Ixodes holocyclus – Параличтік кене және оның зияны

Species of tick
Speciesbox
| image = Tick before and after feeding. jpg
| image caption = Ixodes holocyclus before and after feeding
| taxon = Ixodes holocyclus
| authority = Neumann, 1899 The natural hosts for the paralysis tick include koalas, bandicoots, possums and kangaroos. James Backhouse, a well travelled Quaker during the early colonial period, gave the following account: "At Colongatta, in Shoal Haven district, which, like that of Illawarra, is much more favorable for the grazing of horned cattle than for sheep. Among the enemies of the latter in these rich, coast lands, is the Wattle Tick, a hard flat insect of a dark colour, about the tenth of an inch in diameter, and nearly circular, in the body; it insinuates itself beneath the skin, and destroys, not only sheep, but sometimes foals and calves. Paralysis of the hind quarters often precedes death in these cases. Sometimes it occasions painful swellings, when forcibly removed from the human body, after having fixed its anchor like head and appendages in the skin. To prevent this inconvenience, we several times, made them let go their hold, by smearing them over with oil, or with wet tobacco ashes." Whilst pioneering settlers knew that ticks posed a threat to their dogs and perhaps to themselves, the paralysis tick was not scientifically described until Louis Georges Neumann did so in 1899.). It was further studied by Nuttal and Warburton (1911). By 1921, Dodd had established a definitive link between Ixodes holocyclus and clinical disease in three dogs. His findings were that it took five to six days from time of attachment for clinical signs to develop, with motor paralysis being the major neurological symptom. The life cycle of the tick was studied chiefly by Ian Clunies Ross. Clunies Ross also demonstrated that a toxin produced by the tick, and not some infective agent carried by the tick, was responsible for the paralysis. The life cycle was further studied by Oxer and Ricardo (1942) and later summarised by Seddon (1968). In 1970, Roberts' work Australian Ticks gave the first comprehensive description of Australian ticks, including Ixodes holocyclus. The first confirmed human death in Australia due to tick envenomation was reported by Cleland in 1912, when a large, engorged tick caused flaccid paralysis in a child, progressing to asphyxiation. Headstones at the Cooktown cemetery attribute some human deaths to ticks. In the first half of the 20th century, at least 20 human deaths were attributed to the paralysis tick. Eighty percent of the victims reported in New South Wales between 1904 and 1945 were children aged under four years. Many cases of "infantile paralysis" (later known as poliomyelitis) may well have been misdiagnosed and actually been cases of tick paralysis.

The life cycle of Ixodes holocyclus consists of four stages: egg, larva, nymph, adult. Ixodes holocyclus requires three hosts to complete its life cycle, thus it is a "three host tick". Ticks hatch as six legged larvae after an incubation period of 40 to 60 days. Larvae search for a blood meal from a host, feed for four to six days, then drop from the host and moult to become an eight legged nymph. Nymphs require a second blood meal before they can moult again to become an adult. Female adults then require a further blood meal of up to ten days before dropping off to lay up to 3000 eggs in leaf litter. Male adults will search for females on the host for mating, and to parasitise the females for blood meals. That life cycle takes around a year to complete, with minimum being 135 days, and the maximum 437 days. When a tick is fully engorged it is said to be replete.

Adult females lay between 2000 and 6000 eggs in leaf and branch litter, under the scaly or fibrous bark of certain trees and shrubs, or in dense fine foliage near the tips of branches. They use a wax like substance to make a cohesive mass of eggs and attach them at the selected site. After 40–110 days incubation, a small fraction of the eggs survive and hatch to larvae. Development occurs with suitable warmth and high humidity (e. g. in moist leaf litter).

