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xx Other Protozoa and Disease
« Thread started on: Sep 22nd, 2006, 08:27am »

OVERVIEW Protozoan Disease

Avian Malaria
"Clinical Signs
Infected birds are often weak, depressed, dyspneic and anorexic. Birds may have abdominal protrusion (due to hepatosplenomegaly) and ocular hemorrhage. Central nervous system ischemia may occur with P. gallinaceum due to occlusion of capillaries by exoerythrocytic schizonts in heavily parasitized endothelial cells. Hemolytic anemia, often accompanied by leukocytosis, lymphocytosis, and hemoglobinuria, may also be present. Coma and death may occur quickly when the parasite burden is high. "

MSU article on PROTOZOAL DISEASE (easy to read summaries-excerpt below):
Blackhead (Histomoniasis, Enterohepatitis)

Blackhead is an acute or chronic protozoan disease of fowl, primarily affecting the cecae and liver. The disease is present wherever poultry are raised. Blackhead is one of the critical diseases of growing turkeys and game birds. It may cause stunted growth, poor feed utilization and death. It is of lesser economic importance in chickens since they are more resistant, but the incidence in chickens apparently is increasing.
Blackhead is caused by a protozoan parasite called Histomonas meleagridis. The organism in passed in the fecal material of infected birds. In many instances, the organism is shed within the eggs of the cecal worm of chickens, turkeys and game birds. Free-living blackhead organisms do not survive long in nature, but those in cecal worm eggs may survive for years. Therefore, most blackhead transmission is considered due to ingesting infected cecal worm eggs. Transmission may also occur by the earthworm.

Chickens are frequently infected without showing signs of the disease. These chickens may shed enormous numbers of blackhead organisms, many of which are protected by cecal worm eggs. Outbreaks in turkeys can often be traced to direct or indirect contact with ranges, houses or equipment previously used by chickens. Free-flying birds may also contribute to an infection.

Most blackhead losses occur in young birds (six to sixteen weeks). Among the symptoms are loss of appetite, increased thirst, droopiness, drowsiness, darkening of the facial regions and diarrhea. Morbidity and mortality are variable, but mortality seldom exceeds fifteen percent; however, it may approach one-hundred percent in uncontrolled turkey outbreaks. Losses are usually low in chickens.

Lesions of uncomplicated blackhead are confined to the cecae and liver, thus the reason for the synonymous term, enterohepatitis. The cecae are ballooned and walls may be thickened, necrotic and ulcerated. Caseous (cheesy) cores within the cecae may be blood tinged. Peritonitis may be present if ulcers have perforated the ceca walls. Livers are swollen and display circular depressed areas of necrosis about one-half inch in diameter. Smaller lesions coalesce to form larger ones. Lesions are yellowish to yellow-green and extend deeply into the underlying liver tissue. Healing lesions may resemble those seen in visceral leukosis.

Blackhead diagnosis is made readily on the basis of the lesions. Atypical forms, particularly in chickens, must be differentiated from cecal coccidiosis and Salmonella infections in particular. Medications may interfere with atypical lesions. Laboratory tests may be required for positive diagnosis in such cases.

Good management practices can do much to control the blackhead problem. Do not keep birds of different species on the same premises. Do not range turkeys on ground previously used by chickens unless several years have elapsed. Rotate ranges periodically if possible. Cecal worm control is necessary to reduce blackhead incidence. Wire or slatted floors reduce exposure.

Good management is the only effective method of preventing this disease since many of the effective drugs used in past years are no longer available commercially. Drugs that reduce the presence of cecal worms, and thus reduce the infection rate, are available but do not have an effect on the Histomonas organism. Refer to the cecal worm section for recommended control practices.

Hexamitiasis (Infectious Catarrhal Enteritis)

Hexamitiasis is an acute infectious disease of turkeys, quail, ducks, chukar partridges and pigeons. Heavy losses have been reported in one outbreak in ring-necked pheasants. Chickens apparently are not affected.
Hexamitiasis is a problem in every commercial turkey-producing area. It may be a major problem in localized areas during a particular year, followed by one or more years in which incidence is low.

