EFFECTS OF DIFFERENCE TIMING OF ROUTINE VACCINATION

SCHEDULES ON GROWTH PERFORMANCE, MORTALITY RATE AND

BLOOD PARAMETERS OF BROILERS.

BY

ORAGWU CHIOMA .L.

PG/PGD/06/41933

DEPARTMENT OF ANIMAL SCIENCE

UNIVERSITY OF NIGERIA,

NSUKKA.

FEBRUARY, 2010.

EFFECTS OF DIFFERENCE TIMING OF ROUTINE VACCINATION

SCHEDULES ON GROWTH PERFORMANCE, MORTALITY RATE AND

BLOOD PARAMETERS OF BROILERS.

A THESIS SUBMITTED TO THE DEPARTMENT OF ANIMAL SCIENCE, FACULTY

OF AGRICULTURE, UNIVERSITY OF NIGERIA, NSUKKA IN FULFILLMENT OF

THE REQUIREMENT FOR THE AWARD OF THE DEGREE OF POSTGRADUATE

DIPLOMA DEGREE IN DEPARTMENT OF ANIMAL SCIENCE

BY

ORAGWU CHIOMA .L.

PG/PGD/06/41933

SUPERVISOR: DR. S.O.C. UGWU

FEBRUARY, 2010

ii

CERTIFICATION

We certified that ORAGWU CHIOMA .L. (PG/PGD/06/41933) carried out

research in the poultry unit of the Department of Animal Science of the University. The

Report embodied herein is original and has not been submitted for any other degree of

this or any other university.

……………….. ………………… Dr. S.O.C Ugwu Dr. S.O.C Ugwu Supervisor Head of Department Date…………………….. Date……………… ………………………

External Examiner

Date …………………….

iii

DEDICATION

To Almighty God, for his infinite love and grace.

iv

ACKNOWLEDGEMENT

My heartfelt and sincere gratitude go to Almighty God, the Author and Finisher of

my faith, for his great providence in the course of my studies.

I am greatly indebted to my parents and my sweet husband, for their painstaking effort to

ensure that I lacked nothing in terms of finance, advice, encouragement and prayerful

support.

My profound gratitude goes to my supervisor, Dr S.O.C Ugwu for all his

counselling, assistance, suggestions and encouragement during the course of study,

despite his enormous commitment. May God reward and bless him.

My gratitude goes to all my lecturers especially Prof G.C Okeke and the Head of

Department, Dr A.G Ezekwe for their kindness and advice.

To my colleagues, friends and well wishers, may God continue to bless you all.

v

TABLE OF CONTENTS

Title page ------------------------------------------------------------------------------- i

Certification --------------------------------------------------------------------------- ii

Dedication ----------------------------------------------------------------------------- iii

Acknowledgment ---------------------------------------------------------------------- iv

Table of Contents --------------------------------------------------------------------- v

List of Tables ------------------------------------------------------------------------- vii

Abstract ------------------------------------------------------------------------------- viii

