Feline babesiosis

Introduction

Babesia organisms are tick-borne hemoprotozoal parasites with worldwide distribution. Known hosts include rodents, humans, cattle, horses, dogs, and cats. These piroplasms, or intraerthrocytic parasites, cause severe disease in susceptible mammals. Feline babesiosis is a relatively new clinical entity with little known regarding its epidemiology and disease course. However, it is considered endemic in the coastal regions of South Africa. Multiple species of Babesia organisms have been documented in cats including Babesia felis, B. herpailuri, B. cati, B. canis subsp. presentii, B. canis subsp. canis, Theileria annae, B. pantherae, B. microti-like, and B. leo.^1–5 The majority of these infections are reported in wild felids in Africa, Asia, Europe, and Central America. Infrequent reports of infection have been documented in North America after 2006.^2–6

The objective of this manuscript is to review the etiology, clinical presentation, diagnosis, and treatment of feline babesiosis, particularly with regard to features distinct from canine babesiosis. For a complete review of the pathophysiologic basis of clinical syndromes associated with Babesia spp. in dogs the reader is referred to the companion article in this issue, entitled ‘Clinical Management of Canine Babesiosis.’

Etiology

Although the focus on Babesia spp. in recent literature has largely been on canine infection, increasing numbers of reports documenting Babesia infection in cats have arisen in the past 5 years. The majority of published literature originates from South Africa and includes case reports, restrospective studies of naturally infected cats, and experimental infections.^2,3,5,7–12 In 2006, Yabsley et al⁶ documented a Babesia sp. in Floridian wild cats, marking the first feline report of babesiosis in North America (Table 1).

Four small babesial species cause clinical disease in cats: B. felis, B. cati, B. leo, and B. microti-like spp.^{1–4,9,13–19}B. felis is a small (0.9 × 0.7 μm) highly pathogenic piroplasm. The piroplasm manifests most commonly as singular or paired annular bodies (signet ring); pear-shaped forms and, rarely, tetrads (Maltese cross forms) are also reported.^1,9B. cati (1 × 1.5 μm) occurs morphologically as single or paired annular bodies within the erythrocyte and results in milder clinical disease.^1–3B. leo was recently identified in lions in South Africa.^4,17 This species is 1.05 × 1.0 μm, round to oval in shape, and typically appears as singlets or in pairs within the erythrocyte.^4,17 Maltese cross formations have occasionally been reported. Both natural and experimental infections in domestic cats have been documented in South Africa.^4,17,19 Reports from Spain and Portugal document natural infection of B. microti-like spp. in domestic cats.¹³ The piriform in this babesial infection occurs most commonly as a singlet; however, the distinct morphology is not well characterized.

The large feline babesial species include B. herpailuri (1 × 2.5 μm), B. canis subsp. presentii (2.7 × 1.7 μm), B. pantherae (2.0 × 1.8 μm), and B. canis subsp. canis. Single or paired annular bodies represent the morphology of B. herpailuri, while B. canis subsp. presentii are characterized by single or paired inclusions that are round to oval or ring shaped.^1,5 The clinical course of B. herpauiluri is not well characterized, with only 1 case report of suspected naturally occurring infection in a domestic cat.¹⁴ Infection in domestic cats has been documented under experimental conditions.^2,3,20B. canis subsp. presentii may be asymptomatic or a moderate to severe clinical disease may develop in domestic cats.⁵B. pantherae is not well described either morphologically or clinically. This species has been isolated from leopards in Kenya and has been documented to experimentally cause infection in domestic cats.^1–3,20B. canis subsp. canis, a large babesial species primarily considered a canine pathogen, has also been reported to cause natural infection in domestic cats in Spain and Portugal.¹³

An unidentified Babesia sp. has been reported in Floridian panthers and Texas cougars, with polymerase chain reaction (PCR) analysis indicating a prevalence of up to 90%.⁶ rRNA sequencing (18S) reveals this piroplasm to be genetically distinct from other feline babesial species, and most closely related to the canine Babesia spp. found in Japan: B. odocoileri and B. divergens. No signs of clinical disease have been reported, suggesting a low pathogenecity for panthers.

