Markovchick Vincent J., Pons Peter T., Bakes Katherine M.(ed.) Emergency medicine secrets. 5th ed
Подождите немного. Документ загружается.
Chapter 51 TETANUS, BOTULISM, AND FOOD POISONING358
30. Should antibiotics be used for infectious diarrhea?
The use of antibiotics in acute diarrhea remains controversial. Short courses or single-dose
regimens of broad-spectrum antibiotics (e.g., ciprofloxacin 750 mg, norfloxacin 800 mg, or
levofloxacin 500 mg as single doses) have been shown to reduce the frequency of stool by
50% and duration of illness to 12 to 24 hours. Azithromycin (1,000 mg PO as a single dose,
or weight-based equivalent) can be considered in pregnant women and children, for whom
fluoroquinolones are contraindicated. In areas where amebiasis and giardiasis are prevalent,
consider metronidazole 500 mg three times a day for 5 days. Antibiotic therapy is not
generally recommended in children with bloody diarrhea because of the association with
enterohemorrhagic E. coli (O157.H7) infections, in which antibiotics do not significantly
improve outcome and can promote the development of HUS from increased lysis of
organisms with release of endotoxin and Shiga-like toxin.
31. Which diarrhea-producing agent is associated with febrile seizures in
children?
Shigella infections in young children can present with high fevers, generalized toxic
appearance, abdominal cramps, bloody mucoid stool, and seizures with or without
encephalopathy. Other complications include dehydration, hyponatremia, hypoglycemia, and
surgical emergencies (e.g., toxic megacolon, rectal prolapse, or intestinal perforation).
Endemic Shigella is responsible for 75% of diarrhea-related deaths in developing countries.
ACKNOWLEDGMENT
The editors gratefully acknowledge the contributions of Kevin Dean, MD and Scott Rudkin, MD,
MBA, authors of this chapter in the previous edition.
Figure 51-1. Approach to traveler’s diarrhea.
1
Chapter 51 TETANUS, BOTULISM, AND FOOD POISONING 359
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1. Ahasan HAMN, Mamun AA, Karim SR, et al: Paralytic complications of puffer fish (tetrodotoxin) poisoning.
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2. Ashkenazi S: Shigella infections in children: new insights. Semin Pediatr Infect Dis 15:246–252, 2004.
3. Bleck TP: Clostridium tetani. In Mandell GL, Douglas RG, Bennett JE, editors: Principles and practice of
infectious diseases, ed 5, Philadelphia, 2000, Churchill Livingstone, pp 2537–2543.
4. Brett M: Food poisoning associated with biotoxins in fish and shellfish. Curr Opin Infect Dis 16:461–465,
2003.
5. Centers for Disease Control and Prevention: National Surveillance Team— Enteric Diseases Epidemiology
Branch: National Botulism Surveillance. Retrieved from www.cdc.gov/nationalsurveillance/botulism_
surveillance.html. Accessed August 24, 2009.
6. Fox CK, Keet CA, Strober JB: Recent advances in infant botulism. Pediatr Neurol 32:149–154, 2005.
7. Giannini L, Vannacci A, Missanelli A, et al: Amatoxin poisoning: a 15-year retrospective analysis and follow-up
evaluation of 105 patients. Clin Toxicol 45:539–542, 2007.
8. Gilbert DM, RC Moellering, EM Eliopoulos, et al, editors: The Sanford guide to antimicrobial therapy,
New York, 2004, Antimicrobial Therapy, Inc, pp 43.
9. Hill DR, Ryan ET: Management of travellers’ diarrhoea [review]. BMJ 6:337, 2008.
10. Isbister G, Kiernan M: Neurotoxic marine poisoning. Lancet Neurol 4:219–228, 2005.
11. Kretsinger K, Broder KR, Cortese MM, et al: Preventing tetanus, diphtheria, and pertussis among adults: use
of tetanus toxoid, reduced diphtheria toxoid and acellular pertussis vaccine recommendations of the Advisory
Committee on Immunization Practices (ACIP) and recommendation of ACIP, supported by the Healthcare
Infection Control Practices Advisory Committee (HICPAC), for use of Tdap among health-care personnel.
MMWR Recomm Rep 55(RR–17):1–37. 2006.
