Dirofilariasis is predominantly a veterinary problem. Two species of dirofilariae, Dirofilaria immitis and D. repens, are widely distributed in southern Europe where they cause heartworm disease and tissue nodules, respectively, in dogs, cats and other carnivores. Humans are inadvertent and unsuitable hosts where the parasites usually do not develop to the mature and reproductive adult stage. Instead, in the case of human infection, the worms are generally found encapsulated in subcutaneous, pulmonary and intraorbital nodules induced by the immune defence (McCall et al. 2008; Simón et al. 2009).

Various mosquito species of the genera Aedes, Anopheles, Culex and Ochlerotatus take part in the transmission of dirofilariae in Europe (Pampiglione et al. 1995). In endemic areas in Italy, the most important vectors are probably Oc. caspius and Ae. vexans (Gratz 2004), but the newly introduced species Ae. albopictus also appears to play an important role in the epidemiology of dirofilariasis (Cancrini et al. 2003).

The highest prevalences of human dirofilariasis are to be found in Italy (66%), France including Corsica (22%), Greece (8%) and Spain (4%), but many cases are probably not diagnosed or notified (Pampiglione et al. 1995; Raccurt 1999). Notified human cases of D. repens infections have substantially increased in number during the past two decades or so in the Mediterranean (Pampiglione et al. 1995; Muro et al. 1999; Pampiglione and Rivasi 2000; Simón et al. 2005). Increasing travel seems to favour its emergence outside known endemic areas, and it is possible that both D. immitis and D. repens have spread to the south of Switzerland (Bucklar et al. 1998). Even more northerly, in the Netherlands and Germany, single autochthonous cases of D. repens infections in dogs were recently reported (Hermosilla et al. 2006; Overgaauw and Van Dijk 2009).

The reasons for the observed geographic expansion of Dirofilaria worms are not clear, but climate change, the spread of vectors and increased uncontrolled movement of dogs and cats through Europe are supposed to be important driving forces (Genchi et al. 2005, 2009).

Malaria was endemic in Europe until about the mid-twentieth century (Bruce-Chwatt and de Zulueta 1980). It did not only occur in the subtropical Mediterranean regions but as far north as Scandinavia (Huldén et al. 2005). Plasmodium vivax, P. malariae and, less commonly, P. falciparum were the malarial agents circulating in Europe. After centuries of human and parasitic coexistence (Reiter 2000), malaria was on the decline since the nineteenth century when the intensification of agriculture and livestock farming resulted in the large-scale drainage of swamps, marshes and other wetlands, thus substantially reducing Anopheles breeding sites. A general improvement in living and hygienic conditions as well as the spatial separation of human dwellings and livestock keeping facilities contributed to a further reduction of humans being exposed to mosquito bites. On a pan-European scale, however, malaria disappeared only as a consequence of the additional administration of efficient drugs (chloroquine) and insecticides (DDT) developed in the early twentieth century decades (Alten et al. 2007).

While the WHO declared malaria eradicated from Europe in the 1970s, isolated locally acquired cases continued to occur. Indigenous Plasmodium strains that had evolved in parallel to their European vector mosquitoes, however, appeared to have become extinct. Subsequent autochthonous malaria cases, plenty of which were recorded in continental Europe in the past 20 years or so (Sartori et al. 1989; Nikolaeva 1996; Baldari et al. 1998; Krüger et al. 2001; Cuadros et al. 2002; Kampen et al. 2002; Zoller et al. 2009; Santa-Ollala Peralta et al. 2010; Danis et al. 2011a), were most likely due to transmission of parasites imported with their human hosts from overseas endemic areas. Presumably due to missing coadaptation, experimental infection of European Anopheles species with tropical Plasmodium strains usually failed to produce infective parasite stages (Shute 1940; Ramsdale and Coluzzi 1975; Daškova and Rasnicyn 1982). In more recent studies, An. plumbeus developed P. falciparum oocysts and sporozoites, respectively, though (Marchant et al. 1998; Eling et al. 2003).

