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xx poo~ology
« Thread started on: Sep 17th, 2006, 02:32am »

This information is an AID in diagnosis...many things will affect the color of droppings and the consistency and other general symptoms and history must be considered when attempting to narrow down what is wrong with your birds


Info references specific to poo to help identify illness ...WE ARE LOOKING FOR PHOTOS TO ILLUSTRATE THESE DESCRIPTIONS...YOU CAN POST IN THE PHOTO SECTION THIS CATEGORY OR SEND THEM TO DL AND YOUR ANONYMITY WILL BE ASSURED! grin

http://www.ahc.umn.edu/rar/MNAALAS/Birdcare.html
The color is influenced by the bird's diet. Normal droppings are formed into a coil, reflecting the size and diameter of the intestine. Along with the fecal portion is a variable amount of uric acid or urate ('whitewash') and urine ('water'). The urates are usually in a blob or mixed in with the feces and should be white or beige.
A bird has diarrhea when the fecal portion of the dropping lacks form ('pea soup'). Diarrhea is not very common in birds. A dropping with a normal fecal portion but a large amount of urine around it represents a watery dropping (polyuria), not diarrhea! All diarrheic droppings appear loose, but not all loose or watery droppings constitute diarrhea. This Is a very important distinction. Polyuric droppings may indicate disease (diabetes or kidney disease), but more often they result from increased water consumption or consumption of large amounts of fleshy fruits and vegetables.


http://www.ncsu.edu/project/cvm_avian/notes.html
4. Urine
a. In most birds urine is present as both a watery portion and a solid paste (urates). Desert adapted species, such as budgies, parakeets and cockatiels pass more formed urates. More tropical and frugivorous species, such as Amazon parrots and macaws, pass more watery droppings.
b. Causes of polyuria include excitement, anxiety, consumption of fruits and vegetables, renal disease, increased water consumption (polydypsia), etc.
c. Causes of bloody urine include renal disease, lead poisoning, and bleeding in the cloaca.
d. Causes of green colored urine (biliverdinuria) include liver disease (especially common with psittacosis), and bile staining from feces.
e. Yellow urine is rare. It is usually caused by severe, rapid liver disease


DIARREA> consider rotavirus (see more articles below)

http://www.heidihoefer.com/pages/birds/avian_blood_test.htm
BASIC AVIAN CLINICAL PATHOLOGY-Heidi L. Hoefer, DVM, Dip ABVP-Avian Practice
(excerpt)
Bilirubin testing does not have diagnostic value in most species. This means that birds do not become jaundiced (skin and eyes turning yellow). Birds lack the enzyme which converts the bile pigment biliverdin into bilirubin. Birds with liver disease will therefore have excess levels of biliverdin. Biliverdin does not accumulate in tissues; it is rapidly excreted in the urine. Green/yellow urates represents biliverdin in the urine and can be loosely considered the bird equivalent of jaundice. Birds do not become "yellow" from jaundice like people or other small companion mammals.

http://www.ext.nodak.edu/extpubs/ansci/swine/eb73w.htm#Feeding
Feed Additives
Poultry, particularly growing chickens, are sensitive to the beta-glucans in barley. Beta-glucans form gels in the digestive tract of birds that are not broken down because of the lack of appropriate enzymes and the rapid rate of passage in poultry. [b]Without addition of beta-glucanases to the feed, barley-based diets have been associated with reduced levels of available energy and with wet droppings, pasty vents, and wet litter
.
However, adding beta-glucanases to diets fed to poultry can effectively eliminate the problems with wet, gummy droppings while increasing the availability of dietary energy and reducing the effective variation in energy content.
NOTE:
More info on the above in the NUTRITION category in the ADDITVES thread-DL

http://www.wingwise.com/droppings.htm
ABNORMAL DROPPINGS: This excellent article offers some excellent general descriptions of ABNORMAL DROPPINGS > ( WATERY DROPPINGS (an increase in urine often cofused with diarrhea)as opposed to LOOSE STOOL (or true diaarhea)...short and quick reference.

