Steatitis

[S. Gass]

***
*** PLEASE NOTE - squeamish individuals may not want to read past the
second paragraph
***

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
vet says that it's more likely due to Bubba being unable to properly
utilize vitamin E. I'm not sure that sounds quite right, but it's
irrelevant at this point.

I've been treating him as directed, with vitamin E, 1ml amoxycillin
daily and a steroid (the name of which I've forgotten) every other day
and, of course, changed his diet. He's getting various canned foods,
along with some raw meat - about half chicken, half beef. The beef is
about 4 parts lean round to 1 part liver. Dry, poultry-based food is
always available. His appetite comes and goes, but he at least eats
something. The affected area (the abdominal fat pad) has gotten
considerably smaller and softer, and he seems to be feeling better
overall.



My primary concern now is what appears to be quite a bit of necrotic
tissue. As the weeks have gone by, a number of small holes opened up.
At first there was blood draining from them, but lately it's been a
clear fluid. Eventually, a number of the small holes combined into a
single area of about 1-1/2 x 3", which is now mostly scabbed over.

Part of the scab came off last night, though, revealing an area of
decidedly non-healthy tissue. I'm trying not to be too graphic, but it
basically looks like old hamburger. First of all, am I correct in
assuming that this is necrosis? If so, I suppose it's also safe to
assume that the rest of the area is necrotic as well, correct? We were
last at the vet about a week ago, and I was told that there wasn't any
sign of infection. I can't say that it looks infected now, either -
just dead.

How might such a thing be treated? Is it even possible? I understand
that the tissue could probably be removed, but I'm not sure there
would be enough skin to cover the area.

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'd appreciate any advice. Even the more experienced of my vets has
only seen a handful of cases in 30+ years. Thanks.

Steve

[Liz]

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.

[Liz]

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.

[buglady]

"S. Gass" > wrote in message
om...
He's getting various canned foods,
> along with some raw meat - about half chicken, half beef. The beef is
> about 4 parts lean round to 1 part liver.

.......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

[buglady]

"S. Gass" > wrote in message
om...
He's getting various canned foods,
> along with some raw meat - about half chicken, half beef. The beef is
> about 4 parts lean round to 1 part liver.

.......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

[Liz]

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.

[Liz]

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.

[Marie Fischer]

buglady wrote:
> 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?

well, the original poster wrote she fed a "salmon & tuna
flavored food", but "flavor" in the name means just that
the product must contain an amount sufficient to be able
to be detected (which usually isn't much). before accusing
the manufacturer, i would try to find out how much % of fish
there actually was in the food.

--
marie

[Marie Fischer]

buglady wrote:
> 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?

well, the original poster wrote she fed a "salmon & tuna
flavored food", but "flavor" in the name means just that
the product must contain an amount sufficient to be able
to be detected (which usually isn't much). before accusing
the manufacturer, i would try to find out how much % of fish
there actually was in the food.

--
marie

[S. Gass]

Thank you all for the replies! I'll summarize my response, rather than
sending individual replies.


"buglady" > wrote in message k.net>...
> http://www.afip.org/vetpath/WSC/wsc00/00wsc06.htm
> Ceroid pigment is present as brown/gray globules, mostly within the
> cytoplasm of macrophages

The pathology presented in this link is quite an accurate description
of Bubba's condition when we first discovered it. The vet clipped all
the hair off his abdomen, and the yellow/brown discoloration was very
apparent. At the time, he had one central opening, draining blood. Her
immediate reaction was that it was a necrotic malignancy, beyond hope,
and that I should put him down. I insisted that she run some tests
first, though, and fortunately she consulted with the vet who had seen
steatitis.

The only abnormality on the CBC was an elevated white count, of about
28,000. He hasn't had a fever, and did respond very quickly to
treatment for steatitis. The holes do appear to be the result of fluid
draining from the area, and have usually first manifested as an area
of "thin" skin or a blood blister. It's quite difficult to describe
accurately, and has been changing rapidly. I've been told that the
progression from bloody discharge to clear fluid is a positive sign,
however, and there hasn't really been any drainage at all over the
past few days.

There hasn't been any obvious indication of parasites, and I don't
think the vets have even considered that as a possibility. However, it
is easy to imagine that parasitic growth or some other secondary
condition have occurred since this all began, or that the skin
condition is indeed a result of the medication, and I'll ask the vets
tomorrow. It's gotten to the point where they both look at him
whenever I bring him in.

The reason I've continued the steroid use is that the area appeared to
clear up very quickly when he was first on them. When I stopped the
steroids (as directed), it then quickly erupted, and his overall
condition deteriorated. Restarting the steroids again led to rapid
improvement, and I do have a reference to effusions related to
steatitis. You raise a very valid point, though, Liz, and I'll discuss
the issue with them in depth.

I hope that I'm looking at the healing process for steatitis, but am
concerned that there might be a large area of necrotic tissue,
including the skin. I do understand that necrosis is often associated
with steatitis. There is an odor as well, although the tissue I looked
at yesterday does look just a little less disgusting today - it's
smoother, and the affected area doesn't look as deep, although it's
still a grayish brown.

The vets have been "on alert", so I'm sure we'll be able to get in
there tomorrow morning. I'll still be grateful to receive any
additional thoughts/experiences, though, and again, thanks to all for
replying!

Steve

[S. Gass]

Thank you all for the replies! I'll summarize my response, rather than
sending individual replies.


"buglady" > wrote in message k.net>...
> http://www.afip.org/vetpath/WSC/wsc00/00wsc06.htm
> Ceroid pigment is present as brown/gray globules, mostly within the
> cytoplasm of macrophages

The pathology presented in this link is quite an accurate description
of Bubba's condition when we first discovered it. The vet clipped all
the hair off his abdomen, and the yellow/brown discoloration was very
apparent. At the time, he had one central opening, draining blood. Her
immediate reaction was that it was a necrotic malignancy, beyond hope,
and that I should put him down. I insisted that she run some tests
first, though, and fortunately she consulted with the vet who had seen
steatitis.

The only abnormality on the CBC was an elevated white count, of about
28,000. He hasn't had a fever, and did respond very quickly to
treatment for steatitis. The holes do appear to be the result of fluid
draining from the area, and have usually first manifested as an area
of "thin" skin or a blood blister. It's quite difficult to describe
accurately, and has been changing rapidly. I've been told that the
progression from bloody discharge to clear fluid is a positive sign,
however, and there hasn't really been any drainage at all over the
past few days.

There hasn't been any obvious indication of parasites, and I don't
think the vets have even considered that as a possibility. However, it
is easy to imagine that parasitic growth or some other secondary
condition have occurred since this all began, or that the skin
condition is indeed a result of the medication, and I'll ask the vets
tomorrow. It's gotten to the point where they both look at him
whenever I bring him in.

The reason I've continued the steroid use is that the area appeared to
clear up very quickly when he was first on them. When I stopped the
steroids (as directed), it then quickly erupted, and his overall
condition deteriorated. Restarting the steroids again led to rapid
improvement, and I do have a reference to effusions related to
steatitis. You raise a very valid point, though, Liz, and I'll discuss
the issue with them in depth.

