Ticks
Overview Gary Podolsky MD
Ticks
are the leading carriers of diseases to humans worldwide, second
only to mosquitoes. It is not the tick bite but the toxins or organisms
in the tick's saliva transmitted through the bite that cause disease.
Ticks
like spiders are arthropods. All tick species have a similar life
cycle consisting of four stages: egg, larva (six legs), nymph (eight
legs, sexually immature), and adult.
There
are more than 800 species of ticks throughout the world. They are
responsible for carrying such diseases as Rocky Mountain spotted
fever, Lyme's disease, Babeosis (Texas fever), Ehrlichosis, and
Tularemia (also transmitted via rabbits), as well as Colorado tick
fever and Crimean-Congo Hemorrhagic fever.
In
addition to disease transmission, ticks can also cause tick paralysis.
This condition occurs when neurotoxins in the tick saliva make you
ill; cause paralysis of the body; and in extreme cases, can stop
you from breathing in extreme cases.
Tick
Biology (What makes Ticks, tick?)
Ticks
require blood meals at larval, nymph, and adult stages. If all three
feeding stages occur on one host, the tick is referred to as a “one-host”
tick. Most Ixodidae are “three-host” ticks—each feeding stage is
on a different host. Some ticks are host specific, but most are
opportunists and feed on a variety of hosts.
Ticks
act as amplifiers or reservoirs for infectious agents. Ticks ingest
microorganisms while feeding on an infected host. The organisms
replicate in the tick and are carried to the adult tick stage from
which they are transmitted to other hosts when the tick feeds. Microorganisms
are passed transovarially from one generation of ticks to the next,
and depend solely on the tick to survive.
Some
major organisms vectored by ticks are borrelia, rickettsia, tularemia,
viruses, and protozoan parasites. Ticks may also secrete a neurotoxin
that produces tick paralysis.
Ticks
are divided into two categories: Ixodidae (hard ticks) and Argasidae
(soft ticks).
Ticks
are important to humans because of the diseases they can transmit.
Understanding the biology of the insect is key to anticipating and
preventing diseases.
Hard
Ticks (Ixodidae)
Have
a hard, shield-like scutum that covers the entire dorsal surface
in males but only the anteromedial portion of the females. The head
is visible from above and below.
These
feed slowly over the course of days. Females may ingest over fifty
times their body weight in blood and other fluids.
Hard
ticks transmit all of the major tick-borne disease in North America
with the exception of relapsing fever.
Disease
transmission usually occurs near the end of a meal, as the tick
becomes full of blood. Some of the more common hard ticks are: American
dog tick; Wood tick; Deer tick (they carry Lyme's disease)and Lone
star tick
Soft
Ticks (Argasidae)
Soft
ticks have more rounded bodies without the hard scutum found in
hard ticks. These ticks usually feed for less than 1 hour. Disease
transmission can occur in less than a minute. The bite of some of
these ticks produces intensely painful reactions. Two common soft
ticks found in the United States are the Pajaroello tick and spinose
ear tick. Transmit relapsing fever
Outbreaks
of tick-related illnesses follow seasonal patterns as ticks evolve
from larvae to adults. They hide in low brush to hitch a ride on
a potential host. Ticks require a "blood meal" to grow
and survive, and they are not very particular upon whom or what
they feed. If these freeloaders don't find a host, they may die.
Once
a tick finds a host (animal or person) and a suitable site for attachment,
the tick begins to burrow with its mouthparts barbed into exposed
skin.
Tick
attachment and feeding
Ticks
secrete "cementum" to more firmly anchor their mouthparts
and head to their host. Ticks may secrete or regurgitate small amounts
of saliva that contain neurotoxins. These nerve poisons prevent
pain and irritation of the bite
Saliva
may contain an anticoagulant.
Diseases
of Ticks
Babesiosis
(Human Babesiosis)
Is
caused by a tick borne protozoan infection
Babesia microti . After
an infected nymph bites a human, the organisms enter the host's
red cells, where they multiply and cause hemolysis.
Rodents,
wild animals and cattle are its natural reservoir, with humans rarely
infected. Symptoms start 1-4 weeks after bit and may be mild to
severe. In severe cases - high fever, chills, nausea and vomiting,
may even mimic malaria with future complications such as lung edema,
anemia, kidney failure and bleeding.
Clinical
signs of infection vary considerably; many patients remain asymptomatic.
Symptoms
usually appear one to four weeks following a tick bite and at first
consist of the gradual onset of malaise, anorexia, and fatigue.
Within a week or so, fever that ranges from 37.8 °
to 40.3 °
C (100 °
to 104 °
F) drenching sweats, and myalgia develop.
As
with malaria, nausea, vomiting, headache, shaking chills, hemoglobinuria,
altered mental status, disseminated intravascular coagulation, anemia
with dyserythropoiesis, hypotension, respiratory distress, and renal
insufficiency are common. Pulmonary edema is occasionally found,
and splenomegaly may occur, but is rather atypical.
There
parasites may be seen on a blood smear (as with malaria) and treatment
may be supportive or if severe symptoms, several drugs are used.
This A number of reports of single patients
with concomitant Borrelia and Ehrlichia infection have appeared
in the United States and in Canada.
In
areas where all three infections are present, laboratory testing
of patients with an established diagnosis for the other two infections
would not be unreasonable. For patients with Lyme disease, a single
thick blood smear could be examined for the morules that typify
human granulocytic ehrlichiosis and for the intraerythrocytic parasites
that characterize babesiosis. Immunofluorescent immunoassays or
PCR testing would be more sensitive procedures. disease
often co-exists with Lyme disease in the same ticks, although it
is rare.
Patients
with only mild clinical manifestations of babesios may require no
specific treatment. For those who do need treatment, quinine combined
with clindamycin is the treatment of choice. Parasitemia is consistently
eradicated and babesial infestation does not recur when treatment
is discontinued
Colorado
Tick Fever
Colorado
tick fever is the most common human arbovirus infection. It is transmitted
exclusively by female wood ticks ( Dermacentor andersoni )
in North America.
The
distribution of Colorado tick fever virus roughly approximates that
of its vector tick, D andersoni . The virus has been isolated
from humans and from ticks in California, Colorado, Idaho, Montana,
Nevada, New Mexico, Oregon, South Dakota, Utah, Washington, and
Wyoming, and also in southern Alberta and British Columbia. Physicians
should be aware of the possibility of Colorado tick fever in febrile
patients returning from these regions.
Mammals
involved in the natural cycle of Colorado tick fever virus include
the golden mantled ground squirrel, porcupine, chipmunk, deer mouse,
and bushy-tailed woodrat. Colorado tick fever virus also is transovarially
(adult female to egg) and transstadially (larva to nymph to adult)
transmitted in D andersoni ticks.
