MITES AND TICKS
Mites are among the most diverse and successful of all the invertebrate groups. They have exploited an incredible array of habitats, and because of their small size (most are microscopic) go largely unnoticed. Many live freely in the soil or water, but there are also a large number of species that live as parasites on plants, animals, and some that feed on mold.
A Rather Large Population of a Plant Feeding Mite. Image Courtesy of Eric Gunther.
Some of the plant pests include the so-called spider mites, thread-footed mites, and the gall mites. Among the species that attack animals are members of the Sarcoptic Mange mites, which burrow under the skin. Demodex mites are parasites that live in or near the hair follicles of mammals, including humans. Perhaps the best-known mite, though, is the house dust mite.
Insects may also have parasitic mites. Examples are Varroa destructor, which attaches to the body of the honeybee, and Acarapis woodi, which lives in the tracheae of honey bees. There are hundreds of species of mites associated with other bee species, and most are poorly described and understood. Some are thought to be parasites, while others beneficial symbionts.
There are over 45,000 described species of mites. Scientists believe that we have only found 5% of the total diversity of mites. Mites are believed to have existed for around 400 million years.
Mites cause several forms of allergic diseases, including hay fever, asthma and eczema and are known to aggravate atopic dermatitis. Mites are usually found in warm and humid locations, including beds. It is thought that inhalation of mites during sleep exposes the human body to some antigens that eventually induce hypersensitivity reaction. Dust mite allergens are thought to be among the heaviest dust allergens. However not all types of mites are infectious including the Alaskozetes antarcticus an arctic inhabiting mite. Certain mites can also serve as vectors of disease.
Mites and ticks have 4 pair of legs and a broadly joined cephalothorax and abdomen, which gives the appearance of one body segment. There are over 200 families of mites and some experts feel over a million species, most of which are not discovered. They typically exhibit 4 stages of development, namely the egg, larva, nymph and adult. The larval stage bears 3 pair of legs while the nymph and adult possess 4. Their life cycles are normally brief (2 to 3 weeks) and correspondingly mites can build huge populations in a short period of time.
House Dust Mites. The house dust mite (sometimes referred to by allergists as HDM), is a cosmopolitan in distribution. Dust mites feed on organic detritus such as flakes of shed human skin and flourish in the stable environment of dwellings. They mites are a common cause of asthma and allergic symptoms worldwide. Some of the digestive enzymes (notably proteases) produced by the house mite persist in their fecal matter, and can be strongly allergenic.
The European house dust mite (Dermatophagoides pteronyssinus) and the American house dust mite (Dermatophagoides farinae) are two different species, but are not necessarily confined to Europe or North America; a third species Euroglyphus maynei also occurs widely.
The body of a house dust mite is just visible against a dark background in normal light. A typical house dust mite measures 420 micrometers in length and 250–320 micrometers in width. Both male and female adult house dust mites are creamy blue and have a rectangular shape. The body also contains a striated cuticle. Like all acari, house dust mites have eight legs (except 3 pairs in the first instar). Dust mites can be transported in dust bunnies or by minor air currents generated from normal household activities.
The average life cycle for a male house dust mite is 10 to 19 days. A mated female house dust mite can live for 70 days, laying 60 to 100 eggs in the last 5 weeks of her life. In a 10 week life span, a house dust mite will produce approximately 2000 fecal particles and an even larger number of partially digested enzyme-covered dust particles.
The house dust mite survives in all climates, even at high altitude. A person sheds about 1.5 grams of skin cells and flakes every day (approximately one pound per year), which is enough to feed roughly a million house dust mites under ideal conditions. If trying to control house dust mites, humidity should be kept low. House dust mites thrive in the indoor environment provided by homes, specifically in bedrooms and kitchens. They survive well in mattresses, carpets, furniture and bedding, with figures around 188 mites per gram of dust. Even in dry climates, house dust mites survive and reproduce easily in bedding (especially in pillows), deriving moisture from the humidity generated by human breathing, perspiration, and saliva.
House dust mites consume minute particles of organic matter. Like all acari, house dust mites have a simple gut; they have no stomach but rather diverticulae, which are sacs or pouches that divert out of hollow organs. Like many decomposer animals, they select food that has been pre-decomposed by fungi. House dust mites eat the same particle several times, only partially digesting it each time; between feedings, they leave particles to decompose further. Only when the particles are fully digested do they enter the dust mite's fecal matter.
Allergens produced by house dust mites are among the most common causes of asthma. Some main signs of house dust mite allergies are itchiness, sneezing, inflamed or infected eczema, watering/reddening eyes, runny nose and clogging in the lungs. Avoidance of dust mites and their allergens is the best course of action for those with dust mite allergies. The use of bedding that acts as a barrier to the dust mite and its allergens is a good first step. The bedding should also be breathable and be able to withstand frequent washing. However, a home allergen reduction plan has been recognized as being an essential part to the management of asthma symptoms and therefore all aspects of the home environment should be considered (proper vacuuming, use of air cleaners, off-gassing from paint and cleaning products, etc). The Asthma and Allergy Foundation of America as well as the Asthma Society of Canada certify products that may be used in a home allergen reduction plan in a Program called Asthma and Allergy Friendly.
Most people who have dust mite allergy sneeze when they wake up in the morning. They will generally feel better as they leave their room for the day and then at night when they sleep, the cycle repeats again. Repeated exposure can lead to chronic and long lasting asthma.
It is commonly believed that the accumulated detritus from dust mites can add significantly to the weight of mattresses and pillows. While it is true that the fecal matter of dust mites will increase over time, there is no scientific evidence for these claims. Considering the size of these mites and their products it is doubtful that their presence could add to any measurable weight to a mattress.
Control. Allergy and asthma sufferers are also often advised to avoid feather pillows due to the presumed increased presence of the house dust mite allergen. The reverse, however, is true. A 1996 study from the British Medical Journal has shown that polyester fiber pillows contained more than 8 times the total weight of the mites and their products. Disodium octaborate tetrahydrate powder is often used to eradicate house dust mites.
A simple washing will remove most of the waste matter. Exposure to temperatures over 60 °C (140 °F) for a period of one hour or freezing, exposure to temperatures below 0 °C (32 °F), will typically prove fatal to house dust mites; a relative humidity less than 50 percent may also be fatal. Ten minutes in household clothes dryer at high temperatures has been shown to be sufficient to kill all the dust mites in bedding. House dust mites reproduce quickly enough that their effect on human health can be significant
A house dust mite greatly magnified-normally not visible to the naked eye. Image Courtesy of Clemson Entomology Department.
