EN 
HR Diseases in focus:
Crimean-Congo Haemorrhagic Fever
Lyme Disease
Lyme disease, also known as borreliosis
It is a bacterial disease that is transmitted to humans by the bite of infected ticks. The disease infects humans and, less commonly animals.
The disease is caused by bacteria in the Borreliaceae family, namely Borrelia burgdorferi sensu lato. The B. burgdorferi complex has at least 17 species worldwide, although only five are relevant to humans. All of them can induce erythema migrans, that is an early skin rash. Borrelia afzelii and B. garinii are the most common in Europe, and they are associated with cutaneous symptoms and, less frequently, neurological problems. B. burgdorferi sensu stricto can result in neurological and arthritic symptoms. In Europe, two species, B. bavariensis and B. spielmanii, have been linked to neurological issues. Borrelia valaisiana and B. lusitaniae rarely infect people.
The reported incidence in Europe is about 22.6 cases per 100,000 inhabitants per year with a wide range depending on the geographical area. About 85,000 cases of borreliosis are reported annually in the European Union. According to the data of the Epidemiology Service of the Croatian Institute of Public Health (HZJZ), in 2013, 661 sick people from borreliosis were reported in the Republic of Croatia, in 2014, 470 sick people, in 2015, 437 reports were received, and in 2016, 468 sick people were reported. On average, about a dozen cases in humans are reported annually. The largest number of patients in Croatia was recorded in Zagorje, Međimurje, Koprivnica-Križevci County, and then in the city of Zagreb and the surroundings of Zagreb. Antibodies have been demonstrated in about 0.5% of dogs.
Borrelia is transmitted only by Ixodes ricinus ticks in most of Europe and Croatia (pictures 1 and 2), although Ixodes persulcatus ticks are vectors in the Baltic countries. Because of their abundance and size, nymphs are thought to be the primary vector of B. burgdorferi s.l. The exact time frame required for successful Borrelia transmission to humans has never been identified. Several studies on Borrelia transmission to humans indicate that there is little likelihood of developing Lyme disease even after feeding on an infected tick.
The symptoms in humans are fatigue, chills, fever, headache, pain in muscles and joints with a characteristic skin manifestation called erythema migrans. Within 2 to 30 days, an oval or ring-shaped reddening of the skin appears around the site of the tick bite, which gradually spreads, and gradually fades in the middle, creating a characteristic shape. Erythema migrans can be accompanied by the so-called “minor symptoms” (headache, faintness, dizziness, pain in joints and muscles, difficulty concentrating). If the disease is not treated, the bacteria (spirochetes) can spread and the early extended form of the disease can occur, where 10 to 20% of untreated people develop chronic arthritis. Untreated Lyme disease can also affect the nervous system, causing such symptoms as a stiff neck and severe headache (due to meningitis), temporary paralysis of the facial muscles (Bell’s palsy), insensitivity to stimuli, pain or weakness in the limbs, or poor muscle coordination, and A small number of people may also have heart problems, such as irregular heartbeats, for several weeks after infection. Arthritis may manifest in animals.
If you suspect a disease, contact your doctor or veteinarian
Crimean-Congo Haemorrhagic Fever
CCHF is rare, viral zoonotic disease that spreads to humans by tick bites or infected animal blood. Hyalomma ticks can transmit the virus while feeding on a variety of domestic ruminants (sheep, goats, and cattle), and wild herbivores, hares, hedgehogs and certain rodents.
Disease is caused by a primarily tick-borne CCHF virus of the genus Orthonairovirus of the family Nairoviridae, order Bunyavirales
The first outbreak of the disease in the Crimean Peninsula was described in 1967, while in 1956, virus was isolated from a patient in the former Zaire (now Democratic Republic of the Congo). In 1969, these two outbreaks were proven to be caused from the same virus, hence as a consequence the names of both countries have been used to describe the disease. Distribution of the virus reflects the broad distribution of Hyalomma ticks, the predominant vector of the virus. CCHF is the most widespread viral hemorrhagic fever, found in Eastern and Southern Europe, the Mediterranean, northwestern China, central Asia, Africa, the Middle East, and the Indian subcontinent. CCHF was first diagnosed in Bulgaria and became endemic in some regions of the country. In Greece, the first and so far only autochthonous case was reported in 2008. In 2016, Spain reported its first autochthonous cases in the province of Ávila, Castile-León. According to the European Centre for Disease Prevention and Control (ECDC), currently in Europe (in 2024) there has only been one fatal case of the disease in Spain. Disease has not been confirmed in Croatia.
