Babesiosis

Edited November 3, 2015

 

The Babesiosis guidelines were first published in the J Feline Med Surg (2013) 15: 643-646 by Katrin Hartmann et al.

 

 

Synopsis

 

Babesiosis is a tick-borne protozoan disease affecting domestic and wild animals and humans worldwide. Babesiosis is caused by parasites of the genus Babesia (B.) that belong to protozoan piroplasms.1 The disease is named after the Romanian bacteriologist Victor Babeş. Babesiosis is also known as piroplasmosis (from Latin pirum, meaning “pear”, and plasma, “image, formation”). Babesia spp. are common blood parasites of mammals. Human babesiosis is uncommon, but more cases in people have been reported recently, likely because of rising awareness. Babesiosis is found in dogs worldwide, but only rarely in cats.

 

 

Agent Properties

 

Several Babesia spp. have been detected in domestic cats in different regions of the world, including South Africa, Sudan, Zimbabwe, Israel, India, Thailand, Brazil, France, Poland, and Germany. However, only few Babesia organisms have been characterised.

 

Most reports about babesiosis in cats come from South Africa, where it is mainly found in the coastal areas. There (as well as in other parts of Africa, e.g. the Sudan), infection is caused mainly by B. felis, a small Babesia spp. that causes severe anaemia and icterus.2,3 Most other small Babesia spp. in domestic cats, like the B. cati found primarily in India, are less pathogenic.

 

Babesia leo, another small species, is antigenetically and genetically similar to B. felis and common in lions of the Kruger National Park, South Africa, and in Swaziland4, but also prevalent in domestic cats in these areas. A small babesia was also seen in blood smears of cats in Rio de Janeiro, Brazil, but the species was not identified.

 

Sporadic cases of canine Babesia spp. infections in domestic cats have been reported in Europe, such as B. canis canis from Spain and Portugal, a B. microti-like species from Portugal, and a B. canis-like species from Poland.3 B. canis presentii has been detected in Israel, and B. canis vogeli is common in stray cats in Thailand.5-7

 

In addition to the small B. leo, several large Babesia spp., including B. herpailuri and B. pantherae, have been discovered in wild felids, in lions, cheetahs, and the Florida panther. They can be transmitted experimentally to domestic cats, but their infectivity and pathogenicity under natural circumstances is unknown.3

 

Several new species (e.g. B. venatorum) have been discovered in the last years. A new species, named B. hongkongensis was discovered in kidney sections of a free-roaming cat in Hong Kong.8 The level of genetic divergence within Babesia spp. suggests that new subspecies might represent an “expanding universe”.9 

 

 

Fig. 1. Life cycle of Babesia spp. Copyright Diffomédia-Masure/Royal Canin

Fig. 1. Life cycle of Babesia spp. Copyright Diffomédia-Masure/Royal Canin

 

Life cycle

 

Babesioses are vector-borne diseases usually transmitted by ticks. The vector (or vectors) for Babesia spp. in cats has (have) not yet been identified.

 

Babesiae replicate in erythrocytes, where they produce merozoites. These structures appear as inclusions attached to each other at their ends, thereby forming tetrads. These so-called Maltese Cross formations are essentially pathognomonic of babesiosis. Ticks are infected by ingesting merozoites during feeding, and replication of the parasite within their salivary cells results in sporozoite formation. When infected ticks feed, the sporozoites are regurgitated and fed back into the bloodstream of the host.

 

 

Epidemiology

 

B felis is the most important pathogenic species in cats. It is mainly found in the coastal areas of South Africa.2,3 It usually occurs in cats less than three years of age, without any predilection for sex or breed.10,11

 

Apart from the usual transmission by ticks, Babesia spp. have been transmitted iatrogenically, e.g. through blood transfusions. Virulence is determined primarily by the parasite species involved.

 

 

Clinical signs

 

Severe disease has been described in cats infected with B. felis in South Africa, where feline babesiosis is diagnosed regularly.2 This species has not been reported in Europe so far. Feline babesiosis caused by other Babesia spp. presents rather as a chronic, mild disease.5

 

Common clinical signs are anorexia, lethargy, weakness, and a rough haircoat.10,12 Unlike in dogs, fever and icterus are uncommon. In most instances with fever, a concurrent illness is diagnosed.12 Most clinical signs are secondary to haemolytic anaemia that results from the infection of erythrocytes by the piroplasms. Cats usually cope with the anaemia and may show only mild clinical signs.