Grocer’s Itch. Acarus siro. These mites infest a wide range of food products such as grain, milk products, dried fruits, straw and animal hides in both household and commercial situations. The most important mite in stored products is Acarus siro, a species found throughout the world. Is particularly a pest of processed cereal products rather than whole grain. It is quite small but readily visible to the naked eye. It prefers temperatures ranging from 24 to 332 C. It tends to develop most rapidly under humid conditions (greater than 60% but preferring 85%). The amount of damage is done to grain is directly related to moisture content; grain is only attacked when moisture content is 14% or better. The dermatitis encountered by food handelers infested with this mite is referred to as grocer’s itch. Other names for dermatitis caused by Acarus siro and other related mites are baker’s itch, dried-fruit mite dermatitis, wheat pollard itch and vanillism.
Another common mite in stored products is the cosmopolitan Tyrophagus putrescentiae. It is particularly a problem in food with high protein content, namely cheese, ham, seeds, dried eggs, nuts and fish. These mites feed primarily on fungi that tend to thrive on foods stored at warm temperatures. Under these conditions they can complete one generation in as little as one week and reach huge populations in a month.
Acarus siro Adult Mites.
Ear Mites. This is a group of parasitic mites that attack a variety of animals, including cats, dogs and rabbits. In these animals, infestations are limited to the ears and the mites are typically found feeding in the outer ear canals. As do most parasitic arthropods, ear mites are host-specific and no species attack humans. In rabbits, infestations can become serious if left uncontrolled; the result can be bleeding, secondary infection and possible death. An infestation is easily recognized by a layer of dried ooze on the inner side of the ear. If this crusty ooze is removed, large numbers of mites can be found feeding on ear tissue.
Adult female ear mites are microscopic, pale mites with cup-like structures at the tips of the front four legs and long setae at the tips of the hind four legs. Male ear mites are smaller and have cup-like structures at the tips of all eight legs. Males have a pair of copulatory suckers on the lower rear. The third pair of legs has especially long setae near the tip. The fourth pair of legs of male and female ear mites is noticeably smaller than the other legs. The egg is soft, sticky and pearly white at first, but soon dries and sticks to the substrate. The larvae are microscopic, pale mites with three pairs of legs. The front four legs have cup-like structures at the tips and the hind two legs have long setae at the tips. The protonymph has four pairs of legs with cup-like structures at the tips of the first four legs. The last two legs are very small. Deutonymphs have only three pairs of legs and two small bumps on the rear called copulatory tubercles. This stage has cup-like structures on the front four legs and long setae on the hind two legs.
Ear Mite Adult. Image Courtesy Joel Mills.
Ear mites evidently pierce the lining of the auditory canal or somehow cause excessive production of earwax which becomes fouled with blood and bacteria. Crusts of earwax and blood form in the auditory canal and outer ear. Host animals scratch their ears excessively which causes loss of hair and scabbing. Secondary bacterial infections sometimes cause fever, depression and sullen, ill-tempered behavior. The ears of infected animals have a noticeable foul odor. Heavily infected animals often shake their heads constantly or run in circles in the direction of the most heavily infected ear. The most spectacularly bizarre behavior occurs when heavily infected dogs or cats are brought out of the cold into a warm room. These poor animals apparently "go berserk" with "spasmodic fits." Symptoms tend to be less severe on older host animals.
Cat Ear Mite Infestation.
Life History. Ear mites are passed from one animal to another when mites are dislodged during violent shaking of the head onto nearby animals or contact between animals, especially while nursing. However, it has been shown that ear mites also crawl about on the body of infested animals and that they can survive off of the host as long as hair and other detritus from the host animal are present. Thus, this mite passes from host to host with ease in confined quarters. Adult mites live about four weeks. Eggs hatch in 3 to 4 days and each active developmental stage lasts about one week and is followed by a 24 to 36 hour resting stage. Development from egg to egg laying female takes about three weeks. Ear mites tend to wedge under the edges of scabs for shelter.
Ear mites can be reared successfully from cells, hair, and dried earwax scraped from the ears of host animals. Once the ears of infested animals are secondarily infested with bacteria, the mites leave the suppurating area and tend to infest the outer ear or skin around the eyes. These facts indicate that ear mites do not feed on fluids.
Scabies Mange Mites. Sarcoptes scabei is a parasitic mite that attacks a wide variety of mammals; however, there are many varieties, with each type being host-specific. For example, the variety of scabies that attacks humans does not infest other animals. Similarly the scabies mites that attack dogs do no infest humans. The human scabies mite is almost invisible to the naked eye (about 1/60 inch), cylindrical in shape, and has golf tee-shaped suckers on the tips of the legs
A female human sarcoptic mange mite (Sarcoptes scabei) greatly magnified. Image courtesy of CDC Healthwise Photo Library.
The life cycles of male and female human scabies mites are somewhat different. A young female adult will crawl over the human body until she reaches soft wrinkly skin and, within two to three minutes, bores inward, forming a tunnel about 3/4" in length and parallel to the skin surface. She feeds on body juices and lays eggs (up to 20 per female) in the burrows. With close inspection mature females can be seen in the burrows. As a result of this activity, pimple-like structures develop which eventually rupture after a day or two, releasing the eggs on the skin. Once hatched, the larval and nymphal stages crawl over the skin and periodically feed in sebaceous glands and hair follicles. Male mites also feed in these areas. Generally it takes about two weeks to complete the life cycle from egg to adult.
Scabies is nearly always acquired by skin-to-skin contact with an infested individual. The contact may be quite brief such as holding hands. Frequently it is acquired from children, and sometimes it is sexually transmitted. Occasionally scabies is acquired via bedding or furnishings, as the mite can survive for a few days off its human host.
The majority of the mites (63%) are found on the hands (especially between the fingers) and wrists and about 11% on the elbows. In women the mites are often found burrowing beneath and around the breasts and nipples. In young children, whose skin is still soft, the mites can be found all over the body and frequently on the legs.
Scabies infestation between fingers. Image courtesy of CDC Healthwise Photo Library.
There are no obvious symptoms for the first 30 days after infestation. During that period, treatments are not necessary. However, subsequently, an intense rash and itching begins to occur over many areas of the body, in some cases even in areas where the mites are not found. The itch is characteristically more severe at night and affects the trunk and limbs. It does not usually affect the scalp. Itching can become so intense that the infested person loses sleep and can be affected mentally. Blisters and pustules on the palms and soles are characteristic of scabies in infants. Secondary infection commonly complicates scabies and results in crusting patches and scratched pustules. After about 100 days the mite population drops off and symptoms of the infestation begin to disappear.
Treatment consists of elimination of the mites from the body and treatment of recently worn clothing and bedding. The mites are totally host dependent and cannot live off the host for more than a day or two. Pesticide lotions can be used to kill those mites on the body. Kwell lotion was the standard for control for many years. However due to possible negative side effects of the active ingredient, it has been mostly replaced with more effective products. Recently used clothing or bedding should be laundered, ironed or sealed in large plastic bags for a few days. Symptoms will not disappear completely for a few weeks after the mites are eliminated. This is significant because it is probably not a good idea to over-treat an infestation of these mites. One of our grandkids contacted scabies and the kids next door had the same problem. We instructed the neighbor how to treat her kids. About a week later she indicated that the symptoms had not disappeared and wanted to retreat her kid. This is not a good idea as exposing children too frequently to the prescribed pesticide can lead to overmedicating. Therefore it’s important to know and to follow the directions for such direct contact treatments.
