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What’s Eating You? Ixodes Tick and Related Diseases, Part 1: Life Cycle, Local Reactions, and Lyme Disease
Author(s)
Kelsey D. Wilson, MD
Dirk M. Elston, MD

Ticks are ectoparasitic hemophages that feed on mammals, reptiles, and birds. The Ixodidae family comprises the hard ticks. A hard dorsal plate, scutum, and capitulum that extends outward from the body are features that distinguish the hard tick. 1Ixodes is the largest genus of hard ticks, with more than 250 species localized in temperate climates.2 It has an inornate scutum and lacks festoons (Figure 1).1 The Ixodes ricinus species complex accounts for most species relevant to the spread of human disease (Figure 2), with Ixodes scapularis in the northeastern, north midwestern, and southern United States; Ixodes pacificus in western United States; I ricinus in Europe and North Africa; and Ixodes persulcatus in Russia and Asia. Ixodes holocyclus is endemic to Australia.3,4

Figure 1. Adult Ixodes scapularis tick with identifiable features such as 8 black legs, an inornate scutum, and an absence of festoons.

Figure 2. Geographic distribution of Ixodes species most commonly involved in disease transmission (approximation).

Life Cycle

Ixodes species progress through 4 life stages—egg, larvae, nymph, and adult—during their 3-host life cycle. Lifespan is 2 to 6 years, varying with environmental factors. A blood meal is required between each stage. Female ticks have a small scutum, allowing the abdomen to engorge during meals (Figure 3).

Figure 3. Female adult Ixodes scapularis tick (top) engorges following a blood meal, increasing in size as the light-colored abdomen expands beyond the dark-brown scutum (bottom).

Larvae hatch in the early summer and remain dormant until the spring, emerging as a nymph. Following a blood meal, the nymph molts and reemerges as an adult in autumn. During autumn and winter, the female lays as many as 2000 eggs that emerge in early summer.5 Nymphs are small and easily undetected for the duration required for pathogen transmission, making nymphs the stage most likely to transmit disease.6

The majority of tick-borne diseases present from May to July, corresponding to nymph activity. Fewer cases present in the autumn and early spring because the adult female feeds during cooler months.7

Larvae have 6 legs and are about the size of a sesame seed when engorged. Nymphs are slightly larger with 8 legs. Adults are largest and have 8 legs. Following a blood meal, the tick becomes engorged, increasing in size and lightening in color (Figure 3).1

Ticks are found in low-lying shrubs and tall grass as well as on the forest floor. They search for a host by detecting CO2, warmth, the smell of sweat, and the color white, prompting attachment.8 Habitats hospitable to Ixodes have expanded in the wake of climate, environmental, and socioeconomic changes, potentially contributing to the increasing incidence and expansion of zoonoses associated with this vector.9,10

 

 

Local Reactions

A tick bite may induce local hypersensitivity, leading to a red papule or plaque at the bite site, followed by swelling, warmth, and erythema. A cellular immune reaction induces induration and pruritus. Hard ticks are less likely than soft ticks to cause a serious local reaction.11,12

A variety of clinical and histologic features are observed following an arthropod bite. Histologically, acute tick bites show a neutrophilic infiltrate with fibrin deposition. Chronic reactions demonstrate a wedge-shaped, mixed infiltrate with prominent endothelial swelling. Eosinophilic cellulitis, or Wells syndrome, reveals tissue eosinophilia and flame figures.13 Tick mouthparts may be identified in the tissue. B-cell hyperplasia is seen in Borrelia lymphocytoma and is more common in Europe, presenting as erythematous to plum–colored nodules on the ear and areola.14

Lyme Disease

Disease manifestations vary by location. Lyme disease is associated with Borrelia burgdorferi and the recently identified Borrelia mayonii in the United States15; in Europe and Asia, acrodermatitis chronica atrophicans is associated with Borrelia afzelii and neuroborreliosis, with Borrelia garinii. Lyme disease is the most common tick-borne illness in the United States.16 The I ricinus species complex is the most common vector harboring Borrelia species.17 At least 36 hours of tick adherence is required for disease transmission.18 The incubation period is 3 to 20 days (median, 12 days).19

Clinical Findings
Erythema migrans is the most characteristic sign, seen in 80% of cases of Lyme disease. The typical rash is a centrifugally spreading, erythematous, annular patch with central clearing at the site of the tick bite.20 Atypical rashes include vesicular, indurated, ulcerated, and follicular variants.21 Histopathology commonly shows a superficial and deep perivascular lymphocytic infiltrate with plasma cells, histiocytes, and eosinophils.22 Typically, the rash resolves in 3 to 5 weeks.18

Early disseminated Lyme disease can present with any of the following findings: multiple erythema migrans; neurologic involvement, including cranial nerve palsy and meningitis; and Lyme carditis, which may result in atrioventricular block.23,24 Late findings include arthritis, encephalopathy, and polyneuropathy. A late cutaneous manifestation, acrodermatitis chronica atrophicans, is rare in the United States but occurs in as many as 10% of Lyme disease cases in Europe. An initial inflammatory response manifests as blue-red erythema and edema of the extensor surfaces of the extremities, commonly on the dorsal hands, feet, elbows, and knees. Firm fibrotic nodules may develop later over the olecranon and patella.23,24