12. Long S: Infant botulism. Concise Rev Pediatr Infect Dis July:707–710, 2001.
13. Murphy TV, Slade BA, Broder KR, et al, Advisory Committee on Immunization Practices (ACIP) Centers for
Disease Control and Prevention (CDC): Prevention of pertussis, tetanus, and diphtheria among pregnant and
postpartum women and their infants. Recommendations of the Advisory Committee on Immunization
Practices (ACIP) [review]. MMWR Recomm Rep 57(RR–4):1–51. Erratum in: MMWR Morb Mortal Wkly Rep
57(26):723, 2008.
14. Niyogi S: Shigellosis. J Microbiol 43:133–143, 2005.
15. Oldfield E: Emerging foodborne pathogens: keeping your patients and your families safe. Rev Gastroenterol
Disord 1(4):177–186, 2001.
16. Pawloski SW, Warren CA, Guerrant R: Diagnosis and treatment of acute or persistent diarrhea.
Gastroenterology 136:1874–1886, 2009.
17. Pulido OM: Domoic acid toxicologic pathology: a review. Marine drugs 6(2):180, 2008.
18. Sheffield J, Ramin S: Tetanus in pregnancy. Am J Perinatol 21:173–182, 2004.
19. Sobel J: Botulism. Clin Infect Dis 41(8):1167–1173, 2005.
20. Sobel J, Painter J: Illnesses caused by marine toxins. Clin Infect Dis 41(9):1290–1296, 2005.
360
MOSQUITO- AND TICK-BORNE DISEASES
OF NORTH AMERICA
CHAPTER 52
Andrew M. Kestler, MD, MBA, DTMH
1. Why should I read this chapter?
Mosquitoes are the most important disease vectors worldwide, and ticks are the most
important arthropod vectors in North America. West Nile virus and the Lyme disease
spirochete are common endemic pathogens within the continental United States and Canada.
In the case of rarer diseases, such as Rocky Mountain spotted fever (RMSF) and tularemia,
early recognition and treatment can be life-saving. Other diseases, such as dengue fever and
malaria, frequently occur in travelers and recent immigrants from the tropics who present to
EDs across North America.
2. What are the most important tools in diagnosing these vector-borne
diseases?
A detailed history and a skin examination. Many of these illnesses initially present with a
nonspecific syndrome of fever, headache, and myalgia. A history of travel, exposure to the
vector, or a characteristic rash can provide the key to a difficult diagnosis.
3. Does malaria occur in North America?
Most definitely. The Centers for Disease Control and Prevention (CDC) was established in Atlanta
in 1946 for the specific purpose of controlling malaria in the southeastern United States. Malaria
remains endemic in the Caribbean and parts of Mexico. The CDC registered 1,505 cases of
malaria in the United States for 2007. Anopheles mosquito species, the night-biting vector of
malaria, are still widely found across North America and have caused transmission in the United
States from one household member to another.
4. What causes malaria?
There are four species of the protozoan Plasmodium: Plasmodium falciparum, Plasmodium
vivax, Plasmodium ovale, and Plasmodium malariae. Malaria is usually acquired by the bite
of an infected female Anopheles, but it also may be transmitted by transfusion of infected
blood or from mother to child in utero. P. falciparum, the most common and the most life-
threatening type of infection, causes virtually all of the 1 million annual malaria deaths
worldwide.
5. Can malaria be prevented?
Although no one method of protection is 100% effective, proper use of prophylactic
drugs, bed nets, insect repellent, and proper patient education would prevent most cases
of traveler’s malaria seen in the United States. Tropic-bound travelers should consult a
local travel clinic and the CDC website to assess malaria risk and plan prophylaxis
accordingly.
6. Describe the clinical presentation of malaria.
Symptoms develop 10 to 14 days after P. falciparum infection but may be latent for
1 year with P. vivax. Patients complain of flu-like symptoms, with fever, chills, headache,
nausea, vomiting, abdominal pain, cough, and myalgias. Physical examination may reveal
jaundice, hepatomegaly, or splenomegaly but is often normal. The presence of a rash
or significant lymphadenopathy suggests another diagnosis or a coinfection. Anemia,
Chapter 52 MOSQUITO- AND TICK-BORNE DISEASES OF NORTH AMERICA 361
thrombocytopenia, and hemoglobinuria are common laboratory findings. Patients may
develop renal failure, pulmonary edema, shock, disseminated intravascular coagulation,
profound anemia, acidosis, and hypoglycemia. Cerebral malaria, the most common
fatal manifestation of malaria in adults, presents with altered mental status, seizures,
and coma.
