Peachick Necropsy **WARNING GRAPHIC PICTURES**

[Garden Peas]

A couple of things...

First, this doesn't explain those holes, and I don't know the significance of those holes. That could be more of a peritonitis kind of thing, I will look that up next.

Second, if one of these forms of enteritis was the cause of death, I'm not sure that Baytril (enrofloxacin) -- great drug that it is -- would be the drug of choice, or even effective. It's a different drug class from the drugs they use against these, I think, at least if I am correctly understanding what I am reading.

And since the mortality is partial, that would explain why only some of the birds got sick, and so far only one has died.

But I am speculating here...

 

[Garden Peas]

This looks like a super cool resource:

http://partnersah.vet.cornell.edu/avian-atlas/#/

So here's some other photos:

Fowl cholera

Clinical Description

The presence of blood and severe congestion in the intestinal lumen is commonly associated with acute Pasteurella multocida infection.

Fowl Cholera


Submitted by admin on Thu, 09/04/2008 - 17:28
Fowl Cholera (Pasteurella multocida)

Etiology

Fowl cholera (FC) is a highly contagious disease of domestic and wild birds. The disease is caused by Pasteurella multocida, a gram-negative, non-spore-forming, rod shaped bacteria. There are 16 somatic serotypes of Pasteurella multocida, of which 1, 3, and 3x4 are the most common. The pathogenicity of Pasteurella multocida strains is quite variable and the degree of expression of clinical signs varies by host species as well as variations within the host's immune system.
Host Range

Outbreaks of FC occur most frequently in turkeys, chickens, ducks, and geese. The disease is particularly severe in turkeys. Other bird species raised in captivity, as well as wild avian species, may also develop clinical disease. Some domestic mammals are also susceptible.
Epidemiology

FC is spread via horizontal transmission through contact with infected birds, contaminated equipment, personnel, etc. Pasteurella multocida can enter through mucous membranes, including oral, nasal, and conjunctival, as well as through cutaneous wounds. Chronically infected carriers play a major role in the spread of this disease and infected birds can remain carriers for life. The prevalence of Pasteurella multocida among wild birds, rodents, and other domesticated and non-domesticated species is likely responsible for the introduction of the infection into most domesticated poultry flocks.
FC is widely distributed, with periodic enzootic outbreaks occurring in most countries throughout the world. The disease usually manifests as a septicemia, sometimes with high morbidity and high mortality. However, a more chronic and asymptomatic form of the disease can also occur. Young adults are most susceptible to FC infection and physiologic stresses, such as egg lay cycles and seasonal changes, influence susceptibility. FC is more prevalent in the cooler seasons of the year.
Clinical Signs

Signs vary depending on the course of the disease. In the acute form of FC, infected birds may develop fever, ruffled feathers, anorexia, increased respiratory rate, and cyanosis. Cyanosis is often easiest to appreciate on the non-feathered skin of the comb and wattles. Mucoid discharge from the mouth and diarrhea may also occur. Diarrhea often begins as watery and whitish in color, progressing to a greenish color with mucus. In the acute form, signs may be absent and birds may be found dead in their nests. Birds that survive the acute septicemia may later die of dehydration and emaciation. Some birds may survive but remain chronically infected.
In the chronic form of FC, birds that survive acute infection or birds exposed to a low virulence strain, generally exhibit localized infections. The wattles, sinuses, foot pads, sternal bursa, and leg and wing joints may become swollen. Exudative pharyngeal and conjunctival lesions may be present. Sometimes tracheal rales and dyspnea may occur secondary to respiratory tract infections. Infected birds may also exhibit torticollis from middle ear infections and meningeal involvement. The chronic form of FC may last 3 to 4 weeks and may sometimes persist for years.
Post-mortem Lesions

In the acute form of FC, lesions associated with vascular disturbances are common. The veins of the abdominal viscera, especially the duodenum, may be markedly hyperemic. Petechiael and ecchymotic hemorrhages are frequently found throughout the viscera, most commonly the lungs, intestines, heart, and abdominal fat. Excessive fluid may be found in the pericardium and coelomic cavity. In infections with virulent strains of Pasteurella multocida, there may be liver enlargement and coagulative necrosis. Other findings may include pneumonia, especially in turkeys, and excessive mucous along the digestive tract. Lesions of the ovaries may include flaccid follicles, hyperemia, and egg-yolk peritonitis from ruptured ova.
In the chronic form of FC, localized infections may be found throughout the body including the hock joints, foot pads, oviduct, and coelomic cavity. Suppurative lesions are frequently found in the respiratory tract and pneumatic bones. Pneumonia is especially common in turkeys. Caseous exudate and fibrin may also infiltrate the calvarial bones, middle ear, meninges, and air spaces.
Differential Diagnosis

Fowl cholera must be differentiated from erysipelas, acute colibacillosis, Avibacterium gallinarum and complicated Mycoplasma gallisepticum in turkeys and other birds that may have both diseases. Erysipelas is caused by a gram-positive rod. Cholera can be differentiated from other septicemic diseases by isolation of P. multocida. Related organisms that cause cholera-like diseases in poultry include P. gallinarum, P. haemolytica, and P. anatipestifer.
Diagnosis

Culture samples can be taken from the liver, lungs, spleen, wattles or affected joints at necropsy. Additionally, impression smears of the liver and heart blood can also be obtained. Gram-stained impression smears may reveal bipolar, gram-negative rods suggestive of P. multocida. Use of Wright's stain or methylene blue readily demonstrates the bipolar morphology of P. multocida. Rabbits, hamsters, or mice can be inoculated for pure culture. P. multocida grows readily on blood agar but does not grow on MacConkey agar. Isolates should be tested for antibiotic sensitivity and resistance.
Prevention and Control

