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DL
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xx Related General info
« Thread started on: Oct 6th, 2006, 12:00pm »

This thread will contain general information related to "poo" ... such as digestion etc. to help understand the processes at work!


http://wingwise.com/droppings.htm
(An informative general article on bird droppings)

http://www.petplace.com/article-printer-friendly.aspx?id=502
Polyuria (small excerpt from this excellent article)
"Usually, birds only produce a very small volume of liquid urine, and the majority of the waste from the kidneys will be in the form of semi-solid, white/beige urates. Occasionally, a larger volume of urine is produced (polyuria), which is often mistaken for diarrhea. Birds that are polyuric will have a more liquid dropping, but the fecal component remains solid and formed. Birds with diarrhea have a more liquid consistency to the fecal component."

http://www.wisc.edu/ansci_repro/101equinelab/parasites/parasite_methods/parasite_detection.html
Learn to do your "own" faecal tests with this article!

http://www.rvc.ac.uk/review/Parasitology/poultrEggs/Common.htm
Identify (microscope)> The RVC/FAO Veterinary Diagnostic Parasitology

http://www.finchaviary.com/Maintenance/FecalSmear.htm
Another EXCELLENT article on doing your own faecal smears

http://members.tripod.com/forester_at_large/foresteratlarge/id19.html
How to convert your microscope to take photos

http://www.vin.com/proceedings/Proceedings.plx?CID=WSAVA2002&PID=2589&Category=429
Faecal examination techniques and considerations
« Last Edit: Jul 2nd, 2007, 03:17am by DL » User IP Logged

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xx Re: ENTERIC DISEASE
« Reply #1 on: Jul 19th, 2007, 11:18am »

http://www.avian.uga.edu/documents/pip/2006/PIP-Sept-Oct%202006.pdf
PATHOGENESIS OF ENTERIC DISEASE
(Frederic J. Hoerr,DVM, PhD,Diplomate ACVP,ACPVVeterinaryDiagnostic
LaboratoryAuburnUniversityAuburn, Alabama)

In this article I have excerpted a section out to place at the top of this thread first as it details some basic terminology... the article in its entirety (with the exception of the charts >refer back to article to view these) follows this excerpted section- DL
EXCERPT:
"FEED PASSAGE AND DIARRHEA
Feed passage is undigested particles of feed in the
feces and represents a loss of digestive efficiency.
The economic consequences involve feed conversion, growth, carcass yield, and cost of production.
Feed passage usually occurs with diarrhea, which is
characterized by increases in the mass of feces, the
frequency of fecal passage, and/or the fecal fluidity.
Feed passage represents a malabsorption or
maldigestion syndrome that shares many of the same causes as diarrhea. For the purposes of this discussion, four underlying mechanisms of diarrhea and feed passage will be examined, according to the scheme of Crawford, 1997 (5).
Secretory Diarrhea:
This involves the excessive secretion of fluid from the intestinal mucosa, relative to the fluid absorption capacity of the intestine. This is caused by viruses that destroy mature enterocytes on the tips of the villus, leaving functional secretory enterocytes in the crypt and on the side of the villus. It is also caused by bacterial enterotoxins that affect mediators of intestinal electrolyte transport. In general, the mediators increase chloride secretion from the crypts and decreasing NaCl uptake from the tips of villi (1). As water follows these electrolytes, the net result is fluid overload in the lumen of the intestine.

Osmotic Diarrhea:
This involves excessive osmotic forces exerted by luminal solutes. Poultry diets high in salt are one cause, and some digestive problems associated antinutritional factors (non-starch polysaccharides, NSP) in barley, rye, and wheat, and other ingredients, reviewed by I ji, 1999 (7). These complex carbohydrates are resistant to digestive enzymes, create a viscous environment within the intestinal lumen, increase the mass of luminal
digesta, and produce moist sticky droppings.

Malabsorption:
This is the output of voluminous, bulky feces with increased osmolarity owing to unabsorbed nutrients and, in man, excessive fat. Digestion is inefficient due to either ineffective enzymes or a lack of enzymes. Defective absorption occurs with the loss of mature enterocytes and replacement by immature cells lacking full absorptive function. Increased fluid in the gut dilutes bile acid, impairing lipid absorption and allowing proliferation of bacteria (11). Exudative disease. This is characterized by blood or tissue debris from necrosis and inflammation, such as with severe coccidiosis, clinical salmonellosis, necrotic enteritis, or
histomoniasis. In this situation, the gut experiences severe insult involving the necrosis and loss of enterocytes, loss of fluid, electrolytes and plasma from the damaged mucosa, and inflammation. The host must contend with the escape of pathogens into the vascular system and dissemination to the liver. If the disease is not fatal, anorexia and diversion of nutrients for inflammation and repair will reduce growth and yield,
impair feed conversion, and increase the cost of pro-
duction.
REFERENCES >see below


