Chapter 2

Diseases caused by Bacteria

                         

Many of the common and economically important diseases of fowl are caused by bacterial agents. Fortunately, these infections as a rule are not transmissible to other farm animals, although there are notable exceptions. 

2.1 Salmonellosis & Arizonosis

Avian salmonellosis is divided into three distinct disease groups, namely Pullorum disease, Fowl Typhoid and Paratyphoid. Arizonia infection is most often in turkey poults.

2.1.1 Pullorum Disease.

Synonyms

Bacillary White Diarrhea, BWD

Definition

Primarily an acute disease of chicks during first month of lives, characterized by high mortality. It is often found in mature fowl as a chronic infection.

Etiology

Salmonella pullorum, isolated by Rettger in 1900, he described this disease as a "Fatal septicemia of young chicks". This bacteria is a long slender Gram-negative rod. Resistant to cold. sunlight, drying and disinfectants. The cells occur singly, nonmotile, non-liquefying, non-sporogenic and faculatively anaerobic. Does not ferment maltose and dulcitol.

Susceptibility

Chickens and turkeys are most susceptible. However, natural infections have been reported in pheasants, ducks, sparrows, guinea fowl, quail, canaries and pigeons. Among mammals, rabbits appear to be readily susceptible, and infection has been reported as occurring in hogs, foxes, mink and man. 

Occurrence

World wide distribution. Pullorum is virtually eradicated in poultry in the U.S. since National Poultry Improvement Plan (NPIP) was organized in 1940 for the purpose of controlling pullorum disease. 

Epizootiology.

  • 1. The most important source of infection is the infective egg laid by carrier hen.
  • 2. Mode of dissemination of pullorum disease is described below:
    • a. Infected hen
    • b. Infected egg laid by infected hen.
    • c. Incubator containing infected egg.
    • d. Chick box in which infected chicks may be present.
    • e. Brooder.
    • f. Surviving infected pullet which may be a carrier.

Symptoms:

  • 1. Incubation period of 5 - 7 days.
  • 2. Age: usually under 3 weeks of age.
  • 3. Action: Peracute type, no detectable symptom, die suddenly; Acute in baby chicks, chronic in mature fowls.
  • 4. Mortality: If chicks are hatched from infective eggs, dead and sick chicks may be observed in the hatchery.
  • Those infected after hatching, mortality reach a peak at 7 - 10 days. Mortality as high as 30 - 40% has been recorded.
  • 5. White diarrhea in a small percent of birds. (Septicemia). Dehydration, vent smear with fecal material.
  • 6. Loss of appetite.
  • 7. Squeaky chirp. Appear cold (fever).
  • 8. Difficult breathing (pneumonia).
  • 9. Swelling of joints - arthritis, more common in hens (chronic).

Post-Mortem Lesions.

1. Peracute type - no lesion.

2. Subacute type

  • a. Enlarged and congested liver. The normal yellow color may be streaked with hemorrhage.
  • b. Necrotic foci may be present in the cardiac muscle, liver, lungs, ceca, large intestine and muscles of the gizzard.
  • c. Unabsorbed yolk sac. (During the first few days of life, the yolk sac serves as source of nutrient.)
  • d. Cheesy core in ceca.
  • e. Pericarditis and epicarditis
  • f. Pneumonia - firm grayish nodules.
  • g. Liver is the most constant seat of gross lesions and followed in order by the lungs, heart, gizzard and ceca.

3. Chronic Form - Adult fowl

  • a. Oval and shrunken misshaped, greenish or leaden-colored egg yolk. The yolk is firm as if it has been cooked
  • b. There may be enlargement of heart. Small, grayish firm nodules may also be noted.
  • c. Salpingitis, atrophied testicles
  • d. Arthritis

4. Histopathology:

Infiltration of R.E. and mononuclear cells replacing necrotic parenchymatous cells.

Diagnosis:

  • 1. Go by history, age, symptom
  • 2. Laboratory diagnosis:
    • a. Definitive diagnosis: Isolation and identification of Salmonella pullorum bacteria.
    • b.Tissue samples from liver, spleen, heart, and yolk sac are good source for bacterial culture in septiemic cases.
    • c. In the case of chronic infection or carrier, serological tests are required.

Control and Prevention

  • 1. Any plan for controlling pullorum disease must its principle objective the elimination of the most prolific and constant source of infection, the carrier hen or turkey.
  • 2. Procure eggs and chicks only from known pullorum free flocks.
    • (a) The hatchery should be dust free, cleaned after each hatch.
    • (b) Fumigate between hatch with KMN04 method.

      0.175gm KMN04

      = cubic feet space

      0.35cc. Formalin

    • Fumigate at 18 days of incubation (chicken)
    • 25 days of incubation (turkey)
    • Length - 1-3 hours
    • Also pre-incubation fumigation may be applied.
  • 3. Blood testing breeders - The most important methods.
    • (a) Recent revision of the pullorum program requires 100 percent flock test of foundation breeder (grandparent) flocks and 15% of multiplier breeders if the flock originated from pullorum free parents.
    • (b) All birds over five months of age, should be tested annually. Flocks revealing infection should be retested within two or four weeks until negative. Every reactor regardless of its value, should be removed from the premises.
    • (c) Grade of chickens

    U.S. Pullorum typhoid passed - 1 test with no reactors.

    U.S. Pullorum typhoid clean flock: No reactors.in 2 tests, 6 months apart. No reactors in three tests, 30 days apart.

  • (d) Blood testing: Rapid whole blood stained antigen method. (Agglutination test).

The most widely used method. Consists of mixing 1 part of blood with 2 parts of the strained polyvaient K antigen on a plate. A distinct agglutination in 1 minute is considered positive and in 2 minutes is doubtful.

The rapid serum test: The test is conducted in a manner similar to the rapid whole blood test, but instead, serum and unstained antigen are used. 

Standard tube method:

This method is very accurate but required more skillful laboratory techniques.

Treatment

  • 1. No drug or combination of drugs has been found capable to eliminate infection, thus it is no substitute for eradication program.
  • 2. If chicks showed symptoms of pullorum increase brooder temperature to 100-105 F.
  • 3. Furazolidone (F180) is the drug of choice, it is administered in feed at the level of 0.04 percent for 10 days for treatment and 0.01-0.015 per cent continuously for prevention, or 200 grams/ton feed.
  • 4. Sulfonamides: Sulfadiazine and sulfamerazine are very effective in reducing mortality. 

2.1.2 Fowl typhoid

Synonyms - Typhoid 

Definition

A septiemic disease of domesticated birds. Characterized by an acute and chronic phase, enlarged spleen , mahogany- colored liver, and diarrhea with passing around the vent.

Etiology

Salmonella gallinarum is closely related to Salmonella

Susceptibility

Young adult chickens are very susceptible 2 weeks guineas and a few other species are also susceptible.

Occurrence

The disease is widespread in the poultry producing area of the country, but out breaks are sporadic, depending on the season, environment, and control methods.

Epizootiology

Similar to pullorum disease. Transmission through eggs, carrier hens, flies also play a important role. Discharge from nose, mouth and bowl of infected birds are infectious.

Symptoms

  • 1. Action - Acute to chronic
  • 2. Incubation period - Four to five days, varies considerably with the virulence of the organism.
  • 3. Course of disease about five days
  • 4. High fever of about 110-112°F
  • 5. Loss of appetite, restless, ruffled feathers, increased thirst, unthriftiness, greenish diarrhea.
  • 6. Mortality depends on the resistance of birds may run as high as 75% in untreated flocks.
  • 7. Comb and Wattles - Generally pale and shrunken. In acute cases appeared dark.

Post-Mortem Lesions

  • 1. Peracute type - No lesion
  • 2. Liver - Enlarged 2-3 times, bronze color. Necrotic foci is evident in subacute cases. (Characteristic)
  • 3. Spleen-Enlarged (2-3 times of normal size), mottle, sometimes hemorrhagic (characteristic)
  • 4. Kidney-Enlarged, hard, swollen and congested.
  • 5. Oviduct- Appeared cook, due to high fever, ova-hemorrhagi 

Misshapen and discoloration.