The term chronic Lyme disease has been used to describe the persistence of symptoms after treatment; however, large clinical trials have not detected a difference in symptom frequency between patients with a history of Lyme disease and matched controls.25,26 Many patients with chronic Lyme disease may instead have posttreatment Lyme disease syndrome, described as nonspecific symptoms including fatigue, arthralgia, and decreased mental acuity following treatment of confirmed Lyme disease. Symptoms generally improve within 1 year.27

Laboratory Testing
The gold standard for laboratory diagnosis of Lyme disease is 2-tiered serologic testing. First, an enzyme immunoassay or immunofluorescence assay is used to screen for antibodies. A Western blot follows if the result of the screen is positive or equivocal. Western blot testing for IgM and IgG is used when illness duration is less than 4 weeks; after 4 weeks, a Western blot for IgG alone is sufficient.27,28 The 2-tiered test has 99% specificity. Sensitivity increases with duration of disease (29%–40% with erythema migrans; 42%–87% in early disseminated disease; 97%–100% in late disease).29,30 A false-positive result can occur in the presence of infectious mononucleosis, an autoimmune disorder, and syphilis. If serologic testing is negative and suspicion remains high, testing should be repeated in 2 to 4 weeks.31 When a patient in a Lyme-endemic area presents with typical erythema migrans, serologic testing is unnecessary prior to treatment.32

Management
Treatment of Lyme disease centers on antibiotic therapy (Table). First-line treatment of early disseminated disease is doxycycline for 14 days (range, 10–21 days).27 In pregnant women, children younger than 8 years, and tetracycline-allergic patients, amoxicillin or cefuroxime axetil for 14 days (range, 14–21 days) may be used.33 For erythema migrans without complications, doxycycline for 10 days is effective. Complications that require hospitalization are treated with intravenous ceftriaxone.27 Re-treatment in patients with posttreatment Lyme disease syndrome is not recommended.34 Prophylaxis with a single dose of doxycycline 200 mg may be indicated when all of the following conditions are met: (1) the patient is in an area where more than 20% of Ixodes ticks are infected with B burgdorferi, (2) the attached tick is I scapularis, (3) the tick has been attached for more than 36 hours, and (4) treatment is begun within 72 hours of tick removal.27

References
  1. Anderson JF, Magnarelli LA. Biology of ticks. Infect Dis Clin North Am. 2008;22:195-215.
  2. Jongejan F, Uilenberg G. The global importance of ticks. Parasitology. 2004;129(suppl):S3-S14.
  3. Xu G, Fang QQ, Keirans JE, et al. Molecular phylogenetic analyses indicate that the Ixodes ricinus complex is a paraphyletic group. J Parasitol. 2003;89:452-457.
  4. Swanson SJ, Neitzel D, Reed DK, et al. Coinfections acquired from Ixodes ticks. Clin Microbiol Rev. 2006;19:708-727.
  5. Mathison BA, Pritt BS. Laboratory identification of arthropod ectoparasites. Clin Microbol Rev. 2014;27:48-67.
  6. Falco RC, Fish D, Piesman J. Duration of tick bites in a Lyme disease-endemic area. Am J Epidemiol. 1996;143:187-192.
  7. Centers for Disease Control and Prevention. Lyme disease graphs. http://www.cdc.gov/lyme/stats/graphs.html. Updated November 21, 2016. Accessed November 21, 2017.
  8. Randolph SE. The impact of tick ecology on pathogen transmission dynamics. In: Bowman AS, Nuttall PA, eds. Ticks: Biology, Disease and Control. Cambridge, UK: Cambridge University Press; 2008:40-72.
  9. Ostfeld RS, Brunner JL. Climate change and Ixodes tick-borne diseases of humans. Philos Trans R Soc Lond B Biol Sci. 2015;370. pii:20140051. doi:10.1098/rstb.2014.0051.
  10. Medlock JM, Hansford KM, Bormane A, et al. Driving forces for changes in geographical distribution of Ixodes ricinus ticks in Europe. Parasit Vectors. 2013;6:1.
  11. McGinley-Smith DE, Tsao SS. Dermatoses from ticks. J Am Acad Dermatol. 2003;49:393-396.
  12. Middleton DB. Tick-borne infections. What starts as a tiny bite may have a serious outcome. Postgrad Med. 1994;95:131-139.
  13. Melski JW. Wells’ syndrome, insect bites, and eosinophils. Dermatol Clin. 2015;8:287-293.
  14. Castelli E, Caputo V, Morello V, et al. Local reactions to tick bites. Am J Dermatopathol. 2008;30:241-248.
  15. Pritt BS, Mead PS, Johnson DK, et al. Identification of a novel pathogenic Borrelia species causing Lyme borreliosis with unusually high spirochaetaemia: a descriptive study. Lancet Infect Dis. 2016;16:556-564.
  16. Orloski KA, Hayes EB, Campbell GL, et al. Surveillance for Lyme disease—United States, 1992-1998. MMWR CDC Surveill Summ. 2000;49:1-11.
  17. Gray JS. The ecology of ticks transmitting Lyme borreliosis. Exp Appl Acarol. 1998;22:249-258.
  18. Piesman J, Mather TN, Sinsky RJ, et al. Duration of tick attachment and Borrelia burgdorferi transmission. J Clin Microbiol. 1987;25:557-558.
  19. Richardson M, Elliman D, Maguire H, et al. Evidence base of incubation periods, periods of infectiousness and exclusion policies for the control of communicable diseases in schools and preschools. Pediatr Infect Dis J. 2001;20:380-391.
  20. Myers SA, Sexton DJ. Dermatologic manifestations of arthropod-borne diseases. Infect Dis Clin North Am. 1994;8:689-712.
  21. Ducroux E, Debarbieux S, Boibieux A, et al. Follicular borreliosis: an atypical presentation of erythema chronicum migrans. Dermatology. 2009;219:84-85.
  22. Miraflor AP, Seidel GD, Perry AE, et al. The many masks of cutaneous Lyme disease. J Cutan Pathol. 2016:43:32-40.
  23. Lenormand C, Jaulhac B, Debarbieux S, et al. Expanding the clinicopathological spectrum of late cutaneous Lyme borreliosis (acrodermatitis chronica atrophicans): a prospective study of 20 culture and/or polymerase chain reaction (PCR) documented cases. J Am Acad Dermatol. 2016;74:685-692.
  24. Zajkowska J, Czupryna P, Pancewicz SA, et al. Acrodermatitis chronica atrophicans. Lancet Infect Dis. 2011;11:800.
  25. Seltzer EG, Gerber MA, Cartter ML, et al. Long-term outcomes of persons with Lyme disease. JAMA. 2000;283:609-616.
  26. Shadick NA, Phillips CB, Sangha O, et al. Musculoskeletal and neurologic outcomes in patients with previously treated Lyme disease. Ann Intern Med. 1999;131:919-926.
  27. Wormser GP, Dattwyler RJ, Shapiro ED, et al. The clinical assessment, treatment, and prevention of Lyme disease, human granulocytic anaplasmosis, and babesiosis: clinical practice guidelines by the Infectious Diseases Society of America. Clin Infect Dis. 2006;43:1089-1134.
  28. Schriefer ME. Lyme disease diagnosis: serology. Clin Lab Med. 2015;35:797-814.
  29. Wormser GP, Nowakowski J, Nadelman RB, et al. Impact of clinical variables on Borrelia burgdorferi-specific antibody seropositivity in acute-phase sera from patients in North America with culture-confirmed early Lyme disease. Clin Vaccine Immunol. 2008;15:1519-1522.
  30. Leeflang MM, Ang CW, Berkhout J, et al. The diagnostic accuracy of serological tests for Lyme borreliosis in Europe: a systematic review and meta-analysis. BMC Infect Dis. 2016;16:140.
  31. Sanchez E, Vannier E, Wormser GP, et al. Diagnosis, treatment, and prevention of Lyme disease, human granulocytic anaplasmosis, and babesiosis: a review. JAMA. 2016;315:1767-1777.
  32. Lantos PM, Brinkerhoff RJ, Wormser GP, et al. Empiric antibiotic treatment of erythema migrans-like skin lesions as a function of geography: a clinical and cost effectiveness modeling study. Vector Borne Zoonotic Dis. 2013;13:877-883.
  33. Smith GN, Gemmill I, Moore KM. Management of tick bites and Lyme disease during pregnancy. J Obstet Gynaecol Can. 2012;34:1087-1091.
  34. Berende A, ter Hofstede HJ, Vos FJ, et al. Randomized trial of longer-term therapy for symptoms attributed to Lyme disease. N Engl J Med. 2016;374:1209-1220.
Article PDF
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Author and Disclosure Information

