Mycoplasma Registry Reports- 7 Tick-Borne Diseases: symptoms & treatment

[Guest guest]

Rocky Mountain spotted fever, Lyme disease, ehrlichiosis, tularemia,

babesiosis, Colorado tick fever, relapsing fever

* * * * * * * * * * * * * * * * * * * * * * * * * * *

MYCOPLASMA REGISTRY REPORTS

for gulf war syndrome & chronic fatigue syndrome

© Dudley & Leslee Dudley 2005. All rights reserved.

MycoplasmaRegistry/ MycoReg@...

* * * * * * * * * * * * * * * * * * * * * * * * * * *

Tick-Borne Disease

ROBERT L. BRATTON, M.D., Mayo Clinic, sdale, Arizona

G. RALPH COREY, M.D., Duke University Medical Center, Durham, North

Carolina

RedNova.com - Dallas,TX,USA - June 26, 2005

http://www.rednova.com/news/health/158202/tickborne_disease/

Tick-borne diseases in the United States include Rocky Mountain

spotted fever, Lyme disease, ehrlichiosis, tularemia, babesiosis,

Colorado tick fever, and relapsing fever. It is important for family

physicians to consider these illnesses when patients present with

influenza-like symptoms. A petechial rash initially affecting the

palms and soles of the feet is associated with Rocky Mountain spotted

fever, whereas erythema migrans (annular macule with central

clearing) is associated with Lyme disease. Various other rashes or

skin lesions accompanied by fever and influenza-like illness also may

signal the presence of a tick-borne disease. Early, accurate

diagnosis allows treatment that may help prevent significant

morbidity and possible mortality. Because 24 to 48 hours of

attachment to the host are required for infection to occur, early

removal can help prevent disease. Treatment with doxycycline or

tetracycline is indicated for Rocky Mountain spotted fever, Lyme

disease, ehrlichiosis, and relapsing fever. In patients with clinical

findings suggestive of tick-borne disease, treatment should not be

delayed for laboratory confirmation. If no symptoms follow exposure

to tick bites, empiric treatment is not indicated. The same tick may

harbor different infectious pathogens and transmit several with one

bite. Advising patients about prevention of tick bites, especially in

the summer months, may help prevent exposure to dangerous vector-

borne diseases. (Am Fam Physician 2005;71:2323-30, 2331-2. Copyright

2005 American Academy of Family Physicians.)

Because people continue to interact with nature, patients will

continue to present to physician offices with tick-borne diseases. It

is important for family physicians to recognize these illnesses

because early, accurate diagnosis may lessen the morbidity and

mortality of these treatable diseases. This article provides an

update on the more common tick-borne diseases. Agents and

characteristics of tick-borne disease are summarized in Tables 1 and

2.1

-------------------------------------

Rocky Mountain Spotted Fever

-------------------------------------

EPIDEMIOLOGY

Rocky Mountain spotted fever is caused by Rickettsia rickettsii and

is the most common rickettsial disease in the United States.2 The

disease is limited to the Western hemisphere and occurs in all states

except Maine, Hawaii, and Alaska. The disease is more common in the

coastal Atlantic states from April to September, although infections

may occur year-round further south.3 The wood tick (Dermacentor

andersoni) is the principal vector in the western United States,

whereas the dog tick (Dermacentor variabilis) is the most common

vector in the eastern and southern United States. Transmission from

person to person is not thought to occur. The incidence of Rocky

Mountain spotted fever is highest in children five to nine years of

age.4

SIGNS AND SYMPTOMS

Typically in tick-borne diseases, a tick bite is recalled by 50 to 70

percent of patients.3,4 The onset of symptoms of Rocky Mountain

spotted fever usually begins five to seven days after inoculation.

