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By Roderick D. Balce, RMT
I. Introduction A. History B. Epidemiology C. Overview II. Description of the Organism A. Taxonomy B. Morphology C. Life Cycle D. Comparison Between Babesia and Plasmodium
III. Pathogenesis A. Vector B. Modes of transmission C. Mechanisms of Injury IV. Pathobiology A. Clinical features B. Infection in Immunocompromised Host C. Immunology V.Laboratory Diagnosis VI. Clinical Management VII. Prevention and Control VIII. Recent Updates
A. Brief History
1888 – Victor Babes discovered microorganisms in the erythrocytes of cattle. 1893 – Smith and Kilbourne established Pyrosoma as the first identified arthropod-born protozoan. 1957 – Skrabalo and Deanovic described the first confirmed human case of babesiosis caused by B.
Most cases of babesiosis have been reported from the USA usually caused by B. microti In Europe, 84% of cases have occurred in splenectomized individuals In Nigeria and Mozambique, over half of the persons tested were seropositive for Babesia Several cases were also reported in Asia and South Africa
Babesiosis is a malaria-like, hemoparasitic infection caused by the protozoan genus Babesia. Causative agent: B. microti and related organisms Infective Stage: Sporozoite Mode of Transmission: Skin inoculation Vector: Ticks (Ixodes spp.) Reservoirs: Rodent, cattle, deer Diagnostic Procedures: Thick & Thin Blood Smear, Serological tests, PCR
II. CAUSATIVE AGENT
Class Sporozea Subclass Coccidia Suborder Hemosporiina Plasmodium
Class Aconoidasida Subclass Piroplasmia
Suborder Eimeriina Isospora, Cyclospora, Cryptosporidium, Sarcocystis, Toxoplasma
C. Life Cycle
piriform, round or oval depending upon the species resembles P. falciparum but has several distinguishing features: pleomorphic, can be vacuolated, and does not produce pigment tetrad form is a diagnostic feature
(A and B) B. microti ring forms, about 1.5– 2.5 nm in diameter (Giemsa-stained). (C ) Tetrads, about 1–2.5 nm in diameter.
(D) Rings; (E) Pyriforms; (F) Band forms
(G) B. microti rings ; (H) Plasmodium vivax young ring; (I) Plasmodium falciparum multiple parasites; Maurer’s dots can be seen.
Babesia sp. in a thin blood smear stained with Giemsa. Note the tetrads, a dividing form pathognomonic for Babesia, in both images.
D. Comparison Between Babesia and P. falciparum
Babesia spp. Ring forms Larger, usually pearshaped, can contain a central vacuole, tetrad forms diagnostic Absent Absent Budding (forming tetrads of trophozoites) Ticks (Ixodes dammini or scapularis) Asynchronous erythrocytic cycle P. falciparum Smaller, no central vacuole, applique or acole forms diagnostic Present Present Schizogony (forming schizonts and merozoites) Mosquito (Anopheles minimus flavirostris) Undergoes exoerythrocytic and synchronous erythrocytic schizogony
Schizonts and gametocytes Hemozoin pigment Asexual division Vector Life cycle
A. The Tick Vector 3 developmental forms exist – larva, nymph, and adult blood meal is required to progress to the next developmental stage
all 3 forms may feed on humans but the nymph is the main vector of babesiosis
B. Modes of Transmission
Skin inoculation or tick bite Co-transmission with B. burgdorferi Blood transfusion – Babesia can survive for 21-35 days under standard blood storage conditions; 60 cases have been documented in 2006 Transplacental – 2 cases have documented on humans
C. Mechanisms of Injury
and resultant anemia – due to humoral mechanisms resulting from the production of anti-erythrocyte membrane antibodies Cytoadherence of erythrocytes within the vasculature – due to a cryofibrinogen complex present in the plasma of patients Release of harmful mediators – due to the production and release
A. Clinical Features
Symptoms: fever, malaise, fatigue, anorexia, rigors, headache, myalgia, arthralgia, nausea, vomiting, abdominal pain, photophobia, conjunctivitis, sore throat, and cough Physical Findings: splenomegaly, hepatomegaly, skin changes, jaundice
Laboratory Findings: hemoglobinuria, decreased haptoglobin, increased reticulocyte count, thrombocytopenia, high ESR, (+) direct Coomb’s test, proteinuria, increased BUN and creatinine, increased bilirubin, ALP, AST, ALT, and LD Disease is more fatal in splenectomized individuals. American cases are less severe than European ones.
