Chapter 7 Protozoan Diseases

 

 

                  

 Two of the most destructive disease of poultry, coccidiosis and blackhead, as well as several less Important pathological conditions are caused by protozoa. Poultry men and turkey growers are all too familiar with the ravages of coccidiosis and blackhead, the losses from these two diseases being widespread and relatively enormous.

7.1 Coccidiosis.

a. Synonyms:

Coxy, pink spot, red spot.

b. Definition:

Coccidiosis is probably the most prevalent infectious disease confronting the poultry industry, and as such it is a protozoan disease of the intestinal tract of chickens and other birds, usually subact or chronic in its course, but sometimes acute in its manifestation. It is most injurious to young chicks, although older fowls are often seriously affected. In rate cases the disease in geese assumes an unusually and highly fatal form in which the kidneys are the organ principally involved.

c. General information about Coccidia

Class: Protozoa

Subclass: Sporozoa

• 1. Of the many known genera of the coccidia there are but two of importance: Eimeria and Isospora.
• 2. The freshly passed oocysts of both genera consist of little more than a compound all and a rounded mass of nucleated protoplasm separated by a jelly-like material. In the presence of moisture and oxygen there characteristics developed from the protoplasm mass of Eimeria, four spores, or sporocysts, each containing of more of less banana shaped sporozoites. The matured cysts Isospora contains but two Spores, each holding 4 sporozoites

Asexual life cycle.

• 1 The oocyst is passed out with the droppings of the infected fowl. These oocysts are not yet infective. However, under favorable conditions they undergo sporulation.
• 2. Ideal condition for sporulation is temperature at 84°F and humidity at 70% +, so this disease occurs in warm and moist weather.
• 3. In favorable conditions it takes about 18-72 hours for the oocysts to sporulate into infective stage. 
• 4. Development continues after infection, with the formation of sporozoites.
• 5. In the fowl these sporozoites are released from the oocyst shell due to the mechanical action of gizzard and enzyme action of pancreatic juice and bile, (release of sporozoites in 2 hours after infection).
• 6. Liberated sporozoites penetrate surface epithelium of mucosa and into the lamina propria, later through the basement membrane to the epithelial cells lining the glands of Liberkuhn. Within the epithelial cell, the parasite, now known as a trophozoite, round up, divides by a process of a sexual multiple fission known as schizony which contains many merozoites. The development and activity of the merozoites in the epithelial cells of the intestine resulted in destruction of these cells and liberation of the first generation merozoites into the intestinal canal, (60-72 hours).
• 7. The 1st generation merozoites enter intestinal epithelial cells each merozoite develop into a second generation schizont, it is this stage causing most hemorrhage and damage, usually hemorrhage appear about 96 hours after infection. Extensive hemorrhage may occur on the 5th day, if infection is severe.
• 8. This schizont - to merozoite - to - schizont phase of the life cycle is repeated several times, resulting in severe damage to the intestinal mucosa.

Sexual Cycle.

• 1. After several generations of a sexual cycle to change in cycle which characterized by the formation of gametocytes.
• 2. The merozoites that enter epithelial cells developed in to gametocytes (round bodies). The microgametocytes and macrogametocytes.
• 3. From the microgametocyte there may develop as many micro gametes as nuclei, each of which is a minute flagellated body. Fertilization is accomplished by the penetration of the microgamete into the macrogamete through a microplye
• 4. Tile resulting zygote secretes a wall about itself, a process in which certain cytoplasmic granules are involved, and it is known as an oocyst.
• 5. The time necessary for completion of life cycle varies, but under average condition it is from 4-10 days,
• 6. The younger the coccidia culture the shorter the disease cycle. Oocysts in unshaded soil live up to 14 months, shaded area up to 21 months.
• 7. Sporulated oocysts are quite resistant to external influences and have found to exist in a viable state for as long as six months in the soil of poultry lots.
• 8. Disinfectants in the strengths ordinarily employed, do not kill the oocysts, although continued contact with strong solutions of such disinfectants will eventually destroy them. Dryness, putrefaction and ammonia can kill coccidia oocysts.

d. Occurrence:

Coccidiosis occurs wherever poultry is raised and it is prevalent in flocks all over the world. Because of the favorable conditions offered for development of the oocysts during the spring and summer and also because young, highly susceptible chicks are being reared at the time, the incidence of the disease is greater during those seasons than at other times of the year. Outbreaks are more likely to occur during periods of we weather.

e. Susceptibility:

All kinds of fowls. Coccidia itself is species specific.

f. Severity of the disease. 