Given the still increasing travel activities to and from tropical countries with endemic malaria and a global warming scenario that allows both a higher reproduction rate of the mosquitoes, resulting in higher population densities, and a shorter developmental time of the malaria parasites in the mosquito (extrinsic incubation period) with rising temperatures, an increase in autochthonous malaria cases in Europe must be expected for the future. However, due to the high health standards, the lack of a zoonotic reservoir of the human plasmodia and their relatively short incubation period that makes disease cases quickly apparent, it is very unlikely that malaria ever becomes endemic again in central Europe.

Although West Nile virus (WNV; Flaviviridae, Flavivirus, Japanese encephalitis antigenic complex) was reported from the French Rhone delta already in the early 1960s (Hannoun et al. 1964) and Europe has henceforth faced occasional WNF epidemics, WNF is commonly considered emergent. This is probably due to the fact that, since the middle of the 1990s, outbreaks tend to occur increasingly often and more regularly present with severe neurological manifestations (Gubler 2007). While the majority of the majority remains asymptomatic, 20–40% of infected persons may develop clinical illness with about 1% displaying encephalitis, meningitis and flaccid paralysis (Kramer et al. 2003). Of the neuroinvasive cases, a substantial percentage will suffer from long-term disability or even die (Klee et al. 2004).

In addition to humans, equines and corvid birds are particularly susceptible to the virus. Numerous fatal cases of disease and several outbreaks among humans and equines with high morbidities and mortalities were observed during the past 15 years or so in various countries of Europe, for example, Romania in 1996 (Tsai et al. 1998), Russia in 1999 (Platonov et al. 2001), France in 2000 (Murgue et al. 2001), Italy in 2002, 2008 and 2009 (Autorino et al. 2002; Macini et al. 2008; Barzon et al. 2009; Rizzo et al. 2009; Angelini et al. 2010) and Greece in 2010 and 2011 (Danis et al. 2011b, c).

WNV is widely distributed in Africa and Eurasia where a lot of mosquito species have been found infected (Hubálek and Halouzka 1999). Principal vectors in Europe are Cx. pipiens, Cx. modestus and Cq. richardii (Reiter 2010), with Cx. p. pipiens biotype molestus being the most important bridge vector transmitting the virus from birds to humans (Kilpatrick et al. 2005; Hamer et al. 2008, 2009). Transovarial transmission of WNV has been observed, for instance, in Ae. albopictus and Cx. pipiens (Baqar et al. 1993; Goddard et al. 2003), and overwintering was documented to occur in Cx. pipiens (Nasci et al. 2001).

Vertebrate reservoir hosts of WNV are mainly wild birds, with most of the species displaying no clinical signs after infection (Malkinson and Banet 2002). Migratory birds seem to play a particular role in virus transportation over long distances, for example, from Africa to the European continent (Rappole et al. 2000). WNF outbreaks are often connected to wetlands where huge numbers of migratory and non-migratory birds aggregate and come into contact with myriads of mosquitoes. In addition to this rural transmission cycle where amplification of the virus occurs and ornithophilic mosquitoes are involved, an urban cycle with less host-specific mosquito vector species appears to exist (Hubálek and Halouzka 1999; Koopmans et al. 2007).

While only exceptionally WNF has been diagnosed and virus could be isolated north of about latitude 49° in Europe (Hubálek 2008), there is evidence of more widespread virus circulation, for example, in Great Britain and Germany (Buckley et al. 2006; Linke et al. 2007), from serological studies on resident birds.

Contrasting the common assumption that dengue virus (DENV; Flaviviridae, Flavivirus, dengue antigenic complex) is associated with tropical regions, it used to be endemic in southern Europe as long as Ae. aegypti was present. In 1926–1927, DENV caused a major outbreak in Greece with more than 1,000 deaths due to dengue haemorrhagic fever among an estimated total of close to one million disease cases (Cardamatis 1929; Rosen 1986). With a low mortality rate, dengue fever probably also occurred in Spain at the beginning of the eighteenth century (Eritja et al. 2005). It disappeared from Europe together with its vector, and both here and elsewhere the absence of dengue epidemics in former endemic regions has been ascribed to successful mosquito/Ae. aegypti control (Gubler 1989).