It should be mentioned that medical doctors frequently misdiagnose scabies mite infestations. As discussed above, several of the neighbors of the lady suffering from delusory parasitosis were convinced by her that they had scabies and were actually diagnosed and treated for them. I was once suffering from itching of the skin and went to a M. D. who immediately, upon hearing my symptom, stated that I had scabies and prescribed Kwell. I told him that I really didn’t have any of the other symptoms other than itching. His response was "sometimes there are no other symptoms," which may or may not be true. The point is that he didn’t even look at me. Upon hearing "itching" he stepped back about two feet (they are fairly contagious) and muttered "scabies.” After using the Kwell with no relief, I consulted a dermatologist who correctly diagnosed my problem as dry skin.
I was recently contacted by a convalescent home about a scabies infestation. They had approximately 100 patients half of which were diagnosed with scabies. This was a real problem. Public Health had quarantined the hospital because this is a communicable disease. Of course this was devastating and confusing to the older residents as their relatives couldn’t visit them. The people who worked there were very concerned and fearful that they might carry the disease home with them and give it to their own families. With this in mind, the hospital wanted me to come up with a viable treatment program. Treatment was several fold. Everyone involved had to be treated with Kwell lotion-the chemical that at that time was preferred. Treatment included all the patients and individuals who worked there as symptoms of an active infestation do not appear immediately. There was no need to treat the premises itself as the mites are host-dependent and can only live off the host for a day or two. However, recently worn clothing and bedding had to be treated as a potential source of infestation. We considered sending these to a commercial laundry, but that created the potential of infesting the individuals who worked there. Instead, we took all the clothing and bed sheets and sealed them in large trash bags for three days, keeping in mind that the mites can only survive off the host for a day or two.
Permethrin 5% is topical medication of choice. Toxicity may resemble allergic reactions. It is usually applied to the skin before bedtime and left on for about 8 to 14 hours, then showered off in the morning. Package directions or doctor's instructions should be followed, but one application is normally sufficient to cure an infection.
Lindane lotion (e.g. Kwell) is approved in the U.S. for use as a second-line treatment where first-line medications like permethrin have failed, are not well tolerated or otherwise contraindicated. It is illegal in 17 other countries, and 33 more countries have restricted its use. Though rare, serious side effects have resulted from product misuse. The FDA has confirmed 3 deaths that all involved use of lindane not in accordance with the label, including excessive topical applications and oral ingestions.
There is some evidence that a 10% sulfur ointment in petroleum jelly applied topically is effective. It is cheap and readily available over-the-counter. It also has the advantage of being able to be used in pregnant women and infants under two months of age.
Neem oil is deemed very effective in the treatment of scabies although only preliminary scientific proof exists which still has to be corroborated, and is recommended for those who are sensitive to permethrin, a known insecticide which might be an irritant. Also, the scabies mite has yet to become resistant to neem, so in persistent cases neem has been shown to be very effective.
A single dose of Ivermectin has been reported to reduce the load of scabies but another dose is required after 2 weeks for full eradication. In 1999, a small scale test comparing topically applied Lindane to orally administered Ivermectin found no statistically significant differences between the two treatments. As Ivermectin is easily administered (not requiring a rub down of the whole body like lindane or permethrin twice per treatment), compliance is much better. Ivermectin is used in eradication programs of many parasites of both human and animal. Side effects may include mild abdominal pain, nausea, vomiting, myalgia and/or arthralgia, which subside. The product is considered safe for use in children over five months of age. There is no vaccine available for scabies, nor are there any proven causative risk factors. Therefore, most strategies focus on preventing re-infection. All family and close contacts should be treated at the same time, even if asymptomatic. Cleaning of environment should occur simultaneously, as there is a risk of reinfection. Therefore it is recommended to wash and hot iron all material (such as clothes, bedding, and towels) that has been in contact with scabies infestation.
Cleaning the environment should include: Treatment of furniture and bedding; Vacuuming floors, carpets, and rugs; Disinfecting floor and bathroom surfaces by mopping; Cleaning the shower/bath tub after each use; Daily washing of recently worn clothes, towels and bedding in hot water, drying in a hot dryer and steam ironing. Options to combat itchiness include antihistamines such as chlorpheniramine.
Arthropod bites can be mistaken for mite bites. Some
arthropods that commonly bite humans are chiggers, also known as redbugs (Eutrombicula
alfreddugesi ); mosquitoes; cat fleas and bedbugs. Chigger bites commonly
occur beneath areas of restrictive clothing such as belts, underwear, and
socks. Morphologically, the chigger bite resembles the scabies bite except that the
chigger itself frequently appears as a tiny red dot in the center of the
urticarial lesion. Chigger bites are usually few in number, compared with the
large number of scabies bites on many
patients. Chiggers do not burrow; they feed at the base of a hair follicle or
in a pore. The bites commonly cause itching in three to six hours, and
dermatitis develops in 10 to 16 hours. In the South, chiggers are active
virtually year-round and commonly are encountered in woodlands and along
swamps. Chiggers feed on skin tissue over a period of several days. Mosquito bites are
usually associated with itchy wheals of short duration. They are generally
found on uncovered portions of the body and do not tend to be grouped.
Considerable variation in clinical appearance can be noted in the bites of the
160 species of U.S. mosquitoes.
Cat-flea ( Ctenocephalides felis) bites usually are located only on the lower extremities of the body--the legs and ankles. The lesions are grouped, itchy, and reared, with a central round minute spot differing in color from the surrounding tissue. Secondarily infected lesions are commonly found. Generally the patient is aware of having been bitten. Bedbug (Cimex lectularius) bites are usually found upon arising in the morning. They appear as grouped, itchy papules around the waist or on other areas not covered by clothing. Because of their complex nutritional requirements, bedbugs--which emit an offensive odor--come in contact with their human host only during feeding. During feeding, injected saliva produces an allergic reaction. The reaction causes delayed swelling, itching, and burning that may continue for seven days or longer.
Dog Mange. This is persistent contagious skin diseases caused by parasitic mites. The term is sometimes reserved for the infestation of domestic animals. Another term used to describe mite infestation is acariasis. These mites embed themselves either in hair follicles or skin, depending upon the type of mange. They generally infect domestic animals, commonly dogs and other canines, but can also affect wild animals and even humans. Two types of mites produce canine mange, and each type has characteristic symptoms.
Demodectic Mange Mite. Image Courtesy Joel Mills. Demodectic Mange in Dog. Image Courtesy Skabb.
Minor cases of demodectic mange usually do not cause much itching but might cause pustules on the dog's skin, redness, scaling, hair loss, or any combination of these. It most commonly appears first on the face, around the eyes, or at the corners of the mouth, and on the forelimbs and paws.