People
with recreational or occupational exposure to ticks in the period
April through June have a higher incidence of infection. Males in
general, and people aged 20 to 29 had the highest risk of acquiring
the disease.
The
incubation period ranges from less than one to nineteen days (average,
about four days), possibly dependent on the number of colorado tick
fever virions the individual receives from the infecting tick. The
onset is usually abrupt and is characterized by high fever, chills,
joint and muscle pains, severe headache, ocular pain, conjunctival
injection, nausea, and occasional vomiting. The spleen and liver
may be palpable. A transitory petechial or maculopapular rash is
seen in a few individuals.
No
specific signs or symptoms, physical findings, laboratory abnormalities,
radiographic or electroencephalographic features define Colorado
tick fever. However, the diagnosis of Colorado tick fever is strongly
suggested if the illness is interrupted by an afebrile, symptom-free
interval that lasts two to three days. Fifty percent of the individuals
with clinical illness manifest this interval.
A
history of travel to an endemic area suggests the diagnosis. Ninety
percent of infected individuals recall having had a tick attached
or having seen a tick crawling on their body or clothing.
Colorado
tick fever is rarely a life-threatening illness, but may cause severe
discomfort, and symptoms may last for weeks. Treatment is symptomatic.
A
few individuals have a more severe illness that produces extended
prostration, anorexia, continuing fatigue, and convalescence for
several more weeks. Children may have hemorrhagic manifestations
ranging from a more pronounced rash to a disseminated intravascular
coagulopathy and gastrointestinal bleeding. Central nervous system
involvement, including aseptic meningitis and encephalitis, has
been observed in severely affected children. Rarely, adult orchitis,
pericarditis, hepatitis, and symptoms mimicking myocardial infarction
have been reported.
Because
the illness is relatively mild, extensive diagnostic studies are
not usually performed. Leukopenia and, in some instances, thrombocytopenia
have been observed, as has toxic granulation of neutrophils. Immature
granulocytes may appear in the peripheral blood..
Serologic
conversion from a negative, or low titer to a positive or high titer
is most often used for confirmatory diagnosis. However, antibody
to Colorado tick fever virus is not detected until one or two weeks
after the onset. IgM antibody to Colorado tick fever virus does
not cross-react with any other North American virus, so that detecting
such antibody, even in a single serum, can be considered presumptive
evidence of recent infection
Isolating
Colorado tick fever virus from the patient is a more dependable
basis for laboratory confirmation. Colorado tick fever virus replicates
in erythrocytes and is sequestered from antibodies. Viremia may
last for several months. Early in the infection, virus can be isolated
from both serum and blood clots with about the same frequency, but
about a month after onset it is more easily isolated from blood
clots.
Crimean
Congo Hemorrhagic Fever
Occurs
in Africa, Asia, and the Middle East. It is common in many animals
but rare, yet serious in people.
It
is caused by a virus transmitted by infected ticks or by direct
contact with infected animal body fluids. There is no vaccine. Risk
to travellers in low. Symptoms start after an incubation period
of 1-3 days. Non-specific symptoms like fever, dizziness, headache,
neck stiffness; aches, abdominal pain, diarrhea, nausea, sore eyes
and photophobia develop. Generalized bleeding can develop. Diagnosis
is confirmed with a blood test. Treatment is supportive only.
Ehrlichiosis
(Human Erlichoiosis)
Ehrlichiosis
is a bacterial infection transmitted by tick bites.
Symptoms
are similar to Rocky Mountain spotted fever and Lyme disease. Onset
of symptoms occurs 5-10 days after the tick bite with sudden fever,
headache, chills, aches and nausea and vomiting. A generalized rash
occurs more often in affected children compared to adults. Untreated
meningitis, kidney and liver disease may occur, and rarely it is
fatal.
Diagnosis
is with blood tests, which may take some time. Doxycycline is effective
treatment (which will also cover Rocky Mountain Spotted Fever and
Lyme disease), while waiting for confirmation of blood work.
The
ehrlichia are obligate intracellular bacteria that infect a variety
of animals and are usually vectored by ticks.
The
first case of human ehrlichiosis in the United States occurred in
1986, and was reported in 1987. Because the organism produces characteristic
colonies (morules) in monocytes, the disease was labeled human monocytic
ehrlichiosis (HME).
The
first case of human granulocytic ehrlichiosis (HGE), so-called because
the organisms form morules in granulocytes instead of monocytes,
was reported in 1995. (Both organisms will infect stem cells, but
maturation into mature cells select against the specific organisms.)
The
clinical courses of infections by either organism are quite similar.
Typically the first manifestation is an acute febrile illness associated
with headache and myalgia. Approximately 75 percent of patients
have a history of tick exposure. Laboratory studies usually disclose
leukopenia and thrombocytopenia, sometimes anemia, and hepatic aminotransferases
are usually elevated. A nonspecific rash occurs in approximately
one-third of the patients with HME, but is less common in patients
with HE.
The
diagnosis is aided by finding typical organisms in peripheral blood
smears, but typical morules are found in only about 80 percent of
serologically confirmed infections. Infections are most often diagnosed
by immunofluorescence assay (IFA), although polymerase chain reaction
(PCR) assays are being used more commonly.
A
confirmed diagnosis is defined as:
A fourfold increase in antibody titer by IFA
in acute- and convalescent-phase sera;
PCR amplification of ehrlichial DNA; or
Detection of intraleukocyte morules and
a single IFA titer ³
64 |
Most
patients have a mild illness that rapidly responds to Doxycycline
(100 mg BID). Defervesence usually occurs in twenty-four to forty-eight
hours.
Some
older patients, have adult respiratory distress syndrome (ARDS),
renal failure, neurologic disorders, and disseminated intravascular
coagulation (DIC).
Case-fatality
ratios as high as 10 percent for HGE and 5 percent for HME have
been reported.
The
white-footed mouse (or deer mouse, Peromyscus leucopus) is
a significant animal reservoir for the agent associated with HGE
US
Army centre for health promotion and preventative medicine
http://chppm-www.apgea.army.mil/ento/erlichio.htm
CDC
http://www.cdc.gov/ncidod/dvrd/ehrlichia/
Familydoctor.org
http://familydoctor.org/056.xml
Lyme's
Disease
Lyme
Disease is an infection by the spirochete Borrelia burgdorferi
that is associated with variable, complex clinical features.
It is transmitted by the bite of Ixodes ticks
Lyme
Disease was first recognized after two women called the Connecticut
State Health Department's attention to an incidence of juvenile
rheumatoid arthritis at least 100 times higher than expected in
the vicinity of Lyme, CT, in 1975.