The overall predisposition for contracting the disease is lower in cats than in dogs. Young (<3 years of age) cats appear to be predisposed to infection in endemic areas, suggesting early exposure with age-related immunity.^3,9,12 Older cats are susceptible to the disease following relocation to an endemic area or in conjunction with concurrent disease, immunosuppression, or severe trauma.^9,12 A predilection for the Oriental and Siamese breeds has been reported.^3,12 Incidence appears to be highest in the summer months, most likely due to the vector life cycle.³ Splenectomy does not appear to have an effect on the transmission rate; but, splenectomized cats exhibit a more severe clinical disease.^10,11 Retrovirus infections, including feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV), are suspected to increase host susceptibility via immunosuppression.^5,13 Coinfection with other erythrocytic pathogens, including multiple Babesia spp., Mycoplasma spp., and Cytauxzoon felis, has been reported in up to 30% of cases.^5,13,19 Although unreported in cats, coinfection with Bartonella spp. has been documented in dogs with babesiosis.²¹ As vectors and biohabitats for Bartonella spp. and Babesia spp. overlap, coinfection may also exist in cats.

Transmission, Life Cycle, and Pathogenesis

While defined transmission studies in cats do not exist, all babesial species are assumed to be transmitted via a tick vector.^3,17,19 Ticks of the genera Ixodes, Dermacentor, Rhipicephalus, Amblyomma, and Haemophysalis are known to infest cats and are likely vectors for transmission.^2,5 Mechanical transmission via other biting insects and arthropods may also occur. Transmission via blood transfusion or cat bites/fights have not been reported, but these remain plausible modes of transmission. Evaluation of blood smears in kittens born to infected mothers revealed no parasitemia. However, blood smear evaluation was performed only during the first 3 hours of life.⁹ In a survey by Jacobson et al,³ 1 respondent documented vertical transmission from queen to kittens.

As in dogs, Babesia organisms multiply in the definitive host via multiple fission to produce merozoites. Ticks are subsequently infected following ingestion of parasitized host erythrocytes. The babesial merozoites undergo a complex life cycle in the tick. During this process, multiple fission of merozoites results in the production of sporozoites (infective undeveloped cells) within the arthropod salivary glands.^1,22,23 The adult female tick is considered most important in vector transmission as transstadial and transovarial (multiplication in the ovaries and eggs perpetuating the life cycle over multiple generations) infections occur.^1,22,24 These sporozoites are then passed via tick saliva into the host circulation. Maturation of the sporozoites occurs at the time of tick attachment, thus requiring an attachment time of 2–3 days before transmission can occur.²⁴

Once in the definitive host, Babesia organisms attach to the erythrocyte membrane and are subsequently engulfed by endocytosis.²³ Within the erythrocyte, the host membrane surrounding the parasite disintegrates, granting subsequent stages of the organism direct contact with the cytoplasm. The loss of this host cell membrane is characteristic of Babesia spp. and allows for assumption of a wide variety of shapes.^23,25 Repeated binary fission occurs within the erythrocyte, resulting in up to 16 merozoites. It is the hosts' response to these reactions within their erythrocytes that determines the clinical disease course.²⁵ A prepatent period of 3–28 days is reported for B. felis.²⁶

The pathogenicity of Babesia spp. is dependent on many variables including species, strain, host age, and immunologic response. The species and strain appears to be the most important factors in determining pathogenicity.²⁶ The most and least virulent species in felines are B. felis and B. cati, respectively.¹

Clinical Syndromes Associated with Feline Babesiosis

Because of a paucity of scientific reports, little is known regarding clinical presentation and disease course. The majority of studies and case series documenting both natural and experimental infection originate from South Africa and address B. felis.^3,8–12 The information contained in this section refers to a summary of these reports of B. felis infection in domestic cats. Additional information on other species is specifically stated and referenced. An acute, complicated, and a chronic, subclinical, form of the disease exist with the latter being more typical.