In the more severe form, hair loss can occur in patches all over the body and might be accompanied by crusting, pain, enlarged lymph nodes, and deep skin infections.
A Dog with Severe Demodectic mange. Image Courtesy of Julie Knicely.
Demodectic mange is not generally contagious to people, other animals, or even other dogs (except from mother to pup). However, the mite is zoonotic, and, upon infesting a human, will generally live in the hair follicles of the eyelashes and eyebrows. These mites thrive only on very specific hosts (dogs) and transmission usually occurs only from the mother to nursing puppies during the first few days after birth. The transmission of these mites from mother to pup is normal (which is why the mites are normal inhabitants of the dog's skin), but some individuals are sensitive to the mites, which can lead to the development of demodectic mange.
Some breeds appear to have an increased risk of mild cases as young dogs, including the Afghan Hound, American Staffordshire Terrier, Boston Terrier, Boxer, Chihuahua, Shar Pei, Collie, Dalmatian, Doberman Pinscher, Bulldog, English Bull Terrier, Miniature Bull Terrier, German Shepherd Dog, Great Dane, Old English Sheepdog, American Pit Bull Terrier, West Highland White Terrier, Rat Terrier, and Pug.
Demodectic mange also occurs in other domestic and wild animals. The mites are specific to their hosts, and each mammal species is host to one or two unique species of Demodex mites. There are two types of demodectic mange in cats. Demodex cati causes follicular mange, similar to that seen in dogs, though it is much less common. Demodex gatoi is a more superficial form of mange, causes an itchy skin condition, and is contagious amongst cats.
Treatment. Localized demodectic mange is considered a common puppyhood ailment, with roughly 90% of cases resolving on their own with no treatment. Minor, localized cases are often treated with medicated shampoos and not treated with agents aimed at killing mites as these infestations often resolve within several weeks in young dogs.
Demodectic mange with secondary infection is treated with antibiotics and medicated shampoos as well as parasiticidal agents. Amitraz is a parasiticidal rinse that is licensed for use in many countries for treating canine demodicosis. It is applied weekly or biweekly, for several weeks, until no mites can be detected by skin scrapings.
Demodectic mange in dogs can also be managed with ivermectins, although there are few countries which license these drugs, which are given by mouth, daily, for this use. Ivermectin is used most frequently; collie-like herding breeds often do not tolerate this drug due to a defect in the blood-brain barrier, though not all of them have this defect. Other drugs that can be used include doramectin and milbemycin.
Cats with Demodex gatoi must be treated with weekly or bi-weekly sulfurated lime rinses. Demodex cati are treated similarly to canine demodicosis.
Sarcoptic Mange Also known as canine scabies, sarcoptic mange is a highly contagious infestation of Sarcoptes scabiei canis, a burrowing mite. The canine sarcoptic mite can also infest humans and cats, pigs, horses, sheep and various other species.
These mites dig into and through the skin, causing intense itching and crusting that can quickly become infected. Hair loss and crusting frequently appear first on elbows and ears. Skin damage can occur from the dog's intense scratching and biting. Secondary skin infection is also common. Dogs with chronic sarcoptic mange are often in poor condition.
Sarcoptic Mange Mite. Image Courtesy Joel Mills.
Affected dogs need to be isolated from other dogs and their bedding, and places they have occupied must be thoroughly cleaned. Other dogs in contact with a diagnosed case should be evaluated and treated.
There are a number of parasiticidal treatments useful in treating canine scabies. Sulfurated lime rinses applied weekly or bi-weekly are effective. Selamectin is licensed for treatment by veterinary prescription in several countries; it is applied as a drip-on directly to the skin. Unlicensed, but frequently used, ivermectin, given by mouth for two to four weekly treatments; this drug is not safe to use on some collie-like herding dogs, however. Other ivermectin drugs are also effective, but none is licensed for use on dogs.
Veterinarians usually attempt diagnosis with skin scrapings from multiple areas, which are then examined under a microscope for mites. Sarcoptes, because they may be present in relatively low numbers, and because they are often removed by dogs chewing at themselves, may be difficult to demonstrate. As a result, diagnosis in Sarcoptic mange is often based on symptoms rather than actual confirmation of the presence of mites. A common and simple way of determining if a dog has mange is if it displays what is called a "Pedal-Pinna reflex", which is when the dog moves one of its hind legs in a scratching motion as the ear is being manipulated and scratched gently by the examiner; because the mites proliferate on the ear margins in nearly all cases at some point, this method works over 95% of the time. It is helpful in cases where all symptoms of mange are present but no mites are observed with a microscope. In some countries, a serologic test is available that may be useful in diagnosis.
For demodectic mange, properly performed deep skin scrapings generally allow the veterinarian to identify the microscopic mites. However because the mite is a normal inhabitant of the dog's skin, the presence of the mites does not conclusively mean the dog suffers from demodex. Rather abnormally high numbers of the mite are more useful. In breeds such as the West Highland white terrier, relatively minor skin irritation which would otherwise be considered allergy should be carefully scraped because of the predilection of these dogs to demodectic mange. Skin scrapings may be used to follow the progress of treatment in demodectic mange.
Face Mange Cats. Feline scabies is caused by a tiny mite called Notoedres cati. This mite affects cats very much like the sarcoptic mange mite affects dogs; in fact, their life cycles and treatments are very similar. While many cat owners do not realize that cats get mange, as veterinarians, we see and treat this on a regular basis. If your cat suffers from severe itching or hair loss on the head and neck, you should consider having her examined for this mange mite. The mites spend their entire life on a cat. The female mite burrows into the skin and lays eggs several times as she continues burrowing. These tunnels can actually reach the length of several centimeters. After she deposits the eggs, the female mite dies. In 3-8 days, the eggs hatch into larvae which have 6 legs. The larvae mature into nymphs which have 8 legs. The nymph then molts into an adult while it is still in the burrow. The adults mate, and the process continues. The entire life cycle requires 2-3 weeks.
Symptoms of Cat’s Face. Image Courtesy of Department of Parasitology, University of Sao Paulo, Brazil.
Notoedres can infect cats of all ages, breeds, and colors. It infects both males and females and often will infect an entire litter of kittens. Because this mite is transmitted directly from cat to cat, it is more common in outdoor cats that come in contact with strays. The mite only lives a few days off of the cat, but transmission through grooming, boarding, and sharing bedding is possible. N. cati can also infest foxes, dogs and rabbits
The symptoms usually start with hair loss and itching on the ears and then spread rapidly to the face, eyelids, and neck. The mites can also spread to the feet and lower abdomen. This characteristic spread probably occurs from the cat's habit of grooming, and sleeping curled up in a ball. As the disease progresses, the skin will become thickened, wrinkled, and covered with grayish/yellow crusts. Because of the intense itching, the infected cat will often scratch and irritate the skin causing secondary infections to develop. The surrounding lymph nodes may also become enlarged as the problem worsens. The characteristic itching and hair loss pattern help to diagnose Notoedric mange in the cat. Skin scrapings are performed to confirm the diagnosis. There are usually a large number of mites present on the skin and the resulting skin scrapings.