Common symptoms include generalized malaise, myalgias (especially in

the back and leg muscles), fever, frontal headaches, nausea, and

vomiting. Other symptoms may include nonproductive cough, sore

throat, pleuritic chest pain, and abdominal pain. The classic

presenting symptoms include sudden onset of headache, fever, and

chills accompanied by an exanthem appearing within the first few days

of symptoms. Initially, lesions appear on the palms, soles, wrists,

ankles, and forearms. The lesions are pink and macular and fade with

applied pressure. The rash then extends to the axilla, buttocks,

trunk, neck, and face, becoming maculopapular and then petechial

(Figure 1(5)). The lesions may then coalesce to form large areas of

ecchymosis and ulceration. Respiratory and circulatory failure, as

well as neurologic compromise, may occur.6 Patients with glucose-6-

phosphate dehydrogenase (G6PD) deficiency are at especially high risk

for complications and poor outcomes.7

Strength of Recommendations

DIAGNOSIS

The diagnosis of Rocky Mountain spotted fever is based primarily on

clinical signs and symptoms. If a rash is present, the use of skin

biopsy and immunofluorescent staining for Rickettsia is highly

specific, although with only slightly more than 60 percent

sensitivity. Laboratory testing is of limited usefulness but may

include thrombocytopenia and hyponatremia.8 Elevation of specific

enzyme-linked immunosorbent assay (ELISA) and latex agglutination

titers usually is delayed until the convalescence period.

TABLE 1 Causative Agents, Vectors, and Geographic Distribution of

Tick- Borne Diseases

TABLE 2 Clinical Characteristics of Tick-Borne Diseases

Figure 1. Image of a patient with Rocky Mountain spotted fever; note

late rash on trunk.

TREATMENT

Fever and headache during peak months of tick exposure in endemic

areas should suggest Rocky Mountain spotted fever. Rash,

thrombocytopenia, and hyponatremia make immediate treatment

imperative. Antimicrobial agents for the treatment of Rocky Mountain

spotted fever include tetracycline, doxycycline (Vibramycin), and

chloramphenicol (Chloromycetin) for a minimum of seven days.9

Fluoroquinolones also may be effective, but are not recommended for

routine use in patients with Rocky Mountain spotted fever because of

a lack of evidence.10 For optimal effect, it is critical to treat

patients early in the course of their illness. According to the

Centers for Disease Control and Prevention, appropriate antibiotic

treatment should be initiated immediately when there is a suspicion

of Rocky Mountain spotted fever on the basis of clinical and

epidemiologic findings. Treatment should not be delayed until

laboratory confirmation is obtained.7

-------------------------------------

Lyme Disease

-------------------------------------

EPIDEMIOLOGY

Lyme disease is the most common vector-borne infectious disease in

the United States.9 The disease is caused by the spirochete Borrelia

burgdorferi. In the United States, the main vector is Ixodes

scapularis (Figure 2(11)), commonly referred to as the black- legged

or deer tick because the female tick often attaches itself to the

white-tailed deer during the winter. Natural reservoirs for B.

burgdorferi include the white-footed mouse and other small mammals.

The larvae or nymphs of the tick feed on the white-footed mouse and

become infected. Adult ticks or, more commonly, nymphs may then

infect humans. Studies using animals have shown that infected

nymphalstage ticks must remain attached for 36 to 48 hours or longer,

and infected adult ticks must remain attached for 48 to 72 hours or

longer, before the risk of transmission of B. burgdorferi becomes

substantial.12-15 There is no evidence that Lyme disease can be

transmitted by mosquitoes, flies, or fleas. Blood products have never

been associated with transmission of Lyme disease.16

SIGNS AND SYMPTOMS

Lyme disease typically develops in three stages. Stage 1 (early

localized) Lyme disease occurs seven to 10 days after tick bite.

Findings include typical rash (erythema migrans) in 75 percent of

patients at the site of the tick bite. The rash typically develops as

an annular macule or papule with central clearing that may expand to

a diameter of up to 50 cm. Other indications include influenza- like

symptoms of low-grade fevers, fatigue, arthralgias, headaches, cough,

and regional lymphadenopathy. Stage 2 (early disseminated) Lyme

disease occurs a few weeks after the initial infection. Symptoms

include multiple secondary cutaneous annular lesions, fever,

adenopathy, and central nervous system symptoms. Cough and

pharyngitis may occur. Stage 3 (late chronic disease) symptoms

include chronic arthritis, central nervous system impairment,

dermatitis, and keratitis. Other symptoms may include neurologic

abnormalities such as meningoencephalitis, Bell's-like palsy, and

radiculopathies, and myocardial abnormalities such as

atrioventricular block, pericarditis, and cardiomegaly.8

DIAGNOSIS

Early diagnosis of Lyme disease in a patient with typical erythema

migrans in an endemic area does not require laboratory confirmation.