This reference guide to droppings from MSSTATE symptom chart:
http://www.msstate.edu/dept/poultry/diagext.htm#drop
DroppingsSymptom............Possible Cause

Profuse................. Enteritis; excess roughage in diet
Bloody.................. Cecal coccidiosis; Newcastle disease
Green................... Feed intake low; bile not diluted
Sulfur yellow......... Blackhead (MAINLY a problem in TURKEYS-chickens will frequently be infected and show no signs of the disease > please read here:
http://dlhunicorn.conforums.com/index.cgi?board=articles&action=display&num=1158931641&start=0#1158931641
Light yellow or yellowish-green... Fowl typhoid; fowl cholera
Foamy................... Intestinal parasites (protozoa)

http://www.petplace.com/article-printer-friendly.aspx?id=502
Lack of feces in the dropping. These droppings appear as only urates and urine. When they appear following an episode of diarrhea, it may indicate an obstruction in the intestinal tract.

http://edis.ifas.ufl.edu/PS044
watery,streaked with urates......Ulcerative enteritis
diarrea/pasted vent.....fowlcholera/pullorum/necrotic enteritis/staphylococcus

http://www.unley.sa.gov.au/webdata/resources/files/poultryguide1.pdf#search='Droppings%20mustard%20%20poultry'
"Internal Parasites
Birds appearing listless, pale in the face, losing condition and producing mustard-coloured
droppings
can be suspected as having worms"

http://gallus.tamu.edu/workshop%20proceedings/Texas%20Broiler%20Symposium%202006/Cervantes%20Phibro%20-%20RSS%20-%202006%20TBS.pdf#search='helicopter%20stunting%20poultry'
WATERY YELLOW TO ORANGE DROPPINGS and/or CLOACAL PASTING > Malabsorption Syndrome ((ILLUSTRATED WITH PHOTOS OF SYMPTOMS)

http://www3.sympatico.ca/davehansen/digest.html
Gizzard erosion can be suspected in vague illnesses accompanied by indigestion and loose, greenish, mucoid and intermittently bloodstained droppings. Distension and flabbiness of the gizzard musculature occurs mostly in debilitated birds, specially when the exit into the small intestine is impacted with hard fibrous ingesta. Such an obstruction soon causes depression, loss of appetite, and soft droppings which rapidly become smaller in amount, and are passed progressively less frequently. If the condition is not relieved, death can result from toxaemia even before the effect of starvation is felt. Birds affected in this way are generally those kept in planted aviaries or where little food and an abundance of coarse fibrous material is present. Liquid paraffin given slowly by mouth in liberal amounts using a dropper (10-20 drops per 100 gram body weight) is the most effective and safest treatment. This tends to ease and soften the obstruction, and soothe the mucous membrane of the gut. Diagnosis is difficult and has to be based on careful observation, and consideration of all the circumstances.

http://www.addl.purdue.edu/newsletters/2003/fall/avchlamid.htm
Avian Chlamydiosis
When clinical signs occur in birds, they include yellow-to-greenish or watery gray droppings,

CHRONIC BROWN/WATERY DROPPINGS:

AVIAN INTESTINAL SPIROCHATOSIS
http://www.octagon-services.co.uk/articles/poultry/AIS.htm
EXCERPT:
causes chronic brown watery droppings...previous studies have shown that 70% of flocks have spirochaetes but only 30% have pathogenic or disease-causing strains."
http://www.octagon-services.co.uk/poultryposters/WVPA2005.htm
excerpt:
B.pilosicoli is potentially a serious chronic pathogen...faecl contact is the major factor in the spread of the infection...studies show that tiamulin is particularly effectivce as treatment .
http://www.bioagrimix.com/haccp/html/tiamulin.htm
Info on TIAMULIN
http://www.wattnet.com/Library/ViewLib.cfm?PG=1&ST=0&libNum=1100
(MORE ON TREATMENT Spirochaetes)
Both the tiamulin and lincomycin treatments were effective in removing the BP infection, while untreated infected birds remained infected. The use of zinc bacitracin in flocks with avian intestinal spirachaetosis (AIS) caused by BP should be avoided. However, if the infection is caused by B. intermedia, zinc bacitracin is effective in reducing colonization. This emphasizes the importance of differential diagnosis between the two species of spirochaetes in flocks with AIS.
http://search.yahoo.com/search?ei=utf-8&fr=slv8-msgr&p=zink%20Bacitracin%20veterinary

http://www.rirdc.gov.au/comp02/eggs1.html#UMU-23J
(excerpt)
"This project has improved the Australian capacity to rapidly identify and type intestinal spirochaetes from chickens. It has demonstrated that strains of the various spirochaete species vary in their susceptibility to antimicrobials, but in general there is little antimicrobial resistance present. Care should be taken with the use of zinc bacitracin, as it may predispose chickens to infections with B. pilosicoli. Both tiamulin and lincomycin are effective in treating intestinal spirochaete infections, but addition of dietary enzyme with xylanase activity also can reduce colonisation with B. intermedia."
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xx Re: poo~ology
« Reply #1 on: Dec 11th, 2006, 06:11am »

