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#1
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Steatitis
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*** 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
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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
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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
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"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
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"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
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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
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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
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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
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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
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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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