 

From the Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina, Charleston, South Carolina.

The authors report no conflict of interest.

This article is the first of a 3-part series. The next part will appear in the April 2018 issue.

The images are in the public domain.

Correspondence: Dirk M. Elston, MD, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina, 135 Rutledge Ave, MSC 578, Charleston, SC 29425 (elstond@musc.edu).

Issue
Cutis - 101(3)
Publications
Cutis
MDedge Dermatology
Topics
Infectious Diseases
Page Number
187-190
Sections
Environmental Dermatology
Author(s)
Kelsey D. Wilson, MD
Dirk M. Elston, MD
Author(s)
Kelsey D. Wilson, MD
Dirk M. Elston, MD
Author and Disclosure Information

 

From the Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina, Charleston, South Carolina.

The authors report no conflict of interest.

This article is the first of a 3-part series. The next part will appear in the April 2018 issue.

The images are in the public domain.

Correspondence: Dirk M. Elston, MD, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina, 135 Rutledge Ave, MSC 578, Charleston, SC 29425 (elstond@musc.edu).

Author and Disclosure Information

 

From the Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina, Charleston, South Carolina.

The authors report no conflict of interest.

This article is the first of a 3-part series. The next part will appear in the April 2018 issue.

The images are in the public domain.

Correspondence: Dirk M. Elston, MD, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina, 135 Rutledge Ave, MSC 578, Charleston, SC 29425 (elstond@musc.edu).

Article PDF
CT101003817.PDF
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Ticks are ectoparasitic hemophages that feed on mammals, reptiles, and birds. The Ixodidae family comprises the hard ticks. A hard dorsal plate, scutum, and capitulum that extends outward from the body are features that distinguish the hard tick. 1Ixodes is the largest genus of hard ticks, with more than 250 species localized in temperate climates.2 It has an inornate scutum and lacks festoons (Figure 1).1 The Ixodes ricinus species complex accounts for most species relevant to the spread of human disease (Figure 2), with Ixodes scapularis in the northeastern, north midwestern, and southern United States; Ixodes pacificus in western United States; I ricinus in Europe and North Africa; and Ixodes persulcatus in Russia and Asia. Ixodes holocyclus is endemic to Australia.3,4

Figure 1. Adult Ixodes scapularis tick with identifiable features such as 8 black legs, an inornate scutum, and an absence of festoons.

Figure 2. Geographic distribution of Ixodes species most commonly involved in disease transmission (approximation).

