Babesia
 

Classification: Taxonomic ranks under review (cf. Illustrated Guide to Protozoa, 2000. Allen Press)

Protista (unicellular eukaryotes)
Apicomplexa (cells with cluster of organelles known as apical complex)
Haematozoea (vector-borne parasites infecting blood cells of vertebrates)
Piroplasmorida (form pear-shaped bodies in blood cells, tick vectors)

Family: Babesiidae
This group of parasites is transmitted to mammalian hosts by arachnid (tick) vectors. They do not produce spores, flagella, cilia or pseudopodia but move by body flexion or gliding. The apical complex is reduced (conoid absent) and no stages produce haemozoin pigment. In mammals, the parasites do not undergo exoerythrocytic schizogony but multiply by binary fission and schizogony forming small characteristic pear-shaped (piroplasm) stages in blood cells. When ingested by ticks, the parasites form unique paired bodies (strahlenkorper) which give rise to numerous schizonts leading to the production of numerous sporozoites in the salivary glands. Infections persist in ticks during metamorphosis (trans-stadial transmission) and are passed by female ticks to their progeny (trans-ovarian transmission). Many babesial species have been associated with severe disease syndromes.

Babesia spp. [these species cause babesiosis (tick fever) in domestic and wild animals]

Parasite morphology: Intraerythrocytic stages appear singly as small round, ovoid or elongate trophozoites (2-4µm), in pairs as pear-shaped (= pyriform, hence piroplasm) merozoites, or in tetrads as cruciform merozoites.

Host range: Infections have been detected in most domestic animals (cattle, sheep, goats, horses, pigs, dogs, cats) and numerous wild animals (over 70 species) and humans. Three species cause tick fever in cattle, B. bovis (B. argentina), B. bigemina, and B. divergens. Some parasite species are not host specific and can be transmitted among different mammals; some are zoonotic. Infections in humans have been attributed to B. microti from rodents in North America and B. divergens from cattle in Europe. All parasite species are limited in their distribution in accordance with that of their tick vectors.

Parasite species

Vertebrate hosts

Disease

Pathogenicity

Vectors

Distribution

B. bovis
(argentina)

cattle, deer

redwater fever

high

Ixodes,
Rhipicephalus (Boophilus)

Europe, Africa, Australia,
South & Central America

B. bigemina

cattle, deer

redwater fever

moderate

Haemaphysalis, Rhipicephalus (Boophilus)

Europe, Africa, Australia,
South & Central America

B. divergens

cattle

redwater fever

moderate

Ixodes

Western & Central Europe

B. major

cattle

low

Rhipicephalus (Boophilus)

Europe, Russia

B. equi

horses, zebra

biliary fever

high

Dermacentor,
Hyalomma,
Rhipicephalus (Boophilus)

Southern Europe, Africa,
Asia, South America

B. caballi

horses

moderate

Dermacentor,
Hyalomma,
Rhipicephalus (Boophilus)

Dermacentor,
Hyalomma,
Rhipicephalus (Boophilus) Southern Europe, Russia,
Africa, Asia

B. ovis

sheep, goats

low

Rhipicephalus (Boophilus),
Ixodes

Southern Europe, Africa,
Asia, tropical America

B. motasi

sheep, goats

moderate

Rhipicephalus (Boophilus), Haemaphysalis, Dermacentor

Southern Europe, Africa,
Asia, tropical America

B. trautmanni

pig

moderate

Rhipicephalus

Southern Europe, Africa

B. canis

canids

tick fever

high

Rhipicephalus, Dermacentor, Haemaphysalis

Southern Europe, Africa,
Asia, South & North America

B. gibsoni

canids

tick fever

high

Rhipicephalus, Haemaphysalis

India, Ceylon, China

B. felis

cats, lion, leopard

moderate

Haemaphysalis

Africa, India

B. microti

rodents

low

Ixodes

worldwide

B. rodhaini

rodents

low

unknown

Africa


Site of infection: Parasites infecting host erythrocytes undergo transformation to form trophozoites which divide by binary schizogony and undergo differentiation to form merozoites. The host cell is ultimately lysed and the merozoites infect new cells, repeating the cycle of development.