 

Complications of babesiosis include renal failure, pulmonary oedema, hepatopathy, and CNS signs.12 Concurrent infection with Mycoplasma hemofelis, feline leukaemia virus, or feline immunodeficiency virus may contribute to the clinical presentation and severity of disease.

 

The typical laboratory findings in cats with babesiosis are a consequence of haemolytic anaemia, which is usually regenerative, macrocytic, and hypochromic. Haemolysis can be caused by both extravascular and intravascular erythrolysis.11 Anaemia is most pronounced approximately three weeks after an experimental infection.13 Blood smears can show increased polychromatophils, Howell-Jolly bodies, nucleated erythrocytes, and anisocytosis.12 Erythrophagocytosis by monocytes is also observed,12 and intra-erythrocytic parasites can sometimes be detected.11 Secondary, immune-mediated haemolytic anaemia with anti-erythrocyte antibodies can be occasionally seen, leading to a positive Coomb’s test and auto-agglutination.11

 

Infected cats usually show no changes in the white blood cells. Thrombocytopenia is common in other species but is an inconsistent finding in cats.11,13

 

In serum biochemistry, ALT activity is elevated in most cases, whereas ALP activity is generally within reference values.2,11 Total bilirubin concentration is commonly increased,11 most likely as a result of haemolysis, but secondary hepatocellular injury may be a contributing factor.2 Feline babesiosis does usually not alter urea, creatinine, cholesterol concentrations, or blood pH.14 Polyclonal gammopathy has been observed in cats with hypergammaglobulinaemia also leading to increased total protein concentrations.11 

 

 

Immunity

 

The host generates a specific immune response against most Babesia spp., but this does not eliminate the parasite. Cats that recover from the clinical signs usually remain chronic carriers.

 

Fig. 2. Blood smear of a cat with Babesia spp. in erythrocytes (courtesy of Katrin Hartmann, Medizinische Kleintierklinik, Ludwig-Maximilians-Universität München, Germany).

Fig. 2. Blood smear of a cat with Babesia spp. in erythrocytes (courtesy of Katrin Hartmann, Medizinische Kleintierklinik, Ludwig-Maximilians-Universität München, Germany).

 

Diagnosis

 

Babesiosis is suspected when merozoites are detected in blood smears. Parasites are best identified in thin smears examined at maximum magnification under oil, using Romanovski (methylene blue and eosin) or Giemsa stains (Fig. 2). Sometimes the characteristic “Maltese cross” tetrad formation can be seen (Fig. 3). The different Babesia spp. and other blood parasites, including Cytauxzoon felis, are morphologically indistinguishable.3 When the level of parasitaemia is low, which is often the case, detection of the organism in blood smears can be difficult.

 

Fig. 3. Characteristic "Maltese cross" tetrad formation in infected erythrocyte.

Fig. 3. Characteristic “Maltese cross” tetrad formation in infected erythrocyte.

Testing for anti-Babesia antibodies is widely used in dogs, but not in cats so far.

 

Currently, the best method for a definitive diagnosis of Babesia spp. infection in cats is detecting the organisms’ nucleic acid in blood samples by PCR.9 Techniques have been developed for simultaneous detection of several Babesia spp., but differentiation between species, e. g. through nucleotide sequence differences of the 18S ribosomal subunit, is equally possible.3,5,9 

 

 

Treatment

 

Prognosis depends on the severity of disease, which in turn depends on both organism and host factors. Mortality rates of 15-20 % have been reported.15 Concurrent infection with Mycoplasma hemofelis, feline leukaemia virus, or feline immunodeficiency virus has a negative impact on the response to treatment and outcome of disease.11

 

Antiprotozoal drugs and supportive care are the mainstays of therapy. Cats infected with B. felis should always be treated, as the infection is commonly fatal if left untreated. In a review of 20 cats with experimentally induced babesiosis and 70 natural cases, all untreated animals eventually died.12 Response to treatment is generally good, but recurrence of clinical signs and chronic persistent infections are possible,14 and repeated or extended treatment may be necessary.2

 

Most antibabesial drugs are not effective in cats and, when used in experimental studies to treat B. felis infection, showed variable or questionable results.16,17 Currently, the drug of choice is primaquine phosphate, an antimalaria compound. Administration of 0.5 mg/kg orally or intramuscularly has been found effective.1,2 However, although primaquine phosphate is capable of reducing parasitaemia, it does not eliminate B. felis from the host’s organism. Also, it frequently causes vomiting when administered orally. Due to its narrow therapeutic window in cats it has to be administered carefully, as dosages exceeding 1 mg/kg can be lethal.16 Rifampicin and sulfadiazine-trimethoprim showed some anti-parasitic effect but were less active than primaquine phosphate, while buparavaquone, enrofloxacine, and danofloxacin did not show any anti-babesial effect.17 

 

 

Prevention

 

As Babesia spp. are transmitted by different tick species, tick control is the best way to prevent infection. Since cats do not tolerate permethrin, other drugs (e. g. fipronil) need to be used.