The newly moulted adult female becomes increasingly active during the first 6 or 7 days and seeks a host. It attaches to the final host after 7 to 9 days (but possibly up to 77 days). After insemination by a male tick, or sometimes before, a female feeds on blood to gain the nutrients for the egg mass to mature. Adult females engorge for a period of 6–30 days, the time again being temperature dependent. (The 30 day engorgement time is derived from laboratory culture colonies.) Under natural conditions, the time taken for an adult female to engorge while on the host varies from 6 to 21 days, the period being longest in cool weather. When replete, the adult female drops off the host to the ground. After 11–20 days the gravid female starts to lay a batch of 2000 to 6000 eggs (20–200 eggs per day over 16–34 days) into moist vegetation such as leaf and branch litter, under the bark of trees and shrubs, or in foliage near the tips of branches. The eggs are attached as a mass with a wax like substance. The female tick dies one or two days after egg laying is complete. Under laboratory conditions, female ticks have been kept alive for more than two years. Due to the variation in time taken for the female to engorge, a host may carry a tick for up to three weeks without the tick becoming significantly engorged or causing paralysis. However, in warm weather, the female engorges rapidly and, at the same time, injects her toxin into the host, thus causing paralysis if the host is susceptible. The adult female does not usually inject detectable amounts of toxin until the third or fourth day of attachment to the host, with peak amounts being injected on days five and six. Diagnosis: A very large tick when fully engorged; scutum about as long as broad and broadest a little posterior to mid length, with strong lateral carinae; capitulum relatively long porose areas deep, cornua usually absent, but when present at most only mild and rounded; auriculae present; hypostome lanceolate, dentition mainly 3/3; no sternal plate; anal grooves meeting at a point behind; all coxae with an external spur decreasing in size posteriorly; trochanters III and IV usually with small, pointed ventral spurs. Body: Unfed specimens, oval, flat, yellowish, 2.6 × 1.1 mm – 3.8 × 2.6 mm; marginal groove well developed and continuous; hairs small, scattered, most numerous in region of marginal fold. Semi engorged specimens frequently with body widest behind coxa IV and with a waist at level of spiracles. Fully engorged specimens broadly oval, attaining 13.2 × 10.2 mm, living ticks with blue grey alloscutum, the dorsum light in colour, a dark band in region of marginal groove. Capitulum: Length 1.00–1.035 mm. Basis dorsally 0.60–0.68 mm in width, the lateral submarginal fields swollen and frequently delimited from the depressed, median field by ill defined carinae; posterior margin sinuous, posterolateral angles swollen, sometimes mildly salient; porose areas large, deep subcircular or oval, the longer axis directed anteriorly, interval frequently depressed, at most about the width of one; basis ventrally with posterior margin rounded and with well defined, blunt, retrograde auriculae. Palps long and slender, some long hairs ventrally; article I rounded and somewhat salient laterally, inner 'ring' with dorsal tongue like prolongation and ventrally semicircular and plate like, the posterior margin of the plate extending beyond the palp; articles 2 and 3 with no apparent suture, 0.75–0.85 mm in length and about four times as long as wide, narrowly rounded distally. Hypostome lanceolate and bluntly pointed; dentition mainly 3/3, the innermost file of small, spaced teeth, basally 2/2. Scutum: As wide as or a little wider than long, widest a little posterior to mid length, 1.6 × 1.7 mm – 2.4 × 2.4 mm, flat medianly, convex external to the long, strong lateral carinae; anterolateral margins practically straight, posterolateral margins mildly concave; posterior anle broadly rounded. Punctations numerous, fine, sometimes a little coarser medianly and laterally, shallow rugae frequently present posteriorly. Cervical grooves well defined but short. Emargination moderate. Scapulae blunt. Genital aperture: On a level with coxa IV, but in engorged specimens sometimes just posterior to this level. Anal grooves: Rounded anteriorly, curving behind anus to meet in a somewhat elongate point. Spiracular plate: Subcircular, greatest dimension 0.40–0.45 mm. Legs: Coxae smooth, I and II sometimes with mild rounded ridges externally, each with a row of long hairs posteriorly and an external spur, longer and more pointed than in male, and decreasing in size posteriorly. Trochanter IV (and sometimes III) frequently with a small, ventral spur. Tarsi tapering a little abruptly; length of tarsus I 0.70–0.80 mm, and of tarsus IV 0.60–0.78 mm.

