The first cat I ever had was fed only raw muscle, this was over 11
years ago. He developed steatitis and vitamin E alone cured him. I
gave him 400mg per day and in two weeks he was already moving around
(he got to the point where he didn't move at all and it took many vets
to get him diagnosed - seems vets are not very familiar with nutrient
deficiencies). One thing he did *not* have were holes openning up
throughout his body. His skin was just fine. Are you sure steatitis is
the only thing your cat has? You know for a fact the tissue is
necrotic by its smell. Necrotic tissue has a very characteristic smell
- smells very much like the liquid skunks use to drive away their
enemies. It's nothing like gas (fart) - sorry for the word. It's a
more pungent smell. I would have a vet look at it because dead tissue
can cause serious infection.

What I do know is that vitamin C deficiency causes hemorrhages and
skin ruptures but cats can make their own vitamin C. What I do not
know is what is the precursor of vitamin C for cats so if the
precursor is missing in the diet, they wouldn't be able to synthesize
vitamin C. With the change in diet this should be automatically
corrected.

He's getting various canned foods,

......Normally, liver shouldn't exceed 10% of the diet.

Apparently lots of fluid can build up with inflammation - could be why the
skin broke open to discharge it.   Perhaps the color of what you are seeing
is due to ceroid pigmentation:

Scroll down to Case III, where you'll note this cat also ate a canned tuna
diet - back in 2000/2001.  Don't these manufacturers learn anything?  Also
note they mention liver as a possible cause, so I'd cut that liver amount in
the diet back.

http://www.afip.org/vetpath/WSC/wsc00/00wsc06.htm
Ceroid pigment is present as brown/gray globules, mostly within the
cytoplasm of macrophages

buglady
take out the dog before replying

I found something that looks worth considering. Since cats are natural
hosts of the parasite toxoplasma gondii, it is common to find cats
infected with this parasite. The vet prescribed steroids, which
weakened your cat's immune system and this may have allowed T. gondii
to cause infection - see below. I would have your cat tested for T.
gondii and stop using steroids right away if he tests positive. If it
were my cat, I'd stop the steroids immediately but NOTE that I'm not a
vet!

CASE IV – H99-2875 (AFIP 2737304)
Signalment: 12-year-old, castrated male, domestic shorthair cat, Felis
cattus.
History: The cat was referred to “Exclusively Dermatology”
for a multifocal, nodular and ulcerative dermatopathy of 3-4 weeks
duration. The cat had been anorexic for 6 days and was systemically
unwell and pyrexic (400C).
Gross Pathology: None given.
Laboratory Results: CBC: Severe lymphopenia
Biochemistry: Hypercalcemia, hypercholesterolemia, hyperglycemia,
pre-renal azotemia, myopathy.
PCR for feline calicivirus, Chlamydia sp. & Neospora caninum: Negative
PCR for Toxoplasma gondii & feline herpesvirus-1: Positive
Witness  antibody detection kit (Agen) for feline
immunodeficiency virus: Positive
Contributor’s Diagnosis and Comment: The submission was a 6mm
skin biopsy of haired skin. There was mild, irregular epidermal
hyperplasia accompanied by moderate, diffuse, spongiosis and
multifocal epidermal necrosis. Multifocal intra-epidermal pustules
were associated with multifocal, subepidermal vesicle and pustule
formation. There was diffuse superficial dermal degeneration and
necrosis associated with a moderate, perivascular to diffuse, mixed,
predominately neutrophilic and plasmacytic, dermatitis and
panniculitis. Extensive vascular degeneration and necrosis was evident
within the dermis and there was pyogranulomatous thrombosis of deep
dermo-hypodermal venules. Scattered throughout the dermis and
hypodermis there were individual and aggregated intra-
and extracellular protozoal zoites measuring between 1-2 um diameter
and 2-6 um length.
Morphologic Diagnosis: Severe, acute, diffuse, dermal vascular
necrosis and hypodermal thrombosis with a subacute, diffuse,
necrotizing, mixed neutrophilic and plasmacytic dermatitis containing
intracytoplasmic and extracellular protozoal zoites: Toxoplasma
gondii.
Cutaneous disease is an uncommon manifestation of clinical
toxoplasmosis in both humans and cats. A review of 100 cases of
clinical toxoplasmosis in cats identified only two cats with cutaneous
toxoplasmosis. The reported incidence of cutaneous manifestations of
toxoplasmosis in humans is also <10%. Toxoplasmosis in cats is usually
characterized clinically by fever, dyspnea, polypnea, anorexia,
lethargy and abdominal discomfort. The histological changes described
in feline cutaneous toxoplasmosis are a toxoplasmic vasculitis and
associated infarction.
Acute toxoplasmosis in humans is usually characterized by isolated,
asymptomatic lymphadenopathy without a rash. Cutaneous manifestations
of toxoplasmosis are variable with maculopapular, nodular, purpuric,
papulopustular, lichenoid, vegetative or erythema-multiforme-like
lesions described. Histologically, varied combinations of vasculitis,
perivasculitis, necrosis, periadnexal inflammation, and rare
granulomas have been described.
As in this case, persistent fever is a frequent finding with feline
toxoplasmosis. The significance of the positive serological test for
FIV with concurrent clinical toxoplasmosis is controversial. Lappin et
al (1996 and 1992) found there was no difference between FIV-naive and
FIV-infected cats in terms of clinical illness and duration of oocyst
shedding following primary exposure with T. gondii. However, the
parenteral administration of T. gondii to FIV-infected cats will
induce severe, generalized toxoplasmosis, whereas FIV-negative cats
only developed a mild transient disease. Non-congenital toxoplasmosis
in humans occurs most commonly in immunocompromised patients suffering
from either a neoplastic disorder, collagen vascular disease, organ
allograft transplant, or HIV.
Felidae are the definitive hosts of T. gondii. Humans and animals
become infected mainly by ingesting bradyzoites from infected meat or
by sporulated oocysts from cat feces. The sexual cycle of T. gondii
only occurs in the intestine of cats. Ingestion of sporulated oocysts
or bradyzoites by humans and animals, including cats, will result in
local multiplication in the intestine and lymph nodes before
dissemination of tachyzoites to other organs and tissues where they
may continue to reproduce asexually or encyst as bradyzoites.