I hope that I'm looking at the healing process for steatitis, but am
concerned that there might be a large area of necrotic tissue,
including the skin. I do understand that necrosis is often associated
with steatitis. There is an odor as well, although the tissue I looked
at yesterday does look just a little less disgusting today - it's
smoother, and the affected area doesn't look as deep, although it's
still a grayish brown.

The vets have been "on alert", so I'm sure we'll be able to get in
there tomorrow morning. I'll still be grateful to receive any
additional thoughts/experiences, though, and again, thanks to all for
replying!

Steve

[buglady]

"S. Gass" > wrote in message
om...
> Update: There now seems to be a more normal color returning to the
> open area, i.e. pink rather than brown. And it doesn't really smell
> acrid or skunk-like
> There is still an open area of about 1" in diameter, though, with the
> likelihood of becoming quite a bit larger. Tomorrow I'll learn how
> best to treat it, or if surgical intervention is necessary/possible.

.......Personally if things are improving, i think I'd leave it alone.
Surgery makes bigger holes than that!. Since fatty acids play such a big
role in skin permeability/integrity. I think the accumulated fluid weighing
on fragile, too porous skin, probably just caused it to open. This, after
all, is what most infected wounds will do - find the easiest point to drain
and rupture the skin. Glad to hear thinks are pinking up.

buglady
take out the dog before replying

[buglady]

"S. Gass" > wrote in message
om...
> Update: There now seems to be a more normal color returning to the
> open area, i.e. pink rather than brown. And it doesn't really smell
> acrid or skunk-like
> There is still an open area of about 1" in diameter, though, with the
> likelihood of becoming quite a bit larger. Tomorrow I'll learn how
> best to treat it, or if surgical intervention is necessary/possible.

.......Personally if things are improving, i think I'd leave it alone.
Surgery makes bigger holes than that!. Since fatty acids play such a big
role in skin permeability/integrity. I think the accumulated fluid weighing
on fragile, too porous skin, probably just caused it to open. This, after
all, is what most infected wounds will do - find the easiest point to drain
and rupture the skin. Glad to hear thinks are pinking up.

buglady
take out the dog before replying

[Karen Chuplis]

Oh my goodness. I am SO sorry :(( So sorry. My thoughts and prayers are
with you.
Karen

"S. Gass" > wrote in message
om...
> We just got back from the vet. It is gangrene. We're not going to
> subject him to surgical attempts to correct it. Thanks all.
>
> Steve

[Karen Chuplis]

Oh my goodness. I am SO sorry :(( So sorry. My thoughts and prayers are
with you.
Karen

"S. Gass" > wrote in message
om...
> We just got back from the vet. It is gangrene. We're not going to
> subject him to surgical attempts to correct it. Thanks all.
>
> Steve

[Dee]

On 28 Jul 2003, S. Gass wrote:

> We just got back from the vet. It is gangrene. We're not going to
> subject him to surgical attempts to correct it. Thanks all.


I'm very sorry Steve.

Dee

[Dee]

On 28 Jul 2003, S. Gass wrote:

> We just got back from the vet. It is gangrene. We're not going to
> subject him to surgical attempts to correct it. Thanks all.


I'm very sorry Steve.

Dee

[Steve Gass]

On Mon, 28 Jul 2003 20:03:45 +0000, buglady wrote:

> Oh, how awful, I'm so sorry. I know you won't feel up to answering questions
> now, but was this a complication of the steatitis? Is there any chance of
> saving him?

Yes, it is apparently a result of the steatitis. After much thought, and
discussing it with my wife, we've decided to seek a second opinion. These vets
explained that they can excise the tissue, leaving an open wound of 5 - 6" in
diameter, and involving a very long, difficult and painful recovery, if recovery
is even possible. We can't put him through that.

It was a nice day, so I took him outside and sat with him, figuring that a dirty
environment could do him no more harm. He rolled in the grass, then laid on his
back, purring and kneading the air as I skritched his chin and rubbed his ears.
Overnight, the open area had become genuinely appalling, but we can't give up
just yet. I spoke to another vet, who doesn't see why there wouldn't be enough
skin to at least mostly close the wound after excision, which would give Bubba a
chance of living in enough comfort to give recovery a shot.

At this point there is, of course, no way of knowing how far the gangrene has
spread. If organs are involved then there truly is no hope, but if it's still
limited to the fat pad, and if the skin can be closed, he may have a chance. I
have another appointment tomorrow morning, and will see what a different vet has
to say. Thanks again.

Steve

[Steve Gass]

On Mon, 28 Jul 2003 20:03:45 +0000, buglady wrote:

> Oh, how awful, I'm so sorry. I know you won't feel up to answering questions
> now, but was this a complication of the steatitis? Is there any chance of
> saving him?

Yes, it is apparently a result of the steatitis. After much thought, and
discussing it with my wife, we've decided to seek a second opinion. These vets
explained that they can excise the tissue, leaving an open wound of 5 - 6" in
diameter, and involving a very long, difficult and painful recovery, if recovery
is even possible. We can't put him through that.

It was a nice day, so I took him outside and sat with him, figuring that a dirty
environment could do him no more harm. He rolled in the grass, then laid on his
back, purring and kneading the air as I skritched his chin and rubbed his ears.
Overnight, the open area had become genuinely appalling, but we can't give up
just yet. I spoke to another vet, who doesn't see why there wouldn't be enough
skin to at least mostly close the wound after excision, which would give Bubba a
chance of living in enough comfort to give recovery a shot.

At this point there is, of course, no way of knowing how far the gangrene has
spread. If organs are involved then there truly is no hope, but if it's still
limited to the fat pad, and if the skin can be closed, he may have a chance. I
have another appointment tomorrow morning, and will see what a different vet has
to say. Thanks again.

Steve

[Betsy]

Oh, I am SO VERY VERY GLAD you are going to another vet.

Cats are very resilient. They can tolerate a lot, and will recover just to
be "with you". I've seen my cats recover from horrible things many times,
apparently to please me. Please give Bubba a chance! And do keep us
posted.

"Steve Gass" > wrote in message
...
> On Mon, 28 Jul 2003 20:03:45 +0000, buglady wrote:
>
> > Oh, how awful, I'm so sorry. I know you won't feel up to answering
questions
> > now, but was this a complication of the steatitis? Is there any
chance of
> > saving him?
>
> Yes, it is apparently a result of the steatitis. After much thought, and
> discussing it with my wife, we've decided to seek a second opinion. These
vets
> explained that they can excise the tissue, leaving an open wound of 5 - 6"
in
> diameter, and involving a very long, difficult and painful recovery, if
recovery
> is even possible. We can't put him through that.
>
> It was a nice day, so I took him outside and sat with him, figuring that a
dirty
> environment could do him no more harm. He rolled in the grass, then laid
on his
> back, purring and kneading the air as I skritched his chin and rubbed his
ears.
> Overnight, the open area had become genuinely appalling, but we can't give
up
> just yet. I spoke to another vet, who doesn't see why there wouldn't be
enough
> skin to at least mostly close the wound after excision, which would give
Bubba a
> chance of living in enough comfort to give recovery a shot.
>
> At this point there is, of course, no way of knowing how far the gangrene
has
> spread. If organs are involved then there truly is no hope, but if it's
still
> limited to the fat pad, and if the skin can be closed, he may have a
chance. I
> have another appointment tomorrow morning, and will see what a different
vet has
> to say. Thanks again.
>
> Steve

[Betsy]

Oh, I am SO VERY VERY GLAD you are going to another vet.

