Ticks

Ticks

There are 2 common families of ticks, the Argasidae or soft ticks and the Ixodidae or hard ticks. The hard ticks differ from the soft ticks in that the formers’ head (capitulum) is visible from a dorsal angle and that they possess a plate like structure (scutum) on the dorsal side of the cephalothorax. The scutum typically covers 1/3 of the back of the female and in the male; it covers almost the entire dorsal surface. In the soft ticks, the capitulum is not visible from above and there is no scutum present. Both types of ticks prefer warm-blooded animals, but will attack cold-blooded animals such as reptiles. The life cycle of the tick includes eggs, larva (seed tick) with 3 pair of legs, nymph, and adult.

A Hard Tick characterized by a well-developed Scutum and Dorsally Visible Capitulum (Head)

Soft Ticks

Soft ticks feed primarily on the blood of birds. They are typically nightly feeders and return to protected locations to hide during the day. One of the more damaging species is the fowl tick (Argas periscus), which is one of the more important worldwide poultry pests. Nymphs and adults of this tick are very active at night. It is not unusual to see large numbers of these ticks crawling up the roosts, filling with blood and before daybreak leaving for their daytime hiding places. The larval stage, once attached to the host, remains to engorge with blood for several days. Under favorable conditions the entire life cycle may be complete in as little as 30 days. In the absence of an available host this can be extended to several months.

A Soft Tick (Argas persicus) Lacks the Scutum and Capitulum Not Visible From a Dorsal Angle. Image Courtesy of Matt Pound, ARS, Bugwood.

Heavy infestations of these ticks may result in a rundown condition, loss of weight and reduced egg production. Secondary infections may occur which can result in the death of the animals. Fowl ticks will attack humans, especially in the absence of their preferred hosts.

Tick Born Relapsing Fever.

There are two forms of this disease being caused by bacteria in the genus Borrelia and transmitted through louse or soft-bodied tick bites. Borrelia recurrentis is the agent of louse-borne disease vectored by Pediculus humanus, namely the body louse. It is more severe than the tick-borne variety. Epidemics most commonly occur with poor living conditions, famine and war in the developing world; it is currently prevalent in Ethiopia and Sudan. Mortality rate is 1% with treatment; 30-70% without treatment. Prognostic signs include severe jaundice, severe change in mental status and severe bleeding.

Lice that feed on infected humans acquire the Borrelia organisms that then multiply in the gut of the louse. Subsequent the bacterium can be passed onto another human by crushing the louse or by the feces which are scratches into feeding wounds. B. recurrentis can also infect a victim via mucous membranes and then invades the bloodstream. No other animal reservoir exists.

Tick-borne relapsing fever is found primarily in Africa, Spain, Saudi Arabia, Asia, and certain areas in the Western U.S. and Canada. It is vectored by soft ticks and caused by Borrelia duttoni.

Most people who are infected get sick around 5-15 days after they are bitten by the tick. The symptoms may include a sudden fever, chills, headaches, and muscle or joint aches, and nausea; a rash may also occur. These symptoms continue for 2-9 days, and then disappear. This cycle may continue for several weeks if the person is not treated. Relapsing Fever is easily treated with 1-2 weeks of antibiotics. Most people improve within 24 hours of starting antibiotics. Complications and death due to relapsing fever are rare.

Relapsing fever is a candidate etiology for a mysterious series of plagues in late medieval and early renaissance-era England referred to at the time as sweating sickness but which have not recurred in epidemic form since the 16th Century.

Antibiotics of the tetracycline class are most effective, but may induce a Jarisch-Herxheimer reaction, which occurs in over 50% of patients. This reaction produces apprehension, diaphoresis, fever, tachycardia, and tachypnea with an initial response followed rapidly by hypotension. Recent studies have shown that tumor necrosis factor-alpha (TNF-alpha) may be partly responsible for the reaction.

Hard Ticks

Unlike soft ticks, hard ticks only have 3 feeding periods during their life cycle. A typical life cycle of a hard tick is as follows. The female will deposit up to 7,000 eggs in a cluster in the soil. The larval stage (seed tick) crawls up on a twig or other surface and waits for an available host. Once it attaches itself to the host, it typically crawls until it encounters a ridge and then buries its head beneath the skin and begins to feed on blood. Hard ticks feed to engorgement, swelling to many times their original size. They only feed once for 3 to 5 days during each of their developmental stages. After feeding, the larva drops off the host and eventually molts into an eight-legged nymph. After digesting the blood the nymph again crawls up and waits for another host. After engorging on blood the nymphs drop off and molt into adults. The adult repeats the feeding sequence.

Engorged Tick

The length of the life cycle primarily depends on the availability of food. These ticks can survive extended periods of time (up to a year) without feeding. As a consequence the life cycle can be completed in less than a few months or can be extended for years if a host is not readily available. These ticks are excellent vectors of pathogens. Hard ticks are especially good vectors because of their wide host range and high reproductive potential. Hard ticks are also slow feeders and are easily dispersed by hosts.

Wood Tick. (Dermacentor adersoni) Vectors Various Serious Diseases.

Tick Paralysis. This is the only tick-borne disease that is not caused by an infectious organism. Tick paralysis results from inoculation of a toxin from tick salivary glands during a blood meal. The toxin causes symptoms within 2-7 days, beginning with weakness in both legs that progresses to paralysis. The paralysis ascends to trunk, arms, and head within hours and may lead to respiratory failure and death. The disease can cause acute ataxia without muscle weakness.

Tick paralysis is believed to be due to toxins found in the tick’s saliva that enter the bloodstream while the tick is feeding. The two ticks most commonly associated with North American tick paralysis are the Rocky Mountain wood tick (Dermacentor andersoni) and the American dog tick (Dermacentor variabilis); however, 43 tick species have been implicated in human disease around the world. Most North American cases of tick paralysis occur from April to June, when adult Dermacentor ticks emerge from hibernation and actively seek hosts. In Australia, tick paralysis is caused by the tick Ixodes holocyclus. Up to 1989 20 fatal cases have been reported in Australia.

Tick paralysis has killed thousands of animals, mainly cows and sheep, in other parts of the world. Although tick paralysis is of concern in domestic animals and livestock in the United States as well, human cases are rare and usually occur in children under the age of 10.

Tick paralysis occurs when an engorged and gravid (egg-laden) female tick produces a neurotoxin in its salivary glands and transmits it to its host during feeding. Experiments have indicated that the greatest amount of toxin is produced between the fifth and seventh day of attachment (often initiating or increasing the severity of symptoms), although the timing may vary depending on the species of tick.

Unlike Lyme disease tick paralysis is chemically induced by the tick and therefore usually only continues in its presence. Once the tick is removed, symptoms usually diminish rapidly usually within several hours to days. However, in some cases, profound paralysis can develop and even become fatal before anyone becomes aware of a tick’s presence. Diagnosis is based on symptoms and upon finding an embedded tick, usually on the scalp.

