STARI, or Masters Disease: Lone Star Tick–Vectored Lyme-like Illness

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Lyme-like illness (also known as southern tick–associated rash illness [STARI] or Masters disease) is vectored by the Lone Star tick (Amblyomma americanum). Lyme-like illness lesions, which are similar to the erythema migrans rash of Lyme disease, tend to have lymphocytic dermal infiltrates. With the exception of Borrelia lonestari, the possible causative agent or agents of Lyme-like illness have not been cultured. More research is needed to fully understand this newly recognized zoonosis. Clinicians are encouraged to increase their knowledge and awareness of this Lyme disease mimic.

Section snippets

Epidemiology

Lyme-like illness does not appear to be caused by Borrelia burgdorferi sensu stricto. The exact etiology or etiologies are still uncertain. One putative bacterial cause of Lyme-like illness is Borrelia lonestari found in Amblyomma americanum ticks [11], [12]. One case implicating this bacterial species has been published [13]. In addition, Borrelia lonestari has been detected in Lone Star ticks removed from humans [14]. In one polymerase chain reaction (PCR) DNA screen of 312 southeastern

Appearance

The annular lesions in Lyme-like illness have many similarities to Lyme erythema migrans. This similarity is the primary basis for the term “Lyme-like” (Fig. 2, Fig. 3, Fig. 4). Although the lesions of each illness can differ clinically as a group—Lyme-like lesions tend to be smaller and more circular, have more central clearing, are more likely to have a patchy irregular border (see Fig. 2J, K), and are less commonly seen in multiples—it is difficult to use appearance to differentiate

Clinical sequelae

With the etiology of Lyme-like illness still uncertain and with no definitive test available, it is impossible to absolutely prove rash sequelae; however, the authors' impressions are that Lyme-like illness results in far less severe arthritis than Lyme disease. In an early study, Missouri patient data were compared with national Lyme disease data, and the frequency of signs and symptoms was roughly comparable [26]. Although no long-term follow-up study of Lyme-like illness has been done, the

Histology

In Fig. 5, the histologic differences between dermal cellular infiltrates of Lyme erythema migrans and Lyme-like illness rashes are shown. It is evident that when stained with hemotoxylin-eosin, the Lyme-like rashes have a predominantly lymphocytic infiltrate. In contrast, Lyme erythema migrans often shows an abundance of plasma cells [31].

Serology

Because Lyme-like illness—by definition—is not caused by infection with Borrelia burgdorferi sensu stricto [1], it is not surprising that conventional serologic tests such as ELISAs and Western blots, which are based on Borrelia burgdorferi sensu stricto, are usually negative. Cross-reactivity can occur, however, and Lyme tests are known to have false-positive and false-negative results. A 3-year comparative study illustrates the different results. Using a baseline ELISA, none of the 25

Incubation time

Of the physician-diagnosed Lyme-like illness cases published, the authors identified 128 in which the incubation times were able to be calculated [3], [7], [19], [22], [24], [25], [29]. Being careful to count patients only once, 45 Lyme-like illness patients had a mean incubation time of 9.2 days. Another 83 patients had a median incubation time of 6.6 days. The most recent 18 patients had a mean incubation time of 6.1 days [7].

The authors found no evidence that larger adult tick bites (with

Treatment

The causative agent or agents of Lyme-like illness are not definitively known. The authors believe that this Lyme-like illness deserves Lyme-like treatment, and that standard Lyme treatment recommendations apply [35]. Therefore, the authors prescribe 10 to 30 days of oral doxycycline at 3 mg/kg in divided doses, amoxilcillin 500 mg three times daily, or cefuroxime 500 mg orally twice daily [3]. Because there is evidence that cephalexin is not efficacious for Lyme disease [36], the authors do

Coinfection

Our current appreciation of the Lone Star tick (Amblyomma americanum) as a vector of human pathogens is relatively recent [37]. Just as physicians in the northeastern United States should be aware of coinfections resulting from the Ixodes scapularis deer tick transmitting more than one pathogen [38], doctors should be aware that the Lone Star tick can similarly transmit more than one pathogen.

Three published cases of Lyme-like illness coinfection (two with HME due to Ehrlichia chaffeensis and

Clinical differentiation

Although Lyme-like rashes can have mild pruritis, the common presence of intense pruritis in hypersensitivity reactions can help distinguish them. Many patients present with an asymptomatic Lyme-like bull's-eye rash on their back. Due to patients’ infrequent examination of their own back, they may be unaware of the rash until a family member calls it to their attention. Similarly, the absence or presence of any prior rash reaction to tick bites is helpful in differentiation (eg, a person has

Discussion

The current definition of Lyme disease in the United States is an infection caused exclusively by Borrelia burgdorferi sensu stricto [1]. Even though the precise etiology of Lyme-like illness is unknown, there is overwhelming evidence that it is not caused by Borrelia burgdorferi sensu stricto. This fact mandates that Lyme-like illness be classified as a separate condition or disease.

Borrelia burgdorferi sensu stricto has been documented in nature in areas nonendemic for Lyme disease [51], [52]

Summary

The Lone Star tick (Amblyomma americanum) is the vector of Lyme-like illness, also known as STARI or Masters disease. The spread of this aggressive tick through the Northeast [59], even into Maine [60], has caused some to reconsider calling this STARI (see Fig. 1). There is concern that this acronym might cause problems similar to those caused by the Rocky Mountain spotted fever misnomer. The authors anticipate that as the Amblyomma americanum tick expands its territory, the Lyme-like illness

Acknowledgments

The authors acknowledge the following contributors who assisted in the preparation of this article: Karen Angotti, Peggy and David Bird, Sally Mitchell Lape, Dr. Susan E. Little, and Dr. James H. Oliver.

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