Well. We just got back from our new vet, and it was quite an eye-opening
experience. We saw an outstanding feline vet, who says that the surgery itself,
while a rather radical excision of the entire fat pad, would be quite
recoverable.

However (big however), he is concerned about the _anemia_, about which we had
previously known nothing. He diagnosed anemia first by the color of Bubba's
gums, etc. and confirmed it by looking at _the bloodwork done by the first vet_.
This has never been mentioned to us as being an issue. Perhaps they assumed that
it was a result of Bubba's condition at the time.

The leukemia test was negative, thank God, but he has ordered another workup to
try to determine the cause of the anemia before we proceed with surgery. In
addition to reducing the chances of survival, there wouldn't be much point to it
if something else is killing Bubba.

His blood sugar was a little high on the last test - 160 - although nobody has
yet classified him as diabetic. I am curious to see what the level is now that
he's eating more like a carnivore should, rather than the "balanced diet" we've
always been told to feed him. It could be that the lack of real carnivore food
might have caused the anemia in the first place, which is the likely cause of
the gangrene.

I also wonder if the steatitis did clear up weeks ago, and what I've seen since
then was merely gangrene setting in. A number of you have tried to tell me that
it wasn't the steatitis, for which I thank you again, but the vet told me that
it was. "No sign of infection," indeed.

I will update tomorrow. Once again, thanks to all!

Steve

*Our 12 year old male DSH Bubba has steatitis, possibly as a result of
*eating salmon & tuna flavored food from a well-known manufacturer. The

That's very odd.

Feline nutritional steatitis is a well-described, and today, rarely seen,
condition.

Historically, people would feed cats a canned-tuna-only diet, and cats fed
that way could get get this disease - the high unsaturated fat content of
the all-tuna diet (or other inappropriate, unbalanced diet, of course) is
the problem. The high amount of polyunsaturated fats overwhelms the normal
antioxidant abilities of vit E and selenium to scavenge free radicals,
free radicals cause peroxidation of lipid membranes, leading to sort of a
cascading problem, where walls of cells are broken down, causing a lot of
necrosis of fat throughout the body, abdomen, subcutis, etc. The result
is, you get this very distinctive gross and histologic appearance. For
pathology buffs.... because you have all this necrosis, and sort of self
digestion, you get a secondary inflammatory infiltrate of neutrophils and
macrophages, and
characteristic deposition of ceroid, a type of lipofuscin, whcih is a type
of broken down membrane. The ceroid is acid fast, so you can stain for it.

We still (obviously as per the original post) occasionally see this in
cats but now it is more often seen in waterfowl. There was a big outbreak
in herons at the SD zoo which had been scavenging on fish left at the
docks. Anyway, in the cat, this causes a distinct looking nodular yellow
green lesion, and the lesions smell fishy. also seen in mink and swine.
it's also very very painful. In cats the skin usually looks kind of ripply
and you can feel nodules in abdomen, and cat may be crying out from pain

*The vets won't be in until Monday. Should I try to clean it in the
*meantime, or just leave it alone? I didn't catch the name of the pads
*they gave me, but I think they're saturated with an antiseptic
*cleaning solution.

I hope your vet has helped you already, since it is now Wednesday. I'll
skim down and see if you reported back! Sorry I didn't see this sooner....

So many of you have replied with valuable information, advice and well wishes.
Please forgive me for not replying individually - it's been a very rough week,
but I truly appreciate that you have all taken the time.

The current update:
Bubba is having surgery tomorrow morning. We don't have all the facts yet
regarding possible cancer, etc., but realized that he certainly won't survive
the vile mess on his belly for much longer. I think the vet has been very
conservative in his assessment and recommendations, which is understandable
given that we have had no previous relationship.

While I certainly respect his instinct that an underlying condition caused the
anemia, which in turn caused the gangrene, my instinct is that the steatitis (in
combination with the naturally limited bloodflow in a large fat pad) caused the
gangrene, which in turn caused the anemia. I apologized for being pushy about
it, and his response indicated to me that he probably thought I made the right
decision.

I guess at this point I'm sort of writing a diary here, but in addition to
keeping you all updated, I'm hoping that someone will someday find Bubba's story
helpful.

Thanks all.

Steve