However, ELISA testing is 89 percent sensitive and 72 percent

specific. Positive results on ELISA testing should be confirmed with

Western blotting. Polymerase chain reaction testing, although not

widely available, may be useful for the diagnosis, especially with

fluid from the joints of the affected patient.3 Isolation of B.

burgdorferi from most tissues and body fluids by culture is difficult

to achieve and requires weeks to grow before it can be analyzed.

TREATMENT

The risk of infection with B. burgdorferi after a recognized tick

bite is minimal, and is almost nonexistent if the tick was attached

less than 36 hours. Routine antibiotic prophylaxis is not

indicated.8,16 A cost-effectiveness analysis showed that prophylaxis

with one 200-mg dose of doxycycline was cost-effective only if the

likelihood of infection exceeded 3.5 percent, much higher than in the

typical practice setting.17 If symptoms develop, antibiotic treatment

is curative in most cases. Recommended antibiotic treatment includes

doxycycline (100 mg orally twice per day if patient is older than 12

years) or amoxicillin (500 mg orally three times per day or 50 mg per

kg per day orally for patients 12 years and younger). Cefuroxime

(Ceft\in; 500 mg orally, twice per day) or erythromycin (250 mg

orally, four times per day) can be prescribed for persons who are

allergic to penicillin or cannot take tetracyclines. Treatment

usually lasts 14 to 21 days for uncomplicated cases. Late or severe

disease, particularly with neurologic or cardiovascular

manifestations, requires treatment with intravenous antibiotics, with

a switch to oral therapy once the patient is no longer in high-degree

atrioventricular block. Treatment in these advanced cases should be

administered for at least 30 days. Late disease may be associated

with treatment failures, and re-treatment may be necessary.18

-------------------------------------

Ehrlichiosis

-------------------------------------

EPIDEMIOLOGY

Human ehrlichiosis has been reported in the United States with two

identifiable subtypes. Human monocytic ehrlichiosis (HME) is caused

by Ehrlichia chaffeensis, and human granulocytic ehrlichiosis (HGE)

is caused by Anaplasma phagocytophilum (formerly called Ehrlichia

equi or Ehrlichia phagocytophila). The two subtypes are clinically

indistinguishable but epidemiologically distinct.19

HME occurs most frequently in the south-central and southeastern

United States. It occurs year-round with the highest incidence in

June and July. In contrast to the tendency of Lyme disease and Rocky

Mountain spotted fever to occur in children, HME typically affects

adults. E. chaffeensis is found in Amblyomma amencanum (Lone Star

tick) and D. variabilis (dog tick). The white-tailed deer is the

principal animal reservoir.

The majority of cases of HGE occur in the upper midwestern and

northeastern United States. Adults who live in rural areas or have

exposure to tick-infested areas are most likely to be affected. The

I. scapularis species are the principal vectors, and the white-

footed mouse and white-tailed deer are the principal hosts.

SIGNS AND SYMPTOMS

The signs and symptoms of ehrlichiosis include an influenza-like

syndrome consisting of fever, chills, cough, malaise, headache, and

myalgia. Symptoms begin approximately seven days after tick bite and

include a maculopapular, macular, or petechial rash that affects the

trunk and upper extremities and, in rare cases (less than 5 percent),

the palms and soles. HME and HGE present with similar signs and

symptoms, but HGE rarely presents with the rash. Clinical

differentiation from Rocky Mountain spotted fever is difficult.

DIAGNOSIS

Laboratory findings in patients with HME and HGE include leukopenia,

thrombocytopenia, and elevated serum transaminase levels. Patients

presenting with a nonspecific influenza-like syndrome of fever,

chills, malaise, headache, and myalgia coupled with leukopenia and

thrombocytopenia should be treated empirically. The principal method

of diagnosing human ehrlichiosis is detection of seroconversion

during convalescence. A fourfold rise or fall in antibody titer with

a minimum peak of 1:64 and a single serum antibody titer greater than

or equal to 1:128 is necessary for the diagnosis.