7. How is malaria diagnosed?
A high index of suspicion is the key to an early clinical diagnosis and survival because early
initiation of treatment is a time-critical action. Definitive diagnosis is established with light
microscopy visualization of protozoa on blood smears. Thick blood smears are more sensitive,
but thin blood smears are necessary for speciation and calculation of a parasitemia percentage.
Repeat blood smears at least three times at 12-hour intervals, although false-negatives will still
occur. Antigen rapid detection kits are useful in case of limited access to an experienced
laboratory technician.
8. How is malaria treated?
Unless P. falciparum infection can be ruled out, prompt treatment should be initiated
empirically and the patient admitted. Severe malaria is treated with intravenous quinine
(quinidine in the United States), or with artesunate (investigational new drug through CDC in
the United States). There are several oral options for treating uncomplicated malaria, including
mefloquine, atovaquone-proguanil (Malarone), and artemether-lumefantrine (Coartem,
licensed by the Food and Drug Administration in 2009). Those receiving intravenous
medications should receive telemetry monitoring because quinine and quinidine cause
dysrhythmogenic QT prolongation. The latter two drugs also require combination therapy with
clindamycin or tetracyclines to avoid recurrence and resistance.
KEY POINTS: MALARIA
1. Malaria is a common and lethal disease of the returning traveler or recent immigrant.
2. Normal blood smears do not rule out the disease.
3. Begin early empirical treatment in a sick patient with the right travel history.
4. More people die from malaria than from any other bite- or sting-induced disease.
9. What is dengue and where does it occur?
Dengue is a mosquito-borne flavivirus endemic to tropical regions the world over. Only
41 U.S. cases were confirmed by the CDC in 1999 and 2000, but given that many symptoms
are nonspecific and that the disease is not reportable on a national level, it is thought to be
significantly underdiagnosed and under-reported. Of note, Florida, Texas, and Hawaii report
autochthonous transmission, meaning that the disease was acquired within the state. Puerto
Rico has a few thousand cases per year. The principal vector, Aedes aegypti, is found across
the southeastern United States.
10. How do dengue fever and dengue hemorrhagic fever (DHF) present?
Many infections, especially in children, are asymptomatic or go unnoticed as a mild febrile
illness. Classic dengue fever occurs after 5 to 6 days of incubation and lasts about 1 week,
presenting with fever, retro-orbital headache, nausea, vomiting, arthralgias, and severe
myalgias, earning it the nickname of “breakbone fever.” A confluent blanching, macular rash is
characteristic but only occurs in 50% of cases. The illness provides immunity to one of the
four virus serotypes, but reinfection with another serotype may lead to the more severe form,
Chapter 52 MOSQUITO- AND TICK-BORNE DISEASES OF NORTH AMERICA362
DHF. DHF is characterized by capillary leakage and thrombocytopenia, manifesting with dermal
and mucosal hemorrhage or pleural and peritoneal effusions. DHF can develop into dengue
shock syndrome, which if untreated carries a mortality of more than 40%.
11. How do I diagnose and treat dengue fever?
The diagnosis is usually made with enzyme-linked immunosorbent assay (ELISA) serology,
which is often negative during the acute illness. The ELISA assay may cross-react with
antibodies to other arboviruses such as West Nile. Laboratory abnormalities include
thrombocytopenia, which occurs frequently even in the absence of DHF, nonspecific elevation
of liver enzymes, and hemoconcentration in the case of DHF. Treatment is supportive: fluids
and analgesics for dengue fever and intensive care for DHF, which in experienced centers can
reduce the mortality below 1%. Nonsteroidal anti-inflammatory drugs (NSAIDs) and aspirin
are to be avoided because of platelet inhibition.
12. What is West Nile virus?
The West Nile virus is a flavivirus that is acquired through the bite of Culex mosquitoes.
