Babesia life cycle Babesia parasites reproduce in red blood cells, where they can be seen as cross-shaped inclusions

(fourmerozoites asexually budding, but attached together forming a structure looking like a "Maltese cross")[3] and cause hemolytic anemia, quite similar to malaria. Unlike the Plasmodium parasites that cause malaria, Babesia species lack an exoerythrocytic phase, so the liver is usually not affected. In animals, Babesia canis rossi, Babesia bigemina, and Babesia bovis cause particularly severe forms of the disease, including a severe haemolytic anaemia, with positive erythrocyte-in-saline-agglutination test indicating an immune-mediated component to the haemolysis. Common sequelae include haemoglobinuria "red-water", disseminated intravascular coaguation and "cerebral babesiosis" caused by sludging of erythrocytes in cerebral capillaries. In bovine species, the organism causes hemolytic anemia, so an infected animal will show pale mucous membranes initially. As the levels of billirubin (a byproduct of red blood cell lysis) continue to increase, the visible mucous membranes will become yellow in color (icterus) due to the failure of the liver to metabolise the excess bilirubin. Hemoglobinuria will be seen due to excretion of red-blood-cell lysis byproducts via the kidneys. Fever of 40.5C (105F) develops due to release of inflammatory byproducts. Diagnosis[edit] Only specialized laboratories can adequately diagnose Babesia infection in humans, and as a result Babesia infections are considered highly under-reported. It develops in patients who live in or travel to an endemic area or receive a contaminated blood transfusion within the preceding 9 weeks, so this aspect of the medical history is vital.[4] Babesiosis may be suspected when a person with such an exposure history develops persistent fevers and hemolytic anemia. The definitive diagnostic test is the identification of parasites on a Giemsa-stained thin blood smear.[4] So-called "Maltese cross formations" on the blood film are essentially diagnostic of babesiosis, since they are not seen in malaria, the primary differential diagnosis.[3] Careful examination of multiple smears may be necessary, since Babesia may infect less than 1% of circulating red blood cells and thus be easily overlooked.[5] Serologic testing for antibodies against Babesia (both IgG and IgM) can detect low-level infection in cases with a high clinical suspicion, but negative blood film examinations. Serology is also useful for differentiating babesiosis from malaria in cases where people are at risk for both infections. Since detectable antibody responses require about a week after infection to develop, serologic testing may be falsely negative early in the disease course.[6] A polymerase chain reaction (PCR) test has been developed for the detection of Babesia from the peripheral blood.[7] PCR may be at least as sensitive and specific as blood film examination in diagnosing babesiosis, though it is also significantly more expensive.[8] Most often, PCR testing is used in conjunction with blood film examination and possibly serologic testing.[4] Other laboratory findings include decreased numbers of red blood cells and platelets on complete blood count.

