Southern Tick-Associated Rash Illness (STARI)



Adult female Lone Star tick. Photo courtesy of the Centers for Disease Control.

Since the late 1980s, physicians in the south central and southeast United States have observed Lyme disease-like rashes on patients with a recent history of tick bite. However, the tick vector associated with these lesions is Amblyomma americanum, the Lone Star tick, rather than either of Ixodes tick species – I. scapularis or I. pacificus - known to transmit Lyme disease in the United States. In the absence of proof that the causative agent of Lyme disease, Borrelia burgdorferi sensu stricto, is associated with these rashes (and considerable evidence that it is not), this clinical entity has been differentiated from Lyme disease and is called Southern Tick-Associated Rash Illness, or STARI. It is also sometimes referred to as Masters disease, in honor of Edwin Masters, the Missouri family physician who first reported these cases to his state’s Department of Health.

Despite vigorous efforts, the causative agent of STARI has never been cultured and is not currently known. However, some evidence exists that a recently discovered spirochete, Borrelia lonestari, may be responsible: B. lonestari has been detected by polymerase chain reaction (PCR) in Lone Star ticks removed from humans, as well as in Lone Star ticks collected during general epidemiological studies. More convincingly, B. lonestari DNA was detected by PCR in the biopsied skin lesion of a patient with a history of recent Lone Star tick bite, while B. burgdorferi DNA was absent in the same sample. However, other studies have been unable to confirm this finding; in one Missouri investigation, biopsies from the lesions of 31 patients with Lone Star tick bites were negative by both culture and PCR for B. lonestari. Thus, the etiology of STARI remains elusive. It is possible that multiple borrelial species may be responsible.

The known geographic range of the Lone Star tick has expanded over the past two decades and now stretches northward into both New England and the southern Great Lakes area. As a result, there are now regions of the country where both STARI and Lyme disease are endemic, making it difficult sometimes to distinguish between the two diseases on epidemiological grounds alone.

The true incidence of STARI is unknown, as the illness in not nationally reportable.

Signs and Symptoms


STARI rash on the back of adult male patient from Missouri. Photo by Dr. Edwin Masters, courtesy of Infectious Disease Clinics of North America

The hallmark of Southern Tick-Associated Rash Illness is the Lyme-like lesion. The rash usually appears within seven days of a Lone Star tick bite, and similar to the Lyme lesion, expands in a circular or elliptical fashion. Patients with STARI can also have constitutional symptoms, such as fever, headache, stiff neck, myalgias and joint pain, but these are less frequent and generally less severe in STARI patients than in patients with Lyme disease.

The full clinical picture of STARI is not well understood, but there is general consensus that the post-rash sequelae of STARI are significantly milder than those of Lyme disease. Some physicians in areas endemic for STARI have reported post-rash neurologic and cardiac manifestations in rare cases, but these are not universally accepted findings. Long term follow up studies of STARI patients have never been performed.

As Lone Star ticks are also vectors of Q fever and human monocytic ehrlichiosis, physicians should be alert to the possibility of coinfection. Cases of coinfection of STARI and these illnesses exist in the academic literature.


In the absence of a known etiological agent, it is impossible to develop serologic tests for STARI. Thus, the diagnosis of STARI is clinical and based primarily on the existence of the typical rash, ideally after a known Lone Star  tick bite.

There appear to be some very subtle differences between Lyme and STARI rashes. STARI lesions are smaller on average and less variable in shape than those of Lyme disease, and also tend to have more central clearing – ironically, making them more likely to consistently resemble the iconic “bull’s eye” rash of Lyme disease than Lyme rashes themselves. Another difference in rash presentation is that secondary (multiple) lesions tend to be less common in STARI than in Lyme disease. In general, however, it is almost never possible to distinguish between Lyme and STARI rashes on the basis of appearance alone.

Although PCR tests have been developed to probe for B. lonestari DNA in tissue or blood samples, they are not commercially available and are of limited usefulness in any case as long as doubts remain about B. lonestari’s role in the etiology of STARI.


Despite the lack of a known causative agent for STARI, the skin lesion’s similarity to the rash associated with Lyme disease has led most physicians and health agencies to conclude that STARI should be treated similarly to early Lyme disease. Thus, antibiotic therapy is the treatment of choice, and is usually continued for two to three weeks. Doxycycline and amoxicillin are the most commonly prescribed antibiotics. If signs and symptoms of disseminated illness (fever, headache, lymphadenopathy, etc.) are present, some physicians will treat for slightly longer periods.

Most cases of STARI respond completely with timely antibiotic treatment.

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