A
history of a tick bite from a few patients, close geographic clustering,
and a predominant onset in summer or early fall led to suspicion
of an arthropod vectored infection. The distribution of subsequent
cases was similar to that of the deer tick Ixodes dammini
(now named Ixodes scapularis ).
Spirochetes
were found in the midguts of the ticks by Willy Burgdorfer, thus
the name Borrelia burgdorferi .
Subsequently,
organisms were recovered from the blood of patients with typical
Lyme disease at State University of New York.
The
name was changed from Lyme arthritis to Lyme disease, and the disorder
was recognized to be identical to a syndrome long known in Europe.
Buchwald described the skin lesions known as dermatitis chronica
atrophicans in 1883.
Afzelius
described erythema chronicum migrans, the typical erythematous rash,
in 1921. Spirochetes were found in the skin lesions in 1948, and
reports of benefits from penicillin therapy appeared in 1951, 1955,
and 1958. Benign lymphocytic infiltration of the skin was reported
in 1953. Garin and Bujadoux described the neurologic features in
1922, and the condition has been known in Europe as Barnwarth's
syndrome since his 1941 report.
Lyme
disease has been reported from at least forty-four states in the
United States, including some states in which the tick vectors are
not known to exist, and is widespread in Europe, Asia, and Australia.
When CDC surveillance started in 1982, only about 500 cases were
reported. The incidence has increased steadily. In 2002, 23,763
cases of Lyme disease were reported, and total reported cases is
over 157,000. (Approximately 60,000 infections occur each year in
Europe.) Some of these cases are undoubtedly erroneous diagnoses,
but CDC considers Lyme disease under reported. The overall incidence
rate in 2002 was seven infections per 100,000 population.
In
the Northeast and Midwest, most cases occur from May to August;
in the Pacific region, the incidence is evenly distributed throughout
the year. In the Northeast and Midwest have the highest incidence
in individuals younger than 15 years; the second highest incidence
is in the 25 to 44 year age group, which reflects peridomestic exposure.
In California the highest incidence is in the 25 to 44 year age
group, which reflects recreational or occupational exposure.
In
Canada, the greatest number of confirmed cases (199) has been in
Ontario; while no confirmed cases have been reported in Newfoundland,
Prince Edward Island, Nova Scotia, the Yukon and the Northwest Territories.
http://www.arthritis.ca/types%20of%20arthritis/lyme%20disease/default.asp?s=1
According to the Canadian Lyme Disease Foundation, Lyme disease
carrying ticks have been found in every Canadian Province. Ixodes
scapularis have been found as far north and west as Slave
Lake Alberta. http://www.canlyme.com/
Lyme disease is transmitted largely by Ixodes ticks, Ixodes
scapularis in New England and the Midwest, I. pacificus
in California, I. ricinus in Europe, I. persulcatus
in China.
Ixodes
ticks are much smaller than common dog ticks. The nymphs, which
are responsible for most human bites, are smaller than the adults
— about the size of a poppy seed. As a rule of thumb, arthropods
easily identified as ticks by individuals who are not familiar with
the appearance of Ixodes ticks are not of that species.
After
hatching, ticks go through three stages: larval, nymph, and adult.
Blood
meals are required at all three stages and provide opportunities
for infection. The larvae attach to mice and acquire the infection.
Nymphs
attach to a wide variety of animals and transmit the infection.
Most
human bites are by nymphs, which are small and usually undetected.
Only
30 percent of patients with Lyme disease can recall a tick bite.
Nymphs
must remain attached for at least twenty-four hours and possibly
48 hours to transmit infection.
Infection
rates approach 100 percent only after more than 100 hours attachment.
Adult
ticks usually attach to deer. Eliminating the deer population greatly
reduces the incidence of Lyme disease.
The
white-footed mouse, Peromyscus leukopus , is the most significant
host for Lyme disease spirochetes in the Northeastern and north
central regions, and provides the reservoir for infection. (Wild
animals usually are not affected by the organisms
The
clinical aspects of Lyme disease are divided into three stages or
phases.
In
stage one, the acute localized phase ,
which is characterized by the typical skin rash, the organisms are
limited to the area in which the tick bite occurred.
In
stage two, the acute disseminated phase ,
the organisms are spread throughout the body and produce widespread
skin lesions as well as cardiac and neurologic disorders. Stage
three, the chronic disseminated phase, is characterized by arthritis.
The
typical skin rash of Lyme disease is a single red plaque that has
been named, Erythema Chronicum Migrans ,
or ECM. This plaque usually appears 2-14 d (range: 3-21d) after
the tick (nymph) bite.
It
starts as a red papule or macule and expands outwardly, often with
central clearing. The ultimate diameter is usually 5 to 20 cm but
these lesions range from 3 to 68. Usually the plaque is asymptomatic
except for its appearance, minor burning, itching, or pain may be
present.
The
plaque appears at the site of bites, which usually is where clothing,
such as underwear on the thigh, groin or the axilla, or a belt at
the waist, stopped the tick's progress.
The
plaque does not vesiculate, which helps distinguish it from erythema
multiforme. If the patient receives no treatment (antibiotics) the
plaque fades after four weeks (range: 1 to 14 weeks).
With
treatment, it disappears more rapidly. The rash occurs in over 80
percent of infected individuals, and possibly more, particularly
individuals who are aware of the possibility of infection and are
watching for a plaque.
A
flu-like syndrome typically accompanies the skin lesions, and is
characterized by malaise, fatigue, a low-grade intermittent fever,
arthralgias and myalgias. Tender lymphadenopathy is often present
near the ECM.
Serology
is usually nonreactive at the time ECM appears, but often becomes
positive while the lesion is present.
IgM
antibodies appear first; IgG appears later.
Organisms
can be cultured from the leading edge of ECM lesions, the only site
where organisms can be found with significant frequency. Special
culture media is required; few laboratories outside endemic areas
stock that media.
The
second stage begins 4 wks (Range: 0-10 wks) after ECM appears, but
often overlaps the first and third stages.
Manycharacteristic
yndromes affecting different systems are described:
Multiple
skin lesions termed secondary ECM
appear in 10 to 15 percent (as high as 50 percent in some studies)
of untreated patients. The secondary skin lesions are smaller than
the primary and migrate less. They can be located anywhere, and
number from twenty to over one hundred.
Nervous
system infection occurs in 15 to
20 percent of untreated patients:
Peripheral
nervous system involvement
is most common and is characterized by radicular pain most often
in the limb that was the site of the bite.
Meningoencephalitis
("Aseptic
Meningitis") appears in 8 to 15 percent of untreated individuals
and is characterized by a fluctuating headache, photophobia, and
meningismus. The cerebrospinal fluid may contain leukocytes (10–100/mm
3 ) and increased protein. Organisms are rarely cultured from the
CSF.