• 1. Depends upon kinds or species of coccidia infected. Tenella is most pathogenic specie.
• 2. Number of coccidia oocysts ingested
• 3. Heavy breed chickens are more resistant to this disease.
• 4. Age: Fowls do not build up immunity, unless exposed to coccidia.
• 5. Improper feeding.
• 6. Improper housing, management problem, especially in wet
• 7. Amount of immunity are variable to this disease.
• 8. Vitamin A and K level affect the severity of this disease.

g. Transmission:

• 1. Ingestion of contaminated droppings, litter, water, and feed.
• 2. Mechanical carrier.
• 3. flies.
• 4. Carrier chickens. 

7.1.1 Chicken coccidiosis.

1. There are 9 known Eimeria species parasite the chicken intestine.

2. Symptoms:

• 1. Action: Acute-chronic in extremely acute cases, the first thing noticed will be dead birds.
• 2. Unusually droopiness and depression are the first symptoms
• 3. The chicks stand hudles, with wings dropped, feathers ruffled and eyes closed
• 4. Diarrhea is commonly present and the loose droppings are frequently mixed with blood.
• 5. In the later stages of the disease there is paleness of the comb and wattles.
• 6. The greatest losses occurs within 6-10 days following the onset of symptoms.
• 7. In older fowl the chronic intestinal type of the disease is most common, Leg weakness is commonly manifested and in some cases is so severe that the affected fowl may be practically paralyzed.

3. Lesions:

• 1 E. acervulina infection. The commonest of all coccidia, it frequently causes extensive morbidity among broiler flocks and replacement pullets. Mortality generally is low, but affected birds may degenerate into culls
• In light and moderate infection, there are numerous whitish patches in the upper half of the small intestine. These lesions can be seen on serosa and mucosa. Heavy infections show severe enteritis with no white patches Thick intestinal wall, white bans or petechial hemorrhages also noted.
• 2. E . necatrix. May be acute or chronic. In acture cases the birds may die in 5-7 days after infection. In chronic cases, the birds may linger on for a long time with a wasting illness. During an acute attack, blood may be noted in the droppings.

  Ballooning, or severe swelling, of the small intestine. Hemorrhagic areas are easily seen on serosal surface of the intestine. The organ contain profuse bloody mucus and the ceca are usually blood-filled, the blood having passed from the intestine into the ceca.

  Location: middle part of small intestine, oocysts found in ceca.

• 3. E. tenella Causes cecal coccidiosis, commonly call "bloody coccidiosis". The hemorrhage usually commence about the fifth day after infection. Birds huddly, their heads drawn in and their feathers ruffled. It is a disease primarily among young chicks, but seldom in those under 10-11 days old. Death loss may be high.

  The ceca are swollen and filled with a blood mass, the result of hemorrhage of the blood vessels of cecal lining surviving birds have white or pink cores in the ceca; these are formed from rbc, oocysts, pus and fecal material.

• 4. E. brunetti. In moderate infection, there is a thickening in the lower half of the small intestine the rectum, cloaca and ceca. There may be a blood tinged catarrhal exudate and short red streaks in the lower intestine and rectum.

  In severe infections, the lining of the small intestine may slough off. Cheese-like cores may be found plugging the narrow portion of the ceca, but the rest of the ceca seems to be a little affected aside from swelling.

• 5. E. maxima. Dilation of the small intestine and a thickening of the wall. Intestinal content takes the form of a thick mucous, which may be grayish, brownish or pinkish in color.

  Location: Middle portion of S. I.

• 6. E. mivati. Congestion, pinpoint hemorrhages and whitish patches in the upper third of the small intestine with some spread into lower portion of the small intestine, ceca, and rectum.
• 7. E. hagani. Upper-half of the small intestine, small, round hemorrhagic spots and severe catarrhal enteritis in the duodenum and upper half of the remainder of the small intestines.
• 8. E. praexox. Upper third of small intestine. no appreciable tissue damage.
• 9. E. Mitis. Entire length of the small intestine without causing appreciable damage.

4. Diagnosis

• 1. Based on symptom and autopsy lesions.
• 2. A positive diagnosis of coccidiosis is dependent upon finding one or more of the various stages of the organisms by microscopic examination of a thin film of fecal material and intestinal mucosa.

5. Prevention, Treatment, and Control:

• 1. Sound management, dry litter, clean house, keep the house dry. Don't crowd the chicken. Proper feeding of Vitamin A and K.
• 2.Treatment with drugs.

