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Poultry diseases and treatment

Dr. Mujeeb Ather Asst. Director (Pathologist)
Veterinary Biological Research Institute, Hyderabad .

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  • Disease challenges by viruses, bacteria, parasites and toxic compounds are common in poultry. Although out rate clinical disease may not occur but the immune system is impaired resulting in susceptibility to other infections and vaccination failure against ND and IB.
  • Despite advance in diagnostic procedures vaccinations and medication CRD remains one of the most important diseases in many poultry producing areas of the world.
  • It is a very challenging disease and difficult to prevent under typical field conditions.
  • Mycoplasma Gallisepeticum & Mr. Synoviae are the two significant species affecting poultry.


  • CRD caused by M. Gallisepeticum and Synoviae and Airsaculitis die to M. Synoviae infection occurs worldwide. These conditions are responsible for extensive losses especially losses especially where concurrent viral respiratory diseases occur.
  • Despite all out efforts to control and eradicate mycoplasmosis, this troublesome disease continuos to inflict heavy economic losses in poultry flocks.
  • CRD became most troublesome following disease situation (like vaccination stress, secondary stress, secondary bacterial invaders etc.) The annual losses also do occur due to poor production of eggs and meat and low hatchability in the flock that survive and increased medication cost make this one of the costliest disease problems confronting the poultry industry.
  • Commercial broilers between 3 - 7 weeks of age are more susceptible with severe infection at 5 th week, mortality 12-12%. Commercial layers are susceptible from 3 rd week onwards with severe infection between 16-18 weeks and 21-23 rd weeks, Mortality 5-6%.

Pathological and Economical losses due to Mycoplasma Infections:

DIRECT LOSSES:

  • Embryo Mortality 15 - 20%
  • Chick Mortality 10 - 15%
  • Depressed Weight gain 10 - 20%
  • Depressed feed consumption 10 - 20%
  • Egg Drop 10%

INDIRECT LOSSES:

Increased sensitivity to

  • E.coli and other bacterial infection
  • Immuno suppression
  • Vaccine failure particularly against ND & IB

TRANSMISSION

  • The most important method of mycoplasma transmission is vertical from the hen through the eggs to the broiler flock. Frequency of mycoplasma contamination in eggs is dependent upon the degree of infection in the hen. It has been shown that, Mycoplasma do not infect every egg passed from an infected hen. This is because every yolk does not pick up the organism, but the greater the Mycoplasma infection in the bird the greater the chances of transmission.
  • Bird to bird transmission is the second most important method of Mycoplasma spread Mycoplasma causes lesions in the upper respiratory tract, nostrils, sinuses and trachea. Wherever the lesions occur Mycoplasma also occur and serve as a source of infection for other birds.
  • Mycoplasma can be carried on droplets of water. The most logical source of infection is from the breath of chickens. Any snacking, coughing or sneezing resulting from the upper respiratory lesions can cause the spread of Mycoplasma.
  • Spread also takes place by contaminated feed and equipment.

Pathogenesis:

  • Mycoplasma penetrates the protective cells of the living membranes of the air passage; they begin killing these cells initiating an inflammatory reaction of the entire area and in some instance penetrates into the blood stream. Lesions caused by Mycoplasma become entryways for other microorganisms. During the invasion, Mycoplasma pass through the air passage into the air sacs, their favorite site of infection. Air sac membranes have virtually no defense since they are made up of only two thin layers of cells without any protective covering. The first lesions on the air sac membranes appear as very small, slightly cloudy swelling that look like a drop of dew. The lesions multiply so that by 3-7 days they join together and become cloudy or opaque.
  • Generally under field conditions bacteria begins their entry soon after Mycoplasma lesions appear. By the end of 7-10 days the lesions become very thick with the formation of heavy yellowish pus, which may be foamy.
  • Bacteria invasion of Mycoplasma lesions causes much more severe infections. E.coli is the most commonly recognized secondary bacterial invader, but several others including pseudomonas, klebsellia, proteus streptococci and staphylococci can be involved.

ASSOCIATED BACTERIAL INFECTION:

  • E. Coli 70%
  • Pseudomonos 20%
  • Proteus 5%
  • Klebseilla 3%
  • Streptococci 1%
  • Staphylococci %

Symptoms:

  • Incubation period: 6-21 days under natural condition. It is very difficult to determine the exact date of exposure. Numerous chicken flocks develop clinical infection near the onset of egg production suggesting a low level of inherent infection (probably due to egg transmission). This apparent long extension of the incubation period is especially common in off springs of infected chicken hatched from the eggs dipped in antibotic solution for control of M.G. infection.
  • Clinical manifestation develops slowly and in winter months the disease has long course.
  • Coughing, snicking and sneezing
  • Oedema of head with nasal and eye discharges
  • Retarded growth
  • Reduced feed conversion
  • Moderate-high mortality
  • Decreased quantity of Poultry meat
  • Reduced egg production
  • Increased severity of vaccine reactions against RD & IB.
  • Increased susceptibility to stress particularly chilling.
  • MG infected layers remains septicemic throughout life and therefore has lower production levels thereafter.
  • The hens develop antibodies bit the infection remains active. So no benefits are derived from the immunity.
  • MS infected hens tend to for through the infection, recover and develop immunity after which they return to normal production rates.
  • Medication against MG will improve the production but medication must be maintained continuously to prevent production slumps.

Pathology:

  • Oedema of the head
  • Catarrhal exudate in the nasal passages, air sacs and in the trachea
  • Yellowish cheesy material in the air sacs (thoracic and abdominal)
  • Fibrinous peri hepatitis
  • Thickening of the respiratory mucosa, congestion with infiltration of mononuclear cells.
  • Lymphoid hyperplasia of the submucosa of the bronchi and the wall of the air sacs.
  • M.Synoviae causes severe arthritis.

 


Perihepatitis

Diagnosis

  • Symptoms and lesions
  • Serological tests like SPA, HI and ELISA
  • Isolation and identification
  • Histopathological studies