Cats are very resilient. They can tolerate a lot, and will recover just to
be "with you". I've seen my cats recover from horrible things many times,
apparently to please me. Please give Bubba a chance! And do keep us
posted.

"Steve Gass" > wrote in message
...
> On Mon, 28 Jul 2003 20:03:45 +0000, buglady wrote:
>
> > Oh, how awful, I'm so sorry. I know you won't feel up to answering
questions
> > now, but was this a complication of the steatitis? Is there any
chance of
> > saving him?
>
> Yes, it is apparently a result of the steatitis. After much thought, and
> discussing it with my wife, we've decided to seek a second opinion. These
vets
> explained that they can excise the tissue, leaving an open wound of 5 - 6"
in
> diameter, and involving a very long, difficult and painful recovery, if
recovery
> is even possible. We can't put him through that.
>
> It was a nice day, so I took him outside and sat with him, figuring that a
dirty
> environment could do him no more harm. He rolled in the grass, then laid
on his
> back, purring and kneading the air as I skritched his chin and rubbed his
ears.
> Overnight, the open area had become genuinely appalling, but we can't give
up
> just yet. I spoke to another vet, who doesn't see why there wouldn't be
enough
> skin to at least mostly close the wound after excision, which would give
Bubba a
> chance of living in enough comfort to give recovery a shot.
>
> At this point there is, of course, no way of knowing how far the gangrene
has
> spread. If organs are involved then there truly is no hope, but if it's
still
> limited to the fat pad, and if the skin can be closed, he may have a
chance. I
> have another appointment tomorrow morning, and will see what a different
vet has
> to say. Thanks again.
>
> Steve

[Liz]

Steve, very very sorry to hear that. :( Is your cat diabetic?

[Liz]

Steve, very very sorry to hear that. :( Is your cat diabetic?

[buglady]

"Steve Gass" > wrote in message
...
I spoke to another vet, who doesn't see why there wouldn't be enough
> skin to at least mostly close the wound after excision, which would give
Bubba a
> chance of living in enough comfort to give recovery a shot.

........I'm glad you're checking in with another vet. Hope your kitty
recovers.

buglady
take out the dog before replying

[buglady]

"Steve Gass" > wrote in message
...
I spoke to another vet, who doesn't see why there wouldn't be enough
> skin to at least mostly close the wound after excision, which would give
Bubba a
> chance of living in enough comfort to give recovery a shot.

........I'm glad you're checking in with another vet. Hope your kitty
recovers.

buglady
take out the dog before replying

[Steve Gass]

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

[Steve Gass]

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

[Arjun Ray]

In >, "Steve Gass"
> wrote:

| Well. We just got back from our new vet, and it was quite an
| eye-opening experience.

Nothing like a second opinion!

| His blood sugar was a little high on the last test - 160 - although
| nobody has yet classified him as diabetic.

It could have been high due to stress, such as the vet visit. What is
the reference range associated with the 160 number?

[Arjun Ray]

In >, "Steve Gass"
> wrote:

| Well. We just got back from our new vet, and it was quite an
| eye-opening experience.

Nothing like a second opinion!

| His blood sugar was a little high on the last test - 160 - although
| nobody has yet classified him as diabetic.

It could have been high due to stress, such as the vet visit. What is
the reference range associated with the 160 number?

[Dee]

On Tue, 29 Jul 2003, Steve Gass wrote:

> 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 think you're absolutely right Steve. I come more and more to believe
that the crap we're lead to believe is good for our animals is causing
more ailments than we can possibly imagine. All the best to you and
Bubba. I know what you're going through. Hang in there.


Dee

[Dee]

On Tue, 29 Jul 2003, Steve Gass wrote:

> 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 think you're absolutely right Steve. I come more and more to believe
that the crap we're lead to believe is good for our animals is causing
more ailments than we can possibly imagine. All the best to you and
Bubba. I know what you're going through. Hang in there.


Dee

[PawsForThought]

>Steve Gass wrote:
>
>> 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 wouldn't be a bit surprised, Steve. Good luck and healing purrs to Bubba.

Lauren
________
See my cats: http://community.webshots.com/album/56955940rWhxAe
Raw Diet Info: http://www.holisticat.com/drjletter.html
http://www.geocities.com/rawfeeders/ForCatsOnly.html
Declawing Info: http://www.wholecat.com/articles/claws.htm

[PawsForThought]

>Steve Gass wrote:
>
>> 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 wouldn't be a bit surprised, Steve. Good luck and healing purrs to Bubba.

Lauren
________
See my cats: http://community.webshots.com/album/56955940rWhxAe
Raw Diet Info: http://www.holisticat.com/drjletter.html
http://www.geocities.com/rawfeeders/ForCatsOnly.html
Declawing Info: http://www.wholecat.com/articles/claws.htm

[Liz]

After your "thanks all" I was afraid you had put your kitty to sleep,
glad you didn't. I believe he can recover from all his conditions
providing the vet is good and the food is adequate to correct his
anemia and glucose. How are those holes? Did the vet close them or
kept them open? I'm glad he did not develop an infection so far. My
choice would be to keep the holes open and wash three or four times a
day with a very dilute solution of oxygen peroxide. The more oxygen in
the holes, the faster it heals and less chance of infection. Is the
necrotic area too extensive? I'm cheering for you both! :)

[Liz]

After your "thanks all" I was afraid you had put your kitty to sleep,
glad you didn't. I believe he can recover from all his conditions
providing the vet is good and the food is adequate to correct his
anemia and glucose. How are those holes? Did the vet close them or
kept them open? I'm glad he did not develop an infection so far. My
choice would be to keep the holes open and wash three or four times a
day with a very dilute solution of oxygen peroxide. The more oxygen in
the holes, the faster it heals and less chance of infection. Is the
necrotic area too extensive? I'm cheering for you both! :)

[Hillary Israeli]

In >,
S. Gass > wrote:

*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....

--
hillary israeli vmd http://www.hillary.net
"uber vaccae in quattuor partes divisum est."
not-so-newly minted veterinarian-at-large :)

[Hillary Israeli]

In >,
S. Gass > wrote:

*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....

--
hillary israeli vmd http://www.hillary.net
"uber vaccae in quattuor partes divisum est."
not-so-newly minted veterinarian-at-large :)

[Steve Gass]

On Wed, 30 Jul 2003 15:29:58 +0000, buglady wrote:

> "Steve Gass" > wrote in message
> ...
>> Well. We just got back from our new vet, and it was quite an eye-opening
>> experience
> ........I am so relieved you found a more responsive vet. BTW I did run
> across one reference WRT gangrene (a particular kind) which mentioned
> something about steroid abuse, so I wonder if the steroids made the situation
> worse.

Yes, this vet is exceptional, although Bubba's prognosis is quite poor. He is
too anemic to be able to survive the surgery without a transfusion, and the
cause of the anemia is not yet known. Liver and kidney functions are normal, but
there is a good chance of a bone marrow problem or cancerous process. The vet is
having one last test done to see if the anemia might be indicative of a
treatable condition - sorry, being outside my realm, I didn't fully understand
the specifics. He doesn't seem to suspect diabetes as a cause. It is very
unlikely that the anemia is related to diet, because it has worsened despite
Bubba's new diet.