CCHF virus can spreads through: Tick bites from infected hard ticks (Ixodidae), contact with blood or body fluids of infected animals or humans, improperly sterilized medical equipment. Viraemia in livestock is short-lived, and of low intensity. Animals play a crucial role in the life cycle of ticks, and in the transmission and amplification of the virus and are, therefore, in the focus of veterinary public health. The natural cycle of CCHFV includes transovarial and transstadial transmission among ticks and a tick-vertebrate-tick cycle involving a variety of wild and domestic animals. Infection can also be transferred between infected and uninfected ticks during co-feeding on a host; so called ‘non-viraemic transmission’ phenomenon.
As animals do not develop clinical signs, CCHFV infections have no effect on the economic burden regarding livestock animal production. In contrast to animals, infections of humans can result in the development of a severe disease. People with CCHF are usually sick for about two weeks. Around the fourth day of illness, large areas of severe bruising, severe nosebleeds, and uncontrolled bleeding at injection sites can develop. Up to 50% of people hospitalized with CCHF will die, unfortunately there is no specific treatment or cure. Recovery is slow, and the long-term effects are not well studied.
If you suspect a disease, contact your doctor or veterinarian
More information:
https://www.nature.com/articles/s41579-023-00871-9
https://www.osmosis.org/answers/crimean-condo-hemorrhagic-fever
Q Fever
Q fever is an infectious disease of animals and humans caused by the bacterium Coxiella burnetii. It produces airborne spores, which are highly infectious (1-10 bacteria cause the disease) and is therefore considered a potential biological weapon. Cattle, small ruminants, cats and humans are primarily affected, but other mammal and bird species can also be affected. The disease is considered the most important cause of infectious abortions in ruminants and is a dangerous zoonosis that spreads quickly and easily and is difficult to eradicate. In humans, the disease is transmitted during an autopsy, blood transfusion, and bone marrow transplantation in an immunocompromised patient. During pregnancy, the disease can be transmitted from the mother to the fetus and to people present at the birth (Figure 1).
Bacteria Coxiella burnetii is a type of intracellular, pathogenic bacteria. It is a small gram-negative bacterium with two growth phases and also exists in the form of spores that are inactive in soil. Ticks are also considered to be carriers of the disease.
The “Q” in the name of the disease stands for a question. It got its name when the first people got it (in the 1930s in Australia and in the 1940s in the USA) because doctors did not know what caused the disease. Therefore, they had many questions (or “queries”) about the cause of the fever. The disease occurs regularly on the territory of the Republic of Croatia and has been described in most European countries (Figure 2). It is an endemic disease in the coastal part of the Republic of Croatia, and micro-endemic areas have been established during outbreaks in the continental part (Čazma, Đurđevac…). In March 2022, around 20 human cases were confirmed in the Rijeka area, with one death. About 15 years ago, an epidemic of Q fever in small ruminants was recorded in the Netherlands, which caused damage amounting to 307 million euros and resulted in a large number of sick people. In Croatia, the number of sick people ranges from a few to slightly more than 20 sick people a year. Every year, positive disease cases are determined in cattle and sheep, and occasionally in goats.
Despite the asymptomatic infection, the animals excrete the pathogen via the placenta, amniotic fluid, urine, feces and milk. When the disease first enters the farm, it spreads rapidly and causes abortions on a large scale. The biggest problem is resistant spores that survive for years in the environment and are a constant source of infection. People become infected through contact with an infected placenta, fetus, lochia, and inhalation of spores and can be infected through aerosols in a contaminated environment. Ticks are also considered to be carriers of the disease.