Following discovery of anticoccidial activity of the sulfa drugs in 1939, attention was directed toward treatment of coccidiosis. However, anticoccidial agents (coccidiostats) show activity so early in the life cycle that few benefits are derived from treatment after symptoms appear. For this reason the preventive approach for use of drugs has largely supersede- the treatment approach. S Q (Sulfaquinoxaline) is the drug of choice for treating this disease. Other commonly used drugs are Sulfamethazine, Sulfaquanidine, Sulfamerazine, Nitrofura-zone, ureomycine, Terramycin, Amprolium etc.

There a various kinds of coccidiostats in the market for preventing tative use against coccidia. Long term continuation administration of cocidiostats in water of feed will induce resistance to a specific drug thus, changing of coccidiostats after using it for certain period of time is important, among the commonly used cocidiostate, monensin is the only drug that has not been running into the drug resistant problem, so far.

Special of developing resistant of coccidia to various

cocidiostats and different.

(1). Glycomide - very rapid

(2). Quinines - rapid

(3) Clopidoless rapid.

(4) Sulfonamides - moderate.

(5) amproimin - slow.

(6) Nicariazin - very slow.

(7) Moenrin absent. 

Commercial available vaccine is made by Sterwin Laboratories with the trade Coccivac.

7.12 Turkey Coccidios

In turkeys only the species of coccidia are generally considered of concern - E. megrimitis, E . adenoeides and E .gallopavonis.

1 E. meleagrimitis

After the 4th day infection, birds begin to chirp, huddle together with drooping wings and ruffled feathers. Droppings become fluid and may contain blood. There is a severe weight loss and high mortality in young poults. Necrotic enteritis appears in the duodenum and upper jejunum wall of the intestine is thickened and the lower portion, may contain a greenish mucous.

Mortality usually occurs on the fifth, sixth and seventh days after infection. 

2. E . adenoeides

After the 4th day of infection droppings become fluid, contain mucus and a small amount of blood. By the 6th or 7th day, feces are composed almost entirely of yellow cheesy exudate.

A severe enteritis in the lower small intestine, ceca and large intestine. The infection may result in up to 100% mortality in young poults. Death occurs late on the fifth day and continues at least through the seventh day after infection.

3. E. gallopavonis.

Droppings are watery and may contain tinges of blood. This species is highly pathogenic for 3-6 weeks -old poults. Causing marked signs and some mortality in birds as old as 11 weeks

A typical creamy-white mucous in the ceca large intestine, and lower one-third of the small intestine. The wall of the intestine is usually damage, thickened and devoid of food.

4. E. melagridis

Lower small intestine and ceca. low pathogenicity.

5. E. dispersa

Upper one-half of small intestine, low pathogenicity.

6. E. subrothunda

Upper two-third of small intestine, low pathogenicity.

7. E. innocua

Small intestine low pathogenicity.

7.1.3 Goose conccidiosis: E. truncata

• 1. Age: 3 weeks - 3 months.
• 2. In epithelium of the uriniferous tubules
• 3. Oocysts in tubules
• 4. Very acute 2-3 days.
• 5. Mortality very high. 

7.2 HISTOMONIASIS.

a. Synonyms:

Infectious enterohepatitis, or blackhead.

b. Definition:

One of the most destructive infectious disease to which turkeys are extremely susceptible, and is responsible for large losses in the turkey industry.

c. Etiology:

• 1. Hiistomaonas meleagridis, a protozoa, is classified as a flagella but is one of the few that likewise has an amoeboid stag 
• 2. The organisms are passed out of the body of an infected fowl in the droppings and in some instances are enclosed within the eggs of the cecal worm Heterakis gallinad.
• 3. The organism does not survive long in an unprotected state outside the body of the fowl.

d. Occurrence:

Blackhead is widespread, being found in practically every section where turkeys are raised.

e. Susceptibility:

• 1. Young turkeys from one to three months of age are highly susceptible, and it is in poults of this age that the severest losses occur.
• 2. Chickens are also subject of infection, but the disease is far less severe and not so common as it is in turkeys. 

f. Transmission:

• 1. By ingestion of the cecal worm or its eggs both of which frequently harbor the infectious organisms. Earthworm also could transmit the disease.
• 2. By carrier turkeys, chickens whose droppings contaminate the environment.

g. Symptoms:

• 1. Age: 1-3 months of 15 days after infection.
• 2. Action: Acute in young poults, more chronic in mature birds.
• 3. Inappetence, increased thirst, ruffled feather, droopy wings and drowsiness.
• 4. Diarrhea is practically always present and the droppings vary from a light green to a brownish color.
• 5.. Orangd-colored or sulfur diarrhea is characteristic, the diarrhea may be foamy.
• 6. Weakness and emaciation are evident and in some, but not all instances the skin of the head becomes dark in color.

h. Lesions:

• 1. Ulcerative enteritis - raised lumpy area in the walls of the pouches, entire cecum may be enlarged, inflamed and filled with a cheesy, core-like mass. The lining membrane is seriously damaged and blood is frequently found on the core of cellular debris in the gut.
• 2. Ulcerative hepatitis - enlargement of the liver, with round, depress, ulcer-like areas of yellowish or salmon color over the surface. These lesions may be few in number of so plentiful as to cover the greater part of the surface of the organ.
• 3. Peritonitis in cases where liver is extensively involved.

i. Diagnosis:

• 1. Go by age, ,history, and lesion.
• 2. Differential diagnosis:

Characters	TB	Blackhead	Coccidiosis
Age	Old	Young	Young
Action	Chronic	Acute to Chronic	Acute to Chronic
Transmitted to other species	Yes	Yes	No
Common species infected	Chicken	Turkey	Chicken, Turkey
Emaciation	+	+ -	- +
Diarrhea	-	Sulfur, Foaming	Mucous blood
Liver	Nodule	Ulcer(circular)	-
Spleen	+	-	-
Intestine	Nodule	Ulcer (Circular)	Enlarged, Hemor-rhagic Necrotic
Occurence in Turkey	Rare	Very Common	Common

   

3. Laboratory diagnosis:

Direct microscopic examination of fresh fecal material will reveal Histomonas meleagridis.

j. Prevention:

• 1. Do not raise turkey near to chicken (isolation of rearing)
• 2. Raise turkey in strict or semi confinement for 10-14 weeks.
• 3. Rotate the range, do not use the same range if they had an outbreak the previous year.
• 4. Control cecal worms with medication, phenothiazine or hygromycin.
• 5. Preventive for Blackhead,

Hepzide (Merk), Ipropan (Ipronidazole, Roche). Furox (Furazolidone, Norwich), Carb-o-Sep (Arsenic, Whitmoyer).

k. Treatment:

Same as preventative medication, except, different in dosage used. 

7.3 LEUKOCYTOZOON.

a. Definition:

Acute, highly fatal disease, primarily of young ducklings and turkeys, characterized by the fact that the causative protozoan parasites invade the circulatory system of the victims and do great damage to the blood cells.

b. Etiology:

• Different species of Leucocytozoon attack different species of birds
• Leucocytozoon simondi- in ducks.
• Leucocytozoon smithi- in turkeys. L. andrewsi- chicken.

c. Distribution:

It is a very important disease in the Southeast, especially South Carolina where there are a lot of turkeys raised.

d. Transmission:

• 1. Transmitted by Leucocytozoon carrying black flies, turkey gnats by biting birds. At least three species have been shown to transmit this disease. Simulium occldentale,S. nigoparvum, and S. slossonae.
• 2. Wild turkeys as reversoir. 

e. Symptoms:

• 1. Turkey: Under 12 weeks of age, most susceptible. Ducklings: From 2 weeks to 2 months.
• 2. Action: Acute, symptoms may be shown for only a short time.
• 3. Inappetence, droopiness, weakness, and a tendency to sit down.
• 4. Some birds lie prone with the head and neck extended and the wings spread out from the body.
• 5. Thirst is increased and breathing rapidly becomes labored.
• 6. Eventhough the affected birds appear drowsy, if made to move they become greatly excited, show loss of equilibrium and may go into convulsions followed by coma.
• 7. Moist tracheal rales are common in chronic cases, and the affected birds make repeated attempts to clear their throat when excited.

f. Lesions:

• 1. Slight inflammation of the duodenum is the only consistent gross lesion noted in young birds.
• 2. Hemorrhagic spots in breast muscles.
• 3. Enlarged congested spleen.
• 4. Emaciation and anemia, flesh is yellowish in color.
• 5. Increase in the amount of pericardial fluid and the heart muscle is paler than normal.

g. Diagnosis:

• 1. In the field, the presence of blackflies, and symptoms and excitable of turkey.
• 2. Laboratory microscopic direct examination, reveal large number of leucocytozoon in RBC or WBC.

h. Prevention:

• 1. Confinement rearing in houses screened against simulids until the poults are several weeks old.
• 2. Keep blackflies away by spraying insecticide or repellents.
• 3. Complete segregation of breeding and brooding operations will do much to prevent transmission from adult carriers to poults carrier for months.

i. Treatment:

No satisfactory treatment. 