Natural predators of I. holocyclus include insectivorous birds and wasps.

Humid conditions are essential for survival of the paralysis tick. Dry conditions, relatively high temperatures (32 °C) and low temperatures (7 °C) are lethal for all stages after a few days. An ambient temperature of 27 °C and high relative humidity is thought to be optimal for rapid development. Very dry or very wet conditions are not ideal. The tick population in a given year is probably governed by the rainfall in the previous year if temperature variation has been moderate. North easterly weather, with moisture laden sea breezes on the east coast of the continent, provides ideal conditions. This pattern usually sets in during spring and early summer. Tick envenomation in animals (especially pets) peaks in spring to mid summer. Typically, larvae appear late February to April or May, followed by nymphs from March to September or October and then gradually the adult population from August to February, peaking around December. Under favourable conditions a second cycle may result in a second peak in May. However, infestation by adults can occur at any time of the year when conditions are suitable, even in mid winter. Only in the very hot summer months are they difficult to find. Small numbers of each instar are present throughout the year, with the numbers in each life cycle segment rising to plateau levels at particular times and then falling away again. Winter occurrence of gravids varied from nil to very small numbers in two of eight years studied.

Ticks generally are obligate blood feeders. Active stages (larvae, nymphs and adults) of Ixodes holocyclus require blood as a source of nutrition. Adults also require the blood for sperm or egg production. The feeding process of ixodid ticks has first a slow phase for several days followed by a fast phase in the last 12–24 hours before detachment. There may be a tenfold increase in fed versus unfed weights by the end of the slow phase, but there is another tenfold increase by the end of the final fast phase. Leaving the full engorgement as late as possible reduces the chances of detection and removal by the host. The hypostome has a groove along its dorsal surface forming a food canal (also known as the preoral canal) through which blood is drawn from the host and passed on to the mouth and pharynx. During blood feeding by ixodid ticks, the liquid portion of the meal is first concentrated by removal of water and excess ions, which move across the gut epithelium and enter the tick's body cavity (hemocoele). These components are then taken up by the salivary glands, which produce a watery saliva that is injected back into the host