In humans, Q fever can go unnoticed, but it can also have an acute or chronic course. Acute infection is manifested by headache, febrility, bone pain, pneumonia, while chronic infection manifests itself in hepatitis, endocarditis and neurological symptoms. In domestic ruminants, the disease is usually mild or asymptomatic, and the most serious consequence is abortion in late pregnancy. It regularly occurs at the end of winter or in spring, during lambing/kids. The disease is a dangerous zoonosis that in the acute phase has a flu-like clinical picture and leads to hepatitis, osteomyelitis and endocarditis and even death in the chronic phase. The disease already has a significant negative impact on human and animal health and poses a significant risk to public health in the Republic of Croatia.
If you suspect a disease, contact your doctor or veterinarian
More information:
https://www.woah.org/en/disease/q-fever
Echinococcosis
Human echinococcosis is a disease caused by the larval stages of tapeworms of the genus Echinococcus (family: Taeniidae, order: Cyclophyllidea, class: Cestoda). Human cystic echinococcosis is caused by the larval stages of the tapeworm Echinocoscus granulosus sensu lato (photo 1).
E. granulosus s.l., a tapeworm, parasitises the small intestine of dogs and other canids but causes no apparent clinical signs. Various herbivores and omnivores serve as intermediate hosts in which cysts are formed (picture 2). Humans are considered accidental intermediate hosts since they can be invaded in the same way as other intermediate hosts but are not involved in transmission to the final host.
The tapeworm Echinococcus granulosus sensu lato (small dog tapeworm) represents a complex of ten known genotypes classified into five species: E. granulosus sensu stricto (former “sheep genotype”, G1 to G3), Echinococcus equinus (horse genotype, G4), Echinococcus ortleppi (cattle genotype, G5), Echinococcus canadensis (camel genotype, G6; pig genotype, G7; G9, and cervid genotypes G8 and G10) and Echinococcus felidis (“lion genotype”). So far, two species have been molecularly proven in the Republic of Croatia: E. granulosus sensu stricto and E. candensis.
Historically, Croatia was a highly endemic area of cystic echinococcosis, particularly in Dalmatia and the islands. Today, the incidence ranges from 0.1-0.99 cases per 100,000 individuals, with an average of about ten cases reported in humans per year. From 1994 to 2018, an average of 20 cases were reported (from 11 to 26), while for the last five years up to 10 cases have been reported per year (from 3 to 7).
Dogs and other canids are infected when they ingest hydatid cysts harbouring protoscolexes (picture 3) from intermediate hosts (e.g. sheep, goats, cattle, or pigs). Tapeworms mature in the small intestines of final hosts in the which the grow into adult tapeworms in the intestine and excret eggs with the faeces into the environment. During feeding, the intermediate hosts become infected by egg-contaminated food or water. Oncospheres emerge from eggs in the intestines, enter the animal’s bloodstream, and develop into cysts in the internal organs, mainly liver. Food and water contaminated with tapeworm eggs infect humans in the same way.
Hydatid cysts are most commonly found in the liver (60%) followed by the lungs (25%), and other organs and tissues (15%). Symptoms vary depending on the affected organs, size, and number of cysts. Invasions can be asymptomatic for years before the cysts become large enough to cause symptoms in the affected organs. When a cyst ruptures, the patient may experience fever, urticaria, eosinophilia, and suffer anaphylactic shock.
If you suspect a disease, contact your doctor or veterinarian
Hepatitis E
Hepatitis E (HE) is a liver disease caused by viral infection. Humans and wide range of domestic (horses, domestic pigs, dogs, cats) and wild animals (wild boars, wild canids) can be infected.