Life Cycle

Ixodes species progress through 4 life stages—egg, larvae, nymph, and adult—during their 3-host life cycle. Lifespan is 2 to 6 years, varying with environmental factors. A blood meal is required between each stage. Female ticks have a small scutum, allowing the abdomen to engorge during meals (Figure 3).

Figure 3. Female adult Ixodes scapularis tick (top) engorges following a blood meal, increasing in size as the light-colored abdomen expands beyond the dark-brown scutum (bottom).

Larvae hatch in the early summer and remain dormant until the spring, emerging as a nymph. Following a blood meal, the nymph molts and reemerges as an adult in autumn. During autumn and winter, the female lays as many as 2000 eggs that emerge in early summer.5 Nymphs are small and easily undetected for the duration required for pathogen transmission, making nymphs the stage most likely to transmit disease.6

The majority of tick-borne diseases present from May to July, corresponding to nymph activity. Fewer cases present in the autumn and early spring because the adult female feeds during cooler months.7

Larvae have 6 legs and are about the size of a sesame seed when engorged. Nymphs are slightly larger with 8 legs. Adults are largest and have 8 legs. Following a blood meal, the tick becomes engorged, increasing in size and lightening in color (Figure 3).1

Ticks are found in low-lying shrubs and tall grass as well as on the forest floor. They search for a host by detecting CO2, warmth, the smell of sweat, and the color white, prompting attachment.8 Habitats hospitable to Ixodes have expanded in the wake of climate, environmental, and socioeconomic changes, potentially contributing to the increasing incidence and expansion of zoonoses associated with this vector.9,10

 

 

Local Reactions

A tick bite may induce local hypersensitivity, leading to a red papule or plaque at the bite site, followed by swelling, warmth, and erythema. A cellular immune reaction induces induration and pruritus. Hard ticks are less likely than soft ticks to cause a serious local reaction.11,12

A variety of clinical and histologic features are observed following an arthropod bite. Histologically, acute tick bites show a neutrophilic infiltrate with fibrin deposition. Chronic reactions demonstrate a wedge-shaped, mixed infiltrate with prominent endothelial swelling. Eosinophilic cellulitis, or Wells syndrome, reveals tissue eosinophilia and flame figures.13 Tick mouthparts may be identified in the tissue. B-cell hyperplasia is seen in Borrelia lymphocytoma and is more common in Europe, presenting as erythematous to plum–colored nodules on the ear and areola.14

Lyme Disease

Disease manifestations vary by location. Lyme disease is associated with Borrelia burgdorferi and the recently identified Borrelia mayonii in the United States15; in Europe and Asia, acrodermatitis chronica atrophicans is associated with Borrelia afzelii and neuroborreliosis, with Borrelia garinii. Lyme disease is the most common tick-borne illness in the United States.16 The I ricinus species complex is the most common vector harboring Borrelia species.17 At least 36 hours of tick adherence is required for disease transmission.18 The incubation period is 3 to 20 days (median, 12 days).19

Clinical Findings
Erythema migrans is the most characteristic sign, seen in 80% of cases of Lyme disease. The typical rash is a centrifugally spreading, erythematous, annular patch with central clearing at the site of the tick bite.20 Atypical rashes include vesicular, indurated, ulcerated, and follicular variants.21 Histopathology commonly shows a superficial and deep perivascular lymphocytic infiltrate with plasma cells, histiocytes, and eosinophils.22 Typically, the rash resolves in 3 to 5 weeks.18

Early disseminated Lyme disease can present with any of the following findings: multiple erythema migrans; neurologic involvement, including cranial nerve palsy and meningitis; and Lyme carditis, which may result in atrioventricular block.23,24 Late findings include arthritis, encephalopathy, and polyneuropathy. A late cutaneous manifestation, acrodermatitis chronica atrophicans, is rare in the United States but occurs in as many as 10% of Lyme disease cases in Europe. An initial inflammatory response manifests as blue-red erythema and edema of the extensor surfaces of the extremities, commonly on the dorsal hands, feet, elbows, and knees. Firm fibrotic nodules may develop later over the olecranon and patella.23,24

The term chronic Lyme disease has been used to describe the persistence of symptoms after treatment; however, large clinical trials have not detected a difference in symptom frequency between patients with a history of Lyme disease and matched controls.25,26 Many patients with chronic Lyme disease may instead have posttreatment Lyme disease syndrome, described as nonspecific symptoms including fatigue, arthralgia, and decreased mental acuity following treatment of confirmed Lyme disease. Symptoms generally improve within 1 year.27

Laboratory Testing
The gold standard for laboratory diagnosis of Lyme disease is 2-tiered serologic testing. First, an enzyme immunoassay or immunofluorescence assay is used to screen for antibodies. A Western blot follows if the result of the screen is positive or equivocal. Western blot testing for IgM and IgG is used when illness duration is less than 4 weeks; after 4 weeks, a Western blot for IgG alone is sufficient.27,28 The 2-tiered test has 99% specificity. Sensitivity increases with duration of disease (29%–40% with erythema migrans; 42%–87% in early disseminated disease; 97%–100% in late disease).29,30 A false-positive result can occur in the presence of infectious mononucleosis, an autoimmune disorder, and syphilis. If serologic testing is negative and suspicion remains high, testing should be repeated in 2 to 4 weeks.31 When a patient in a Lyme-endemic area presents with typical erythema migrans, serologic testing is unnecessary prior to treatment.32