No vaccine is currently available for any tick-borne disease, except for Tick-borne encephalitis. Individuals should therefore take precautions when entering tick-infested areas, particularly in the spring and summer months. Preventive measures include avoiding trails that are overgrown with bushy vegetation, wearing light-colored clothes that allow one to see the ticks more easily, and wearing long pants and closed-toe shoes. Tick repellents containing DEET (N,N, diethyl-m-toluamide) are only marginally effective and can be applied to skin or clothing. Rarely, severe reactions can occur in some people who use DEET-containing products. Young children may be especially vulnerable to these adverse effects. Permethrin, which can only be applied to clothing, is much more effective in preventing tick bites. Permethrin is not a repellent but rather an insecticide; it causes ticks to curl up and fall off of the protected clothing.

Although several attempts have been made to isolate and identify the neurotoxin since the first isolation in 1966 the exact structure of the toxin is still unknown.

Below are descriptions of four documented cases of this condition,

Case 1. On May 15, a girl aged 6 years from Weld County awoke with symptoms of bilateral lower extremity weakness. She attended school as usual but needed assistance from a friend to walk outside for recess, where she fell down and was unable to get up. Her mother took her to an outpatient clinic, and a neurology appointment was arranged for the next day. She awoke the next day with a tingling sensation in her hands and feet, an inability to sit or stand on her own, and difficulty swallowing. The girl was admitted to the intensive-care unit on May 16 with a presumed diagnosis of Guillain-Barré syndrome and subsequently required intubation. On the evening of May 17, a nurse who was bathing the girl found a tick along her hairline. Investigators later learned that the tick had been visible on magnetic resonance imaging of the girl’s head earlier that day. The tick was removed immediately, and the girl’s symptoms improved; she was discharged home 1 week later. The tick was identified as a female Dermacentor andersoni. The girl often had visited her grandmother in the mountains in Larimer County and frequently hiked in the area. Seven days before symptom onset, the girl had visited her grandmother and played outside in the yard.

Case 2. On May 22, a man aged 86 years from the mountains in Larimer County began to have increased difficulty standing and transferring to and from his motorized scooter. The man was homebound as a result of chronic polyneuropathy and weakness from spinal stenosis. The next morning, his weakness worsened, and he was unable to walk or grasp objects. He called for emergency services and was admitted to the local hospital with a diagnosis of progressive worsening of his chronic neuropathy. Physical examination revealed normal cranial nerve function but generalized weakness; deep-tendon reflexes were absent. On the evening of May 23, a nurse who was changing the man’s gown noticed a tick on his back. After tick removal, his symptoms improved during the next 4 days, and he was discharged home on May 27, although 2 weeks later he did not feel he had yet recovered to his baseline condition. The man did not report any recent travel or spending any time outdoors, with the exception of daily visits to his mailbox using his scooter. He owned a dog that was often outside, and he believed this was the likely source of the tick; the dog had no signs of tick paralysis.

Case 3. On May 22, a woman aged 78 years from the mountains in Grand County had generalized weakness and difficulty walking. During the next few days, her signs and symptoms progressed to facial weakness, slurred speech, decreased taste, and confusion. While the woman was preparing to go to the ED on May 25, her roommate noticed a tick on the back of the woman’s neck below the hairline. Physical examination in the ED revealed normal cranial nerve function and no appreciable weakness, but the patient did have decreased deep-tendon reflexes. The ED physician removed the tick by cutting the surrounding tissue with a scalpel. The patient was discharged home to recover. The patient subsequently reported that within 24 hours her weakness, alteration in taste, and confusion were resolved; however, 3 weeks after discharge, she still became tired easily. The woman reported that she hiked or walked outside daily.

Case 4. A man aged 58 years from Larimer County with a history of chronic renal failure traveled to southern Texas on April 20. On April 24, he had a tingling sensation in his hands and perioral numbness. Three days later, he collapsed while trying to stand and was unable to get up. While helping him off the floor, his wife discovered a tick on the man’s back. She removed the tick before transporting him to a local ED. He was transferred and admitted to an intensive-care unit but did not require intubation. Several hours later, he began to regain feeling in his hands and was able to walk with assistance. He was discharged home on May 5, but 6 weeks later he still reported residual subjective weakness. The patient reported that he frequently performed yard work and various outdoor recreational activities.

Rocky Mountain Spotted Fever. This is the most lethal and most frequently reported rickettsial illness in the United States. It is present throughout the Americas. Some names for Rocky Mountain spotted fever in other countries include “tick typhus,” “Tobia fever” (Colombia), “São Paulo fever” or “febre maculosa” (Brazil), and “fiebre manchada” (Mexico). It is distinct from the viral tick-borne infection Colorado tick fever. The disease is caused by Rickettsia rickettsii, a species of bacterium that is spread to humans by Dermacentor ticks. Initial signs and symptoms of the disease include sudden onset of fever, headache, and muscle pain, followed by development of rash. The disease can be difficult to diagnose in the early stages, and without prompt and appropriate treatment it can be fatal.

The name “Rocky Mountain spotted fever” is somewhat of a misnomer. Beginning in the 1930s, it became clear that this disease occurred in many areas of the United States other than the Rocky Mountain region. It is now recognized that this disease is broadly distributed throughout the continental United States, and occurs as far north as Canada and as far south as Central America and parts of South America. Between 1981 and 1996, this disease was reported from every U.S. state except Hawaii, Vermont, Maine, and Alaska.

Rocky Mountain spotted fever remains a serious and potentially life-threatening infectious disease today. Despite the availability of effective treatment and advances in medical care, approximately 3% to 5% of individuals who become ill with Rocky Mountain spotted fever still die. However, effective antibiotic therapy has dramatically reduced the number of deaths; before the discovery of tetracycline and chloramphenicol in the late 1940s, as many as 30% of individuals infected with R. rickettsii died.

Rocky Mountain spotted fever, like all rickettsial infections, is classified as a zoonosis. Zoonoses are diseases of animals that can be transmitted to humans. Many zoonotic diseases require a vector (e.g., a mosquito, tick, or mite) in order to be transmitted from the animal host to the human host. In the case of Rocky Mountain spotted fever, ticks are the natural hosts, serving as both reservoirs and vectors of R. rickettsii. Ticks transmit the organism to victims primarily by their bite. Less commonly, infections may occur following exposure to crushed tick tissues, fluids, or tick feces.

A female tick can transmit R. rickettsii to her eggs in a process called transovarial transmission. Ticks can also become infected with R. rickettsii while feeding on blood from the host in either the larval or nymphal stage. In this case after the tick molts into the next stage, the R. rickettsii may be transmitted to the second host during the feeding process. Furthermore, male ticks may transfer R. rickettsii to female ticks through body fluids or spermatozoa during the mating process. These types of transmission represent how generations or life stages of infected ticks are maintained. Once infected, the tick can carry the pathogen for life.

Rickettsiae are transmitted to a vertebrate host through saliva while feeding. It usually takes about 24 hours of attachment and feeding before the rickettsiae are transmitted to the host. The risk of exposure to a tick carrying R. rickettsii is low. In general, about 1%-3% of the tick population carries R. rickettsii, even in areas where the majority of human cases are reported.