Previously endemic in Africa, it first was reported in the United States in an outbreak in
New York City in 1999, where it was associated with a die-off of infected crows. Since that
time, the disease has spread westward to the Pacific, with a U.S. peak incidence of 9,862 in
2003, decreasing to 720 cases in 2009.
13. What are the symptoms of West Nile infections?
Only one in five infections is symptomatic, and only 1 in 140 to 320 present with central nervous
system involvement. Symptomatic infection with the West Nile virus occurs 3 to 15 days after
exposure. Initial symptoms include fever, headache, weakness, nausea, vomiting, and rash.
Those with central nervous system involvement present most frequently with an encephalitic
syndrome, for example, altered mental status and/or seizures. Isolated aseptic meningitis also
occurs. More rarely, patients suffer polio-type paralysis or Parkinsonian movement disorders.
The elderly are at much higher risk for severe disease and death. Neuropsychiatric sequelae
occur in more than 50% of those with severe disease.
14. How is West Nile encephalitis diagnosed and treated?
Diagnosis is made with ELISA antibody assays on serum or cerebrospinal fluid (CSF).
Treatment is supportive. Young, nontoxic patients without central nervous system involvement
may safely be discharged home.
15. Are ticks a significant vector of disease?
Yes. They are responsible for the greatest variety and number of cases of vector-borne human
illness in North America. Tick-transmitted Lyme disease is the most common vector-borne
illness in the United States, with more than 28,921 confirmed cases in 2008 and an additional
6,277 probable cases. There are two major families of ticks: the hard ticks and the soft ticks
(Ornithodoros). Hard ticks transmit all tick-borne diseases, with the exception of relapsing
fever. Ticks typically spread disease in the summer months, when ticks are actively seeking
blood meals, and when most potential human hosts are engaged in outdoor activities.
16. List the principal vectors and distribution of tick-borne diseases.
See Table 52-1.
17. How is Lyme disease transmitted?
Ixodes scapularis ticks transmit Lyme disease in eastern and central North America, whereas
Ixodes pacificus is the vector on the Pacific Coast. Tick nymphs pick up the Borrelia
spirochetes from mice, then transmit the Lyme infections to people. Transmission of Lyme
disease rarely occurs before 48 hours of attachment. Although white-tailed deer do not harbor
the disease, they are the preferred hosts of the adult tick. New cases of acute Lyme disease
peak between April and September, when nymphs are feeding.
Chapter 52 MOSQUITO- AND TICK-BORNE DISEASES OF NORTH AMERICA 363
RMSF, Rocky Mountain spotted fever; STARI, southern tick-associated rash illness.
Disease Vector Pathogen U.S. Distribution
First-Line
Treatment
Babesiosis Ixodes
scapularis
Babesia
microti
Northeast Quinine plus
clindamycin
Colorado tick
fever
Dermacentor
andersoni
Coltivirus Western
mountains
Supportive
Ehrlichiosis Amblyomma
americanum
Ehrlichia
chaffeensis
Southeast,
south-central
Doxycycline
Anaplasmosis Ixodes species Anaplasma
phagocytophila
Same as Lyme Doxycycline
Lyme disease Ixodes species Borrelia
burgdorferi
Northeast,
midwest, west
Doxycycline
Relapsing fever Ornithodoros
species
Borrelia
species
Western
mountains
Doxycycline
RMSF Dermacentor
species
Rickettsia
rickettsii
Nationwide,
mostly Southeast
Doxycycline
STARI A. americanum Borrelia
lonestari
Southern United
States
Doxycycline
Tick paralysis Multiple Toxins Nationwide Tick removal
Tularemia A. americanum
and Dermacentor
species
Francisella
tularensis
West,
south-central
Streptomycin
TABLE 52–1. PRINCIPAL VECTORS AND DISTRIBUTION OF THE TICK-BORNE DISEASES
18. Describe the three clinical stages of Lyme disease.
n
Early acute or localized infection. The classic skin lesion, erythema migrans (EM),
develops at the bite site within 3 to 32 days in 80% of infections. If rash develops at the
bite site in less than 48 hours, it is a hypersensitivity reaction (or cellulitis) not Lyme. More
than 50% of patients will not recall a tick bite. EM expands slowly as an erythematous
macule to a size of at least 5 cm and often much larger. Central clearing is common; it is
usually painless but at times pruritic. Many individuals will develop systemic flulike
symptoms with fever, suggesting some degree of early dissemination. Untreated, EM will
typically resolve spontaneously over 3 to 4 weeks.