The acute form of B. felis infection is characterized by a severe clinical disease course. Parasitemia levels vary and appear to depend on the immunocompetence of the host, chronicity of infection, and concurrent disease. Splenectomy results in a dramatic increase in both the degree of parasitemia and the severity of anemia. Additionally, parasitemia is negatively correlated with packed cell volume (PCV); as the PCV decreases, parasitemia rises.

Anemia, and its associated clinical signs, is the predominant clinical syndrome seen in the acute form of the disease. Cats show a remarkable ability to adapt to the disease with clinical signs generally appearing only in the terminal stages. Patients with severe anemia cope well if kept unstressed, exhibiting a rapid and uneventful recovery with only 8% requiring blood transfusions.^2,3,9 A possible explanation for cats' ability to tolerate a high parasitemia may be their relative resistance to endotoxin, as species resistant to endotoxin are less susceptible to babesiosis.^27,28 Common presenting complaints include depression, inappetance, a roughened hair coat, exercise intolerance, weight loss, weakness, pallor, tachycardia, tachypnea, pica, vomiting, and diarrhea. Fever is uncommonly reported, documented in only 5% and 7% of infected cats in 2 case series.^9,29 The majority of cats exhibiting febrile responses in 1 study had concurrent diseases including respiratory infections, stomatitis, and gingivitis. Splenomegaly, in contrast to dogs, is a less common physical examination finding, reported in 24% of cats.³ Clinical icterus is uncommon, reported in 18–21% of naturally infected domestic cats and none of the experimentally infected cats.^11,12 Twenty-five percent of naturally infected cats are reportedly asymptomatic at presentation.¹²

The anemia of B. felis infection is multifactorial, resulting from both intravascular and extravascular hemolysis. Erythrophagocytosis is commonly evident on blood smear evaluation and is thought to play a significant role in pathogenesis. Immune-mediated hemolytic anemia may occur secondary to the inappropriate production of antierythrocyte membrane antibodies. A saline agglutination test was reported to be positive in 16% of domestic cats infected with B. felis involving mainly nonparasitized erythrocytes as well as reticulocytes.¹² Spherocytosis has not been documented in these patients, and Coombs testing has not been evaluated. Patients with positive saline agglutination tests have statistically significantly lower hematocrits that nonagglutinating cats.¹² While these tests are suggestive of immune-mediated destruction of erythrocytes, these cats have responded to antibabesial therapy alone without immunosuppressive therapy. Although undocumented in cats, parasitic activity may directly damage the erythrocyte cell membrane, resulting in increased osmotic fragility and subsequent intravascular hemolysis as is the case in dogs.^2,30

Hematologic abnormalities include anemia, thrombocytopenia, and alterations in white blood cell count. The most common abnormality is anemia, which follows a fluctuating course. A rapid drop in erythrocyte count occurs less commonly than in dogs, and is most frequent in splenectomized cats. Forty-three percent of naturally infected cats displayed a normal hematocrit, 23% a moderate anemia, and 34% a severe anemia.¹² Macrocytic, hypochromic erythrocyte indices are the most common change, seen in 57% of cats, with the greatest anomalies in splenectomized cats.^10,12 Erythrocytic changes consistent with a regenerative response are commonly evident on blood smear examination. These include reticulocytosis, polychromasia, Howell–Jolly bodies, nucleated red blood cells, anisocytosis, and basophilic stippling. Nucleated erythrocytes are reported in 70% of cases.¹² Thrombocytopenia is an inconsistent finding in cats. Although 98% of cats appear to be thrombocytopenic via automated methods, only 25% are confirmed thrombocytopenic via manual count.¹² This discrepancy is not surprising as automated counts are notoriously inaccurate in cats. Leukocytosis (inflammatory, stress-induced, or physiologic) is seen in 11% of patients, and leukopenia in 17%.¹² These changes in the leukogram appear to be related to concurrent disease rather than the babesial infection.¹²

