Page 44 - Withrow and MacEwen's Small Animal Clinical Oncology, 6th Edition

CHAPTER 1 The Etiology of Cancer 23

Like most retroviruses, FeLV is rapidly inactivated by heating and The Rickard strain of FeLV (FeLV-R), although similar to
most disinfectants. 317 Given these characteristics, environmen- MYC-containing recombinant strains in its ability to rapidly pro-
duce mediastinal lymphoma, does not recombine with the MYC
tal contamination (e.g., examination tables, cages, and waiting
VetBooks.ir rooms) is unlikely to be a potential source of FeLV infection. 310 gene. 306,337 Instead, it exerts some of the biologic effects by inte-
306
Although saliva may contain up to 100,000 virus particles per
grating adjacent to the MYC gene, causing its overexpression.

milliliter, prolonged, intimate contact with infected cats usually
is required for transmission. The factors most frequently incrimi- Feline Oncornavirus-Associated Cell Membrane Antigen
nated in the transmission of FeLV are licking, biting, grooming, FOCMA is a protein found on the surface of FeLV and FeLV-
and sharing of litter pans, food bowls, and water dishes. Intimate induced neoplasms but not on nonneoplastic feline cells. 338,339
contact is enhanced in catteries and multiple-cat households, FOCMA is detected serologically when cells expressing it react
where infection rates may be very high. 319 to immunoglobulins produced in cats that have regressed FeSV-
Before vaccines and routine testing became available, the over- induced fibrosarcoma or FeLV infection. The presence of the
all prevalence of FeLV infection in the United States was estimated FOCMA antibody is determined by the ability of the serum to
at 1% to 3% of the cat population. 308,309 The prevalence of FeLV react with FL74 cells, a transformed infected feline lymphocyte
infection was less than 1% in single-cat households and as high line. 340 Antibodies to FOCMA protect against neoplastic and
as 30% in multiple-cat households. 327 The incidence of FeLV- myeloproliferative disease. Some FeLV vaccines contain FOCMA
positive test results in sick cats in the United States was approxi- and elicit an anti-FOCMA response. 341 The relative importance of
mately 11.5%. 328 Several studies have reported a decline in the this in preventing disease in vaccinates is unknown.
prevalence of FeLV by as much as 50% over the past 20 years; this
decrease may be attributed partially to the widespread use of FeLV Neoplastic Diseases Caused by Feline Leukemia Virus
vaccination. 307,329,330 Much has yet to be learned about the genetic basis for the vast
Although cats may be infected with FeLV subgroups A, B, or C diversity of tumor types produced by FeLV and its recombinants.
or other recombinants, only subgroup A has been found in cell-free We now know that FeLV, through one or another of its recombi-
fluids and is thought to be associated with natural transmission of nants, may cause virtually any hematopoietic neoplasm in the cat.
FeLV. Subgroups B and C and other recombinants are more cell The only hematopoietic neoplasms not yet associated with FeLV
associated and are not thought to be transmitted in nature. 323–326 in nature are mast cell leukemia, eosinophilic leukemia, plasma
The FeLV subgroups are characterized by their cross-interfer- cell tumors, and polycythemia vera. 306
ence with homologous but not heterologous subgroups of FeLV Although FeLV infection is considered the most significant
and by their host range and other factors. All naturally infected infectious cause of morbidity and mortality in cats, only 20%
FeLV cats have subgroup A, 50% of infected cats have a combina- of cats persistently infected with FeLV develop lymphoid can-
tion of subgroups A and B, and 1% of infected cats in nature have cer. 342,343 The cat has the highest incidence of hematopoietic
a mixture of subgroup C, either as AC or ABC. 308,328,331 neoplasms of domestic animals, and the prevalence of lymphoma
The relevance of subgroups in strains is essential to an under- ranges from 44 to 200 cases per 100,000 cats, six times the rate of
standing of the biodiversity of the clinical disease caused by this disease in humans. 306 Twenty years ago 70% of lymphomas in
FeLV infection. Although subgroups A, B, and C maintain 85% cats were believed to be caused by FeLV.
genomic homology, cats infected with various combinations of Some cancers are more commonly associated with FeLV infec-
these subgroups may manifest vastly different diseases. tion than others. Large granular lymphoma and globular leuko-
Subgroup A has a variety of strains that range from nonpatho- cyte tumors usually test negative for FeLV, 344–345 whereas 70% to
genic to very pathogenic. 332 Although most strains of subgroup A 90% of cats with nonlymphoid hematopoietic neoplasia (myelo-
have limited pathogenicity, their pathogenicity increases dramati- proliferative disease) test positive for FeLV. 306 The percentage of
cally if they are present with other subgroups. lymphomas that test positive for FeLV also varies, depending on
Subgroup B is created when subgroup A recombines with the anatomic location of the tumor. 346–347 Cats with spinal, medi-
endogenous FeLV envelopes at sequences already in the feline astinal, ocular, and renal lymphoma frequently tested positive for
genome. 333–335 Each recombination is unique, resulting in many FeLV before routine vaccination (more than 70%). 349 Extranodal
strains of FeLV-B. The combination of subgroups A and B is more lymphomas, such as those of the nasal cavity and the alimentary
contagious and pathogenic than subgroup A alone. 328,331,332 Cats tract, frequently test negative for FeLV infection. 306 Over the
infected with subgroups A and B often develop thymic lymphoma past 20 years, the multicentric FeLV-positive form has declined
and myeloproliferative disease. 333 in young cats, and the FeLV-negative alimentary form in older
Subgroup C arises from the mutation of subgroup A. 336 Cats cats has increased. 350,351 Although the alimentary form most often
may be infected with a combination of C and other subgroups, is FeLV negative, as assessed by IFA and ELISA testing, some of
although these combinations are uncommon and are found in only these lesions have been shown by PCR to be FeLV positive, which
about 1% of naturally infected cats. FeLV-C is antigenically simi- suggests that the disease may be related to previous FeLV exposure.
lar to the associated membrane antigen (feline oncornavirus-asso- Although not all lymphomas are caused by FeLV, the relative
ciated cell membrane antigen [FOCMA]); cats carrying FeLV-C risk of developing lymphoma is 62 times higher in FeLV-positive
have developed severe erythroid hypoplasia and anemia and usu- cats, and cats that are FeLV negative but that have had previous
ally die within 1 to 2 months. 323 Further complicating the biodi- exposure to FeLV have a fortyfold increase in the risk of devel-
versity of subgroups and strains is the fact that subgroups A and B oping lymphoma. 352 Most spontaneous lymphomas of cats that
can recombine with proto-oncogenes, such as MYC or TCR, pro- test positive for FeLV arise from T cells, whereas FeLV-negative
ducing FeLV-MYC or FeLV-TCR. 306 Both of these recombinants lymphoma frequently is of alimentary or B-cell origin. 353,354 The
are considered more potent tumor producers than their nonre- time from infection to tumor development varies and may depend
combinant FeLV parent. Another subgroup, T, is highly cytolytic on the age at which the cat is infected or on other factors, such as
for T lymphocytes and causes severe immunosuppression. 324–326 strain, anatomic location, and viral subgroup. 306 The range from