Vectors include Dermacentor variabilis, Dermacentor andersoni, Rhipicephalus sanguineus, and Amblyomma cajennense. However, not all of these are of equal importance, and most are restricted to certain geographic areas.

There are two major vectors of R. rickettsii in the United States, the American dog tick and the Rocky Mountain wood tick. American dog ticks (Dermacentor variabilis) are widely distributed east of the Rocky Mountains and also occur in limited areas on the Pacific Coast. Dogs and medium-sized mammals are the preferred hosts of adult D. variabilis, although it feeds readily on other large mammals, including humans. Rocky Mountain wood ticks are found in the Rocky Mountain States and in southwestern Canada. Its life cycle may require up to 2 to 3 years for completion. Adult ticks feed primarily on large mammals while larvae and nymphs feed on small rodents.

There are only approximately 800 cases reported in the U.S. a year. Rocky Mountain spotted fever can be very difficult to diagnose in its early stages, even among experienced physicians who are familiar with the disease. Individuals infected with R. rickettsii usually notice symptoms following an incubation period of one to two weeks after a tick bite. The early clinical presentation of Rocky Mountain spotted fever is nonspecific and may resemble a variety of other infectious and non-infectious diseases. These include fever, nausea, emesis, severe headaches, muscle pain, lack of appetite, with advance symptoms including abdominal and joint pain and maculopapular and petechial rashes (red spotted).

The classic triad symptoms for this disease are fever, rash and history of tick bite. The rash has an inward pattern of spread, meaning it begins at the extremities and works towards the trunk. The rash first appears 2-5 days after the onset of fever and is often very subtle. Younger patients usually develop the rash earlier than older patients. Most often it begins as small, flat, pink, non-itchy spots on the wrists, forearms, and ankles. These spots turn pale when pressure is applied and eventually become raised on the skin. The characteristic red, spotted rash of Rocky Mountain spotted fever is usually not seen until the sixth day or later after onset of symptoms, but this type of rash occurs in only 35% to 60% of patients with Rocky Mountain spotted fever. The rash involves the palms or soles in as many as 50% to 80% of patients; however, this distribution may not occur until later in the course of the disease. As many as 10% to 15% of patients may never develop rash.

Rocky Mountain spotted fever can be a very severe illness and patients often require hospitalization. Because R. rickettsii infects the cells lining of blood vessels throughout the body, severe manifestations of this disease may involve the respiratory system, central nervous system, gastrointestinal system, or renal system. Host factors associated with severe or fatal Rocky Mountain spotted fever include advanced age, male sex, African-American race, chronic alcohol abuse, and glucose-6-phosphate dehydrogenase (G6PD) deficiency. Deficiency of G6PD is a sex-linked genetic condition affecting approximately 12% of the U.S. African-American male population; deficiency of this enzyme is associated with a high proportion of severe cases of Rocky Mountain spotted fever. This is a rare clinical course that is often fatal within 5 days of onset of illness.

Long-term health problems following acute Rocky Mountain spotted fever infection include partial paralysis of the lower extremities, gangrene requiring amputation of fingers, toes, or arms or legs, hearing loss, loss of bowel or bladder control, movement disorders and language disorders. These complications are most frequent in persons recovering from severe, life-threatening disease, often following lengthy hospitalizations.

Appropriate antibiotic treatment is initiated immediately when there is a suspicion of Rocky Mountain spotted fever on the basis of clinical and epidemiological findings. Treatment should not be delayed until laboratory confirmation is obtained. In fact, failure to respond to a tetracycline antibiotic argues against a diagnosis of Rocky Mountain spotted fever. Severely ill patients may require longer periods before their fever resolves, especially if they have experienced damage to multiple organ systems. Preventive therapy in non-ill patients who have had recent tick bites is not recommended and may, in fact, only delay the onset of disease.

Rocky Mountain spotted fever was first recognized in 1896 in the Snake River Valley of Idaho and was originally called “black measles” because of the characteristic rash. It was a dreaded and frequently fatal disease that affected hundreds of people in this area. By the early 1900s, the recognized geographic distribution of this disease grew to encompass parts of the United States as far north as Washington and Montana and as far south as California, Arizona, and New Mexico.

Colorado Tick Fever. CTF, (also called Mountain tick fever, Mountain fever, and American mountain fever) is an acute viral infection transmitted from the bite of an infected wood tick (Dermacentor andersoni). It should not be confused with the bacterial tick-borne infection, Rocky Mountain Spotted Fever.

The type species of the genus Coltivirus, Colorado tick fever virus (CTFV) infects haemopoietic cells, particularly erythrocytes, which explains how the virus is transmitted by bloodsucking ticks and also accounts for the incidence of transmission via blood transfusion.

The disease develops from March to September, with the highest infections occurring in May and June. The disease is found almost exclusively in the western United States and Canada, mostly in high mountain areas such as Colorado and Idaho. The CTFV was first isolated from human blood in 1944.

The virus particle, like other Coltiviruses, is ~80 nm in diameter and is generally non-enveloped. The double stranded RNA viral genome is ~20,000bp long and is divided into 12 segments, which are termed Seg-1 to Seg-12. Viral replication in infected cells is associated with characteristic cytoplasmic granular matrices. Evidence suggests that viral presence in mature erythrocytes is a result of replication of the virus in hematopoitic erythrocyte precursor cells and simultaneous maturation of the infected immature cells rather than off direct entry and replication of CTFV in mature erythrocytes.

The wood tick is usually found attached to a host, but when it is without a host it hides in cracks and crevices as well as soil. If for some reason the tick is not able to find a host before the winter months, it will stay under groundcover until spring when it can resume its search. The wood tick typically does not seek out available hosts in the hottest summer months as well. Adult ticks, for the most part, tend to climb to the top of grass and low shrubs to attach themselves to a host that is wandering by. These ticks are able to attach to their hosts by secreting a cement-like substance from their mouths and inserting it into the host.

Colorado Tick Fever is acquired by tick bite. There is no evidence of natural person-to-person transmission. However, rare cases of transmission from blood transfusions have been reported. The virus which causes Colorado Tick Fever may stay in the blood for as long as four months after onset of the illness.

First signs of symptoms can occur about 3-6 days after the initial tick bite, although it can have incubation periods of up to 20 days. Patients usually experience a two-staged fever and illness which can continue for three days, diminish, and then return for another episode of 1-3 days. The virus has the ability to live in the blood stream for up to 120 days; therefore coming in contact without proper precautions and the donation of blood are prohibited.

Initial symptoms include: fever, chills, headaches, pain behind the eyes, light sensitivity, muscle pain, generalized malaise abdominal pain, nausea, vomiting as well as a flat or pimply rash.[2] During the second phase of the virus a high fever can return with an increase in symptoms. CTF can be very severe in cases involving children and have even required hospitalization. Complications with this disease have included aseptic meningitis, encephalitis, and hemorrhagic fever, but these are rare.