  • 6. Heart - Necrotic foci in myocardium and pericardium.
  • 7. Intestine - Catarrhal inflammation.
  • 8. In young chicks, grayish-white foci may sometimes be observed in the lungs, heart, and gizzard.

Diagnosis

  • 1. There are similarities with pullorum, fowl cholera, monocytosis (pullet disease) or fowl plague.
  • 2. Differential diagnosis:
    • a. The marked congested and enlarged organs are not found in pullorum disease, fowl cholera or fowl plague.
    • b. High fever does not present in pullorum.
    • c.The bronze colored liver is very diagnostic.
  • 3. Laboratory diagnosis
    • a. Cultivation and identification of the organism
    • b. Serological identification.
    • c. Salmonella pullorum and gallinarum are serologically undifferentiated. However, S. gallinarum Ferments Maltose, most strains of S. pullorum do not attract this sugar. S. gallinarum acidifies dulsitol. S. gallinarum is anaerogenic, but S. pullorum is erogenic. 

Control:

  • 1. Start with Salmonella clean flocks.
  • 2. Blood test breeders.
  • 3. Sanitation
  • 4. Immunization with killed fowl typhoid bacteria, not effective.

Treatment

  • 1. Medication

    Chicken - NF 180 is the best drug for Salmonella infection. #2/ton of feed for one week or l#/ton of feed, 6-8 days.

  • Turkey-Birds that have fever should put on treatment with NP 180.
  • 2. Move affected birds to another area.
  • 3. Change water and feed more often.
  • 4. Disinfect premise is with lye water (1%).
  • 5. Do not keep the flock for breeding purpose.

2.1.3 Para-Typhoid

Synonyms - Salmonellosis

Definition

A large group of acute or chronic diseases caused by one or more of the normally motile members of the Salmonella genus.

Etiology

There are about 1,700 serological types of motile Salmonella involved. The bacteria can be differentiating form S. Pullorum and S. gallinarum by biochemical reactions, but species identification depends on serology.

Susceptibility

This is a group of diseases which have public health importance. Salmonellosis is infectious to human and many other animals.

Occurrence

Occurs in all parts of the world, although certain serotypes are usually predominant in a region.

Epizootiology

  • 1. Rodents reptiles and flies are the source of infection in the chickens house.
  • 2. Turkey is particularly notorious for harboring Salmonella organisms.
  • 3. Egg shell transmission with the possibility of shell penetration.
  • 4. Contaminated environment, hatchery, feed, water, litter, and animal by products.

Symptoms

1. Young chickens and turkeys (A few days to one month old).

  • 1. Action: Acute to peracute
  • 2. High fever, 110°-112°F. Appeared cold, watery diarrhea, and dehydration.
  • 3. Somonlence, head lowered, eyes closed, wings drooping, and the feathers ruffled.
  • 4. Marked anorexia and increased water consumption.

2. Adult chickens and turkeys.

  • 1. Adults generally do not exhibit outwards signs of infection. However, they are often chronic carriers of partyphoid organism both in their internal organs and intestinal tracts.
  • 2. In natural infection, mortality is low in chickens but higher in poults.
  • 3. Ducklings- die slowly, tremble and gasp for air. Also called , keel disease .
  • 4. Pigeons - arthritis is commonly observed. Most often in wing joints and is evident as soft, subcutaneous swellings.

Postmortem Lesions

  • 1. No lesion in peracute type.
  • 2. Unabsorbed yolk, coagulated yolk.
  • 3. Congested, enlarged liver, spleen with hemorrhagic streaks or pin point necrotic foci.
  • 4. Congested kidney.
  • 5. Pericarditis with adhesion, air sac infection.
  • 6. Hemorrhagic enteritis, cecal cores are occasionally observed.

Diagnosis.

  • 1. Clinical observations and necropsy findings may be suggestive of paratyphoid infection when a supportive history is available, early treatment or control recommendations.
  • 2. Final diagnosis dependent on the isolation and identification of the causative organisms.
    • 1. The tissue most frequently selected for culture are heart, liver, lungs, gall bladder, ovary, testes, oviduct, pancreas, spleen, and intestinal content.
    • 2. Polyvalent - antiserum may be used to identify the bacteria isolates from infected tissues.

Control

  • 1. Hatchery and egg sanitation is the most important factor in the prevention and control of paratyphoid infection of poultry. (Fecal contamination, egg bourn). 
  • 2. Sanitation during brooding period.
  • 3. Flock sanitation, keep rodents away from the chicken house.
  • 4. Serological testing. Procedures for the serological detection of adult carriers of paratyphoid infections have not been accepted or applied on the scale of those employed for the detection of punorum disease and fowl typhoid. The tube agglutination test for S. typhimurium has been most frequently used as a supplementary measure to other means of control or as a method for locating infected flocks.
  • 5. A flock with the history of paratyphoid infections should not be retained for breeding. Do not wash eggs from infected flocks, because the shell is contaminated.

Treatment

  • NF 180 #2 per ton of feed
  • NF 180 #4 per ton of feed in S. typhimurium infection.

2.1.4 Arizonosis

Synomyme: Paracolon infection

Definition:

Disease of pults primarily, chronic intestinal disease of all-age birds. Characterized by focal necrosis of the abdominal organs.

Etiology:

Arizona bacterial comprise a large group of serologically and biochemically related organisms of the family Enterobacteriaceae. Occupying a position intermediate between typical coliforms and the paratyphoids. Gram negative, nonsporogenic rods which are usually motile.

Susceptibility:

Young poults and chicks are very susceptible up to 4 weeks or age. Other birds as well as animals are also susceptible.

Occurrence: World wide.

Epizootiology

  • 1. Egg shells contaminated by diseased birds.
  • 2. Contaminated feeds (feather meal, meat scrap, and others).

Symptoms:

Identical to paratyphoid infection

Postmortem lesion

  • 1. Mottled yellow liver, discolored heart muscles, peritonitis and unabsorbed yol sac.
  • 2. Infected birds do not remain carriers and the infection is usually overcome in one month.

Diagnosis:

Isolation and identification of the organisms.

Control:

  • 1. Fumigation of eggs.
  • 2. General strict and good management.

Treatment

  • 1. Treatment is advocated as the birds do not usually remain carriers.
  • 2. Turkey breeder 4 #NF 180 per ton of feed for two weeks then reduce to 2 # per ton of feed for continuous medication. Young birds use 2 # per ton of feed for two weeks.

2.1.5 Isolation and identification of Salmonella and Arizona bacteria.

2.1.5.1 Bacterial culture:

Enrichment media - Selective media for Gram negative bacteria, and Gram positive bacteria are inhibited. (Selenite broth).

Primary Isolation media or selective media - support the growth of several types of organisms but each will have different characteristics. (S S agar, desoxycholate agar, Bismuth sulfite agar).

Differential media

Indicate fermentation of carbohydrates, production of H2S etc. (Triple sugar iron agar, Urea broth, citrate broth).

Salmonella organisms aremotile, except for Sal. pullorum and gallinarum. Non-lactose ferment, appeared as small colorless colonies. Red colonies are formed by lactose fermenter (B. coli etc).

Differentiate from proteus or urease activity. Salmonella is negative.

2.1.5.2 Serological identification

Although some species of Salmonella can be identified biochemically, most can only be identified serologically.

  • 1. Somatic (0) antigens designated by Arabic numerals.
  • 2. Flagella (h) antigens: Divided into 2 phase 1, designated by small letters of the alphabet. Specific for Salmonella. Phase 2, designated by Arabic numeral, less specific.

Most veterinary diagnostic laboratories, based on the possession certain somatic antigens, divide Salmonella cultures into groups A through I. Approximately 80% of all salmonella types isolated from turkeys and chickens in the United States are members of B. C. D. and E. The greatest number of paratypes belong to group C, followed by group E, B, and n in sequence. Both Salmonella: pullorum and S. gallinarum belong to group n. Salmonella typhlmurium (group I) being the single organism most oftenly isolated from poultry and other animals.

