I’d like to begin by saying thanks to several readers for their
thought-provoking questions/comments….I’ve been in-and-out of the lab for
the past few weeks so I apologize for the long delay between posts, so
thanks also to everyone for bearing with me. In my last post I provided
a little info about basic puma and bobcat ecology and how it pertains to the
NSF project on which I’m working. We are particularly interested in disease
transmission dynamics between domestic and wild felid populations across
multiple landscapes. These populations are known to be susceptible to
numerous viral, bacterial, and protozoal pathogens. These animals can also
be reservoirs for several zoonotic agents, which we discussed in the
comments section of my last post. (*Side note: From here on I will focus
primarily on the viral agents that are capable of causing disease in felines
only. I certainly hope all the bacteriologists and parasitologists out there
continue reading though*.*)

Our lab investigates two notable feline retroviruses, feline
immunodeficiency virus (FIV) and feline leukemia virus (FeLV). FIV is the
feline analogue to HIV, demonstrating affinity for similar cell types as
well as displaying comparable clinical symptoms and outcomes. Infection in
domestic cats can cause immunosuppression ultimately resulting in death.
However, many animals remain asymptomatic carriers for the duration of their
lives. The fitness impacts on wild felines have yet to be fully understoood,
but seroprevalence rates across our study areas are found to be quite high.
A major objective of our project is to determine the impacts of this disease
on the health and behavior of large carnivore populations facing varying
environmental stressors.

FeLV is similar to FIV in that it is also a horizontally-transmitted,
immunosuppressive retrovirus. The similarities pretty much end there though.
Whereas in FIV infection depletion of T-cells is the major clinical symptom,
FeLV infected animals may experience cytosuppressive (aplastic anemia) or
cyotproliferative (lymphoma) disorders. The majority of exposed felines will
be able to mount a sufficient immune response to the infection. These
animals are known to have regressive or latent infections and usually show
no signs of disease. But for roughly 30% of those exposed, a progressive
infection ensues marked by persistent viremia and FeLV-related disease.
While cases in nondomestic felids are rare, there have been
several incidents which have raised concerns. Most notably, a recent
epizootic among the protected Florida panther (*Puma concolor coryi)*
population
caused wildlife officials to implement a FeLV vaccination program. This was
the first such program of its kind among free-ranging nondomestic felid
populations. The real interesting thing about this outbreak was that virus
isolated from the Florida panthers was genetically linked to a particularly
virulent domestic cat strain of FeLV, thus illustrating the organism’s
ability to cross species. This cross-species transmission indicates that
some kind of interaction took place between domestic and wild felines,
which provides us with a very unique oppotunity to gain insight into the
details of such host/pathogen relationships.

The bulk of my work focuses on FeLV exposure events in Florida, California,
and Colorado. In my next post, I’ll get into some more details lab work that
goes into determining the status of all these animals. I’ll be posting at
least once a week for the rest of the Summer, so be sure to check back often
and don’t hesitate to send me any comments or questions you may have. I hope
you’ve enjoyed reading as much as I’ve enjoyed sharing.

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