The elimination of reservoirs of Pasteurella multocida (such as rats, mice, cats, raccoons, skunks, etc.) in contact with domesticated and commercial poultry is one of the most effective management procedures to control the disease.
Both live and inactivated Pasteurella multocida vaccines are available for use in chickens. Three live products are available in the United States; the Clemson University CU low virulent strain; M-9, a mutant of CU of very low virulence; and PM-1, a mutant of CU intermediate in virulence between CU and M-9. Inactivated bacterins are primarily trivalent whole cell products containing the most common serotypes. Autogenous vaccines are also commonly used. A combination of inactivated and live vaccines can reduce the incidence of fowl cholera in susceptible broiler breeder flocks. Since FC is primarily a disease of older birds, broilers are not commonly vaccinated.
Selected References

1. Brogden, K.A., K.R. Rhoades, and K.L. Heddleston. 1978. A new serotype of Pasteurella multocida associated with fowl cholera. Avian Dis 22:185-90.
2. Charlton, B. R. (ed). 2006. Avian Disease Manual, 6th ed. American Association of Avian Pathologists (AAAP), 953 College Station Road, Athens, Georgia 30602-4875.
3. Glisson. J.R., C.L. Hofacre, and J.P. Christensen. 2008. Pasteurellosis and other respiratory bacterial infections. In Diseases of Poultry, 12th ed. Y.M. Saif. et al. (ed.). Blackwell Publishing, Ames, Iowa.
4. Glisson, JR. 1998. Bacterial respiratory disease of poultry. Poult Sci Aug;77(8):1139-42. Review.
5. Harper, M., J.D. Boyce and B. Adler. 2006. Pasteurella multocida pathogenesis: 125 years after Pasteur. FEMS Microbiol Lett. Dec;265(1):1-10. Review.
6. World Organization for Animal Health (OIE) website. 2008. www.oie.int

Thank you to the following individuals for reviewing these materials:
Charles Hofacre
Jaime Ruiz
Jose Bruzual
Differentials:
Colibacillosis
Erysipelas
Infectious Coryza
Mycoplasma gallisepticum
Pasteurella anatipestifer
Pasteurella gallinarum
Pasteurella haemolytica
Etiology:
Fowl Cholera

 

[Garden Peas]

The Cornell resource also has interesting photos of Marek's disease showing the effect on various organs, but I didn't copy any over to here, since they generally had no resemblance to the necropsy pix.

But still nothing that would relate to those puzzling holes... If they are signficant?

 

[Garden Peas]

This site also looks like a very helpful resource:

http://www.thepoultrysite.com/

Here's more info on Fowl Cholera:

The thing that I thought was interesting was the internal bleeding followed by necrosis, and the "congestion" which it says is overfilling of the liver by red blood cells.

http://www.thepoultrysite.com/publications/6/diseases-of-poultry/181/fowl-cholera

FOWL CHOLERA

68. 69.. Fowl cholera is an infectious disease in domestic fowl, waterfowl and other avian species. It is manifested either in acute septicaemic form with a high morbidity and death rates or as chronic local forms (independently or secondary to acute ones). Acute fowl cholera. The sudden and unexpected death could be the first sign of the disease. In this form, the lesions are predominantly related to vascular injuries.

70. Commonly observed signs are anorexia, ruffled feathers, oral and nasal mucus discharge, cyanosis and white or greenish watery mucoid diarrhoea. Frequently, subserous petechial or ecchymosed haemorrhages in the anterior part of the small intestine, the gizzard or the abdominal fat are discovered.

71. 72. Congestion (overfilling of blood vessels with red blood cells) of the liver as an initial manifestation of E. coli septicaemia in a broiler chicken. H/E, Bar = 40 µm.

73.In layers (commercial or breeders), acute oophorites with regressing follicles and consequently, diffuse peritonites are commonly observed.

74. Chronic fowl cholera. It is characterized by local inflammations. The periorbital sinuses are frequently affected by a serofibrinous inflammation.

75. 76. 77. Another local form is the injury of wattles that are strongly distended because of their filling with fibrinous caseous content. The flocks that recuperated from fowl cholera continue to carry and shed Pasteurella multocida. The carriers store the organism in nasal choanas and contaminate the forage, water and the environment with oral discharges. Wild birds and some mammals (swine) could also carry the agent and introduce it into poultry flocks. Cannibalism is an essential route of spreading the infection.

78. In turkeys a common finding is the unilateral or bilateral croupous pleuropneumonia

79. the fibrinous caseous exuate accumilated in wattles sometimes leads to gangrene of the covering skin.

80. 81. possibly be spread from sinuses to adjacent air-filled skull bones with subsequent necrosis and onset of neurological signs (opisthotonus and torticolis). The diagnosis is made on the basis of disease history, clinical signs, the lesions and the results of bacteriological studies. Fowl cholera should be differentiated from acute E. coli septicaemia, erysipeloid, fowl typhoid etc. The immunization of birds at the age of 8 -12 weeks gives very promising results. Many antibiotics and sulfonamides could lower death rate, but at discontinuation of the treatment, the disease could recur. Sulfonamides are appropriate for treatment, but they inhibit egg-laying.

 

[Peafowlssssssss]

@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.

Well, he was the biggest in size in that pen, i don't know anything about parasites, but last month we got many wet days, the humidity was so high, not sure if this related to parasites or not.