While the Notoedres mite can be killed with many of the same products used to treat dogs with scabies, most of them are NOT safe to use in a cat. Cats are much more sensitive to some of the insecticides that are safe to use in the dog. The current recommended treatment for cats is to clip all long hair and then bathe the cat with a gentle cleansing shampoo. After the shampoo, a 2 to 3% lime sulfur dip (Lymdip) is applied to the entire surface of the cat. Some cats may require a sedative to be properly bathed and treated. This is repeated every seven days until the condition resolves and may require 6 to 8 weeks of treatment.
Some veterinarians have successfully used an amitraz dip to cure this disease, but this is anoff-label use of this product and may make some cats sick. Recently, ivermectin has also been used successfully, much as it has been for sarcoptic mange in dogs. Ivermectin is not approved for use in cats, but under close veterinary care, it may provide a viable form of treatment. If there are multiple cats in the household it is often recommended that all cats in the household are treated because they may be harboring the mites. Unlike allergies, the intense scratching caused by Notoedres responds poorly to steroids.
Prevention is best accomplished by preventing your cat from coming in contact with stray or infected cats. Indoor cats are much less likely to contract this disease. Avoid boarding or grooming your cats at locations that do not provide good sanitation and insist that all grooming tools be disinfected between uses. At the first signs of infection, seek prompt treatment and isolate the infected cat from other cats in the household.
As with other mites in the Sarcoptes family, Notoedres can infect humans. The disease, though, is generally self-limiting, causing only temporary itching.
Human Follicle Mite. Demodex. This is a genus of tiny parasitic mites that live in or near hair follicles of mammals. About 65 species of Demodex mites are known; they are among the smallest of arthropods.
Demodectic Mange Mite. Image Courtesy Joel Mills.
Demodex folliculorum and Demodex brevis are typically found on humans. It is extremely rare to see a human infected with a different species of mite, such as Demodex canis, though a few instances have occurred. D. folliculorum was first described in 1842; D. brevis was identified as separate in 1963. D. folliculorum is found in hair follicles, while D. brevis lives insebaceous glands connected to hair follicles. Both species are primarily found in the face, near the nose, the eyelashes and eyebrows, but also occur elsewhere on the body.
The adult mites are only between 0.3 mm and 0.4 mm long, with D. brevis slightly shorter than D. folliculorum. They have a semi-transparent elongated body that consists of two fused segments. Eight short segmented legs are attached to the first body segment. The body is covered with scales for anchoring itself in the hair follicle, and the mite has pin-like mouth-parts for eating skin-cells, hormones and oils (sebum) which accumulate in the hair follicles. The mite's digestive system is so efficient and results in so little waste that there is no excretory orifice. The mites can leave the hair follicles and slowly walk around on the skin, at a speed of about 8–16 cm/hour, especially at night; they try to avoid light.
Female Demodex folliculorum are somewhat shorter and rounder than males. Both male and female Demodex mites have a genital opening, and fertilization is internal. Mating takes place in the follicle opening, and eggs are laid inside the hair follicles or sebaceous glands. The six-legged larvae hatch after 3–4 days, and it takes about seven days for the larvae to develop into adults. The total lifespan of a Demodex mite is several weeks. The dead mites decompose inside the hair follicles or sebaceous glands.
Older people are much more likely to carry the mites; it is estimated that about 1/3 of children and young adults, 1/2 of adults, and 2/3 of elderly people carry the mites. The lower rate of children may be due to the fact that children produce much less sebum. It is quite easy to look for one's own Demodex mites, by carefully removing an eyelash or eyebrow hair and placing it under a microscope.
The mites are transferred between hosts through contact of hair, eyebrows and of the sebaceous glands on the nose. Different species of animals host different species of demodex; and demodex is not contagious between different species.
In the vast majority of cases, the mites go unobserved, without any adverse symptoms, but in certain cases (usually related to a suppressed immune system, caused by stress or illness) mite populations can dramatically increase, resulting in a condition known as demodicosis or Demodex mite bite, characterized by itching, inflammation and other skin disorders. Blepharitis (inflammation of the eyelids) can also be caused by Demodex mites.
Tropical Rat Mite. The tropical rat mite commonly occurs on rats in most tropical parts of the world and some temperate areas. This mite has characteristic long legs and is known for painful bites. Itching follows the bite and can result in severe dermatitis. These mites do not vector any known disease. The preferred host of these ectoparasites is rats. However when rats are killed these mites will leave their bodies and travel considerable distances, particularly along heating pipes in wall. Under these conditions human inhabitants may be attacked in great numbers.
Psoroptic Rat Mites. These mites have shorter legs than the sarcoptic mange mites and do not burrow under the skin. These mites inhabit the base of hairs and pierce the skin introducing toxic saliva with resultant inflammation. An exudate oozes out and forms a scab. The skin becomes hardened and thickened especially on the scalp of humans and in the ears of domestic animals.
Pymotes Itch Mite. There are two species of Pymotes mites that cause itch in humans, namely Pyemotes tritici, the straw itch mite and Pyemotes herfsi, the oak leaf gall mite. The former is parasitic on a variety of insects including pests of wheat, alfalfa and other crops. The mite is usually microscopic, but the gravid females are visible. Problems commonly exist when alfalfa straw or other agricultural commodities containing these pests and their parasites are brought in from the field. Straw itch mites are found in stored grain, dried beans and peas, wheat straw, hay and other dried grasses. The mites are actually beneficial because they attack insects that feed on stored grain and similar materials. The mites bite individuals handling these materials resulting in dermatitis. The infested area itches, but some victims have an allergic reaction with a fever. Bites from these mites can be confused with chicken pox because of eruptions with both maladies
A straw itch mite. Image courtesy of John Moser, USDA Forest Service.
These mites have a very unusual life cycle. The males are microscopic and not visible to the naked eye. They wander continuously over the relatively giant body of a pregnant female feeding on her parasitically. The eggs hatch and 200 to 300 mites develop to adulthood within the enlarged female’s abdomen. They are released from her at a rate of about 50 a day. Only about 3% are males but they emerge first and remain clustered around the genital opening of the female. With the aid of their hind legs they drag newly emerging females through the opening even though they can exit on their own. Copulation is immediate and once eggs develop inside the new females they swell to many times their original size thus repeating the cycle.
Humans, particularly in grain growing areas, are bitten when handling infested straw, crops (beans, cotton, and small grains) or crop residues, or similar materials harboring the mites and those who make dried plant arrangements. Straw itch mites can travel through the air, so anyone in these areas can be at risk. Bites occur more often when straw itch mites become separated from their insect hosts or their hosts become scarce, itch mites may bite other animals, and humans. A person who is severely infested may have thousands of bites from itch mites that cannot be detected by the naked eye. Fortunately, the mites cannot live on humans and do not remain long. There is no evidence that the bites transmit disease, or that there is a person-to-person transmission of the mite.
