Poultry Diseases Management.

Poultry Diseases Management article is a comprehensive guide to poultry diseases cause,sign, diagnosis, treatment and control. Poultry Diseases Management is a most read article for poultry owners & doctors for on time diagnosis and treatment of poultry diseases. 

Under the Following Points We Have Described About Major Poultry Diseases Management :

Aspergillosis

Cause

• The disease is caused by a fungus, Aspergillus fumigatus.

Transmission

• Transmission is by inhalation of fungus spores from contaminated litter (e.g. wood shavings) or contaminated feed.
• Hatcheries may also contribute to infection of chicks.

Species Affected

• Young chicks are very susceptible, older chickens are more resistant to infection.
• Turkey poults, pheasant chicks, quail chicks, ducklings, and goslings may also become infected.

Clinical Signs

• Infected chicks are depressed and thirsty.
• Gasping and rapid breathing (“pump handle breathing”) can be observed.
• Mortality is variable, from 5 to 50%.
• Gross lesions involve the lungs and airsacs primarily.
• Yellow-white pin-point lesions can be found.
• Sometimes all body cavities are filled with small yellow-green granular fungus growth.

Diagnosis

• The presence of Aspergilllus fumigatus can be identified microscopically or sometimes even with the naked eye in the air passages of the lungs, in the air sacs or in lesions of the abdominal cavity.

Treatment and Control

• There is no treatment for aspergillosis.
• Affected chicks should be removed and destroyed.
• Strict hygiene in breeder and hatchery management is necessary.
• Choice of litter material is important so that no spore-bearing wood shavings are used.
• Should regularly spray Viraclean in the farm.

Marek’s Disease (MD, Neurolymphomatosis)

Cause

• Marek’s disease is caused by a herpes virus.

Transmission

• Main transmission is by infected premises, where day-old chicks will become infected by the oral and respiratory routes.
• Dander from feather follicles of MD-infected chickens can remain infectious for more than a year.
• Young chicks are particularly susceptible to horizontal transmission.
• Susceptibility decreases rapidly after the first few days of age.

Species Affected

• The domestic fowl.

Clinical Signs

• Infected birds show weight loss. or may exhibit some form of paralysis.
• Mortality varies from 5 to 50% in unvaccinated birds.
• The classical form (paralysis) with leg nerve involvement causes a bird to lie on its side with one leg stretched forward and the other backward.
• When the gizzard nerve is involved, the birds will have a very small gizzard and intestines and will waste away.
• Mortality usually occurs between 10 and 20 weeks of age.

Diagnosis

• The presence of tumours in liver, spleen, kidneys, lungs, ovary, muscles, or other tissues is indicative of MD, but they can also be indicative of lymphoid leucosis.
• However, nerve involvement, either grossly (swelling of leg, wing or other nerves) or microscopically, is typical of MD.
• Eye involvement can be visible as an irregular constriction of the iris (ocular lymphomatosis).
• Skin involvement (skin leucosis) often consists of tumours of feather follicles or in between follicles.
• Skin leucosis is a reason for broiler condemnation in certain parts of the world.
• A proper diagnosis to differentiate MD from LL requires histological examination.

Treatment and Control

• Vaccination of day-old chicks is an effective mean of control.
• It has been demonstrated that MD vaccine only prevents the appearance of Marek’s disease tumours and paralysis, it does not prevent the birds from becoming infected with MD -virus.
• It is therefore of major importance to maintain high hygienic and sanitary measures by good management to avoid early exposure of young chickens.

Control & Factors Influencing Outbreak of Marek’s Disease (M.D.)

Factors of 1st Order

• Presence of pathogenic M.D. virus at the farm is the biggest etiologic factor of M.D The infection is followed by a quick and heavy multiplication of the virus in the defense organs of the body such as bursa, thymus, spleen etc.
• This explains why M.D. is an immunosuppressive disease. Then a stage comes when multiplication of virus decreases and now we can see formation of tumors and affection of the nerves.

Factors of 2nd Order

Genetics

• Several lines of chickens with genetic resistance to MD have been selected and maintained experimentally.
• Spencer et al (1976) found genetically resistant chickens were protected by vaccination to a greater extent than more susceptible ones.
• Breeding for genetic resistance may be a valuable adjunct to immunization for control of MD.