Subarachnoid
Nerve Root Inflammation . Facial
nerve palsy is most common and is often bilateral. It lasts from
weeks to months, but recovery is usually complete. Other cranial
nerves that may be involved: III, IV, and VI are involved more often
than V and VIII, which are involved more often than IX through XII.
Chronic
Confusional State may interfere with
daily cognitive function and memory. It is seen with "some
frequency," but more precise incidence data apparently is unavailable.
The cerebrospinal fluid, CT and MR scans, and neurologic examination
often are completely normal. Only detailed neuropsychological testing
discloses cognitive defects, and these are usually reversible with
antibiotic therapy.
Multifocal
leukoencephalitis resembling multiple
sclerosis is extremely uncommon. It may be acute and fulminant or
slowly progressive.
Cardiac
abnormalities appear in 4 to 8 percent of
untreated infected persons. EKG evidence of myocarditis or pericarditis
is present in 60 percent. Mild left ventricular dysfunction occurs
in half, but congestive heart failure is infrequent. Conduction
defects are common, and atrioventricular (AV) block—first to third
degree—is most frequent. Hospitalisation is usually required for
monitoring, and some patients require transvenous pacing. The cardiac
abnormalities usually resolve completely, but three of the four
reported deaths resulting from Lyme disease have been caused by
cardiac involvement. (The fourth resulted from ARDS.)
Arthritis
is common and occurs in 60 percent of untreated
patients. It begins up to two years after onset, and is characterized
by recurrent, asymmetric, oligoarticular pain and swelling.
Only
one joint at a time is involved, but as many as ten joints can be
involved at once. The median duration of the arthritic episodes
is eight days.
The
frequency of joint involvement is: Knee > Shoulder > Elbow
> TMJ > Ankle > Wrist > Hip > Hands and Feet.
The
diagnosis of Lyme disease is based primarily on clinical findings,
and treating patients with early disease solely on the basis of
objective signs and a known exposure is appropriate.
B
burgdorferi can be cultured from 80
percent or more of biopsy specimens taken from early erythema migrans
lesions. However, the diagnostic usefulness of this procedure is
limited because of the need for a special bacteriologic medium (modified
Barbour-Stoenner-Kelly medium) and protracted observation of cultures.
When
serologic testing is indicated, CDC recommends testing initially
with a sensitive first test, either an enzyme-linked immunosorbent
assay (ELISA) or an indirect fluorescent antibody (IFA) procedure,
followed by testing with the more specific Western immunoblot (WB)
test to corroborate equivocal or positive results with the first
test. Antibodies often persist for months or years following successfully
treated or untreated infection. Seroreactivity alone cannot be used
as a marker of active disease.
Neither
positive serologic test results nor a
history of previous Lyme disease assures that an individual
has protective immunity. Repeated infection has been documented.
Treatment
of Lyme Disease
Treatment
of early stage disease (ECM or secondary skin lesions) is almost
always successful and stops progression of lesions and prevents
development of subsequent disorders.
Doxycycline,
except in pregnant patients, or amoxicillin are the antibiotics
of choice.
Treatment
for arthritis consists of oral or intravenous antimicrobials given
for much longer periods. The success rate is much lower—apparently
30 to 60 percent.
Controversies:
Chronic Lyme disorder or “Post Lyme Syndrome”
According
to a recent report 20 percent of the individuals with a typical
erythema migrans skin lesion will get well and have no further problems
without any treatment.
Of
those treated at this early stage, over 90 percent develop no subsequent
evidence of Lyme disease.
Lyme
disease ranks behind only AIDS in media coverage and may be greatly
overdiagnosed. Only 20 percent of the patients referred to Allen
Steere's Lyme disease clinic at New England Medical Center actually
have the disease.
Alternative
views of diagnostic criteria and treatment strategies have been
presented by patient advocacy groups and in newsletters devoted
to Lyme disease.
Steere
has stated in publications that the chronic fatigue syndrome and
fibromyalgia are not part of the spectrum of Lyme disease. This
disabling syndrome is similar to chronic fatigue syndrome or fibromyalgia.
Persistent
complaints are generally non-specific and include arthralgias, myalgias,
cognitive difficulties, fatigue, malaise, dizziness, stiff neck
and photophobia.
Some
patients are totally disabled. Such persistent disability is most
common in individuals who have not been treated in the early stages
of their infection. In some the treatment has been delayed for almost
a year. Additional patients have had symptoms of early dissemination
of the infection to the nervous system.
Does
chronic Lyme disease really exist? If so, how should it be treated?
At the present time no definite answer can be given and cases should
be referred to an Infectious Disease specialist. General treatments
for chronic pain should be utilized.
Lyme
disease Prevention
A
successful Lyme disease vaccine for humans was developed. But the
vaccine was expensive and recommendations for its use by the Advisory
Committee for Immunization Practices would have limited it to approximately
1 percent of the population. Some concern about its safety apparently
existed also, although the available data on outcomes did not support
these concerns. Sales of the Lyme vaccine for humans were so small
that the product was withdrawn from the market in February 2002.
A
Lyme disease vaccine for dogs has been available since 1990. This
vaccine, a chemically inactivated, whole-cell preparation of B.
burgdorferi formulated with a polymer-based adjuvant, is not
considered suitable for humans because it may induce immunopathology
through cross-reactions with human antigen
The
current status of prophylactic antibiotics is unresolved, but the
administration of a single 200 mg oral dose of doxycycline following
the discovery of an attached and engorged tick—not just an attached
tick—appears reasonable.
Mediterranean
spotted fever
Mediterranean
spotted fever is also known as Marseille fever, South African tick
bite fever, Kenya tick bite fever, India tick typhus, and Boutonneuse
fever. It is endemic in the Mediterranean and is caused by Rickettsii
conorii. The major vector is the dog tick Rhipicephalus
sanguineus.
As
so all spotted fevers, it usually occurs during warm weather months.
Infections are usually mild in children and young adults. Individuals
at greatest risk are the elderly, alcoholics, and individuals with
glucose-6-phosphodehydrogenase (G-6-PD) deficiency.
Tick-borne
encephalitis
(TBE)
is caused by members of the flavivirus family that can affect the
central nervous system. Although TBE is most commonly recognised
as a meningo-encephalitis, mild febrile illnesses can also occur.
TBE
is transmitted to humans by the bite of an infected tick or, less
commonly, by ingestion of unpasteurised milk from infected animals,
especially goats
The
virus is maintained in nature by small mammals, domestic livestock
and certain species of birds.
Men
tend to be infected than women and most of these infections are
caused by leisure activity such as hiking and walking.
