Hantavirus – from Puumala to Andes
Hantaviruses are a family of zoonotic viruses found worldwide. Rodents are the primary natural reservoirs for hantaviruses, but humans can become infected through exposure to some of these viruses. Nearly all human infections are acquired by inhalation of dust or aerosols contaminated with rodent urine or faeces (1). Andes virus is one of many hantaviruses and the only one known to be capable of human-to-human transmission (2).
Hantaviruses cause a range of clinical syndromes, broadly divided into two main groups. In Europe and Asia, hantaviruses cause haemorrhagic fever with renal syndrome, whereas in the Americas they cause hantavirus cardiopulmonary syndrome (3). There is some overlap in clinical presentation, and disease severity varies according to viral variant, host factors, the type and degree of exposure, and early access to intensive care (3).
Only one hantavirus is known to be endemic in Norway: Puumala virus, first identified in Puumala, Finland, in the 1980s. This virus causes nephropathia epidemica ('mouse fever'). Typically, 10–40 cases of the virus are reported annually in Norway, but this likely only includes the more severe cases, as individuals with mild and non-specific symptoms are probably not diagnosed (1). Puumala virus usually causes a mild illness, with fever, headache, back and abdominal pain, although some patients experience renal involvement (1). Infection is caused by exposure to virus shed by bank voles and, probably, field voles, for example during outdoor activities, stacking firewood, or removing rodent droppings in holiday cabins (1). Variants of hantavirus found in Asia and other parts of Europe, such as Hantaan, Dobrava and Seoul viruses, cause a more severe form of haemorrhagic fever with renal syndrome than Puumala virus (3).
Only one hantavirus is known to be endemic in Norway: Puumala virus, first identified in Puumala, Finland, in the 1980s. This virus causes nephropathia epidemica ('mouse fever')
Disease caused by Andes virus infection was first described in Argentina and Chile in 1995. Since then, more than 1200 cases have been reported in South America, with an increasing incidence in recent years (4). The rodent Oligoryzomys longicaudatus is the natural reservoir of Andes virus and is found only in South America. The incubation period is uncertain but is estimated at 1–6 weeks (3).
Clinical presentation is often non-specific at onset. Patients typically present with fever, marked malaise, fatigue, myalgia, headache, dizziness and gastrointestinal symptoms including nausea, vomiting, diarrhoea or abdominal pain (3). In some cases, this can progress within a few days – typically around one week – to cough, dyspnoea, hypoxia, hypotension, or other signs of rapidly progressive respiratory or circulatory compromise. At this stage, the disease may present as a severe acute respiratory infection or atypical pneumonia, and patients should be admitted to hospital for close monitoring for rapid clinical deterioration (5).
The fatality rate for Andes virus infection has been reported at 20–50 %, although estimates vary substantially depending on outbreak setting, availability of diagnostics and early access to treatment (3,6). Early diagnosis and organ support in intensive care, including extracorporeal membrane oxygenation (ECMO), can improve outcomes (3). There is no proven antiviral treatment, although experimental treatments may be an option, including the unlicensed influenza drug favipiravir, which has shown promising results in animal studies (7). The bradykinin B2 receptor antagonist icatibant has also been used in some patients with severe Puumala virus (8). There are currently no approved vaccines for Andes virus.