Bites produce a rash which includes red welts with a small white pustule (head) at the center. The bite is not felt and can take from two to 24 hours for resulting welts to appear. Severe cases can cause infection, fever, vomiting, and joint pain. Severe itching and possible infection can occur if bites are scratched open. Itching may last up to a week or more and will normally disappear within a few weeks. The bites of straw itch mites are characteristically found on the trunk of the body and on the arms.
To prevent straw itch mite bites, avoid grassy areas and shower with plenty of soap after being in grassy or weedy areas. An insect repellent containing DEET is effective in preventing the bites. The best control strategy is to eliminate the mite's host insects. If possible, clean storage areas thoroughly and treat with a pesticide, such as cyfluthrin. If necessary, stored commodities can be fumigated to disinfest them. Mite populations should decrease or completely disappear with the onset of the first frost. Many people believe the mites infest their beds or homes, but this is not true.
Oral antihistamines such as diphenhydramine and topical anti-itch creams such as hydrocortisone have been useful in alleviating the discomfort caused by the
bites. In most cases the bites
Pyemotes herfsi, also known as the oak leaf gall mite or itch mite, is an ectoparasitic mite, identified in central Europe in 1936, whose presence in the United States was confirmed during the 1990s. The United States Centers for Disease Control estimated that during an outbreak in August 2004, 54% of the population of Crawford County, Kansas, or about 19,000 people, suffered from its bites. Other states in the US where humans have been affected during the 2000s are Nebraska, Oklahoma, Missouri, Tennessee Shelby County, Texas, and Illinois. Currently in August 2008 an outbreak is being reported in the northern suburbs of Cincinnati, Ohio by the Hamilton County Public Health Department.
This species has biology very similar to the straw itch mite. The mites' reported hosts have included Anobium punctatum, the pink bollworm, Grapholita molesta, Tineola bisselliella and various pests of stored grain, as well as humans and their pets. Their usual hosts in the United States are oak midge larvae. Newly emerged and mated females inject aneurotoxin-containing saliva into their hosts, which paralyzes the host and enables the pregnant female mites to feed on the host's hemolymph. A single mite can paralyze and kill an insect larva 166,000 times its own weight; within a few days, up to 250 adult mites emerge from the female. A life cycle can be completed within seven days. Conditions that are cooler and moister than average favor its population growth. Outbreaks of attacks on humans in the United States have been attributed to fluctuations in the supply of oak midge larvae.
The closely related straw itch mite (Pyemotes tritici), was initially suspected, as the culprit in the Kansas infestation but no specimens of this species were found. The reports indicated that the bites occurred on people after being outdoors in or near wooded areas. Based on this information, a search was initiated and resulted in the discovery of Pyemotes herfsi preying on midge larvae in leaf galls on pin oak trees.
Humans typically report itching from mite bites within 10 to 16 hours after contact. The victims often do not recall being bitten. The rash that results from the bites is usually described as a red patch with a small blister in the center, most often found on the neck, face, arms, or upper torso. A secondary bacterial infection sometimes arises when the bite is scratched. The suggested treatments include the application of calamine lotion, an antihistamine cream such as Benadryl, or a corticosteroid cream; a suggested preventive measure is the application of DEET before outdoor activity. Anecdotal reports from the Kansas outbreak, however, suggest that DEET might not provide complete protection against P. herfsi.
The bites are not life-threatening, but a few individuals suffering 100 or more bites have undergone brief hospitalizations.
This is a group of parasitic mites that attack a variety of animals, including cats, dogs and rabbits. In these animals, infestations are limited to the ears and the mites are typically found feeding in the outer ear canals. As are most parasitic arthropods, ear mites are host specific and no species attacks humans. In rabbits, infestations can become serious if left uncontrolled; the result can result in bleeding, secondary infection and possible death. An infestation is easily recognized by a layer of dried ooze on the inner side of the ear. If this crusty ooze is removed, large numbers of mites can be found feeding on ear tissue.
As discussed, ear mites are common in dogs and cats. Young animals appear to be more susceptible to the feeding of these arachnids. Typical symptoms include frequent shaking of the head, lowered ears (in cats), and nearly black coloration in the outer ear canal (this gives the appearance that the animal has very dirty ears).
In all cases a few applications of several drops of mineral oil to the infested area will give considerable relief and control; most veterinarians suggest this should be followed by applications of medications specifically used for ear mite control. It should also be noted that bacterial and fungal infections of the ears result in similar symptoms.
HUMAN FOLLICLE AND SEBACEOUS MITES
Follicle mites are long and skinny with short legs (Figure 30). These microscopic mites infect many species of mammals, and they seem to have a high degree of host specificity (i.e., mites from one host species will not infect another host species). Humans are infected with Demodex folliculorum, which lives in hair follicles and sebaceous (oil) glands, especially around the face (particularly in and around the nose, eyes, and forehead). This mite occurs in a high percentage of the population (nearly 100% in older people), but, fortunately, it normally does not cause "problems." In those cases in where follicle mites do cause problems, they are most often associated with skin rashes, hair loss (particularly the eyelashes), and acne.
In other animals, infections with follicle mites can be more serious. Dogs are infected with D. canis (the dog follicle mite), which can cause red or canine demodectic mange. This mite can cause severe skin problems in infected dogs, including significant loss of hair and skin rashes. In severe cases infected dogs may be euthanized.
A human follicle mite. Image courtesy of Life Science Dept., University of South Africa.
Trombiculidae (pronounced /trɒmbɨˈkjuːlɨdiː/) is a family of mites called trombiculid mites (also called berry bugs; harvest mites; red bugs; scrub-itch mites; and, in their larval stage, chiggers). The term chigger is sometimes used to refer to a different animal, the Chigoe flea. Trombiculidae live in the forests and grasslands and are also found in low, damp areas where vegetation is rank such as woodlands, berry bushes, orchards, along lakes and streams, and even in drier places where vegetation is low such as lawns, golf courses, and parks. They are most numerous in early summer when grass, weeds and other vegetation are heaviest. A common species of harvest mite in Northern America is Trombicula alfreddugesi; in the UK the most prevalent harvest mite is Trombicula autumnalis.
Trombiculid mites are found throughout the world. In Europe and North America, they tend to be more prevalent in the hot and humid parts. In the more temperate regions, they are found only in the summer (in French, harvest mites are called aoûtat, or "August" flies . In the United States, they are found mostly in the southeast, the south, and the Midwest. They are not present, or barely found, in far northern areas, in high mountains and in deserts. In the British Isles, the species Trombicula autumnalis are called harvest mites, in North America the species Trombicula alfreddugesi, and the species Trombicula (eutrombicula) hirsti which are found in Australia and are commonly called the scrub-itch mite.
