A dog & canine forum. DogBanter

If this is your first visit, be sure to check out the FAQ by clicking the link above. You may have to register before you can post: click the register link above to proceed. To start viewing messages, select the forum that you want to visit from the selection below.

Go Back   Home » DogBanter forum » Dog forums » Dog health
Site Map Home Register Authors List Search Today's Posts Mark Forums Read Web Partners

Need some QUICK ideas



 
 
Thread Tools Display Modes
  #1  
Old April 5th 07, 10:33 PM posted to rec.pets.dogs.health
Suja
external usenet poster
 
Posts: 2,483
Default Need some QUICK ideas


A fellow volunteer just called to say that his brother's dogs got into some
grass clippings that had been sitting around for a couple of weeks, and got
really sick from it. One of the dogs (a boxer mix) died from it, and his
145 lbs. GSD is at the vet's and barely hanging on. The vet has started the
dog on IV antibiotics, and is doing blood tests. I don't have a lot of
information, but the symptoms appear to be lethargy, vomiting and blood in
the feces.

Phenolic acid, benzoic acid and hydroxyphenylpropionic acids can all be
released during plant decay, but they shouldn't be in large enough doses to
kill 60 pound dogs. It's been warm here the past week, and it's possible
there were mushrooms mixed in there that could be causing this. Don't know
if there could be some other fungus or mold that could cause these symptoms.

The dog can't be impacted if it is still passing stool, can it? I've asked
the owners to check the grass to see if there is anything growing in there,
and to call poison control for how to deal with that if they find anything.
Any other ideas?

Suja


  #2  
Old April 5th 07, 10:48 PM posted to rec.pets.dogs.health
Suja
external usenet poster
 
Posts: 2,483
Default Need some QUICK ideas


"Suja" wrote in message:

Forgot to mention, no chemicals of any sort was used on the lawn, so that's
not it.

Suja


  #3  
Old April 6th 07, 12:23 AM posted to rec.pets.dogs.health
buglady
external usenet poster
 
Posts: 863
Default Need some QUICK ideas


"Suja" wrote in message
...

A fellow volunteer just called to say that his brother's dogs got into

some
grass clippings that had been sitting around for a couple of weeks, and

got
really sick from it. One of the dogs (a boxer mix) died from it, and his
145 lbs. GSD is at the vet's and barely hanging on. The vet has started

the
dog on IV antibiotics, and is doing blood tests. I don't have a lot of
information, but the symptoms appear to be lethargy, vomiting and blood in
the feces.

Phenolic acid, benzoic acid and hydroxyphenylpropionic acids can all be
released during plant decay, but they shouldn't be in large enough doses

to
kill 60 pound dogs. It's been warm here the past week, and it's possible
there were mushrooms mixed in there that could be causing this.


.................yeah, wonder if that isn't it. In which case the liver
needs huge support. Do they really think they ate some of the clippings or
was the pile just disturbed? Any nasty neighbors?

There's a list of fungi present in compost:
http://www.annmicro.unimi.it/full/53...oer_53_349.pdf

We got bad toads here in FL - any reptiles they could have eaten?

But this is silly. She should call ASPCA poison control hotline and open an
account. Cripes, hope his pup is OK

buglady
take out the dog before replying


  #4  
Old April 6th 07, 12:41 AM posted to rec.pets.dogs.health
Suja
external usenet poster
 
Posts: 2,483
Default Need some QUICK ideas


"buglady" wrote in message:

................yeah, wonder if that isn't it. In which case the liver
needs huge support. Do they really think they ate some of the clippings

or
was the pile just disturbed? Any nasty neighbors?


I think it's no on the nasty neighbors, and they seem absolutely convinced
that whatever is causing this is/was in the grass clippings. The symptoms
of mushroom poisoning in humans is similar.

There's a list of fungi present in compost:
http://www.annmicro.unimi.it/full/53...oer_53_349.pdf


I'll pass it along.

We got bad toads here in FL - any reptiles they could have eaten?


Not that I know of. Another avenue to explore, however.

But this is silly. She should call ASPCA poison control hotline and open

an
account.


That's what I said, and he said that the thought never occured to them.

Cripes, hope his pup is OK


Me too. I'll let you know how it turns out.

Wonder if necropsy of the dog that died would've given them the answers
they're looking for.

