Increasing incidence and changing epidemiology of babesiosis in the Hudson Valley region of New York State: 2009-2016.

Babesiosis is an emerging infection in parts of New York State. From 2009 through 2016, there was a significant increase in the incidence rate of babesiosis in the Hudson Valley region of New York State (P = 0.002), an inland geographic location in which babesiosis only first emerged in 2001. A significant increase in cases was found for both the Upper Hudson Valley (UHV) region (P < 0.001) as well as for the Lower Hudson Valley region (P = 0.03). The greatest increase in the incidence rate was found for the UHV, with a 16.8-fold increase in incidence over the 8-year time period. In conclusion, babesiosis is a rapidly emerging infection in the Hudson Valley region of New York State, the geographic region now accounting for more cases than any other single geographic area in the state.

Babesia--a historical overview.

The history of the genus Babesia is briefly outlined. The classical differences with the main other genus of non-pigment-forming hemoparasites, Theileria, are the absence of extra-erythrocytic multiplication (schizogony) in Babesia and the cycle in the vector tick, which includes transovarial transmission in Babesia but only transstadial transmission in Theileria. Also, the multiplication in the red cell of Babesia, by budding, most often results in two daughter cells (merozoites), while that of Theileria gives four merozoites, often as a Maltese cross. In particular this means that what is still commonly called Babesia microti is not a Babesia and that it would be just as logical to speak of human theileriosis as of babesiosis. The small piroplasm of horses, long known as Babesia equi, is already commonly designated as Theileria equi. However, on molecular grounds, it may be necessary to create a new genus for these parasites. The Babesia species of domestic animals are briefly discussed and presented in a table.

Theobald Smith--the discoverer of ticks as vectors of disease.

The cause of Texas fever in cattle, which is characterised by lysis of erythrocytes leading to anaemia, icterus, haemoglobinuria, and death, remained unsolved for many decades and assorted theories were proposed as an explanation for a disease being transmitted by apparently healthy animals. From 1889 to 1893, Theobald Smith and Frederick L. Kilbourne could demonstrate in elegantly conducted experiments how the disease was spread from cattle to cattle by ticks serving as the vector of transmission. Furthermore, they were able to identify the pathogen of Texas fever, an intra-erythrocytic protozoan which Smith named Pyrosoma bigeminum. Today it is recognised that either of two species of the now renamed genus Babesia, Babesia bigemina and Babesia bovis, may be involved in Texas fever and that babesiosis is generally transmitted by ticks. In animals, genera like Boophilus spp., Dermacentor spp. and Rhipicephalus spp. are possible vectors. The first case of tick-transmitted babesiosis in a human was reported by Skrabalo and Deanovic in 1957 and occurred near Ljubliana in the small town of Strmec, Croatia. In humans, the vectors of most reported cases are ticks of the genus Ixodes, which are among the most predominant ticks in Austria. However, cases of human babesiosis in Austria remain to be studied. Smith and Kilbourne's work was the first demonstration that ticks transmit disease of any kind. Furthermore, by proving that ticks carry Babesia microti--which causes babesiosis in animals and humans--this is the first account of a zoonotic disease and the foundation of all later work on the animal host and the arthropod vector.

Development of effective living vaccines against bovine babesiosis--the longest field trial?

Between 1959 and 1996, research was performed to change a vaccine against babesiosis in Australia and to improve it as actual or threatened untoward field responses became apparent. The most significant change occurred in 1964 with the traditionally used carriers of Babesia being replaced as vaccine donors by acutely infected splenectomised calves. This ensured the infectivity of the vaccine and was fortuitously associated with a reduction in the virulence of Babesia bovis in vaccine. Since then, more than 27 million doses of highly infective vaccine have been supplied from the laboratory at Wacol near Brisbane. This vaccine reduced serious losses from babesiosis in vaccinated cattle in Australia to very low levels and has now gained acceptance worldwide. Research to ensure the continuing effectiveness of the vaccine has proved to be essential.

Long odyssey of babesiosis.

The history of babesiosis is traced from the discovery of the parasite in 1888, to its present endemic niche. The author uncovers clinical and epidemiological features of human babesiosis in a patient hospitalized in New Jersey.

Erythema migrans: a chronicle.

Arvid Afzelius first described and named erythema migrans (EM), a clinical entity that he assumed to be caused by an agent transmitted by the bite of a tick (Ixodes reduvius). Certain neurologic, cutaneous, and other syndromes observed in Europe were recognized in the 1920s and 1930s to be disabling sequelae of EM. In the 1940s and 1950s the effectiveness of penicillin as therapy for EM was demonstrated. In 1968 the first patient with EM and neurologic sequelae in North America benefited from treatment with penicillin. In 1975, an epidemic arthropathy appeared in the area of Lyme, Connecticut. Despite resemblance to EM (the initial appearance of cutaneous lesions), the complex was called Lyme disease because of the occurrence of cardiac, neurologic, and arthritic sequelae. The vector of Lyme disease, Ixodes dammini--a tick that harbors agents that cause Lyme disease and babesiosis--was identified and characterized in 1979. The spirochete that causes Lyme disease was designated Borrelia burgdorferi. The North American and European species of spirochete and the clinical syndromes to which they are related are described.