Proceedings of the fifth mountain lion workshop: 27

32 PROCEEDINGS OF THE FIFTH MOUNTAIN LION WORKSHOP
Several testing procedures are commonly employed
to diagnose feline leukemia infection. Notably, most tests rely
on detection of viral antigen denoted p27 in blood, serum, or
tears. The commercially available ELISA has the advantage
of being very fast and easily performed in the field, but has a
slight risk of false positives. Confirmation of FeLV
antigenemia may be performed with IFA.
Despite a few isolated reports of feline leukemia in
nondomestic felids, overall seroprevalence approaches zero.
In California, the mountain lion seroprevalence by antigen
ELISA was 0 (Paul-Murphy et al. 1994), as it was in Florida
panthers (Roelke et al. 1993).
Clearly, future rates of feline leukemia infection in
mountain ions are likely to be related to rates in domestic cats
with which they are sympatric. Domestic cat FeLV
seroprevalence has been reported from 5.1% in mid-Atlantic
states (Glennon et al. 1991, who themselves claimed that there
might be a bias towards "healthy cats" in their sample"), to
10.7% (Stark et al. 1987). Specific rates of FeLV in
California domestic cats have not been reported.
FELINE IMMUNODEFICIENCY VIRUS
Feline immunodeficiency virus (FIV) and the related
puma lentivirus (PLV) have incited concern and controversy
regarding their potential impacts on populations of free
ranging felids. Genetically, FIV and PLV are similar to HIV,
the agent responsible for acquired immune deficiency
syndrome (AIDS) in humans. AIDS (i.e. very low CD4 Tlymphocyte
counts, increased susceptibility to opportunistic
infections, etc.) has also been observed in FIV-infected
domestic cats, but it remained controversial whether any
clinical disease in non-domestic felids could be attributed to
FIV/PLV infection. PLV is genetically and biologically
distinct from FIV (Olmstead et al. 1992), with one study
reporting similar structural genes between the virus but
distinctly shorter long terminal repeats (LTRs) in PLV
(Langley et al. 1994). Domestic cats which were
experimentally inoculated with PLV became viremic but had
no change in T cells or appreciable disease after 6 months
(VandeWoude et al. 1996).
FIV in domestic cats is transmitted by "intimate
contact": saliva inoculated via a bite wound and sexual
transmission. For large cat species, it is reasonable that
ingestion of FIV-infected small felids could also transmit the
infection. The disease course in cats is similar to that in
humans with HIV, including an initial high level of bloodborne
virus associated with local enteritis, followed by low
levels of viremia and eventual oscillatory dynamics of virus
load and antibody titer, eventually culminating in high viremia
again and frank immunosuppression (Ackley et al. 1990).
Onset of AIDS is variable, occurring approximately 8 years
after initial infection of kittens (Pedersen, UC Davis pers.
commun.).. Thus the two concerns for potential impact of
FIV on mountain lions are whether acutely infected, marginal
mountain lions would be "pushed over the edge" by transient
diarrhea, and whether chronically infected, asymptomatic
mountain lions would survive long enough to succumb to
AIDS.
Numerous tests are available for diagnosing infections
with FIV, including ELISA, western blot, and IFA.
Additionally, viremia may be confirmed by co-cultivating
patient blood with domestic cat peripheral blood mononuclear
cells (PBMCs). PLV and FIV apparently cross-react in
serologic tests (Olmstead et al. 1992). Screening procedures on
many felid species have identified seropositive individuals in
mountain lions, cheetahs (Acinonyx jubatus), bobcats, tigers,
African lions, jaguars, and others. Rates of seroprevalence
vary. California lion seroprevalence of FIV was reported as 0
in one study (Paul-Murphy et al. 1994), while Olmstead et al.
(1992) reported a California seroprevalence of PLV and FIV of
56.25% (n=9) using immunoblot. They also found 80%
seropositivity in Arizona, 50% in New Mexico, and 20% in
Wyoming. Florida panther seroprevalence varied from 30%
(Barr et al. 1989) to 37% (Roelke et al. 1993).
To date, confirmation of clinical disease attributable
to FIV is controversial. Kennedy-Stoskopf et al. (1996)
documented inverted CD4/CD8 ratios, indicative of virally
induced adverse immune effects. It is not known whether
natural pathogenicity differs between PLV and FIV.
A likely source of FIV in mountain lion populations
in the west is infected domestic cats. The seroprevalence of
FIV in cats in the US varies from 1.2% (Yamamoto et al.
1989), 4.7% (Glennon et al. 1991), 8.06% (Courchamp and
Pontier 1994), to as high as 11.3% in a high risk population in
Texas (Cohen et al. 1990)
In summary, further data need to address pathogenicity
of PLV and FIV in mountain lions before we can adequately
assess the risk these diseases have for lion populations. It is
fascinating to note that FIV seroprevalence is very high in some
populations, even in the absence of FeLV. Thus we cannot
attribute high rates of FIV solely to exposure to infected
domestic cats. Interesting future research should concentrate
on the molecular epidemiology of domestic cat and mountain
lion PLV and FIV infections.
FELINE INFECTIOUS PERITONITIS
Significant confusion exists regarding the origin and
epidemiology of feline infectious peritonitis (FIP) in
populations of domestic cats, where FIP is common and
thoroughly described. Thorough understanding of FIP biology
in non-domestic felids is even more poorly understood. FIP
occurs as a mutant form of the ubiquitous, highly infectious
feline enteric coronavirus (FECV) (Poland et al. 1996). Viral
strain differences and intrinsic differences in susceptibility of
hosts both further complicate FIP epidemiology.