Peachick Necropsy **WARNING GRAPHIC PICTURES**

[zazouse]

I was wearing gloves, so when we finished i just took off my gloves and got some photos with my phone, but also a gopro camera will be a great option for you.

I do also but these rubber gloves i get, tear real easy and even though i bring extra they usually all get ripped in the process

then i have messy hands and i can't touch my camera.
I do not even bother with gloves most of the time when processing cause it is just a waist ,but if something dies then i will most defiantly wear them the entire time.

 

[Garden Peas]

@q8peafowl , I know that you have been asked lots of questions, and this whole thing has been difficult.

I am completely baffled by the apparent holes and necrotic (dying) tissue that @zazouse pointed out on the enlarged photos. That would not be expected (I don't think) on any regular necropsy (for example, the one of her bird that died of a sinus infection), and I am fairly certain that the bird could not have decayed that fast after death. And decay wouldn't produce holes like that, so very quickly, I don't think.

I have pondered this and banged my head about it, and I have only been able to come up with two things that could have caused this.

The first would be some kind of external injury, which may not have produced an obvious surface wound. For example, when there is a bite injury, sometimes the animal's teeth do injury below the skin (and in this case feathers), without tearing the skin. I can say from experience that both dog and cat bites can leave damage below the skin which results in bleeding and bruising and apparently some tearing of tissue, without breaking the skin itself, or with minimal injury to the surface. Also, puncture wounds, particular if inflicted with a sharp object, don't always leave gaping openings on the surface, and sometimes have remarkably little bleeding. And even bullets.... Decades back, someone shot one of my dogs with a .22 -- with the vet's help and xrays, we eventually identified 7 holes (six were in pairs, entry + exit), so the dog had been shot 4 times, but we were hard pressed to find the holes or the source of his injuries until we had the xrays. I would have thought a bullet would leave a bigger hole... Piercing wounds from knives or perhaps an exposed nail or sharp surface in the pen could be similarly difficult to locate from the exterior of the bird.

Is there any possibility another pea could have inflicted injuries with its feet or spurs? Or by pecking very hard?

The second thing that I am wondering about is some kind of hideous internal parasite. I don't know what sorts of parasites may exist in the local environment. One reads about horrible worm parasites in Africa which burrow through muscle and exit people's skin... I haven't seen one in many years, but we used to have screw worms here which would erupt from the side of a horse or dog... looked like an abscess and then there was a huge disgusting hole... truly gross. I think the holes looked a bit like the holes on the bird. Othman, are there any parasites in Kuwait which might have tunneled through the bird's abdominal cavity and organs? I think those holes are too large for roundworms, aren't they?

If the order in which things happened was that the bird suffered an injury (physical or parasitic), then there was some minor bleeding internally, then necrosis set in, killing the surrounding tissue, it seems like the bird could easily die from the internal infection and even copious quantities of Baytril would not save it. That would explain @AugeredIn 's observation and comment that the necrosis looked like it came up towards the liver from somewhere else, rather than starting at the liver.

So then I am wondering if the source of injury could be repeated, in other words, if other birds in the pen could be similarly injured or could get the parasite, if that's what it was.

Just grasping at straws here, but I am worried about the rest of the birds, as I'm sure you are, and I am just trying to puzzle this out. I will be interested to see what @casportpony 's expert can tell us.

 

[casportpony]

That level of decay can occur with peritonitis and/or necrotic enteritis. Lost a chicken hen to peritonitis and she smelled like death *before* she died!

-Kathy

 

[casportpony]

Also lost a horse to the same thing, was probably septic, too. 24 hours later and the smell from him was something I hope none of you ever experience.

Haven't sent the pictures off to UC Davis yet, but will do this weekend for sure.

-Kathy

 

[Garden Peas]

That level of decay can occur with peritonitis and/or necrotic enteritis. Lost a chicken hen to peritonitis and she smelled like death *before* she died!

-Kathy

Exactly.... but am stymied on what would be the cause or source of the peritonitis or necrotic enteritis? Injury? Parasite? What instigated the necrotic process here in this bird's abdominal cavity?

Those holes wouldn't have come from a passing bacteria... or if they did, the level of decay and abscess would have been visible with lots of pus nearby, like an abscess when it's opened, right? If I'm interpreting the photos correctly, there's dead, necrotic tissue, but not pus?

I keep coming back to physical or parasitic injury, but I don't know anything about necrotic enteritis. I'm thinking that would be a possibility, I just don't know anything about it. What can you tell us about that disease process?

 

[Garden Peas]

Hey, look what I found:

http://www.thepoultrysite.com/publications/6/diseases-of-poultry/184/necrotic-enteritis

There's some interesting photos:

NECROTIC ENTERITIS

113.. Necrotic enteritis (NE) is an acute Clostridium infection characterized by severe necroses of intestinal mucosa. The disease begins suddenly, with a sharp increase in death rate. A strong dehydration is observed. The skin is sticked on or adhered to body musculature and is hardly removed.