I don't know what to think about the steroid use, although the vet doesn't seem
to consider it a potential cause of the gangrene. In fact, he mentioned that
steroids, specifically prednisone, can be used to treat anemia. I've been giving
Bubba 1/2 cc of dex-something every 2-3 days, depending on how he's been
feeling. Without steroids his discomfort was obvious, and the first vet had said
that he needed it, and that it "should be safe". Then again . . .

I've been giving him 1cc of amoxicillin daily throughout, even after I was told,
a couple of weeks ago, that it wasn't really necessary because there was "no
sign of infection."

I do believe that this all started as steatitis, which was cleared up weeks ago.
The anemia prevented proper healing, though, so the area died. I try not to
dwell on what might have been, had I known he was anemic.

At this point, if the test shows that the anemia might be treatable, and if
Bubba survives the transfusion and surgery, he might live long enough to treat
the anemia and recover to the point of living a comfortable life. I can't say
that I'm optimistic, but at least we'll be able make a decision based on a full
understanding of the situation.

Steve

[Steve Gass]

On Wed, 30 Jul 2003 15:29:58 +0000, buglady wrote:

> "Steve Gass" > wrote in message
> ...
>> Well. We just got back from our new vet, and it was quite an eye-opening
>> experience
> ........I am so relieved you found a more responsive vet. BTW I did run
> across one reference WRT gangrene (a particular kind) which mentioned
> something about steroid abuse, so I wonder if the steroids made the situation
> worse.

Yes, this vet is exceptional, although Bubba's prognosis is quite poor. He is
too anemic to be able to survive the surgery without a transfusion, and the
cause of the anemia is not yet known. Liver and kidney functions are normal, but
there is a good chance of a bone marrow problem or cancerous process. The vet is
having one last test done to see if the anemia might be indicative of a
treatable condition - sorry, being outside my realm, I didn't fully understand
the specifics. He doesn't seem to suspect diabetes as a cause. It is very
unlikely that the anemia is related to diet, because it has worsened despite
Bubba's new diet.

I don't know what to think about the steroid use, although the vet doesn't seem
to consider it a potential cause of the gangrene. In fact, he mentioned that
steroids, specifically prednisone, can be used to treat anemia. I've been giving
Bubba 1/2 cc of dex-something every 2-3 days, depending on how he's been
feeling. Without steroids his discomfort was obvious, and the first vet had said
that he needed it, and that it "should be safe". Then again . . .

I've been giving him 1cc of amoxicillin daily throughout, even after I was told,
a couple of weeks ago, that it wasn't really necessary because there was "no
sign of infection."

I do believe that this all started as steatitis, which was cleared up weeks ago.
The anemia prevented proper healing, though, so the area died. I try not to
dwell on what might have been, had I known he was anemic.

At this point, if the test shows that the anemia might be treatable, and if
Bubba survives the transfusion and surgery, he might live long enough to treat
the anemia and recover to the point of living a comfortable life. I can't say
that I'm optimistic, but at least we'll be able make a decision based on a full
understanding of the situation.

Steve

[Steve Gass]

On Wed, 30 Jul 2003 15:54:06 +0000, Hillary Israeli wrote:
> 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.

Thank you Hillary - this has been a very important clue. I've known that
necrosis is often associated with steatitis, and have assumed that's what I've
been seeing. I don't know the difference between necrosis and gangrene, but
assume that there is a distinction.

Anyway, a little research has turned up the fact that one of the symptoms of gas
gangrene is _acute anemia_! If Bubba developed a necrotic situation as a result
of the steatitis, in an area where there isn't much blood flow to begin with,
then it seems to me that it could easily progress to full-blown gangrene,
resulting in acute anemia, which is now the primary concern.

Without being familiar with the history of this condition, and probably having
little experience with steatitis, this vet, as good as he is, is assuming that
the gangrene is a result of the anemia rather than, quite possibly, the other
way around.

He said that a transfusion would probably get Bubba through the surgery, but it
would be pointless if Bubba isn't producing red blood cells properly due to a
serious underlying condition. I'm going to press for the surgery regardless of
the last test result. A ray of hope . . .

Steve

[Steve Gass]

On Wed, 30 Jul 2003 15:54:06 +0000, Hillary Israeli wrote:
> 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.

Thank you Hillary - this has been a very important clue. I've known that
necrosis is often associated with steatitis, and have assumed that's what I've
been seeing. I don't know the difference between necrosis and gangrene, but
assume that there is a distinction.

Anyway, a little research has turned up the fact that one of the symptoms of gas
gangrene is _acute anemia_! If Bubba developed a necrotic situation as a result
of the steatitis, in an area where there isn't much blood flow to begin with,
then it seems to me that it could easily progress to full-blown gangrene,
resulting in acute anemia, which is now the primary concern.

Without being familiar with the history of this condition, and probably having
little experience with steatitis, this vet, as good as he is, is assuming that
the gangrene is a result of the anemia rather than, quite possibly, the other
way around.

He said that a transfusion would probably get Bubba through the surgery, but it
would be pointless if Bubba isn't producing red blood cells properly due to a
serious underlying condition. I'm going to press for the surgery regardless of
the last test result. A ray of hope . . .

Steve

[Steve Gass]

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

[Steve Gass]

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

[Karen Chuplis]

in article , Steve Gass at
wrote on 7/30/03 9:46 PM:

> 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

Please keep us updated. I will pray that surgery goes well, but I know we
all understand how serious this is and a worry for you.

Karen

[Karen Chuplis]

in article , Steve Gass at
wrote on 7/30/03 9:46 PM:

> 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

Please keep us updated. I will pray that surgery goes well, but I know we
all understand how serious this is and a worry for you.

Karen

[Liz]

> 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.

Polyunsaturated fatty acids are themselves antioxidants, neutralizing
(scavenging) free radicals just as vitamin E, C, A, beta-carotene,
etc. How do they interfere with the antioxidant properties of vitamin
E?

[Liz]

> 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.

Polyunsaturated fatty acids are themselves antioxidants, neutralizing
(scavenging) free radicals just as vitamin E, C, A, beta-carotene,
etc. How do they interfere with the antioxidant properties of vitamin
E?

[Karen Chuplis]

I'm so sorry. Prayers for Bubba and for your family. It's obvious he was
well loved.

Karen

"Steve Gass" > wrote in message
...
> I am very sorry to have to report this, but we eased Bubba's passage at
around
> 10:00 this morning. The vet went to give him a pill last night, and the
skin
> literally tore off of his neck, a strong indicator of Cushing's disease.
The
> steroids may very well have played a role, although I find it difficult to
> believe that such a drastic symptom would have manifested after about 4
weeks of
> minimal steroid use. I didn't ask, but will sometime.
>
> At this point, I would also like to express my thanks to, and record my
highest
> recommendations for, the doctors and staff at Smoketown Veterinary
Hospital in
> Smoketown, PA. It is obvious that Bubba ended up in the most
compassionate,
> gentle and competent hands he could have been in, and he knew it, too. In
stark
> contrast to the other vet, he calmly laid on his back, kneading, as the
doctors
> examined him. The experience has taken a bit of the edge off of my grief.
>
> We will miss Bubba. He was a wonderful creature.
>
> Steve

[Karen Chuplis]

I'm so sorry. Prayers for Bubba and for your family. It's obvious he was
well loved.