2.2 Pasterellosis

2.2.1 Fowl Cholera

Synonyms: Avian Cholera, avian pasteurellosis, avian hemorrhagic septicemia.

Definition:

Acute septicemic disease of somestic fowls and wild birds caused by Pasterurella multocida (P. aviseptica) Characterized by high morbidity and morality.

Etiology:

Pasterurella multocida P. avicida, P. aviseptica) Small, non-motile, Gram-negative, ovoid or elongated rod, encapsulated. Wright's Giemasas, methylene blue, or carbolfuchsin stains will show the characteristic bipolar morphology of the organism. The organism grows well in blood agar, but not in MacConkey agar.

The organism survives several months in soil, litter as decayed matters, but is killed by disinfectants.

Susceptibility:

Chicken, turkey and ducks are most commonly affected. However, domestic fowls, game birds, cage birds and wild birds are susceptible.

Occurrence:

Fowl cholera occurs sporadically or enzootically in most countries of the world. It is a serious problem in turkey and chicken.

Epizootiology:

  • 1. The mode of transmission among water fowl is unknown.
  • 2. In domestic Fowls, "healthy" nasal carriers provide a source of infection.
  • 3. The natural spread of the disease among domestic fowl is believed to be by ingestion, inhalation and transmitted by vectors mechanically.

Symptoms:

  • 1. Age: Semimature to mature.
  • 2. Peracute type: Fowl died suddenly, usually in good flesh.
  • 3. Acute:
    • 1. Birds may live for a day or longer
    • 2. Greenish and yellowish diarrhea. Thirst, increased water consumption, anorexia.
    • 3. Fever, 100-112°F.
    • 4. Mucous in mouth and nostrils.
    • 5. Cyanotic combsand wattles.
    • 4. Chronic
      • 1. Linger for weeks or months and act as Carriers.
      • 2. Swollen wattles and eyes.
      • 3. Inflammation of joints, tendon sheath of the legs or wings.
      • 4. Torticollis

Postmortem Lesions

1. Acute type:

  • 1. A sticky mucous in the mouth and nasal passage may be found.
  • 2. Reddish discoloration of the skin and breast muscles is a common but not constant finding. In general the abdominal organs appear congested and darken.
  • 3. Hemorrhage of various sizes are found on the heart muscles, particularly around the coronary groove, abdominal subcutaneous tissue and gizzard fat.
  • 4. The pericardial sac often contains an excess of yellowish fluid.
  • 5. Liver, either very dark or lighter than usual, its surface may be spotted with many white necrotic foci.
  • 6. Severe inflammation and hemorrhage in the lining of the duodenum are lesions frequently present. In lower section a yellow sticky material is found.
  • 7. Lung, consolidation and congestion with numerous small hemorrhage.
  • 8. Cheesy, yellowish deposits are often observed in various parts of the body, especially on the membrane of the air sacs and the intestine.

2. Chronic type:

  • l) Dried cheesy, yellow yolk material is found free in the abdominal cavity or adherent to some organ, ruptured yolk.
  • 2) Hemorrhages of the ovary, soft, flabby, irregular in outline and pedunculated ova, greenish colored ovum is observed occasionally. Salpingitis.
  • 3) Caseous, swollen wattles and joints.
  • 4) Supportive meningitis as a result of the organism localized at the base of the skull and ear.

3. Histopathology:

Coagulation necrosis of parenchymataus cells and heterophilic infiltration.

Diagnosis:

1. Field differential diagnosis.

1)Age

Typhoid Chicks+

Cholera

2)Action

fast

very fast to chronic

3)Species

chicken,turkey

chicken,turkey,duck

4)Pullorum test

+

-_ _ _

5)comb

pale

cyanotic

6)Temperature

110-112 F

110-112 F

7)Breathing

Normal

Rattling

8)Wattle, joints

Normal

swollen,enlarged

9)Diarrhea

Greenish

Greenish

10)Liver, sive

enlarged 2-3X

Normal to slightly enlarged

color

brown

red

Necrotic foci

+

++

11)Spleen, size

Enlarged 2-3X

Typhoid

Normal

Cholera

12)Heart

Nodule

Hemorrhage 

13)Ceca

Core

Normal

14)Ovary

Cooked

Cooked

2. Laboratory Diagnosis:

  • l) Finding bipolar characteristic organisms in Wright or Giemsa stained smear of circulating blood.
  • 2) Isolation and characterization of bacteria from circulating blood liver or other viscera.
  • 3) Whole blood strained antigen agglutination test.
  • 4) Laboratory animal inoculation, chicks and mice.

 Control:

  • 1. Water sanitation
  • 2. This is a stress disease, good management would help.
  • 3. Control flies and rodents.
  • 4. Vaccination at 12-16 weeks for placement flocks in problems area and repeat 4-8 weeks later, subcutaneous injection of autogenous bacteria in the neck or thighs. Action of immunity develops within 4-5 days, length of immunity is about 6 months. 

Treatment :

  • 1. Sulfonamides especially sulfaquinoxalene (SQ); sulfamenthazine, sulfamer SQ in the feed at 0.33% level for 14 days.
  • 2. Teramycin in water or feed is also effective.

2.2.2 New Duck Disease

Synonyms:

Infections serositis, New Duck Disease, duck septicemia,

Definition:

A relatively new and serious disease of ducks. It is a septicemic disease characterized by fibrinous peritonitis, pericarditis, and airsacculitis.

Etiology:

Pasteurella anatipestifer (Moraxella anatipestifer).

Symptoms:

1. Age:

Growing ducklings 4-9 weeks old. 

2. Mortality rate:

Very high, May reach 70% death ensuring with 6-12 hours after the first symptoms were noted.

3. Depression:

  • Sleepiness, ruffling of feathers, greenish diarrhea, jerking of the head.
  • Serous discharge from the eyes and weakness followed by prostration.

4. Ataxia.

Postmortem lesions:

  • 1. Hemorrhages on the spleen, liver and heart 
  • 2. Pibrinous perihepatitis, and pericarditis (characteristic).
  • 3. The spleen may be enlarged and mottle, the kidneys are congest
  • 4. Severe hemorrhagic enteritis may occur.
  • 5. Fibrinous meningitis.

Control and treatment:

  • 1. lOOgm. Chlorotetracyline/l ton mesh for 5 days.
  • 2. 0.1% Sulfadimidine in water for 2 days. 

2.3. Pseudotuberculosis

Definition:

An acute, rapidly fatal disease in wild birds as well as chickens.

Etiology:

Yershinia pseudotuberculosis. Gram negative, motile small rod or coccobacilli. Aerobic, non-spareforming. Species of this genus share many of the characteristics of the Enterobacteriaceac.

  • 1. Entrance through digestive tract. 
  • 2. Skin injuries may also form portals of entry.

Symptoms:

Rapid onset, usually rapid death following onset of signs, bronzing of skin, malaise, diarrhea, inappctence anorexia and occasionally lameness. (General septicemia)

Postmortem Lesions:

  • 1. The characteristic multiple grayish white foci in spleen liver, kidneys and breast Muscle are pathognomonic.
  • 2. There are caseating granulomatous or necrotizing focal lesions.

Diagnosis:

  • Direct isolation and identification of the agent.
  • Control.
  • Unknown.
  • Treatment:
  • Wide spectrum antibiotics are effective.

 

2.4 Tuberculosis of Poultry

a. Synonyms:

TB, Avian T.B.

b. Definition:

Chronic infectious disease of mature fowls, characterized by granulomatous lesions in the viscera.

c. Etiology:

Mycobacterium tuberculosis var. acian. The organism is acid fast, measures 1-3 1! long, grows best on media containing glycerin, egg medium, the colonies being oily and most, Grampositive.