 

The soluble parasite antigen of several Babesia spp. has been used experimentally as a vaccine against the clinical manifestations of babesiosis, with variable success against bovine and canine species; no feline vaccines exist.

 

 

References

 

  1. 1 Birkenheuer AJ. Babesiosis. In: Greene CE (ed). Infectious Diseases of the Dog and Cat. 4th ed. St. Louis: Elsevier Saunders, 2012, pp 771-784.
  2. 2 Penzhorn BL, Schoeman T, Jacobson LS. Feline babesiosis in South Africa: a review. Ann N Y Acad Sci 2004; 1026: 183-186.
  3. 3 Yabsley MJ, Murphy SM, Cunningham MW. Molecular detection and characterization of Cytauxzoon felis and a Babesia species in cougars from Florida. J Wildl Dis 2006; 42: 366-374.
  4. 4 Bosman AM, Venter EH, Penzhorn BL. Occurrence of Babesia felis and Babesia leo in various wild felid species and domestic cats in Southern Africa, based on reverse line blot analysis. Vet Parasitol 2007; 144: 33-38.
  5. 5 Baneth G, Kenny MJ, Tasker S, Anug Y, Shkap V, Levy A, et al. Infection with a proposed new subspecies of Babesia canis, Babesia canis subsp. presentii, in domestic cats. J Clin Microbiol 2004; 42: 99-105.
  6. 6 Simking P, Wongnakphet S, Stich RW, Jittapalapong S. Detection of Babesia vogeli in stray cats of metropolitan Bangkok, Thailand. Vet Parasitol 2010; 173: 70-75.
  7. 7 Solano-Gallego L, Baneth G. Babesiosis in dogs and cats–expanding parasitological and clinical spectra. Vet Parasitol 2011; 181: 48-60.
  8. 8 Wong SS, Poon RW, Hui JJ, Yuen KY. Detection of Babesia hongkongensis sp. nov. in a free-roaming Felis catus cat in Hong Kong. J Clin Microbiol 2012; 50: 2799-2803.
  9. 9 Criado-Fornelio A, Gonzalez-del-Rio MA, Buling-Sarana A, Barba-Carretero JC. The “expanding universe” of piroplasms. Vet Parasitol 2004; 119: 337-345.
  10. 10 Jacobson LS, Schoeman T, Lobetti RG. A survey of feline babesiosis in South Africa. J S Afr Vet Assoc 2000; 71: 222-228.
  11. 11 Schoeman T, Lobetti RG, Jacobson LS, Penzhorn BL. Feline babesiosis: signalment, clinical pathology and concurrent infections. J S Afr Vet Assoc 2001; 72: 4-11.
  12. 12 Futter GJ, Belonje PC. Studies on feline babesiosis. 2. Clinical observations. J S Afr Vet Assoc 1980; 51: 143-146.
  13. 13 Futter GJ, Belonje PC, van den Berg A. Studies of feline babesiosis 3. Haematological findings. J S Afr Vet Assoc 1980; 51: 271-280.
  14. 14 Futter GJ, Belonje PC, Van den Berg A, Van Rijswijk AW. Studies on feline babesiosis. 4. Chemical pathology; macroscopic and microscopic post mortem findings. J S Afr Vet Assoc 1981; 52: 5-14.
  15. 15Ayoob AL, Prittie J, Hackner SG. Feline babesiosis. J Vet Emerg Crit Care (San Antonio) 2010; 20: 90-97.
  16. 16 Potgieter FT. Chemotherapy of Babesia felis infection: efficacy of certain drugs. J S Afr Vet Assoc 1981; 52: 289-293.
  17. 17 Penzhorn BL, Lewis BD, Lopez-Rebollar LM, Swan GE. Screening of five drugs for efficacy against Babesia felis in experimentally infected cats. J S Afr Vet Assoc 2000; 71: 53-57.

 

 

 

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