Tickborne diseases in the United States are a significant public health problem, and in the past 50 years scientists have detected at least a dozen new such infections. With more than 30,000 cases diagnosed each year, Lyme disease is the most commonly reported vector-borne illness in the United States, and in 2015 it was the sixth most common nationally notifiable disease.1
Due to increased education and recognition, most practitioners are familiar with the symptomatic presentation of Lyme disease. In stage 1, patients usually exhibit the classic erythematous expanding annular “bulls-eye” rash known as erythema migrans, and approximately 50% experience constitutional flu-like symptoms. In stages 2 and 3, or disseminated Lyme disease, patients may present with Bell’s palsy or other cranial nerve deficits, arthritis, peripheral neuropathies, and cardiac manifestations such as transient heart block and carditis. Borrelia burgdorferi, the spirochete that causes Lyme disease, is not the only pathogen spread by the deer tick Ixodes scapularis in the northeastern United States: Babesia microti, the agent of babesiosis, and Anaplasma phagocytophilum, the agent of human granulocytic anaplasmosis (HGA; formerly human granulocytic ehrlichiosis) are asserting a presence in similar geographic regions. Coinfection with these organisms is possible. Human monocytic ehrlichiosis (HME), caused by Ehrlichia chaffeensis, is another emerging tickborne disease with similar geography to HGA. The incidence of babesiosis,HGA,and HME is increasing, and the geographic areas for their tick vectors are expanding. HME and HGA can be serious infections with high rates of hospitalization and complications, particularly when diagnosis or treatment is delayed.
Babesia microti is the predominant protozoan cause of babesiosis in the United States; occasional sporadic cases of babesiosis caused by other species have been reported. Babesiosis is transmitted by the bite of an infected I scapularis (commonly known as the black-legged or deer tick) (Figure 1), usually in the nymphal or adult stage. The primary carrier of Babesia are white-footed mice, although it is found in other small mammals. Although white-tailed deer are the most important food source for the adult stage of the tick, deer are not infected with B microti.2 Babesia is rarely transmitted by blood transfusion, organ transplant, or vertically during pregnancy. The incidence of transfusion-transmitted babesiosis in the United States is 1.1 cases per million red blood cell units distributed.3
HME is caused by Ehrlichia chaffeensis, anobligate intracellular gram-negative species of rickettsial bacteria that grows within membrane-bound vacuoles in human and animal leukocytes.4,5 Less commonly, human disease is caused by E ewingii, the organism responsible for canine granulocytic ehrlichiosis. The principal vector of E chaffeensis is the lone star tick (Amblyomma americanum) (Figure 2). Other ticks occasionally have been found to contain DNAof E chaffeensis, but their role in transmission is unlikely.4 The white-tailed deer is the main competent reservoir for E chaffeensis, although domestic goats, dogs, raccoons, and coyotes may also carry the bacterium.
HGA is caused by the gram-negative bacterium Anaplasma phagocytophilum, which is transmitted by I scapularis, the same vector of Lyme disease and babesiosis. I pacificus, the western black-legged tick, is the primary vector of HGA in the western United States. Also similar to Lyme disease, deer and the white-footed mouse are the principal animal hosts for HGA.
This article originally appeared on Clinical Advisor