Blood meal digestion in ticks is similar in all species. The digestive system is histologically divided into foregut, midgut and hindgut. The foregut comprises the sucking pharynx and the oesophagus. The midgut contains a ventriculus with a valve, a variable number of blind diverticula (caeca), and a rectal tube. The hindgut is divided into a rectal bulb and the rectum itself. The mouthpart section of the tick is known as capitulum ("little head"). The capitulum is not a true 'head' in the sense that the structures one normally associates with the head (primitive brain, salivary glands) are not contained within it; these structures are located in the 'body' of the tick. Ixodes holocyclus has no eyes. The palps are the paired tactile and positioning limbs, which are not inserted into the skin but splayed out on the surface. The chelicerae are the paired cutting jaws, which cut a channel into skin for the hypostome. The hypostome is the single feeding tube, which also anchors the tick by its reverse barbs. The basis capituli forms the basal ring of cuticle to which the palps, chelicerae and hypostome are attached. The basis capituli moves in the dorsoventral plane and articulates with the body proper. Once it has chosen a feeding site, a tick positions itself with its legs so as to elevate its body at a sharp angle. Guided by the palps, the chelicerae cut into the skin with their horizontal cutting action. These rip and tear at the epidermal layers and a small pool of blood is formed. The hypostome is inserted, and this provides the initial attachment strength. In the case of Ixodes holocyclus, the hypostome is inserted very deep into the dermis. The process by which such ticks feed is termed telmophagy (pool feeding). (This contrasts with the process of solenophagy, used by mosquitoes, in which feeding is direct from a small venule.) The resultant pool expands as a result of the anticoagulants released from the salivary glands. The host reacts against the tick lesion by haemostasis, inflammation and cell mediated immunity. An array of pharmacologically active substances is injected with the saliva of the tick, including anticoagulants, prostaglandin E2, prostacyclin, apyrase and, in certain tick species, antihistamines. Prostaglandin E2 and prostacyclin inhibit platelet aggregation and dilate blood vessels. Feeding is almost continuous, with pulses of salivation alternating with periods of feeding to ensure continued suppression of host defences. There is a concentration of saliva and presumably toxin in the granulomatous reaction around the tick mouth parts. It is thought by some experimenters that the residual toxin located in this granuloma is at least partially responsible for the increasing paralysis which occurs after the tick is removed. By comparison, the North American paralysis tick Dermacentor andersoni (found in the Rocky Mtns) does not produce a granuloma at the site of attachment, and in this case the paralysis rapidly regresses after the tick is removed. The distribution map gives only an approximation of the tick's distribution as the situation is not static. There are reports from inland Victoria, including north eastern suburbs of Melbourne. This may reflect general movement of insects and ticks from equatorial to polar latitudes which in turn may be related to climate change. The need for humid conditions largely determines the botanical niche of this species. Low, leafy vegetation provides higher humidity levels by reducing the desiccating effects of wind and direct sunlight. This environment also suits the tick's major host, the bandicoot, as it seeks out grubs and worms in the leaf litter. Certain vegetation may be conducive to paralysis ticks. There are mixed reports about whether paralysis ticks climb trees. Some references mention ticks climbing to the tops of trees, while others report that they stay within 50 cm of the ground.

The kinds of effects caused by bites of Ixodes holocyclus vary in their frequency according to the type of host and whether the tick is at the stage of larva, nymph or adult. Humans are most notably affected by local irritation and numbness, allergic reactions and tick transmitted infectious diseases. Tick paralysis is possible but not common. Domestic animals (pets and livestock) are most notably affected by tick paralysis. Allergic reactions and tick transmitted infectious diseases are possible but rarely diagnosed. Native animals are most notably affected by anaemia caused by carrying heavy burdens of ticks drawing large quantities of blood. Tick paralysis is possible but mainly recognised in captive animals where there has been a discontinuity in exposure and so a drop in immunity. Although there is the possibility of innate differences between species, the variations in effects can largely be explained by how often and how heavily hosts are exposed.

At the site of a bite by an adult female Ixodes holocyclus one can expect there to be local numbness and an itchy lump which lasts for several weeks. Although most cases of tick bite are uneventful in humans, some can produce life threatening effects including severe allergic reactions, tick transmitted infectious diseases such as Rickettsial Spotted Fever (also known as Queensland tick typhus), and tick paralysis. Larvae and nymphs, as well as adults, are capable of causing very dramatic allergic reactions. Dramatic local redness and swelling may develop within 2–3 hours of attachment of even one larva. People have experienced allergic reactions after coming in contact with both live and dead tick products. Having a tick simply walk over a person's hand produces in some people an intense discomfort and itching. What particular components of the tick body cause these reactions is unknown, but it could be a water soluble component that is excreted through the cuticular canals. In south east Queensland a 'maddening rash' (known locally as 'scrub itch') is caused by infestation by many tick larvae. This especially affects people clearing leafy bushland such as lantana scrub. Whilst systemic paralysis is possible in humans, it is now a relatively rare occurrence. This is because an engorging adult female tick needs to remain attached for several days. This was more likely to occur in the past because there was less medical and public awareness of the problem and perhaps because it was more likely to be misdiagnosed as polio. Paralysis is more likely to occur in children and in situations where ticks are attached in places where they are not easily detected (e. g., under bandages). Up through 1989, 20 human fatalities had been reported in Australia. If an unusual black scab (eschar) develops at the site of a tick bite, or if there are any other signs of illness occurring within a few weeks of a tick bite (especially flu like symptoms, fever, generalised skin rash, or muscular or joint pain), a doctor should be consulted and informed about the tick bite. A rickettsial infection (Rickettsia australis or Rickettsia honei) may be the cause. Whilst many such rickettsial infections are self limiting, early treatment with antibiotics can prevent longer term problems in some individuals. Doctors may also wish to investigate the possibility of a Lyme like disease, particularly if there is also a 'bullseye' or target shaped skin rash (erythema migrans).