CHAPTER ONE: INTODUCTION

1.1 Background of the Study -------------------------------------------------------- 1

1.2 Objectives of the Study ---------------------------------------------------------- 4

1.3 Justification ----------------------------------------------------------------------- 4

CHAPTER TWO: LITERATURE REVIEW

2.1 Some Common Diseases of Poultry. ------------------------------------------- 6

2.1.1 New Castle Disease:------------------------------------------------------------ 6

2.1.2 Infectious Bursal Disease (Gumboro Disease): ----------------------------- 9

2.1.3 Fowl Pox ------------------------------------------------------------------------ 11

2.2 Vaccines and Vaccination ------------------------------------------------------- 12

2.3 The Importance of Vaccination ------------------------------------------------- 13

2.4 Deciding Whether or not to Vaccinate ---------------------------------------- 14

2.5 Types of Vaccines: --------------------------------------------------------------- 15

2.6 Administration -------------------------------------------------------------------- 16

2.7 Types of Vaccination Programmes --------------------------------------------- 18

2.8 Tips For Successful Vaccination ----------------------------------------------- 20

2.9 Vaccine Distribution ------------------------------------------------------------- 21

2.10 Factors Which Interfere With Vaccine Efficacy ----------------------------- 21

CHAPTER THREE: MATERIALS AND METHODS

3.1 Location and Duration of the Study -------------------------------------------- 25

3.2 The Experimental Animals. ---------------------------------------------------- 25

3.3 General sanitation and Health measures --------------------------------------- 26

vi

3.4 Experimental Design: ------------------------------------------------------------ 26

3.5 Data Collection Analysis -------------------------------------------------------- 27

3.6 Analysis of Data ------------------------------------------------------------------ 31

CHAPTER FOUR

Results --------------------------------------------------------------------------------- 32

CHAPTER FIVE

Discussion ----------------------------------------------------------------------------- 37

CHAPTER SIX

Summary Conclusion and Recommendation -------------------------------------- 39

References ----------------------------------------------------------------------------- 41

Appendices

vii

LIST OF TABLES

Table 1: The vaccination programme for common diseases of poultry ............ 19

Table 2: The day of vaccination and the treatments used................................. 20

Table 3: Weekly live body weight of broiler subjected to varying vaccination

Schedule ............................................................................................. 32

Table 4: Mean of daily live weight gain of broilers subjected varying vaccination

Schedule ............................................................................................. 33

Table 5: Weekly shank length of broilers subjected to varying vaccination

Schedule ............................................................................................. 34

Table 6: Mean daily shank length gain of broilers subjected to varying

vaccination schedule ........................................................................... 35

Table 7: Mortality rates of broilers subjected to different vaccination schedule 35

Table 8: Mean values for blood parameters of broilers subjected to different

vaccination schedules ..................................................................................... 36

viii

ABSTRACT

This study was conducted to find the effect of the delayed routine vaccination

schedules on growth performance, blood parameters and immunity levels of broilers

reared in a humid tropical part of Nigeria. A total of 90 broiler chickens were procured

and sorted into three treatments (control, 1 week delay in vaccination and 2 weeks delay

in vaccination). The results showed significant differences (P < 0.05) in all growth

parameters studied with lower values for broilers with delayed vaccination schedules

(Treatment 2 and 3). Shank length and gains in shank length were not significantly

(P>0.05) affected by delayed vaccination schedule. The blood parameters (PCV and

WBC) values were significantly (P<0.01) lower in birds whose vaccination schedule was

delayed for two weeks, (Treatment 3) compared to other treatments while immunity

levels were significantly (P<0.01) lower in Treatment 3 compared to Treatments 2 and 1

respectively. It was concluded that delayed vaccination schedule of up to two weeks

considerably affected growth performance and immunity status of broilers.

1

CHAPTER ONE

INTODUCTION

1.1 Background of the study

The poultry industry in Nigeria is characterized by a mixture of backyard,

peasant, household-oriented and modern large scale poultry farms which dot our country

side and urban centres today. It can be said that poultry keeping has become a business in

Nigeria since Poultry is now kept by practically every household in Nigeria especially in

rural communities (Obioha 1992). Broilers are meat type chickens that reach market size

at about 8-10 weeks of age. Nearly 80% of all commercial chicks hatched in Nigeria are

broilers (Bundy et al 1975).

Poultry occupies a unique position in Nigeria animal production programme for several

reasons. The most important of these is the fact that poultry are relatively free from the

many pathological, ecological and economic constraints which affect the commercial

production of other breeds and classes of livestock in Nigeria (Obioha 1992). The

occurrence of disease in a poultry flock is a serious event and one that causes a lot of

anxiety to a poultry farmer due to the fact that most commercial poultry are reared

intensively with a large number of birds occuping a relative small area, a disease can

spread rapidly among the whole flock causing a high level of mortality and huge financial

loss to the farmer. The prevention of disease therefore is a decisive factor to the success

or failure of a poultry enterprise. Diseases of poultry can be caused by four major factors

namely: pathogens, poor management, deficiency of nutrients and metabolic disorders.