Management
Treatment of Lyme disease centers on antibiotic therapy (Table). First-line treatment of early disseminated disease is doxycycline for 14 days (range, 10–21 days).27 In pregnant women, children younger than 8 years, and tetracycline-allergic patients, amoxicillin or cefuroxime axetil for 14 days (range, 14–21 days) may be used.33 For erythema migrans without complications, doxycycline for 10 days is effective. Complications that require hospitalization are treated with intravenous ceftriaxone.27 Re-treatment in patients with posttreatment Lyme disease syndrome is not recommended.34 Prophylaxis with a single dose of doxycycline 200 mg may be indicated when all of the following conditions are met: (1) the patient is in an area where more than 20% of Ixodes ticks are infected with B burgdorferi, (2) the attached tick is I scapularis, (3) the tick has been attached for more than 36 hours, and (4) treatment is begun within 72 hours of tick removal.27

Ticks are ectoparasitic hemophages that feed on mammals, reptiles, and birds. The Ixodidae family comprises the hard ticks. A hard dorsal plate, scutum, and capitulum that extends outward from the body are features that distinguish the hard tick. 1Ixodes is the largest genus of hard ticks, with more than 250 species localized in temperate climates.2 It has an inornate scutum and lacks festoons (Figure 1).1 The Ixodes ricinus species complex accounts for most species relevant to the spread of human disease (Figure 2), with Ixodes scapularis in the northeastern, north midwestern, and southern United States; Ixodes pacificus in western United States; I ricinus in Europe and North Africa; and Ixodes persulcatus in Russia and Asia. Ixodes holocyclus is endemic to Australia.3,4

Figure 1. Adult Ixodes scapularis tick with identifiable features such as 8 black legs, an inornate scutum, and an absence of festoons.

Figure 2. Geographic distribution of Ixodes species most commonly involved in disease transmission (approximation).

Life Cycle

Ixodes species progress through 4 life stages—egg, larvae, nymph, and adult—during their 3-host life cycle. Lifespan is 2 to 6 years, varying with environmental factors. A blood meal is required between each stage. Female ticks have a small scutum, allowing the abdomen to engorge during meals (Figure 3).

Figure 3. Female adult Ixodes scapularis tick (top) engorges following a blood meal, increasing in size as the light-colored abdomen expands beyond the dark-brown scutum (bottom).

Larvae hatch in the early summer and remain dormant until the spring, emerging as a nymph. Following a blood meal, the nymph molts and reemerges as an adult in autumn. During autumn and winter, the female lays as many as 2000 eggs that emerge in early summer.5 Nymphs are small and easily undetected for the duration required for pathogen transmission, making nymphs the stage most likely to transmit disease.6

The majority of tick-borne diseases present from May to July, corresponding to nymph activity. Fewer cases present in the autumn and early spring because the adult female feeds during cooler months.7

Larvae have 6 legs and are about the size of a sesame seed when engorged. Nymphs are slightly larger with 8 legs. Adults are largest and have 8 legs. Following a blood meal, the tick becomes engorged, increasing in size and lightening in color (Figure 3).1

Ticks are found in low-lying shrubs and tall grass as well as on the forest floor. They search for a host by detecting CO2, warmth, the smell of sweat, and the color white, prompting attachment.8 Habitats hospitable to Ixodes have expanded in the wake of climate, environmental, and socioeconomic changes, potentially contributing to the increasing incidence and expansion of zoonoses associated with this vector.9,10

 

 

Local Reactions

A tick bite may induce local hypersensitivity, leading to a red papule or plaque at the bite site, followed by swelling, warmth, and erythema. A cellular immune reaction induces induration and pruritus. Hard ticks are less likely than soft ticks to cause a serious local reaction.11,12

A variety of clinical and histologic features are observed following an arthropod bite. Histologically, acute tick bites show a neutrophilic infiltrate with fibrin deposition. Chronic reactions demonstrate a wedge-shaped, mixed infiltrate with prominent endothelial swelling. Eosinophilic cellulitis, or Wells syndrome, reveals tissue eosinophilia and flame figures.13 Tick mouthparts may be identified in the tissue. B-cell hyperplasia is seen in Borrelia lymphocytoma and is more common in Europe, presenting as erythematous to plum–colored nodules on the ear and areola.14

Lyme Disease

Disease manifestations vary by location. Lyme disease is associated with Borrelia burgdorferi and the recently identified Borrelia mayonii in the United States15; in Europe and Asia, acrodermatitis chronica atrophicans is associated with Borrelia afzelii and neuroborreliosis, with Borrelia garinii. Lyme disease is the most common tick-borne illness in the United States.16 The I ricinus species complex is the most common vector harboring Borrelia species.17 At least 36 hours of tick adherence is required for disease transmission.18 The incubation period is 3 to 20 days (median, 12 days).19

Clinical Findings
Erythema migrans is the most characteristic sign, seen in 80% of cases of Lyme disease. The typical rash is a centrifugally spreading, erythematous, annular patch with central clearing at the site of the tick bite.20 Atypical rashes include vesicular, indurated, ulcerated, and follicular variants.21 Histopathology commonly shows a superficial and deep perivascular lymphocytic infiltrate with plasma cells, histiocytes, and eosinophils.22 Typically, the rash resolves in 3 to 5 weeks.18