Evaluation of the biochemical profile is considered to be of little diagnostic value. Total plasma protein concentrations are typically normal, with inconsistent changes in γ, α, and β globulins. Elevations of alanine aminotransferase are reported in 35–89% of naturally infected cats, with elevations of alkaline phophatase and γ-glutamyl transferase in 25% and 4%, respectively.^11,12 Mild to moderate hyperbilirubinemia is noted in 50–86% of cats, with only 21% being clinically icteric.^3,11,12 Both direct and indirect bilirubin are elevated suggesting the contributory role of both intrahepatic cholestasis and hemolytic anemia. Elevated alanine aminotransferase, hyperbilirubinemia, clinical icterus, and a severe anemia are significantly correlated.¹² Hepatocellular hypoxia and necrosis is the most likely cause of hepatic cystosolic enzyme activity, secondary to both anemia and inflammatory mediators. Albumin concentrations tend to be increased, consistent with dehydration. Blood urea and creatinine concentrations remain essentially unchanged throughout the course of the disease, with 7–25% of cats exhibiting a moderate increase during the terminal stages.^3,11,12 Electrolyte abnormalities occur in the majority of cases, with no consistent patterns reported. The severe acid-base disturbances reported in dogs are rarely reported in cats.

Sixty percent of veterinary clinicians in South Africa reported occurrence of the acute complicated form of the disease with 5% reporting frequent, 34% occasional, and 38% rare occurrence.³ Various sequelae are documented in this form of the disease. Hepatopathy is reported in 34% with histopathologic evidence of centrolobular necrosis, bile stasis, extramedullary hematopoiesis, and hemosiderosis.^3,11,12 Renal involvement is reported in 31% of patients, typically during the terminal stages. Pulmonary edema (16%), cerebral dysfunction (12%), thromboembolism (3%), bleeding diathesis (3%), heart failure (2%), and gastric ulceration (2%) also occur.^3,11,12 Although immune-mediated hemolytic anemia is only reported in 4% of cases, the actual incidence is likely higher as slide agglutination and Coombs testing are not routinely performed. Concurrent infections including Mycoplasma hemofelis (11%), FIV (14%), and FeLV (32%) are frequently seen.^3,12 The typical clinical course is one of a progressive anemia with clinical signs manifesting during the late stages of severe disease (PCV<13%) followed by a moribund state and death. It is difficult to predict the clinical decline, as it is rapid, often associated with stress, and leads to an unexpected death.

B. felis infected cats may be chronic asymptomatic carriers, with documentation of parasitemia evident on serial blood smear evaluations of at least 2 years duration.²⁹ This is especially true in cats living in endemic regions. Exposure is thought to occur at an early age in these animals. While immunocompromised cats succumb to infection, the immune system in immunocompetent hosts prevents the development of clinical disease. As the immune system is incapable of completely eradicating the disease, the host reverts to the chronic carrier state with the production of antibabesial antibodies persisting to act as a form of premunity.¹ However, stress or concurrent illness may result in acute onset of signs and a clinical decline.

Isolated reports of infection with other babesial species exist in the veterinary literature.^4,5,8,14 Natural infection caused by Babsesia canis subsp. presentii has been documented in 1 domestic cat in Israel.⁵ Clinical signs included acute lethargy, anorexia, pyrexia, and icterus. Clinicopathologic testing revealed marked parasitemia, a severe normocytic, hypochromic anemia, leukopenia, and elevations in aspartate aminotransferase and creatinine kinase. Coinfection with FIV and (Candidatus Mycoplasma haemominutum) was documented. Resolution of clinical signs and clinicopathologic abnormalities followed antibabesial therapy. The housemate to this cat had low-grade infection of B. canis subsp. presentii, but remained asymptomatic without treatment.