Suja


  #5  
Old April 6th 07, 12:47 AM posted to rec.pets.dogs.health
buglady
external usenet poster
 
Posts: 863
Default Need some QUICK ideas


"buglady" wrote in message
link.net...

This doesn't sound the same, but I will note that gastric lavage was done -
and may have saved this dog.
Roquefortine can occur in silage:
http://www.pubmedcentral.nih.gov/art...i?artid=339273
Acute penitrem A and roquefortine poisoning in a dog
A 45-kg, 4-year-old, castrated male, Labrador retriever had vomited once and
was presented for lethargy, excessive panting, trembling, and
incoordination. That morning, the dog had been outside unsupervised, with
access to restaurant garbage.

The dog was anxious, ataxic, and full-body tremors were evident. The heart
rate was elevated but difficult to determine due to the polypnea. Body
temperature was elevated (40.9癈) and both pupils were dilated. Mucous
membranes were pink, and capillary refill time (CRT) was normal (1 s).
Collection and immediate freezing of the vomitus was requested to help with
diagnosis, treatment, and prognosis. Because of the severity of its
condition, the dog was to be transferred to an emergency clinic for 24-hour
care, but convulsions began before this was possible. Seizures, but no
foreleg paddling, and hyperesthesia were controlled by administration of
diazepam (Valium 10; Rocher, Mississauga, Ontario), 3 boluses, each 0.22
mg/kg body weight (BW) given, IV, at 3-minute intervals. Lactated Ringer's
solution (Baxter, Toronto, Ontario) was administered, IV, at a rate of 90
mL/kg BW/h. All tremor activity ceased after administration of phenobarbitol
sodium (Phenobarbitol; Abbott Laboratories, Toronto, Ontario), 2 boluses,
each 2.7 mg/kg BW given, IV, at a 5-minute interval.

Acute toxicosis was suspected. Because of the possibility of septic shock,
or anaphylactic shock, or both, the dog was treated with ampicillin sodium
(Ampicillin; Novopharm, Toronto, Ontario), 22.2 mg/kg BW, IV, and
tripelennamine HCl (Vetastim; rogar/STB, Montreal, Quebec), 0.5 mL/10 kg BW,
IM. In addition, prednisolone sodium succinate (Soludelta Cortef; Upjohn,
Orangeville, Ontario), 22.2 mg/kg BW, was given IV. Gastric lavage with warm
water was performed, after anesthesia had been induced with a bolus of
propofol (Rapinovet; Schering-Plough, Pointe-Claire, Quebec), 2 mg/kg BW,
IV, and was maintained with isoflurane (Aerrane; Janssen, Toronto, Ontario).
Activated charcoal (50 g) was administered. Hyperthermia was treated by
placement of cold wet towels over the animal's body during anesthesia. Heart
rate (96 beats/min) and body temperature (38.1?C) were normal before
transport to the emergency clinic. Diazepam (Valium; Sabex, Boucherville,
Quebec) was administered in an IV drip (0.2 mg/mL) before and during the
30-minute trip.

On arrival at the emergency clinic, the dog was panting and had begun to
paddle with his forelegs. Rectal temperature (38.5癈), CRT ( 2 s), and
mucous membranes were normal. An electrocardiogram revealed a regular
cardiac rhythm with an increased heart rate (160 beats/min). The dog was
maintained on diazepam, 0.5 mg/kg BW/h, IV, for 4 h. Administration rate was
halved at 2-hour intervals during the next 6 h. Intravenous electrolytes
(Plasma-lyte 148; Baxter, Toronto, Ontario) were administered, as required.
Ampicillin sodium was continued at 22.2 mg/kg BW, IV, q8h, for 24 h. Lateral
and dorsoventral thoracic radiographs taken on day 2 revealed signs of
aspiration pneumonia. Ampicillin was discontinued and cefoxitin sodium
(Cefoxitin; Novopharm, Toronto, Ontario) was prescribed at 22.2 mg/kg BW,
IV, q6h, for 24 h, then q8h for 24 h. Pulse oximetry readings of blood
oxygen saturation were below normal (80%). Nasal catheterization with 100%
oxygen therapy (112 mL/kg BW/min for 20 h) increased blood oxygen saturation
to levels greater than 95%. By day 4, the dog was free of abnormal
neurological signs and the pneumonia was treated at home with amoxicillin
and clavulinic acid (Clavamox; Pfizer, London, Ontario), 11.1 mg/kg BW, PO,
q12h, for 14 d.