7.4 Trichomoniasis.

There are two, distinct types of the condition, each caused by a different portions of the intestinal tract.

a. Trichomonasis of the upper digestive tract.

1. Etiology: 

Trichomonas gallinae.

2. Species.

Turkeys, pigeons, also chickens.

3. Transmission:

• l) Pigeon and wild birds as carrier.
• 2) Mechanical transmission by flies.
• 3) Contaminated feed, water, especially stagnant water.

4. Symptoms:

• l) Droopiness and depression.
• 2) Little or no appetite, sagging wings, emaciation and drooling.
• 3) The disease may be very acute in young birds with death coming as soon as one day after the appearance of symptoms. While the older fowls the course is usually more prolonged in nature.
• 4) In some cases the crop region ic pendulous and palpation reveals a large quantity of fluid in the organ,
• 5) Action: Chronic, take long time to develop the disease.
• 6) Age: 16 - 20 weeks.
• 7) Dropping had foul smell.
• 8) Cyanotic head.

5. Lesions:

• l) Rough, protruding, yellowish, raised, cheesy areas (cone shaped) which are firmly embedded in the mucosa and submucosa of the crop and esophagus, less frequently in the proventriculus.
• 2) These areas may coalesce and form a continuous large lesion with complete destruction of the membranes.

6. Diagnosis:

• 1) Symptom and lesion. 
• 2) Microscopic examination of fresh material from the lesion.

7. Prevention:

• l) Sanitation problem. Should raise young birds at least one mile from the mature.
• 2) Control flies, pigeons, doves.
• 3) Feed high level of Vitamin A.

8. Treatment:

• l) Give 1:2000 dilution of CuS04 for 5-7 days. 
• 2) Increase level of Vitamin A; 

b. Trichomoniasis of the lower digestive tract.

• 1. Etiology: Trichomonas gallinarum.
• 2. Species. Severe infections in turkey, other birds such as chicken, guineas are also affected.
• 3. Transmission: Ingestion of contaminated feed and water.
• 4. Symptoms:
  • l) Action: Chronic in older birds. Young may die in 4-18 days.
  • 2) Mortality sometimes high in turkeys.
  • 3) Affected birds are droopy,lose weight, and show a diarrhea characterized by yellowish fluid droppings.
• 5. Lesion.
  • l) Liver, elevated focal lesions, cheesy, granular in appearance.
  • 2) Similar lesion may be present on the walls of the ceca.
• 6. Diagnosis: Direct microscopic examination.

 7.5 HEXAMITIASIS.

a. Synonyms:

Infectious catarrhal enteritis.

b. Definition:

Acute infectious disease, primarily of turkeys but which also occurs in quail, and in chukar partridges.

c. Etiology:

Hexamita meleagridis.

d. Susceptibility:

Primarily a disease of poults under three months of age. Young quails, chicks, ducklings and pigeons.

e. Transmission:

• 1. Ingestion of contaminated material, such as feed, soil and water.
• 2. Because of large percentage of recovered birds remain carriers, a ready reservoir of the organism is always present where such fowls are kept.

f. Symptoms:

• 1. Age Usually 3-8 weeks.
• 2. Mortality: From 20-90% have been reported.
• 3. Action: Acute.
• 4. Subnormal body temperature, require more heat in the house.
• 5. Watery and foamy diarrhea is present.
• 6. Some birds continue to eat but despite this emaciation is rapid.
• 7. Listless and droopy, and walk with stilted gait.

g. Lesions.

• 1. Emaciation, dehydrated.
• 2. Marked catarrhal enteritis, the walls of the intestine are flabby and the contents are watery.

h. Diagnosis:

Direct microscopic examination, finding and identifying the organism.

i. Prevention:

• 1. Sell all mature turkeys 2 weeks before young turkeys arrive.
• 2. Keep wild pigeons and quails out.

j. Control.

• 1. Remove all dead turkeys from the premises and burn them.
• 2. Move turkeys to grossly clean range.
• 3. Divide turkeys into two pens, rotate them daily.

k. Treatment:

• 1. Do not flush, because of dehydration.
• 2. Treatment with drugs.
  • Aureomycin 200 gm/ton feed.
  • Soluble aueramycin 10 gm/ton feed.
  • 3 lbs. of dried whey 121/2 tablespoonful of CuSO4. stock
  • solution 121/2 gal. water.