Pathogenesis: Infected animals develop a high persistent fever becoming dull, listless and anorexic. Parasites cause extensive intravascular haemolysis (erythrocyte rupture) producing progressive signs of anaemia. Erythrocyte destruction may be as high as 75% in fatal cases and even milder infections produce severe anaemia. Haemoglobin clearance mechanisms become overloaded, resulting in jaundice and haemoglobinuria (red discolouration of the urine, ‘red water’ in bovine babesiosis). Haemolysis involves the release of many pharmacologically active agents (e.g. proteolytic enzymes) which affect microcirculation (vasodilatation, increased permeability) leading to hypotension and oedema, and affect blood (viscosity, coagulation, cytoadherence) leading to ischaemia (congestion and degenerative changes in tissues/organs). Infected animals may exhibit diarrhoea, abortion if pregnant, cerebral signs, muscle tremors, wasting, coma and death. Chronically infected animals remain weak, thin and out of condition for several weeks before recovery. Animals that recover are usually immune for life, sometimes thought to be due to complete cure (sterile immunity) but more often associated with the persistence of small numbers of parasites (premunitive immunity). There is an inverse age-resistance to infection and disease, with young cattle being less susceptible than older cattle. There is also a genetic component to resistance, with Bos taurus cattle being more susceptible than Bos indicus (zebu) cattle. Infections in humans have proven severe and fatal in asplenic individuals, with symptoms appearing 10-20 days after tick bite and presenting as a fulminant febrile haemolytic disease, characterized by general malaise, then fever, shaking chills, sweating, arthralgias, myalgias, fatigue, weakness, occasional hepatosplenomegaly, and jaundice.

Mode of transmission: Infections are transmitted by ixodid (hard-bodied) ticks which may be one-, two- or three-host ticks. Ingested parasites develop into large motile vermicules which migrate through the body of the tick and then undergo sporogony. Parasites undergo trans-stadial transmission, whereby infections persist during metamorphosis from larvae to nymphs to adults. They also undergo transovarian transmission, where parasites infect developing eggs in engorged female ticks, so nearly all the progeny are born already infected. Eventually, hundreds of small pyriform bodies (sporozoites) are formed within salivary cells and are injected into mammalian hosts during feeding.

Differential diagnosis: Infections are conventionally diagnosed by the detection of intraerythrocytic stages in smears of peripheral blood stained with any of the Romanowsky’s stains, notably Giemsa. However, once the acute febrile phase has passed, parasites may be difficult to find as they are rapidly removed from the circulation. Recourse has therefore been made to immunoserological tests to detect specific host antibodies against the parasites. Molecular biological techniques have also been developed to parasite DNA following the polymerase chain reaction (PCR) amplification of specific gene sequences.

Treatment and control: Timely chemotherapy is generally effective, although the small virulent species (such as B. bovis) are usually more difficult to treat than other less aggressive species. One of the first successful treatments for bovine babesiosis was the azonaphthalene dye, trypan blue, but it was not very effective against B. bovis. The most commonly used compounds are the diamidines (diminazene diaceturate, imidocarb, amicarbalide), and quinuronium and acridine derivatives. Macrolide antibiotics (clindamycin) and tetracyclines (oxytetracycline, chlortetracycline) have shown variable effects against human infections. Treatment can facilitate recovery, leaving latent infections or complete cure. However, elimination of all parasites may also eliminate premunitive immunity. Because young animals in endemic areas develop infection-immunity (premunition), this has been exploited for immunological control either through premunization/chemoimmunization (infect animals then treat them) or vaccination using whole parasites (attenuated strains) or subcellular (subunit) fractions. Several commercially available preparations have proven effective in regional areas, but a universal vaccine is not yet available. Prevention strategies involving tick control programmes have been relatively effective in several countries in controlling or eliminating infections in domestic stock.

 

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