CTF is seasonal, mostly occurring in the Rocky Mountain region of the United States and usually in altitudes from 4,000 to 10,000 feet. Patients with CTF are mostly campers and young males, who most likely have been bitten because of their occupational activities.

A combination of clinical signs, symptoms and laboratory tests can confirm the likelihood of having CTF. Some tests include complement fixation to Colorado tick virus, Immunofluoresence for Colorado tick fever, and some other common laboratory findings suggestive of CTF including leucopenia, thrombocytopenia, and mildly elevated liver enzyme levels.

To avoid tick bites and infection, experts advise:

  • Avoid tick infested areas, especially during the warmer months.
  • Wear light colored clothing so ticks can be easily seen. Wear a long sleeved shirt, hat, long pants, and tuck pant legs into socks.
  • Walk in the center of trails to avoid overhanging grass and brush.
  • Check your body every few hours for ticks when you spend a lot of time outdoors in tick infested areas. Ticks are most often found on the thigh, arms, under arms and legs. Ticks can be very small (no bigger than a pinhead). Look carefully for new “freckles”.
  • Use insect repellents containing DEET on your skin or permethrin on clothing. Be sure to follow the directions on the container and wash off repellents when going indoors.
  • Remove attached ticks immediately.

Contracting the CTF virus is thought to provide long lasting immunity against reinfection. However it is always wise to be on the safe side and try to prevent tick bites.

Lone Star Tick-Amblyomma americanum. The lone star tick is a species of tick in the genus Amblyomma. It is very widespread in the United States ranging from Texas to Iowa in the Midwest and east to the coast where it can be found as far north as Maine. It is most common in wooded areas, particularly in forests with thick underbrush.

Like all ticks, it can be a vector of diseases including human granulocytic ehrlichiosis (Ehrlichia chaffeensis), canine and human granulocytic ehrlichiosis (Ehrlichia ewingii), tularemia (Francisella tularensis), and Southern tick-associated rash illness (STARI, possibly caused by the spirochete Borrelia lonestari). STARI exhibits a rash similar to that caused by Lyme disease but is generally considered to be less severe.

Though the bacteria responsible for Lyme disease, Borrelia burgdorferi, has occasionally been isolated from lone star ticks, numerous vector competency tests have demonstrated that this tick is extremely unlikely to be capable of transmitting Lyme disease. There is evidence that the A. americanum saliva inactivates Borrelia burgdorferi more quickly than the saliva of Ixodes scapularis

Lone Star Tick. Image Courtesy of U.S. Center Disease Control.

Tularemia.This disease (also known as Pahvant Valley plague, rabbit fever, deer fly fever, Ohara’s fever) is a serious infectious disease caused by the bacterium Francisella tularensis which has several subspecies with varying degrees of virulence. The most important of those is F. tularemia tularensis (Type A), which is found in wild rabbits in North America and is highly virulent for humans and domestic rabbits. F. tularensis palaearctica (Type B) occurs mainly in aquatic rodents (beavers, muskrats) in North America and in hares and small rodents in northern Eurasia. It is less virulent for humans and rabbits. The primary vectors are ticks and deer flies, but the disease can also be spread through other arthropods. The disease is named after Tulare County, California.

F. tularensis was discovered in 1911 during an outbreak of rabbit fever, when the disease killed a large number of ground squirrels in the area of Tulare Lake in California. The bacterium was first isolated by GW McCoy of the US Public Health Service plague lab and reported in 1912. Scientists determined that tularemia could be dangerous to humans; a human being may catch the infection after contacting an infected animal. The ailment soon became frequent with hunters, cooks and agricultural workers.

The disease is endemic in North America, and parts of Europe and Asia. The most common mode of transmission is via arthropod vectors. Rodents, rabbits, and hares often serve as reservoir hosts, but waterborne infection accounts for 5 to 10% of all tularemia in the US. Tularemia can also be transmitted by biting flies, particularly the deer fly Chrysops discalis. Individual flies can remain infective for 14 days and ticks for over 2 years. Tularemia may also be spread by direct contact with contaminated animals or material, by ingestion of poorly cooked flesh of infected animals or contaminated water, or by inhalation. The most likely method for bioterrorist transmission is through an aerosol.

In the United States, although records show that tularemia was never particularly common, incidence rates continued to drop over the course of the 20th century so that between 1990 and 2000, the rate was less than 1 per 1,000,000, meaning the disease is extremely rare in the US today.

Depending on the site of infection, tularemia has six characteristic clinical syndromes: ulceroglandular (the most common type representing 75% of all forms), glandular, oropharyngeal, pneumonic, oculoglandular, and typhoidal.

The incubation period for tularemia is 1 to 14 days; most human infections become apparent after 3 to 5 days. In most susceptible mammals, the clinical signs include fever, lethargy, anorexia, signs of septicemia, and possibly death. Animals rarely develop the skin lesions seen in people. Subclinical infections are common and animals often develop specific antibodies to the organism. Fever is moderate or very high and tularemia bacillus can be isolated from blood cultures at this stage. Face and eyes redden and become inflamed. Inflammation spreads to the lymph nodes, which enlarge and may suppurate (mimicking bubonic plague). Lymph node involvement is accompanied by a high fever. Death occurs in less than 1% if therapy is initiated promptly.

The bacteria can penetrate into the body through damaged skin and mucous membranes, or through inhalation. Humans are most often infected by tick bite or through handling an infected animal. Ingesting infected water, soil, or food can also cause infection. Tularemia can also be acquired by inhalation; hunters are at a higher risk for this disease because of the potential of inhaling the bacteria during the skinning process. It has been contracted from inhaling particles from an infected rabbit ground up in a lawnmower (see below). Tularemia is not spread directly from person to person.

Francisella tularensis is an intracellular bacterium, meaning that it is able to live as a parasite within host cells. It primarily infects macrophages, a type of white blood cell. It is thus able to evade the immune system. The course of disease involves spread of the organism to multiple organ systems, including the lungs, liver, spleen, and lymphatic system. The course of disease is similar regardless of the route of exposure. Mortality in untreated (pre-antibiotic-era) patients has been as high as 50% in the pneumoniac and typhoidal forms of the disease, which however account for less than 10% of cases. Overall mortality was 7% for untreated cases, and the disease responds well to antibiotics with a fatality rate of about 1%. The exact cause of death is unclear, but it is thought to be a combination of multiple organ system failures.

The drug of choice is Streptomycin. Tularemia may also be treated with gentamicin for ten days, tetracycline-class drugs such asdoxycycline for 2-3 weeks, chloramphenicol or fluoroquinolones. An attenuated, live vaccine is available, but its use is restricted to high risk groups. Its use as post-exposure prophylaxis is not recommended.