ARTICLE:
"The digestive tract is a tube lined by specialized epithelial cells that are continuous with the epithelial layers covering the skin. Thus, the digestive tract is open to the external environment and to exposure from ingested organisms and toxins. Along the length of the tract, the epithelial cells differentiate and acquire a variety special functions that include the secretion of fluid, electrolytes, and enzymes, and in the gizzard,
physical disruption of particulate digesta. The cells form a semipermiable surface that selectively allows passage of fluid, electrolytes, and dissolved nutrients.Regardless of its specialized function, every digestive epithelial cell is part of a continuous physical barrier to protect against the entry of foreign materials and organisms into the bloodstream and gaining access to other
viscera. The integrity of the protective barrier is broken when organisms and toxic agents damage epithelial cells This epithelial lining continually sheds cells into the
center of the digestive tube (lumen) with ongoing
regeneration of new cells that differentiate to assume the functions of those lost. The surface area of intestinal lining (mucosa) is greatly expanded from the extensive microscopic folding to form a carpet of finger-like projections called villi. Villi exist throughout the length of the small and large intestine, steadily decreasing in height along the way. The luminal surface of each enterocyte is also increased by many microvilli to facilitate absorption.

Each villus is lined with epithelial cells (enterocytes) that are differentiated according to location on the villus to absorb fluids and nutrients (tip), secrete electrolytes and fluids (side and crypt), and to regenerate and replace damaged cells or those lost to normal attrition (crypt).

Mucus and Fluid Secretion:
Mucus that is secreted onto the epithelial surface lubricates movement of digesta along the digestive tract. It is secreted by specialized epithelial cells arranged into glands in the mouth and esophagus, and by individual goblet cells in the proventriculus and intestine. Mucus is not secreted in the crop or gizzard, however, digesta arrives in those organs softened and lubricated by the previous upstream site.

Mucus is a viscous material composed of water and glycoprotein. It protects the mucosal cells in the stomach and intestine from autodigestion by gastric acid, pepsin and other digestive enzymes (4). The protective effect of mucus is further evidenced by increased secretion on the mucosal surface and goblet cell hypertrophy in response to noxious stimuli. Mucus is one of the barriers to bacterial and fungal invasion. Virulent strains of Candida albicans, the agent of thrush, have a mucinolytic enzyme that dissolves the mucin barrier to enhance adherence to and penetration of epithelial cells (3). Helicobacter pylori, the agent causing gastric ulcers in humans,secretes urease that breaks down the protective layer of gastric mucus (10). Urease can be present in poultry feeds from improperly processed (underheated) soy meal (8).

In addition to mucus, the gut secretes a large volume of water and dissolved electrolytes. For every gram of food ingested, the gut secretes about 2 grams of water that facilitates digestion and absorption. The excessive water in the lumen is reabsorbed in the lower small intestine, cecum, and colon. The fluid in the upper small intestine, however, is protective in that it keeps bacteria in suspension and washes them downstream.

The Lamina Propria:
The epithelial lining of the gut is supported by the lamina propria, which contains the connective tissue that underlies the specialized surfaces, the vascular and lymphatic channels, and the immune system, or gut-associated lymphoid tissue (GALT). The blood vessels going into and away from the tip of the villus form a countercurrent mechanism that creates a hyperosmolar condition to facilitate absorption of fluid. Throughout the gut, the rich vascular supply serves to rapidly dilute and carry away any agents or chemicals (endogenous or
exogenous) that may breach the mucosal barrier.

Agents that directly damage the components of blood vessels may cause ischemic injury to the mucosa (infarction) or hemorrhage. Virulent forms of Newcastle disease and avian influenza, invasive
candidiasis, coccidiosis caused by Eimeria tenella,
and the more pathogenic forms of salmonellosis are
examples of diseases that can injure the gut vascu-
lar system.

GALT represents the largest secondary immunological organ in the body. In the chicken, the immunological tissues are distributed in specific sites at the junction of the proventriculus and gizzard, and
cecal tonsils; at concentrated ectopic locations; diffusely scattered through lamina propria; and as scattered individual intraepithelial lymphocytes.
GALT is composed of B and T lymphocytes, plasma
cells, macrophages, and dendritic cells (resident,
antigen-processing macrophages). One important
function of GALT is the secretion of secretory antibody (IgA) onto the mucosal surface in response to the heavy exposure of the gut to foreign antigens on
infectious agents and ingesta.

