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Steatitis



 
 
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  #1  
Old July 26th 03, 08:56 PM
S. Gass
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Posts: n/a
Default Steatitis

***
*** 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
  #2  
Old July 27th 03, 04:15 AM
Liz
external usenet poster
 
Posts: n/a
Default

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.
  #3  
Old July 27th 03, 04:15 AM
Liz
external usenet poster
 
Posts: n/a
Default

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.
  #4  
Old July 27th 03, 11:17 AM
buglady
external usenet poster
 
Posts: n/a
Default


"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


  #5  
Old July 27th 03, 11:17 AM
buglady
external usenet poster
 
Posts: n/a
Default


"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


  #6  
Old July 27th 03, 01:25 PM
Liz
external usenet poster
 
Posts: n/a
Default

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.
  #7  
Old July 27th 03, 01:25 PM
Liz
external usenet poster
 
Posts: n/a
Default

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.
  #8  
Old July 27th 03, 04:36 PM
Marie Fischer
external usenet poster
 
Posts: n/a
Default

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

  #9  
Old July 27th 03, 04:36 PM
Marie Fischer
external usenet poster
 
Posts: n/a
Default

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

  #10  
Old July 27th 03, 08:01 PM
S. Gass
external usenet poster
 
Posts: n/a
Default

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


"buglady" wrote in message rthlink.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
 




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