http://www.omafra.gov.on.ca/english/livestock/poultry/facts/flushing.htm
(excerpt)
"...A flushing problem can be described as a diuresis, a diarrhea, or a combination of both conditions. Diuresis is excessive urination as evidence of the excretion of much clear fluid or white uric acid with the fecal dropping. Diuresis can result from feeding a diet containing too much salt or protein nitrogen. Diuresis is usually a normal mechanism of eliminating excess electrolytes, body nitrogen, and toxins by increasing water consumption and flushing these compounds out of the body through the kidneys. Diarrhea is excessive excretion of fluids from the gastrointestinal tract. This condition is more complex than diuresis because it can be caused by many different factors. Diarrhea can be caused by one of three types of agents: infectious, noninfectious osmotic, and noninfectious nonosmotic.

Infectious agents are microorganisms that either irritate or damage the absorptive intestinal lining (eg coccidia, c.albicans, rotavirus), or excrete toxins that interfere with the normal electrolyte and water exchange in intestinal cells (eg E.coli, clostridium, cholera, salmonella).

Noninfectious osmotic agents cause feed intolerance, maldigestion, or malabsorption. These agents are osmotically active in the but because birds do not produce the appropriate enzymes to digest and absorb these compounds. In osmotic diarrhea, an excess amount of water is retained in the lumen of the gut and gut motility increases to eliminate the osmotically active compounds, expelling other feed components that would otherwise be digested. Examples of osmotic agents that cause diarrhea include excess levels of dietary magnesium (carbonate, sulfate, and oxide forms), and non-starch carbohydrates (eg raffinose in soybean meal, lactose in whey, pentosans in small grains, or sucrose).

Noninfectious nonosmotic agents are chemical, physical, or physiological in nature. Some pharmaceutical chemicals and toxins cause diarrhea in ways similar to the toxins produced by E.coli and cholera. An excessive amount of some ioniphore coccidiostats can cause a flushing response unless dietary electrolytes are adjusted appropriately. The biogenic amines, histamine and tyramine, can cause a diarrhea if they exceed 100 ppm in the diet. These compounds are often found in protein by-product meals produced from spoiled fish or animal by-products. Mycotoxins, such as citronen, can cause severe flushing even after on small dose in the feed. Physical irritations in the gut by tumors or parasites (eg ascarids) will cause diarrhea. Some types of physical or physiological stress cause acute or chronic diarrhea. Some acute stressors increase gut motlity or alter intracellular messengers that ultimately reduce the absorption of sodium, chloride, water, and other nutrients from the lumen of the gut. Some chronic stressors increases the birds’ susceptibility to enteric pathogens. Stressors that can cause flushing include moving or handling turkeys, extremes in environmental temperature, vaccinations, and drastic changes in diet formulation. Therefore, management practices can have a significant impact on the manifestation of a flushing problem.

The flushing syndrome is often a seasonal problem and is observed most prevalently during spring and fall. These seasons typically have warm days and cool nights, so a consistent temperature in a facility is difficult to maintain. Temperature stress (either heat stress of chilling) can predispose a poultry flock to flush (Ferket 1994). Moreover, the seasonal effects of flushing in 10- to 16-week old turkeys may be related to an intestinal bloom of coccidiosis or other organisms. Since coccidiostats are withdrawn from the feed by the time the birds are 8 weeks of age, the birds may shed a ‘spike’ in oocysts from 11 to 17 weeks (Ferket 1995). This oocyst spike is often associated with some fecal looseness. However, maintaining birds on a coccidiostat-medicated feed most often does not prevent an episode of flushing.