The length of the mite's cycle depends on species and environment, but normally last 2 to 12 months (but may be longer). The number of cycles in a year depends on the region. For example, in a temperate region, there might only be 3 a year, but in tropical regions, the cycle might be continuous all year long. Adult mites overwinter in protected places such as slightly below the soil. Females become active in the spring, and once the ground temperature is regularly above 60 ℉ (15.6 ℃), she lays eggs, up to 15 eggs per day in vegetation when soil temperatures are 60 ℉ (15.6 ℃). It follows that from April through early autumn up until the first frost, humans are susceptible to chigger bites. The larvae congregate in groups on small clods of earth, in matted vegetation and even on low bushes and plants, where they have more access to a prospective host. The eggs are dormant for about six days, after which the non-feeding pre-larvae emerge, with only three pairs of legs. After about six days, the pre-larva grows into its larval stage.
The larvae, commonly called chigger, is tiny (0.007–0.008 in) in diameter, normally light red, covered in hairs, and move quickly relative to size. Chigger is also an alternate term for the chigoe flea (Tunga penetrans), a sand flea found in tropical and subtropical climates in the Americas and Africa. The name chigger originated as a corruption of chigoe. The larval stage is the only parasitic stage of the mite's life cycle. They are parasites various animals, including amphibians, reptiles, birds, and mammals, and feed on skin. This often causes an intensely itchy red bump in humans (who are accidental hosts). Chiggers attach to the host, pierce the skin, inject enzymes into the bite which subsequently form a hardened tube called a that digest stylostome. Once formed the digested cell are sucked up through the hardened tube. They do not burrow into the skin or suck blood, as is commonly assumed. Itching from a chigger bite may not develop until 24–48 hours after the bite, so the victim may not associate this symptom with the bite itself. Tiny red welts are also formed due to this feeding. The red welt/bump on the skin is not where a chigger laid eggs, as is sometimes believed. The larva remains attached to a suitable host for 3 to 5 days before dropping off to molt into the nymph stage. There are three nymphl instars, namely the protonymph, deutonymph, and tritonymph.. The protonymph is an inactive transitional stage. The active deutonymph develops an additional pair of legs (for a total of eight) subsequently re-entering inactivity during its transitional tritonymph phase before growing to adulthood. The deutonymph and adult are predatory feeding on small arthropods and their eggs and occasionally feeding on plant material. They live in soil, often found when digging in yards and gardens. Adults can be beneficial to human beings, since they often eat the eggs of other pests, such as mosquitoes.
Although chigger usually does not carry diseases in North American temperate climates, they are considered a dangerous pest in East Asia and the South Pacific because they vector Oriental tsutsugamushi,, a bacterium that causes scrub typhus, which is known alternatively as the Japanese river disease, scrub disease, or tsutsugamushi.
An adult chigger, unlike the larvae, these are predatory. Image courtesy of Susan Ellis, Bugwood.
Chiggers typically feed around the ankles or behind the knees and tend to congregate where clothing comes in restrictive contact with the skin. They may crawl as high as the crotch. If someone were to sit or lie down in chigger-infested grass, their bites could occur all over the body. These mites do not burrow into the skin, but rather secrete digestive enzymes that dissolve tissue just under the skin. Chigger bites initially appear as small-reddened areas but soon develop into small water blisters. The accompanied itching that can last up to 36 hours. Some people suffer from nausea.
Chiggers are more common in the South and other tropical or semitropical areas of the world, but can be encountered in most states. Individuals who live in chigger-infested areas may become somewhat immune to their bites. When a chigger feeds it injects saliva that causes the tissues to harden around its mouthparts. This hardened area is referred to as a feeding tube and functions to facilitate the chiggers feeding. However, if someone has a history of chigger bites, he or she may become hypersensitive to their saliva and when the chigger begins to feed, a massive hardened area (instead of the feeding tube) quickly develops. This, in turn, blocks the chigger’s ability to further feed. As a consequence little saliva is injected and typical symptoms do not develop.
Currently available treatments are few with applications of benzocaine the most effective. Prevention of infestation by this mite is the best strategy and is accomplished staying away from grasses and fields in chigger-infested areas. Also, placing socks outside of pant legs and applications of insect repellants are also effective. Chiggers are known to vector scrub typhus (Rickettsia tsutsugamushi). This disease is also known as Japanese river fever and is found primarily in Southeast Asia. It is fairly well controlled now, but was problematic during WWII, before antibiotics were routinely used.
Chigger bites commonly occur beneath areas of restrictive clothing such as belts, underwear, and socks. Morphologically, the chigger bite resembles the Pyemotes bite except that the chigger itself frequently appears as a tiny red dot in the center of the urticarial lesion. Chigger bites are usually few in number, compared with the large number of Pyemotes bites on many patients. Chiggers do not burrow; they feed at the base of a hair follicle or in a pore. The bites commonly cause itching in three to six hours, and dermatitis develops in 10 to 16 hours. In the South, chiggers are active virtually year-round and commonly are encountered in woodlands and along swamps. Chiggers feed on skin tissue over a period of several days.
Scrub typhus is transmitted by some species of trombiculid mites ("chiggers", particularly Leptotrombidium deliense), which are found in areas of heavy scrub vegetation. The bite of this mite leaves a characteristic black eschar (piece of dead skin that is cast off from the surface) that is useful to the doctor for making the diagnosis. Scrub typhus is endemic to a part of the world known as the "tsutsugamushi triangle", which extends from northern Japan and far-eastern Russia in the north, to northern Australia in the south, and to Pakistan and Afghanistan in the west.
The precise incidence of the disease is unknown, as diagnostic facilities are not available in much of its native range. In rural Thailand and in Laos, murine and scrub typhus accounts for around a quarter of all adults presenting to hospital with fever and negative blood cultures. The incidence in Japan has fallen over the past few decades, probably due to decreasing exposure, and many prefectures report fewer than 50 cases per year. It affects females more than males in Korea, but not in Japan.
Symptoms include fever, headache, muscle pain, cough, and gastrointestinal symptoms. More virulent strains of O. tsutsugamushi can cause hemorrhaging, intravascular coagulation. Macuopapular rash, eschar, splenomegaly and lymphadenopathies are typical signs. Leukopenia and abnormal liver function tests are commonly seen in the early phase of the illness. Pneumonitis, encephalitis, and myocarditis occur in the late phase of illness. Acute scrub typhus appears to improve viral loads in patients with HIV. This interaction is refused by an in vitro study.
In endemic areas, diagnosis is generally made on clinical grounds alone. Where there is doubt, the diagnosis may be confirmed by a laboratory test such as serology.
Without treatment, the disease is often fatal. Since the use of antibiotics, case fatalities have decreased from 4%–40% to less than 2%. The drug most commonly used is doxycycline; but chloramphenicol is an alternative. There are currently no licensed vaccines available.
Severe epidemics of the disease occurred among troops in Burma and Ceylon during World War II (WWII). Several members of the U.S. Army's 5307th Composite Unit (Merrill's Marauders) died of the disease; and in 1944, there were no effective antibiotics or vaccines available. The disease was also a problem for US troops stationed in Japan after WWII, and was variously known as "Shichitō fever" (by troops stationed in the Izu Seven Islands) or "Hatsuka fever" (Chiba prefecture).
