Pyroplasmosis is a transmissible protozoal disease of humans and animals caused by intracellular protozoa of the genus Babesia, parasitizing in erythrocytes. The disease develops in individuals with a reduced immune response. The course of pyroplasmosis is accompanied by fever, chills, headaches and muscle pains, arthralgia, hepatomegaly, anemia. The diagnosis of pyroplasmosis is confirmed by the detection of the parasite in a smear and a thick drop of blood, as well as by the methods of ELISA. The therapeutic effect against the causative agent of pyroplasmosis is provided by the combined administration of clindamycin and quinine, azithromycin and atovaquone.
Pyroplasmosis (babesiosis, babesiellosis) is a parasitic zoonotic infection occurring with febrile, anemic and jaundice syndromes. As an infectious disease, pyroplasmosis is an urgent problem for veterinary medicine, since it mainly affects small and large cattle, dogs and other animals. Human babesiosis is relatively rare (several hundred cases are known in the world). Human pyroplasmosis was first diagnosed in 1957 in Yugoslavia. Since then, human cases have been identified in Asia, Africa, Europe, and America.
Pathogens of pyroplasmosis belong to the type of protozoa, the family Babesiidae, the genus Babesia. According to their morpho-physiological properties, babesias resemble malaria pathogens: they also parasitize in red blood cells, and outwardly resemble plasmodia. In the erythrocyte, babesias are located on the periphery or in the center; they have a different (pear-shaped, ring-shaped, oval, dot-shaped, amoeboid, lanceolate) shape, diameter from 2-3 to 4-5 microns. Human pyroplasmosis can be caused by 3 types of pathogen: Babesia divergens and Babesia rodhaini in Europe, Babesia microti – on the American continent.
Pathogens of pyroplasmosis parasitize in the body of wild and domestic animals (rodents, dogs, cats, small and cattle), and are transmitted to humans by transmissible means, through the bites of infected ixodes and argass ticks. In the body of ticks, babesia persists for life and is even transmitted transovarially to offspring. In addition, a possible infection of a person with blood transfusion from persons with asymptomatic parasitemia is not excluded. Shepherds, agricultural workers, tourists are at increased risk of infection with pyroplasmosis during the period of seasonal tick activity (from May to September). Sometimes there is a mixinfection of babesias and spirochetes of the genus Borrelia – Lyme disease pathogens transmitted by the same species of ticks.
The life cycle of babesia development takes place in the body of vector ticks and vertebrates. In the tick’s body, parasites leave the erythrocytes of the vertebral host and undergo a complex and multiple cycle of division in the lumen and epithelial cells of the intestine, hemolymph, various organs of the tick. The process of development of babesia to the invasive stage (mononuclear sporozoites) occurs in the salivary glands of the tick and is stimulated by blood sucking. Once in the blood of humans or animals, pyroplasmosis pathogens penetrate into red blood cells, where they multiply by binary division or budding. By increasing their numbers, the parasites destroy the host’s red blood cells, then penetrate into new red blood cells, repeating the division cycle.
Clinical manifestations of pyroplasmosis develop when 3-5% of erythrocytes are affected by babesias. Together with the destroyed erythrocytes, parasite waste products and protein substances are released into the bloodstream, causing a pronounced general toxic and pyrogenic reaction. Anemia, tissue hypoxia, microcirculation disorders are increasing, mainly in the renal capillaries, where free hemoglobin and erythrocyte membranes settle. The defeat of 10-15% of red blood cells leads to death from acute renal failure.
In individuals with normal immunity, pyroplasmosis occurs as an asymptomatic carrier, despite parasitemia of 1-2%. Severe manifest course is mainly observed in people with reduced immune responses: elderly people, patients who have undergone splenectomy, HIV-infected, etc.
The incubation period for infection with pyroplasmosis lasts 1-3 weeks (in rare cases, several months). With a mild clinical form of pyroplasmosis, flu-like symptoms are noted: fever, weakness, bruising, body aches. With a severe course of infection, an acute fever develops with a temperature of 40-41 °With and terrific chills, severe headaches and muscle pains, arthralgia. Against the background of high fever, nausea, vomiting, epigastric pain, alternation of constipation and diarrhea, hepatosplenomegaly, jaundice, weight loss occur. From the 6th-7th day of the disease, hemoglobinemia, hemoglobinuria, oligoanuria and acute renal failure increase. Pyroplasmosis caused by B.divergens has a particularly severe course: even with timely specific treatment, mortality reaches 50%. The death of patients with pyroplasmosis is usually associated with uremia, renal-hepatic insufficiency or the addition of bacterial infections (pneumonia, sepsis).
Chronic pyroplasmosis occurs with periodic feverish reactions, impaired appetite, weakness, decreased attention, fatigue, depression, which can be mistakenly regarded as hypochondria or depression.
Diagnosis and treatment
Since cases of pyroplasmosis are rare in clinical practice, the disease is taken for hemorrhagic fever with renal syndrome, malaria, sepsis, blood diseases, manifestations of AIDS, etc. To make a clinical diagnosis, it is important to take into account epidemiological information (being in endemic areas, the fact of tick bites), as well as a combination of pathognomonic symptoms (prolonged fever, anemia, hepatomegaly).
Laboratory confirmation of pyroplasmosis is based on microscopy of a thick drop or smear of blood when they are stained according to Romanovsky-Giemsa: in this case, the nucleus of babesia is colored red, and the cytoplasm is blue. With the help of serological tests (ELISA), diagnostic antibody titers are detected 3-8 weeks after the onset of the disease. In chronic pyroplasmosis, the detection of babesia DNA by PCR is most indicative. The biological method of diagnosing pyroplasmosis – the introduction of the patient’s blood to splenectomized hamsters with subsequent isolation of the pathogen is effective, but long (takes from 2 to 4 weeks).
Mild, benign forms of pyroplasmosis do not need specific therapy. In severe cases, it is recommended to prescribe clindamycin together with quinine, or azithromycin and atovaquone, or a combination of pentamidine, diisocyanate, sulfamethoxazole and trimethoprim. With anemia, iron preparations, hemotransfusion are indicated; with high fever, detoxification therapy and antipyretics are indicated. In the case of acute kidney injury, hemodialysis is performed.
Without treatment, severe forms of pyroplasmosis almost always end in the death of the patient. With timely antiparasitic therapy, the chances of recovery are high. Immunoprophylaxis of pyroplasmosis has not been developed. Non-specific measures are reduced to the fight against vectors of infection, protection from ticks, urgent removal of stuck ticks.