On a global scale, dengue has been spreading and numbers of cases have been rising continuingly for decades, not the least because of the global spread of Ae. albopictus and ongoing urbanization (Guzman and Istúriz 2010). For this reason and for the re-emergence of Ae. aegypti in former endemic areas such as Madeira (Almeida et al. 2007) and the Georgian Black Sea coast (Iunicheva et al. 2008), concern about dengue resurgence is growing in Europe.

However, while the spread of Ae. aegypti is limited by its cold intolerance, this is obviously not the case with Ae. albopictus (Grist and Burgess 1994). Due to the continuing spread of Ae. albopictus in Europe, dengue is presently also regarded a risk to temperate climatic zones. Although located in warm regions of Europe, first autochthonous cases of DENV transmission, most likely caused by Ae. albopictus, after decades of absence of the disease have been reported from Croatia (Schmidt-Chanasit et al. 2010; Gjenero-Margan et al. 2011) and southern France (Gould et al. 2010; La Ruche et al. 2010).

Aedes aegypti is highly anthropophilic and must be accounted for the vast majority of cases of DENV transmission to humans. It is a particularly synanthropic mosquito species and prefers breeding in urban surroundings in small artificial water containers (Christophers 1960). Independent of this human urban dengue cycle driven by Ae. aegypti, a sylvatic cycle among wild primates exists in Southeast Asia and West Africa with other zoophilic Aedes mosquito species as vectors (Vasilakis et al. 2011). In rural areas, both cycles are connected by peridomestic Aedes species such as Ae. albopictus whose developmental stages are also frequently found in small man-made containers (Hawley 1988).

There is no DENV vertebrate reservoir other than humans and non-human primates.

Dengue can present with a broad spectrum of clinical illness, ranging from mild non-specific symptoms to severe and fatal disease (Halstead 2002). According to WHO case definitions, three clinical developments are possible: classical dengue, dengue haemorrhagic fever and dengue shock syndrome. Classical dengue occurs in most cases of infection when a host undergoes a primary infection with DENV. It is asymptomatic or causes a self-limited febrile syndrome with undifferentiated symptoms such as the sudden onset of fever, nausea, vomiting, headache, retro-orbital pain and rash, accompanied by severe joint and muscle pain (“breakbone fever”). In some cases, usually after a second DENV infection with another serotype (Halstead 1980), classical dengue proceeds as dengue haemorrhagic fever. This often happens around the time of defervescence and presents with haemorrhagic manifestations (petechiae, mucosal bleedings) and cavitary effusions. Up to about 10% of cases that develop shock (dengue shock syndrome) are fatal (WHO 2005).

Yellow fever indeed is a disease of the tropics and subtropics, resulting from the thermophilic mosquito species Ae. aegypti being the principal vector of the causative agent, yellow fever virus (YFV; Flaviviridae, Flavivirus), in the human-to-human urban cycle. Similar to DENV, there is a jungle cycle in endemic regions in Africa and South America, respectively, where tree-hole-breeding mosquito species, such as Ae. africanus (Africa) and Haemagogus species (South America), transmit the virus between monkeys. In the moist savanna regions, the zones of emergence, a rural cycle takes place where the virus is transferred by various Aedes species, including Ae. africanus and Ae. simpsoni, from the jungle cycle monkey reservoirs to humans (Vainio and Cutts 1998). The virus is maintained in the mosquito population by vertical transmission via the eggs (Beaty et al. 1980; Fontenille et al. 1997).

Yellow fever may clinically present with a broad spectrum of symptoms ranging from non-specific flu-like illness to fatal haemorrhagic fever. Typical signs of a febrile illness, such as headache, myalgia, malaise, nausea, etc., appear during a first phase, the period of infection, which lasts several days. A short period of remission may follow in which the disease symptoms disappear. About a fourth of the people affected enter a more severe third phase, the period of intoxication, with fever, vomiting, jaundice, renal failure, haemorrhages, hypotension and coma. Up to 50% of the patients with hepatorenal dysfunction die within 1–2 weeks (Monath 2001).

In Europe, yellow fever outbreaks were recorded in Portugal, Spain, Italy and France in the eighteenth and nineteenth centuries (Strode 1951; Eritja et al. 2005). Although potential mosquito vectors spread and numbers of travellers returning from yellow fever endemic regions rise, the disease is not regarded a high priority risk in Europe since safe and efficacious vaccines are available (Roukens and Visser 2008).