Most poultry diseases are brought about by the presence of one or more pathogens or

2

causative organisms. These organisms are always present in any poultry environment but

they attain a virulent stage when the resistance of the chicken is low due to internal or

external stress. The stress condition may be created by mismanagement, transportation,

handling, internal parasite or even excessive excitement (Obioha 1992). The infectious

organism may also gain easy access to the tissue of the birds following wound that may

be cause by cannibalism. Some of the common sources of stress are lack of feed and

water, poor ventilation, inadequate floor space, poor sanitation, high internal and external

parasitic load, extremes of weather, vaccination failure, sudden changes in feed or

environment, pests, flies, ants, nutritional deficiencies etc.

Apart from encouraging the invasion of pathogens, bad management may cause

disease directly. Examples of bad management are over crowding, poor ventilation,

failure to vaccinate at the right time, failure to remove dead birds promptly, failure to

remove droppings regularly leading to accumulation of ammonia and breeding site of

pathogens and parasites, cannibalism, uncontrolled access of visitors to poultry farms and

absence of disinfectant troughs or dips.

Poultry disease maybe caused by lack of or deficiency of one or more essential

nutrients. This is why poultry feeds should be balanced. Where one element is deficient

or excessive it can induce or cause the body to show symptoms relevant to such

deficiency or excessesive availability of the nutrient. A group of diseases may be caused

by faulty metabolic process in the body. These include the fatty liver syndrome. Animal

diseases are important limitation to edible protein production. It is the goal of veterinary

medicine to reduce losses due to animal diseases and in cooperation with animal

scientists, to develop positive live stock /poultry health programme (Oyenuga et al 1973).

3

Vaccination of poultry is very important disease prevention programme in poultry

farming. Vaccines have varying expiration dates, depending on the storage temperature

and nature of production. The expiration date is based on holding the vaccine under

optimum conditions, frequently involving refrigeration. Vaccines that are expired have

lost part of their antigenic properties and are ineffective as immunizing agents.

Vaccination of poultry animals are programmed based on age of birds and are

administered based on age and body weight. Although vaccination is an important

weapon in the control of many livestock diseases, the immunity produced is overcome by

massive exposure of birds to infection, by moderate contact with a highly virulent strain

of the infecting agent or by stress, e.g. poor environment conditions.

Moreover it is not the purpose of a vaccine to protect an animal that is inoculated

while in the incubation stage of a disease. Vaccination should not be considered as a

panacea in disease control. It should be supplemented with sanitary measures designed to

prevent the introduction and spread of disease. Some poultry diseases can not be treated

properly by medication but can be controlled by vaccination; therefore vaccination of

poultry against certain diseases and at the right timing help in proper growth rate as well

as reduced morbidity and mortality in the flock. Evidence has shown that there are

delayed vaccination programmes for broilers reared by some farmers in remote villages

or farmers that rear their birds in locations where veterinary care is limited or non

existent; that is why this research is aimed at knowing the effect of those delayed

vaccination on growth and mortality rate of affected birds.

4

1.2 Objectives of the Study

The objectives of this study are as follows

1. To find out the effects of irregular timing of vaccination on the growth

performance of broilers.

2. To determine the mortality rate of broilers subjected to irregular vaccination

schedules.

3. To determine the Haemagglutination inhibition values and the Haematological

values (Packed cell volumes and White blood cell counts) of birds not

vaccinated at the appropriate times.

1.4 Justification

Vaccination is an effective means of preventing or reducing the adverse effect of

specific diseases in poultry especially viral diseases. The control of viral disease is

dependent upon prevention through sanitation, biosecurity and by vaccination. In some

areas or small farms, vaccination is seldom practiced because of some reasons namely;

low cases of disease problems in farms, lack of proper diagnosis and expensive cost of

vaccines as poultry vaccines usually come in 100-1000 dose vials. Vaccines come in

either live or inactivated forms which have their advantages and disadvantages. What

normally brings about vaccination failure include, breaking the cold chain by poor

storage since they come in freeze dried forms, exposing the vaccine directly to sunlight or

heat and lack of adoption of proper route of vaccination. These can reduce the potency of

a vaccine. The timing or schedule of vaccination can also affect the performance of the

birds. These factors leading to vaccination failures abound with little or no information to

