Avian Mycoplasmosis

Avian Mycoplasmosis develops reduced hatchability, sub optimal egg production and poor carcass quality there by impose economic loss.

Avian Mycoplasmosis is mainly a disease of respiratory system, characterized by coryza, sneezing, moist rales and open mouth breathing.

Etiology

The disease is caused by Mycoplasma belongs to mollicutes, order Mycoplasmatale.

It is a small, self-replicating prokaryotes measures about 300-800nm in diameter. They lack the cell wall, but surrounded by a triple layered plasma membrane.

Some species of mycoplasma are pathogenic. There are 22 species of mycoplasma recovered from avian sources but only four of them are found affecting domestic poultry.

There is difference exists in virulence and tropism of the strains. The organism is highly sensitive to external environment and survival is restricted to a few days or less under normal poultry house condition. It is also sensitive to detergent.

• M. gallisepticum (Mg) – Chicken and Turkey
• M. synovieae (Ms) – Chicken and Turkey
• M. meleagridis (Mm)- Turkey s and family Mycoplasmataceae

Epidemiology

Predisposing factors

• Virulence of the organism.
• Number of organism taken by the host Species and age of the host.
• Debilitating factors.
• The disease usually occurs in association with other pathogens such as New castle disease (live virus), Infectious bronchitis, Turkey rhinotracheitis, pathogenic strains of E.coli and Haemophilus paragallinarum.
• Nutritional deficiency, excessive enivironmental anoxia, dust, and social stress.

Source of infection

Mostly intensive method of rearing of birds found to establish the form of respiratory complex disease in association with other pathogens and predisposing factors. The disease is present in poultry species for many years.

Transmission

• Lateral transmission occurs from birds to birds.
• Transovarian transmission occurs in chickens and turkey.
• Fomites, and air borne transmission play a crucial role  for the spread of infection.

Host Affected

• Chicken and turkey are the natural host for this infection. However, turkey and very young birds are more susceptible to the disease.
• Intensively reared birds mostly infected.
• In addition, the organism has been isolated from ducks and free flying birds
• It is also isolated from the oviduct of fowls, turkey hens, cockerel and turkey semen.

Pathogenesis

M gallisepticum outbreaks occurs by lateral transmission from infected chickens; some times egg transmission becoming a major source of infection.

The incidence of egg transmission is highly variable, ranging up to 30-40% during the first 2 months after infection of susceptible birds in production.

The transmission rate then lessens and is inconsistent (0-5%) until the end of production. Birds infected before the onset of production transmit through the egg at a much lower rate, if at all. The infection may be dormant in the infected chick for days to months, but when the flock is stressed, aerosol transmission occurs rapidly and infection spreads through the flock.

All mycoplasma species enter the body either congenitally In the respiratory tract M. gallisepticum initially attached to the epithelial cells and causes cellular damage and interference with cilial activity. Injury to the cell membrane, impairment of cell nutrition and the production of hydrogen peroxide by the organisms are observed.

The infiltration of subepithelial tissues with monocytes is a non specific inflammatory response where as specific inflammatory response occurs by infiltration with large numbers of lymphocytes.

Initially, toxin is produced by high concentration of organism and later resulted with immune response. The possibility that a toxin is involved.

In acute anaemia in chickens infected with M. synoviae the rapid onset and the absence of extramedullary erythropoiesis suggest a haemolytic cause rather than suppression of erythrogenesis.

The epithelium of the upper air passages is most susceptible to infection; however, in severe, acute disease the infection is also found in the lower respiratory tract. Live virus vaccination, natural virus infection, cold weather, or crowding may initiate the spread.

In addition, the infection may be carried by personnel, fomites, or introduction of infected birds. In many flocks, the source of infection cannot be determined.

The epithelium of the upper air passages is most susceptible to infection; however, in severe, acute disease the infection is also found in the lower respiratory tract.

There is a marked interaction between respiratory viruses, Escherichia coli , and M gallisepticum in the pathogenesis of chronic respiratory disease. Once infected, birds remain carriers for life.

Clinical Signs

• Young birds Coryza, sneezing and moist rales.
• Open mouth breathing increase during concurrent infection.
• Coryza is more severe in turkey than in chickens.
• In turkeys sinusitis with swelling of one or both of infraorbital sinuses is noticed.
• Complete closure of eyes.
• Nasal exudate often join with sinusitis.
• Soiling of wing feathers of turkey.
• Swelling of infraorbital sinuses rare in chicks.
• Conjunctivitis, exudate in eyes seen in both chicks and turkey visible.
• Adult birds Decrease egg production in layers.
• Ataxia and swelling of hock and lameness is noticed in turkey.