Age

• Prevention of early exposure of vaccinated birds with virulent M.D virus (MDV) enhances the efficacy of the vaccine.
• If one can achieve his, he will definitely emerge victorious over M.D.

Factors of 3rd Order

Sex

• It is interesting to know that females are more sensitive to M.D. than males. This is indicated by a shorter duration incubation period, higher frequency of clinical manifestations and larger no.of females with tumors.

Maternal Antibodies

• The presence of maternal antibodies (MABs) significantly impedes the multiplication of MDV during the first stage of disease.
• The degree of this procection depends on the antibody titre. Maternal antibodies also impede propagation of MD vaccine virus.

Factors of 4th Order

Viral Infections

• Chicken anaemia agent (CAA) and Reo virus can predispose the birds to or aggravate MD.

Bacterial Infections

• Mycoplasma synovie can act as a predisposing factor for MD

Factors of 5th Order

• Aflatoxin induced immunosuppression can make the birds prone to MD.
• Sanitation and biosecurity play very important role in the occurrence of Marek’s disease.

Epzootiology

• All strains of MDV develop in an infectious form in the cells of feather follicles. Therefore, the no.of produced and released MD viruses increase during the chicks, a young animal and layer’s moult.
  From the feather follicles, MDV reach the air and get settled in the dust. In dust, the effectively of MDV is preserved for a very long time.
• The dust usually concentrates on the ceiling and walls but also in the ventilation of the chicken house. A through mechanical removal and an innocuous disposal (heating) of the infectious dust are important measures against further infections.
• Various insects which live in the litter as for ext. black lesser mealworm is a carrier of MDV. If these insects (beetles) are eaten by chickens, they might be infected.
• The most significant way of MDV transmission is the inhalation of infected dust. Any alternate ways of infection (mentioned below) which are common with other viral diseases, are meaningless for MD.
  1. Vertical spread (Vertical via the hatching eggs)
  2. Genital spread (during the mating of a male and female)
  3. Oral communication (through feed or drinking water)

Prevention

The occurrence of Marek’s disease can be successfully prevented if one carefully studies the following points:

Preventing the Pathogen’s Introduction

• MDV strains are never vertically transmitted (i.e. via the hatching eggs). The only source for infection for chicks and chickens of all age groups is dust containing the virus.
• They get infected in an environment which is contaminated with MDV Cleaning and disinfecting can decontaminate the chicken houses.
• The interested readers can obtain the protocol of disaffection program from our office. The introduction and spreading of MDVs in farms can be effectively and continuously prevented by appropriate architectural measures.
• This method is used by the producers of specific pathogen free (S.P.F) hatching eggs. SPF flocks are kept in positive pressurized houses having filters to nullify possibility of entry of any microorganisms.

Proper Vaccination

• Faulty application of the vaccine such as dilution mistakes during the preparation, faults in the technique of injection, too long times of storage or too high ambient temperate of reconstituted vaccines.
• In the modern hatchery practices possibility of such lapses is very minimum. · Too low content of viruses in the vaccine. The protection by inoculation depends on the dose of injected viruses.
• Ventri’s MD vaccine contains minimum 4000 to 5000 P.F. US/ dose as against British pharmacopea (Vet), standards of 1500 PFU/close. A higher content of viruses does not lead to any significant improved protection. In case of severely affected farms, a booster dose of MD vaccine may be tried on 18th day. There are some reports of encouraging outcome with such practice of MD booster vaccination.
• If an infection with virulent MDV occurs simultaneously with or a few days after the vaccination, there can be no sufficient protection from the vaccine. In our opinion, this applies to all available vaccines. The older the chicks are at the time of infection by MDV, the lower the rate of spread of field strain (pathogenic) is. This can be achieved only with the help of accurate cleaning / disinfection and strict biosecurity measures, for first 15 days post hatchery vaccination. ·
• As it is known of other live virus vaccines, the contamination of a vaccine can lead to damage to the inoculated chick by concurrently present microorganisms. This explains the need of accurate sterilization of injection appliances before being used.
• The presence of high maternal antibodies can also impede the development of immunity in the vaccinated chicks.
• In short, occurrence of MD cases despite of vaccination can be attributed to
  1. Improper sanitation and poor biosecurity.
  2. Early exposure to virulent MDV
  3. High maternal antibody
  4. Poor vaccination procedures
• In 1982, two American scientists found that vaccination of 18-day-old embryos accelerated development of protective immunity by several days and proposed this technique for controlling detrimental effects of early exposure to virulent MDV. This technique is named as: In ovo Mark’s vaccination”. The in ovo method eliminated the need for manual post-hatch inoculation of day old chicks and result in healthier chicks due to earlier introduction of disease preventing vaccines and less stress to the chicks. Tri-bio laboratories, U.S.A. (collaborator of Ventri biologicals Divn) have already produce one such in ovo MD vaccine.