Moist heat destroys the organism rather rapidly but cold does not affect it. It is readily destroyed by direct sunlight. Chemical disinfectants are effective when it is present in material which contains no protein.

d. Susceptibility:

  • 1. Chickens and turkeys are very susceptible.
  • 2. All species of birds are capable of being infected.
  • 3. Mammal, are susceptible. Other animals such as sheep, rabbit, rodents and calves are also susceptible.
  • 4. Chickens are resistant to M. bovis, while parrots and parrotlike birds are highly susceptible. Parrots may also become infected with human strains.
  • 5. Birds other than psitiacinea are resistant to infection by human bacilli

e. Occurrence:

  • 1. World wide.
  • 2. Serious problem in the midwest states of U.S. where young birds have contact with older birds or with swine.

F. Epizootiology:

  • 1. Through alimentary route, contaminated feed and water.
  • 2. Contact with hogs and sheep that habour the bacilli.
  • 3. Feeding raw garbage to hogs.
  • 4. Cannibalism.

g. Symptoms:

  • 1. Age: fowls may become infected at any age, but because of the chronic nature of the disease symptoms are not usually observed in birds less than one year of age.
  • 2. Action: Chronic
  • 3. Temperature: Within normal range.
  • 4. One of the first indications of tuberculosis in fowl is loss of weight ("going light ")
  • 5. Combs, wattles, skin and mucous membranes of the head become pale, and the feathers are ruffled, listless and unthrifty.
  • 6. Lameness in one or both legs due to tuberculosis abscess in the joints.
  • 7. Diarrhea often appears in the later stages.

h. Postmortem lesions:

  • 1. Location of lesions seen most oftenly in liver, spleen, intestine, mesentery, bone marrow and lung.
  • 2. Grossly, there are irregular grayish yellowish or grayish white nodules.
  • 3. Histopathology: The avian tubercule consists of a center of caseation necrosis, without calcification, a giant tell zone, epithelioid (histiocyte) cells zone, and encapsulated by fibrous tissue, epitheliod cells and lymphocytes at the margin.
  • 4. The tubercle nodules in poultry are firm but are incised easily since mineral salts are not present.
  • 5. Enlarged thymus.
  • 6. Postmortem disposition : Condemn, disregard the extensiveness of lesions.

i. Diagnosis:

  • 1. Go by history and the chronic condition.
  • 2. Typical tubercle lesions.
  • 3. Should differentiate this disease from:
    • 1. Blackhead disease - ulcer like lesion in liver and cecum.
    • 2. Marek's disease - young age and histopathology.
    • 3. Raillietina echinobothrida (tapeworm). lesion in intestinal wall.
    • 4. Laboratory diagnosis:
      • 1. Microscope examination of affected tissue, acid fast bacteria on fresh smears. Confirmed by histopathology of typical granulomatous lesion.
      • 2. Culture of bacteria.

J. Control

  • 1. Raise fowls away from hogs and sheep.
  • 2. Only keep young layers. Do not keep birds of several ages in one chicken hours.
  • 3. Tuberculin test to identify reactors.

Site

Wattle for chicken, wing web for turkey Intradermal).

Preparation

Wash wattle with 70% alcohol.

Syringe, needle - tuberculin syringe, 25-26 GT needle.

Amount

0.03 - 0.05 c.c.

Check reaction

at 48 hours after inoculation.

Interpretation

Positive reactor indicated by a soft. swelling in the injection site.

If reactors were found, retest in 30- 45 days.

k. Treatment:

  • 1. Medication - Not effective
  • 2. Vaccination - Not effective

2.5 Avian Mycoplasmosis (Mycoplasma gallisepticum, Mycoplasma Meleagridis and Mycoplasma Synoviae).

2.5.1 Mycoplasma gallisepticum infection.

Synonyms:

M G (Mycoplasma gallisepticum).

  • 1. CRD (Chronic respiratory disease), air sac cold, air-sacculitis in chicken.
  • 2. Infectious sinusitis in turkey.

Definition:

An infectious and contagious disease of poultry characterized by respiratory rales, coughing, and nasal discharge. The clinical manifestations are slow to develop and the disease has a long course.

Etiology:

  • 1. Mycoplasma gallisepticum is the cause of uncomplicated airsaculitis, It is a small coccoid filterable organism about 0.5 U in diameter and does not have a rigid cell wall, stains with Giemsa's stain and requires a medium enriched with (10-20%) serum or serum fraction for its growth. It is resistant to penicillin, thallous acetate, can be propagated in embryonating chicken eggs where it may or may not cause death of the embryo. The organism researches its highest concentration in the yolk sac and in the choriollantoic membrane. This organism survives in lyophilized forms and frozen state for a long time. It lives only a short time outside the chicken body, killed by 113°F heat for one hour. Another species of mycoplasma commonly isolated from chickens, but not pathogenic, is g. m. gallinarum.
  • 2. Mycoplasma my produce disease by itself or its action may be enhanced by the following factors.
    • a. Escherichia coli, Hemophilias gallinarum
    • b. Virus infection or vaccination of infectious bronchitis. New castle disease and perhaps other viruses.
    • c. Stress and environmental changes

Susceptibility:

Chickens, turkeys, pigeons, ducks and pea fowl of all ages.

Occurrence:

Widespread in U.S.A. and other countries.

Epizootiology:

  • 1. It is primarily transmitted through eggs.
  • 2. Spread by air-borne dust or droplets and contact.
  • 3. Outbreak of the disease are often started by carriers. 

Symptoms:

1. Chickens.

  • a. It is a seasonal disease, more often seen in winter and fall.
  • b. Age: Four weeks or older.
  • c. Action: Chronic
  • d. Nasal discharge with no odor, Foamy exudate in eyes and swollen periorbital sinuses.
  • e. Persistent cough, trachea rale, sneeze and gasp.
  • f. Loss of appetite. Retarded growth and down grade of carcasses. Flock uneven in sizes.
  • g. Delaying birds, egg production drop 20-30%
  • h. Mortality variable, depending on environmental climate condition and the type of secondary infection.

2. Turkeys.

Sinusitis Type

  • a. Age Four weeks and older
  • b. Action: Chronic
  • c. Excessive amount of nasal discharge. Foamy eyes, closing of eyes due to secretion in the sinuses. This secretion may later become cheesy and yellow
  • d. Swelling of the infra-orbital sinus -(one or both sides). 

Postmortem lesions: 

1. Chicken 

  • a. Catarrhal exudate in respiratory tract. 
  • b The air sacs frequently contain caseous exudate and may present a "beaded" appearance. 
  • c. Birds that have a secondary infection show figrinous exolate in the pericardial sac and liver surface, in addition to the above lesions.
  •  d. Histopathology: Marked thickening of mucous membrane, infiltrated by mononuclear cells, and hyperplasia of mucous glands. 

2. Turkeys 

  • a. Muco-caseous exudates appear in the nostrils, eyes sinuses, and trachea. 
  • b. Infra-orbital sinuses are swollen, in named, and filled with exudate, the exudate becomes dry and caseous. 

Diagnosis: 

  • 1. Air sacs are involved more extensive than any other disease . 
  • 2. Very chronic disease. 
  • 3. Serology (blood test) and isolation of the organism. Serum plate agglutination test is reliable. 

Control. 

  • 1. Eradication is the best method of controlling Mycoplasmosis. 
    • a. Start baby chicks from a PPLO free flock 
    • b. Do not use PPLO recovered birds for breeders
    • c. Blood testing breeders, using serum agglutination plate test, stained M.M. G. and M. S. antigens.
  • 2. Delay vaccination of birds with ND, IB virus at times birds were under stress. 
  • 3. Proper ventilation. 
  • 4. Using PPLO vaccine - Not reliable, dangerous, not recommended. 
  • 5. Egg heating to inactivate PPLO, initially eggs are warmed up to room temperature then later incubated during a 12-24 hour period to just reach an internal temperature of 115°F. 

Treatment: 

  • 1. The tetracycline group is effective in treatment 100-400 gm/ton feed. 
  • 2. Tylosin is the drug of choice, the dosage usually used for adult fowl is 25 mg/kg 
  • 3. If the broilers are ready to be sold, sell them and take the loss in condemnation. 