Causative agent of HE is Hepatitis E virus (HEV). HEV is a small (27-34 nm) non-enveloped icosahedral single-stranded virus, with a linear positive-sense RNA of approximately 7.2 kb in length. HEV is classified in the genus Orthohepevirus of the family Hepeviridae, and it shows a relatively strict host specificity. The human-associated genotypes, which are the leading cause of acute hepatitis worldwide, as well as zoonotic genotypes originating from domestic animals and wild-living mammal species (pig, wild boar, rabbit, deer, mongoose, and camel species), are grouped into the species Orthohepevirus A, which includes a total of eight genotypes (HEV1–8). Orthohepevirus B contains the avian hepatitis E virus species causing the “splenomegaly syndrome” as well as the “big liver and spleen disease” in poultry, whereas Orthohepevirus C viruses were isolated from rodents (rats, mice, voles, and shrew) and carnivores (such as ferrets, mink, and foxes). HEV from bats is classed in the species Orthohepevirus D. Finally, fish-related HEV belongs to the genus Piscihepevirus. Four genotypes of HEV cause illness in humans, each displaying different epidemiologic and clinical characteristics in developing and developed countries. Cases of hepatitis E typically present in one of two ways: either as large outbreaks and sporadic cases in areas where HEV is endemic (genotype 1 in Asia and Africa, genotype 2 in Mexico and west Africa, and genotype 4 in Taiwan and China) or as isolated cases in developed countries like the United States (genotype 3). Even though contaminated water is the main source of HEV infection, zoonotic potential has been recognized for the genotypes 3 and 4.
Hepatitis E was suspected for the first time in 1980 during a waterborne epidemic of acute hepatitis in Kashmir, India. In Croatia, the first samples of animal origin were tested for the presence of HEV RNA in 2007, and a comprehensive survey based on viral RNA detection in domestic and wild animals and mollusks with the aim of exploring the possible role of wild animals in the spread of the zoonotic HEV genotypes was carried out in 2009. HEV RNA was detected in domestic pigs and wild boars, but it was not confirmed in any other domestic or wild animals. In Croatia, the first autochthonous human case of hepatitis E was reported in 2012.
Hepatitis E has mainly a fecal-oral transmission route, similar to hepatitis A, although the viruses are unrelated. Contaminated water, undercooked meat (especially pork), and poor sanitation contribute to its spread.
The average incubation period for hepatitis E in humans is 40 days, ranging from 2 to 8 weeks. Most HEV infections are asymptomatic, but symptoms may include jaundice, fatigue, and nausea. Elevated hepatic aminotransferase levels coincide with the symptomatic phase. There is no specific antiviral therapy for acute hepatitis E. Hepatitis E usually resolves on its own without treatment, three to six monts usually leads to virus clearance from the blood , although the virus may persist in stool for longer period (from 1 week prior to onset to 30 days after the onset of jaundice). Elevated hepatic aminotransferase levels coincide with the symptomatic phase.
Most infected animal species show no clinical signs but viremia and anti-HEV antibodies are detected in serum samples from infected animals. Avian HEV can cause symptomatic disease (hepatitis-splenomegaly) but is not dangerous to humans.
If you suspect a disease, contact your doctor or veterinarian
More information:
https://www.visavet.es/en/articles/hepatitis-e-zoonotic-emerging-disease-industrialized-countries.php
https://en.wikipedia.org/wiki/Hepatitis_E
https://britishlivertrust.org.uk/information-and-support/liver-conditions/hepatitis-e
Swine Influenza
Swine influenza (SI) is a highly contagious acute viral respiratory disease in pigs which is distributed worldwide. However, sporadic human infections have occurred with influenza viruses that normally circulate in pigs and not in humans. When this happens, these viruses are referred to as “variant viruses”.
Swine influenza viruses (swIAVs) belong to the species Influenza A virus (IAV), genus Alphainfluenzavirus, family Orthomyxoviridae with a segmented RNA genome.
After the Spanish flu in 1918, the human influenza virus was introduced into the pig population in the United States. It was isolated in 1931 and named the “classical swine” H1N1. This virus is still present in America and Asia, but has not been present in Europe since the early 1980s, when it was replaced by the avian-like H1N1 subtype. The most common subtypes of swine influenza viruses (swIAVs) circulating worldwide are H1N1, H1N2 and H3N2. The distribution of subtypes and genotypes varies in different geographical regions.