In animals, babesiosis is suspected by observation of clinical signs (haemoglobinuria and anaemia) in animals in endemic areas. Diagnosis is confirmed by observation of merozoites on thin film blood smear examined at maximum magnification under oil using Romonovski stains (methylene blue and eosin). This is a routine part of the veterinary examination of dogs and ruminants in regions where babesiosis is endemic. Babesia canis and B. bigemina are "large babesias" that form paired merozoites in the erythrocytes, commonly described as resembling "two pears hanging together", rather than the "Maltese Cross" of the "small babesias". Their merozoites are approximately twice the size of small babesias. Cerebral babesiosis is suspected in vivo when neurological signs (often severe) are seen in cattle that are positive for B. bovis on blood smear, but this has yet to be proven scientifically. Outspoken red discolouration of the grey matter post mortem further strengthens suspicion of cerebral babesiosis. Diagnosis is confirmed post mortem by observation of babesia-infected erythrocytes sludged in the cerebral cortical capillaries in a brain smear. Treatment[edit] Most cases of babesiosis resolve without any specific treatment. For ill patients, treatment is usually a two-drug regimen, quinine and clindamycin.[9] As these drugs are often poorly tolerated, recent evidence suggests a regimen of atovaquone and azithromycin can be equally effective.[10] In lifethreatening cases, exchange transfusion is performed. In this procedure, the infected red blood cells are removed and replaced with uninfected ones. Imizol is a drug trade mark ICI is best against Babesiosis in Veterinary. Epidemiology[edit] Babesiosis is a vector-borne illness usually transmitted by Ixodes scapularis ticks. Babesia microti uses the same tick vector as Lyme disease and ehrlichiosis, and may occur in conjunction with these other diseases.[2] The organism can also be transmitted by blood transfusion.[11][12] Ticks of domestic animals, especially Rhipicephalus (Boophilus) microplus and R. (B.) decoloratustransmit several species of Babesia to livestock animals, causing considerable economic losses to farmers in tropical and subtropical regions. In North America, the disease is primarily found in eastern Long Island, Fire Island, Nantucket Island and Martha's Vineyard off of the coast of Massachusetts. More generally, it can be found in the northern midwestern and New England states.[13][14][15][16][17] It is sometimes called "The Malaria of The Northeast."[18] Cases of babesiosis have been reported in a wide range of European countries. Disease in Europe is usually due to infection with Babesia divergens, while in the United States Babesia microti andBabesia duncani are the species most commonly associated with human disease. Babesiosis has also been observed in Korea.[19] Babesiosis has emerged in Lower Hudson Valley, New York since 2001.[20] In Australia, babesiosis of types B. duncani and B. microti, has recently been found in symptomatic patients along the eastern coastline of the continent.[21] A similar disease in cattle, commonly known as tick fever, is spread by Babesia bovis and B. bigemina in the introduced cattle tick Rhipicephalus microplus. This disease is found in eastern and northern Australia.[2

pathophysiology Babesiosis is a zoonotic disease maintained by the interaction of tick vectors, transport hosts, and animal reservoirs. The primary vectors of the parasite are ticks of the genus Ixodes. In the United States, the black-legged deer tick, Ixodes scapularis (also known as Ixodes dammini; see the image below), is the primary vector for the parasite; in Europe, Ixodes ricinus appears to be the primary tick vector. In each location, the Ixodes tick vector for Babesia is the same vector that locally transmits Borrelia burgdorferi, the agent implicated in Lyme disease.

Ixodes scapularis, tick vector for babesiosis. Image courtesy of Centers for Disease Control and Prevention. I scapularis has 3 developmental stageslarva, nymph, and adulteach of which requires a blood meal for development into the next stage. As a larva and nymph, the tick feeds on rodents (eg, the whitefooted mouse, Peromyscus leucopus); however, as an adult, the tick prefers to feed on the white-tailed deer. Female ticks are impregnated while obtaining their blood meal on the deer, with the formation of up to 20,000 eggs. (In Europe, by way of contrast, cattle constitute the primary animal reservoir). The clinical signs and symptoms of babesiosis are related to the parasitism of RBCs by Babesia. The ticks ingest Babesia from the host during feeding; they then multiply the protozoa in their gut wall and concentrate them in their salivary glands. When they feed again on a new host, they inoculate the new host withBabesia. Entering the hosts bloodstream during the tick bite, the parasite infects RBCs, and differentiated and undifferentiated trophozoites are produced. Upon infection of the host erythrocyte, mature B microti trophozoites undergo asynchronous asexual budding and divide into 2 or 4 merozoites. As parasites leave the erythrocyte, the membrane is damaged. The precise mechanism of hemolysis is unknown. Babesia species in the host erythrocyte range from 1 to 5 m in length. B microtimeasures 2 1.5 m, B divergens measures 4 1.5 m, and B bovis measures 2.4 1.5 m. As noted, the organisms are pearshaped, oval, or round. Their ring form and peripheral location in the erythrocyte frequently lead to their being mistaken for Plasmodium falciparum. However, they differ from P falciparum in that the schizogony is asynchronous and massive hemolysis does not occur. Alterations in RBC membranes cause decreased conformability and increased RBC adherence, which can lead to development of noncardiac pulmonary edema and acute respiratory distress syndrome (ARDS) among those severely affected.[1]