Babesiosis (babesiosis,) is a zoonotic parasitic disease characterized by chills, fever, splenomegaly, jaundice and hemolysis caused by Babesia ticks infecting vertebrate erythrocytes through tick vectors. Pathogenesis Babesia is a tick-mediated protozoa that parasitizes the red blood cells of vertebrates. Since Babesia was discovered in 1888, more than 90 species of Babesia have been known to infect wild and domestic animals. At least three species infect humans. The parasitic stage of the protozoa within the red blood cells of vertebrates is a process of asexual budding (budding), in which they continuously destroy red blood cells. After being ingested by ticks, the developmental stage in ticks is sexual, forming zygotes that divide and proliferate to produce large numbers of vermicules. From the tick intestinal epithelial cells escape into the intestinal lumen, and then into the tick salivary gland cells, that is, through the schizogony proliferation (schizogony) and semi-circular pear-shaped body. This glandular protozoan can infect vertebrates by sucking blood from ticks. Epidemiology in some areas of the United States, Ireland and Yugoslavia and other regions have Babesia patients. China’s Yunnan Province also found in patients with this disease. 1, the source of infection This disease is a typical disease of animal origin, diseased livestock, such as cattle, horses, sheep, pigs, dogs and other infected rodents with worms, such as voles, mice, mice, gophers and asymptomatic gopher and people with worms, can be a source of infection. 2.Transmission pathway People are infected by ticks with protozoa. Babesia can be transmitted to the larvae through tick eggs, so hard ticks are not only vectors, but also storage hosts. Importation of blood from carriers is also a mode of transmission. In addition, it can be transmitted from mother to fetus via placenta. 3. Susceptibility of the population is universal regardless of race, age and sex. Splenectomized persons are more susceptible. People engaged in animal husbandry may be occupationally exposed. Livestock babesiosis is widely distributed in China, for example, cattle babesiosis is found in twelve provinces in central, southern, eastern and southwestern China. Horse babesiosis is also found in seven provinces in northeast, north and northwest China. Tiny babesioses are found in wild rats. If conditions are favorable, the disease can be transmitted through tick bites. Pathogenesis and pathological changes Under the electron microscope, the schizonts of Babesia microti are firstly close to the erythrocytes with their anterior ends. When it rapidly invades the erythrocyte, it brings part of the erythrocyte membrane into it, making it concave and forming a vacuole. The vacuole then disappears until the erythrocyte membrane is cleaved. The protozoa are then distributed in the cytoplasm, eventually leading to lysis of the erythrocytes. A large number of erythrocytes containing protozoa collect on the walls of small blood vessels and capillaries, leading to vascular lumen blockage and ultimately localized ischemic necrosis of the affected organs. Due to the stagnation of blood flow in the hepatic sinusoids, hepatocytes become swollen, degenerated and necrotic, which is most common around the central vein. In addition, hematopoietic tissues such as liver, spleen and bone marrow are proliferated, spleen can be enlarged up to 2-5 times, and kidneys can be enlarged with hemorrhagic spots. The meninges and brain parenchyma are congested and edematous. Clinical manifestations Latent period 1~6 weeks. The incubation period of babesiosis transmitted through blood transfusion is 1~9 weeks. The severity of clinical symptoms is related to the species of Babesia and the immune function of the host. Asymptomatic infections may persist for months to years, especially in healthy individuals under 40 years of age who may remain subclinical throughout. Clinical types: 1. Mild: Mostly self-limiting, typically presenting with progressive malaise and malaise. Fever may be present, usually around 38?C. It may be accompanied by chills, sweating, headache, myalgia, arthralgia and anorexia. Lymph nodes are not enlarged. 2.Medium size: The onset of the disease is acute, with high fever of 39?C to 40?C, chills and trembling, and profuse sweating. Severe headache, myalgia, and even peripheral joint pain. Sometimes photophobia, mental depression or agitation, trance. Nausea and vomiting may occur, but there is no meningeal irritation. There is mild to moderate enlargement of the spleen and no abnormalities in the lymph nodes. There is no rash.3. Severe: Clinical manifestations at onset are the same as medium. In critically ill patients, hemolytic anemia develops rapidly, accompanied by jaundice, proteinuria, hematuria and renal dysfunction. Splenectomized patients, patients receiving immunosuppressive therapy, patients with combined HIV infection and patients older than 50 years old often have more severe clinical manifestations. Fatal complications such as acute respiratory distress syndrome (ARDS), DIC, congestive heart failure, renal failure, myocardial infarction, splenic infarction or splenic rupture may occur. The severe type mostly dies within 5-8 days after the onset of the disease. Laboratory tests and diagnosis 1. Laboratory tests show hemolytic anemia with decreased erythrocyte volume, decreased hemoglobin, increased total and indirect bilirubin levels, decreased conjugated bead protein, and/or increased reticulocytes. Platelets are decreased, peripheral blood leukocytes are usually normal, and transaminases such as ALP, AST, ALT, and LDH are elevated. 2.Diagnosis (1), may have a history of tick bite. (2) There may be typical clinical manifestations: chills, fever, sweating, headache, muscle and joint pain, anemia and splenomegaly. (3) The diagnosis is confirmed when Babesia is found in the blood smear. Detection of Babesia DNA by PCR is also helpful for diagnosis. Serological tests: Indirect immunofluorescence assay (IFA) or enzyme-linked immunosorbent assay (ELISA) can be used to detect specific IgM antibody titer ≥ 1:64 or specific IgG antibody titer ≥ 1:1024 for diagnosis of acute or recent infections, and ≥ 4-fold dynamic elevation of antibody titer is of greater diagnostic significance. Treatment Many patients need only symptomatic treatment, but severe patients with persistent high fever, dramatically increased protozoaemia and rapidly decreasing erythrocyte pressure volume should be given special treatment such as blood transfusion, blood exchange, etc. Recommended pathogen-specific treatments: 1. Quinine 650mg 3 times/d orally plus clindamycin 600mg 3 times/d orally or 300-600mg 4 times/d intravenously, for 7 to 10 days. Children’s dose is quinine 8mg/kg, Q6h～Q8h orally plus clindamycin 7-10mg/kg daily, Q6h～Q8h. Adverse effects include diarrhea and tinnitus, hearing loss and vertigo, and 1/3 of the patients had dosage reduction or discontinuation of the drug due to serious adverse effects. 2, atovaquone 750mg, Q12h and azithromycin, the first day 500 ~ 1000mg, the second day to start 250mg / d combination therapy, the course of 7-10 days. This regimen is well tolerated. Adverse reactions include diarrhea and rash. In immunocompromised patients azithromycin may be increased to 600-1000 mg/d. The dose of the two-drug combination in children is atovaquone 20 mg/kg, Q12h, and azithromycin 10 mg/(kg.d) on the first day, and 5 mg/(kg.d) beginning on the second day. Prevention Avoid entering the infected area during the active season of vector ticks. Collective and individual tick prevention measures should be taken, such as taking care to detect ticks from clothing, wearing protective clothing and socks, and using tick killers and tick repellents. Regular tick control should be carried out on domestic animals, including tick control on the body of the animal and the barn and its environment. Strengthen quarantine between animals, detect the affected animals at an early stage, take effective isolation measures and provide active treatment. Avoid contact with wild rodents as much as possible. Blood donors in infected areas should be carefully examined, and anyone with a history of suspected disease and those who have lived in infected areas for a long time should not donate blood. Strict checks should be made on the blood sources of those receiving blood transfusions to ensure that they are not infected.