Evolution of swIAVs in Europe and Asia has been distinct from that in North America. SwIAVs are also different from human influenza viruses, and although they have the same nomenclature, they can be distinguished from them genetically and antigenically.
In 2009, the H1N1 pandemic virus (H1N1pdm09), commonly referred to as “swine flu”, highlighted the zoonotic potential of swIAVs and IAVs in general. The emergence of the H1N1pdm09 virus was the result of a reassortment event between a North American “triple-reassortant” (TRA) swine influenza virus and a Euroasian “avian-like” H1N1. Since its introduction into the European swine population, it has largely reassorted with the circulating swine subtypes.
The data from a Croatian survey in 2016 shows that the seroprevalence of swIAVs in Croatian pig herds was estimated at 30.3%. The predominant subtypes were avian-like H1N1 (44.6%), followed by H3N2 (42.7%) and human-like H1N2 (26.3%). Although the H1N1pdm09 strain was probably introduced into Croatian pig herds, it could not be detected by HI assay due to the diversity of circulating swIAVs. Due to the lack of samples, only the Euro-Asian avian H1N1 swine virus was isolated from Croatian pigs. According to the World Health Organisation (WHO), two cases of variant SI viruses were recorded in humans in 2023, in the United Kingdom (vH1N2) and the Netherlands (vH1N1), and a vH1N1 infection was detected in Spain in early 2024. The virus variant has never been identified in Croatia.
In both humans and pigs, the virus is transmitted through direct contact with infected animals, contaminated objects and the environment or through aerosolised particles. It is important to emphasise that human-to-human transmission of variant influenza viruses is rare and most human infections do not result in further transmission. The emergence of the last pandemic IAV strain in 2009 was probably the result of a series of reassortments in mammals over a period of years before the pandemic was recognised.
In both humans and pigs, the virus is transmitted by direct contact, contaminated objects and the environment, or via aerosol particles. The disease is not transmitted through the meat of infected pigs. It is important to emphasize that human-to-human transmission of VIA variants is rare and that most human infections do not result in further transmission. The appearance of the last pandemic swIAVs in 2009 was probably the result of several years of gene rearrangement and adaptation of the newly created virus to the human body so that it could be transmitted from person to person.
In pigs, it causes symptoms such as fever, coughing, nasal discharge, lethargy and reduced appetite. Although the mortality rate in pigs is generally low, morbidity in infected swine herds can be as high as 100% and can cause significant economic losses due to reduced weight gain and secondary infections.
Human infection with variant influenza viruses usually results in mild clinical symptoms similar to seasonal influenza, such as fever, headache, lethargy and respiratory symptoms.
If you suspect a disease, contact your veterinarian
More information:
https://www.ecdc.europa.eu/en/swine-influenza/factsheet
https://www.sciencedirect.com/science/article/pii/S1931312820304029
Rift Valley Fever
Rift Valley fever (RVF) is a vector-borne zoonosis. It can cause severe disease in humans and ruminants such as cattle, goats, sheep, buffalo and camels.
RVF is caused by the Rift Valley fever virus (RVFV), which belongs to the genus Phlebovirus, the order Bunyavirales and the family Phenuiviridae
RVFV was first identified in 1931 in the Great Rift Valley in Kenya during the investigation of a major outbreak in sheep on a farm. The disease is widespread in Sub-Sahar Africa and is also spreading in the Comoros archipelago (including Mayotte), Madagascar, Saudi Arabia and Yemen. The largest outbreaks were reported in Egypt in 1977-78, with around 18,000 cases and 598 human deaths, and in East Africa in 1997, when 90,000 people were infected and 500 died. In 2000, 516 people with suspected severe RVF were reported from primary health centres and hospitals in Saudi Arabia, 87 of whom died.
According to the European Centre for Disease Prevention and Control (ECDC), no cases were reported from EU/EEA countries between 2017 and 2020 France reported three imported cases in 2016. Prior to that, imported cases were reported from the UK and France in 2012 (two cases), from the UK in 2013 (one case) and from France in 2015 (one case). No case of human-to-human transmission of RVFV has ever been reported.