5

the farmers as to why they occur and the extent of loss caused to the farmer. Nigeria is

largely a country where minimum attention is paid to quality control or adherence to

prescribed conditions for storage of drugs and for vaccines. As such, the poultry farmers

and their enterprises are limitlessly at the mercy of agencies that procure vaccines/drugs

and fail to adhere to manufacturer’s specifications about storage and shelf life since

nobody actually monitors them to ensure that there specification are adhered to. The best

that can be done to inform farmers could be to document the affects of vaccination

failures to the birds being reared to create awareness which may lead to asking pertinent

questions about storage life of each vaccine before procuring them for use in a poultry

enterprise.

6

CHAPTER TWO

LITERATURE REVIEW

2.1 Some Common Diseases of Poultry.

In Nigeria and other tropical countries, some diseases of poultry are more

common than others. Some of the important poultry diseases are hereby described.

2.1.1 New Castle Disease:

New castle disease, is a disease of poultry caused by paramyx virus type -1

(Pmv-1) but for international control purpose, it is now accepted that New Castle disease

is an infection by an avian pmv-1 with an intercerebral paterogenicity index (ICPI) of

over 0.7 (McCracken, et al., 1992)

The disease was first recognized in 1926 in three widely separated countries-

England (Doyle, 1927), Java (kraneveld, 1927) and Korea (Konno, et at., 1927). Ever

since then, it has been recognized in other countries of the world. In Nigeria, the disease

was reported in 1951 (Kirkby, 1951), later diagnosed in Ibadan (Hill, 1953). Ever since

the virus was first recognized in New Castle upon Tyne by Doyle in 1927, it has

constituted a major threat to poultry production worldwide, hence the need for continuous

research into its control. The control of New castle disease (ND) is based on

complementary hygienic and medical measures. Full protection can only be assured if

vaccination programmes are combined with hygienic precautions (Meulemans, 1988).

The phenomenon of vaccination is to confer acquired immunity on the birds. This

phenomenon of acquired immunity was first observed by the Chinese. These they did by

nasal inoculation of small pox virus and the production of disease in the individual in

other to render them immune (Noble, 1946).

7

New Castle disease one of the most serious poultry diseases in Nigeria. It is

caused by a group of closely related viruses which form the avian paramyxovirus type 1.

A striking feature of New Castle disease(ND) strains is their ability to cause quite distinct

signs and severity of diseases, even in the same host species (Jordan 1990). NDs have

been placed under five pathotypes.

a) Viscerotypic velogenic ND’s which causes a highly virulent form of the

disease in which haemorrhagic lesions are characteristically present in the

intestinal tract,

b) Neurotropic velogenic ND’s which causes high mortality following

respiratory and nervous signs.

c) Mesogenic ND’s which causes respiratory and sometimes nervous signs with

low mortality.

d) Lentogenic respiratory ND’s which causes mild or inapparant respiratory

infection and

e) Asymptomatic enteric ND’s which causes inapparant enteric infection.

Spread of the Virus/Disease

The mode of transmission from bird to bird is by

1. Inhalation of the virus (Hofestad, 1953; Okoye and Shoyinka, 1984)

2. Ingestion of contaminated faeces, either directly or indirectly in contaminated

food or water

3. Movement of people, equipment and poultry product

The importance of any of these factors will depend on the situation in which the

epizootic occurs (Lancaster et al., 1975).The virus spreads more rapidly in an

8

intensive system of production. A major factor in the rapid spread of NDV is the

ability of the virus to survive in the dead host or excretions for several weeks.

