| Babesiosis | |
|---|---|
| Other names | Babesiasis, Texas fever |
 | |
| Blood smear ofBabesia microti | |
| Pronunciation |
|
| Specialty | Infectious disease |
| Symptoms | fever,chills, headache, fatigue[1] |
| Risk factors | Removedspleen, weakened immune system, doing outdoor activities[1] |
| Differential diagnosis | Malaria |
Babesiosis orpiroplasmosis is amalaria-likeparasitic disease caused by infection with aeukaryotic parasite in the orderPiroplasmida, typically aBabesia orTheileria, in thephylumApicomplexa.[2] Human babesiosistransmission via tick bite is most common in theNortheastern andMidwestern United States and parts of Europe, and sporadic throughout the rest of the world. It occurs in warm weather.[3] People can get infected withBabesia parasites by the bite of an infectedtick, by getting a blood transfusion from an infected donor of blood products, or by congenital transmission (an infected mother to her baby).[4]Ticks transmit the human strain of babesiosis, so it often presents with other tick-borne illnesses such asLyme disease.[5] Aftertrypanosomes,Babesia is thought to be the second-most common bloodparasite of mammals. They can have major adverse effects on the health of domestic animals in areas without severe winters. In cattle, the disease is known asTexas cattle fever orredwater.[6]
Half of all children and a quarter of previously healthy adults withBabesia infection are asymptomatic. When people do develop symptoms, the most common are fever andhemolytic anemia, symptoms that are similar to those of malaria.[5] People with symptoms usually become ill 1 to 4 weeks after the bite, or 1 to 9 weeks after transfusion of contaminated blood products. A person infected with babesiosis gradually developsmalaise and fatigue, followed by a fever. Hemolytic anemia, in which red blood cells are destroyed and removed from the blood, also develops. Chills, sweats, andthrombocytopenia are also common symptoms. Symptoms may last from several days to several months.[7]
Less common symptoms and physical exam findings of mild-to-moderate babesiosis:[5]
In more severe cases, symptoms similar to malaria occur, with fevers up to 40.5 °C (105 °F), shaking chills, and severe anemia (hemolytic anemia). Organ failure may follow, includingadult respiratory distress syndrome. Sepsis in people who have had asplenectomy can occur rapidly, consistent withoverwhelming post-splenectomy infection. Severe cases are also more likely to occur in the very young, very old, and persons withimmunodeficiency, such asHIV/AIDS patients.[9]
A reported increase in human babesiosis diagnoses in the 2000s is thought to be caused by more widespread testing and higher numbers of people with immunodeficiencies coming in contact with ticks, the disease vector.[6] Little is known about the occurrence ofBabesia species in malaria-endemic areas, whereBabesia can easily be misdiagnosed asPlasmodium. Human patients with repeat babesiosis infection may exhibitpremunity.[10]
Babesia species are in thephylumApicomplexa, which also has the protozoan parasites that causemalaria,toxoplasmosis, andcryptosporidiosis.[5] Four clades ofBabesia species infect humans. The main species in each clade are:[citation needed]
Babesia parasites reproduce inred blood cells, where they can be seen as cross-shaped inclusions (fourmerozoites asexually budding, but attached forming a structure looking like a "Maltese cross")[11] and cause hemolytic anemia, quite similar to malaria.
Unlike thePlasmodium parasites that cause malaria,Babesia species rarely exhibit an exoerythrocytic phase with trophozoite forms.[12]
In nonhuman animals,Babesia canis rossi,Babesia bigemina, andBabesia bovis cause particularly severe forms of the disease, including 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 coagulation, and "cerebral babesiosis" caused by sludging of erythrocytes in cerebral capillaries.[citation needed]
In bovine species, the organism causes hemolytic anemia, so an infected animal shows pale mucous membranes initially. As the levels ofbilirubin (a byproduct of red blood cell lysis) continue to increase, the visible mucous membranes become yellow (icterus) due to the failure of the liver to metabolize the excess bilirubin. Hemoglobinuria is seen due to the excretion of red-blood-cell lysis byproducts via the kidneys. A fever of 40.5 °C (105 °F) develops due to the release of inflammatory byproducts.[citation needed]
Only specialized laboratories can adequately diagnoseBabesia infection in humans, soBabesia infections are considered highly under-reported. It develops in patients who live in or travel to an endemic area or receive a contaminatedblood transfusion within the preceding 9 weeks, so this aspect of the medical history is vital.[13] 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 aGiemsa-stainedthin-film blood smear.[13]
So-called "Maltese cross formations" on the blood film are diagnostic (pathognomonic) of babesiosis since they are not seen in malaria, the primary differential diagnosis.[11] Careful examination of multiplesmears may be necessary, sinceBabesia may infect less than 1% of circulating red blood cells, thus be easily overlooked.[14]
Serologic testing forantibodies againstBabesia (bothIgG andIgM) can detect low-level infection in cases with 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.[15]
Apolymerase chain reaction (PCR) test has been developed for the detection ofBabesia from the peripheral blood.[16] PCR may be at least assensitive and specific as blood-film examination in diagnosing babesiosis, though it is also significantly more expensive.[17] Most often, PCR testing is used in conjunction with blood film examination and possiblyserologic testing.[13]
Other laboratory findings include decreased numbers of red blood cells andplatelets oncomplete blood count.[18]
In animals, babesiosis is suspected by observation of clinical signs (hemoglobinuria and anemia) in animals in endemic areas. Diagnosis is confirmed by observation of merozoites on a 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.[citation needed]