n
Early disseminated disease. This may occur in untreated individuals days to weeks after
the tick bite. Most will have fever and adenopathy, and many will have multiple secondary
skin lesions that are smaller than the initial EM. Lyme arthritis is the most common
secondary Lyme manifestation in the United States, occurring in 70% of patients with
untreated EM. This mono- or oligoarticular process most commonly produces effusions
in the knee and other large joints. Neurologic manifestations include cranial neuritis,
Chapter 52 MOSQUITO- AND TICK-BORNE DISEASES OF NORTH AMERICA364
such as unilateral or bilateral facial nerve palsy (Bell’s), and aseptic meningitis.
Radiculoneuritis, similar to postherpetic neuralgia, with burning and paresthesias also
occurs. Carditis occurs in less than 10% of cases and presents most typically with
atrioventricular blocks.
n
Late or chronic disease. Late manifestations occur months to years after infection. Lyme
arthritis is the most common, presenting in 10% of those with untreated EM. The arthritis
typically does not cause joint destruction and may resolve spontaneously after several
years. Chronic neurologic disease may include polyneuritis, multiple-sclerosis-like
encephalomyelitis (0.1%), and subtle encephalopathy. Chronic dermatitis (acrodermatitis
chronicum atrophicans) and keratitis are relatively rare in the United States.
19. Does Lyme disease remind you of another spirochetal disease?
Primary, secondary, and tertiary phases, and the organ systems involved, are reminiscent of
syphilis.
20. How is Lyme disease diagnosed?
The typical EM rash in an endemic area is sufficient for diagnosis. For disseminated disease,
ELISA serology is used to detect Lyme antibodies. Suggestive clinical findings are key because
positive serology does not prove active infection in an endemic area. A positive test in an
asymptomatic individual is not an indication for treatment.
21. How is Lyme disease treated?
Oral therapy with doxycycline or amoxicillin is effective for early disease and for mild early
disseminated disease, such as arthritis. Neurologic and cardiac manifestations (with the
exception of an isolated Bell’s palsy) typically require parenteral therapy with ceftriaxone over
2 to 3 weeks, with a good prognosis. Admission to telemetry is recommended in Lyme
carditis even for a first-degree atrioventricular block if the PR interval is greater than 300 ms,
given the risk of progression. Temporary pacing may be needed for third-degree blocks. Late
Lyme disease may not always respond to treatment.
22. Can Lyme disease be prevented?
The mainstays of prevention remain avoiding tick exposure (difficult for outdoor enthusiasts),
preventing attachment with protective clothing, and removing ticks promptly if they attach
(twice daily tick checks). The only vaccine was removed from the market in 2002.
23. An ED patient presents with a tick bite; should you treat prophylactically for
Lyme disease?
Yes and no. If you practice in an endemic area, if you can identify the tick as Ixodes
scapularis, and if it likely was attached for more than 48 hours (suggested by engorgement,
or known exposure time), treatment with a single 200 mg dose of doxycycline is effective in
preventing Lyme. If you cannot meet these three conditions, simply give your patient
appropriate return precautions.
KEY POINTS: LYME DISEASE
1. It is the most common vector-borne disease in the United States.
2. A classic erythema migrans rash develops at site of tick bite.
3. Heart block, Bell’s palsy, and arthritis develop in advanced disease.
4. Positive serology test is not diagnostic of infection.
5. Treatment is doxycycline, amoxicillin, or ceftriaxone.
Chapter 52 MOSQUITO- AND TICK-BORNE DISEASES OF NORTH AMERICA 365
24. What on earth is STARI and what can be done about it?
STARI stands for southern tick-associated rash illness because it causes EM just like Lyme
disease. It is caused by a nonculturable spirochete, Borrelia lonestari, transmitted by the
lone star tick, Amblyomma americanum. If a patient presents with EM in the southern
United States, a Lyme nonendemic area, the diagnosis is likely to be STARI. Treat just as
you would early localized Lyme disease.
25. What is relapsing fever?
Relapsing fever is caused by several Borrelia species transmitted by soft ticks. Most cases are
linked to stays in rural, rodent-infested cabins, in the mountains of the western United States.