In humans, RVFV is mainly spread by Aedes and Culex mosquito species, but can also be transmitted by direct or indirect contact with the blood or organs of infected animals, by handling animal tissues and body fluids, by assisting animal births or by disposing of carcasses or foetuses. The transmission of RVFV from person to person has not been proven.
Among animals, RVFV is mainly spread by the bite of infected mosquitoes, which can acquire the virus by feeding on infected animals. The female mosquito is also able to transmit the virus directly to her offspring via the eggs, so that new generations of infected mosquitoes hatch from the eggs. RVFV can also be spread by livestock movement or passive mosquito dispersal.
The clinical signs of Rift Valley fever are usually non-specific, which makes it difficult to recognise individual cases.
In animals, the RVF is characterised by high fever, lethargy and a high abortion rate in pregnant animals. The mortality rate in young animals is high (90%–100%) and they usually die within 2–3 days. Adult animals are less susceptible and have a mortality rate of 10–30%. RVF should be suspected when there are abortions and neonatal mortality in domestic ruminants, especially sheep,following unusually heavy rainfall and flooding.
Symptoms in humans appear 2-6 days after infection. Most symptoms in humans are non-specific, mild and flu-like, such as fever, muscle and joint pain and headache. However, a small percentage of cases can progress to more severe forms, including haemorrhagic fever with hepatitis, gum and nose bleeding, encephalitis and eye disease (retinitis). The mortality rate for severe RVF can be as high as 10-20%. No specific treatment is required for patients with mild symptoms, while general supportive therapy is recommended for the more severe cases.
If you suspect a disease, contact your doctor or veterinarian
More informations:
https://www.cdc.gov/rift-valley-fever/about/index.html
https://www.who.int/health-topics/rift-valley-fever#tab=tab_1
https://www.mdpi.com/2227-9059/12/3/540
Tick-borne Encephalitis (TBE)
Tick-borne encephalitis (TBE) is a viral infectious disease that affects the central nervous system and is transmitted through the bite of infected ticks. In its natural cycle, the tick-borne encephalitis virus (TBEV) is transmitted from infected ticks (Ixodes ricinus – mainly in Europe) to small mammals, which serve as reservoir hosts. Humans are only incidental and dead-end hosts and play no role in the maintenance of the virus. Various domestic animal species can become infected, and neurological symptoms are sporadically observed in dogs and horses. More important for public health is the infection of domestic ruminants, which is asymptomatic, but during an acute infection the virus can be excreted in milk. Consequently, unpasteurised milk and milk products from infected animals can be a source of infection for humans in sporadic cases.
TBEV is an arbovirus belonging to the family Flaviviridae, genus Orthoflavivirus, tick-borne encephalitis serocomplex. There are three main subtypes of TBEV, European, Siberian and Far-Eastern, and two additional subtypes (Baikalian and Himalayan) have recently been proposed. Different subtypes are present in different regions of the world and the severity of clinical symptoms depends on the virus subtype.
TBE is endemic in Euro-Asia, from Western Europe to the easternmost regions of Asia. TBE is endemic in 27 European countries, including Croatia, where the disease was first described in the north-western continental region in 1953 and clinical cases have been reported ever since. Most cases in Croatia are associated with transmission through the bite of infected ticks, but recently two outbreaks of TBE have also been confirmed where goat’s milk and dairy products were the source of infection. In recent years, the first human cases of TBE have been confirmed in several regions of Europe and an increase in cases has been observed in the known endemic regions. This general trend is likely to continue in the future.
In most cases, humans can become infected through bites from infected ticks. Less common routes of transmission have also been described, such as the consumption of unpasteurised dairy products from infected domestic ruminants. In any case, infected humans are dead-end hosts and cannot be a source of infection for other humans. Animals are also infected by bites from infected ticks and are generally also dead-end hosts. An exception is domestic ruminants, which can serve as a source of infection during the acute viraemic phase when the virus is spread via milk.