 

2.5.2 Mycoplasma meleagridis:

2.5.3 Infectious Synovitis

Synonyms: Synocitis.

Definition:

Infectious disease of chickens and turkeys, characterized as joint infections and respiratory disease.

Etiology:

Mycoplasma synoviae which is a PPLO and closely related to M. gallisepticum and M. meleagridis 

Susceptibility:

Birds of all ages can be infected, but it is of foremost concern in chicks and poults form 4 to 12 weeks. 

Occurrence:

Widespread in U.S.A. 

Epizootiology:

  • 1. Spread through eggs.
  • 2. Spread by infected birds.

Symptoms:

  • 1. Age: Usually 4-12 weeks
  • 2. Incubation period - caries from 24-80 days.
  • 3. Retarded growth, emaciation, pale comb, lamess, and distended joints of legs and wings.
  • 4. Swollen of hock joints and foot pads.
  • 5. Breast blisters may be seen.
  • 6. Greenish diarrhea common in severely affected birds.
  • 7. Respiratory distress may occur.
  • 8. High morbidity but low mortality.

 Postmortem lesions:

  • 1. Exudate in the joints at first is mucoid and later becomes creamy, caseous and yellowish. 
  • 2. If chicks are infested early in life there is a septicemic stage, the liver is enlarged and greenish and the kidneys become swollen.
  •  3. Respiratory form - air sacs may be filled with caseous exudate.

Diagnosis:

  • 1. History and postmortem appearance are diagnostic.
  • 2. Serological tests, to differentiate M.S. from M.G. and M.M. 

Control.

  • 1. Do not save breeder replacements form flocks that were infected with M. synoviae. 
  • 2. Eradication is the best way to control this disease. 

Treatment

  • 1. Infected breeder flocks should be sold, due to the chronic nature of this disease, recovery is slow. 
  • 2. Antibiotics such as Tylosin, Erythromycin, Spectinomcin and Lincomycin are effective. Chlortetracycline in feed at 200 gm/ton for 14 days. 

2.6 Infectious Coryza. 

a. Synonyms:

Coryza, roug, cold. 

b. Definition:

Acute severe Catarrbal inflammation of the mucous membranes of the upper respiratory tract.

 c. Etiology:

Hemo hilus gallinarum. Hemophlic, pleomorphic, Gram-negtive, non-motile bacterium. This organism is found in the sinus exudate of infected chicken, has bipolar characteristics. In young cultures it occurs as a short coccoid rod, but after 24-48 hours many long forms are found. It does not live long outside the host body. Hemonhilus organism require special nutrients for growth. X-factor-Hemine, cysteine. V factor, DPN (Diphosphorpyridine nucleotide). Horse serum contains both factors. The X factor is not essential for H. gallinarum. 

d. Susceptibility:

Chicken only. Chickens 14 weeks of age and older are most susceptible.

 e. Occurrence:

All parts of this country. However, as serious problem only in the pacific coast area. 

f. Epizootiology. 

  • 1. Transmission through carrier birds. 
  • 2. Contact transmission 
  • 3. Within a flock, contaminated water and feed are probably the mode of transmission.

 g. Symptoms: 

  • 1. Age: Any age, usually growing or laying fowls. 
  • 2. Action: Acute, rapid onsets, spread rapidly. 
  • 3. Thin watery discharge from nostril, soon becomes thick and sticky, with an offensive odor, and has tendency to dry in yellowish crusts around the nasal openings. 
  • 4. As the inflammation extends, the adjacent sinuses become filled with mucus. This is unable to drain away and changes to be rather dry cheesy form which accumulates in large quantities and to cause prominent bulging about the eye Ocular roup
  •  5. If the air passages are involved, rattling noises is evident.
  •  6. Sneeze cough, swollen wattles
  •  7. Affected fowls set quietly with feathers ruffled, have little or no appetite, shake their heads frequently in an effort to dislodge the mucus.

 h. Postmortem lesions: 

  • 1. Acute catarrhal inflammation of the mucous membranes of the nasal passages and sinuses.
  •  2. Catarrhal conjuntivities and subcutaneous edema of the face and wattles.
  •  3. Chronic inflammatory process accompanied by caseous exudate in the sinuses, nasal passages and conjunctival sacs.
  •  4. Histopathology-Sloughing, hyperplasia of the mucosal and glandular epithelial cells. Heterophil infiltration of upper respiratory tract including infraobital sinus, trachea and nasal cavity.

I Diagnosis:

Based on history, field symptoms and particularly had odor of exudate. 

1. Differential diagnosis:

  •  a. Fowl pox - yellowish patches in the throat are easily removed in roup, while in pox they are adherent to lower layer.
  •  b. Other diseases also produce this type of lesions are chronic cholera, vit. A deficiency and GRD. 

2. Bacterial and isolation.  

J. Control  

  • 1. Strict sanitation program 
  • 2. Feed high level of Vitamin A 
  • 3. Remove any carrier or recovered birds. 
  • 4. Do not mix birds with different ages. 
  • 5. Depopulate, empty chicken house for at least 2 weeks before using again. (Break the cycle). 

K. Treatment: 

  • 1. Medication: Sulfathizole when given in mash or drinking water is effective. (1/2 lb. sulfathiazole/100 lb. feed). 
  • 2. Severe swelling (edema) in the eye or sinus must be treated individually.

2.7 Avian Hepatitis 

a. Synonyms: 

Infectious hepatitis, Avian vibronic hepatitis. 

b. Definition:

Acute to chronic infectious disease of adult chickens characterized by hepatitis. 

c. Etiology:

Vibrio hepaticus produces yolk sac congestion and necrosis of liver and enlargement of spleen of embryonating chicken eggs. It is a Gram-negative, motile organism, short comma, S-shaped forms, and long spirals. 

d. Susceptibility:

Chickens only. 

e. Occurrence:

Incidence low in the U.S. 

f. Epizootiology:

Oral transmission 

g. Symptoms: 

  • 1. Age: Growing chicks and laying pullets. 
  • 2. Action: From acute to chronic. 
  • 3. Incubation period-Varies from 2-15 days. 
  • 4. Increased in the number of cuts due to emaciation. Listlessness, shrunken comb, and loss of flesh 
  • 5. Drop in egg production of 20-30% within a period of 2-3 weeks
  •  6. Low mortality, form 5-15%. (High morbidity). 

h. Postmortem lesions: 

  • 1. Liver is the primary site of gross lesion. Congested, hemorrhagic and necrotic areas in liver.
  •  2. Myocardial necrosis, splenic infarction. 
  • 3. In chronic cases, varying degrees of ascites and cardiacy hypertrophy of pericardiocites.
  •  4. Histologically, the liver shown lymphocytic and heterophilic infiltration around the veins of hepatic triad, fatty degeneration of liver cells, and focal necrosis.

 i. Diagnosis: 

  • 1. A sudden drop of egg production without any noticeable disease symptom. 
  • 2. Increase amount of culls as many as 50% chickens in a month
  • 3. Should differentiate this disease from leukosis. There are tumors and intestinal involvements in leukosis.
  • 4. Laboratory diagnosis: Culture organism in 5-7 day old embryonating chicken eggs, from liver or heart blood of affected birds. Enrichment media, reduced O2 tension.

 j. Control. 

  • 1. No specific methods are available for the control of this disease  
  • 2. Improvement of general hygienic measure.

k. Treatments:

Furazolidone is the drug of choice. (NF-180)

Dosage:

200-400g./ton of feed for several weeks.  

2.8 Erysipelas 

a. Synonyms: None

b. Definition:

Acute infectious bacterial disease of most fowl.