The Centers for Disease Control and Prevention regard F. tularensis as a viable bio-weapons agent, and it has been included in the biological warfare programs of the USA, USSR and Japan at various times. A former Soviet biological weapons scientist, Kenneth Alibek, has alleged that an outbreak of Tularemia among German soldiers shortly before the siege of Stalingrad was due to the release of F. tularensis by Soviet forces, but this claim is rejected by others who have studied the outbreak. In the US, practical research into using tularemia as a bio weapon took place in 1954 at Pine Bluff Arsenal, Arkansas, an extension of the Camp Detrick program. It was viewed as an attractive agent because:

  • it is easy to aerosolize
  • it is highly infective; 10-50 bacteria are required to infect
  • it is non-persistent and easy to decontaminate (unlike anthrax)
  • it is highly incapacitating to infected persons
  • it has comparatively low lethality, which is useful where enemy soldiers are in proximity to non-combatants, e.g. civilians

The Schu S4 strain was standardized as Agent UL for use in the U.S. M143 bursting spherical bomblet. It was a lethal biological with an anticipated fatality rate of 40 to 60 percent. The rate-of-action was around three days, with a duration-of-action of 1 to 3 weeks (treated) and 2 to 3 months (untreated) with frequent relapses. UL was streptomycin resistant. The aerobiological stability of UL was a major concern, being sensitive to sun light, and losing virulence over time after release. When the 425 strain was standardized as agent JT (an incapacitant rather than lethal agent), the Schu S4 strain’s symbol was changed again to SR.

No vaccine is available to the general public. The best way to prevent tularemia infection is to wear rubber gloves when handling or skinning lagomorphs (such as rabbits), avoid ingesting uncooked wild game and untreated water sources, wear long-sleeved clothes, and use an insect repellent to prevent tick bites.

In the summer of 2000, an outbreak of tularemia in Martha’s Vineyard resulted in one fatality, and brought the interest of the CDC as a potential investigative ground for aerosolized Francisella tularensis. Over the following summers, Martha’s Vineyard was identified as the only place in the world where documented cases of tularemia resulted from lawn mowing.

An outbreak of tularemia occurred in Kosovo in 1999-2000.

In 2004, three researchers at Boston University Medical Center were accidentally infected with F. tularensis, after apparently failing to follow safety procedures.

In 2005, small amounts of F. tularensis were detected in the Mall area of Washington, DC the morning after an anti-war demonstration on September 24, 2005. Biohazard sensors were triggered at six locations surrounding the Mall. While thousands of people were potentially exposed, no infections were reported.

Q Fever. Q fever is a disease caused by infection with Coxiella burnetii, a bacterium that affects humans and other animals. This organism is uncommon but may be found in cattle, sheep, goats and other domestic mammals, including cats and dogs. The infection results from inhalation of contaminated particles in the air, and from contact with the milk, urine, feces, vaginal mucus, or semen of infected animals. The incubation period is 9-40 days. It can be considered the most infectious disease in the world, as a human being can be infected by a single bacterium. The bacterium is an obligate intracellular pathogen.

It was first described by Edward Holbrook Derrick in abattoir workers in Brisbane, Queensland, Australia. The “Q” stands for “query” and was applied at a time when the causative agent was unknown; it was chosen over suggestions of “abattoir fever” and “Queensland rickettsial fever”, to avoid directing negative connotations at either the cattle industry or the state of Queensland.

The pathogen of Q fever was discovered in 1937, when Frank Macfarlane Burnet and Mavis Freeman isolated the bacterium from one of Derrick’s patients. It was originally identified as a species of Rickettsia. It is a zoonotic disease whose most common animal reservoirs are cattle, sheep and goats. Coxiella burnetii is no longer regarded as closely related to Rickettsiae but as similar to Legionella and Francisella and is a proteobacterium.

Incubation period is usually 2 to 3 weeks. The most common manifestation is flu-like symptoms with abrupt onset of fever, malaise, profuse perspiration, severe headache, myalgia (muscle pain), joint pain, loss of appetite, upper respiratory problems, dry cough, pleuritic pain, chills, confusion and gastro-intestinal symptoms such as nausea, vomiting and diarrhea. The fever lasts approximately 7 to 14 days.

During the course, the disease can progress to an atypical pneumonia, which can result in a life threatening acute respiratory distress syndrome (ARDS), whereby such symptoms usually occur during the first 4 to 5 days of infection.

Less often the Q fever causes hepatitis which may be asymptomatic or becomes symptomatic with malaise, fever, liver enlargement (hepatomegaly) and pain in the right upper quadrant of the abdomen. Whereas transaminase values are often elevated, jaundice is uncommon. Retinal vasculitis is a rare manifestation of Q fever.

The chronic form of Q fever is virtually identical to inflammation of the inner lining of the heart (endocarditis), which can occur months or decades following the infection. It is usually fatal if untreated. However, with appropriate treatment the mortality falls to around 10%.

The pathogenic agent is to be found everywhere except New Zealand. In Europe it appears as hepatitis rather than pneumonia as in the United States. The bacterium is extremely sustainable and virulent: a single organism is able to cause an infection. The common way of infection is inhalation of contaminated dust, contact with contaminated milk, meat, wool and particularly birthing products. Both hard and soft ticks can transfer the pathogenic agent to other animals. Transfer between humans seems extremely rare and has so far been described in very few cases. They are naturally infected with the bacterium. Sub-adult ticks while feeding on an infected host develop a general infection in their tissues. The bacterium can then be passed on subsequent molts or even to developing eggs by an infected female. Feeding by an infected tick can transmit the bacterium to mammal hosts including humans. More importantly the bacterium remains active in tick feces for up to six years which of course can biome airborn and transmitted to victims via inhalation. Argasid ticks also can disseminate the organism via infectious coxal fluids.

Some studies have shown more men to be affected than women, which may be attributed to different employment rates in typical professions. “At risk” occupations include, but are not limited to veterinary personnel, stockyard workers, farmers, shearers, animal transporters, laboratory workers handling potentially infected veterinary samples or visiting, people who cull and process kangaroos, hide (tannery) workers.

Treatment of the acute Q fever with antibiotics is very effective and should take place in consultation with an infectious diseases specialist. Commonly used are doxycycline, tetracycline,chloramphenicol, ciprofloxacin, ofloxacin, and hydroxychloroquine. The chronic form is more difficult to treat and can require up to four years of treatment with doxycycline and quinolones or doxycycline with hydroxychloroquine.

Q fever in pregnancy is especially difficult to treat because doxycycline and ciprofloxacin are contraindicated in pregnancy. The preferred treatment is five weeks of co-trimoxazole. Protection is offered by Q-Vax, a whole cell inactivated vaccine developed by an Australian vaccine manufacturing company CSL. The intradermal vaccination is composed of killed Coxiella burnetii organisms. Skin and blood tests should be done before vaccination to identify preexisting immunity; the reason is that vaccinating subjects who already have immunity can result in a severe local reaction. After a single dose of vaccine, protective immunity lasts for many years. Revaccination is not generally required. Annual screening is typically recommended. In 2001, Australia introduced a national Q fever vaccination program for people working in “at risk” occupations.