Karen

"Steve Gass" > wrote in message
...
> I am very sorry to have to report this, but we eased Bubba's passage at
around
> 10:00 this morning. The vet went to give him a pill last night, and the
skin
> literally tore off of his neck, a strong indicator of Cushing's disease.
The
> steroids may very well have played a role, although I find it difficult to
> believe that such a drastic symptom would have manifested after about 4
weeks of
> minimal steroid use. I didn't ask, but will sometime.
>
> At this point, I would also like to express my thanks to, and record my
highest
> recommendations for, the doctors and staff at Smoketown Veterinary
Hospital in
> Smoketown, PA. It is obvious that Bubba ended up in the most
compassionate,
> gentle and competent hands he could have been in, and he knew it, too. In
stark
> contrast to the other vet, he calmly laid on his back, kneading, as the
doctors
> examined him. The experience has taken a bit of the edge off of my grief.
>
> We will miss Bubba. He was a wonderful creature.
>
> Steve

[buglady]

"Steve Gass" > wrote in message
...
> I am very sorry to have to report this, but we eased Bubba's passage at
around
> 10:00 this morning. The vet went to give him a pill last night, and the
skin
> literally tore off of his neck, a strong indicator of Cushing's disease.

.........oh geez, I am so sorry, such a long road. My condolences to you and
your family.

You might want to visit this site, which gives me comfort still (especially
the book excerpts from (My Cat Saved My Life
http://www.mycatsavedmylife.com/Textonly.html ) for all the 4 footed
friends who have passed through my house:
http://www.griefhealing.com/Granimallovers.htm

my highest
> recommendations for, the doctors and staff at Smoketown Veterinary
Hospital in
> Smoketown, PA. It is obvious that Bubba ended up in the most
compassionate,
> gentle and competent hands he could have been in

..........Now that you have a wonderful vet, I hope you'll have many more
kitties pass into your life.

We who choose to surround ourselves
with lives even more temporary than our own
live within a fragile circle, easily and often breached.
Unable to accept its awful gaps,
we still would live no other way.
We cherish memory as the only certain immortality,
never fully understanding the necessary plan.

-- Irving Townsend, in The Once Again Prince

buglady
take out the dog before replying

[buglady]

"Steve Gass" > wrote in message
...
> I am very sorry to have to report this, but we eased Bubba's passage at
around
> 10:00 this morning. The vet went to give him a pill last night, and the
skin
> literally tore off of his neck, a strong indicator of Cushing's disease.

.........oh geez, I am so sorry, such a long road. My condolences to you and
your family.

You might want to visit this site, which gives me comfort still (especially
the book excerpts from (My Cat Saved My Life
http://www.mycatsavedmylife.com/Textonly.html ) for all the 4 footed
friends who have passed through my house:
http://www.griefhealing.com/Granimallovers.htm

my highest
> recommendations for, the doctors and staff at Smoketown Veterinary
Hospital in
> Smoketown, PA. It is obvious that Bubba ended up in the most
compassionate,
> gentle and competent hands he could have been in

..........Now that you have a wonderful vet, I hope you'll have many more
kitties pass into your life.

We who choose to surround ourselves
with lives even more temporary than our own
live within a fragile circle, easily and often breached.
Unable to accept its awful gaps,
we still would live no other way.
We cherish memory as the only certain immortality,
never fully understanding the necessary plan.

-- Irving Townsend, in The Once Again Prince

buglady
take out the dog before replying

[buglady]

"Steve Gass" > wrote in message
...
> steroids may very well have played a role, although I find it difficult to
> believe that such a drastic symptom would have manifested after about 4
weeks of
> minimal steroid use. I didn't ask, but will sometime.

...........Tuck these away for when you need answers. You may decide it's
not really important in the end. Years ago I finally threw away a whole
pile of lab reports I kept going over after one of my oldster pups died. I
realized it was serving no purpose to try and figure out why he wasn't here
any more.

.....May your Bubba loll around in green grass on the other side.

http://maxshouse.com/Endocrine_System_&_Disorders.htm#Hyperadrenocorticism
http://www.marvistavet.com/html/cushing_s_disease.html
http://www.kween.net/foundation/cushings.htm
Warning - very graphic pix in one below:
http://www.lbah.com/Canine/cushingsummary.htm#Felcush
People site - Exogenous Cushings:
http://www.pennhealth.com/ency/article/000389.htm
Steroids/Vet Use/Side Effects:
http://www.vet.utk.edu/hnilica/pdf/AppropriateSteroiduse.pdf
Feline Adrenal Disease:
http://www.vin.com/VINDBPub/SearchPB/Proceedings/PR05000/PR00106.htm

buglady
take out the dog before replying

[buglady]

"Steve Gass" > wrote in message
...
> steroids may very well have played a role, although I find it difficult to
> believe that such a drastic symptom would have manifested after about 4
weeks of
> minimal steroid use. I didn't ask, but will sometime.

...........Tuck these away for when you need answers. You may decide it's
not really important in the end. Years ago I finally threw away a whole
pile of lab reports I kept going over after one of my oldster pups died. I
realized it was serving no purpose to try and figure out why he wasn't here
any more.

.....May your Bubba loll around in green grass on the other side.

http://maxshouse.com/Endocrine_System_&_Disorders.htm#Hyperadrenocorticism
http://www.marvistavet.com/html/cushing_s_disease.html
http://www.kween.net/foundation/cushings.htm
Warning - very graphic pix in one below:
http://www.lbah.com/Canine/cushingsummary.htm#Felcush
People site - Exogenous Cushings:
http://www.pennhealth.com/ency/article/000389.htm
Steroids/Vet Use/Side Effects:
http://www.vet.utk.edu/hnilica/pdf/AppropriateSteroiduse.pdf
Feline Adrenal Disease:
http://www.vin.com/VINDBPub/SearchPB/Proceedings/PR05000/PR00106.htm

buglady
take out the dog before replying

[Liz]

When you said the skin of his neck came out on the vet's hand the
first thing that occurred to me was leprosy. I did not know cats can
have leprosy but they can and you will find many sites on the net
discussing the disease. Apparently it is transmitted by contact with
rats or rat bites. I believe your cat was misdiagnosed. He never had
steatitis. The steroids weakened the immune system and the microbes
took over his body quickly. When you told the vet Bubba was fed tuna
flavored food, the vet probably jumped to the conclusion it was
steatitis since steatitis may also show lumps under the skin. :(

Feline leprosy

Feline leprosy is caused by Mycobacterium lepraemurium. It is thought
infection is via rat bites or contact with rats.

Lesions appear as soft, fleshy, freely movable nodules in the skin.
They are nonpainful and the cat is generally in good health. These
lumps can however become ulcerated and surrounding lymph node (glands)
may become enlarged. Most lesions are seen on the head and lower legs.

Surgical removal is the treatment of choice however antituberculosis
drugs such as Dapsone and Clofazimine (3mg/kg daily for 6 weeks) may
also be effective.