Abrupt onset of flulike symptoms (i.e., fever, myalgias, headache, and vomiting) occurs 2 to
18 days after exposure. A generalized macular rash or a pruritic eschar at the bite site may
develop. After 3 days of fever, symptoms resolve and then relapse on a weekly basis up to
10 times, with declining severity. Diagnosis is made by detection of spirochetes on stained
thick and thin blood smears or by special culture. The very young and very old suffer
increased morbidity and mortality. The disease responds well to doxycycline, penicillin, and
erythromycin, but a Jarisch-Herxheimer reaction may occur (malaise and hypotension.)
26. What is RMSF?
RMSF is a life-threatening infection caused by Rickettsia rickettsii and transmitted by
Dermacentor, or dog ticks. Its name derives from its original description in Montana and
Idaho in the late 19th century and from the typical petechial rash occurring initially on the
wrists and ankles. Currently, most cases are reported from the southeastern and south-central
United States. The rash later involves the palms and soles, then spreads to the trunk, and
often progresses into purpuric lesions. About 60% of infections will present with the classic
triad of rash, fever, and tick exposure, although the rash is rarely present during the first
3 days of the illness. Abrupt onset fever, severe headache, and myalgias are the most
common presenting symptoms, 5 to 7 days after the tick bite.
27. How dangerous is RMSF? What can be done about it?
Untreated, RMSF mortality hovers around 25%. In 2003, 1,091 cases were reported in the
United States. The rickettsial pathogen induces a vasculitis that leads to end-organ
dysfunction, including confusion, respiratory failure, and renal failure, and most typically kills
by disseminated intravascular coagulation. Appropriate and timely antibiotics can reduce the
mortality to below 5%, but delay is frequent because of the relatively late onset of the
characteristic rash. Doxycycline remains the drug of choice, whereas chloramphenicol is
recommended for younger children (younger than 8 years). Because antibody production lags
behind clinical disease, serology is confirmatory rather than diagnostic. Consider early empiric
treatment in the spring and summer in endemic regions.
28. What are ehrlichiosis and anaplasmosis?
Ehrlichiosis and anaplasmosis are tick-borne diseases caused by the rickettsia-like bacteria,
Ehrlichia chaffeensis, which infects monocytes, and Anaplasma phagocytophila (formerly
known as Ehrlichia phagocytophila or Ehrlichia equi), which infects neutrophils. Ehrlichiosis is
transmitted by A. americanum in the southeastern and south-central United States, whereas
anaplasmosis is transmitted by Ixodes ticks in a similar distribution to Lyme disease. Around
600 cases of each were reported to the CDC in 2006. Both diseases present with fever and
flulike symptoms, progressing to respiratory and renal failure, and coma in severe cases.
Rash may occur in ehrlichiosis but not in anaplasmosis. Both diseases preferentially attack
older or immunocompromised adults, but anaplasmosis induces additional
immunosuppression and has a greater case fatality rate.
29. How are ehrlichiosis and anaplasmosis diagnosed and treated?
High clinical suspicion is needed in endemic areas during the summer months.
Thrombocytopenia, leukopenia, and mildly elevated liver enzymes, in the context of possible
Chapter 52 MOSQUITO- AND TICK-BORNE DISEASES OF NORTH AMERICA366
tick exposure or bites, are highly suggestive and should prompt treatment in an ill patient.
Microscopic examination of buffy coat or peripheral blood may reveal characteristic inclusion
bodies in monocytes or neutrophils. Separate serologic and polymerase chain reaction (PCR)
tests exist for both pathogens but are only useful for confirmation of diagnosis. First-line
therapy consists of doxycycline. Chloramphenicol, fluoroquinolones, and rifampin have also
been reported to be effective.
30. What is Colorado tick fever?
Colorado tick fever is caused by an RNA Coltivirus transmitted by Dermacentor ticks in the
western United States. Patients present 3 to 6 days after a bite, with sudden fever, headache,
myalgias, and photophobia. A transient petechial rash may occur. In about 50% of cases,
symptoms resolve and then recur after 3 days. Prognosis is excellent, although complications
such as encephalitis, meningitis, and pericarditis have been reported. Diagnosis is by
serology, although many cases go undiagnosed. Treatment is supportive.