Early disseminated Lyme disease can present with any of the following findings: multiple erythema migrans; neurologic involvement, including cranial nerve palsy and meningitis; and Lyme carditis, which may result in atrioventricular block.23,24 Late findings include arthritis, encephalopathy, and polyneuropathy. A late cutaneous manifestation, acrodermatitis chronica atrophicans, is rare in the United States but occurs in as many as 10% of Lyme disease cases in Europe. An initial inflammatory response manifests as blue-red erythema and edema of the extensor surfaces of the extremities, commonly on the dorsal hands, feet, elbows, and knees. Firm fibrotic nodules may develop later over the olecranon and patella.23,24

The term chronic Lyme disease has been used to describe the persistence of symptoms after treatment; however, large clinical trials have not detected a difference in symptom frequency between patients with a history of Lyme disease and matched controls.25,26 Many patients with chronic Lyme disease may instead have posttreatment Lyme disease syndrome, described as nonspecific symptoms including fatigue, arthralgia, and decreased mental acuity following treatment of confirmed Lyme disease. Symptoms generally improve within 1 year.27

Laboratory Testing
The gold standard for laboratory diagnosis of Lyme disease is 2-tiered serologic testing. First, an enzyme immunoassay or immunofluorescence assay is used to screen for antibodies. A Western blot follows if the result of the screen is positive or equivocal. Western blot testing for IgM and IgG is used when illness duration is less than 4 weeks; after 4 weeks, a Western blot for IgG alone is sufficient.27,28 The 2-tiered test has 99% specificity. Sensitivity increases with duration of disease (29%–40% with erythema migrans; 42%–87% in early disseminated disease; 97%–100% in late disease).29,30 A false-positive result can occur in the presence of infectious mononucleosis, an autoimmune disorder, and syphilis. If serologic testing is negative and suspicion remains high, testing should be repeated in 2 to 4 weeks.31 When a patient in a Lyme-endemic area presents with typical erythema migrans, serologic testing is unnecessary prior to treatment.32

Management
Treatment of Lyme disease centers on antibiotic therapy (Table). First-line treatment of early disseminated disease is doxycycline for 14 days (range, 10–21 days).27 In pregnant women, children younger than 8 years, and tetracycline-allergic patients, amoxicillin or cefuroxime axetil for 14 days (range, 14–21 days) may be used.33 For erythema migrans without complications, doxycycline for 10 days is effective. Complications that require hospitalization are treated with intravenous ceftriaxone.27 Re-treatment in patients with posttreatment Lyme disease syndrome is not recommended.34 Prophylaxis with a single dose of doxycycline 200 mg may be indicated when all of the following conditions are met: (1) the patient is in an area where more than 20% of Ixodes ticks are infected with B burgdorferi, (2) the attached tick is I scapularis, (3) the tick has been attached for more than 36 hours, and (4) treatment is begun within 72 hours of tick removal.27