Prevention of Other Infections

• clinically healthy chicken only can develop protective immunity after the vaccination. This means that in order to have a successful program to control MD., other pathogenic agents must be eliminated. Certain infections which can make the bird susceptible to Mark’s disease are mentioned below:
• Certain species of avian mycoplasma enchase the multiplication of Marek’s disease virus in cell cultures according to Dr. Kaleta Gieban, an eminent European scientist.
• Chicken Anaemia Agent (CAA)- Experimental dual infections with CAA and subclinical doses of MDV caused enhancement of MDV antigen shedding to feather follicles.

Nutritional Prophylakis

• Aflatokins increase susceptibility of poultry to Marek’s disease.
• The mechanism is through depression of the cell-mediated immune response. Certain vitamins like vitamin A, C, E, B6, H etc., are very essential for the development of lymphoid (defense) organs of the body like bursa, thymus, spleen, liver etc., one should always use the vitamins which are procured from a dependable source only because the use of substandard vitamins may lead to immunosuppression. Recommended product of multi vitamins is Growvit Power

Environmental Factors

• According to a study undertaken in hot climates successively for two years by Dr. Raghard Al-Khoja, the heat stress can affect the efficiency of immunity build up against Marek’s disease. He found that the chicks hatched during summer (i.e March to June) are more susceptible to MDV infection. So one should take extra care during summer to prevent MD incidences.
• Mark’s disease vaccination is carried out during the 1st 24 hours of a chick’s life and its effectiveness is determined until the chicks reach the age of at least six weeks. Therefore, chicks should be protected from exposure to field (Pathogenic) MDV for atleast first 6 weeks are even more crucial.
• Only persons working on the farm and dressed in clean protective clothing shall be admitted to the chicken houses.

The Significance of Mark’s Disease 

• Prior to the use of vaccines, MD constituted a serious economical threat to the poultry industry because of heavy mortality and losses. Since vaccine does not mean full proof protection, losses still occur but they are no longer as serious a problem.
• Perhaps the greatest impact of MD is immunosuppression (impairment of immune system) apparently caused by the damage to the bursa, thymus, spleen, liver etc. Both humoral antibody and cell mediated immunity can be depressed by MD. These are reflected by reduced antibody response to a variety of vaccines and by alteration of T cell functions. MDV infection could increase susceptibility to primary and secondary infections with coccidia and reduced antibody response to M. sysnoviae.
• In broilers, MD may exist in sub clinical form if not in clinical form. This may lead to vaccine failure. That is why MD vaccination (at least half dose) is recommended in day old broiler chicks.

Infectious Anaemia (CAA/CIAV)

A very resistant small virus known as CAA (Chicken Anaemia Virus) or CIAV (Chicken Infectious Anaemia Virus) causes infectious Anaemia.

Transmission

• The major mode of transmission of Infectious Anaemia is vertical transmission from infected breeder hens.
• Horizontal transmission from bird to bird or by infected equipment, clothing, etc. is also possible.

Clinical Sings and Lesions

• CAA causes a syndrome in young chicks up to approximately 3 weeks of age.
• Adult birds may get infected but will not develop clinical signs.
• The disease is characterized by increased mortality and anaemia associated with atrophy of the haematopoietic tissues in the bone marrow.
• Subcutaneous and intramuscular haemorrhages can be found accompanied with atrophy of the lymphoid system.
• Affected birds may show focal skin lesions (also known as blue wing disease).
• Mortality rates vary from 20% to 70%.
• Affected flocks will show poor growth reflected in economic losses.