B. cati infection has also been reported and is considered the least virulent of the feline babesial species. A low level of parasitemia is typically observed.⁸ Experimental infection with B. leo in the domestic cat resulted in neither parasitemia nor clinical signs.⁴ Following splenectomy, a parasitemia increased to 45% of visualized RBCs, in conjunction with the development of a mild anemia. The patient remained asymptomatic with a gradual decline in both parasitemia and antibody titer over several months without treatment. A case report from South Africa describes natural infection with suspected B. herpailuri in 1 domestic cat.¹⁴ Diagnosis was based on morphologic descriptions of the parasite, but was not confirmed via serologic or DNA-based testing. Clinical signs included fever, malaise, muddy-appearing mucous membranes, pallor, and constipation. Treatment with antibabesial agents resulted in a rapid resolution of clinical signs.

Diagnosis

Traditionally, diagnosis of feline babesial infection has been accomplished by direct visualization of the organism via light microscopy.³¹ Peripheral (ear-stick) and central blood smears are most commonly utilized; however, visualization of parasitized erythrocytes on evaluation of lymph node, bone marrow, and splenic aspirates are also documented.² Routine evaluation of blood smears in asymptomatic cats on annual examination is recommended in endemic areas.¹² Suggested preparation of blood smears includes a thin preparation, fixation in methyl alcohol, and Romanowsky-type staining. Fresh Giemsa stain in a phosphate buffer is considered the preferred method; Diff-Quick staining has also been reported.^{3–5,9,12,14}

Blood smears (central or peripheral) are useful in providing an estimate of the percentage of parasitemia, with strong correlation between the 2 methods when compared in B. felis infected cats.¹² This suggests that B. felis parasitized erythrocytes in cats do not sequester in capillary beds. This may not hold true in infections with large babesial species, as the large size of the parasite occupies a substantial volume of the erythrocyte, interfering with the normal deformability necessary to traverse capillary beds. Although highly specific, blood smear evaluation is considered an insensitive test for the detection of babesial infections, especially in cats with a low-level parasitemia and in chronic carriers.^2,13 An additional diagnostic modality should be pursued in cats with a strong suspicion of babesial infection and negative blood smear evaluations. Moreover, blood smear evaluation is limited in that it cannot provide a definitive identification of either genus or species, as the morphology of genetically distinct Babesia spp., Theileria spp., and Cytauxzoon felis are similar.^3,17

Nucleic acid-based techniques, including PCR and reverse line blot hybridization assays, are the most sensitive and specific tests for the detection of feline babesial infection.^13,17,19 These tests detect parasitic DNA/RNA, rather than merely the production of antibodies in response to infection. Nucleic acid techniques have been used to detect B. felis, B. leo, an unnamed Babesia spp. in cougars, B. canis subsp. canis, and B. canis subsp. presentii.^5,6,13,17,19 Importantly, these assays are able to discriminate among piroplasm genus and species. As concurrent infection with multiple Babesia spp., Cytauxzoon felis, Theileria spp., and Mycoplasma spp. are frequently reported, this is clinically advantageous.^13,17,19 Detection of the organism is possible in blood, organ tissue, and within tick vectors.¹⁹ PCR is capable of diagnosing babesial infections from small volume blood samples with extremely low parasitemia (0.00005%).¹³ Both nested and semi-nested PCR techniques are available. The semi-nested PCR assay is quicker to perform and less prone to contamination; but detection to the level to species is less reliable than with nested PCR techniques.¹³

Indirect fluorescent antibody (IFA) testing detects antibabesial antibodies in the blood of infected or exposed animals. Serologic diagnosis using IFA in cats has been infrequently described in the literature and is not recommended for routine diagnosis.^2,4,27 As in dogs, false negatives may occur in the very young, immunocompromised patients, or in early acute infection before an immune response is mounted.³² In these cases, the evaluation of convalescent titers can be considered. Positive IFA results in endemic areas should be interpreted with caution as high antibody titers often occur in asymptomatic carriers as well as previously exposed and treated cats.³³