The tick's paralysing toxin has been estimated to affect as many as 100,000 domestic animals annually, with up to 10,000 pets being referred to veterinary surgeons for treatment.

All stages of Ixodes holocyclus are commonly responsible for allergic reactions in humans.

Attachment of a few larvae to a non sensitised host provokes little or no response, even though the contact is prolonged over several days. However, towards the end of feeding some itching, redness and localised swelling may develop at the site of attachment. Repeated infestation with larvae, as occurs in rural and wooded suburban areas where bandicoots are common, rapidly leads to the development of hypersensitivity. Dramatic local redness, numbness, swelling and itching may develop within 2–3 hours of attachment of even one larva if a person has been sensitised by a previous bite. In this case attachment of the larvae leads to formation of intra epidermal blebs and eventually blisters. These eventually rupture and the larvae detach and are lost. A tick embedded over an eyelid may result in gross facial and neck swelling within a few hours. The person can go on to develop tracheopharyngeal compression within 5–6 hours after the first onset of symptoms.

Attachment of the nymphal and adult stages produce variable responses, many of which are allergic in nature. Often, attachment may provoke little or no response and the patient may be unaware of the presence of a tick for some days until eventually minor itching leads to its discovery. Conversely, there is sometimes a locally heightened sensitivity or hyperaesthesia. Such attachment sites are surrounded by redness. The induced allergy is unusual in that the onset of the allergic reaction, which ranges from mild stomach symptoms to life threatening anaphylaxis (skin rashes, swollen tongue and serious drop in blood pressure), can occur up to 3 to 6 hours after eating mammalian meat (typically beef, lamb or pork) and often many months after the tick bite. All mammals except humans and certain apes have a carbohydrate commonly known as alpha gal (galactose α 1,3 galactose) in their tissue fluids. When a tick feeds on the blood of a mammal (bandicoot, possum, cat, dog etc.) it takes alpha gal into the tick's digestive system. When the same tick attaches to the next host (e. g., a human) it transfers the alpha gal to the tissues of that next host. The immune system of some humans recognises alpha gal as foreign and so produces antibodies against it. In this case the antibody produced is IgE, which is the type of antibody responsible for most allergic reactions. Thus the human is primed for a delayed allergic reaction to subsequent ingestion of mammalian meats (but not chicken or fish). Alpha gal allergy in a human can now be recognised through a blood test. The reaction to alpha gal is distinct from any immediate allergic reaction to the tick itself, which is provoked by proteins in the tick's saliva, not the carbohydrate alpha gal. People who have such allergic reactions, however, may have a greater predisposition to also developing the allergy to mammalian meats over the next several months.