B. Infection in Immunocompromised Host HIV infection predisposes to severe babesiosis which can be prolonged and chronic. Patients show high parasitemia and may develop CNS involvement or complications such as CHF, RDS, and renal failure. Relapse of symptoms is possible.
V. LABORATORY DIAGNOSIS
and Thin Blood Smear Serologic Tests
Indirect Immunofluorescent Test ELISA
vitro culture Polymerase Chain Reaction (PCR)
Direct diagnostic method for detection: (A) Photomicrograph of positive BabesiaIFAT, 400 (B) Display detail 1000, oil (zoomed) (C) Negative IFAT control.
Babesia spp.-specific PCR designed for amplification of a highly specific region of the 18S rRNA gene (Armstrong et al., 1998). P – positive control, N – negative, control, S – patient sample, I – inhibition control, M – 123-bp marker.
VI. CLINICAL MANAGEMENT
A. Antiparasitic Treatment Quinine 650 mg p.o. 3 times daily Clindamycin 600 mg p.o., i.v. 3 times daily Azithromycin 500 mg/1st day, 250 mg therafter p.o. once daily Atovaquone 750 mg p.o. twice daily Doxycycline 200 mg p.o. once daily
VII. PREVENTION AND CONTROL
of exposure to the
tick vector Application of insect repellents such as DEET or permethrin Discouraging blood donors from endemic areas
Babesiosis: Recent insights into an ancient disease
K.-P. Hunfeld, A. Hildebrandt, J.S. Gray
International Journal for Parasitology 38 (2008) 1219–1237
New Developments in the Phylogeny of B. microti and B. microti-like organisms
analysis of 18S rRNA and β-tubulin gene fragments of parasites resulted in the identification of three separate clades As a consequence B. microti, long regarded as a single species, is now regarded as a genetically diverse species
New tools for a more rapid molecular diagnosis of Babesia spp. infection
of sensitive and specific multiplex PCR assays that can yield results within one day and can detect as few as three parasites in 100 uL blood Use of a single diagnostic test covering agents such as Babesia spp., Borrelia spp., Anaplasma spp., and Rickettsia spp.
Shared features in the pathobiology of babesiosis and malaria
Peter J. Krause1, Johanna Daily, Sam R. Telford, Edouard Vannier, Paul Lantos and Andrew Spielman
TRENDS in Parasitology
clinical manifestations of malaria and babesiosis are similar. Most cases of babesiosis and malaria consist of a mild to moderate illness characterized by fever, sweats, chills, headache, myalgia, back and abdominal pain, nausea, vomiting, diarrhea and pallor. They differ in the periodicity of
share similar pathology in the brain, lung, kidney and other organs. Erythrocyte cytoadherence and sequestration generally are found in the cerebral vasculature of patients dying of cerebral malaria. Several studies of Babesia cerebral disease have demonstrated extensive erythrocyte cytoadherence and sequestration in the brains of infected animals.
complications are often observed in adults experiencing severe malaria. Likewise, pulmonary disease is the most common complication in people experiencing severe babesial infection with up to 20% of patients suffering from noncardiac pulmonary edema. Studies point to the central role of cytokines, and especially TNF, in babesia and malaria
impairment is a common complication of P. falciparum and babesial infections. Renal failure has been reported in 5% of severe B. microti human infection and even more frequently in patients experiencing severe B. duncani infection. On autopsy of patients dying of malaria, several distinct pathologic patterns are noted in the kidneys, with erythrocyte sequestration contributing to the pathology. Studies in animals infected with
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