Treatment

Controlled clinical studies evaluating the efficacy of therapy in feline babesiosis are lacking. Therapeutic recommendations are based on the results of 2 studies in experimentally infected cats, various isolated case reports, and anecdotal reports^{2,3,5,9,14,27,34} Compounding this, feline babesial infections (especially small Babesia spp.) are difficult to treat with a poor initial response to therapy and a high rate of infection relapse.^13,29 As complete sterilization of babesial infections is rare, the current goal of therapy is the resolution of clinical signs and anemia. Treatment for asymptomatic chronic carriers with persistent parasitemia is not recommended at this time. However, monitoring via routine CBC evaluation and blood smear analysis is indicated.

Primaquine phosphate is a member of the 8-aminoquinolone group of antimalarial drugs. It is the only drug proven to be reliably efficacious in the treatment of small feline babesial infections and is considered the drug of choice.^{2,3,9,12,29,34} Rapid resolution of clinical signs and decreased parasitemia is typically seen within 24–72 hours.^9,29 Published dosages range from 0.5 to 1.0 mg/kg PO, IV, or IM once, or administered daily on 3 consecutive days.²⁹ Long-term therapy has been reported to be safe although it should be emphasized that the duration of therapy should be based on hematologic variables and clinical signs rather than parasitemia. High-dose therapy, doses exceeding 1 mg/kg, should be avoided as fatal toxicity has been reported in 4 out of 4 cats.²⁹ Vomiting following oral therapy is the most commonly reported adverse effect.²⁹ A relapse rate of 20–80% following treatment with primaquine is lower than that of other antibabesial protocols.^3,9 Repeat administration of primaquine for relapse infections has proven efficacious and is well tolerated, with survival rates up to 100%.^3,9,26 In addition, primaquine has proven efficacious as a rescue therapy when resistance to other antibabesial drugs occurs.³⁴ Complete sterilization of the infection does not routinely occur; premunition develops as survivors remain chronic carriers with antibabesial antibody production.^3,12,29 Some practitioners in endemic areas advocate the use of primaquine in combination with doxycycline, diminazine, imidocarb, or trypan blue.³ The comparative efficacy of these combination regimens, however, has not been evaluated.

Diminazine aceturate, an aromatic diaminidine derivative, has shown promise in the treatment of large babesial species in cats. Administration of an unpublished dose to 1 cat with an unnamed large babesial species resulted in a rapid resolution of clinical signs within 24–48 hours.¹⁴ Additional clinical studies are needed to verify efficacy. The use of a single dose of 3.5 mg/kg, IM in the treatment of B. felis has shown extreme variation in clinical efficacy with resistance and relapses commonly reported.²⁹ At this time it is considered unsuitable for the treatment of small babesial species in cats. The use of diminazine in canine babesial infections has shown a very narrow therapeutic range, with inconsistent elimination of the drug and a high rate of toxicity, including severe, fatal neurologic dysfunction.^1,35–37 Moreover, it is cumulative over an extended period. To avoid toxicity the dose should not be repeated with this or another diaminidine derivative within a 6-week period. As diminazine therapy in cats is less common, these same guidelines should be applied in cats until proven otherwise.

Imidocarb diproprionate, a carbanilide member of the diaminidine family, has no proven efficacy in the treatment of B. felis infections in cats.²⁹ However, it has shown efficacy against large babesial infections. A single dose of 2.5 mg/kg, IM or coadministration with doxycycline are both efficacious in the resolution of clinical signs in B. canis subsp. presentii and B. herpailuri infections.^5,29 Although uncommon, adverse effects are severe and anticholinesterase in nature, including salivation, lacrimation, vomiting, diarrhea, muscle tremors, restlessness, tachycardia, and dyspnea.

