Clinical signs

Table 2.1. FHV Disease forms, lesions and clinical signs [Note: concurrent infection with other agents is required to determine the aetiology of chronic rhinitis]

Source: ABCD

FHV infection typically causes acute upper respiratory and ocular disease, which can be particularly severe in young kittens. Viral replication causes the erosion and ulceration of mucosal surfaces, producing rhinitis, conjunctivitis and, occasionally, corneal ulcerative disease, mainly dendritic ulcers which are considered a pathognomonic clinical manifestation (Maggs, 2005).
Typical clinical signs are pyrexia, depression and anorexia, serous or serosanguineous ocular and/or nasal discharge, conjunctival hyperaemia, sneezing and, less frequently, salivation and coughing (Gaskell et al., 2006). Secondary bacterial infection is common in which case secretions tend to become purulent. In certain susceptible kittens, the disease may be more severe and FHV infection has been associated with primary pneumonia and a viraemic state that can produce severe generalized signs and eventually death (Gaskell et al., 2006).
Less frequent clinical signs associated with FHV are oral ulceration or dermatitis and skin ulcers (Hargis et al, 1999) and neurological signs (Gaskell et al., 2006). Abortion may occur as a rare secondary clinical sign, although, in contrast to other herpesviruses, it is not a direct consequence of viral replication.
After reactivation and recrudescent disease, some cats may show acute cytolytic disease as described above. Others may show chronic ocular immune-mediated disease in response to the presence of FHV virus. Strong experimental evidence suggests that stromal keratitis, associated with corneal oedema, inflammatory cell infiltrates and vascularisation and eventually blindness, is an example of this disease mechanism (Nasisse et al., 1989; Maggs, 2005).
Corneal sequestra and eosinophilic keratitis in cats have been linked to the presence of FHV in the cornea and/or blood in some of the affected cats. However, a definite causal association cannot be made since some affected cats are negative to FHV (Cullen et al., 2005, Nasisse et al., 1998). FHV DNA has been also detected in aqueous humor of a larger proportion of cats suffering from uveitis compared to healthy cats, suggesting that FHV may cause uveal inflammation (Maggs et al., 1999).
Chronic rhinosinusitis, a frequent cause of chronic sneezing and nasal discharge in cats, has been associated with FHV infection. Viral DNA can be detected in some affected cats, but is also found in controls without clinical signs (Henderson et al., 2004). Recent investigations show that the virus is not actively replicating in such cats, suggesting that chronic rhinosinusitis might be initiated by FHV infection, but perpetuated by immune-mediated mechanisms producing inflammatory and remodelling phenomena, leading to permanent destruction of nasal turbinates and bone complicated by secondary bacterial infection (Johnson et al., 2005).
Very often, FHV infection occurs combined with feline calicivirus and/or Chlamydophila felis, Bordetella bronchiseptica, Mycoplasma spp. and other micro-organisms, including Staphylococcus spp., Escherichia coli, may lead to secondary infection of the respiratory tract, causing a multi-agent respiratory syndrome (Gaskell et al., 2006).