Regardless of the predisposing factors, flushing is generally caused by a disruption of chloride and/or sodium transport by enterocytes in the intestine or kidney. This results in hyperosmolarity in the lumen of the intestine or excessive fluid excretion through the kidneys. This basic physiological response can be modified by a number of compounds with varying degrees of success. High dietary fiber (10% crude fiber) from oat hulls can improve gut motility and absorb excess fluids, but the high degree of nutrient dilution will reduce feed conversion. Colloidal clay compounds may be helpful if dietary inclusion rate is high enough (2.5% or more). Coccidiostatic ioniphores and growth promotant antibiotics may alleviate a flushing problem if it is due to a bloom in infectious microorganisms (coccidia, cryptospiridia, E.coli, clostridium). Electrolyte supplementation of drinking water may temporarily alleviate a flushing problem by helping the birds regain their electrolyte balance. Finally, flushing can sometimes be alleviated supplementing feed or drinking water with specific osmolytes like betaine....."

http://www.poultry-health.com/fora/inthelth/hoerr01.htm
INTESTINAL INTEGRITY AND THE IMPACT OF LOSING IT
(excerpt)
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, involving the mucosal epithelial cells, immune and mesenchymal cells, enteric neurons, and hormonal and central nervous system. In general, the mediators act by increasing chloride secretion from the crypts and decreasing NaCl uptake from the tips of villi. 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, such as occurs with diets formulated with certain lots of bakery byproduct meal. Osmotic factors may be involved in digestive problems associated with antinutritional factors (non-starch polysaccharides, NSP) in barley, rye, and wheat, and other ingredients, reviewed by Iji, 1999. These complex carbohydrates, typically hexoses and pentoses, 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. It occurs because of defective intraluminal digestion due to ineffective enzymes or a lack of enzymes. Defective absorption could occur with the loss of mature enterocytes that have been replaced with immature cells lacking full absorptive function. Again, NSP may be involved with malabsorption because the gelatinous luminal content blocks the access of enzymes to otherwise digestible nutrients. This problem is also associated with increased mitotic activity and increased crypt depth in the gut mucosa, suggestive of an increased turnover of enterocytes, and a relative increase in secretory enterocytes or a decrease of mature enterocytes. Bile acid concentration within the digesta is also diluted, possibly impairing lipid absorption. The decreased bile concentration is associated with increases in luminal aerobic and anaerobic bacteria.

Exudative Diseases: This is characterized by frequent defecation of variable volume, but with the presence of blood or detritus from necrosis and inflammation. In chickens, this could be observed by severe coccidiosis, clinical salmonellosis, necrotic enteritis, or histomoniasis. In this situation, the gut experiences severe insult involving the necrosis and loss of enterocytes, possible loss of fluid, electrolytes and plasma from the damaged mucosa, and a major inflammatory response. The host must contend with the escape of the primary or secondary pathogens into the vascular system and dissemination to the liver, and possibly beyond. 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 production.



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xx Re: more on ROTAVIRUS (diarrea)
« Reply #2 on: Jun 28th, 2007, 5:59pm »

http://www.sandhillvet.demon.co.uk/rotavirus.htm
(excerpt) : ...."Rotavirus infection can be seen in birds of all ages but its effects are most dramatically seen in young birds between 3 and 14 days old. The infection affects the gut resulting in wet droppings, the birds are rapidly depressed and vent pecking is common. Affected birds often eat the litter and may die because of the damage done to the gut by the virus or by gizzard impaction. A significant number of the birds that survive the infection become stunted. Although disease and deaths are most commonly seen in younger birds all ages can be affected. In the older birds other viruses, in addition to Rotavirus, are often isolated from scouring birds. Many birds suffer from sub clinical disease so the absence of clinical disease does not ensure that Rotavirus is not present within a flock. Falls in egg production due to Rotavirus infection have not been recorded in game birds but have been seen under experimental conditions in chickens and turkeys....
.....There is no specific treatment for Rotavirus infection. Affected birds need to be given re-hydration salts via the water to prevent dehydration and using a water disinfectant that is effective against viruses E.g. SWC V3 or Virkon-S, will prevent birds being infected from a contaminated water supply. In some cases antibiotics may be effective against any secondary bacterial infections but will have no direct impact on the course of the Rotavirus infection......."

http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1516-635X2006000300009&lng=en&nrm=iso&tlng=en
..."In poultry, both in layer hens and broilers, rotavirus has already been established as the etiological agent of enteritis, originated from viral replication in intestinal epithelium, resulting in diarrhea and nutrient malabsorption (Snodgrass et al., 1986), which causes an increase in feed conversion ratio and large economic losses to poultry industry (Barnes, 1997)....In addition, predisposing factors, such as diseases attributed to other pathogens like coronaviruses, reoviruses, enteroviruses, and adenoviruses (Dea & Tijssen, 1988; Hayhow & Saif, 1993); bacteria such as Escherichia coli and Salmonella spp (Porter, 1998); physiological stress; and toxic and environmental factors, such as temperature, ventilation, and husbandry, may directly interfere in the resolution of the disease after rotavirus infection. However, the importance of these asymptomatic chickens is that they are constantly shedding the virus, without being clinically detected, and disseminate the virus to susceptible chickens....."