Since the gut is continuously and heavily exposed
to foreign materials, the lamina propria is quite
active due to the responsiveness of GALT, and is
actually in a normal state of reactivity and mild
inflammation. The transition from normal, mild inflammation to subclinical disease is an important consideration in poultry, not only from an economic standpoint but also as a predecessor to fatal enteric disease. Multiple enteric stresses and disease challenges may occur simultaneously in production environments. (10)

Infectious bursal disease, chicken infectious anemia,
Marek’s disease, and hemorrhagic enteritis of turkeys potentially impact secondary lymphoid tissues of
chickens and turkeys. It is common to have mild clinical coccidiosis in broilers during and immediately following the onset of acute bursal disease. Lymphocytolytic mycotoxins such as T-2 toxin and diacetoxyscirpenol rapidly deplete GALT (6).

(contd. below)
« Last Edit: Nov 30th, 2007, 09:06am by DL » User IP Logged

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xx Re: Related General info
« Reply #2 on: Jul 19th, 2007, 12:23pm »

(contd.)

DIGESTIVE PATHOGENS OF POULTRY
The digestive tract is compromised when the mucus
layer is degraded; epithelial cells are effaced or
destroyed, the vascular supply is interrupted, or the
immune system is compromised. The epithelial layer can be damaged by viruses, bacteria, fungi, myriad parasites, and toxins; reviewed by Moon,1997 (9). This section will focus on specific types of injury to intestinal epithelium.

Viruses:
Infection and replication of an enteric virus usually kills an epithelial cell. In contrast to bacteria, viruses do not produce toxins. Each of the intestinal viruses has a tropism for cells in a specific state of differentiation along the villus: crypts, on the tips and sides of the villus, or only on the tip,respectively. The severity of the clinical disease andthe course of the uncomplicated viral infection are a reflection of target cell injury. For a virus thatdestroys cells on the tip of the villus, the absorptive
function of the gut is lost and surviving epithelium
is secretory. Watery diarrhea occurs until the villi are repaired with mature functional cells on the tips.
A torovirus- like virus isolated from turkeys stimulates the enterocytes to release cytokines that interact with the immune system, and a series of reactions with the inflammatory response, and nerves in the wall of the intestine (Dr. Akbar Ali, personal communication). The result is increased fluid secretion in the gut that
overrides its absorptive capacity,
causing diarrhea and decreased digestive efficiency.

Bacteria:
Bacteria damage epithelium by producing toxins, attaching to the cell, and invading the cell(5). The host can ingest bacterial toxin in contaminated feed. Staphylococcus, Clostridium and Bacillus are possible producers of enterotoxin in feed.

Ingested bacteria can produce toxins as they multi-
ply in the gut. Escherichia coli, Clostridium perfrin-
gens, Clostridium colinum, and Campylobacter spp. produce enterotoxins that are polypeptides capable of causing diarrhea. Some enterotoxins increase fluid secretion and others are cytotoxic, causing cell lysis and death. Some E. coli attach and adhere to the surface of the enterocyte and secrete a toxin that disturbs the water regulation of the cell. This causes a net secretion of chloride, loss of water, and the development of diarrhea. Necrotic enteritis caused by Clostridium perfringens causes severe toxin-induced cell necrosis (death), mucosal destruction and death of the host.

Other bacteria proliferate, invade and destroy
intestinal epithelium. Certain E. coli attach and damage the microvilli, causing the release of cytokines,
inflammation, fluid secretion, and diarrhea. Enteroinvasive bacteria proliferate within cells after invasion, causing cell death and enabling cell-to-cell spread. Salmonella invades and passes through epithelial cells to invade to lymphatic and blood vessels, incites inflammation in the gut, and then disseminates to other organs.

Fungi and Mycotoxins:
Candida colonizes mainly the stratified squamous mucosa of the mouth, esophagus, and crop, and sometimes the gizzard lining (koilin). Fungal infections of the intestinal mucosa are not significant in poultry. Mycotoxins are significant and damage the muscosa and interfere with digestive functions. Trichothecene mycotoxins cause caustic injury to the tips of villi, and
radiomimetic injury to rapidly dividing crypt epithelium. Aflatoxin decreases bile secretion from the liver and bicarbonate secretion from the pancreas. Other toxins that influence digestion include fumonisins, sterigmatocystin, ochratoxin, and undefined toxins of Penicillium.

Protozoa and other Parasites:
Coccidia invade and destroy epithelial cells, and some damage the lamina propria. This results in increased mucus secretion, reduced absorption, hemorrhage and fluid leakage from damaged mucosa, and a dynamic
immune and inflammatory response. Coccidiosis
enhances the adherence of pathogenic bacteria, such as Clostridium perfringens and Salmonella typhimurium and decrease the adherence of nonpathogens such as Bacteroides vulgatus and Bifidobacterium thermophilum (2). The inflammatory response to nematodes brings a
greater involvement of mast cells and the mediators
of acute inflammation, which are also linked to neu-
rological responses (1).