31. What is babesiosis?
Babesiosis is a malaria-like illness, caused by the Babesia microti protozoan. It is transmitted
by Ixodes ticks in the northeastern United States but has also been acquired by transfusion.
Like malaria, the protozoan infects red blood cells, causing fever, drenching sweats, myalgias,
and headache. Though most disease is mild, life-threatening disease occurs in elderly and
asplenic patients. Concurrent infection with Lyme disease occurs in 20%, causing a more
severe illness. Diagnosis is made by serology or by detecting ring forms on stained thin or
thick blood smears. Treatment typically consists of quinine and clindamycin in combination,
although azithromycin and atovaquone together are also effective.
32. What is tularemia?
Tularemia is a rare disease (125 cases/year in the United States) caused by Francisella
tularensis, a virulent gram-negative coccobacillus. Most cases occur in the south-central
United States in hunters through tick bites or contact with infected tissue of rabbits or
rodents. The more common ulceroglandular form manifests with an ulcer at the tick bite,
painful regional adenopathy, fever, headache, and myalgia. The severe typhoidal form presents
with abdominal pain, fever, and prostration without skin and lymphatic manifestations and
carries an untreated mortality of 30% to 60% by septic shock. Transaminitis and patchy
pulmonary infiltrates develop in severe disease.
33. How is tularemia diagnosed and treated?
Prompt diagnosis and life-saving treatment depend on a high index of suspicion because
serology and culture results will not be acutely available. Streptomycin remains the drug of
choice, but if unavailable, other aminoglycosides (gentamicin and tobramycin), tetracyclines,
ciprofloxacin, and chloramphenicol are alternatives.
34. What is tick paralysis?
Tick paralysis is a syndrome caused by neurotoxins in the saliva of gravid females of
many tick species. Young girls in western North America are at highest risk, especially
after prolonged tick attachment. The syndrome usually presents as an ascending paralysis
similar to Guillain-Barré, with sparing of sensorium and sensory function. Mortality does
occur as a result of respiratory failure. Tick removal usually brings about prompt and
complete recovery.
35. What is the proper method for tick removal?
At times, simpler is better: use direct traction with a gloved hand and forceps as close as
possible to the tick mouthparts, avoiding twisting. It is not necessary to dig after embedded
mouthparts. Cleanse the area well after removal. Please forget every other tick removal
method ever devised or imagined.
Chapter 52 MOSQUITO- AND TICK-BORNE DISEASES OF NORTH AMERICA 367
WEBSITES
Malaria, Centers for Disease Control and Prevention: www.cdc.gov/malaria
Stari, Centers for Disease Control www.cdc.gov/ncidod/dvbid/stari
West Nile virus, Centers for Disease Control and Prevention www.cdc.gov/ncidod/dvbid/westnile
World Health Organization www.who.int
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1. Centers for Disease Control and Prevention: Summary of notifiable diseases—United States, 2003. MMWR
52:1–80, 2005.
2. Ettestad PJ, Voorhees RE, Sewell CM, et al: Tickborne relapsing fever outbreak after a family gathering—
New Mexico, August 2002. MMWR 52:809–812, 2003.
3. Greenwood B, Bojang K, Whitty C, et al: Malaria. Lancet 365:1487–1498, 2005.
4. Guzmán MG, Kourí G: Dengue: an update. Lancet Infect Dis 2:33–42, 2001.
5. Haas E, Anderson D, Neu R, et al: Tick paralysis—Washington, 1995. MMWR 45:325–326, 1996.
6. Sexton, DJ: Human ehrlichiosis and anaplasmosis. UpToDate Online, www. uptodate.com, 17.2, 2009.
7. Solomon T: Flavivirus encephalitis. N Engl J Med 351:370–378, 2004.
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9. Stanek G, Strle F: Lyme borreliosis. Lancet 362:1639–1647, 2003.
36. Beside ticks and mosquitoes, do other North American arthropods transmit
disease?
Yes. Fleas transmit plague in the southwestern United States. Deerfly and flea transmission of
tularemia has been reported. Body lice transmit Bartonella quintana, the cause of trench fever,
to the urban homeless. Mites (chiggers) and body lice transmit types of typhus but not in
North America.