http://www.isrvma.org/article/59_3_4.htm
..."To summarize, rotavirus was found by various methods in poultry and in a lesser extent in pet birds, while in poultry it was involved in a syndrome of retarded growth complicated with enteritis and diarrhea. A good correlation was revealed between the different methods of rotavirus diagnosis...."

http://www.ansci.cornell.edu/poultry/ppjan01.pdf
...."...Furthermore, darkling beetles have been shown to
transmit several other infectious agents including Salmonella, Aspergillus spp., Escherichia coli,
Bacillus spp., Streptococcus spp., Reovirus, Rotavirus, Eimeria (coccidiosis), and tapeworms....."









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xx Re: Diarrea due to CRYTOSPORIDUM
« Reply #3 on: Jun 30th, 2007, 8:26pm »

http://parasitology.informatik.uni-wuerzburg.de/login/n/h/2113.html
(excerpt)
"...Species of the genus Cryptosporidium are coccidian parasites that infect epithelial cells (extracytoplasmic) of the intestinal and respiratory tract of vertebrates (see Opportunistic Infections). Although immunocompetent hosts show no or only mild clinical signs after Cryptosporidium infections particularly young birds under stress may suffer from life-threatening watery diarrhea, or severe respiratory symptoms. Cryptosporidiosis in chickens, turkeys, quail, and pheasants is usually manifest as respiratory disease caused predominantly by C. baileyi or as enteritic disease (small intestine) caused by C. baileyi and C. meleagridis. The severity of infection depends on the immunocompetence of the host. Infections are due to aerosol transmission of infective oocysts coughed up by carrier (seeder) birds, or may be transmitted by feed or water supplies containing sporulated oocysts derived from feces of infected birds. Clinical signs in birds are coughing, mucoid discharge, dyspnoe, diarrhea, dehydration, weakness and weight loss.
Causal therapy and chemoprophylaxis of chicken cryptosporidiosis with ionophorous antibiotics is problematic. Many approaches to anticryptosporidial efficacy of commercial drugs have failed to improve symptoms in birds suffering from Cryptosporidium infections. Several other anticoccidials as sulfonamides, lasalocid sodium, halofuginone, and decoquinate, or other antibiotics (e.g., paromomycin) available as additives in-feed (Table 1), or as other dosage forms for oral administration have proved to be insufficiently effective in controlling or even eradicating Cryptosporidium infection in birds. The drugs may exhibit positive short-term effects such as improvement of watery diarrhea and reduction of oocyst output in feces due to their `static' rather than `cidal' action on cryptosporidia."

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xx Water Problems and Sodium/Salt
« Reply #4 on: Nov 9th, 2007, 08:46am »

http://www.canadianpoultry.ca/chapter_ii.htm
(excerpt)
"...Water Problems

Water containing physical particles or dissolved mineral material may interfere with automatic drinkers. Particulate material and iron may be removed by a sand filter and settling tank but dissolved minerals and algae growth in the system are more difficult to control. Regular cleaning and flushing may be necessary. Copper sulfate solution may control fungi and algae growth, but it can be toxic for poultry.

Poultry may be poisoned by minerals or chemicals in the water. The sodium in saline (NaCl) water is the most frequent problem. Young birds are very susceptible to sodium toxicity. Sodium above 500 ppm (0.05%) in the drinking water may cause death in young chickens and turkeys depending on the sodium level in the feed. The young birds usually die from oedema and ascites syndrome. Wet droppings or diarrhea would also occur. Salt in the feed can be reduced to avoid disease from salt in the water up to about 1000 ppm (0.1%) of sodium in the water. Saline water above 1000 ppm should not be used for broilers up to 21 days of age even if no salt is added to the feed. High levels of sodium will kill adult chickens by causing diarrhea and dehydration.

Sodium may be present in water as sodium sulfate (NaSO4) or sodium bicarbonate (NaHCO3). Sulfate may be present as magnesium sulfate (MgSO4) and cause diarrhea and death. All sources of sodium in the feed, whether added as salt or present in the feed ingredients, (particularly animal protein) and water are additive in causing sodium toxicity. If sodium is too high in the feed it will cause disease as it does in the water. Sodium, however, is an essential nutrient and poultry require some sodium to grow and produce eggs.
Nitrate in feed and water may be toxic at high levels but can reduce growth at 50 ppm in water. A variety of other naturally occurring minerals and chemicals may be present in water and may cause problems. Surface water may be contaminated by farm pesticides, fertilizer or by industrial chemicals...."

