Tick borne enciphitalis

patients and the median incubation period is 8 days (range, 4–28 days) after tick bite. Non-specific symptoms of mild fever, malaise, headache, nausea, vomiting and myalgias may be present as first manifestation of the disease and spontaneously resolve within 1 week. After another week the patient may develop neurological symptoms.[4] The virus can result in long neurological symptoms, infecting the brain (encephalitis), the meninges (meningitis) or both (meningoencephalitis).[5] In general, mortality is 1% to 2%, with deaths occurring 5 to 7 days after the onset of neurologic signs.
In dogs, the disease also manifests as a neurological disorder with signs varying from tremors to seizures and death.[3]
In ruminants, neurological disease is also present, and animals may refuse to eat, appear lethargic, and also develop respiratory signs.

the family Flaviviridae. It was first isolated in 1937. Three virus sub-types also exist: European or Western tick-borne encephalitis virus (transmitted by Ixodes ricinus), Siberian tick-borne encephalitis virus (transmitted by I. persulcatus), and Far-Eastern tick-borne encephalitis virus, formerly known as Russian spring summer encephalitis virus (transmitted by I. persulcatus).[6][7]
Russia and Europe report about 5,000–7,000 human cases annually.[1][8]
The former Soviet Union conducted research on tick-borne diseases, including the TBE viruses

Causes

disease
It is transmitted by the bite of several species of infected woodland ticks, including Ixodes scapularis, I. ricinus and I. persulcatus,[9] or (rarely) through the non-pasteurized milk of infected cows.[10]
Infection acquired through goat milk consumed as raw milk or raw cheese (Frischkäse) has been documented in 2016 and 2017 in the German state of Baden-Württemberg. None of the infected had neurological disease.[11]
DIAGNOSIS
Detection of specific IgM and IgG antibodies in patients sera combined with typical clinical signs, is the principal method for diagnosis. In more complicated situations, e.g. after vaccination, testing for presence of antibodies in cerebrospinal fluid may be necessary [12].
PCR (Polymerase Chain Reaction) method is rarely used, since TBE virus RNA is most often not present in patient sera or cerebrospinal fluid at the time of clinical symptoms.

Northern Asia. About ten to twelve thousand cases are documented a year but the rates vary widely from one region to another.[16] Most of the variation has been the result of variation in host population, particularly that of deer. In Austria, an extensive free vaccination program since the 1960s reduced the incidence in 2013 by roughly 85%.[17]
In Germany, during the 2010s, there have been a minimum of 95 (2012) and a maximum of 584 cases (2018) of TBE (or FSME as it is known in German). More than half of the reported cases from 2019 had meningitis, encephalitis or myelitis. The risk of infection was noted to be increasing with age, especially in people older than 40 years and it was greater in men than women. Most cases were acquired in Bavaria (46 %) and Baden-Württemberg (37%), much less in Saxonia, Hesse, Niedersachsen and other states. Altogether 164 Landkreise are designated FSME-risk areas, including all of Baden-Württemberg except for the city of Heilbronn.[11]
In Sweden, most cases of TBE occur in a band running from Stockholm to the west, especially around lakes and the nearby region of the Baltic sea.[18][19] It reflects the greater population involved in outdoor activities in these areas. Overall, for Europe, the estimated risk is roughly 1 case per 10,000 human-months of woodland activity. Although in some regions of Russia and Slovenia, the prevalence of cases can be as high as 70 cases per 100,000 people per year. [17][20] Travelers to endemic regions do not often become cases, with only 5 cases reported among U.S. travelers returning from Eurasia between 2000 and 2011, a rate so low that as of 2016 the U.S. Centers for Disease Control and Prevention recommended vaccination only for those who will be extensively exposed in high risk areas.[21]

therapy for TBE. Symptomatic brain damage requires hospitalization and supportive care based on syndrome severity. Anti-inflammatory drugs, such as corticosteroids, may be considered under specific circumstances for symptomatic relief. Tracheal intubation and respiratory support may be necessary.

