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Feature

A Closer Look at Skin Disease Secondary to Tick Bites

September 2024

When patients spend time outdoors, tick bites can cause lesions that can lead to various cutaneous diseases. Physicians may have difficult identifying the lesions and pairing them with their associated parasites, making the identification of the ticks important.

There are 2 types of ticks that clinicians should become familiar with: hard ticks (Ixodidae family) and soft ticks (Nuttalliellidae family).1 Ixodidae ticks, which cause most skin manifestations in humans, have a shield on their bodies that protects against certain degrees of pressure. Hard ticks attach painlessly to patients via a serrated mouthpart and will not detach until transitioning to a new phase in their life cycle (larvae, nymph, adult). Ticks at all life cycle stages can cause allergic and toxic reactions in humans, and can inoculate various infectious agents such as Rickettsia species, other bacteria, protozoa and fungi.

When the attachment causing the primary lesion is a singular adult tick, one may be able to visualize it while engorged. The lower limbs are commonly impacted, but papules may appear anywhere. Given that ticks have a predilection for body folds, one should carefully examine these areas, such as interdigitally on the feet.

When the infestation is due to tick larvae, the small arthropods may not be visible, and attach simply by brushing against them.1 In these cases, clinicians may note a “comet tail” sign, due to multiple arthropods attaching onto the same site with subsequent movement, widening the bite area. The associated papules are erythematous and firm, and may contain central vesicles. In larval infestations, severe pruritus may be present from the up to hundreds of resulting lesions.

Systemic antihistamines and topical steroids are important symptom management tools, but prescribing systemic steroids may be necessary for multiple bite scenarios. Secondary infections may also arise, which could warrant topical or systemic antibiotics.1 Patients can experience delayed reactions to primary lesions due to how the tick attaches to the skin through the serrated mouthpart. When the mouthpart breaks upon extraction, the skin retains fragments, which causes chronic foreign body–type reactions that can persist for months. Although the nodules tend to resist topical medications, local steroid injections may be an effective option.

Secondary lesions are caused by Rickettsia species, as well as other bacterial, protozoan, or fungal infections inoculated by the ticks. These lesions can include those from Lyme disease, Rocky Mountain spotted fever, tick paralysis, ehrlichiosis, and tularemia.

2
This photo shows a female Ixodes scapularis tick carrying multiple larvae. Ticks at all life cycle stages can cause allergic or toxic reactions in humans.

What You Should Know About Lyme Disease

Tick bites can transmit Lyme disease due to the spirochete Borrelia burgdorferi.1 The initial cutaneous lesion takes the form of erythema migrans. One may see expanding  erythematous macules or papules that evolve into plaques with interrupted borders and a lighter purple and/or scaling center. The dissemination of the spirochete causes the concentric expansion of this center, creating the classic “bullseye” that can have a large diameter. The bullseye can appear anytime from 3–30 days after the initial bite.2 Even though erythema migrans can arise on any area of the skin, it mostly appears on the lower and upper limbs and face.

Hematogenous or lymphatic spread of the spirochetes may result in new erythema migrans lesions days or weeks after the cutaneous manifestations appear.1 One can treat the initial manifestations with doxycycline 100mg twice daily for 14 days, but initial lesions may disappear even without treatment. This is a complicating factor that could confound early diagnosis. However, it is important to note that patients can experience late manifestations months or years after the initial Lyme disease infection, but rarely appear at the same time as erythema migrans. Patients can also experience chronic cutaneous involvement in the form of acrodermatitis chronica atrophicans.1 

Insights on Rocky Mountain Spotted Fever

Rocky Mountain spotted fever (RMSF), caused by Rickettsia rickettsii, has a sudden onset in the form of flu-like symptoms lasting 2 to 3 weeks.1 An erythematous, macu-lopapular rash will be visible on the third or fourth day. Lesions that become purpuric with the formation of petechiae indicate severe disease and generalized vasculitis as the agent multiplies in endothelial cells of small vessels.1 RMSF can manifest with no or only mild symptoms; however, some patients can progress to extensive cutaneous necrosis in areas of hemorrhage. If RMSF goes untreated, the mortality rate can be about 20 percent. Treating RMSF with antibiotics—doxycycline for mild to moderate infection and chloramphenicol IV in severe infection—can reduce mortality.1

Tick Paralysis, Erlichosis, and Tularemia: Important Insights

Toxins in the saliva of certain ticks may cause tick paralysis, resulting from a rapid-onset block of neuromuscular transmission, leading to ascending flaccid paralysis.1 If untreated, the patient may experience respiratory failure or death. Tick paralysis is well-described in domesticated animals but can also affect humans, although rarely. To confirm the diagnosis, the tick must be attached to the patient. Removing the arthropod leads to a dramatic regression of symptoms, with potentially no sequelae. Treatment is symptom-based, especially in severe cases.1

Ehrlichiosis and tularemia are bacterial infections that cause high fever, nausea, vomiting and an erythematous or erythematous-purplish non-specific rash.1 Treatment is typically with doxycycline. Patients with tularemia may also have a deep ulcer on the site of the bite and swollen regional lymph nodes. Streptomycin is another antibiotic documented to treat tularemia.

Advising Patients on Tick Removal

In general patients should remove ticks promptly.1 Prolonged tick attachment has a direct relationship with resulting inflammation and with the transmission of infection or toxins. Nymphs and adult ticks may favor moist and warm areas, and thin skin such as the axillae, inguinal regions, ankles, and scalp. Curved, fine forceps may contribute to accurate removal. One should take care to only grasp the tick just below its head, near the skin level, not the body or head itself. Too much pressure on the body or head may result in further spread of saliva from the tick. Slow, steady extraction by pulling straight and upward as atraumatically as possible is advisable. Proper hand washing both before and after removal is also wise.

After removal, inspect for any residual parts of the tick on the skin surface, and consider antiseptic cleansing and topical antimicrobial ointment if indicated. Picaridin or DEET on the skin and permethrin on the external surface of clothes, shoes, and tents may be used as repellents.1

Concluding Thoughts

It is important for podiatrists to be aware of tick-related clinical symptoms and possible resultant conditions, as they may often have lower extremity manifestations. It is wise to maintain an index of suspicion when noting characteristic lesions or constellations of symptoms. Further learning about differential diagnoses and diagnostic testing may also enhance clinical protocols, but are outside the scope of this piece.

Dr. DeLauro is a Diplomate of the American Board of Podiatric Medicine and the American Board of Foot and Ankle Surgery. She is in private practice in New York and New Jersey.

References

1.    Haddad V Jr, Haddad MR, Santos M, Cardoso JLC. Skin manifestations of tick bites in humans. An Bras Dermatol. 2018;93(2):251-255. doi:10.1590/abd1806-4841.20186378
2.    American Academy of Dermatology. Signs of Lyme disease that appear on your skin.
3.    Spach DH, Liles WC, Campbell GL, Quick RE, Anderson DE Jr, Fritsche TR. Tick-borne diseases in the United States. N Engl J Med. 1993; 329(13):936-47.
4.    McGinley-Smith DE, Tsao SS. Dermatoses from ticks. J Am Acad Dermatol. 2003; 49(3):363-92.

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