TREATMENT

As with other tick-borne diseases, treatment of ehrlichiosis should

be started before laboratory tests confirm the diagnosis. Doxycycline

at a dosage of 100 mg twice per day for adults or 4.4 mg per kg per

day in two divided doses for children who weigh less than 45.4 kg (99

lb, 14 oz) is the treatment of choice.20 Tetracycline 500 mg orally

four times per day is an alternative. Chloramphenicol is considered

an alternative to prevent tooth staining, but there is a small risk

of aplastic anemia with its use. Treatment should be continued for at

least three days after fever subsides and until evidence of clinical

improvement, for a minimum of five to seven days.20 Severe cases may

require longer treatment courses.

-------------------------------------

Tularemia

-------------------------------------

EPIDEMIOLOGY

Francisella tularensis is the bacterium that causes tularemia (also

known as rabbit fever). The tick vectors include A. americanum and D.

variabilis in the southeastern and south-central United States and D.

andersoni in the west. Transmission of the bacteria occurs by

ingestion, inoculation, inhalation, or contamination. In the winter,

the most common route is through microlesions in the skin of hunters

who have skinned infected rabbits. In the summer, transmission occurs

via ticks, deer flies, and horse flies. Although less common,

consumption of undercooked infected meat and contaminated water also

can lead to infection.

SIGNS AND SYMPTOMS

Clinical manifestations of tularemia can be divided into various

syndromes, including ulceroglandular (the most common),

oculoglandular, oropharyngeal/gastrointestinal tract, pulmonary, and

typhoidal tularemia.8 Illness usually begins three to five days after

inoculation, with rapid onset of fever, chills, headache, malaise,

fatigue, and myalgias. Cough is present in about one third of

patients. Other findings may include skin ulcers, sore throat,

pleural effusions, pneumonia, acute respiratory distress syndrome,

and pericarditis.21 Nausea and vomiting also may occur. Within 24 to

48 hours, an inflamed papule appears at the infected site (e.g.,

finger, arm, eye, roof of the mouth) except in glandular or typhoidal

tularemia. The papule becomes pustular and ulcerates, producing an

ulcer crater with colorless exudate. Regional lymphadenopathy occurs

and may suppurate and drain. In children, the cervical or posterior

auricular nodes commonly are affected. In adults, the inguinal and

femoral nodes are more likely to be affected.

DIAGNOSIS

Tularemia should be suspected if the patient has been exposed to

rabbits, wild rodents, or ticks; has characteristic symptoms; and has

a primary pustular lesion on an extremity. Isolation of the organism

from skin lesions, lymph nodes, or sputum is diagnostic but dangerous

because the organism can be highly infectious. The disease is

considered a potential biologic weapon. Extreme caution should be

maintained when handling infected tissues or culture media. Acute and

convalescent titers also can confirm the diagnosis. Leukocytosis is

common, but the white blood cell count may be normal. Abnormal chest

radiographic findings (i.e., triad of oval opacities, hilar

adenopathy, and pleural effusions) are more likely with tularemia

than in other tick-borne diseases.22,23

TREATMENT

Treatment should begin before confirmatory laboratory tests are

obtained. If available, the treatment of choice for tularemia is

streptomycin (0.5 g intramuscularly every 12 hours until the

patient's body temperature is normal; thereafter, 0.5 g per day for

five days). Gentamicin (3 to 5 mg per kg per day, intramuscularly or

intravenously in three divided doses for seven to 14 days) also is

effective.24 If renal disease is present, the dose of gentamicin

needs to be reduced. Chloramphenicol or tetracyclines also have been

used, but relapses occasionally occur with these medications, and

they may not prevent node suppuration.3

-------------------------------------

Babesiosis

-------------------------------------

EPIDEMIOLOGY

Babesiosis is the only tick-borne disease in the United States that

is caused by a protozoan (Babesia divergens or Babesia microti).

Transmission occurs by the vector tick (various species of Ixodes).

Most cases occur in the northeastern United States.

SIGNS AND SYMPTOMS

Symptoms are similar to those of other tick-borne diseases and

include influenza-like symptoms one week after inoculation. Fever,

sweating, myalgias, and headache also occur. Babesiosis may resemble

falciparum malaria, with high fever, hemolytic anemia,

hemoglobinuria, jaundice, and renal failure, especially in asplenic

patients. Asymptomatic infection may persist for years in younger

adults.

DIAGNOSIS AND TREATMENT

Babesiosis usually is suspected in a patient with fever, hemolytic

anemia, and an appropriate exposure history. The diagnosis is made by

detection of protozoa in blood smears. A characteristic tetrad,

the " Maltese cross, " appears. Serologic testing and polymerase chain

reaction testing also are available.