Incidence
peaks in spring and early summer, but can occur throughout the year
incubation
period is from two to 28 days
Tick
activity starts when soil temperature rises to 5-70 degrees C in
March or April and ends in fall. In Mediterranean countries ticks
are more active November-January. Ticks are worse in wet summers
and mild winters.
The
risk of infection from specific tick bites ranges from 1:200-1:900.
People at highest risk of being bitten include agriculture/forestry
workers, hikers/ outdoorsmen and collectors of berries and mushrooms.
These ticks attach to humans at hair-covered portions of the scalp,
ears, arms, knee joints, and hands and feet.
TBE
occurs in most or parts of Austria, Germany, southern and central
Sweden, Hungary, France (Alsace region), Switzerland, Norway, Denmark,
Poland, Croatia, Albania, the Baltic states (Estonia, Latvia and
Lithuania), the Czech and Slovak Republics, Hungary, Russia (including
Siberia), Ukraine, some other countries of the former Soviet Union,
and northern and eastern regions of China.
There
are three versions of the disease related to the virus subtypes,
namely European, Far Eastern and Siberian types.
European
version biphasic
with an initial viremic phase of fever and influenza-like symptoms
followed in some cases (after an afebrile period of one to 20 days)
by central nervous system involvement.
Case
fatality rate of the European version is 1% .Long-lasting or permanent
neuropsychiatric sequelae are observed in 10–20% of affected patients.
Far
Eastern version has
a more gradual in onset and normally takes a more severe and longer
course with a reported mortality of 5–20%.
Prevention
is by wearing appropriate clothing, removing ticks before they start
feeding, immunisation (Austria has vaccinated its population and
has lower incidence than neighbouring Czech Republic).
Unvaccinated
individuals bitten by ticks in endemic areas should seek local medical
advice
Unpasteurised
milk should not be drunk. The vaccine is recommended particularly
for spring and summer travel in warm, forested parts of the endemic
areas, when ticks are most prevalent.
Tourists
who hike, camp, hunt and undertake fieldwork in endemic forested
areas should be vaccinated
TBE
vaccine is recommended for those who will be going to reside in
an area where TBE is endemic or epidemic and particularly those
working in forestry, woodcutting, farming and the military.
Relapsing
Fever
Relapsing
fever is a bacterial illness called so because of the unresolved
recurrent fever in untreated people. There are two types:
Louse-borne
variety is found in areas of
poverty with epidemic occurring after natural disasters. They live
and proliferate in the clothing.
The
tick-borne variety is found
in Africa, Southern Europe, Middle East, Asia, Western U.S.A. and
Canada.
Tick
Borne Relapsing Fever
Borreliae,
which belong to the order of Spirochaetales, are helical, actively
motile spirochetes. Strains are not classified by morphology, but
by specificity of the tickspirochete relationship, the range
of animals susceptible to infection, and cross immunity. Human
Borrelia infections occur almost worldwide and produce epidemic
relapsing fever (louse-borne), endemic relapsing fever (tick-borne),
and Lyme disease.
Borrelia
recurrentis , the organism that causes
tick-borne relapsing fever is transmitted to humans by several species
of soft ticks (Argasidae) in the genus Ornithodoros. (Louse-borne
relapsing fever also is caused by Borrelia recurrentis ,
but is called epidemic relapsing fever.) They are leathery, wrinkled,
or granular organisms, often gray in color, that live in deserts
or under dry conditions in wet climates, hiding in crevices in buildings
such as huts, log cabins, cattle barns, and uninhabited houses,
or burrowing into loose soil.
Soft
ticks are adapted for feeding rapidly and leaving promptly; they
are rarely found on a host. Since soft ticks generally feed for
only a short period (thirty minutes or so), the subject may be unaware
of any recent tick bites. They can survive many years without a
blood meal.
Rodents
and other mammals serve as a natural source of infection for the
ticks. The infection is transmitted by the tick bite (saliva), and
also sometimes by contamination of the bite wound with infective
fluid produced by feeding ticks just before they detach. Transtadial
and transovarial transmission of the agent occurs readily; thus,
the ticks also are reservoirs of infection.
Relapsing
fever is endemic across central Asia, most of Africa, parts of the
Middle East, and North and South America. Worldwide, several hundred
cases are reported each year. Approximately thirty to fifty cases
occur annually in the United States, primarily in Oregon, Washington,
and northern California.
Geographic
foci of tick-borne relapsing fever infection are restricted to Ornithodoros-infested
areas. Known vectors of tick-borne relapsing fever in the western
United States include Ornithodoros hermsi, Ornithodoros parkeri,
and Ornithodoros turicata. O hermsi is a rodent parasite
widespread in the Rocky Mountain and Pacific Coast states. Often
found in crevices of vacation or summer cabins. O. turicatais
is found in southwestern United States, extending southward
into Mexico.
These
species are often found in burrows used by rodents or burrowing
owls.
In
Central and South America, Ornithodoros rudis is considered
the most important vector. It feeds on domestic birds and humans.
In Africa, Ornithodoros moubata and Ornithodoros erraticus
are proven vectors. O moubatafeeds on humans, warthogs,
domestic pigs, antbears, and porcupines. It is often found in cracks
in walls, and in earthen floors of huts.
Tick-borne
relapsing fever is characterized by bouts of fever that alternate
with afebrile periods. The onset is usually sudden and is characterized
by fever that often is higher than 39ºC . Often accompanying
the fever are shaking chills, severe headache, myalgias, arthralgias,
nausea and vomiting, muscular weakness, and lethargy. A transitory
petechial rash is common during the initial attack. In some cases,
meningeal inflammation and peripheral facial palsy have occurred.
In
untreated patients, the fever ends in an average of three days (range
one to seventeen), an event accompanied by sweats and intense thirst.
An average of six to seven days later, but with a considerable range,
the fever reappears.
Three
relapses is the average, but as many as ten or more can occur. The
relapses tend to be progressively less severe.
The
relapsing nature of this illness appears to be related to antigenic
variation. As an immune response develops to the predominant spirochetal
antigenic strain, variant strains multiply and cause a recrudescent
infection.
Diagnosis
requires a high index of suspicion. After an incubation period of
about eight days (range, five to fifteen), individuals with tick-borne
relapsing fever may not associate the illness with a visit to a
park or similar location where ticks are encountered. Identifying
the spirochetes in thick or thin blood films, or dark field preparations
of fresh blood usually makes the diagnosis.
Laboratory
findings may include neutrophilic pleocytosis of the cerebrospinal
fluid, peripheral leukocytosis, thrombocytopenia, and hypophosphatemia.
Serologic
testing for tick-borne relapsing fever can be carried out with an
enzyme-linked immunosorbent assay. This procedure is not widely
available.