Gross and microscopic examination of the vomitus revealed blades of grass,
pieces of raw tenderloin, and a cereal-based substance resembling flour. A
thin layer chromatography screen was used for detection of penitrem A (PA),
roquefortine (RQ), or strychnine. Significant levels of PA and RQ ( 10 ppm)
were identified.

Poisoning is the primary differential for a dog with acute onset of
vomiting, polypnea, tachycardia, hyperesthesia, and ataxia, followed by
lateral recumbency, muscle fasciculations, and seizures. Metaldehyde,
mycotoxins, strychnine, zinc phosphide, bromethalin, xanthines, and
insecticides must be considered. The history of garbage consumption in this
case suggested that mycotoxins or xanthines were the most likely toxins. The
dog exhibited mydriasis and tachycardia, clinical signs not associated with
insecticides that cause cholinergic stimulation; the lavage contents lacked
an acetaldehyde odor, making metaldehyde poisoning unlikely; recovery from
bromethalin poisoning rarely occurs in 3 d; and strychnine poisoning is a
rare occurrence.

Mycotoxins are produced by specific fungus. Only certain species of
Aspergillus, Claviceps, and Penicillium produce tremorgenic mycotoxins (1),
such as PA and RQ, which can cause uncontrollable neuromuscular activity in
vertebrates. Different taxonomic classifications of fungal species have made
it difficult for researchers to agree on the species of origin for
individual mycotoxins (2,3). On the basis of morphological and physiological
properties, Penicillium crustosum and Penicillium roquefortii are now
considered the most common producers of PA and RQ, respectively (2). Fungal
synthesis of mycotoxins is factor-dependent. For example, an ambient
temperature of 25癈 and a pH of 5.7 optimize production of PA by P.
crustosum. Similarly, a culture medium containing 2% skim milk, potato
extract, and 2% lactose induces the highest levels of PA when P. crustosum
isolates are incubated for 3 wk (4). Penicillium crustosum may be isolated
from several types of food, including meat, fruit, cereal and cereal
products, cheese, spices, and nuts (4). Lacking appropriate environmental
conditions, fungal mycelia can proliferate but fail to produce a specific
mycotoxin.

Treatment for PA or RQ toxicosis should begin immediately after obtaining a
suspicious history and observation of characteristic clinical signs, which
usually begin 30 min to 4 h after ingestion of garbage, depending on the
amount of mycotoxin consumed (5,6).

Penitrem A intoxication causes ataxia, polypnea, and sustained tremors that
may progress to generalized seizures and death (5,6,7). However, as in this
case, animals may vomit before any of these clinical signs appear (7).
Hyperesthesia may occur, indicated by muscle fasciculations in response to
noise (5). Death of the animal can be avoided by administering phenobarbitol
immediately to control seizures. Clinical signs may resolve within 12 h (7),
but complete recovery may take as long as 21 d (5), depending on the amount
of PA absorbed (6). Without treatment, animals receiving more than 0.5 mg/kg
BW of PA are likely to die within 3.5 h (6). A minimum toxic dose of PA for
the dog has not been determined.

Roquefortine intoxication is characterized by vomiting, panting, muscle
tremors, paddling, hyperesthesia, and seizures (8). Intravenous diazepam
does not alleviate the clinical signs of RQ poisoning as it does similar
signs caused by strychnine and metaldehyde poisoning (8). The prognosis for
dogs with RQ intoxication depends on how soon the toxin is removed from the
stomach. Barbiturate therapy is effective in controlling seizures but may
not prevent death if the toxin remains in the stomach (8). A complete
recovery occurs within a 24- to 48-hour period following vomiting (8).

This dog showed signs typical of both PA and RQ poisoning. Death due to RQ
poisoning was likely prevented by early vomiting, and barbiturate therapy
probably protected the dog against death due to PA-induced seizures. If RQ
levels in the vomitus had been compared with those in the lavage solution,
it might have been possible to show that vomiting did protect the dog
against fatal intoxication. The effectiveness of activated charcoal in
preventing fatality in animals that have ingested RQ is unknown and needs to
be investigated.

The exact mechanism of action by which PA causes symptoms is uncertain. Data
from postmortem examination suggest that some serum enzymes may increase due
to hepatic centrolobular changes (congestion and hepatocyte degeneration and
necrosis) (6). Lungs and large and small intestine are often hemorrhagic and
edematous (6), which may be the result of shock.