114.Chickens at the age of 25 weeks are usually affected, NE is also encountered in hens particularly near the period of the beginning of egg laying or peak egg laying, most commonly associated with coccidiosis. In acute cases, marked congestion of liver, responsible for its dark red to black appearance, is present.

115.The aetiological agent is Clostridium perfringens, mainly from type A and more rarely from type C. The produced a and p" toxins, from C. perfringens type A and type C respectively, are responsible for the necrosis of intestinal mucosa. The small intestine is often distended with gases and the necrotic mucosa is visible through the wall.

116.CI. perfringens is ubiquitous and normally reside into the intestinal tract. The alterations are particularly in the jejunum and the ileum because of their higher pH and the lower oxygen content in these areas. Sometimes, haemorrhages are seen through the intestinal wall.

117.The intestinal lumen is filled with brownish watery content, mixed with gas bubbles.

118.necrotic mucosa acquires a greyish-creamy or greenish appearance. Sometimes the mucosa has a flannelette blanket-like appearance.

119.120.In some cases, the mucosa has a linear pattern similar to the bark of a tree. The predisposing factors are injuries of intestinal mucosa by various Eimeria species, migration of ascarids, immuno¬deficiency states due to CIA, IBD, MD, high content of wheat or fish meal in the diet.

121In cases when NE is associated with small intestinal coccidioses, multiple petechial haemorrhages could be perceived through the wall in different areas along the small intestine.

112.123.124.Throughout the simultaneous occurrence of NE and cocci¬dioses, the content of the lumen is bloody, mixed with necrotic detritus and gas bubbles. The diagnosis is based on the distinctive gross lesions. When necessary, a histological investigation is performed or attempts for isolation of the causative agent. NE should be distinguished from ulcerative enteritis and some small intestinal cocci¬dioses. The control should be aimed at predisposing factors. An appropriate medication of feeds is recommended. A good effect is obtained with oxytetra-cycline dihydrate (OTC 50% premix). NE could be effectively treated with doxy-cycline hydrochloride, amoxicillin etc.

 

[Garden Peas]

And this, from the Merck Manual:

http://www.merckmanuals.com/vet/pou...verview_of_necrotic_enteritis_in_poultry.html


Overview of Necrotic Enteritis in Poultry

inShare​

Necrotic enteritis is an acute enterotoxemia. The clinical illness is usually very short, and often the only signs are a severe depression followed quickly by a sudden increase in flock mortality. The disease primarily affects broiler chickens (2–5 wk old) and turkeys (7–12 wk old) raised on litter but can also affect commercial layer pullets raised in cages. Early mortality is often related to coccidiosis vaccination programs, with Eimeria cycling in these flocks.
Etiology and Pathogenesis

The causative agent is the gram-positive, obligate, anaerobic bacteria Clostridium perfringens. It is usually isolated on blood agar, incubated anaerobically at 37°C (98.6°F), on which it produces a double zone of hemolysis. There are two primary C perfringens types, A and C, associated with necrotic enteritis in poultry. Toxins produced by the bacteria cause damage to the small intestine, liver lesions, and mortality.
C perfringens is a nearly ubiquitous bacteria readily found in soil, dust, feces, feed, and used poultry litter. It is also a normal inhabitant of the intestines of healthy chickens and turkeys. The enterotoxemia that results in clinical disease most often occurs either after a change in the intestinal microflora or from a condition that results in damage to the intestinal mucosa (eg, coccidiosis, mycotoxicosis, salmonellosis, ascarid larvae). High dietary levels of animal byproducts (eg, fishmeal), wheat, barley, oats, or rye predispose birds to the disease. Anything that promotes excessive bacterial growth and toxin production or slows feed passage rate in the small intestine could promote the occurrence of necrotic enteritis. In many cases, concurrent coccidiosis (especially Eimeria maxima, and E acervulina to a lesser extent) is associated with outbreaks in commercial broilers, although recent investigations with NetB-positive isolates have reportedly caused disease without predisposition from Eimeria infections.
Clinical Findings and Lesions

Necrotic enteritis, small intestine, chicken

Most often the only sign of necrotic enteritis in a flock is a sudden increase in mortality. However, birds with depression, ruffled feathers, and diarrhea may also be seen. The gross lesions are primarily found in the small intestine (jejunum/ileum), which may be ballooned, friable, and contain a foul-smelling, brown fluid. The mucosa is usually covered with a tan to yellow pseudomembrane often referred to as a “Turkish towel” in appearance. This pseudomembrane may extend throughout the small intestine or be localized. The disease usually persists in a flock for 5–10 days, and mortality is 2%–50%.
Diagnosis