References
  1. Anderson JF, Magnarelli LA. Biology of ticks. Infect Dis Clin North Am. 2008;22:195-215.
  2. Jongejan F, Uilenberg G. The global importance of ticks. Parasitology. 2004;129(suppl):S3-S14.
  3. Xu G, Fang QQ, Keirans JE, et al. Molecular phylogenetic analyses indicate that the Ixodes ricinus complex is a paraphyletic group. J Parasitol. 2003;89:452-457.
  4. Swanson SJ, Neitzel D, Reed DK, et al. Coinfections acquired from Ixodes ticks. Clin Microbiol Rev. 2006;19:708-727.
  5. Mathison BA, Pritt BS. Laboratory identification of arthropod ectoparasites. Clin Microbol Rev. 2014;27:48-67.
  6. Falco RC, Fish D, Piesman J. Duration of tick bites in a Lyme disease-endemic area. Am J Epidemiol. 1996;143:187-192.
  7. Centers for Disease Control and Prevention. Lyme disease graphs. http://www.cdc.gov/lyme/stats/graphs.html. Updated November 21, 2016. Accessed November 21, 2017.
  8. Randolph SE. The impact of tick ecology on pathogen transmission dynamics. In: Bowman AS, Nuttall PA, eds. Ticks: Biology, Disease and Control. Cambridge, UK: Cambridge University Press; 2008:40-72.
  9. Ostfeld RS, Brunner JL. Climate change and Ixodes tick-borne diseases of humans. Philos Trans R Soc Lond B Biol Sci. 2015;370. pii:20140051. doi:10.1098/rstb.2014.0051.
  10. Medlock JM, Hansford KM, Bormane A, et al. Driving forces for changes in geographical distribution of Ixodes ricinus ticks in Europe. Parasit Vectors. 2013;6:1.
  11. McGinley-Smith DE, Tsao SS. Dermatoses from ticks. J Am Acad Dermatol. 2003;49:393-396.
  12. Middleton DB. Tick-borne infections. What starts as a tiny bite may have a serious outcome. Postgrad Med. 1994;95:131-139.
  13. Melski JW. Wells’ syndrome, insect bites, and eosinophils. Dermatol Clin. 2015;8:287-293.
  14. Castelli E, Caputo V, Morello V, et al. Local reactions to tick bites. Am J Dermatopathol. 2008;30:241-248.
  15. Pritt BS, Mead PS, Johnson DK, et al. Identification of a novel pathogenic Borrelia species causing Lyme borreliosis with unusually high spirochaetaemia: a descriptive study. Lancet Infect Dis. 2016;16:556-564.
  16. Orloski KA, Hayes EB, Campbell GL, et al. Surveillance for Lyme disease—United States, 1992-1998. MMWR CDC Surveill Summ. 2000;49:1-11.
  17. Gray JS. The ecology of ticks transmitting Lyme borreliosis. Exp Appl Acarol. 1998;22:249-258.
  18. Piesman J, Mather TN, Sinsky RJ, et al. Duration of tick attachment and Borrelia burgdorferi transmission. J Clin Microbiol. 1987;25:557-558.
  19. Richardson M, Elliman D, Maguire H, et al. Evidence base of incubation periods, periods of infectiousness and exclusion policies for the control of communicable diseases in schools and preschools. Pediatr Infect Dis J. 2001;20:380-391.
  20. Myers SA, Sexton DJ. Dermatologic manifestations of arthropod-borne diseases. Infect Dis Clin North Am. 1994;8:689-712.
  21. Ducroux E, Debarbieux S, Boibieux A, et al. Follicular borreliosis: an atypical presentation of erythema chronicum migrans. Dermatology. 2009;219:84-85.
  22. Miraflor AP, Seidel GD, Perry AE, et al. The many masks of cutaneous Lyme disease. J Cutan Pathol. 2016:43:32-40.
  23. Lenormand C, Jaulhac B, Debarbieux S, et al. Expanding the clinicopathological spectrum of late cutaneous Lyme borreliosis (acrodermatitis chronica atrophicans): a prospective study of 20 culture and/or polymerase chain reaction (PCR) documented cases. J Am Acad Dermatol. 2016;74:685-692.
  24. Zajkowska J, Czupryna P, Pancewicz SA, et al. Acrodermatitis chronica atrophicans. Lancet Infect Dis. 2011;11:800.
  25. Seltzer EG, Gerber MA, Cartter ML, et al. Long-term outcomes of persons with Lyme disease. JAMA. 2000;283:609-616.
  26. Shadick NA, Phillips CB, Sangha O, et al. Musculoskeletal and neurologic outcomes in patients with previously treated Lyme disease. Ann Intern Med. 1999;131:919-926.
  27. Wormser GP, Dattwyler RJ, Shapiro ED, et al. The clinical assessment, treatment, and prevention of Lyme disease, human granulocytic anaplasmosis, and babesiosis: clinical practice guidelines by the Infectious Diseases Society of America. Clin Infect Dis. 2006;43:1089-1134.
  28. Schriefer ME. Lyme disease diagnosis: serology. Clin Lab Med. 2015;35:797-814.
  29. Wormser GP, Nowakowski J, Nadelman RB, et al. Impact of clinical variables on Borrelia burgdorferi-specific antibody seropositivity in acute-phase sera from patients in North America with culture-confirmed early Lyme disease. Clin Vaccine Immunol. 2008;15:1519-1522.
  30. Leeflang MM, Ang CW, Berkhout J, et al. The diagnostic accuracy of serological tests for Lyme borreliosis in Europe: a systematic review and meta-analysis. BMC Infect Dis. 2016;16:140.
  31. Sanchez E, Vannier E, Wormser GP, et al. Diagnosis, treatment, and prevention of Lyme disease, human granulocytic anaplasmosis, and babesiosis: a review. JAMA. 2016;315:1767-1777.
  32. Lantos PM, Brinkerhoff RJ, Wormser GP, et al. Empiric antibiotic treatment of erythema migrans-like skin lesions as a function of geography: a clinical and cost effectiveness modeling study. Vector Borne Zoonotic Dis. 2013;13:877-883.
  33. Smith GN, Gemmill I, Moore KM. Management of tick bites and Lyme disease during pregnancy. J Obstet Gynaecol Can. 2012;34:1087-1091.
  34. Berende A, ter Hofstede HJ, Vos FJ, et al. Randomized trial of longer-term therapy for symptoms attributed to Lyme disease. N Engl J Med. 2016;374:1209-1220.
References
  1. Anderson JF, Magnarelli LA. Biology of ticks. Infect Dis Clin North Am. 2008;22:195-215.
  2. Jongejan F, Uilenberg G. The global importance of ticks. Parasitology. 2004;129(suppl):S3-S14.
  3. Xu G, Fang QQ, Keirans JE, et al. Molecular phylogenetic analyses indicate that the Ixodes ricinus complex is a paraphyletic group. J Parasitol. 2003;89:452-457.
  4. Swanson SJ, Neitzel D, Reed DK, et al. Coinfections acquired from Ixodes ticks. Clin Microbiol Rev. 2006;19:708-727.