Usutu virus (USUV; Flaviviridae, Flavivirus, Japanese encephalitis group) has its origin in sub-Saharan Africa where it occurs within a natural cycle between birds and mosquitoes, mainly species of the genus Culex (Nikolay et al. 2011). After an episode of increased mortality among blackbirds, it was detected for the first time outside of Africa in 2001 in Austria (Weissenböck et al. 2002). From then on, USUV infections were also demonstrated, either directly by isolation/immunohistochemistry/RNA amplification or indirectly by antibody detection, in birds in Great Britain (Buckley et al. 2003, 2006), Hungary (Bakonyi et al. 2007), Italy (Lelli et al. 2008), Czech Republic (Hubálek et al. 2008a), Poland (Hubálek et al. 2008b) and Switzerland (Steinmetz et al. 2011). The virus was found in Cx. pipiens mosquitoes from Spain in 2006 (Busquets et al. 2008), in Cx. pipiens and Ae. albopictus from Italy in 2009 (Busani et al. 2010; Tamba et al. 2010) and in Cx. pipiens from Germany in 2010 (Jöst et al. 2011a). Interestingly, 1 year after the demonstration of the virus in the German culicids, it could be isolated from blackbirds found dead in the same region (ProMED-Mail 2011). For Austria, it could be shown that USUV was able to overwinter and to establish a local transmission cycle (Weissenböck et al. 2003; Meister et al. 2008).

Being highly pathogenic for blackbirds, USUV is of unclear pathogenicity for humans (Vazquez et al. 2011). In addition to two benign infections in central Africa (Nikolay et al. 2011), two cases with involvement of the central nervous system in immunocompromised patients were reported from Italy (Cavrini et al. 2009; Pecorari et al. 2009).

Sindbis virus (SINV; Togaviridae, Alphavirus, western equine encephalomyelitis virus complex) appears to have its main distribution in Fennoscandia and north-western Russia where outbreaks of disease with hundreds of clinical cases have been occurring since the early 1980s (Lundström 1999; Hubálek 2008). Interestingly, a 7-year periodicity could be observed in Finland (Brummer-Korvenkontio et al. 2002). Outbreaks have, however, also been reported from South Africa (McIntosh et al. 1976), and the virus has been demonstrated to also occur in other parts of Africa, the Middle East and even Australia (Niklasson 1989). In central and western Europe, specific antibodies were found in sentinel chickens in Great Britain (Buckley et al. 2006) and, most recently, the virus could be isolated from Cx. torrentium, Cx. pipiens and An. maculipennis s.l. mosquitoes collected in southern Germany (Jöst et al. 2010). While Cx. torrentium, Cx. pipiens and other ornithophilic species such as Culiseta morsitans must be considered to keep the transmission cycle among the passerine bird reservoir of the virus going, non-discriminative species such as An. maculipennis s.l. and Ae. cinereus are probably responsible for transmission to humans in Europe (Lundström 1999). In laboratory experiments, Ae. albopictus has also been proven to be susceptible for SINV (Dohm et al. 1995).

The disease associated with a SINV infection is called “Ockelbo fever” in Sweden (Skog and Espmark 1982), “Pogosta fever” in Finland (Brummer-Korvenkontio and Kuusisto 1981) and “Karelian fever” in north-western Russia (Lvov et al. 1982). It usually presents with headache, myalgia, arthralgia, malaise, conjunctivitis, pharyngitis and rash (Espmark and Niklasson 1984; Kurkela et al. 2005).

Chikungunya virus (CHIKV; Togaviridae, Alphavirus) is one of the most expansive viruses of modern times. Minor outbreaks have sporadically been reported since the 1960s in central and southern Africa and Southeast Asia. Starting in Kenya in 2004, however, major outbreaks almost continuously occurred until 2007 with hundreds of thousands of human cases and a geographical spread to hitherto unaffected islands of the Indian Ocean, India and parts of Southeast Asia (Powers and Logue 2007; Staples et al. 2009).