When
tick-borne relapsing fever is untreated, the mortality rate is between
2 and 10 percent, mostly in infants..
Tetracyclines
are effective against tick-borne relapsing fever. Oral tetracycline
taken for seven days has been reported successful.
Prevention
of relapsing fever consists of avoiding tick-infested areas or,
when this is not possible, reducing the possibility of tick bites
with repellents or insecticides. Additional measures include fumigating
rodent nesting sites in human habitations, rodent-proofing buildings
in areas where the ticks are endemic, and eliminating rodent access
to unnatural food sources
Q
Fever
Q
Fever is a worldwide zoonosis affecting domestic and wild animals
caused by Coxiella burnetii . Tick to human transmission
is rare.
The
infection presents as a flu-like illness with fever, headache, myalgias
and pneumonitis. Infected individuals may have abnormal liver function
tests, jaundice, and hepatomegaly. The infection usually resolves
in 2 to 4; tetracycline may shorten the course. Infections may become
chronic and produce granulomatous hepatitis and culture negative
endocarditis. Diagnosis is dependent upon serologic testing. Treatment
for chronic disease is not always successful; Tetracycline may be
needed for at least twelve months.
Rocky Mountain Spotted Fever
(Choix
fever, new world spotted fever, Pink fever, Tick fever)
This
is a tick-borne illness and usually affects 600-800 people per year
in the United States, mostly in the southeast states (Oklahoma,
Tennessee, the Carolinas, Georgia and Virginia). It is also in Central
and South America.
The
tick responsible is more active in spring and summer. Children between
5-9 years are most commonly bitten. One reason is that they are
more likely to brush against tick carrying shrubbery and get bitten.
Rocky
Mountain Spotted Fever is related to typhus and caused by a rickettsia
(bacteria-like organism) transmitted by ticks (in the eastern U.S
it is the deer tick, while in the western U.S it is the wood tick).
Symptoms
of Rocky Mountain Spotted start 1-2 weeks after the tick bite and
are usually sudden with high fever, chills, muscle aches, severe
headache and vomiting. A crusted, raised, lump may be at the with
lymph nodes swollen. The characteristic rash of Rocky Mountain spotted
fever begins 1-10 days after the onset of fever.
Small
red spots begin at the extremities (hands, feet, ankles) and spread
centrally (towards the trunk) while usually sparing the face. With
progression these rashes became purpuric (bleeding under the skin)
so that they will not blanch with pressure. Complications of this
disease can lead to brain, kidney, liver, lung failure, and death,
if untreated. Treatment is with tetracycline or a suitable alternative.
Diagnosis
is on history and collection of symptoms. Serologic tests take days
to develop.
It
is important to note that although this rash is typical, not all
cases have the rash or it may be very faint or hard to see, so its
absence does not rule out the disease. Prognosis related to speed
of treatment so an antibiotic may be started without a specific
diagnosis (many of the tick borne diseases have similar treatments).
Different
types of rickettsia cause other “spotted fevers” and their name
usually tells of their location.
Avoidance,
diagnosis and treatment are similar to Rocky Mountain spotted fever,
although the severity of symptoms can vary between them :
-Mediterranean Spotted Fever,-Kenyan Tick Typhus,-African
Tick Bite Fever,-Israeli Spotted Fever,-Astrakhan Fever (found in
the Caspian sea), Siberian Tick Typhus, Indian Tick Typhus, Japanese
Spotted Fever, Queensland Tick Typhus,and Flinders Island Spotted
Fever (Australia.
Early
intervention and treatment can reduce morbidity and mortality. Doxycycline
(Tetracycline) is the drug of choice; chloramphenicol is an alternative,
particularly for children and during pregnancy. Neither drug is
rickettsicidal. Antibiotics inhibit the organism until the body
can mount an immune response that eventually eradicates the organism.
The
dose of doxycycline is 25 to 50 mg/kg/day orally in four divided
doses with a maximun of 2gr/day for adults. Dosage for chloramphenicol
is 50 to 75 mg/kg/day orally for adults and children. Treatment
should continue until the individual has been afebrile for at least
48 hours, or a minimum of five to seven days. Relapses are uncommon
but may be treated with the same medication.
Stari
Southern Tick Associated Rash Illness (Master's disease)
In
the late 1980's and 1990's, physicians in the southeastern and south
central United States began to recognize individuals who developed
a rash essentially identical to erythema migrans, the typical earliest
stage of Lyme disease. This did not develop other manifestations
of that infection. The rash was found to be associated with the
bite of the lone star tick, Amblyomma americanum .
This
simulator of Lyme disease has been named Southern Tick-Associated
Rash illness (STAR Illness or STARI).
The
typical clinical finding is a roughly circular erythematous rash
centered on the site of the tick bite. Central clearing may be present.
The rash is identical to erythema migrans.
Other
symptoms that may be present include fatigue (50 percent), headache
(43 percent), muscle stiffness including stiff neck (36 percent),
and fever (29 percent). However, signs and symptoms of the second
or third stages of Lyme disease do not ensue, even in patients who
are not treated.
No
specific laboratory studies are available. Spirochetes have been
seen in lone star ticks with microscopy, and a spirochete has been
detected by DNA analysis and given the name Borrelia lonestari
.
Lone
star ticks, Amblyomma americanum have a life cycle and
ecologic requirements are similar to Ixodes ticks.
All
three stages—larval, nymph, and adult—aggressively bite people.
However, live spirochetes are observed in only 1 to 3 percent of
these ticks. Pictures, including size comparisons, are available
at ent.iastate.edu/imagegal/ticks
Individuals
with the rash have been given a variety of antibiotics, most commonly
doxycycline. The treatment has been successful, but the rash and
other symptoms disappear without therapy.
Serologic
testing for Lyme disease may be advisable. Until the results are
received, doxycycline therapy, which is effective in the early stages
of that infection, appears reasonable. However, Lyme disease is
uncommon in most of the area where lone star ticks are found.
Tick
Typhus
Tick
Typhus is transmitted to humans by ixodid ticks. An eschar scar
develops at the bite site and the rickettsia (small bacteria like
organism) incubates for about 1 week. A fever develops with a maculopapular
rash (which may be very small). This rash and eschar are very typical
of tick typhus but often this illness is confused with malaria or
a traveller's diarrhea infection. A headache is also noted.
Usually
symptoms are mild but kidney, liver and neurological damage can
occur.
Doxycycline
is an effective treatment and doxycycline when given daily for the
prevention of malaria will prevent typhus.
Infective
ticks infest domestic and wild animals particularly dogs in cities.
Walking in brush is risky. Preventative measures for ticks include
wearing the trouser cuffs inside the socks, DEET use, sleeping on
elevated cots and checking each other for ticks.