Mild disease requires only symptomatic treatment. For severe cases

(e.g., persistent high fever, progressive anemia, rising

parasitemia), patients should be treated with quinine (Quinamm; 650

mg of salt orally, three times per day for seven days) plus

clindamycin (Cleocin; 600 mg orally, three times per day or 1.2 g

administered intravenously twice per day for seven to 10 days), or

with atovaquone (Mepron; 750 mg orally twice per day for seven to 10

days) plus azithromycin (Zithromax; 600 mg orally per day for seven

to 10 days).25 Reduced dosing is required in children. Exchange

transfusion has been used in severely ill patients with high

parasitemia.

-------------------------------------

Colorado Tick Fever

-------------------------------------

EPIDEMIOLOGY AND TRANSMISSION

Colorado tick fever is caused by an RNA orbivirus transmitted by the

D. andersoni wood tick. Between 200 and 300 cases are diagnosed each

year, predominantly in the Rocky Mountain region. Because of its

benign presentation, the infection often may go undetected, and the

annual incidence probably is much higher.26 Patients who are

immunocompromised or who have undergone a splenectomy are at

increased risk for severe complications.

SIGNS AND SYMPTOMS

Influenza-like symptoms usually begin within one week after

inoculation. Although approximately one third of patients have a sore

throat, more extensive involvement of the respiratory system rarely

occurs.2 The most significant feature is a biphasic or " saddleback "

fever associated with meningitis, rash, and conjunctivitis.8 The

disease usually lasts seven to 10 days.

DIAGNOSIS

Diagnosis usually is made with blood smears, which are stained for

the virus with immunofluorescence. Other laboratory abnormalities may

include leukopenia and thrombocytopenia.

TREATMENT

Treatment is supportive. No specific medication is indicated. At the

onset of symptoms, most patients will be treated empirically with

tetracycline, doxycycline, or chloramphenicol to cover for other tick-

borne diseases.

-------------------------------------

Relapsing Fever

-------------------------------------

EPIDEMIOLOGY AND TRANSMISSION

Relapsing fever is caused by the spirochete within the genus

Borrelia. Ticks of the Ornithodoros genus are th\e chief vectors.

Hosts include rodents (e.g., rats, mice, chipmunks, squirrels),

rabbits, and hares. In the United States, most cases occur west of

the Mississippi River, especially in mountainous areas. The disease

typically occurs sporadically or in small, often familial, clusters.8

SIGNS AND SYMPTOMS

The average inoculation period is one week. Influenzalike symptoms,

arthralgias (possibly severe), dizziness, nausea, and vomiting are

common. Fever usually is high (greater than 40C [104F]) and irregular

in pattern, and sometimes is associated with delirium. Most patients

have splenomegaly. Meningeal signs may be present. Other

complications can include epistaxis, hemoptysis, iridocyclitis, coma,

cranial nerve palsy, pneumonitis, myocarditis, and rupture of the

spleen.

DIAGNOSIS

Diagnosis is made most easily by detection of spirochetes in blood,

bone marrow, or cerebrospinal fluid during a febrile episode. Other

laboratory findings may include normal or moderate elevations in the

leukocyte count and thrombocytopenia.

TREATMENT

The treatment of choice is doxycycline (100 mg orally, twice per day

for five to 10 days). Alternative therapy includes erythromycin (500

mg orally four times per day for five to 10 days).27 Therapy may lead

to a JarischHerxheimer reaction (i.e., generalized malaise, headache,

fever, sweating, rigors, seizures, or stroke), especially if given

during the late febrile stage. Administering acetaminophen two hours

before and after antibiotic administration may lessen the severity of

the reaction. Steroids and nonsteroidal anti- inflammatory drugs do

not prevent or modify the cardiopulmonary disturbances of the

reaction.8

-------------------------------------

Combined Infections

-------------------------------------

The same tick may harbor different infectious pathogens and transmit

several with one bite.28 For example, I. scapularis may transmit

ehrlichiosis, Lyme disease, and babesiosis. Babesiosis occurs in 23

percent of patients with Lyme disease29; ehrlichiosis occurs in 10 to

30 percent of patients with Lyme disease; and 10 to 30 percent of

patients with ehrlichiosis acquire Lyme disease or babesiosis

concurrently. Combined infections are thought to cause more severe

symptoms.19,28

-------------------------------------

Prevention of Tick Exposure

-------------------------------------

Measures to help prevent tick exposure include avoiding tick-

infested areas (especially during the summer months), wearing long

pants and tucking pant legs into socks, using tick repellents

containing N,N-diethyl-mtoluamide(DEET) for the skin and permethrin

for clothing, and using bed nets when sleeping on the ground or

camping.