Q fever has been described as a possible biological weapon. The United States investigated Q fever as a potential biological warfare agent in the 1950s with eventual standardization as agent OU. At Fort Detrick and Dugway Proving Ground human trials were conducted on Whitecoat volunteers to determine the median infective dose (18 MICLD50/person i.h.) and course of infection. As a standardized biological it was manufactured in large quantities at Pine Bluff. Arsenal, with 5,098 gallons in the arsenal in bulk at the time of demilitarization in 1970. Q fever is a category “B” agent. It can be contagious and is very stable in aerosols in a wide range of temperatures. Q fever microorganisms may survive on surfaces up to 60 days.

Brown Dog Tick -Rhipicephalus sanguineus.

This tick is the most widely distributed of all ticks occurring worldwide except for the most northern and southern extremes. The preferred host is dogs where it commonly feeds around the ears. It attacks a variety of other animals but rarely, if ever, attacks humans. The brown dog tick is known to vector malignant jaundice in dogs and possibly RMFS in the mountains of Mexico. The brown dog tick is found world-wide, but more commonly in warmer climates. This species is unusual among ticks in that its entire life cycle can be completed indoors.

High infestation levels cause skin irritation and damage in dogs. It can transmit Rocky Mountain spotted fever in humans. In the U.S., R. sanguineus is also a vector of the diseases in dogs: canine ehrlichiosis (Ehrlichia canis) and canine babesiosis (Babesia canis). In dogs, symptoms of canine ehrlichiosis include lameness and fever; those for babesiosis include fever, anorexia and anemia. Rhipicephalus sanguineus has not been shown to transmit the bacteria that causes Lyme disease in humans. In parts of Europe, Asia and Africa, R. sanguineus is a vector of Rickettsia conorii, known locally as Mediterranean spotted fever, boutenneuse fever, or tick typhus.

Brown Dog Tick. Image Courtesy USDA.

It is not uncommon to find large infestations in homes. The authors encountered a huge infestation of this tick in a one-bedroom apartment; the owner had gone on vacation and left her German shepherd in a kennel. Apparently an impregnated female tick attached itself to the dog and was brought home. The tick dropped off and deposited from 2000 to 3000 eggs in the home. Because the ticks had a continuous source of food (the dog) and a favorable environment, development was fast. Over 400 ticks were vacuumed from the apartment. Because the preferred host was present, none of the residents were bitten. However, ticks commonly were found crawling around the apartment and frequently were squashed accidentally, leaving blood spots on the furniture and beige rug.

The best management strategy is prevention of infestations in the house or kennel. In addition, the earlier the infestation is discovered, the easier it is to control. Regular grooming and inspection of pets is essential to management, especially when dogs recently quartered or interacted with other dogs.

There are several species of Ehrlichia, but the one that most commonly affects dogs and causes the most severe clinical signs is Ehrlichia canis. This species infects monocytes in the peripheral blood. The brown dog tick, or Rhipicephalus sanguineous, the primary vector is prevalent throughout most of the United States, but most cases tend to occur in the Southwest and Gulf Coast regions where there is a high concentration of this tick. Ehrlichia is found in many parts of the world and was first recognized in Algeria in 1935. During the Vietnam War ehrlichiosis became well known as a dog disease due to the infection and death of many military working dogs. Two types of human ehrlichiosis have been identified in the United States: human monocytic ehrlichiosis and human granulocytic ehrlichiosis.

There are three stages of ehrlichiosis, each varying in severity. The acute stage, occurring several weeks after infection and lasting for up to a month, can lead to fever and lowered peripheral blood cell counts due to bone marrow suppression. The second stage, called the subclinical phase, has no outward signs and can last for the remainder of the dog’s life, during which the dog remains infected with the organism. Some dogs are able to successfully eliminate the disease during this time. In some dogs the third and most serious stage of infection, the chronic phase, will commence including very low blood cell counts ,bleeding, bacterial infection, lameness, neurological and ophthalmic disorders, and kidney disease, can result. Chronic ehrlichiosis can be fatal.

The acute stage of the disease, occurring most often in the spring and summer, begins one to three weeks after infection and lasts for two to four weeks. Clinical signs include a fever, petechiae, bleeding disorders, vasculitis, lymphadenopathy, discharge from the nose and eyes, swelling of the legs and scrotum. There are no outward signs of the subclinical phase. Clinical signs of the chronic phase include weight loss, pale gums due to anemia, bleeding due to thrombocytopenia, vasculitis, lymphadenopathy, dyspnea, coughing, polyuria, polydipsia, lameness, ophthalmic diseases such as retinal hemorrhage and anterior uveitis, and neurological disease. Dogs that are severely affected can die from this disease.

Although people can get ehrlichiosis, dogs do not transmit the bacteria to humans; rather, ticks pass on the ehrlichia organism. Clinical signs of human ehrlichiosis include fever, headache, eye pain, and gastrointestinal upset. It is quite similar to Rocky Mountain spotted fever, but rash is not seen in patients.

The prognosis is good for dogs with acute ehrlichiosis. For dogs that have reached the chronic stage of the disease, the prognosis is guarded. When bone marrow suppression occurs and there are low levels of blood cells, the animal may not respond to treatment.

Supportive care must be provided to animals that have clinical signs. Subcutaneous or intravenous fluids are given to dehydrated animals, and severely anemic dogs may require a blood transfusion. Treatment for ehrlichiosis involves the use of antibiotics such as tetracycline odoxycycline for a period of at least six to eight weeks; response to the drugs may take one month. In addition, steroids may be indicated in severe cases in which the level of platelets is so low that the condition is life threatening.

Tick control is the most effective method of prevention, but tetracycline at a lower dose can be given daily for 200 days during the tick season in endemic regions.

Black Legged Deer Tick-Ixodes scapularis.

Transmission of the spirochete B. burgdorferi, the causative agent of Lyme disease, occurs by the bite of Ixodes ticks. In the United States, the blacklegged tick, affects the greatest number of people for three principal reasons: their geographic distribution coincides in the northeastern United States with the greatest concentration of humans; spirochete infection rates are high, often exceeding 25% (Burgd; and the geographical range of the tick is spreading.

Ixodes scapularis is found along the east coast of the United States. Florida westward into central Texas forms the lower boundary, although there are reports from Mexico. The upper boundary is located in Maine westward to Minnesota and Iowa. The distribution of I. scapularis is linked to the distribution and abundance of its primary reproductive host, white-tailed deer. Only deer or some other large mammal appears capable of supporting high populations of ticks. In the northeastern United States, much of the landscape has been altered. Forests were cleared for farming, but were abandoned in the late 1800s and 1900s causing succession of the fields to second-growth forests. These second-growth forests created “edge” habitats which provided appropriate habitat for deer resulting in increased populations and thus, may have increased populations of the blacklegged tick.

Adult deer ticks have no white markings on the dorsal area nor do they have eyes or festoons. They are very small (3 mm) and dark brown to black in color with black legs. Adults exhibit sexual dimorphism. Females typically have the area behind the scutum with an orange to red color.