[Liz]

When you said the skin of his neck came out on the vet's hand the
first thing that occurred to me was leprosy. I did not know cats can
have leprosy but they can and you will find many sites on the net
discussing the disease. Apparently it is transmitted by contact with
rats or rat bites. I believe your cat was misdiagnosed. He never had
steatitis. The steroids weakened the immune system and the microbes
took over his body quickly. When you told the vet Bubba was fed tuna
flavored food, the vet probably jumped to the conclusion it was
steatitis since steatitis may also show lumps under the skin. :(

Feline leprosy

Feline leprosy is caused by Mycobacterium lepraemurium. It is thought
infection is via rat bites or contact with rats.

Lesions appear as soft, fleshy, freely movable nodules in the skin.
They are nonpainful and the cat is generally in good health. These
lumps can however become ulcerated and surrounding lymph node (glands)
may become enlarged. Most lesions are seen on the head and lower legs.

Surgical removal is the treatment of choice however antituberculosis
drugs such as Dapsone and Clofazimine (3mg/kg daily for 6 weeks) may
also be effective.

[Steve Gass]

On Thu, 31 Jul 2003 21:36:30 -0700, Liz wrote:

> When you said the skin of his neck came out on the vet's hand the first thing
> that occurred to me was leprosy.

Thanks Liz, but he never showed any symptoms like that. I'll never know exactly
what happened, but base my belief that it was (at first) steatitis on the
opinion of a vet who had seen steatitis, and the fact that Bubba responded so
quickly to treatment for it.

When it first became apparent that he wasn't feeling well, his abdominal fat pad
was somewhat enlarged and quite firm, and there was a single bleeding lesion in
the center. When the hair was shaved from his belly, a yellow/brown mottled
discoloration beneath the skin was very apparent.

One thing that wasn't consistent with steatitis was that the condition appeared
to be limited to a single area, and he didn't appear to be in pain, although he
had been somewhat skittish for awhile. He didn't complain much when cornered and
subjected to petting or brushing, but didn't come looking for attention, either.
His activity level and general health appeared to be normal otherwise, until the
day before the first vet visit. We attributed the skittishness to his having
been cooped up in the house all winter and most of the cold, rainy spring - he
only went outside when he thought the weather was nice enough.

Treatment was vitamin E, antibiotics and, for the first 7 days, prednisone.
After 2-3 weeks the discoloration was gone, there was no effusion, and the fat
pad was significantly smaller and softer.

Literally overnight, however, he developed blood blisters and areas of abnormal
skin over the fat pad. The vet who had seen steatitis gave me no indication that
it wasn't a result of the condition, and recommended that I resume steroid
treatment to control the inflammation, in addition to the vit E and antibiotics.
I was told that there was no sign of infection at that point.

Over the next few days, the blood blisters and abnormal areas broke open,
revealing the holes that I previously mentioned. Over the next week or so the
drainage progressed from blood to a clear fluid. I was told that it would be a
long term recovery, and that I'd have to keep on top of it, but that there still
wasn't any sign of infection. The drainage eventually stopped, and what appeared
to ba a normal scab formed where the effusions had been close together.

Late last week, he had groomed off part of the scab, and a different kind of
hole appeared. It was small at first, maybe 1/4", and on Friday I was told to
keep an eye on it. It was larger on Saturday morning, and had the "old
hamburger" appearance. There wasn't an obvious odor at that point, and by
Saturday evening it looked more like normal tissue. Sunday morning it had grown
larger, and the smell started to become apparent, but again looked a bit more
normal by evening. It still seemed possible that it was the ceroid tissue
associated with steatitis.

By Monday there was no question, though, and it went downhill very quickly from
there.

So that's a summary of Bubba's story. It began on June 12, 2003, and ended on
July 31.

Thanks again.

Steve

[Steve Gass]

On Thu, 31 Jul 2003 21:36:30 -0700, Liz wrote:

> When you said the skin of his neck came out on the vet's hand the first thing
> that occurred to me was leprosy.

Thanks Liz, but he never showed any symptoms like that. I'll never know exactly
what happened, but base my belief that it was (at first) steatitis on the
opinion of a vet who had seen steatitis, and the fact that Bubba responded so
quickly to treatment for it.

When it first became apparent that he wasn't feeling well, his abdominal fat pad
was somewhat enlarged and quite firm, and there was a single bleeding lesion in
the center. When the hair was shaved from his belly, a yellow/brown mottled
discoloration beneath the skin was very apparent.

One thing that wasn't consistent with steatitis was that the condition appeared
to be limited to a single area, and he didn't appear to be in pain, although he
had been somewhat skittish for awhile. He didn't complain much when cornered and
subjected to petting or brushing, but didn't come looking for attention, either.
His activity level and general health appeared to be normal otherwise, until the
day before the first vet visit. We attributed the skittishness to his having
been cooped up in the house all winter and most of the cold, rainy spring - he
only went outside when he thought the weather was nice enough.

Treatment was vitamin E, antibiotics and, for the first 7 days, prednisone.
After 2-3 weeks the discoloration was gone, there was no effusion, and the fat
pad was significantly smaller and softer.

Literally overnight, however, he developed blood blisters and areas of abnormal
skin over the fat pad. The vet who had seen steatitis gave me no indication that
it wasn't a result of the condition, and recommended that I resume steroid
treatment to control the inflammation, in addition to the vit E and antibiotics.
I was told that there was no sign of infection at that point.

Over the next few days, the blood blisters and abnormal areas broke open,
revealing the holes that I previously mentioned. Over the next week or so the
drainage progressed from blood to a clear fluid. I was told that it would be a
long term recovery, and that I'd have to keep on top of it, but that there still
wasn't any sign of infection. The drainage eventually stopped, and what appeared
to ba a normal scab formed where the effusions had been close together.

Late last week, he had groomed off part of the scab, and a different kind of
hole appeared. It was small at first, maybe 1/4", and on Friday I was told to
keep an eye on it. It was larger on Saturday morning, and had the "old
hamburger" appearance. There wasn't an obvious odor at that point, and by
Saturday evening it looked more like normal tissue. Sunday morning it had grown
larger, and the smell started to become apparent, but again looked a bit more
normal by evening. It still seemed possible that it was the ceroid tissue
associated with steatitis.

By Monday there was no question, though, and it went downhill very quickly from
there.

So that's a summary of Bubba's story. It began on June 12, 2003, and ended on
July 31.

Thanks again.

Steve

[Dee]

On Thu, 31 Jul 2003, Steve Gass wrote:

> I am very sorry to have to report this, but we eased Bubba's passage at around
> 10:00 this morning. The vet went to give him a pill last night, and the skin
> literally tore off of his neck, a strong indicator of Cushing's disease. The
> steroids may very well have played a role, although I find it difficult to
> believe that such a drastic symptom would have manifested after about 4 weeks of
> minimal steroid use. I didn't ask, but will sometime.

I'm so Sorry Steve. I know how hard it is to lose a loved one. Steroids
are a wonderful, and at the same time terrible drug. I know this from my
own experience. I believe that they also contributed to my Sunny's death.
Sunny was a sweet little cat, and I'm sure she's playing with Bubba now.


Dee

[Dee]

On Thu, 31 Jul 2003, Steve Gass wrote:

> I am very sorry to have to report this, but we eased Bubba's passage at around
> 10:00 this morning. The vet went to give him a pill last night, and the skin
> literally tore off of his neck, a strong indicator of Cushing's disease. The
> steroids may very well have played a role, although I find it difficult to
> believe that such a drastic symptom would have manifested after about 4 weeks of
> minimal steroid use. I didn't ask, but will sometime.