Diagnosis

• The diagnosis can be based on the clinical signs and pathological findings in affected birds.
• Blood serum testing for specific CM antibodies can be carried out (IFT, VN, etc.) Virus isolation is also possible but it is time-consuming and expensive.

Treatment and Control

• No treatment is available for Infectious Anaemia.
• Maternally derived antibodies can offer protection.
• The induction of high maternal immunity in the progency by vaccinating breeders is the best approach to successful CM control.

Inclusion Body Hepatitis

Cause

• The disease is caused by an avian adenovirus (for example the Tipton strain) and is usually simultaneously accompanied by other immunosuppressive diseases such as Infectious Bursal Disease or Infectious Anaemia.
• There are 12 known serotypes of avian adenoviruses that may be involved in the development of this disease.

Transmission

• Egg transmission is an important factor.
• Horizontal transmission from bird to bird by contact with droppings.
• Once the bird becomes immune, the virus can no longer be isolated from the droppings.

Species Affected

• Chickens, turkeys and pheasants and possibly other birds can be affected by avian adenovirus.

Clinical Signs

• Chickens with inclusion body hepatitis are affected at usually 5 to 7 weeks of age.
• The birds are listless, with ruffled feathers.
• Mortality is usually quite severe, up to 25% in the first 10 days of the disease.

Internal Lesions

• Affected chickens have mottled livers, many with pinpoint necrotic and haemorrhagic spots.
• Pale bone marrow and, in some cases in presence of Infectious Anaemia, gangrenous dermatitis can be seen.
• Kidneys are pale and swollen.
• The spleen is usually quite small (atrophy).
• If Gumboro disease (Infectious Bursal Disease) has been present in the birds, even if sub-clinical, the Bursa of Fabricius will be very small (atrophic).
• Such chickens are immune-suppressed and usually have more severe cases of inclusion body hepatitis and/or infectious anaemia.
• Mature birds do not have clinical signs of adenovirus infection, they only start showing antibodies in their blood.

Diagnosis

• Typical mottled livers with pin-point lesions, pale bone marrow and kidneys, small spleen and bursa are good indications of the disease.
• Histological examination (intranuclear inclusion bodies) of liver and/or virus isolation are helpful means of diagnosis.

Treatment and Control

• No treatment exists.
• Antibiotics can be used to prevent secondary bacterial infection and possible gangrenous dermatitis.
• The best method of control is to ensure adequate immunity against other immune suppressive diseases (e.g. Infectious Bursal Disease).
• Breeder chickens may be vaccinated with live vaccine, followed by inactivated oil-emulsion vaccine application before egg production begins.
• This procedure ensures adequate maternal immunity against IBD disease in the offspring which assists in preventing inclusion Body Hepatitis.

Bronchitis

Cause

• Corona-virus is the causal agent.
• Several different serotypes of IB virus are known to exist.

Transmission

• The virus is transmitted from bird to bird through the airborne route.
• The virus can also be airborne between chicken houses and even from farm to farm.

Species Affected

• Only chickens are susceptible to IB virus.

Clinical Signs

• Respiratory signs include wet rales, gurgling, and wheezing.
• Egg production will decrease dramatically, deformed eggs with wrinkled shells will often be laid.

Internal Lesions

• Mucus and redness in tracheas froth in airsacs in older chickens.
• In young chicks a yellow cheesy plug at the tracheal bifurcation is indicative of IB infection.

Diagnosis

• There are three main factors to be considered in order to arrive at a diagnosis
• The clinical picture including post-mortem findings in the flock.
• lsolation of the virus In the laboratory.
• Rising antibody titre when the serum is tested against a known strain of bronchitis virus.

Treatment and Control

• There is no treatment for Infectious Bronchitis.
• Secondary bacterial infections may be prevented by, or treated with antibiotics.
• Prevention by vaccination is the best method to control.