This is a three-host tick; each mobile stage feeds upon a different host animal. In June and July eggs deposited earlier in the spring hatch into tiny six-legged larvae. Peak larval activity occurs in August, when larvae attach and feed on a wide variety of mammals and birds, primarily on white-footed mice. After feeding for three to five days, engorged larvae drop from the host to the ground where they overwinter. In May, larvae molt into nymphs, which feed on a variety of hosts for three to four days. In a similar manner, engorged nymphs detach and drop to the forest floor where they molt into the adult stage, which becomes active in October. Adult ticks remain active through the winter on days when the ground and ambient temperatures are above freezing. Adult female ticks feed for five to seven days while the male tick feeds only sparingly, if at all.

Adult ticks feed on large mammals, primarily upon white-tailed deer. Beginning in May, engorged adult females typically lay between 1000 to 3000 eggs on the forest floor at the site where they detached from their hosts.

Mortality rates for ticks are high. Tick death is caused by density-dependent factors such as parasites, pathogens, and predators, all of which appear to have little impact on tick populations. Density-independent factors causing tick mortality include a variety of adverse climatic and microclimate conditions, which can influence temperature and humidity and have the greatest impact on tick survival. Due to their low probability of finding a host, starvation also would be a major mortality factor of ticks. Host immunity and grooming activity also may affect mortality.

Black Legged Deer Tick. Image Courtesy Scott Bauer, USDA.

Lyme Disease. This is a bacterial illness caused by a bacterium called a “spirochete.” In the United States, the actual name of the bacterium is Borrelia burgdorferi. In Europe, another bacterium, Borrelia afzelii, also causes Lyme disease. Certain ticks found on deer harbor the bacterium in their stomachs. Lyme disease is spread by these ticks when they bite the skin, which permits the bacterium to infect the body. Lyme disease is not contagious from an affected person to someone else. Lyme disease can cause abnormalities in the skin, joints, heart, and nervous system.

Lyme disease only became apparent in 1975 when mothers of a group of children who lived near each other in Lyme, Connecticut, made researchers aware that their children had all been diagnosed with rheumatoid arthritis. This unusual grouping of illness that appeared “rheumatoid” eventually led researchers to the identification of the bacterial cause of the children’s condition, what was then called “Lyme disease” in 1982. It has now been found in the 48 continental United States and is the most prominent tick borne disease. It has been likened to syphilis because of its lengthy developmental cycle. The disease is not sexually transmitted but can be passed from mother to fetus. It has been found in 51 of the 58 counties of California and is most known north of San Francisco. The Eastern states with the highest outbreaks are New York, New Jersey, and Maine. At the time of this writing Lyme disease has been found in an isolated location of Southern California.

This disease affects different areas of the body in varying degrees as it progresses. The site where the tick bites the body is where the bacteria enter through the skin. As the bacteria spread in the skin away from the initial tick bite, the infection causes an expanding reddish rash that is often associated with “flu-like” symptoms. Later, it can produce abnormalities in the joints, heart, and nervous system. It is medically described in three phases as: (1) early localized disease with skin inflammation; early disseminated disease with heart and nervous system involvement, including palsies and meningitis; and (3) late disease featuring motor and sensory nerve damage and brain inflammation as well as arthritis.

In the early phase of the illness, within days to weeks of the tick bite, the skin around the bite develops an expanding ring of unraised redness. There may be an outer ring of brighter redness and a central area of clearing, leading to a “bull’s-eye” appearance. This classic initial rash is called “erythema migrans” (formerly called erythema chronicum migrans). Patients often can’t recall the tick bite (the ticks can be as small as the periods in this paragraph). Also, they may not have the identifying rash to signal the doctor. More than one in four patients never develope a rash. The redness of the skin is often accompanied by generalized fatigue, muscle and joint stiffness, swollen lymph nodes (“swollen glands”), and headache resembling symptoms of a virus infection.

The redness resolves, without treatment, in about a month. Weeks to months after the initial redness of the skin, the bacteria and their effects spread throughout the body. Subsequently, disease in the joints, heart, and nervous system can occur. In early Lyme disease, doctors can sometimes make a diagnosis simply by finding the classic red rash (described above), particularly in people who have recently been in regions in which Lyme disease is common. The doctor might review the patient’s history and examine the patient in order to exclude diseases with similar findings in the joints, heart, and nervous system. Blood testing for antibodies to Lyme bacteria is generally not necessary or helpful in early stage disease, but it can help in diagnosis in later stages. (Antibodies are produced by the body to attack the bacteria and can be evidence of exposure to the bacteria. These antibodies can be detected using a laboratory method called an enzyme-linked immunosorbent assay. Antibodies, however, can be false indicators of disease, since they can remain for years after the disease is cured. Moreover, false-positive tests in patients with nonspecific findings (those that are not specifically suggestive of Lyme disease) can lead to confusion. Currently, the confirmatory test that is most reliable is the Western Blot assay antibody test. More accurate tests are being developed. Generally, Lyme blood testing is helpful in a patient who has symptoms compatible with Lyme disease, who has a history of a tick bite at least a month prior, or who has unexplained disorders of the heart, joints, or nervous system that are characteristic of Lyme disease.

Because Lyme disease is transmitted by ticks attaching to the body, it is important to use tick-bite avoidance techniques when visiting known tick areas. Spraying insect repellant containing DEET onto exposed skin can help. Wearing long pants tucked into boots and long sleeves can protect the skin. Clothing, children, and pets should be examined for ticks. Ticks can be removed gently with tweezers and saved in a jar for later identification. Bathing the skin and scalp and washing clothing upon returning home might prevent the bite and transmission of the disease.

There are various mammalian reservoirs of the disease that include rodents, deer and humans. Unfortunately, only about 1/4 of the cases are reported and there are false-positive laboratory results. There is no lasting immunity to the disease and antibiotics only work in the first stage of the disease. Under laboratory conditions mosquitoes and biting flies have vectored this disease.

Vaccines were formerly on the market; however, as of Feb. 25, 2002, the manufacturer announced that the LYMErixâ„¢ Lyme disease vaccine will no longer be commercially available. Further studies of vaccines are needed. For now, ideal prevention focuses on the recommendations of the preceding paragraph.

Most cases of Lyme disease are curable with antibiotics. This is so true that some authors of Lyme disease research have stated that the most common cause of lack of response of Lyme disease to antibiotics is a lack of Lyme disease to begin with! The type of antibiotic depends on the stage of the disease (early or late) and what areas of the body are affected. Early illness is usually treated with medicines taken by mouth, for example, doxycycline (Vibramycin), amoxicillin, or cefuroxime axetil. Therefore, if a person finds a typical bull’s-eye skin rash (described above) developing in an area of a tick bite, they should seek medical attention as soon as possible. Generally, antibiotic treatment resolves the rash within one or two weeks with no long-term consequences. Later illness such as nervous-system disease might require intravenous drugs; examples are ceftriaxone (Rocephin) and penicillin G.