I'm so Sorry Steve. I know how hard it is to lose a loved one. Steroids
are a wonderful, and at the same time terrible drug. I know this from my
own experience. I believe that they also contributed to my Sunny's death.
Sunny was a sweet little cat, and I'm sure she's playing with Bubba now.


Dee

[Linda E]

My condolences to you........

Linda

[Linda E]

My condolences to you........

Linda

[Liz]

Thanks for going through the details. My cat had steatitis when he was
about 10 or 11 months old. He was very active and playful and all of a
sudden his activity level started dropping on a daily basis. He would
move less and less. He had an alert and happy look, was eating and
drinking as he always had, so I did not think it was something
serious. It got to a point where he did not move at all, he would lay
on the same spot all day long. He appeared happy, looked alert, was
communicative, was still eating and drinking as if nothing, but he
would not move. So I took him to the first vet. Vet was baffled with
the symptoms. He had no fever, his heart was normal, vet did not
notice anything wrong upon physical examination (at that time blood
tests were not done routinely here). Vet wanted to give him steroids
but I did not allow him to. Since I did not have a straight diagnosis,
I did not want to mask the symptoms. So, no medication. Took him to
another vet and he was equally baffled. I ended up going to 4 or 5
different vets in a month and nobody knew what he had - and I
continued refusing any medication. That whole time he would not move
but he looked normal in every other respect. At the time I had bought
Earl Mindell's Vitamin Bible and was reading it and came across
steatitis - he even mentions cats having steatitis because of being
fed only tuna (the canned tuna for us humans). The symptoms matched
but my cat was not fed tuna. But I decided to give him vitamin E
anyway. He improved almost from night to day and in two weeks he was
his old self again. Vitamin E was the only thing he got. He did not
have any other symptom at all except the unwillingness to move. As I
mentioned previously, his skin was normal and remained normal
throughout that entire month he didn't move. Pain is a *must* symptom
of steatitis. When you exercise in excess, you get muscle pain. That
pain is caused by microscopic crystals of lactic acid. That pain can
be so bad that we do not want to move. Now imagine having little
blubber stones in and around your muscle tissue. It must be an
excruciating pain. That's why animals with steatitis do not move and
do not like being touched or forced to move.

You say your cat did not appear to be in pain. That alone rules out
steatitis. According to literature, the head and neck area are spared
in steatitis - most likely because there are no fat deposits in those
areas and Bubba's neck skin came out. You mention he had a hole in his
belly right from the start. Is there any chance he had been bitten by
a rat? Or cut himself while venturing outside? Or maybe bitten in a
fight with another cat? These microbes are commonly found in soil so
getting infected is easy if the immune system is debilitated. If he
already had anemia, he was already debilitated when he got cut or
bitten. You say he responded well to treatment but you did not give
him only vitamin E. These organisms are bacteria so he probably
responded well to antibiotics on one end, and steroids messed him up
on the other end, which brought his overall condition to deteriorate
quickly. Also what you say about the condition being limited to one
area is in fact inconsistent with steatitis. You also say that after 2
or 3 weeks the fat pad was significantly smaller and softer. He
probably had an inflammation in that area - a normal and *wanted*
response to infection - and steroids made the inflammation go away
(this also explains the "fat pad" becoming softer). Inflammation
should *never* be inhibited unless you know for a fact you're dealing
with an auto-immune disease (see below - btw, seems not many vets or
docs know this - they prescribe steroids as if they were candy). You
mention many times that there were no signs of infection. Inflammation
is a sign of infection and not all infections cause pus or fever. To
make a long story short, I am absolutely sure that was not steatitis.
I believe it was some infection with some anaerobic bacteria or
protozoan, maybe leprosy, maybe T. gondii (as posted earlier), maybe
something else. Yet the only disease that I know of that causes the
skin to literally break loose is leprosy. As I mentioned previously,
these microorganisms are everywhere and any person or animal with a
debilitated immune system is at risk. I wish your vet had sent a
sample of his tissue for culture. Then you'd know exactly what it was.

Anyway, again I am sorry for what you and Bubba went through and I
know you did the best you could to help him. I also apologize for
extending this discussion but it seems you are as eager to get answers
as I am. The more we know, the better for our present and future pets.
I hope a loving kitty makes way into your life soon. :)



INFLAMMATION

Inflammation is the body's reaction to an injury such as an invasion
by an infectious agent. In just the same way as it is necessary to
increase the blood supply to active muscles during exercise to provide
glucose and oxygen so it is also necessary to direct elements of the
immune system into sites of infection. Three major events occur during
this response.
1. An increased blood supply to the infected area.
2. Increased capillary permeability caused by retraction of the
endothelial cells. This permits larger molecules to traverse the
endothelium than would ordinarily be capable of doing so and thus
allows the soluble mediators of immunity to reach the site of
infection.
3. Leucocytes, particularly neutrophil polymorphs and to a lesser
extent macrophages, migrate out of the capillaries and into the
surrounding tissue. Once in the tissue, they migrate towards the site
of infection by a process known as chemotaxis.
These events manifest themselves as inflammation.

The immune system is not the only system which protects the body from
injury; the clotting, fibrinolytic and kinin systems are also involved
in mediating inflammation and in the resolution of tissue damage.
These systems interact to maintain the integrity of the vascular
system and to limit the spread of tissue damage whether it is caused
by physical injury or infectious agents.

Immunology, Ivan M. Roitt, Jonathan Brostoff, David K. Male.

[Liz]

Thanks for going through the details. My cat had steatitis when he was
about 10 or 11 months old. He was very active and playful and all of a
sudden his activity level started dropping on a daily basis. He would
move less and less. He had an alert and happy look, was eating and
drinking as he always had, so I did not think it was something
serious. It got to a point where he did not move at all, he would lay
on the same spot all day long. He appeared happy, looked alert, was
communicative, was still eating and drinking as if nothing, but he
would not move. So I took him to the first vet. Vet was baffled with
the symptoms. He had no fever, his heart was normal, vet did not
notice anything wrong upon physical examination (at that time blood
tests were not done routinely here). Vet wanted to give him steroids
but I did not allow him to. Since I did not have a straight diagnosis,
I did not want to mask the symptoms. So, no medication. Took him to
another vet and he was equally baffled. I ended up going to 4 or 5
different vets in a month and nobody knew what he had - and I
continued refusing any medication. That whole time he would not move
but he looked normal in every other respect. At the time I had bought
Earl Mindell's Vitamin Bible and was reading it and came across
steatitis - he even mentions cats having steatitis because of being
fed only tuna (the canned tuna for us humans). The symptoms matched
but my cat was not fed tuna. But I decided to give him vitamin E
anyway. He improved almost from night to day and in two weeks he was
his old self again. Vitamin E was the only thing he got. He did not
have any other symptom at all except the unwillingness to move. As I
mentioned previously, his skin was normal and remained normal
throughout that entire month he didn't move. Pain is a *must* symptom
of steatitis. When you exercise in excess, you get muscle pain. That
pain is caused by microscopic crystals of lactic acid. That pain can
be so bad that we do not want to move. Now imagine having little
blubber stones in and around your muscle tissue. It must be an
excruciating pain. That's why animals with steatitis do not move and
do not like being touched or forced to move.