Epidemic
typhus is more severe but rarer and is caused by human lice. It
is seen in poverty stricken areas (Rwanda, Uganda, and Ethiopia).
Travelers are unlikely to experience epidemic typhus even if backpacking.
North
Asian Tick Typhus
North
Asian tick typhus is also known as Siberian tick typhus. It is endemic
in Siberia and is closely associated with steppe landscapes. The
causative organism is Rickettsia siberica ; the vectors
are several species of Dermacentor and Haemaphysalis
ticks. Humans are accidental and dead-end hosts.
Queensland
Tick Typhus
Queensland
tick typhus is caused by Rickettsia australis , and is
endemic in southern and northern Queensland. The vector is the scrub
tick Ixodes holocyclus
Tick
Typhus links
Masta
http://www.masta.info/library/factsheets/tick_typhus_fact_sheet.pdf
CDC
http://www.cdc.gov/ncidod/diseases/submenus/sub_typhus.htm
Tick
Paralysis
Tick
paralysis has been recognized since 1912, and involves humans and
animals. This disorder is found world
wide, but occurs most often in North America and Australia. The
Pacific Northwest and Rocky Mountain areas account for most cases.
At least forty-three species of ticks have been reported to cause
tick paralysis.
Tick
paralysis occurs during the spring and summer when ticks are feeding.
Children are affected more often than adults, and girls are affected
twice as often as boys, possibly because their long hair hides the
tick. Men are affected more often than women, probably because they
participate in activities that bring them into contact with ticks
more frequently.
Tick
paralysis is thought to be caused by an unidentified venom secreted
by the tick salivary glands during a blood meal. The disorder first
appears five to six days after attachment of the tick. The earliest
symptoms are restlessness, irritability, and paresthesias in the
hands and feet. Twenty-four to forty-eight hours later, an ascending,
symmetric, flaccid paralysis with loss of deep tendon reflexes appears.
Weakness typically is initially worse in the lower extremities .
Within
one to two days, severe generalized weakness develops. Cerebellar
dysfunction with ataxia and in coordination may appear. Dysfunction
may progress to bulbar and respiratory paralysis. Isolated facial
paralysis may occur in individuals with ticks imbedded behind the
ear.
The
paralysis resolves after removal of the tick, which establishes
the diagnosis. In North America, recovery is usually rapid. It starts
within hours and is complete within days. Other than removing the
tick, no therapy other than supportive care is needed (or available).
However, undiagnosed tick paralysis can be fatal.
Australian
tick paralysis may continue to progress for 48 hours after the tick
is removed, and total recovery is much more prolonged
Tularemia
The
peak incidence is in the summer months, which correlates with the
life cycle of the tick vectors, but infections also occur during
the winter months in association with hunting. Over 75 percent of
the infections are in men, generally in adults over the age of thirty.
Humans
are highly susceptible to infection with the organism, which most
commonly occurs through the bite of an arthropod. Infections follow
bites by ticks, fleas, mites, and deer flies. Infection also is
produced by contact with infected animals, most commonly rabbits,
which can be reservoirs because they have a high natural resistance
to the organism and become carriers. F tularensis infects
hundreds of different vertebrates and invertebrates, but most either
die or recover and eliminate the organisms. Just a few have a significant
role in the transmission of infection to humans. In the United States,
these include rabbits, voles, squirrels, muskrats, and beavers.
(Less common routes of infection include aerosol droplets, contact
with water, and animal bites.) Human-to-human spread does not occur.
Ticks
are the most common vector in the United States, particularly in
the central and Rocky Mountain states, where most infections occur.
Biting flies are responsible for many infections in California,
Nevada, and Utah. The most commonly infected ticks are the Lone
Star tick ( Amblyomma americanum ), the dog tick ( Dermacentor
variabilis ), and the wood tick ( Dermacentor andersoni
).
Hunters
contact infected carcasses when skinning, dressing, and eating deer,
rabbits, muskrats, beavers, squirrels, and birds. Domestic cats
have transmitted the organism to humans, probably by transient colonization
of the cat's mouth or claws after killing or feeding on infected
prey. F tularensis can survive freezing for months, but
thorough cooking of game should minimize the risk of transmission.
Francisella
tularensis is a small, gram-negative
coccobacillus. It is an intracellular organism and the immune response
to it is dependent on cell-mediated mechanisms. The organism enters
the body by a local lesion that can vary in location, resulting
in different manifestations of the disease. The sites of inoculation
include the skin, conjunctiva, oropharynx, respiratory tract, and
occasionally, the gastrointestinal tract.
After
the bite of an infected arthropod, the incubation period averages
about three to five days, but the range can be anywhere from one
to twenty-one days. After cutaneous inoculation, F tularensis
multiplies at the local site and produces a papule. Ulceration
follows two to four days later. At this point, organisms spread
locally to regional lymph nodes and then may disseminate through
the blood and lymphatics. Bacteremia is thought to be common during
this early phase, but is rarely documented.
Six
forms of the disease have been described—ulceroglandular, glandular,
oculoglandular, oropharyngeal, typhoidal, and pneumonic—based on
clinical presentation of the illness. These forms frequently overlap
in individual patients.
The
ulceroglandular form is most common in the North
America, and makes up 48 to 75 percent of the infections. The skin
lesion can appear before, during, or after the lymphadenopathy.
The initial lesion is a painful papule, usually red in color that
becomes necrotic and develops into a tender ulcer with a raised
border. Animal bites or scratches usually produce ulcerations on
the hands or forearms; tick bites tend to produce ulcerations on
the trunk, inguinal area, legs, and the head and neck region. Multiple
skin lesions can occur with exposure to more than one animal. If
untreated, the ulcer can take weeks or months to heal and frequently
leaves a scar.
Typhoidal
tularemia resemble acute bacteremia
caused by more common gram-negative organisms. The onset usually
is abrupt. Fever is as high as 39.4°C (103°F), and chills,
headache, generalized aching, vomiting, and occasional photophobia
are present. Fever can persist for weeks if the infection is untreated.
Hepatosplenomegaly is also reported, but rarely occurs in the acute
stages of the infection. Skin rashes are quite common in this form
of infections. Exanthems generally are of the maculopapular type
and are located on the forearm and hand, including the palm and
fingers.
The
usual laboratory procedure is a serologiy.Antibodies are usually
detected in the second week of illness, and peak between the fourth
and fifth week after infection. Routine culturing of this organism
is not encouraged , because it is hazardous for laboratory
workers.
If
tularemia is suspected, laboratory personnel should be notified.
Hunters
and others who handle wild animals should be instructed not to skin,
or dress game without appropriate gloves, masks, and eye covers.
Wild game should be well cooked. Exposure to ticks should be controlled.