Early removal of ticks can help prevent disease because at least 24

to 48 hours of attachment to the host are required before infection

occurs.19 The body of the tick should be grasped gently and vertical

traction applied until it dislodges. Blunt, medium- tipped, angled

forceps offer the best results. Commercially available devices are

recommended over tweezers for tick removal. Tick removal methods that

are not recommended include applying a hot match to the tick body;

covering the tick with petroleum jelly, nail polish, alcohol, or

gasoline; using injected or topical lidocaine; and passing a needle

through the tick. When an improper technique is applied, parts of the

proboscis may remain in the skin, which can lead to infection or

granuloma formation.30

The authors indicate that they do not have any conflicts of interest.

Sources of funding: none reported.

Rocky Mountain spotted fever is more common in the coastal Atlantic

states from April to September.

Figure 2. Deer tick (Ixodes scapularis), also known as black- legged

tick.

Symptoms of ehrlichiosis begin approximately seven days after tick

bite and include a maculopapular, macular, or petechial rash.

-------------------------------------

REFERENCES

-------------------------------------

1. Gayle A, Ringdahl E. Tick-borne diseases. Am Fam Physician 2001;

64:461-6.

2. Byrd RP Jr, Vasquez J, Roy TM. Respiratory manifestations of tick-

borne diseases in the Southeastern United States. South Med J

1997;90:1-4.

3. Beers MH, Berkow R. The Merck manual of diagnosis and therapy.

17th ed. Whitehouse Station, N.J.: Merck Research Laboratories, 1999.

4. DH. Tick-transmitted infectious diseases in the United

States. Annu Rev Public Health 1998;19:237-69.

5. Drage LA. Life-threatening rashes: dermatologic signs of four

infectious diseases. Mayo Clin Proc 1999;74:68-72.

6. Kwitkowski VE, Demko SG. Infectious disease emergencies in primary

care. Lippincotts Prim Care Pract 1999;3:108-25.

7. Centers for Disease Control and Prevention. Rocky Mountain spotted

fever. Accessed online April 11, 2005, at: http://

www.cdc.gov/ncidod/ dvrd/rmsf/index.htm.

8. Steeve AC. Lyme borreliosis. In: Kasper DL on TR. on's

Manual of medicine. 16th ed. New York: McGraw-Hill, 2005:995-9.

9. Shapiro ED. Tick-borne diseases. Adv Pediatr Infect Dis

1997;13:187-218.

10. Thorner AR, DH, Petri WA Jr. Rocky Mountain spotted fever.

Clin Infect Dis 1998;27:1353-9.

11. Black-legged tick. Accessed online April 11, 2005, at:

http:/ /www. enature.com/fieldguide/snowSpecies_Ll.asp?imageID=18509.

12. Piesman J, Mather TN, Sinsky RJ, Spielman A. Duration of tick

attachment and Borrelia burgdorferi transmission. J Clin Microbiol

1987;25:557-8.

13. Piesman J, Maupin GO, Campos EG, Happ CM. Duration of adult

female Ixodes dammini attachment and transmission of Borrelia

burgdorferi, with description of a needle aspiration isolation

method. J Infect Dis 1991;163:895-7.

14. Piesman J. Dynamics of Borrelia burgdorferi transmission by

nymphal Ixodes dammini ticks. J Infect Dis 1993;167:1082-5.

15. Falco RC, Fish D, Piesman J. Duration of tick bites in a Lyme

disease-endemic area. Am J Epidemiol 1996;143:187-92.

16. Centers for Disease Control and Prevention. Lyme disease.

Accessed online April 11, 2005, at: http://www.cdc.gov/ncidod/dvbid/

lyme/ index.htm.

17. Magid D, Schwartz B, Craft J, Schwartz JS. Prevention of Lyme

disease after tick bites. A cost-effectiveness analysis. N Engl J Med

1992;327:534-41.