You say your cat did not appear to be in pain. That alone rules out
steatitis. According to literature, the head and neck area are spared
in steatitis - most likely because there are no fat deposits in those
areas and Bubba's neck skin came out. You mention he had a hole in his
belly right from the start. Is there any chance he had been bitten by
a rat? Or cut himself while venturing outside? Or maybe bitten in a
fight with another cat? These microbes are commonly found in soil so
getting infected is easy if the immune system is debilitated. If he
already had anemia, he was already debilitated when he got cut or
bitten. You say he responded well to treatment but you did not give
him only vitamin E. These organisms are bacteria so he probably
responded well to antibiotics on one end, and steroids messed him up
on the other end, which brought his overall condition to deteriorate
quickly. Also what you say about the condition being limited to one
area is in fact inconsistent with steatitis. You also say that after 2
or 3 weeks the fat pad was significantly smaller and softer. He
probably had an inflammation in that area - a normal and *wanted*
response to infection - and steroids made the inflammation go away
(this also explains the "fat pad" becoming softer). Inflammation
should *never* be inhibited unless you know for a fact you're dealing
with an auto-immune disease (see below - btw, seems not many vets or
docs know this - they prescribe steroids as if they were candy). You
mention many times that there were no signs of infection. Inflammation
is a sign of infection and not all infections cause pus or fever. To
make a long story short, I am absolutely sure that was not steatitis.
I believe it was some infection with some anaerobic bacteria or
protozoan, maybe leprosy, maybe T. gondii (as posted earlier), maybe
something else. Yet the only disease that I know of that causes the
skin to literally break loose is leprosy. As I mentioned previously,
these microorganisms are everywhere and any person or animal with a
debilitated immune system is at risk. I wish your vet had sent a
sample of his tissue for culture. Then you'd know exactly what it was.

Anyway, again I am sorry for what you and Bubba went through and I
know you did the best you could to help him. I also apologize for
extending this discussion but it seems you are as eager to get answers
as I am. The more we know, the better for our present and future pets.
I hope a loving kitty makes way into your life soon. :)



INFLAMMATION

Inflammation is the body's reaction to an injury such as an invasion
by an infectious agent. In just the same way as it is necessary to
increase the blood supply to active muscles during exercise to provide
glucose and oxygen so it is also necessary to direct elements of the
immune system into sites of infection. Three major events occur during
this response.
1. An increased blood supply to the infected area.
2. Increased capillary permeability caused by retraction of the
endothelial cells. This permits larger molecules to traverse the
endothelium than would ordinarily be capable of doing so and thus
allows the soluble mediators of immunity to reach the site of
infection.
3. Leucocytes, particularly neutrophil polymorphs and to a lesser
extent macrophages, migrate out of the capillaries and into the
surrounding tissue. Once in the tissue, they migrate towards the site
of infection by a process known as chemotaxis.
These events manifest themselves as inflammation.

The immune system is not the only system which protects the body from
injury; the clotting, fibrinolytic and kinin systems are also involved
in mediating inflammation and in the resolution of tissue damage.
These systems interact to maintain the integrity of the vascular
system and to limit the spread of tissue damage whether it is caused
by physical injury or infectious agents.

Immunology, Ivan M. Roitt, Jonathan Brostoff, David K. Male.

[Liz]

Steve, you gotta see this site:

http://www.vetmed.ufl.edu/path/teach/vem5162/panni.htm#Nodular

Steatitis is only one of the possible causes of panniculitis. There's
a picture there (warning: *very graphic*) that looks exactly like what
you described. The picture is of a cat infected by a mycobacterium.

[Liz]

Steve, you gotta see this site:

http://www.vetmed.ufl.edu/path/teach/vem5162/panni.htm#Nodular

Steatitis is only one of the possible causes of panniculitis. There's
a picture there (warning: *very graphic*) that looks exactly like what
you described. The picture is of a cat infected by a mycobacterium.

[Steve Gass]

Thank you Liz, I do appreciate your efforts to help me find the answers.

At this point, the only facts I have are that, when Bubba died, the fat tissue
on his abdomen was gangrenous, he was acutely anemic and his skin was "paper
thin", but there was no sign of kidney or liver disfunction. What I observed
throughout was, beyond a shadow of a doubt, a disease process taking place
within the fat tissue on his abdomen.

He became noticeably lethargic on June 11. The next day he stayed in his box,
not moving or accepting any form of nourishment. The exam on the 13th showed no
bite marks, skin disorders or any kind of trauma. There was a yellow-brown
discoloration of the fat tissue visible beneath the skin, and a single bloody
effusion. He was somewhat anemic at that time, although I was never made aware
of it.

Since there was no biopsy I will never know that it was indeed steatitis. It
could have been tissue death due to anemia from some other cause, or the anemia
could have been caused by the tissue death, which might have resulted from
steatitis. I didn't wait for the reticulocyte test, which would have shown if he
was producing red blood cells or not.

The skin tore off of his neck because it was so thin, which is a symptom of
Cushings disease, which is, in turn, often associated with steroid usage. I
can't say if it was the steroids or a genuine problem with his adrenal gland
but, as buglady suggested, perhaps I don't want to know that right now. One
other thing that I do know, however, is that he wouldn't eat without steroids,
and lost over 4 pounds during the illness.

At some point I will ask for more clues from the vets involved but, for now, I
think I need to get on with life. I've realized that it's just not healthy for
me to dwell on the causes too much right now - anger and guilt won't bring Bubba
back.

But again, thank you, and everyone, for your support and advice.

Steve

[Steve Gass]

Thank you Liz, I do appreciate your efforts to help me find the answers.

At this point, the only facts I have are that, when Bubba died, the fat tissue
on his abdomen was gangrenous, he was acutely anemic and his skin was "paper
thin", but there was no sign of kidney or liver disfunction. What I observed
throughout was, beyond a shadow of a doubt, a disease process taking place
within the fat tissue on his abdomen.

He became noticeably lethargic on June 11. The next day he stayed in his box,
not moving or accepting any form of nourishment. The exam on the 13th showed no
bite marks, skin disorders or any kind of trauma. There was a yellow-brown
discoloration of the fat tissue visible beneath the skin, and a single bloody
effusion. He was somewhat anemic at that time, although I was never made aware
of it.

Since there was no biopsy I will never know that it was indeed steatitis. It
could have been tissue death due to anemia from some other cause, or the anemia
could have been caused by the tissue death, which might have resulted from
steatitis. I didn't wait for the reticulocyte test, which would have shown if he
was producing red blood cells or not.

The skin tore off of his neck because it was so thin, which is a symptom of
Cushings disease, which is, in turn, often associated with steroid usage. I
can't say if it was the steroids or a genuine problem with his adrenal gland
but, as buglady suggested, perhaps I don't want to know that right now. One
other thing that I do know, however, is that he wouldn't eat without steroids,
and lost over 4 pounds during the illness.

At some point I will ask for more clues from the vets involved but, for now, I
think I need to get on with life. I've realized that it's just not healthy for
me to dwell on the causes too much right now - anger and guilt won't bring Bubba
back.

But again, thank you, and everyone, for your support and advice.

Steve