For the relief of symptoms, pain-relieving medicines might be added. Swollen joints can be reduced by the doctor removing fluid from them (arthrocentesis). An arthrocentesis is a procedure whereby fluid is removed from a joint using a needle and syringe under sterile conditions. It is usually performed in a doctor’s office. Rarely, even with appropriate antibiotics, the arthritis continues. It has been suggested by researchers that sometimes joint inflammation can persist even after eradication of the Lyme bacteria. This has been explained as an ongoing autoimmune response causing inflammation of the joint that was initially stimulated by the original bacterial infection. The doctor also can use oral medications such as ibuprofen (Motrin, Nuprin) to reduce inflammation and improve function.

The later phases of Lyme disease can affect the heart, causing inflammation of the heart muscle. This can result in abnormal heart rhythms and heart failure. The nervous system can develop facial muscle paralysis (Bell’s palsy), abnormal sensation due to disease of peripheral nerves (peripheral neuropathy), meningitis, and confusion. Arthritis, or inflammation in the joints, begins with swelling, stiffness, and pain. Usually, only one or a few joints become affected, most commonly the knees. The arthritis of Lyme disease can look like many other types of inflammatory arthritis and can become chronic. Researchers have also found that anxiety and depression occur with an increased rate in people with Lyme disease. This is another important aspect of the evaluation.

Early Symptoms of Lyme Disease, a Rash Called Erythematic Migrans. Image Courtesy CDC Photo Library.

Human Granulocytic Anaplasmosis (HGA). (previously known as Human granulocytic ehrlichiosis, or HGE is an infectious disease caused by Anaplasma phagocytophilum, an obligate intracellular bacterium that is typically transmitted to humans by at least three kinds of ticks, including Ixodes scapularis, Ixodes pacificus, and Dermacentor variabilis. These ticks also transmit Lyme disease and other diseases. The bacteria infect white blood cells called neutrophils, causing changes in gene expression that prolong the life of these otherwise short-lived cells. The number of cases in the United States has increased each year since its recognization, with 789 cases reported in 2001 and 2002.

The major mammalian reservoirs for this bacterium in the eastern and western United States are the white-footed mouse and wood rat, respectively. Although white-tailed deer harbor Anaplasma phagocytophilum, evidence suggests that they are not a reservoir for the strains that cause HGA. 0063Anaplasma phagocytophilum shares its tick vector with other human pathogens, and about 10% of patients with HGA are also infected with Lyme disease, babesiosis, or tick-borne meningoencephalitis.

Symptoms may include fever, severe head ache, muscle aches, chills and shaking, similar to the symptoms of influenza. Symptoms may be minor with gastrointestinal symptoms occur in less than half of patients and a skin rash is seen in less than 10% of patients.

If Ehrlichiosis is suspected, treatment should not be delayed while waiting for a definitive laboratory confirmation, as prompt doxycycline therapy has been shown to improve outcomes. Doxycycline is the treatment of choice. Presentation during early pregnancy can complicate treatment. Rifampin has been used in pregnancy and in patients allergic to doxycycline.

Although the infectious agent is known to be from the Anaplasma genus, the term “human granulocytic ehrlichiosis” (HGE) is often used, reflecting the prior classification of the organism. E. phagocytophilum and E. equi were reclassified as Anaplasma phagocytophilum.

Tick-Borne Encephalitis. This virus (TBEV) is a single-stranded RNA virus that belongs to the genus Flavivirus and is closely related to Powassan virus. TBEV has three subtypes: European, Siberian, and Far Eastern. It is transmitted to humans through the bite of an infected Ixodes tick, primarily I. ricinus (European subtype) or I. persulcatus (Siberian and Far Eastern subtypes). The virus is maintained in discrete areas of deciduous forest where both the tick vectors and animal hosts (mainly rodents) are found. It can also be acquired by ingesting unpasteurized dairy products from infected goats, sheep, or cows. Direct person-to-person spread of TBEV does not occur except rarely through blood transfusion or breastfeeding.

TBE is endemic in temperate regions of Europe and Asia (from eastern France to northern Japan and from northern Russia to Albania) and up to about 1,400 m in altitude with the highest incidences reported in Austria, Czech Republic, Estonia, Germany, Hungary, Latvia, Lithuania, Poland, Russia, Slovenia, Sweden, and Switzerland. As might be expected most cases occur during April-November, with peaks in early and late summer when ticks are active. Over the last 30 years, the geographic range of TBEV and the number of reported TBE cases have increased significantly. These trends are likely due to a complex combination of changes in the ecology and climate, increased human activity in affected areas, and increased recognition.

Even though this disease is not present in the United States it does present a potential problem when visiting any of these countries. The overall risk of acquiring TBE for an unvaccinated visitor to an endemic area during the TBEV transmission season has been estimated at 1 case per 10,000 person-months of exposure. Most TBEV infections result from tick bites acquired in forested areas through activities such as camping, hiking, fishing, bicycling; collecting mushrooms, berries, or flowers; and outdoor occupations such as forestry or military training. The risk is negligible for persons who remain in urban or unforested areas and who do not consume unpasteurized dairy products. Vector tick density and infection rates in TBEV-endemic foci are highly variable. For example, TBEV infection rates in I. ricinus in central Europe vary from less than 0.1% to approximately 5%, depending on geographic location and time of year, while rates of up to 40% have been reported in I. persulcatus in Siberia.

Approximately two-thirds of infections are asymptomatic. The median incubation period for TBE is 8 days (range 4-28 days) while the incubation period for milk-borne exposure is usually shorter (3-4 days).Acute neuro-invasive disease is the most commonly recognized clinical manifestation of TBEV infection. However, TBE disease often presents with milder forms of the disease or a biphasic course. The first phase: exhibits headache, myalgia, and fatigue and usually lasts for several days. Up to two-thirds of patients may recover without any further illness. The second phase typically entails central nervous system involvement resulting in aseptic meningitis, encephalitis, or myelitis. Cranial nerve involvement, bulbar syndrome, and acute flaccid paralysis of the upper extremities have also been described. Among patients who develop central nervous system involvement, approximately 10% require intensive care and 5% need mechanical ventilation.

Symptoms and long-term outcome typically varies by subtype of TBEV. The European subtype is associated with milder disease, a case-fatality ratio of 2%, and neurologic sequelae in up to 30% of patients. The Far Eastern subtype is often associated with a more severe disease course, including a case-fatality ratio of 20%-40% and higher rates of severe neurologic sequelae. The Siberian subtype is more frequently associated with chronic or progressive disease and has a case-fatality ratio of 2%-3%.

There is no specific antiviral treatment for TBE; therapy consists of supportive care and management of complications. No TBE vaccines are licensed or available in the United States. Two safe, effective inactivated TBE vaccines are available in Europe, in adult and pediatric formulations: FSME-IMMUN (Baxter, Austria) and Encepur (Novartis, Germany). The adult formulation of FSME-IMMUN is also licensed in Canada. Two other TBE vaccines are produced in Russia, but little information has been published about their safety and efficacy.

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