Necropsy Findings

Accumulation of excess mucous or catarrhal exudate in nares, trachea, lungs and edema of the airsac walls.

Dilatation of the infraorbital sinuses especially in turkeys due to the presence of excess mucous and later filled with caseous materials.

In the presence of other pathogens severity of the disease may be prolonged and leads to chronic condition. With E. coli, colispepticemia, pericarditis, perihepatitis, and airsacculitis is observed in 4-10 weeks old chickens.

There is no gross lesion produced in encepalopathy of turkeys. Tenosynovitis, arthritis (M.sinoviae), salphingitis with caseous exudate occurs in the oviduct.

Diagnosis

• Based on clinical signs and necropsy findings
• Isolation and identification of organism
• Prolonged incubation of 3-4 weeks period is required for cultivation or else if no growth is seen after this time the culture may be discarded as negative
• Antigen and antibody detection by immunofluorescence technique using species specific sera.
• Molecular diagnosis by PCR.
• Differentiation of strain from other stains of mycoplasma.
• Rapid serum agglutination test: Serum from infected birds forms a clumps when mixed with antigen given 1-2 min and in turkeys 3 min given.
• Haemagglutination test using mycoplasma antigen. The titre of 1:40, 1:80 or above is considered as positive.
• Enzyme linked immunosorbent assay: For antibody detection, the test should be repeated in 2-4 weeks time. Frequently they will be found negative.
• In flocks, in which small numbers of positive reactors to the RSA test persists and from which mycoplasma infection has been confirmed by other serological tests or by cultural examination from live birds carcass.
• Biological inoculation: Demonstration of the organism or antibody into number of 8-16 weeks old germ free chickens are essential. The inoculated birds are kept in isolation for up to 6 weeks.
• The serum tested for antibodies and samples tested by culture.
• Examine the samples also for co-infection such as NDV, IBV and other respiratory infection.
• Heterogenicity exists in the species level has been differentiated by SDS-PAGE analysis of proteins and restriction endonuclease analysis of Mg DNA.

Sample Collection

• Samples should be taken are live birds, fresh carcass, frozen and dead in shell embryo / failure to hatch.
• From live birds, swabs from cloaca, oropharynx, oesophagus, trachea, phallus, exudates aspiration from infra orbital sinuses and joints.
• From dead birds, swabs from nasal cavity, airsacs, joints, embryonated eggs and inner surface of vitelline membrane, oropharynx and airsac.
• All the swab must have been dipped in mycoplasma broth before use.

Differential Diagnosis

• Infectious bronchitis
• New Castle disease
• Chronic Respiratory disease
• Infectious Laryngotracheitis

Treatment

• Antimicrobials inoculated into the pointed portion of egg in albumin.
• Immersion of egg in a solution of antimicrobial (egg dipping) creating for 37◦C for 15 -20 minutes.
• Commonly used drugs are:
  • Tetracyline (chlortetracyclin, oxytetracyclin)
  • Aminoglycosides (neomycin, gentamicin, spectinomycin, Lincomycin, and tiamutin)
  • Fluoroquinolones (Enrofloxacin, danofloxacin)

Prevention

• Natural immunity provides some degree of immunity
• Both live and killed bacterin can be used.
• Live vaccines are relatively low virulence for chickens.
• F strain gives protection to broilers when vaccinated by eye drop or aerosol @ 10 days of age and is considered to replace infection with field strains for Mg but can cause disease in turkeys.
• A temperature sensitive mutant mycoplasma vaccine (ts-11) shown to give good protection against virulent mycoplasma for the respiratory and oviduct for at least 40weeks after vaccinations.
• Bacterin for enhancing egg production may be given although the vaccinated birds do not produce more eggs than unaffected birds.
• M. imitans isolated from geese, ducks, patridge shown to cross react with mycoplasma in RSA, growth inhitbition and immunofluorescence tests.

Control

• Eradication is very much important means of control in breeding stock.
• Treatment of hatching eggs to decrease transmission of mycoplasma through embryo and progeny.
• Monitoring of progeny flocks.