Delusory parasitosis is a paranoia, or irrational fear, of small creepy non-existent creatures. Because mites are so small, this condition is often diagnosed as a mite infestation. This phenomenon is more common than one might expect. Frequently, people who are inflicted with this malady are quite normal in all other phases of life and lead productive lives.
I was quite unaware of this phenomenon until one day a man in his mid 40's walked into my office and indicated that the UCLA Medical Center had referred him to me. He indicated that he and his home were infested with small 'bugs' that he could not eradicate. After a short discussion he reached out into the air and indicated I had them in my office also. I responded that he must have brought them with him. He further stated that he had captured some and placed them on a piece of scotch tape. He related collecting each ‘critter.’ The first had bitten him on the leg and then disappeared under his skin, but he dug it out with a sewing needle. The second was on his pants cuff and bit him on the ankle. The third was found swimming around in his toothpaste. After considerable discussion we examined each 'critter' with a microscope. Needless to say, none resembled an insect or mite. Indeed, they were small grains of sand, pieces of lint and so on. However, even after this close inspection and work over a several-week-period, he could not be persuaded that the attacking creatures were imaginary. The situation became so bad that he convinced his wife that she was also infested. They couldn't get them out of their home even though several exterminators were called. Because of the “infestation,” the home was eventually sold at a considerable loss. Eventually, partly because of the turmoil, their marriage ended in divorce.
There have been many similar situations since then. One of the most unusual occurred a few years ago when a city official from Mission Viejo (Orange County) called me and indicated that he had a whole neighborhood infested with scabies mites (see below). Scabies are parasitic mites that commonly infest humans. At the time this didn’t seem questionable because a number of the people had been to medical doctors and had been treated for this mite. These treatments didn’t seem to solve the problem, so I was brought in as a consultant. The main problem was centered on one particular resident. This woman apparently had convinced much of the neighborhood of the widespread infestation. She was using very drastic measures to try to eliminate these mites from her house and family. She would use lye to scrub down the beds on a weekly basis. On several occasions she washed her kids down with gasoline. Of course, upon hearing this, I began to realize that the whole situation was more than a little irrational. The final clincher was when she indicated that the whole problem started when she brought a potted plant back from Arizona and, while it was sitting in her bathroom, a pod grew out of it and blew these tiny critters all over the neighborhood.
A colleague from NCSU, Mike Waldvogel, reports similar experiences. He states he has received a variety of imaginary critters in vacuum cleaner bags, pillows, panty hose, skin samples, glue boards (like the one you use for catching mice) and (the one he described as the ultimate) a bottle (formerly a pint gin bottle) that was labeled " after douching." Needless to say that one wasn’t opened! Neither were the vacuum cleaner bags, as they usually contain pesticide-laden dust from over-treated carpets.
All of these cases have had several symptoms in common. The 'critters' typically fly through the air, crawl on the skin, frequently appear and disappear in the skin, make clicking noises and can be found in soap and toothpaste. Generally, inflicted individuals have gone to several medical doctors to no avail and can almost never be persuaded that the pests are imaginary.
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 (Figure 33). 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 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 Relaspsing 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 pressor response followed rapidly by hypotension. Recent studies have shown that tumor necrosis factor-alpha (TNF-alpha) may be partly responsible for the reaction.
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.
A cluster of a few thousand hard tick eggs behind a picture frame. Image courtesy of James Gathaway, CDC Photo Library.
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 andersoni) 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 progress 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.
Electromyographic (EMG) studies usually show a variable reduction in the amplitude of compound muscle action potentials but no abnormalities of repetitive nerve stimulation studies. These appear to result from a failure of acetylcholine release at the motor nerve terminal level. There may be subtle abnormalities of motor nerve conduction velocity and sensory action potentials.
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. She was taken to a local emergency department (ED) and transferred to a regional children's hospital. A physical examination revealed ophthalmoplegia (i.e., paralysis of muscles controlling eye movement), dysarthria (i.e., slurred or abnormal speech), and areflexia (i.e., absence of neurologic reflexes); nerve conduction studies indicated decreased velocities. 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 a 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 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. 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.
Detection of antibodies is possible.
At this time there is no specific treatment for CTF. The first thing to do is make sure the tick is fully removed from the skin, then Acetaminophen and analgesics can be used to help relieve the fever and pain. Aspirin is not recommended for children it has been linked to Reye’s syndrome in some viral illnesses. Salicylates should not be used because of thrombocytopenia, and the rare occurrence of bleeding disorders. Someone who suspects that they have been bitten by a tick or is starting to show signs of CTF should contact their physician immediately.
Ticks should be removed promptly and carefully with tweezers and by applying gentle steady traction. The tick's body should not be crushed when it is removed and the tweezers should be placed as close to the skin as possible to avoid leaving tick mouth parts in the skin. Ticks should not be removed with bare hands. Hands should be protected by gloves and/or tissues and thoroughly washed with soap and water after the removal process. This should be performed with great care. Putting Vaseline over the tick will prevent air from reaching it, causing the tick to retract itself from the skin. Be ready to grab it off when it does. Make sure after you pull it out that the nose is not left in your skin. This can cause painful infection to occur.
A match or flame should NOT be used to remove a tick. This method, once thought safe, can cause the tick to regurgitate expelling any disease it may be carrying into the bite wound.
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".
§ 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 (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 tularemia (Type A), which is found in wild rabbits in North America and is highly virulent for humans and domestic rabbits. F. tularemia 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 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 skin ninglagomorphs (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. H.R. Cox and Davis isolated it from ticks in Montana, USA in 1938. 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. Subadult 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 become airborne 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 which 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 ordoxycycline 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 gets 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 [ELISA].) 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 LYMErix™ 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 migrants. 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 the white-footed mouse and wood rat in eastern and western United States, respectively. Although white-tailed deer harbor Anaplasma phagocytophilum, evidence suggests that they are not a reservoir for the strains that cause HGA. Anaplasma 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 genusFlavivirus 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:\ in this case 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.
15. House dust mites feed on dead skin and the presence of their dead bodies, feces and living mites can result in allergies in humans.
16. Typical symptoms of a scabies mite infestation are small red dots or pustules between the fingers, on the wrists and breasts of women and intense itching.
17. Scabies mites are almost always found on the host and it does no good to spray for their presence in the home.
18. The most common hosts of ear mites in and around the home are cats, dogs and pet rabbits.
19. Typical symptoms of chiggers are red dots or small water blisters, especially around the ankles accompanied by intense itching.
20. The brown dog tick is commonly found in protected locations such as kennels and prefers to feed on dogs rather than humans.
21. An early symptom of Lyme’s disease is donut shaped blotches on the skin. It is important to diagnose this disease in its early stages because if it becomes too advanced it is very difficult to cure.