Overview
Tick
bites are common both domestically and in travellers. Severe disease
is not commonly considered with the exception of Lyme disease.
A
preventative Algorithm for Ticks can be derived from the similar
ABC method for control of malaria.
A
wareness- The
public is generally aware of the possibility of Lyme disease in
many areas. Physicians need to keep an open differential diagnosis
for other illnesses when confronted with a tick bite. Because the
full spectrum of diseases is not seen (i.e. very little rash in
Rocky Mt spotted fever) routine serolgies should be ordered on patients
with a history of travel to endemic areas. Co-infections with different
Tick borne diseases are possible.
B
ite avoidance (Clothing, Insect repellent,
Insecticide, Behaviours)
Understanding
that Ticks don't jump on people but are often acquired from brushing
against low-lying shrubbery. Wearing longs leaves and pants will
dissuade entry. The tick will migrate to find a suitable feeding
site. Ankle and wristbands treated with permethrin insecticide provide
a contact kill to the tick.
Protective
Clothing Clothing plays a major role
in avoiding tick bites. Long sleeves and long pants are best. Pants
should be worn with gaiters or tucked into high-top boots or socks.
Ticks are more easily seen on such clothing.
Protecting
pets with proper flea collars protects both the pet as well as the
owner from the ticks.
Insect
Repellents The best insect repellent is DEET or N, N-diethyl-meta-toluamide
(N, N-diethyl-3-methylbenzamide). It has been reported to be effective
against chiggers, ticks, fleas, and biting flies in laboratory studies,
but some field studies have found it only about 80 percent as effective
for ticks as it is for mosquitoes. It is not effective against flies.
DEET is removed by sweating, absorption, evaporation, wiping, and
rain, and in its unmodified form must be reapplied several times
a day. However, two newer formulations have been developed: a microencapsulated
product in which DEET is encased in a protein shell, and a polymerized
form. Both persist much longer than standard preparations—at least
twelve hours — and absorption through the skin is also greatly reduced.
The
American Academy of Pediatrics has recently changed its recommendation
to a more concentrated DEET preparation, 30 percent or less rather
than, less than 10 percent, and now considers such preparations
that are safe for infants as young as two months rather than limiting
application at two years.
Insecticides
Permethrin® (permanone tick repellent)
is a pesticide derived from chrysanthemums that is highly effective
against arthropods when used on clothing. This agent can
kill insects so rapidly that it sometimes is thought to be a repellant,
yet by itself, it has essentially no toxicity for humans.
A
number of spray preparations are available. Clothing should be sprayed
until damp and allowed to dry. Although sprays are convenient, they
last only two to three washings.
Sawyer
used to sell a 13.3% Permethrin Solution called PermaKill. Immersing
clothing in a 1.5 percent solution and allowing it to dry, provided
protection through approximately fifty washings, probably the life
of most garments. Permethrin is such an efficient insecticide that
hanging treated clothing in a closet effectively eliminates almost
all arthropods. (When clothing is first removed from the solution
is has a strong organic solvent odor reminiscent of xylene. However,
once the clothing dries the odor completely disappears.)
R+C
spray contains permethrin.
C
ompliance with medications
The
antimalarial and antibiotic doxycycline is effective against many
Tick borne rickettsia, typhus and Lyme disease. Although chemoprophylaxis
against tick bites is not suggested the choice of doxycycline for
malarial chemoprophylaxis would have this benefit.
The
Lyme disease vaccine Lymerix has been discontinued.
The
TBE vaccine is available in Canada and may be considered for high-risk
travellers. Travelers should take care against all ticks since of
course other diseases share the geographic area with TBE.
D
iagnosis
Tick
borne diseases are not commonly thought of first line. Many patients
with encephalitis present without the clear history of a tick bite.
Early
referral to local Infectious disease specialists is recommended
to order the correct serology.
Lyme's
disease is confusing and the possibility of seronegative Lyme's
disease should be acknowledged.
Collecting
blood for acute and convalescent serology is important.
Clinicians
should be aware on co-infections and be prepared to order additional
serolgies and blood smears (babeosis, malaria) even in patients
who have a diagnosis and are responding to treatment.
Tick
Paralysis is worth looking for in all patients with an unexplained
neurological decline and can actually save someone's life by finding
the occult tick!
E
nvironmental Control Tick Control:
The
most effective measure for reducing the number of ticks around residences
is to apply acaricides to the vegetation on which ticks live. A
single application of agents such as carbaryl, cyfluthrin, or deltamethrin
in early May can reduce populations of I. scapularis nymphs
on residential properties by 68 to 100 percent. One well-timed application
is enough.
These
ticks are frequently found along the edges of forests and spill
out into adjacent vegetation and lawns. Because the ticks are extremely
sensitive to desiccation, increasing exposure to sun and air by
removing dead leaves and brush. A border of wood chips where lawns
abut forests reduces the number of ticks on lawns, presumably be
creating a drying barrier. Adult I. scapularis ticks preferentially
feed on deer, and reducing the deer population reduces the number
of such ticks. However, all or nearly all deer must be removed to
decrease the number of ticks substantially. Fencing that, keep deer
out of residential areas is an acceptable alternative in areas where
deer removal is not acceptable or practical. Baited devices that
lure deer to a site where they can be treated with acaricides are
being evaluated.
Devices that lure white-footed
deer mice (reservoir for B. burgdorferi) , into situations
where they can be treated with the acaricide fipronil to kill ticks
have appeared promising in preliminary tests. In one Massachusetts
study, cotton balls treated with permethrin were gathered by mice
and taken back to their dens. Ticks on the mice were killed by the
permethrin.
How
to remove a Tick
Because
some ticks secrete pathogens at the beginning of feeding it is always
better to remove them as soon as possible. But some ticks do not
secrete theirs till after several hours of feeding so it makes sense
to carefully and deliberately remove the tick and not irritate it
so that it might vomit into the wound.
Because
of the cementum it may be difficult to remove a tick without pulling
skin with it.
Some
techniques like smothering it, pouring alcohol on it or poking it
with a hot needle will irritate it and should be avoided.
Longitudinal
traction is best. Avoid crushing the tick with tweezers or twisting
its head off.
Steady
traction is best. Inspect the wound for retained body parts.
Send
the tick in a urinary specimen bottle. Ticks will quickly desiccate
particularly since they may be missing their hypostome that was
ripped open. To avoid desiccation in the specimen bottle put a square
of moistened paper towel inside. If you find one- look for more!
Special
thanks to Dr Jim Wilkerson (Pathology) of Utah who had helped prepare
much of this material for me.
Dr
Terry Galloway (Entemology) of Winnipeg been a great resource in
answering all my bug questions.
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