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xx Enteric Disease
« Reply #5 on: Nov 30th, 2007, 09:07am »

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 ....."
(refer to link for the rest of the article)

http://www.poultry-health.com/fora/inthelth/pattison02.pdf
"....CLINICAL SIGNS:
....is characterised by diarrhoea with the production of abnormally wet droppings. The faeces usually have a larger volume, are pale or viscous with an excess of
fluid around them. The use of litter boxes (described elsewhere) can be helpful in recognising the early stages of the condition... the onset of enteritis ..."
« Last Edit: Jan 17th, 2008, 04:11am by DL » User IP Logged

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xx Enteritis/DYSBACTERIOSIS
« Reply #6 on: Jan 11th, 2008, 02:26am »

http://www.poultry-health.com/fora/inthelth/pattison02.pdf
Mark Pattison,
Ph.D., D.P.M.P., M.R.C.V.S.
(excerpt:
"....CLINICAL SIGNS
....is characterised by diarrhoea with the production of abnormally wet droppings.
The faeces usually have a larger volume, are pale or viscous with an excess of fluid around them. The use of litter boxes (described elsewhere) can be helpful
in recognising the early stages of the condition. At the onset of enteritis there is normally an increase in water intake but sometimes there may actually be a reduction in water consumption. Sometimes birds are huddled with ruffled feathers but this is not a consistent feature. Often selective feeding is reported where birds ‘flick’ feed or whole grains out of the pans onto the litter......
The end result is a reduction in growth and an adverse effect on feed conversion. There are often secondary effects such as an increase in leg problems due to osteomyelitis.

Post mortem features
.... The signs described above are similar for quite a broad range of pathological lesions. The most severe lesions are seen in necrotic enteritis, but these occur less frequently now, as most cases of enteritis occur without mortality.
Where death occurs, the birds are usually in good condition with food in the crop and gizzard indicating that death has been sudden. There is often a
greenish tinge on the abdomen and the intestinal tract is swollen and flaccid, with a thin wall. There are usually focal areas of ulceration or larger patches of necrosis, which ultimately coalesce resulting in sloughing of the intestinal lining.It is much more common to investigate cases of wet litter or enteritis where
no mortality has occurred. .....
.......Where the enteritis is mild the wall of the intestine maybe thinned, ballooned or slightly inflamed. The gut contents may be full of bubbles, watery or contain viscous orange-coloured mucus. Occasionally the contents appear yoghurt-like and the presence of whole grains of wheat is indicative that digestion is not occurring properly. This condition is often referred to as dysbacteriosis.
In many cases, there is no enteritis and the intestine contains an abnormal amount of fluid, which is clear and like water. The caecae may be dilated.
It is important to distinguish this condition from malabsorption syndrome which can produce similar clinical signs, in particular selective feeding behaviour. Also the possibility of coccidiosis either at a clinical or sub-clinical level must be considered.

Prevention and Treatment
Various strategies have been employed within one integration with varying degrees of success. These regimes have to be changed regularly because, not
surprisingly, the antibiotics become less effective over time......"
(refer to link for details of treatments and slide presentation)


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xx Another condition w/"whitish diarrea"
« Reply #7 on: Jan 17th, 2008, 04:16am »

http://ourvetonline.com/disease_category_info.php?discatid=213&ani=Birds
(some excerpts though I highly recommend you read the entire easy-to-read article on this condition from a vet:
"INFECTIOUS BURSAL DISEASE (GUMBORO) << Back


Infectious bursal disease is an acute, highly contagious viral disease of young chickens. It is most often found in highly concentrated poultry producing areas. It causes marked morbidity and mortality in affected flocks. Although the disease causes severe losses, its affect on reducing the bird's ability to develop immunity to other diseases may be the most serious effect produced by this disease....................

.....Birds have ruffled feathers, a slight tremor at onset of the disease, strained defecation, loss of appetite and are dehydrated. Affected birds have a tendency to sit and when forced to move, have an unsteady gait. Vent picking is common and a whitish diarrhea frequently develops. A sudden rise in body temperature is followed by a drop to subnormal temperature, prostration and death. Birds surviving the initial infection will recover rapidly within two weeks.............
...... indiscriminate medication with certain drugs may severely aggravate mortality....."
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