Infectious Bursal Disease (IBD, Gumboro Disease)

Cause

• The disease is caused by a birna virus of serotype.
• Virus strains can be divided in classical and variant strains.
• The virus is very stable and is difficult to eradicate from an infected farm.

Transmission

• IBD virus is very infectious and spreads easily from bird to bird by way of droppings.
• Infected clothing and equipment are means of transmission between farms.

Species Affected

• Chickens and turkeys appear to be natural hosts.

Clinical Signs

• In subsequent infection on the same farm, mortality is lower and eventually, with successive attacks, there is no mortality noted.
• The sub-clinical form caused by the immunosuppressive effect of the IBD virus is now of more economic importance in that the immune system of the bird is damaged.
• In broilers this form of the disease results in bad performance with lower weight gains and higher feed conversion ratios.

Diagnosis

• In acute cases the Bursa of Fabricius is enlarged and gelatinous, sometimes even bloody.
• Muscle haemorrhages and pale kidneys can be seen.
• Infection by variant strains is usually accompanied by a fast bursal atrophy (in 24-48 hours) without the typical signs of Gumboro disease. Also in chronic cases the bursa is smaller than normal (atrophy). The bursa destruction is apparent on histologic examination.
• The lack of white blood cells (lymphocytes) results in a reduction in the development of immunity and decreased resistance of the birds to other infections.
• Typical signs and lesions are diagnostic of IBD.
• Histopathological examination, serology and/or virus isolation are helpful tools. IBD can be confused with sulfonamide poisoning, aflatoxicosis, and pale bird syndrome (vitamin E deficiency).

Treatment and Control

• No treatment is available for IBD.
• Vaccination of parent breeders and/or young chicks is the best means of control.
• The induction of a high maternal immunity in the progeny of vaccinated breeders is the most effective approach to successful IBD control.

Chronic Respiratory Disease (CRD) (Airsacculitis)

Cause

• The underlying cause of CRD is Mycoplasma gallisepticum (Mg). The condition is frequently triggered by respiratory viruses such as NO and 18 and subsequently complicated by bacterial invasion.
• The main agents involved in the infection are Mycoplasma gallisepticum. Stress caused by moving the birds, by de-beaking or other operations or other unfavourable conditions e.g. cold or bad ventilation, make the birds more susceptible.

Transmission

• The main problem is that parent birds infected with Mycoplasma gallisepticum can transmit the organism through the egg to their offspring.
• In addition, infection can occur by contact or by airborne dust or droplets. The incubation period varies from 4 days to 3 weeks.

Species Affected

Chickens and Turkeys.

Clinical Signs

• Young chickens (broiler chicks or layer pullets) will show respiratory distress. The birds frequently show a lack of appetite, decreased weight gain and increased feed conversion ratios.
• In adult birds the most common symptoms are sneezing, coughing and general signs of respiratory congestion. In laying birds a drop of egg production between 20-30% can occur.
• CRD does not normally cause an alarming number of deaths. The effect is more of a chronic nature causing reduced weight gain and feed conversion ratios in broilers and lower egg production in breeders and layers. In this way the overall economic loss can be very great in broilers but less dramatic in breeders and layers.

Internallesions

• A reddish inflamed trachea and/or cheesy exudates in airsacs, especially in complicated cases (e.g. with secondary E. coli infections) are observed. In mild Mg infections the only lesion might be slight mucus in trachea and a cloudy or light froth in the airsacs.
• Turkeys with Mg infection usually have swollen sinuses under the eyes.

Diagnosis

• Diagnosis of Mg infection can be made by blood testing of chickens, post-mortem examination and ultimately by isolating the causative Mg organism from tracheas or airsacs of affected birds.

Differential Diagnosis

• Respiratory virus infection (Newcastle disease or Infectious Bronchitis) with secondary infection (E. coli, etc.) can give similar lesions.

Treatment

• Treatment of Mg-infected chickens or turkeys with suitable antibiotics or chemotherapeutics has been found to be of economic value.
• However, control by medication or vaccination and eradication of Mg infections has been by far the most effective method of combating the disease.
• Fertile eggs from infected birds can be treated with antibiotics such as tylosin to eliminate the Mycoplasma gallisepticum organisms. Methods used are the injection of fertile eggs or egg dipping.
• Blood serum testing of breeder chickens for Mg antibodies has become a routine to test flocks for a Mg infection.Coccidiosis
• Ciprocolen in the condition of Chronic Respiratory Disease (CRD) which most effective and powerful medicine for the treatment of CRD.

