The mink i
nfluenza virus also induced an antibody response and spread between mink by
contact. The same pathogenesis in mink was observed for two avian influenz
a viruses of the H10N4 subtype, circulating in the avian population. When m
ink were infected with the prototype avian H10 influenza virus, A/chicken/G
ermany/N/49, H10N7, the animals responded with antibody production and mild
pulmonary lesions but neither disease signs nor contact infections were ob
served. Detailed studies, including demonstration of viral antigen in situ
by immunohistochemistry, of the sequential development of pathological lesi
ons in the mink airways after aerosol exposure to H10N4 or H10N7 revealed t
hat the infections progress very similarly during the first 24 h, but are d
istinctly different at later stages. The conclusion drawn is that A/mink/Sw
eden/84, but not A/chicken/Germany/N/49, produces a multiple-cycle replicat
ion in mink airways. Since the viral distribution and pathological lesions
are very similar during the initial stages of infection we suggest that the
two viruses differ in their abilities to replicate and spread within the m
ink tissues, but that their capacities for viral adherence and entry into m
ink epithelial cells are comparable. (C) 2000 Elsevier Science B.V. All rig
hts reserved.