The primary target of PA may be at the biochemical level, as a neural lesion
has not been identified microscopically (9). In vitro research has
demonstrated that PA alters central presynaptic release of the excitatory
neurotransmitters (NTs) glutamate and aspartate, and the inhibitory
neurotransmitter gamma-aminobutyric acid (GABA) (9). In response to PA,
release of these NTs by inactive cortical synaptosomes increases, and
release by stimulated synaptosomes decreases (9). Synapses at the
neuromuscular junction are not affected (9). Research is needed to identify
the in vivo synaptic effects and primary site of action of PA.

In electrophysiologic and histologic studies in rodents, seizure-sensitive
areas (the thalamus and hippocampus) exhibited no abnormalities to account
for PA-induced seizures (10). Rather, dose-related lesions of the cerebellar
cortex may be implicated. At a dose of 0.5 mg/kg BW of PA, some
degeneration of Purkinje cells were observed (10). After inoculation with a
low dose of PA, animals appeared to be most severely affected within 30 min
and recovered within 24 h (10). High doses of PA caused extensive loss of
Purkinje cells and vacuolization of the molecular layer of the cerebellar
cortex (10). Lesions of this magnitude caused significant neuromotor
deficits that persisted for more than a week (10). Breton et al (10)
theorized that the cerebellar lesions are caused by PA's interference with
release mechanisms for glutamate and aspartate, the neurotransmitters for
the primary excitatory inputs to Purkinje cells. These inputs are believed
to be secreting or transmitting GABA (GABAergic). Upon exposure to PA,
excitotoxic cell damage to the Purkinje cells occurs. The GABAergic axons of
the Purkinje cells form inhibitory synapses with the cerebellar nuclei,
which, in turn, activate the cells of the medial thalamic nucleus (10). This
may be the mechanism by which lesions in the cerebellum, a structure
responsible for motor coordination, cause seizures, a clinical sign specific
to thalamocortical damage.

No studies have investigated the mechanism of action of RQ. Clinical signs
are similar to those of strychnine poisoning. Strychnine competes with
glycine at the postsynaptic site in the spinal cord and medulla. Research
investigating the site of action of RQ is needed to aid clinicians further
in effectively treating affected animals.

The possibility of intoxication with PA or RQ may be overlooked by
clinicians presented with a dog exhibiting convulsions. A history of garbage
consumption and sudden ataxia progressing to generalized tremors and
seizures should raise suspicion of intoxication by PA, RQ, or both. Further
investigation into the action of PA and RQ will allow veterinarians to make
a faster diagnosis and more appropriate selection of treatment.

Hillary's (vet from alt.med.vet) class notes on poisonous plants:
http://www.hillary.net/school/spring...m.lec.04.20.98

The other thought is that new green plant growth can have a lot of
nitrogen - perhaps nitrates.

buglady
tak eout the dog before replying


  #6  
Old April 6th 07, 12:53 AM posted to rec.pets.dogs.health
Melinda Shore
external usenet poster
 
Posts: 7,732
Default Need some QUICK ideas

In article , Suja wrote:
Any other ideas?


Some time after reading this post I remembered that we were
always told not to let the horses eat cut grass because of
..... and I couldn't remember what. It just came to me that
it's botulism, which is rare but can get into the grass from
dead animals (in this case possibly moles, mice, etc., that
met an early demise at the hands of the lawnmower). I'd
guess it's a long shot but I don't think it's impossible.
--
Melinda Shore - Software longa, hardware brevis -

Prouder than ever to be a member of the reality-based community
  #7  
Old April 6th 07, 01:04 AM posted to rec.pets.dogs.health
buglady
external usenet poster
 
Posts: 863
Default Need some QUICK ideas


"Suja" wrote in message
...

Wonder if necropsy of the dog that died would've given them the answers
they're looking for.


..........Absolutely - they could have at least looked at stomach contents
and the liver.