Hexamitiasis is caused by a one-celled parasite of the genus Hexamita. Hexamita meleagridis is the cause in turkeys; in pigeons it is Hexamita columbae. Experimentally, the Hexamita of turkeys can be transmitted to young quail, chicks and ducklings, and that of quail and partridges can be transmitted to poults. However, poults cannot be infected with the organism isolated from pigeons.

This disease is found primarily in young birds, and outbreaks seldom occur in poults past ten or eleven weeks. Losses are most severe in birds three to five weeks old. Apparently, resistance develops rapidly with increasing age, regardless of previous exposure.

The primary infection source is droppings from carrier birds. About a third of recovered birds become carriers. Most outbreaks result from a buildup of organisms through several broods of poults, making exposure of the following brood overwhelming. Indirect transmission may result from fecal material carried from one location to another on shoes or equipment. Free-flying birds also may be carriers.

Primary symptoms are listlessness and foamy or watery diarrhea with rapid weight loss due to the dehydrating effect. Birds often huddle together near the heat source and cry or "chirp" constantly as though in pain. Convulsions due to lowered blood sugar levels shortly precede death. Affected birds suffer losses in weight and survivors remain stunted.

Dehydration and emaciation are the principal gross lesions. Muscles are dark and dry. The intestine usually appears to have lost muscle-tone. Intestinal contents are usually thin and watery, or may contain mucus.

Diagnosis depends upon history, symptoms and microscopic examination of intestinal contents. A definite diagnosis cannot be made unless typical flagellated organisms can be detected in intestinal contents of the duodenum. Most flagellate organisms in the cecae are not disease producers.


(see below)
« Last Edit: Apr 4th, 2007, 04:44am by DL » User IP Logged


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xx Re: TRICHOMONASIS ( sometimes called "canker")
« Reply #1 on: Nov 14th, 2006, 08:51am »

Mainly called canker in pigeons but referred to as trichomoniasis in fowl (it is often reported in the poultry literature as being somewhat uncommon in chickens however the backyard flock will experience this more often and it is often confused with "sour crop" and needs to be differentiated also from vitamin A deficiency and Candidiasis (thrush/yeast) and wet pox ... :
"White plaques in the mouth, esophagus, or crop may be caused by capillaria worms, yeast infection (candidiasis, moniliasis), or possibly trichomoniasis or vitamin A deficiency, but most frequently by fowl pox (wet form). White plaques beside the tongue in the mouth are common in hens and turkey breeders and may be caused by mycotoxin or low humidity. Vomitoxin may produce similar lesions in young chickens and turkeys."

".....Clinical signs:
.... include lowered feed consumption, spitting up of feed, high mortality, listless, ruffled feathers and emaciation.... A large crop filled with fluid, difficulty in swallowing, stretching of neck, drooling greenish to yellowish fluid. Diarrhoea (yellow and watery) and a drop in egg production can occur.....
Dimetridazole (0.05%), ipronidizole and nitrasone and effective treatments."

TRICHOMONIASIS (excerpt below)
How to Know When Birds are Infected
In acute cases, there may be little indication that the bird is infected, and death may occur quite suddenly. In other cases, infected pigeon squabs may stop feeding, lose weight, look ruffled and dull, and be unable to stand or maintain their balance.

Diarrhea may also occur. Death may occur within three weeks of infection. Greenish fluid or cheesy material may accumulate in the mouth and crop, and this material may exude from the beak. A pendulous crop may develop in turkey poults and chickens.

How to Know if Birds are Infected with T. gallinae
Characteristic yellowish-white nodules in the oral cavity, esophagus and crop strongly suggest trichomoniasis. The infection is confirmed by finding the organism during microscopic examination of the greenish fluids, cheesy material or the lesion

