Hemobartonellosis - The Merck Veterinary Manual

Hemobartonellosis
(Feline infectious anemia)

Etiology, Transmission, and Pathogenesis

Feline infectious anemia (FIA) is an acute or chronic disease of domestic cats, seen in many parts of the world, caused by a rickettsial agent that multiplies within the vascular system.

Etiology, Transmission, and Pathogenesis:

FIA is caused by an epicellular RBC rickettsial parasite, Haemobartonella felis (termed Eperythrozoon felis in Europe and Australia). Based on genetic similarities, it has recently been proposed to move this organism to the genus Mycoplasma. It is gram-negative and nonacid-fast and reproduces by binary fission. In blood smears, H felis typically appear as cocci in thick areas of the film and as rings or rods in thin areas. The dimensions vary from 0.2-1 µm in diameter for the coccoid forms and up to 3 µm in length for the rod forms.

The causative organisms are usually found in varying numbers on the surface of the RBC but are occasionally seen free in the plasma. They appear as dark red-violet bodies in thin blood smears stained with Wright-Giemsa stain or as purple to blue organisms attached to RBC when using the May-Grunwald-Giemsa staining procedure; this procedure appears to be superior to other Romanowsky staining techniques. Acridine orange staining and direct immunofluorescence techniques have also been recommended for diagnosis of H felis ; unfortunately, these techniques require special equipment and training and are not commercially available.

The number of RBC affected varies with the severity of the infection and the stage in the life cycle of the parasite. Blood films should be examined daily for 5-10 days if infection with H felis is suspected because organisms are recognized in only 50% of cats in the acute phase of the disease. During the acute phase, numbers of H felis organisms increase gradually, then disappear rapidly; clearance of organisms may occur within 2 hrs. In chronically infected cats, organisms appear only sporadically and in small numbers.

FIA can be transmitted experimentally by parenteral or oral transfer of small amounts of infected whole blood into susceptible cats. Intrauterine transmission can also occur, and infections can be transmitted iatrogenically via blood transfusions. However, the natural mode of transmission is believed to be via bloodsucking arthropods (such as fleas) and possibly via bite wounds.

In experimental cases, the incubation period is 1-5 wk, and recovery does not induce immunity to reinfection. Incidence of the naturally occurring disease appears to be higher among 1- to 3-yr-old cats, particularly males. A significant portion of the feline population may carry the infection in a latent form, which becomes exacerbated during debilitating disease or stress. Underlying infection with feline leukemia ( Feline Leukemia Virus and Related Diseases: Introduction) or feline immunodeficiency virus ( Viral-induced Immunodeficiencies) should always be investigated in cats with hemobartonellosis.

It is thought that H felis may not cause illness in healthy cats, but that it leads to acute disease only when an infected cat is stressed by concurrent illness. Similarly, recovered carrier cats are believed to be prone to relapse with stress.

Immune-mediated mechanisms of RBC injury are also important in the pathogenesis of FIA. Parasitized RBC may be damaged by antibody-complement interactions against H felis antigens. In addition, parasite-induced exposure of hidden or altered RBC antigens may lead to RBC destruction; erythrophagocytosis by the reticuloendothelial system appears to be more important than intravascular hemolysis. In experimental infection, the Coombs’ test becomes positive 7-14 days after organisms appear in the blood and remains positive throughout the acute phase; the Coombs’ test becomes negative during the carrier phase of the disease.

Clinical Findings and Lesions:

Any anemic cat may be suspected of having FIA. In acute cases, fever usually reaches 103-106°F (39-41°C); the temperature may drop to subnormal in moribund cats. Experimentally, cats have ≥2 parasitemic episodes before the resulting anemia leads to clinical signs. The severity of clinical signs correlates with the rapidity of onset of anemia. Pallor or jaundice, anorexia, lethargy, depression, weakness, and splenomegaly are common. In chronic or slowly developing cases, there may be normal or subnormal body temperature, weakness, depression, and weight loss or emaciation, but there is less likely to be jaundice and splenomegaly. Dyspnea varies with the degree of anemia. Gross necropsy findings are not pathognomonic; splenomegaly is common, and mesenteric lymph nodes may be enlarged. Hyperplasia of the bone marrow may be seen on histopathologic examination.

Diagnosis:

Haemobartonella felis, feline blood smear

Laboratory confirmation depends on identification of the parasite in the peripheral blood or bone marrow. A series of smears stained with Wright-Giemsa stain over several days may be required for an accurate diagnosis because the erythrocytic bodies exhibit periodicity. Certain artifacts such as Howell-Jolly bodies may be mistaken for blood parasites. The slides should be clean, and the stains should be filtered immediately before use because dirt particles and stain precipitates can mimic the appearance of the organism.

In the southeastern USA, differentiation from feline cytauxzoonosis ( Cytauxzoonosis) should be made. Cytauxzoon felis appears as an intracellular ring, rod, or coccoid-shaped protozoan 0.5-2 µm in diameter within RBC, while H felis tends to form chains on the surface of RBC. A PCR test that detects the organism in blood is also available; a positive result confirms active infection.

Expected laboratory abnormalities include a regenerative anemia; typical changes include diffuse basophilic granules in larger erythrocytes, nucleated RBC, polychromasia, anisocytosis, Howell-Jolly bodies, and an increased reticulocyte count. However, if the onset of anemia is rapid, a nonregenerative anemia may be present. RBC counts may fall as low as 1 × 10⁶ /µL, and hemoglobin values of ≤7 g/dL may be seen. Mean corpuscular volume may be increased. There may be moderate leukocytosis with monocytosis in acute forms, normal counts in chronic forms, and leukopenia in moribund cases. Erythrophagocytosis and autoagglutination may be present in peripheral blood. Serum biochemical changes often include increased ALT, AST, bilirubin, and total protein levels; moribund cats may be hypoglycemic.

Treatment:

Treatment involves both supportive and specific therapies. Without treatment, one-third of acutely ill cats may die. Severely dyspneic cats may require oxygen, and whole blood or packed RBC transfusions may be needed in cats with a PCV of ≤15%, particularly if the anemia is acute. The decision to transfuse should be based on the cat’s clinical condition rather than on the PCV.

Tetracycline (20 mg/kg, PO, tid for 21 days) is recommended as a specific antirickettsial agent. Doxycycline (10 mg/kg, PO, sid for 21 days) is also effective. Unfortunately, H felis is not completely eliminated by tetracycline therapy, resulting in chronically infected carrier animals. Thiacetarsamide sodium (1 mg/kg, IV, every 48 hr for 2 treatments) has also been recommended for the treatment of hemobartonellosis; however, some reports suggest that this agent is less effective than previously thought. Although chloramphenicol has also shown efficacy against H felis , it can cause a significant but reversible erythroid hypoplasia that may interfere with the regenerative response.

The use of glucocorticoids is recommended based on the evidence of immune-mediated RBC injury. Prednisone or prednisolone (2-4 mg/kg, PO, sid) should be used in conjunction with antibiotic therapy, and the dose should be gradually tapered as the PCV increases.