It is thought the toxins of Ixodes holocyclus cause a failure of secretion of neurotransmitter acetylcholine at neuromuscular junctions. In experiments where nerve–muscle preparations were incubated in solution containing toxin, the paralysis effect was delayed for six to seven hours after the addition of toxin. As in live test animals, this effect was temperature dependent, paralysis being more rapid at higher temperatures. Live mice injected with toxin did not develop signs of paralysis for some 8 to 12 hours after the injection. The cause of the delayed toxicity is unknown. Several toxic fractions have been isolated from the salivary glands of Ixodes holocyclus, but there has been variation in the reported molecular size of the principal paralysing toxin or toxins. Early work suggested that the most neurotoxic fraction was a protein (molecular weight 40–60 kilodaltons, stable when freeze dried, originally named holocyclotoxin) Another toxin was found to be lethal but non paralysing. A more recent study isolated three low molecular weight toxins, all three of which were able to cause hind limb paralysis in baby mice. Only one, however, could be isolated in quantities permitting further research. The molecule was relatively small at 6 kilodaltons, corresponding to a protein of approximately 50 amino acids like those in scorpion and spider toxins. The benefit conferred by the paralysing toxin is not clear. Being arachnids, ticks are related to predatory arthropods (spiders, scorpions and mites). Spiders and scorpions have retained toxins and developed specialised delivery structures (fangs and telsons) while mites and ticks have lost this feature. Of the 800 species of ticks, only 40–64 species (across 10 genera) have been reported as causing some form of toxicosis. As ticks have moved from a predatory existence to a parasitic existence, most species have lost their toxin, which would have been a disadvantage for a parasitic lifestyle (parasites in general do not benefit from killing their hosts). The gene sequence of the tick toxin shows high homology to scorpion toxins. The saliva of Ixodes holocyclus also contains an anti coagulant.

Dogs and cats on the east coast of Australia commonly succumb to the tick paralysis caused by Ixodes holocyclus. A similar tick species, Ixodes cornuatus, appears to cause paralysis in Tasmania. Development of a vaccine to protect dogs against the tick toxin has been attempted but has not yet been successful.

The number of paralysis ticks required to paralyse a horse is unknown, but in one study there were cases of large horses with only one to two ticks being paralysed and unable to stand. Horses of any age and size can be affected by tick paralysis. In the same study, 26% of the horses died and, of the surviving horses, 35% developed one or more complications including pressure sores, corneal ulcers, pneumonia and sepsis. The relatively high mortality rates in horses in this study could be due to a range of factors, including horses being badly affected before vets are called, difficulties associated with nursing a recumbent horse, difficulties with owners needing to deliver the bulk of nursing care, and lack of information to veterinarians managing the disease in horses.

Several bacterial diseases are spread by Ixodes holocyclus. As yet no viral or protozoal diseases associated with this vector are known. Vector competence for hard (ixodid) ticks is believed to require that the microorganism be able to replicate within the tick. These ticks tend to not take multiple blood meals from different hosts in one stage, and passing an organism between tick stages (trans stadial transmission) seemingly requires that an organism be able to propagate as the tick matures.

Ixodes holocyclus is the main vector for rickettsial spotted fever (also known as Queensland tick typhus) (causative organism Rickettsia australis) and Flinders Island spotted fever (causative organism Rickettsia honei). Rickettsia australis is an obligate intracellular bacterial parasite that proliferates within the endothelial cells of small blood vessels, causing a vasculitis. Spotted fever is probably more common than the tick borne Lyme like disease found in Australia. Sometimes infection with Rickettsia australis occurs without a rash; there may just be a high fever. Usually (in 65% of cases) there is a black spot (known as an eschar, usually 2–5 mm in diameter) at the site of the tick bite. This looks like a scab with redness and swelling around it. Usually there is only one eschar unless there has been more than one tick bite. Often lymph glands nearby are enlarged and painful. Fever starts 1–14 days (usually 7–10 days) after the tick bite, followed within a few days by a rash. The rash can look like chicken pox as the spots may contain some fluid. Other symptoms include headache, stiff neck, nausea, vomiting, mental confusion, and aching muscles and joints. The illness may be more severe in adults and elderly persons. Spotted fever is diagnosed by two blood tests (immunoglobulin M and Weil Felix tests) taken 10 days apart. PCR analysis of skin biopsies is a more recent testing method. The disease runs its course in two weeks or so but can be cured more quickly with tetracycline antibiotics. As antibiotic treatment is very effective, many persons feel so well that they do not return to have the second blood sample collected. But this second blood test is important as it is the only way of proving the diagnosis of spotted fever. Spotted fever rarely, if ever, occurs more than once because someone infected once usually becomes immune for life. In rare instances there may be a repeated infection after recovery; it is not known whether this is caused by another strain. It is also presently unknown whether chronic infections occur. The disease is rarely fatal. Australian spotted fever was first described in 1946 when 12 soldiers contracted the disease during training exercises in north Queensland; it was at that time known as Queensland tick typhus. Infections generally arise in rural areas, but 10% of reported cases appear to have been acquired in cities. It is commonly seen in tick collectors in southern Queensland. It mostly occurs during the winter and spring, but can occur at any time in temperate areas.