  5. Mathison BA, Pritt BS. Laboratory identification of arthropod ectoparasites. Clin Microbol Rev. 2014;27:48-67.
  6. Falco RC, Fish D, Piesman J. Duration of tick bites in a Lyme disease-endemic area. Am J Epidemiol. 1996;143:187-192.
  7. Centers for Disease Control and Prevention. Lyme disease graphs. http://www.cdc.gov/lyme/stats/graphs.html. Updated November 21, 2016. Accessed November 21, 2017.
  8. Randolph SE. The impact of tick ecology on pathogen transmission dynamics. In: Bowman AS, Nuttall PA, eds. Ticks: Biology, Disease and Control. Cambridge, UK: Cambridge University Press; 2008:40-72.
  9. Ostfeld RS, Brunner JL. Climate change and Ixodes tick-borne diseases of humans. Philos Trans R Soc Lond B Biol Sci. 2015;370. pii:20140051. doi:10.1098/rstb.2014.0051.
  10. Medlock JM, Hansford KM, Bormane A, et al. Driving forces for changes in geographical distribution of Ixodes ricinus ticks in Europe. Parasit Vectors. 2013;6:1.
  11. McGinley-Smith DE, Tsao SS. Dermatoses from ticks. J Am Acad Dermatol. 2003;49:393-396.
  12. Middleton DB. Tick-borne infections. What starts as a tiny bite may have a serious outcome. Postgrad Med. 1994;95:131-139.
  13. Melski JW. Wells’ syndrome, insect bites, and eosinophils. Dermatol Clin. 2015;8:287-293.
  14. Castelli E, Caputo V, Morello V, et al. Local reactions to tick bites. Am J Dermatopathol. 2008;30:241-248.
  15. Pritt BS, Mead PS, Johnson DK, et al. Identification of a novel pathogenic Borrelia species causing Lyme borreliosis with unusually high spirochaetaemia: a descriptive study. Lancet Infect Dis. 2016;16:556-564.
  16. Orloski KA, Hayes EB, Campbell GL, et al. Surveillance for Lyme disease—United States, 1992-1998. MMWR CDC Surveill Summ. 2000;49:1-11.
  17. Gray JS. The ecology of ticks transmitting Lyme borreliosis. Exp Appl Acarol. 1998;22:249-258.
  18. Piesman J, Mather TN, Sinsky RJ, et al. Duration of tick attachment and Borrelia burgdorferi transmission. J Clin Microbiol. 1987;25:557-558.
  19. Richardson M, Elliman D, Maguire H, et al. Evidence base of incubation periods, periods of infectiousness and exclusion policies for the control of communicable diseases in schools and preschools. Pediatr Infect Dis J. 2001;20:380-391.
  20. Myers SA, Sexton DJ. Dermatologic manifestations of arthropod-borne diseases. Infect Dis Clin North Am. 1994;8:689-712.
  21. Ducroux E, Debarbieux S, Boibieux A, et al. Follicular borreliosis: an atypical presentation of erythema chronicum migrans. Dermatology. 2009;219:84-85.
  22. Miraflor AP, Seidel GD, Perry AE, et al. The many masks of cutaneous Lyme disease. J Cutan Pathol. 2016:43:32-40.
  23. Lenormand C, Jaulhac B, Debarbieux S, et al. Expanding the clinicopathological spectrum of late cutaneous Lyme borreliosis (acrodermatitis chronica atrophicans): a prospective study of 20 culture and/or polymerase chain reaction (PCR) documented cases. J Am Acad Dermatol. 2016;74:685-692.
  24. Zajkowska J, Czupryna P, Pancewicz SA, et al. Acrodermatitis chronica atrophicans. Lancet Infect Dis. 2011;11:800.
  25. Seltzer EG, Gerber MA, Cartter ML, et al. Long-term outcomes of persons with Lyme disease. JAMA. 2000;283:609-616.
  26. Shadick NA, Phillips CB, Sangha O, et al. Musculoskeletal and neurologic outcomes in patients with previously treated Lyme disease. Ann Intern Med. 1999;131:919-926.
  27. Wormser GP, Dattwyler RJ, Shapiro ED, et al. The clinical assessment, treatment, and prevention of Lyme disease, human granulocytic anaplasmosis, and babesiosis: clinical practice guidelines by the Infectious Diseases Society of America. Clin Infect Dis. 2006;43:1089-1134.
  28. Schriefer ME. Lyme disease diagnosis: serology. Clin Lab Med. 2015;35:797-814.
  29. Wormser GP, Nowakowski J, Nadelman RB, et al. Impact of clinical variables on Borrelia burgdorferi-specific antibody seropositivity in acute-phase sera from patients in North America with culture-confirmed early Lyme disease. Clin Vaccine Immunol. 2008;15:1519-1522.
  30. Leeflang MM, Ang CW, Berkhout J, et al. The diagnostic accuracy of serological tests for Lyme borreliosis in Europe: a systematic review and meta-analysis. BMC Infect Dis. 2016;16:140.
  31. Sanchez E, Vannier E, Wormser GP, et al. Diagnosis, treatment, and prevention of Lyme disease, human granulocytic anaplasmosis, and babesiosis: a review. JAMA. 2016;315:1767-1777.
  32. Lantos PM, Brinkerhoff RJ, Wormser GP, et al. Empiric antibiotic treatment of erythema migrans-like skin lesions as a function of geography: a clinical and cost effectiveness modeling study. Vector Borne Zoonotic Dis. 2013;13:877-883.
  33. Smith GN, Gemmill I, Moore KM. Management of tick bites and Lyme disease during pregnancy. J Obstet Gynaecol Can. 2012;34:1087-1091.
  34. Berende A, ter Hofstede HJ, Vos FJ, et al. Randomized trial of longer-term therapy for symptoms attributed to Lyme disease. N Engl J Med. 2016;374:1209-1220.
Issue
Cutis - 101(3)
Issue
Cutis - 101(3)
Page Number
187-190
Page Number
187-190
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Cutis
MDedge Dermatology
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Cutis
MDedge Dermatology
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Infectious Diseases
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What’s Eating You? Ixodes Tick and Related Diseases, Part 1: Life Cycle, Local Reactions, and Lyme Disease
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What’s Eating You? Ixodes Tick and Related Diseases, Part 1: Life Cycle, Local Reactions, and Lyme Disease
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Practice Points

  • Lyme disease is transmitted by Ixodes ticks in the northeastern, midwestern, and far western United States.
  • Most tick-borne illnesses, including Lyme disease, respond to treatment with doxycycline.
  • Babesiosis, a malarialike illness, can be transmitted concurrently with Lyme disease.
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