Babesia canis andB. bigemina are "largeBabesia species" that form paired merozoites in the erythrocytes, commonly described as resembling "two pears hanging together", rather than the "Maltese cross" of the "smallBabesia species". Their merozoites are around twice the size of small ones.[citation needed]
Cerebral babesiosis is suspectedin vivo when neurological signs (often severe) are seen in cattle that are positive forB. bovis on blood smear, but this has yet to be proven scientifically. Outspoken red discoloration of the grey matterpost-mortem further strengthens suspicion of cerebral babesiosis. Diagnosis is confirmedpost-mortem by observation ofBabesia-infected erythrocytes sludged in the cerebral cortical capillaries in a brain smear.[citation needed]
Treatment of asymptomatic carriers should be considered if parasites are still detected after 3 months. In mild-to-moderate babesiosis, the treatment of choice is a combination ofatovaquone andazithromycin. This regimen is preferred toclindamycin andquinine because it has fewer side effects. The standard course is 7 to 10 days, but this is extended to at least 6 weeks in people withrelapsing disease. Even mild cases are recommended to be treated to decrease the chance of inadvertently transmitting the infection by donating blood.[5] In severe babesiosis, the combination of clindamycin and quinine is preferred. In life-threatening cases,exchange transfusion is performed.[19] In this procedure, the infected red blood cells are removed and replaced with uninfected ones; toxins produced by the parasites may also be removed.[20]
Imidocarb is a drug used for the treatment of babesiosis in dogs.[21]Extracts of the poisonous,bulbous plantBoophone disticha are used in thefolk medicine ofSouth Africa to treatequine babesiosis.B. disticha is a member of the daffodil familyAmaryllidaceae and has also been used in preparations employed asarrow poisons,hallucinogens, and inembalming. The plant is rich inalkaloids, some of which display an action similar to that ofscopolamine.[22]
Babesiosis is avector-borne illness usually transmitted byIxodes scapularisticks.B. microti uses the same tick vector as Lyme disease, and may occur in conjunction with Lyme.[6] The organism can also be transmitted by blood transfusion.[23][24]Ticks of domestic animals, especiallyRhipicephalus (Boophilus) microplus andR. (B.) decoloratus transmit several species ofBabesia to livestock, causing considerable economic losses to farmers in tropical and subtropical regions.[citation needed]
In the United States, the majority of babesiosis cases are caused byB. microti, and occur in the Northeast and northern Midwest from May through October.[5] Areas with especially high rates include easternLong Island,Fire Island,Nantucket Island, andMartha's Vineyard.[25][26][27][28][29]TheCenters for Disease Control and Prevention now requires state health departments to report infections usingForm OMB No. 0920-0728.[30] In 2014, Rhode Island had an incidence of 16.3 reported infections per 100,000 people.[31]
In Europe,B. divergens is the primary cause of infectious babesiosis and is transmitted byI. ricinus.[5]
Babesiosis has emerged in the Lower Hudson Valley, New York, since 2001.[32]
In Australia, one locally-acquired case ofB. microti has been reported, which was fatal.[33] A subsequent investigation found no additional evidence of human Babesiosis in over 7000 patient samples, leading the authors to conclude that Babesiosis was rare in Australia.[34] A similar disease in cattle, commonly known as tick fever, is spread byBabesia bovis andB. bigemina in the introduced cattle tickRhipicephalus microplus. This disease is found in eastern and northern Australia.[35]
A table of isolated cases of babesiosis, which may be underestimated given how widely distributed the tick vectors are in temperate latitudes.[5]
| Location | Species |
|---|---|
| Pacific Coast (northern California to Washington) | B. duncani |
| Kentucky,Missouri, andWashington | B. divergens |
| Austria,Germany,Italy | B. venatorum |
| Canary Islands | B. microti |
| Africa (Egypt,Mozambique,South Africa) | Uncharacterized spp. |
| Asia (Taiwan,Japan) | B. microti |
| South Korea | Babesia KO1[36] |
| Australia | B. microti[34] |
| South America (Brazil, Colombia) | Uncharacterized spp. |
The disease is named for the genus of the causative organism,[37] which was named after theRomanianbacteriologistVictor Babeș.[38] In 1888, Victor Babeș identified the microorganisms in red blood cells as the cause of febrilehemoglobinuria in cattle.[5] In 1893,Theobald Smith and Frederick Kilborne discovered that a tick was the vector for transmission in Texas cattle. The agent wasB. bigemina. This was the first demonstration that anarthropod could act as adisease vector to transmit an infectious agent to a vertebrate host.[citation needed]
In 1957, the first human case was documented in asplenectomized Croatian herdsman.[5] The agent wasB. divergens. In 1969, the first case was reported in animmunocompetent individual on Nantucket Island. The agent wasB. microti, and the vector was the tickI. scapularis.[citation needed]Equine babesiosis (caused by the protozoanTheileria equi) is also known as piroplasmosis (from theLatinpiro, meaningpear +Greekplasma, a thing formed).[39]
Veterinary treatment of babesiosis does not normally use antibiotics. In livestock and animals,diminazen (Berenil),imidocarb, ortrypan blue would be the drugs of choice for treatment ofB. canis rossi (dogs in Africa),B. bovis, andB. bigemina (cattle in Southern Africa). In acute cases in cattle, a blood transfusion may be carried out. A vaccine is effective againstB. canis canis (dogs in the Mediterranean region), but is ineffective againstB. c. rossi.B. imitans causes a mild form of the disease that frequently resolves without treatment (dogs in Southeast Asia).[citation needed]