The inflammatory response to nematodes brings a
greater involvement of mast cells and the mediators
of acute inflammation, which are also linked to neu-
rological responses (1). Toxic Injury. Oxidized, rancid fats produce free radicals (8) that cause sublethal injury to cells throughout the body, including gut epithelium. The most obvious clinical evidence of fat rancidity is vitamin E deficiency expressed as encephalomalacia.
Biogenic amines, generated by bacterial spoilage of
improperly handled fish and rendered substrates,
target gastroenteric tissues.

FEED PASSAGE AND DIARRHEA
Feed passage is undigested particles of feed in the
feces and represents a loss of digestive efficiency.The economic consequences involve feed conversion, growth, carcass yield, and cost of production.
Feed passage usually occurs with diarrhea, which is
characterized by increases in the mass of feces, the
frequency of fecal passage, and/or the fecal fluidity.
Feed passage represents a malabsorption or
maldigestion syndrome that shares many of the same causes as diarrhea. For the purposes of this discussion, four underlying mechanisms of diarrhea and feed passage will be examined, according to the scheme of Crawford, 1997 (5).

Secretory Diarrhea: This involves the excessive secretion of fluid from the intestinal mucosa, relative to the fluid absorption capacity of the intestine. This is caused by viruses that destroy mature enterocytes on the tips of the villus, leaving functional secretory enterocytes in the crypt and on the side of the villus. It is also caused by bacterial enterotoxins that affect mediators of intestinal electrolyte transport. In general, the mediators increase chloride secretion from the crypts and decreasing NaCl uptake from the tips of villi (1). As water follows these electrolytes, the net result is fluid overload in the lumen of the intestine.

Osmotic Diarrhea:
This involves excessive osmotic forces exerted by luminal solutes. Poultry diets high in salt are one cause, and some digestive problems associated antinutritional factors (non-starch polysaccharides, NSP) in barley, rye, and wheat, and other ingredients, reviewed by I ji, 1999 (7). These complex carbohydrates are resistant to digestive enzymes, create a viscous environment within the intestinal lumen, increase the mass of luminal
digesta, and produce moist sticky droppings.

Malabsorption:
This is the output of voluminous, bulky feces with increased osmolarity owing to unabsorbed nutrients and, in man, excessive fat. Digestion is inefficient due to either ineffective enzymes or a lack of enzymes. Defective absorption occurs with the loss of mature enterocytes and replacement by immature cells lacking full absorptive function. Increased fluid in the gut dilutes bile acid, impairing lipid absorption and allowing proliferation of bacteria (11).

Exudative disease:
This is characterized by blood or tissue debris from necrosis and inflammation, such as with severe coccidiosis, clinical salmonellosis, necrotic enteritis, or
histomoniasis. In this situation, the gut experiences severe insult involving the necrosis and loss of enterocytes, loss of fluid, electrolytes and plasma from the damaged mucosa, and inflammation. The host must contend with the escape of pathogens into the vascular system and dissemination to the liver. If the disease is not fatal, anorexia and diversion of nutrients for inflammation and repair will reduce growth and yield,
impair feed conversion, and increase the cost of pro-
duction.

REFERENCES:refer to article link.
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xx Re: COCCI
« Reply #3 on: Jul 25th, 2007, 12:53pm »

The impact of Coccidiosis on the intestines and visual signs in faecal content vary according to the species of cocci... in addition to the section specifically dealing with cocci read this EXCELLENT article in regards to its impact on intestinal health and visual clues in the faecal contents :
http://www.avian.uga.edu/documents/pip/2003/0903.pdf
(a few excerpts)
>>> ..."The two species that cause intestinal
hemorrhage and pullet death are E. tenella and E. necatrix.
E. tenella is also the species that causes bloody droppings, along with mortality; it is often the easiest
for flock supervisors to recognize due to the characteristic blood-filled ceca of dead pullets
.....
>>>"...Perhaps the more economicallyimportant coccidia species the world over for pullet and rooster
frame-size and body uniformity are those that do not cause death but have an impact on the bird’s
ability to absorb nutrients from feed.
The most commonly recognized are E. acervulina and E. maxima.
The signs of these two species are not as obvious, so their effects are often overlooked until it is too late..."
>>>(re: vaccine) "...Keep in mind that death and bloody droppings are not the only signs to watch for during this period of “vaccine reaction.” Reaction to E.
acervulina and E. maxima can affect the pullet’s ability to absorb vitamins, especially fat-soluble A, D, E
and K. This is one reason that rickets may develop and that an increase may be seen in leg problems around 4 weeks of age.
One solution is to routinely add vitamins to the pullets drinking water during the
vaccine reaction period...."
« Last Edit: Jul 25th, 2007, 1:08pm by DL » User IP Logged

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