18. Treatment of Lyme disease. Med Lett Drugs Ther 2000;42:37-9.

19. Belman AL. Tick-borne diseases. Semin Pediatr Neurol 1999;6:249-

66.

20. Centers for Disease Control and Prevention. Human ehrlichiosis in

the United States. Accessed online April 11, 2005, at:

http://www.cdc. gov/ncidod/dvrd/ehrlichia/index.htm.

21. ME, DW, Schaffner W, McGee ZA. Tularemia: a 30-

year experience with 88 cases. Medicine (Baltimore) 1985;64:251-69.

22. RP, Bates JH. Pleuropulmonary tularemia. A review of 29

patients. Am Rev Respir Dis 1969;99:31-41.

23. Rubin SA. Radiographic spectrum of pleuropulmonary tularemia. AJR

Am J Roentgenol 1978;131:277-81.

24. Dennis DT, Inglesby TV, DA, Bartlett JG, Ascher MS,

Eitzen E, et al. Tularemia as a biological weapon: medical and public

health management. JAMA 2001;285:2763-73.

25. Drugs for parasitic infections. Med Lett Drugs Ther 2004.

Accessed online April 11, 2005, at: http://www.medletter.com/

freedocs/parasitic.pdf.

26. Emmons RW. An overview of Colorado tick fever. Prog Clin Biol Res

1985;178:47-52.

27. Gilbert DN, Moellering RC, Eliopoulos GM, Sande MA. The Sanford

guide to antimicrobial therapy. 34th ed. Hyde Park, Vt.:

Antimicrobial Therapy, 2004:39.

28. DH, Barbour AG, Oliver JH, Lane RS, Dumler JS, Dennis DT,

et al. Emerging bacterial zoonotic and vector-borne diseases.

Ecological and epidemiological factors. JAMA 1996;275:463-9.

29. Meldrum SC, Birkhead GS, White DJ, Benach JL, Morse DL. Human

babesiosis in New York state: an epidemiological description of 136

cases. Clin Infect Dis 1992;15:1019-23.

30. Gammons M, Salam G. Tick removal. Am Fam Physician 2002;66:643-5.

-------------------------------------

The Authors

-------------------------------------

ROBERT L. BRATTON, M.D., Mayo Clinic, sdale, Arizona

G. RALPH COREY, M.D., Duke University Medical Center, Durham, North

Carolina

ROBERT L. BRATTON, M.D., is a consultant in the Department of Family

Medicine at the Mayo Clinic, sdale, Ariz., and associate

professor of family medicine at the Mayo Medical School, Rochester,

Minn. He received his medical degree from the University of Kentucky,

Lexington, and completed a residency in family medicine at the Mayo

Clinic, Rochester, Minn.

G. RALPH COREY, M.D., is professor of medicine and infectious

diseases at Duke University Medical Center, Durham, N.C. He received

his medical degree at Baylor University, Waco, Tex., and completed

his internship, residency, and chief residency in internal medicine,

and an infectious disease fellowship at Duke University Medical

Center.

Address correspondence to L. Bratton, M. D., Mayo Clinic

Family Medicine - Thunderbird, 13737 N. 92nd St., sdale, AZ

85260. Reprints are not available from the authors.

Copyright American Academy of Family Physicians Jun 15, 2005

Source: American Family Physician

* * * * * * * * * * * * * * * * * * * * * * * * * * *

FREE BROCHURE: " How to Get an Accurate Polymerase Chain Reaction (PRC)

Blood Test for Mycoplasmal and Other Infections-with a List of

International Laboratories " © by and Leslee Dudley

is sent automatically and immediately to all new subscribers. It is

updated with current information and the new version is posted to the

Mycoplasma Registry Reports & News list each month.

MycoplasmaRegistry-subscribe

FAIR USE: In accordance with Title 17 U.S.C. Section 107, this

material is distributed without profit to those who have expressed a

prior interest in receiving the included information for research and

educational purposes. The Mycoplasma Registry has no affiliation with

the originator of this article nor is the Mycoplasma Registry

endorsed or sponsored by the originator. If you wish to use

copyrighted material from this site for purposes of your own that go

beyond 'fair use', you must obtain permission from the copyright

owner.

* * * * * * * * * * * * * * * * * * * * * * * * * * *