Clinical Signs

The species of birds, the immune status, age and conditions under which they are

reared may greatly affect the disease signs seen while the presence of other organisms

may greatly exacerbate even the mildest forms of the disease. As a consequence, no

disease signs may be regarded as pathognomonic (Calnek et al., 1997).The symptoms of

NDV include: gasping, coughing, rattling of the wind-pipe and some nervous disorder

which may show as paralysis of legs and wings. An incidence of this disease may cause

up to 50% or more reduction in production through mortality, drop in egg production, and

laying of shelless eggs. Young chicks show more strenuous symptoms like tucking the

heads between the legs, rotating of the head and tumbling. They also produce greenish-

yellow droppings.

In unvaccinated chickens, there is sudden death and marked drop in egg

production with high mortality within 1-12 days upto 10-15% within the first day. Birds

that survived after 12-14 days show paralysis of wings, torticollis and ataxia, egg

production does return to previous levels. In vaccinated chickens or chicks with maternal

antibodies (MA), the signs are less severe and proportional to the level of protective

antibodies (Abdu,2005).

Hygiene and Disease Security:

According to Jordan & Pattison 1996, there is no cure for New castle disease;

therefore prevention with appropriate vaccination is the best method of control. Birds

9

should be vaccinated with B1 strain of New castle disease vaccine preferably between

day-old and 14 days of age and followed by a programme of repeat vaccinations.

Under field conditions vaccination alone is insufficient to bring about effective

control of New castle disease and must be accompanied by good hygiene (Allan et al,

1972). In good management practice over crowding, poor ventilation and inevitable

underlying bacteria infections should be avoided.

2.1.2 Infectious Bursal Disease (Gumboro Disease):

This is an important viral disease of poultry throughout the world. According to

Obori (2005) once a farm is infected by Gumboro disease, it is difficult to eradicate.

Clinically it affects young chickens, usually up to 6 weeks of age. The name Gumboro

disease was initially given to the condition because it was first recognized in the

Gumboro district of Delaware, USA. Infectious Bursal Disease (IBD) is caused by a

birnavirus. The virus is resistant to many disinfectants and environmental factors, and

remains infectious for at least four months in the poultry house environment (Jordan

1990). Because of the resistant nature of the IBD virus, once a poultry house becomes

contaminated, the disease tends to recur in subsequent flocks.

Spread of Infectious Bursal Disease

It is an infectious and highly contagious disease and the virus is persistent in the

environment of poultry house (Benton et al., 1967). The affected chicks excrete virus in

their dropping for up to two weeks after infection but after this time faeces seem to be

uninfected. Chickens infected with the IBD virus also shed the virus into the feed, water,

and poultry house litter become contaminated. Other chickens in the house become

10

infected by ingesting the virus. Because of the resistant nature of the IBD virus, it is

easily transmitted mechanically among the farms by inter movement of people,

equipments and vehicles (Jordan et al., 1996).

Clinical Signs

The clinical form of IBD usually occurs in chickens from 3 to 6 weeks of age.

The clinical stage of the disease has a sudden onset, and are seen within 2-3 days after

exposure and the mortality rate in the flock increases rapidly. (Helmboldt et al., 1964).

Clinical signs of the disease include dehydration, trembling, ruffled feathers, vent

pecking, and depression. Affected chickens experience a transient immunosuppression.

The acute form is characterized by sudden onset, short course and extensive destruction

of lymphocytes particularly in the bursa of fabricius and also in other lymphoid tissue

(Jordan, 1990). Milder forms of the disease exist and include the unapparent infectious

forms.

Prevention and Control of IBD

Effective control of IBD in commercial broilers requires that field virus exposure

be reduced by proper clean-up and disinfection between flocks; and that traffic (people,

equipment and vehicles) onto the farm be controlled. The development and enforcement

of a comprehensive biosecurity program is the most important factor in limiting losses

due to IBD. Phenolic and formaldehyde compounds have been shown to be effective for

disinfection of contaminated premises. Efforts at biosecurity (cleaning, disinfecting,

traffic control) must be continually practiced, as improvement is gradual and often only

seen after 3 or 4 flocks. The sanitary precautions that are applied to prevent the spread of

most poultry infection must be rigorously used in the case of IBD (Calnek et al., 1997).