Since there is no chemotherapy or specific treatment available targeting the TBE virus itself, symptomatic or supportive treatment (e.g. maintenance of the water and electrolyte balances) is required. This lack of targeting treatment emphasizes the necessity of tick prophylaxis. Repellent parasiticides may be the right choice to minimize attachment and subsequent feeding of the tick vector.
In the case of diseased dogs emphasis has to be put on preventing secondary harm to the patient itself as well as the owner during convulsions and aggressive behavior. For that reason, therapy should include resting as well as anticonvulsive and sedative medication (Pfeffer and Dobler, 2011). Non-steroidal anti-inflammatory drugs (NSAID) are best used to combat the high fever, and antibiotics should be given to prevent secondary bacterial infections, in particular pneumonia (Kritz et al., 2001). Most of the few dogs, that survived a clinical TBE needed between a hal

is between 7 and 14 days. Clinical canine TBE is a febrile illness with multifunctional neurological manifestations such as ataxia, uncoordinated movements, abnormal reflexes, convulsions, tremor, paresis, paralysis, and cranial nerve deficits such as facial paresis. The neurobiological signs are often progressive and TBE may lead to death.
In general the risk for a tick-infected dog to develop clinical manifest TBE is very small. A serological survey performed in dogs from Sweden in 1992 proved 18 of 225 dogs (8%) to be seropositive and 16 of these 18 dogs showing neurological signs (Bjöersdorff, 2002).
Human TBE
The incubation period is between 3 and 28 days. The course of disease is often asymptomatic. An estimated 30% will exhibit clinical disease, mainly as a feverish flu-like disease. 10-15% of cases (increasing rate with age) will have neurological disorders with the most severe form of persisting paresis and psychiatric sequelae.
In central Europe, the typical case of encephalitis has a biphasic course, with an early, viremic, flu-like stage, followed about a week later by the appearance of signs of meningoencephalitis. CNS disease is relatively mild, but occasional severe motor dysfunction and permanent disability occur. The case fatality rate is 1% to 5%.
Russian spring-summer encephalitis (sometimes referred to as the "Far Eastern form") normally does not show a biphasic course but is characterized by massive headache, high fever, nausea, and vomiting. Delirium, coma, paralysis, and death may follow; the mortality rate is approximately 25% to 30%.
Louping ill infection is generally mild and also displays a biphasic pattern. The virus infects sheep; few cases are reported in humans.   

seen in children. The symptoms in humans are similar to the clinical signs in dogs. About two thirds of human cases are seen in young females. The tick bites are most often found at the head and there at the transition of hair and neck. The clinical presentation appears as typical ascending flaccid paralysis. After aprodromal phase (paraesthesias, restlessness, irritaility, fatigue, and myalgias) neurological symptoms will start with paralysis of the lower extremities. The deep tendon reflexes are weak or absent. Duirng the next 12 to 24 hours the muscles innervated by facial nerves become weak. Without removal of the tick, finally the respiratory muscles will fail  and the patient will die of respiratory failure. Rare forms of illness include focal muscles paralysis (facial muscles, arm muscles, pupillary dilation, and acute cerebellar syndrome). Sensory findings are generally absent and therefore form an important differential diagnostic symptom to the Guillain-Barré syndrome where sensory findings are frquently found during the prodromal stage of disease.

ticks, mosquitoes, and fleas -- tripled to roughly 650,000 cases between 2004 and 2016. The vast majority -- or 75% -- were caused by ticks. The report says seven new tick-caused illnesses were discovered between 2004 and 2016.

How many tick borne diseases are there?

is potentially life-threatening, and may lead to permanent brain damage or death.

herpes simplex encephalitis (HSE) has a mortality rate of up to 30% even with specific anti-viral treatment, and 70-80% without the treatment. When death happens it is usually because of the brain swelling as a result of its severe inflammation.

[3–7]. Other associated symptoms and signs may include headache, mild depression, irritability, fatigue, or excessive daytime sleepiness

– with the very young and very old particularly at risk – and the particular virus that caused the disease. While many people make a full recovery, in severe cases, the illness may be fatal or result in brain damage.

example, some herpesviruses have an incubation period of about three to seven days on average but may range from about one to three weeks.

Am. 2008, 22, 397-414
Gordon BM, Giza CC: Tick paralysis presenting in an urban environment. Pediatr Neurol. 2004, 30, 122-4
Malik R, Farrow BR: Tick paralysis in North America and Australia. Vet Clin North Am Small Anim Pract. 1991, 21, 157-71
Wright IG, Stone BF, Neish AL: Tick (Ixodes holocyclus) paralysis in the dog – induction of immunity by injection of toxin. Aust Vet J. 1983, 60, 69-70