OK more on molds in silage:

http://www3.interscience.wiley.com/c.../1382/ABSTRACT
Wilted grass and whole-crop maize silages taken from farm silos in northern
Germany were analysed for fermentation pattern, mould counts and composition
of mycoflora as well as for roquefortine C. In general, increasing DM
contents of visibly unmoulded silages resulted in decreasing amounts of
volatile fatty acids and a greater portion of samples with a high number of
mould propagules. The average mould count of these silages was found to be
1򉚕04 cfu g-1, whereas visibly moulded samples contained about 1108 cfu
g-1. Penicillium roqueforti was the predominating fungal species in silages
occasionally accompanied by species of the genera Aspergillus, Mucor,
Monascus and/or Geotrichum. Penicillium roqueforti was detected in 89% of
the visibly moulded and in 85% of the visibly unmoulded samples. Of 24
visibly moulded silages tested, 21 samples contained roquefortine C, a
mycotoxin known to be produced by P roqueforti. The highest level of
roquefortine C found was 36 mg kg-1

...........Nothing here but the title, but apparently it does have an effect
on the liver:
Inhibitory Effects of Roquefortine on Hepatic Cytochromes P450
Aninat, C. Delaforge, M.
ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY
Bibliographic details 2001, VOL 500, pages 331-334

List of fungal toxins and fungi that produce them:
http://www.aerobiology.net/Mycotoxin.html

Some fungal toxins and their effects - more useful than one above::
http://www.aerias.org/DesktopDefault...dex=4&tabid=66

......OK I'm done

buglady
take out the dog before replying




  #8  
Old April 6th 07, 01:12 AM posted to rec.pets.dogs.health
buglady
external usenet poster
 
Posts: 863
Default Need some QUICK ideas


"buglady" wrote in message
link.net...

OK, ONE more!
Mycotoxins in sileage - usually a combo:
http://www.das.psu.edu/dairynutritio...nts/kuldau.pdf

buglady
take out the dog before replying


  #9  
Old April 6th 07, 02:04 PM posted to rec.pets.dogs.health
flick
external usenet poster
 
Posts: 568
Default Need some QUICK ideas


"Suja" wrote in message
...

A fellow volunteer just called to say that his brother's dogs got into
some
grass clippings that had been sitting around for a couple of weeks, and
got
really sick from it. One of the dogs (a boxer mix) died from it, and his
145 lbs. GSD is at the vet's and barely hanging on. The vet has started
the
dog on IV antibiotics, and is doing blood tests. I don't have a lot of
information, but the symptoms appear to be lethargy, vomiting and blood in
the feces.

Phenolic acid, benzoic acid and hydroxyphenylpropionic acids can all be
released during plant decay, but they shouldn't be in large enough doses
to
kill 60 pound dogs. It's been warm here the past week, and it's possible
there were mushrooms mixed in there that could be causing this. Don't
know
if there could be some other fungus or mold that could cause these
symptoms.

The dog can't be impacted if it is still passing stool, can it? I've
asked
the owners to check the grass to see if there is anything growing in
there,
and to call poison control for how to deal with that if they find
anything.
Any other ideas?


Suja -

If it isn't too late, if there was clover (I think) or certain weeds growing
in the lawn, I believe coumadin or a substance close to it can be formed.
In that case the dog needs vitamin K, stat. That would cause internal
bleeding and blood in the stool.

Abnormal clotting would be evident by blood tests - I think PT/PTT.

flick 100785


  #10  
Old April 7th 07, 12:03 AM posted to rec.pets.dogs.health
buglady
external usenet poster
 
Posts: 863
Default Need some QUICK ideas - SUJA SUJA


"buglady" wrote in message
thlink.net...

Have you gotten any feedback on bloodwork and how the pup is doing?

buglady
take out the dog before replying


 




Thread Tools
Display Modes

Posting Rules
You may not post new threads
You may not post replies
You may not post attachments
You may not edit your posts

vB code is On
Smilies are On
[IMG] code is On
HTML code is Off
Forum Jump

Similar Threads
Thread Thread Starter Forum Replies Last Post
Scared pup needs help quick! heather Dog rescue 2 January 10th 06 11:31 PM
They grow so quick! Cin Dog behavior 0 July 12th 04 03:23 AM
They grow so quick! Cin Dog behavior 0 July 12th 04 03:23 AM
They grow so quick! Cin Dog behavior 0 July 12th 04 03:23 AM
Now, that was Quick! (Was NADAC reg. #) Shelly & The Boys Dog behavior 6 September 1st 03 01:42 AM


All times are GMT +1. The time now is 06:30 PM.


Powered by vBulletin® Version 3.6.4
Copyright ©2000 - 2019, Jelsoft Enterprises Ltd.Search Engine Optimization by vBSEO 3.2.0 (Unregistered)
Copyright 2004-2019 DogBanter.
The comments are property of their posters.