Characterized by erhthematous lesions on the skin, swollen snood in turkey toms, and visceral congestion.

c. Etiology:

Erysipelothrix insidiosa, Gram-positive when first isolated from birds. Prolonged cultivation in artificial media changed to gram-negative, short rod, non-motile, non-spore forming organism. 

d. Susceptibility: 

  • 1. Turkeys are very susceptible, it is more common in male turkeys nearing marketing age.
  •  2. Other fowls infected are chicken, ducks, pigeon, pheasant, quail, peacocks and a number of wild birds.
  •  3. Swine, sheep and human are also susceptible. 

e. Occurrence: World wide. 

f. Epizootiology: 

  • 1. Considered soil-born disease, the organism lives in soil for a long time, so that infected premises are a source of infection. 
  • 2. Animals such as hogs, sheep and wild birds are reservoirs. 
  • 3. Organisms enter the body through scratches-mosquito bite or fighting.
  •  4. The organism has been recovered from fish meal so mixed feeds may be a source of infection. 

g. Symptoms: 

  • 1. Age: Turkeys usually 4-7 months of age. 
  • 2. Action: Acute, septicemia 
  • 3. Listlessness, anorexia, cyanotic head. 
  • 4. Greenish to yellowish diarrhea 
  • 5. Swollen snood and carnucles, purplish color. 

h. Postmortem lesions: 

  • 1. The most pathognomonic lesion in turkey is a turgid, reddish purple carbuncle and snood.
  •  2. In poults, hemorrhages in pectoral, thoracic, abdominal muscles, thigh muscle, pericardia, pleural and peritoneum.
  •  3. Liver and spleen-enlarged, congested and friable.
  • 4. Enteritis

 i. Diagnose: 

  • 1. Symptoms similar to blackhead, paratyphoid and other diseases.
  • 2. In turkey, swollen carbuncles and snood is pathognomonic.
  • 3. Confirmation diagnosis depends on the isolation of causative agent.

 j. Control: 

  • 1. Isolation: Do not allow birds to come in contact with sheep or swine, nor should they be allowed to run over ground on which these animals have ranged.
  •  2. Sick birds should be removed and destroyed by burning and the apparently well fowls move to uncontaminated premises.
  •  3. Stop birds gighting with each other by debeaking and desnood.

 k. Treatment: 

  • 1. Use high level penicillin therapy. 50,000 units per bird/IM.
  • 2. Aureomycin is also effective Summer- use 100 gm per ton of feed or 2 ounces per 50 gallon of drinking water. Winter-double the dose.
  • 3. Vaccination: Formalin kelled, aluminum hydroxide absorbed bacteria has been used successfully to immunize turkeys. Several biologic companies produces Erysipelas bacteria for example: 
    • a) Duvox - Lederle vaccine, as preventive
    • b) American Scientific Laboratories
    • c). Sasbury Laboratories.  

Inject 1/2 cc for birds up to 10 lbs., 1 cc for birds over 10 lbs . If erysipelas is an early problem, vaccinate at 8 weeks or whenever poults are moved to range, then revaccinate within 3 months. Birds kept for breeding should be vaccinated again at the time of selection. Do not vaccinate within 21 days before slaughter. 

2.9 Disease caused by anaerobic spore-forming bacteria. 

2.9.1 Ulcerative Enteritis. 

Synonyms:

Quail Disease 

Definition:

Highly infectious and cirulent diseases of game birds, characterized by intestinal ulceration and liver necrosis. 

Etiology:

The etiology of Quail disease has been controversy for many years. However, recent detailed studies established convincingly that the cause is clostridium colinum, a gram positive, spore forming rod shape bacteria. 

Susceptibility:

Quail most susceptible, chicken, turkey, partridge, and grouse are also susceptible. 

Occurrence:

Widely scattered in the U.S,,particularly in quail raising area. 

Epizootiology: 

  • 1. Natural condition - transmitted by ingestion of contaminated feed litter and water. 
  • 2. Experimentally transmitted through feeding suspensions of intestinal contents from infected birds.

 Symptoms: 

  • 1. Age All ages 
  • 2. Action: Acute, birds sometimes died without manifesting symptoms.
  • 3. Chronically infected quails are listless, lumped up with the eyes partly closed, and the feathers are dull and ruffled. 
  • 4. Watery droppings containing urates - one of the first sign. 
  • 5. Decrease in feed consumption and emaciation. 
  • 6. Course of this disease is approximately 3 weeks with the peak of mortality between 5-14 days post-inculation in experimentally infected birds.

 Postmortem Lesions:

  •  1. Acute - birds died early, lesions limited to hemorrhagic enteritis of the upper portion of intestine. 
  • 2. Ulceration may occur in any portion of the intestine and ceca The ilium and rectum are most commonly affected.
  •  3. The ulcers originated as small yellow foci with a hemorrhagic border and are visible on the serosal and mucosal surfaces, or large necrotic dipheratic lesions that may be superficial and have raised edges. 
  • 4. Liver had light yellow mottling to large irregular yellow area of necrosis along the edges, gray foci or small yellow circumscribed foci which sometimes surrounded by a light yellow haloeffect - crater like ulcer. 
  • 5. Spleen, congested, enlarged, hemorrhagic and necrotic. 
  • 6. Lung congested, sometimes consolidated 
  • 7. Histopathology: Large focal areas of coagulation necrosis granulocytic and lymphocytic infiltration.

Diagnosis: 

  • 1. Presumptive diagnosis could be made on the basis of finding ulcerations in the ceca and intestine, accompanied by necrotic foci in the liver and an enlarged hemorrhagic spleen.
  •  2. Bacterial isolation and identification. 
  • 3. Blood smears and histological sections revealing Gram positive and subterminal spore bearing organisms.

 Treatment and Control 

  • 1. Recovered birds serve as carrier 
  • 2. Scrupulous cleanliness about the pens. 
  • 3. Streptomycin is quite effective 
Prophylactic 2gm/gal. drinking water for 25 days. 

Treatment -4-5 gm/gal. drinking water for 5-10 days 

  • 4. Bacitracin and neomycin are also effective 
  • 5. Chloromycetin at a level of 500 gm per ton of mash gave complete protection.

2.9.2 Botulism. 

Synonyms:

Limberneck, western duck sickness, duck disease, and bulbar paralysis.

 Definition:

Acute intoxication of fowl caused by ingestion of spoiled food containing toxin produced by Clostridium  botulinum, characterized by flaccid paralysis of the neck weakness and prostration.

 Etiology:

Clostridum botulinum bacilli, Gram positive rods with peririchous flagella. Occurs singly in pairs and in short to long chains, obligate anaerobes. Cl. botulinum produces many types of exotoxin, the most common type of toxin affects poultry is the C type which is subdivided into C a and C b. C a affect birds only, but C b affects birds and mammals.

 Susceptibility:

All animals are susceptible. The turk vulture is the only known animal to be resistant.

 Occurrence: Outbreaks of botulism in fowls have been reported from widespread areas in the United States. 

Epizootiology: 

  • 1. The disease is more prevalent during warm weather because of the favorable conditions for toxin production but the feeding of spoiled foods may produce the disease at any time
  • 2. Decaying bird carcasses on poultry ranges, wet litter, or other organic matter and fly maggots from decaying substances may habor botulism. 

Symptoms: 

  • 1. Age: Any age, usually adult. 
  • 2. Action: Acute
  •  3. Symptom depend upon volume of toxin .ingested 
    • 1. Sleepy, dull and cyanosis of the head 
    • 2. Neck, leg and wing muscle paralysis. Limbernec ducks might drown. 
    • 3. The feathers are found to be loose and easily plucked.
    •  4. Paralysis of the nifating membrane is pathognomonic of botulism but this symptom was observed in only a few cases out of many affected birds. 

Postmortem Lesions: 

  • 1. Botulism produces no diagnostic changes in the organs of an affected fowl. 
  • 2 varying degrees of catarrhal enteritis may be present 
  • 3. Hemorrhage of the heart also may be seen. 
  • 4. Usually the crop is full. 