11

A third factor to consider in the IBD prevention and control program is

vaccination of the broilers to prevent clinical IBD. Three categories of vaccines, based on

their pathogenicity, have been described: mild, intermediate, and virulent vaccines. The

intermediate type IBD vaccines are most commonly used. These vaccines can stimulate

the broiler to produce antibodies earlier than the mild-type vaccines, without significant

damage to the BF as may occur with the virulent type vaccines.

2.1.3 Fowl Pox

This disease is caused by a virus Avian poxviruses which are members of the

genus avipovirus of the family poxviridae but spread slowly (Calnek et al., 1997).

Spread

Poxvirus infection occurs through mechanical transmission of the virus to the

injured or lacerated skin. Individuals handling birds at the time of vaccination may carry

the virus on their hands and clothing and may unknowingly deposit the virus in the eyes

of the susceptible birds. Insects serve as mechanical vector of the virus (Calnek et al.,

1997). Spread of virus from one chicken to another is by direct contact of the infested

chicken (Jordan et al., 1996) and by contact with wild birds and flies (Obioha, 1992).

Signs

The disease may occur in one of the two forms, cutaneous or diphtheritic or both.

The signs vary depending on susceptibility of the host, virulence of the virus, distribution

of the lesions and other complicated factors (Calnek et al., 1997). The cutaneous lesions

can vary in appearance. First is a papule, which rapidly progresses through the vesicle to

the pustule and finally to the crust or scab stage. After about two weeks, the scab will

12

drop off and a healed lesion is left which may or may not leave the scar (Jordan et al.,

1996). It is characterized by appearance of nodular lesions on the comb, wattle, eyelids

and other non fathered areas of the body. In the diphtheritic form of the disease, small

white nodules are observed in the upper respiratory and digestive tracks. These nodules

coalace to form raised yellow plagues on the mucous membrane. Most lesions are found

in the mouth but others are present in the larynx, trachea and Oesophagus (Obioha,

1992).

Control

There is no satisfactory treatment. However, avipox can be prevented by

vaccination. The two main routes used are the wing web and thigh muscle (Jordan et al

1996). Other major infections diseases that can be vaccinated against include marek’s

disease, pullorum, Typhoid, Cholera, Coccidiosis, Fowl paralysis (Neural

lymphomatosis) etc.

2.2 Vaccines and Vaccination

According to Butcher and Miles (2008) Vaccines are used to prevent or reduce

problems that can occur when a poultry flock is exposed to field disease organisms.

Vaccinations should be thought of as insurance. Like any other insurance programme,

there is a price to be paid for protection against a potential threat. These include, price of

the vaccine, time spent designing the vaccination schedule, administering the vaccines,

and losses due to vaccine reactions from the live-type vaccines and localized tissue

damage from killed-type vaccine injections. As with insurance, if the risk of a particular

disease is low in the area, it makes little sense to vaccinate against that disease, as the

13

costs may outweigh the benefits. Once a decision is made to vaccinate, many factors have

to be considered to ensure that vaccinations are successful.

According to Calnek et al 2007, the factors include,

1. Stress which may reduce the birds ability to reach an immune response. Stress include

environmental extremes (temperature, relative humidity), inadequate nutrition, parasitism

and other diseases. Birds should not be vaccinated during periods of stress.

2. Live vaccines may be inactivated due to improper handling or administration.

3. If there is a breakdown in the biosecurity programme and a disease outbreak occurs,

the vaccination programme needs to be adequate and effective to limit resulting losses.

2.3 The Importance of Vaccination

Vaccination is an effective means to prevent and/or reduce the adverse effects of

specific diseases in poultry (Jacob et al 2003). Poultry refers to birds that people keep for

their use, and generally includes chicken, turkey, duck, goose, quail, pheasant, pigeon,

guinea fowl, pea fowl, ostrich etc. Disease-causing organisms in poultry can be classified,

as viruses, mycoplasma, bacteria, fungi, protozoa, and parasites. All these organisms are

susceptible to chemotherapy, except viruses. Control of viral diseases is dependent upon

prevention through sanitation, biosecurity, and by vaccination.