Here is what the MERCK had to say about it:
Trichomoniasis in domestic fowl, pigeons, doves, and hawks is characterized, in most cases, by caseous accumulations in the throat and usually by weight loss. It has been termed “canker,” “roup,” and, in hawks, “frounce.”
The causative organism is Trichomonas gallinae , a flagellated protozoan that lives in the sinuses, mouth, throat, esophagus, and other organs. It is more prevalent among domestic pigeons and wild doves than among domestic fowl, although severe outbreaks have been reported in chickens and turkeys. Some strains of T gallinae cause high mortality in pigeons and doves. Hawks may become diseased after eating infected birds and commonly show liver lesions, with or without throat involvement. Pigeons and doves transmit the infection to their offspring in contaminated pigeon milk. Contaminated water is probably the most important source of infection for chickens and turkeys.
Clinical Findings:
Trichomoniasis, pigeon
The disease course is rapid. The first lesions appear as small, yellowish areas on the oral mucosa. They grow rapidly and coalesce to form masses that frequently completely block the esophagus and may prevent the bird from closing its mouth. Much fluid may accumulate in the mouth. There is a watery ocular discharge and, in more advanced stages, exudate about the eyes that may result in blindness. Birds lose weight rapidly, become weak and listless, and sometimes die within 8-10 days. In chronic infections, birds appear healthy, although trichomonads can usually be demonstrated in scrapings from the mucous membranes of the throat.
Lesions: The bird may be riddled with caseous, necrotic foci. The mouth and esophagus contain a mass of necrotic material that may extend into the skull and sometimes through the surrounding tissues of the neck to involve the skin. In the esophagus and crop, the lesions may be yellow, rounded, raised areas, with a central conical caseous spur, often referred to as “yellow buttons.” The crop may be covered by a yellowish, diphtheritic membrane that may extend to the proventriculus. The gizzard and intestine are not involved. Lesions of internal organs are most frequent in the liver; they vary from a few small, yellow areas of necrosis to almost complete replacement of liver tissue by caseous necrotic debris. Adhesions and involvement of other internal organs appear to be contact extensions of the liver lesions.

Lesions of T gallinae infection are characteristic but not pathognomonic; those of pox and other infections can be similar. Diagnosis should be confirmed by microscopic examination of a smear of mucus or fluid from the throat to demonstrate the presence of trichomonads. Trichomonads can be cultured easily in various artificial media such as 0.2% Loeffler’s dried blood serum in Ringer’s solution or a 2% solution of pigeon serum in isotonic salt solution. Good growth is obtained at 98.6°F (37°C). Antibiotics may be used to reduce bacterial contamination.

Because T gallinae infection in pigeons is so readily transmitted from parent to offspring in the normal feeding process, chronically infected birds should be separated from breeding birds. In pigeons, recovery from infection with a less virulent strain of T gallinae appears to provide some protection against subsequent attack by a more virulent strain. Successful treatments include metronidazole (60 mg/kg body wt) and dimetridazole (50 mg/kg body wt, PO; or in the drinking water at 0.05% for 5-6 days). Neither of these drugs is approved for use in birds in the USA."

Parasites of the Esophagus and Crop in Birds-CH 13
« Last Edit: Jul 22nd, 2007, 3:16pm by DL » User IP Logged


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xx Re: Avian Malaria
« Reply #2 on: Jan 8th, 2010, 04:04am »

"...Many birds can serve as a definitive host for these parasites. Plasmodium can be pathogenic to penguins, domestic poultry, ducks, canaries, falcons, and pigeons, but is most commonly carried asymptomatically by passerine birds. Avian malaria has a worldwide distribution and is of great economic significance is to the poultry industry. Organisms such as P. gallinaceum, P. juxtanucleare and P. durae may cause up to 90% mortality in poultry. Incidentally, birds with avian malaria have been used as model systems for studying the pathogenesis and treatment of malaria in humans...
...Affected flocks can be treated with Chloroquine (5-10mg/kg) potentiated with primaquine (0.3mg/kg). Chloroquine can also be added to the drinking water at a dose of 250mg/120ml. Grape or orange juice may be needed to override the bitter taste of the medication. Quinacrine at a dose of 1.6 mg/kg given IM for 5 days is another treatment possibility. Additional treatments include sulfonamides combined with trimethoprim, pyrimethamine, and chlorguanil. Due to strain differences in susceptablity, different anti-malarial drugs can be tried. It is important to remember that malaria can be prevented by screening chicken houses to prevent contact with the mosquito vectors.."

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