A controlled clinical trial performed by Penzhorn et al³⁴ evaluated the efficacy of 5 chemotherapeutic agents in cats experimentally infected with B. felis and is the only comparative treatment study in cats that has been published. In this study, the efficacy of buparvaquone, rifampin, sulphadiazine-trimethoprim, enrofloxacin, and danofloxacin were compared with primaquine phosphate. Buparvaquone therapy initially resulted in a decrease in parasitemia equal to that of primaquine; however, an abrupt rise in parasitemia occurred between 48 and 72 hours post-therapy. Treatment with rifampin and sulphadiazine-trimethoprim prevented an increase in parasitemia with no substantial improvement, followed by an abrupt drop in PCV. Both fluoroquinolones had no effect on parasitemia with a steady increase seen in all patients. Primaquine was used as both a control and rescue therapy in this study, proving to result in a dramatic decrease in parasitemia in both instances.

The use of other or adjunctive antimicrobials and anti-protozoal drugs have been reported in endemic areas with varying success.^3,9,14 Transient improvements in clinical signs have been reported in cats infected with small Babesia spp. treated with trypan blue, chloroquine, euflavine, doxycycline, phenamidine, quinuronium, cephalordine, buparavaquone, rifampin, sulfadiazine-trimethoprim, enrofloxacin, danofloxacin, chlortetracycline, and oxytetracycline at a wide range of dosages.^3,9,14,26,34 However, these agents appear less efficacious than primaquine in the reduction of clinical signs and parasitic load, and are considered unsuitable for definitive therapy.

Controlled clinical trials evaluating therapeutic regimens in feline babesiosis are desperately needed. Combination therapy with azithromycin and atovaquone has proven to be highly efficacious in the treatment of small Babesia spp. infections in humans and dogs and is currently considered the treatment of choice in these species.^38–42 Antimicrobials with antiprotozoal properties, such as doxycycline, clindamycin, and metronidazole, have shown efficacy against Babesial spp. in humans and dogs.^43–46 The combination of clindamycin and quinine therapy is the standard of care in the treatment of severe babesiosis in humans.³⁸ To the authors' knowledge no literature exist documenting the use of these chemotherapeutics in feline babesiosis. Future studies should be aimed at development of a standardized treatment protocol incorporating but not limited to the aforementioned therapies.

Supportive care is required for feline babesiosis, especially with severe forms of the disease. As stress and handling are associated with rapid, unexpected death in infected cats, quiet housing in a nonstressful environment and prevention of excessive patient handling is paramount during the hospitalization of these patients.^3,9 Fluid therapy is indicated for maintenance of blood volume and adequate end-organ perfusion, correction of acid-base and electrolyte abnormalities, diuresis, and prevention of RBC sludging in capillaries.^3,5 Blood transfusion may become necessary if clinical signs referable to anemia are significant.^3,9 As the anemia results from hemolysis, packed red blood cells are the blood component of choice. Anecdotal adjunctive supportive therapies have included: vitamin and mineral preparations, corticosteroids, anabolic steroids, nonsteroidal anti-inflammatory drugs, antioxidant therapy, nutritional support, and appetite stimulants.³ The efficacy of these therapies have yet to be critically evaluated.

Prognosis

Mortality rates of 15–20% are reported in naturally occurring B. felis infections, while a 100% mortality is reported in untreated experimentally infected cats (both intact and splenectomized).^3,9 A higher rate of mortality is seen in nonendemic regions and mortality does not appear to correlate to the severity of anemia or parasitemia.^9,11 Concurrent infection is associated with a poor response to therapy, clinical recurrence, the complicated form of the disease, and death.^3,12 Survival of 1 cat with B. canis subsp. presentii and 1 cat infected with a large unidentified babesial organism has been documented in case reports.^5,14 While little is known about the true virulence of Babesia spp. in domestic cats, it is expected that increased clinician awareness will lead to increased testing in cats and subsequently a better understanding of the disease, as has been the case in dogs with babesiosis.