Ixodes holocyclus is also commonly mentioned as a potential vector of Q fever (Coxiella burnetii). The ornate kangaroo tick (wallaby tick) Amblyomma triguttatum has also been implicated in Q fever.

Lyme disease was first described in Europe in 1883 and in the 1970s in North America. It is an illness caused by a spiral shaped bacterium called a spirochaete. The best known culprit is Borrelia burgdorferi, but many different Borrelia species cause Lyme disease worldwide. An Australian spirochaete has not been found in humans yet, and may be quite different from Borrelia burgdorferi. Despite clinical case reports, it is still controversial as to whether Lyme disease occurs in Australia. Some doctors and health authorities believe it does, while others are adamant that it does not. Until the controversy is resolved, patients with suspected Lyme like disease should be treated with an appropriate course of antibiotics because early treatment of Lyme disease invariably results in a complete cure. Some vector competence studies have been undertaken on Ixodes holocyclus with respect to the Lyme disease pathogen Borrelia burgdorferi sensu stricto (a United States strain). These suggested that the tick can not transmit this strain of spirochaete. Despite this, there is a strong belief that some kind of Lyme like spirochaete causes a Lyme like disease in Australia and that it is carried by Ixodes holocyclus. At the Royal North Shore Hospital in Sydney the Tick borne Diseases Research Unit continues its study into this issue. Cases of Lyme like disease are being diagnosed on the basis of clinical signs (often musculoskeletal, chronic fatigue, neurological and dermatological), exclusion of other infections, serology (which is supportive but not conclusive), and response to antibiotic treatment. Initially, antibiotics may cause a worsening of symptoms (the Herxheimer reaction), as spirochaetes are destroyed, which in part supports the diagnosis. This putative Australian form of Lyme like borreliosis is associated with a different clinical picture from true Lyme disease of North America.

Early symptoms in the first four weeks after a tick bite include a rash or red patch that gradually expands over several days. It may get quite large (up to 50 mm or more in diameter). This rash is called erythema migrans or EM. It can be difficult to distinguish from an allergic reaction at the site of the bite. Allergic rashes usually occur within 48 hours of the bite, then fade. EM usually first appears after a delay of 48 hours following the tick bite and gets bigger over a few days or weeks. As it expands, the EM rash often has a 'target' or 'bullseye' appearance, clearing in the middle with a more obvious red edge. EM can persist for months or years, coming and going in that time. Sometimes many small EM rashes occur. EM may occur in as few as 20% of persons with Lyme disease.

More common than EM are symptoms due to invasion by the spirochaete of the nervous system, heart, muscles and joints. These may start weeks or months after the tick bite. Initially, they may include flu like illness, fever, headache, sore throat, fatigue, aching muscles and joints. More serious are meningitis, Bell's palsy (weakness of the face muscles), swelling of joints, and heart problems with palpitations and breathlessness. Lyme disease is difficult to distinguish from many other illnesses, such as chronic fatigue syndrome, because the symptoms may be similar. If a patient has symptoms that could be Lyme disease, even if no tick bite was ever noticed, it is important to see a doctor. Diagnosis is helped by a blood test called a western blot test, but a doctor may do other tests to determine whether any other illness could be causing the symptoms.

Early treatment with antibiotics is important to prevent more serious problems. Pregnant women bitten by a tick should see a doctor. Some data suggests that Lyme disease can affect the foetus, but two large studies in the US and Europe showed no increased risk of adverse effects on the foetus.