A presumptive diagnosis is based on gross lesions and a gram-stained smear of a mucosal scraping that exhibits large, gram-positive rods. Histologic findings consist of coagulative necrosis of one-third to one-half the thickness of the intestinal mucosa and masses of short, thick bacterial rods in the fibrinonecrotic debris. Isolation of large numbers of C perfringens, from intestinal contents that produce the double zone of hemolysis as described above, can confirm the diagnosis. Double zone hemolysis should not be used as the sole criterion for identification of C perfringens, because some strains do not produce both toxins responsible for the hemolysis characteristics. Differential media specifically designed for isolation of C perfringens is available and may be useful for diagnosis.
Necrotic enteritis must be differentiated from lesions produced by Eimeria brunetti and also from ulcerative enteritis. Uncomplicated coccidiosis rarely produces lesions as acute or severe as those seen with necrotic enteritis. Ulcerative enteritis caused by C colinum usually produces focal lesions from the distal portion of the small intestine (ileum) to the ceca and is almost always accompanied by hepatic necrosis.
Prevention, Control, and Treatment

Because C perfringens is nearly ubiquitous, it is important to prevent coccidiosis, especially E acervulina and E maxima infections, as well as changes in the intestinal microflora that would promote its growth. This has traditionally been accomplished by adding antibiotics in the feed such as virginiamycin (20 g/ton feed), bacitracin (50 g/ton feed), and lincomycin (2 g/ton feed), as well as ionophore-class anticoccidial treatments. The recent move by many producers to antibiotic-free feeds has also been associated with markedly increased use of coccidiosis vaccines, resulting in early circulation of mixed Eimeria infections that are associated with the recent resurgence in incidence of necrotic enteritis. Avoiding drastic changes in feed and minimizing the level of fishmeal, wheat, barley, or rye in the diet can also help prevent necrotic enteritis. When higher amounts of wheat, barley, or rye are necessary, use of enzymes for nonstarch polysaccharides in the feed has reduced the level of necrotic enteritis in flocks fed these cereals. Administration of selected probiotics or competitive exclusion cultures has been used successfully to both prevent and treat clinical necrotic enteritis (presumably by preventing proliferation of C perfringens).
Treatment for necrotic enteritis is most commonly administered in the drinking water, with bacitracin (200–400 mg/gal. for 5–7 days), penicillin (1,500,000 u/gal. for 5 days), and lincomycin (64 mg/gal. for 7 days) most often used. In each case, the medicated drinking water should be the sole source of water. Moribund birds should be removed promptly, because they can serve as a source of toxicosis or infection due to cannibalism.

 

[casportpony]

I am no expert, but the photos in those links do look a little like this:


-Kathy

 

[Garden Peas]

Apparently there is a similar disease, ulcerative enteritis, caused by another version of clostridium, but I couldn't find any good pictures.

The common thread between them is coccidial infections that become excessive... apparently clostridium are everywhere, bu the disease takes hold when the coccidia gives it a chance, so good coccidia control is one way to help prevent this.

 

[Garden Peas]

Here's what little I could find on it:

http://www.thepoultrysite.com/diseaseinfo/162/ulcerative-enteritis-quail-disease

(I couldn't get anything from there to copy)

And also this:

http://www.extension.org/pages/68120/necrotic-and-ulcerative-enteritis-in-poultry#.VJ22Nv-vEA

Necrotic and Ulcerative Enteritis in Poultry

Small and Backyard Flocks June 13, 2013|Print

Necrotic enteritis and ulcerative enteritis (UE) are similar diseases, although they are caused by different organisms. UE usually affects gamebirds—quail in particular—and is caused by the bacterium Clostridium colinum. Necrotic enteritis affects chickens and turkeys and is caused by Clostridium perfringens.
These diseases are transmitted through clostridial spores that can remain dormant in the environment for years. Once ingested by birds, the spores germinate and become capable of causing disease. The birds then shed the organism in feces. Other birds in the flock become infected from fecal material in the litter, water, or feed.
Clinical Signs

Enteritis is an inflammation of the digestive tract. Infected birds fail to thrive and have diarrhea and weight loss. In severe cases, death can ensue.
Treatment

Antibiotics, specifically those designed to affect gram-positive bacteria (such as antibiotics containing virginiamycin, bacitracin, or lincomycin), can be used to treat necrotic and ulcerative enteritis. As with any medication, it is important to read the label and follow all instructions. Enteritis is often a secondary infection in a flock with a coccidial problem. For this reason it is important to treat an infected flock for coccidiosis as well.
Prevention and Control

To prevent infection, it is important to maintain effective sanitation and biosecurity. Avoid mixing birds of different ages in the same pen or placing new flocks in a pen without cleaning and disinfecting from the previous flock. Using an acidifying litter treatment to disinfect a pen can reduce the bacterial load.