Diagnosis: 

  • 1. A presumptive diagnosis may be made by observation of the typical flaccid paralysis. 
  • 2. Mouse protection test. 
    • l) Serum from affected birds is inoculated I.P in 0.5 1.0 ml amounts into groups of mice. Death is a positive test. 
    • 2) One group of mice is protected by prior injection of 150 units of botulism antitoxin before injected the serum. Survival of these mice confirm the diagnosis. 

Control

  • 1. Avoid low, wet and stagnant areas. 
  • 2. Watch for spoiled feed. 
  • 3. Pick up dead birds if they are on range. 

Treatment: 

  • 1. Laxatives such as castor oil or Epson salt are a value in the treatment of exposed birds which have not yet shown symptoms of the disease. 
  • 2 Antitoxin is not practical in fowl.
  • 3. Remove stagnant water. 

2.9.3 Gangrenous dermatitis

 Synonyms: kin necrosis, wing rot.. 

Definition:

Necrosis of the skin and deeper tissues 

Etiology:

Several species of clostridial bacteria are responsible. Involved most often is C. septicum. Also encountered are C. perfringens, C. nocy, and C. sporogenes. These clostrida are also part of the normal microflora of the soil and the intestine. These bacteria are large anaerobic gram-positive rods with spores. 

Susceptibility:

Commonly seen in chickens and turkeys. However, this condition also exists in other birds.

 Occurrence:

Almost spontaneously in 4-16 week-old chickens and turkeys.

 Signs:

All parts of skin may be involved. 

Postmortem Lesions: 

  • 1. Necrosis of skin and deeper tissue of the thigh, lumbar area, breast, and extremities. 
  • 2. The necrotic area are hemorrhagic, may contain gas and presence considerable edema. 
  • 3. Livers are often swollen, greenish brown, and contain focal areas of necrosis. 
  • 4. Many large gram-positive rods are present in the subcutaneous tissue, muscle, and liver. 

Diagnosis: 

  • 1. Stained smears: Large gram-positive rods, with spores in carious necrotic tissues.
  •  2. Anaerobic culture and identification of the bacteria. 

Treatment: 

  • 1. Tetracyclines 
  • 2 Penicillin and bacitracin.

2.9.4 Necrotic enteritis 

Etiology:

Caused by type C strains of Clostridum perfringens. 

Occurrence:

In 6-8 week-old chickens. 

Signs:

Rapid loss of condition (emaciation), anorexia and blood-stained feces.

 Postmortem:

  •  1. Thickened distal thread of the small intestine lumen contained bloody exudate. 
  • 2. A necrotic layer consisting of degenerate cells and large numbers of gram-positive rods adheres to the surface or in the lumen of the S.I. 
  • 3. The liver is congested and contains variable numbers of 2-3 mm sharply defined necrotic areas. 

Diagnosis:

Same as the other Clostridial infections.

 Treatment:

Same as necrotic dermatitis. 

2.10 Staphylococcosis. 

a Synonyms:

  • Stap infection, septicemia, staph arthritis. 

b. Definition:

  • Acute or chronic infection caused by stanhylococc; characterized by septicemia, arthritis, vesicular - dermatitis and Bubble foot. 

c. Etiology:

  • Staphylococcus aureus. Gram-positive cocci, the pathogenic strins will coagulate rabbit serum and produce hemolysis on blood agar.

 d. Susceptibility:

  • All fowls are susceptible. However, avian pathogenic strains do not affect human and mammals.
  •  e. Occurrence: World wide. 

f. Epizootiology: 

  • 1. Soil-borne disease 
  • 2. Direct with carrier birds. 
  • 3. Bacteria are passed in droppings of sick birds. 
  • 4. Dirty general environment. 

g. Symptoms for different types of infections. 

  • 1. Arthritis and periostitis, chronic form, lameness, hobbling gait, and frequent resting on the hock, usually one or more joints were swollen. Erosion of the articular surface, with cheesy pus present.
  •  2. Vesicular dermatitis. (Staphylococcus and Clostridial bacteria -are the two organisms most commonly isolated from poultry skin). Appearance of vesicles on the comb wattles, face, feet and shank in early stage and later change to amber-colored scales.
  •   3. Bumble foot. 
  • Abscess of the foot, the primary cause is a bruise or cut on the bottom of the foot through which organisms gain entrance.
  •  4. Omphalitis in baby chicks and turkeys.

 h. Postmortem Lesions: 

  • 1. Acute form- Septicemia, with dark swollen liver, small ambercolored liver, abscesses, watery intestinal content large amount of yellow pus in the affected joints.
  •  2. Chronic form - arthritis, breast blisters, bumble foot, and earlobe infections.

 i) Diagnosis:

Confirmed diagnosis by cultivation and identification of the bacteria. 

j ) Treatment:

  • 1. Erythromycin, novobiocin and penicillin are effective.
  • 2. Novobiocin must be administered in the feed, 350 grams per ton for 5 -7 days.
  • 3. Erythromycin and penicillin can be administered in the water 3 - 5 days, or in the feed at 200 gm per ton for 15 days.  

2.11 Colibacillosis.

2.12 Avian Streptococcosis.

a) Synonyms:

Strep infection.

b) Definition:

Acute or chronic infection of chicken by Streptococci.

c) Etiology:

Streptococcus gallinarum,(Strep. zooepidemicus), belong to Lancefield group C; Gram positive cocci, in chains of 6 to 8 cells

d) Susceptibility:

chickens are natural host.

e) Transmission:

Infection in natural outbreak is by way of nasal cavity.

f) symptoms:

  • l. Applectiform septicemia - sudden death in peracute cases.
  • 2. Sleep and depressed.

g) Lesions.

  • l. Diffuse hemorrhage of breast muscles and skin.
  • 2. Enlarged spleen, slightly enlarged liver.
  • 3. Perihepatitis and pericarfitis.
  • 4. Catarrhal inflammation of intestine.

h) Diagnosis:

Isolation of Streptococcus qallinarum from infected birds

i) Control.

Avoid introduction of affected birds, and institute strict sanitary measures.

 j) Treatment. 

Drugs such as penicillin, erythromycin, novobiocin, eleodromycin,tetracylines and nitrofurans have proved of value, particularly in acute infections.

2.13 Omphalitis

 a) Synonyms:

Navel ill, mushy chick disease.

b) Definition:

Naval infection of baby chicks involving improper closure of the naval with subsequent bacterial infection lead to septicemia.

c) Etiology:

Staphylococcus aureus, Streptococci, coliform bacteria, Pseudomonas are the common bacterias incriminated into this condition.

d) Occurrence

  • 1. Faulty incubator and hatchery sanitation
  • 2. Hatching eggs with dirty shell or poor egg shell quality.

e) Epizootiology:

  • 1. Primary infection source is dirty eggs.
  • 2. Baby chicks are infected in the hatchery during hatching.
  • 3. Does not spread from chick to chick.

f) Symptoms:

  • 1. Age: A few hours old to several days.
  • 2. Action: Acute.
  • 3. Inflammation of the navel. 

g) Forms of infection.

  • 1) Wet form - soft, blowed, mashed, decomposed with bad odor due to gas production. 
  • 2) Dry form - birds linger for two or three days, scars occur at the navel region. Body cavity appears dry. 

h) Postmortem Lesions. 

  • 1. Large amounts of fluid in the muscles, internal organs and body cavity.
  • 2. Dead body liquidies rapidly.
  • 3. Unabsorbed yolks - peritonitis.  

i. Diagnosis: 

  • l. Tentative diagnosis can be made based on age & postmortem lesions.
  • 2. Culture yolk sac material for bacteria.  

j) Control

  • 1. Do not handle green chicks.
  • 2. Clean up incubator on every hatch.
  • 3. Do not place chicks on moist, dirty environment.  

k ) Treatment.

None. Most affected birds die the first few days of their lives. 