Cause

• Coccidiosis is caused by protozoa, unicellular parasites.
• In chickens there are 9 different species of coccidia of which the main 5 are Eimeria acervulina, Eimeria necatrix, Eimeria tenella, Eimeria maxima, Eimeria brunetti.

Transmission

• Infected droppings, containing oocysts of coccidia are the main means of transmission between birds.
• The incubation period is 4 to 6 days.

Species Affected

• Chickens have their own specific coccidiosis types, which do not cross-infect other bird species.

Clinical Signs/Diagnosis

Coccidiosis can be divided into 2 groups.

1. The caesium is involved (Caecal coccidiosis) Mainly caused by E. tenella in chickens up to 12 weeks. Mortality may run as high as 50%.Infected birds are listless, have bloody droppings, a pale comb and show a lack of appetite.Laboratory examination will show haemorrhages in the caecal wall. After severe bleeding a core will be formed in the lumen.
2. The small intestine is involved (small intestinal coccidiosis) Caused by E. acervulina, E. brunet ti, E. maxima, E. necatrix.

Acervulina

• Acervulina is not normally very pathogenic, but in some cases considerable mortality may be seen.
• Birds infected show loss of weight, combs may be shrivelled and a drop or even cessation of egg production in layers may be seen.
• At necropsy, haemorrhagic lesions of E. acervulina are seen throughout the upper portion of the affected intestine and also grey or whitish patches may be present.
• May affect birds of any age.

Brunetti

• May affect birds of any age.
• brunetti is definitely pathogenic, in severe infections
• Mortality can be high. Birds infected show emaciation and diarrhoea.
• At necropsy a white cheese-like material is found in the lumen of the lower intestine and rectum.
• The caeca and cloaca are inflamed. The gut wall is thickened.

Maxima

• May affect birds of any age.
• maxima is less pathogenic than E. acervulina, necatrix and brunetti, mortality is generally low.
• Diarrhoea, loss of weight and a drop in egg production of layers, will be seen; bloody droppings are common.
• At necropsy the lower portion of the small intestine is dilated and the wall is thickened; the gut is filled with thick mucus, greyish, brownish or pinkish in colour.

Necatrix

• Mainly in chickens up to 4 months of age.
• necatrix is very pathogenic.
• Infection with E. necatrix may result in a two stage clinical outbreak of coccidiosis.
• In the acute stage mortality may be high in the first week after infection.
• In the chronic stage blood may be seen in the droppings, the birds are listless and lose weight.
• In layers a drop in egg production will be observed.
• At necropsy the middle portion of the intestine is affected, haemorrhage will be seen.
• The unopened intestine looks spotty, white areas (schizonts) intermingled with bright or dull red spots (haemorrhages) will be observed.

Treatment and Control

• This is most appropriate in the case of coccidiosis as there is no disease group in poultry where both control and treatment are employed more.
• The well-established principles of good management and husbandry are of basic importance.
• It is common practice to include low levels of chemotherapeutics in the feed of birds.
• These chemicals are referred to as coccidiostats and as such keep in check the development of the parasites so that a pathological situation does not develop.
• It should, however, be taken into account that coccidia can develop a resistance to all chemicals so far used for this purpose and for this reason it is necessary to change from one chemical to another periodically.
• Treatment of infected flocks may be carried out by the administration of coccidostats at a higher therapeutic level to the affected birds.
• There are certain products available which are specifically designed for treatment and which are not satisfactory for prevention.
• These chemicals are sometimes referred to as coccidiocidal agents. Whenever administering these products, particular attention should be paid to the dosage recommendation of the manufacturer .

Cause

• The bacterium causing this disease is Hemophilus paragallinarum.

Transmission

• The disease spreads from bird to bird and flock to flock by contact and airborne infected dust particles and via the drinking water.
• Spread by equipment and personnel has also been reported.
• The incubation period varies from 1 to 3 days.