TBEV infection in humans is often asymptomatic. In clinical cases in humans infected with the European subtype of TBEV, the disease is usually biphasic. The first phase corresponds to viraemia and clinical symptoms such as fever, fatigue, malaise, headache, muscle and joint pain occur. After a few days of improvement, the second phase begins, characterised by symptoms of the central nervous system (CNS). The most common clinical manifestations of the neuroinvasive disease are meningitis, meningoencephalitis and meningoencephalomyelitis.
In animals, TBE virus infections are also usually asymptomatic. Some sporadic cases have been reported in horses with non-specific neurological clinical signs. More frequently, clinical signs are reported in dogs, with non-specific clinical signs preceding the onset of neurological symptoms, similar to the biphasic clinical picture known from TBEV in humans. The fatality rate of clinical TBE cases in dogs was 33% and long-term neurological sequelae were observed in 17% of animals.
If you suspect a disease, contact your doctor or veterinarian
West Nile Fever (WNF)
West Nile fever is a zoonotic, emerging mosquito-borne viral disease caused by the West Nile virus (WNV). WNV is maintained in nature in a cycle that involves transmission between birds and mosquitoes. Many bird species can become infected with WNV, but species in the Corvidae family (e.g. crows and jays) are considered most susceptible to severe disease and death from WNV. Although many birds of prey (e.g. owls, hawks and eagles), some songbirds, waterfowl and other birds can become fatally ill. Many bird species serve as WNV reservoir hosts due to high level viraemia. In addition to birds, many different animal species can also be infected. The disease is of public health and veterinary importance as it manifests in horses and humans with neurological clinical signs that can be fatal.
West Nile virus belongs to the genus Orthoflavivirus of the Flaviviridae family, which also includes other zoonotic viruses such as tick-borne encephalitis virus, Zika virus, Usutu virus, dengue virus and yellow fever virus.
WNV was first isolated in 1937 from a febrile patient in the West Nile district of northern Uganda and has since spread worldwide. Until the end of the 20th century, the spread of WNV infections in humans and animals in Europe was mainly associated with sporadic cases. In the last 20 years, WNV has become endemic in many European countries as it spreads in the bird population and can overwinter in mosquitoes. The first sporadic WNV infections in humans and animals in Croatia were described in the last century, but continuous infections in horses have been reported since 2010, mainly in eastern and central Croatia. The first clinical cases in humans were confirmed in 2012 and since then 116 cases have been reported, including some with fatal outcomes.
As WNV is widely distributed in Africa, Europe, the Middle East, North America, and Western Asia, this virus is the most widespread zoonotic mosquito-borne virus in the world. In the last two decades, WNV has also become endemic in Croatia.
WNV is usually transmitted through the bite of a mosquito that becomes infected when feeding on viraemic birds. The most important vectors for WNV are mosquito species of the Culex genus, which are widespread in Croatia. Mosquitoes can transmit WNV among birds and occasionally to humans and horses, which are ‘dead-end’ hosts. This means that an infected horse or human cannot serve as a source of infection for others.
The disease associated with WNV in birds may manifest clinically as a non-specific or neurological disease characterised by loss of coordination, head tilt, tremors, weakness and lethargy. Infected birds often die within a few days, with the severity of the disease depending on the species infected.
Most of the WNV infected horses do not display overt clinical signs (about 80%). Some infected animals have non-specific, flu-like symptoms, but up to 90% of symptomatic cases develop a neurological form with viral encephalitis, which is fatal in up to 50% of cases. Neurological symptoms include ataxia, muscle twitching, seizures, drooping lips, falling, weakness, teeth grinding and hypersensitivity. Cases with recumbence and paralysis are usually fatal.
Although most WNV infections in humans are asymptomatic (80%) or present as self-limited febrile disease (20%), some patients develop WNV neuroinvasive disease, which includes meningitis, encephalitis or flaccid paralysis. The fatality rate for patients with WNV neuroinvasive disease is 10%, and the fatality rate increases significantly with age.