Feline infectious anemia: What's new? (Proceedings) - Veterinary Healthcare
  • SEARCH:

ADVERTISEMENT

Feline infectious anemia: What's new? (Proceedings)


CVC IN BALTIMORE PROCEEDINGS

Introduction

Causes of anemia in cats include decreased red blood cell (RBC) production, blood loss, and increased RBC destruction. The first is always non-regenerative; blood loss and increased RBC destruction are generally followed by a regenerative response 3-5 days after the initial insult, although chronic gastrointestinal blood loss may become non-regenerative due to iron deficiency. Increased RBC destruction may result from:

1. Primary immune-mediated disease, which is less common in cats than in dogs

2. Immune-mediated disease that is secondary to infection, neoplasia, or drugs

3. Inherited defects of RBC osmotic fragility, such as that seen in Somali and Abyssinian cats

4. Metabolic disease, such as hypophosphatemia

5. Toxic causes that result in Heinz body formation, such as acetaminophen, zinc, onions, garlic, and local anesthetic. Feline erythrocytes are more sensitive to such oxidative insults than canine erythrocytes.

Compared with canine RBCs, feline RBCs are smaller and lack central pallor, so spherocytes are not normally identified in the cat. Two types of reticulocytes circulate following the regenerative response to anemia in cats: aggregate and punctate reticulocytes. Aggregate reticulocytes are the most immature form of reticulocytes. The presence of > 1% of these in the peripheral blood indicates active regeneration; they behave much like canine reticulocytes. Laboratories that report a single reticulocyte count for cats generally are reporting the aggregate reticulocyte count. Punctate reticulocytes are more mature and increased numbers (> 10%) suggest a previous regenerative response (within the last 1-2 weeks).

There are several infectious causes of anemia in cats, the most common in the United States being feline leukemia virus and feline immunodeficiency virus infections, feline hemotropic mycoplasma infection, FIP, and the protozoal organism Cytauxzoon felis.

Feline leukemia virus and feline immunodeficiency virus

Feline retroviruses can cause anemia through multiple different mechanisms, including decreased RBC production (bone marrow disease and anemia of inflammatory disease) and increased RBC destruction. Cats infected with FeLV may have a macrocytic, normochromic, nonregenerative anemia that arises from disordered red cell maturation. Increased destruction can occur through secondary immune-mediated hemolytic anemia, or as a result of immunosuppression and infection with other hemolytic pathogens.

Feline infectious peritonitis virus

FIP can cause mild to severe anemia. Multiple mechanisms are likely, including anemia of inflammatory disease and increased RBC destruction.

Hemotropic mycoplasmas

The hemotropic mycoplasmas (hemoplasmas) that infect cats include Mycoplasma haemofelis (Mhf), 'Candidatus Mycoplasma haemominutum' (Mhm), and Mycoplasma turicensis (Mtc). Diagnosis of hemoplasmosis is based on cytologic examination of blood smears, which has very low sensitivity, PCR, or both. The mode of transmission of these organisms remains enigmatic. The most prevalent organism is Mhm, which infects approximately 15-25% of all cats, and is generally considered non-pathogenic or only mildly pathogenic in immunocompetent cats. More severe anemia may be observed in immunosuppressed cats that are infected with Mhm, such as those concurrently infected with FeLV. Using light microscopy, Mhm is very small (0.3 (m), and difficult to identify. Mhf is the least common pathogen, occurring in < 5% of cats, but appears to be the most virulent. Initial infection with Mhf is associated with severe hemolytic anemia, marked reticulocytosis, normoblastosis, and sometimes leucopenia and thrombocytopenia, even in immunocompetent cats. Using light microscopy, Mhf appears as small (0.3 – 0.6 (m) basophilic coccoid bodies on the surface of erythrocytes, sometimes forming short chains of organisms. Mtc was recently discovered in Switzerland, and studies suggest it has a worldwide distribution. It has a similar prevalence in Californian cats as Mhf. It can cause anemia in immunocompetent cats, but may be somewhat less pathogenic than Mhf. It has never been identified on blood smears.

PCR tests for hemoplasmas vary in their ability to detect and identify different species, and so it is best to consult with your diagnostic laboratory to determine the species identified. Treatment of hemoplasmosis involves use of doxycycline (10 mg/kg PO q24h) for 2 weeks. Cats that do not tolerate doxycycline may be treated with enrofloxacin as an alternative. Blood transfusions may also be necessary. Concurrent prednisone therapy to treat secondary immune-mediated hemolytic anemia is controversial and should be avoided if possible, as glucocorticoids have the potential to reactivate latent hemoplasma infections. Although anemia resolves in treated cats, most cats remain latently infected, and disease may reappear following immunosuppression or concurrent illness. Antimicrobials may be less effective in cats infected with Mhm.

Cytauxzoon felis

Cytauxzoon felis is a protozoal organism that belongs to the family Theileriidae. Infection most commonly occurs in cats with access to the outdoors in southern and some Midwestern states, and has been recently recognized along the Atlantic coast. It is transmitted by the bite of an infected tick (Dermacentor variabilis), and infection of cats generally results in rapid death within days of initial illness. The reservoir host is the bobcat, Lynx rufus. The organism initially forms schizonts in mononuclear phagocytes, which can become extremely large and obstruct venules throughout a variety of organs. Merozoites that are then released from the schizonts infect erythrocytes. The schizogonous phase in the bobcat host is brief and non-fatal, but in domestic cats is associated with disseminated intravascular coagulation (DIC) and multiple organ failure. The tick vector appears to be necessary for disease to occur. Clinical signs occur approximately 2 weeks after infection and include anorexia, lethargy, pyrexia (which may be pronounced), icterus, and pallor. Laboratory findings include non-regenerative anemia, leukocytosis, thrombocytopenia, hyperbilirubinemia, hyperglycemia, liver enzyme elevations, hypoalbuminemia, and evidence of DIC. Erythrocytic piroplasms may be seen on blood smears, or schizonts may be seen in tissue monocytes on spleen or liver aspirates. PCR assays are also available. Antiprotozoal therapy has not been proven to be useful for treatment of these infections. Azithromycin and atovaquone are currently being examined for their efficacy, with initial promising results. In recent years, some cats have been identified that have survived infection, possibly because of appearance of less virulent strains or better host immunity.

ADVERTISEMENT

Source: CVC IN BALTIMORE PROCEEDINGS,
Click here