2.14 Avian Listeriosis

a) Synonyms:

  • None.

b) Definition:

  • A chronic or subacute disease of domestic fowl, characterized by septicemia, massive necrosis of the heart muscle.Nervous signs are seldom seen.

c) Etiology:

  • Listeria monccytagenes, a small motile, Gram positive rod, non-spore forming bacteria. Minute colonies, surround by B-type hemolysis (narrow zone).

d) Occurrence:

  • Sporadic.

e) Symptoms

  • 1. Some affected birds died suddenly.
  • 2. Slow wasting is evident in young naturally affected chickens.

f) Postmortem Lesions

  • 1. Massive necrosis of heart muscle. Pericarditis.
  • 2. Necrotic foci in the liver.
  • 3. General edema.
  • 4. Monocytosis in many cases.
  • 5. Histopathology: Necrotic areas frequently contain bacteria. In filtration with lymphoid cells, macrophages and plasma oells.

g ) Diagnosis: 

  • 1. Massive necrotic areas in the heart muscle are suggestive of listeriosis.
  • 2. Positive diagnosis can be established by isolating the organism from the heart blood in blood agar plates.

h) Control

General hygienic environment

i) Treatment:

Chlorotetracycline (Aureomycin) is the drug of choice, lOOg/ton of feed. 

2.15 Spirochaetosis. 

a) Definition:

Acute infectious disease in fowls characterized by fever, locomotor disturbance, and progressive paralysis. Usually seen in tropical or subtropical countries. 

b) Etiology:

Borelia anserina, a spirochete. The family Treponematocea consists of three Genera, Rorrelia, Treponema and Leptosnira. These organisms are difficult to culture in vitro.

 Borrelia anserina is loosely spiraled with 5-6 spirals. The length caries form 7-21 M with an average of 14 M. Motile by a single, short, delicate flagellum at each end. The spirochete has terminal hook which differentiate it from leptospira. Readily stains with aniline dyes as well as with Giesmsas stain.

 c) Susceptibility:

  • 1. Chickens and turkeys are readily susceptible.
  • 2. Ducks and geese are occasionally affected.

d) Transmission:

  • 1. Transmitted by fowl tick Agras pers icus, ingesting infected ticks, their eggs,or contaminated food.
  • 2 Through infected biting flies, insects, or mosquitoes.
  • 3. Transocarian transmission.

e) Symptoms:

  • 1. Signs of incubation period 5-9 days. About 21 days for chronic forms. 
  • 2. Fever 110°
  • 3. Swelling of the feet and claws.
  • 4. Pale comb, listless, greenish diarrhea
  • 5. Anemia, emaciation

f) Postmortem Lesions:

  • 1. Spleen markedly enlarged, mottling and hemorrllagic
  • 2. Liver is pale and contain numerous caseous foci
  • 3. Fibrinous pericarditis and myocarditis.
  • 4. Anemia and enteritis.

 g) Diagnosis: 

  • 1. At the height of the disease the organisms can be demonstrated in the peripheral blood smears stained with Giemsa . 
  • 2. In chronic cases, the organisms can be demonstrated in the pericardial fluid.
  •  3. Agglutination and complement fixation tests may also be used.

h) Control:

  • 1. Eradication of the vector Argas persicus.
  • 2. Control other biting insects

i) Treatment:

  • 1. Atoxyl (sodium arsanilate), the arsenobenzol group of drugsSoamin and Novarsenobillion, penicillin and Tetracycline are effective
  •  Bacterial endocarditis
  •  Etiology: Streptococcus fecalis, Staphylococcus aureus, Pasterurella multocida. Erysipelothrix insidiosa. 

j) Symptoms:

  • 1. Depressed, pale shrunken combs and wattles.
  • 2. High heterophils blood count. 120,000 or more.

k) Lesions:

  • 1. Vegetations On heart valves. The mitral and aortic valves are most frequently involved. 
  • 2. Liver infarct, septic emboli. 

2.17 ORNITH0SIS OR PSITTACOSIS. 

a) Synonyms:

Chlamydiosis, Parrot fever. 

b) Definition:

Psittacosis is primarily a disease of psittacine birds. Ornithosis has been accepted as a broad term to cover the infections of all birds and psittachsis has been used to designate the disease in man.

 c) Etiology: 

  • 1. It is caused by an agent belonging to the rickettsial group. Miyagawenella. psittaci or Chalamydia psittaci. 
  • 2. The order Richettsiales contain organisms produce intracellular elementary bodies. They are intermediate between bacteria and viruses. Non-filterable, gram negative.
  •  3. Can be cultivated in vitro only in living cells. The most common host for cultivation is chick embryo.
  •  4. Rickettsial organisms are classified as bacteria due to the following properties.
    •  1. Multiply by binary fission. 
    • 2. Contain both DNA and RNA 
    • 3. Possess a number of indigenous enzymes. 
    • 4. There are two genera under the family of Chlamydozoaceae.
      •  l) Miyagaiwenella or Bedsonia - Psittacosis and Lymphogranuloma cenerum group.
      •  2) Chlamydozooni-traChoma, inclusion conjuntivities.

 d) Susceptibility: 

  • 1. Primarily disease of parakeets, parrots, love birds and other members of the psittacin group. 
  • 2. Canaries, finches, pigeons, ducks, chickens and turkeys.
  •  3. Human beings are susceptible and people of middle age are more likely to contract the malady than are children.

 e) Transmission: 

  • 1. Spread of the infection occurs primarily by means of body excrete 
  • 2. Contamination of feed and water takes place readily and in this manner transmission is affected from disease to healthy birds.
  •  3. Man contract the disease by inhaling infectious particles of dust or droplets originating from a sick bird.
  •  4. Latent carriers.

 F. Symptoms: 

Turkey 

  • 1. Age: In birds 10 weeks and over 
  • 2, Action: Chronic 
  • 3. Emaciation 
  • 4. Feverish, sleepy, dull 
  • 5. Difficult in breathing, rale. 
  • 6. Yellowish diarrhea. 
  • 7. Many show no symptom. 

g. Lesions. 

  • 1. Emaciation 
  • 2. Spleen and kidney enlarged. 
  • 3. Saffron-colored liver with fibrinous exudates covering the liver surface. 
  • 4. Thickened pericardium and accumulation of exudate in the air sac and on the pericardium and epicardium. 
  • 5. Birds introduction may have accumulation of egg yolk material in the peritoneal cavity.
  •  6. Diffuse pneumonia may occur, but pulmonary edema was more often noticed.
  •  7. Histopathology: Two types of changes are significant , necrotizing

change of parenchlymatous cells and proliferative change of R.E. cells. Also, extensive infiltrations of mononuclear cells, lymphocytes, and heteroophils in the lamina propria and submucosa of the respiratory tract. 

h) Diagnosis: 

  • 1. The extreme infectiousness of the condition for both birds and human handling must be extremely cautious. 
  • 2 It is impossible to recognize orinthosis clinically or by gross anatomical inspection, laboratory diagnosis is rerequired.
  •  3. Birds scatter infected material in dried feces and nasal discharges attached to feathers. Dead birds or birds killed with chloroform should be immersed completely in 5% lysol solution.
  • 4. Smears prepared during necropsy from pericardium, serous surface of the liver, hepatic lesions, or spleen are fixed for 5 minutes with methyl alcohol and then stain with Giemsa for 3 to 20 minutes. Look for elementary bodies. 
  • 5. Material form birds with gross lesions in which elementary bodies are microscopical, are excellently suited for isolation of the virus by inoculation of mice.
  •  6. Identification of the organism.
    •  l) Complement fixation test- mouse spleen or yolk sac material rich in elementary bodies is used as antigen.
    •  2) Pathogenicity tests - inoculation of mice, guinea pigs, hamsters parakeets, pigeons.
    •  3) Fluorescent antibody test. 

i) Treatment:

The organism is susceptible to penicillin, chloramphenicol, and tetracycline. However, only tetracyclines are both economically feasible and effective for large scale treatment of poultry flocks. 100-300 g/ton feed for 2 weeks.

 j) Prevention and Control: 

  • 1. Through management method, blocking air transmission
  •  2 Isolation of sick birds with therapy at the same time.
  •  3. Vaccination not effective
  •  4. Reportable disease, interstate movement of birds form infected flocks is prohibited.