Strict sanitation and biosecurity are essential for successful poultry production.

Thus vaccination is no substitute for effective management. It is important to note that

vaccines may be effective in reducing clinical disease, but exposed birds, in most cases,

still become infected and shed disease organisms (Allan et al., 1978). It is also very

important in reduction of spread of diseases to other farms, production of healthy meat

14

for human consumption and prevention of zoonotic effects of the disease as in bird flu

etc.

Unfortunately, small poultry flocks do suffer from many diseases which could be

controlled through appropriate vaccination. These diseases may result in loss of income

from the sale of eggs, meat or stock (Butcher et al .,2003). Other losses may include

death of valuable breeding stock.

2.4 Deciding Whether or not to Vaccinate

Commercial poultry are usually vaccinated to protect them against a variety of

diseases. Vaccination, however, is seldom practiced by small flock owners. There may be

several reasons for this, including:

They may rarely have disease problems in their farms

They may be unaware that disease is present in their farms

They may not get the disease properly diagnosed

They often do not know where to purchase vaccines

For small scale producers, vaccines may be too expensive because poultry

vaccines usually come in 100 to 1000 dose vials.

Vaccination causes a stress on poultry especially individual vaccination cause

more stress on the bird than flock treatment (Gillespie,1997)

Deciding whether or not to vaccinate against a disease depends on the likelihood that

the birds in a flock may be exposed to that specific disease. If a flock is closed, such that

new birds are never introduced and the birds that leave the farm are not permitted to

15

return, the likelihood of many diseases is greatly reduced. In these cases, since the risk is

small, the owner may decide not to vaccinate (Butcher et al., 2003).

2.5 Types of Vaccines:

Vaccines for poultry are of two types; either live or killed (inactivated), each

having specific advantages and uses.

According to Siddique and Ullah (2004) killed Vaccines are prepared from

bacteria or viruses that have been inactivated and processed. They are usually produced

from infective allantoic fluid treated with B-propiolactone or formalin to kill the virus

and then mixed with a carrier adjuvant (Cross, 1988). These vaccines cannot spread from

bird-to-bird and require individual injection. Several advantages of the killed vaccines

are; administration of a uniform dose, safety (the organism is inactivated), development

of uniform levels of immunity (each bird receives the same dose), no chance for spread of

vaccinal organisms, increased product stability and choice for a wider variety of virus

strains. Inactivated oil –emulsion vaccines are not as adversely affected by maternal

immunity as live vaccines and can be used in day old chicks (Box et al., 1970). Various

disadvantages of the killed vaccines are; increased costs (labor and product), slower onset

of immunity, narrow spectrum of protection and localized tissue damage at the site of

injection. Inactivated vaccines must be administered by injection; success of vaccination

is thus dependant on the skills of the vaccine administrator in administering a full dosage

of vaccine to each bird (Bruytenbach, 2005).

Live vaccines are usually sold as freeze-dried allantoic fluid from infected

embryonated eggs (Calnek et al., 2007).The live vaccines first infect the chicken,

multiply and produce immunity. The live vaccines have got several advantages such as

16

ease of administration, low price, rapid onset of immunity and broader scope of

protection because chickens are exposed to all stages of the replicating virus. Several

disadvantages associated with the live vaccines are; problems with uniform vaccine

application, excessive vaccine reactions, unwanted spread of the vaccinal viruses and

extreme handling requirements needed to maintain viability of the vaccinal organisms

(Jordan,1990). Live vaccines may be easily killed by chemicals, heat and if not carefully

controlled during production, can contain contaminating viruses (Calnek et al., 2007).

They usually contain only one antigen and are administered by spraying (aerosol), via

drinking water, and as eye drop (Jordan 1990). The antigen may be either the disease

organism which has been deliberately attenuated, (made less virulent) by some suitable

means. Both live and killed vaccines are used in Nigerian poultry industry. Live vaccines

provide short-term immunity, which is relatively fast to develop. In comparison, the

immunity afforded by individually administered killed vaccines lasts longer and takes

longer to fully develop.

Allan et al (1972) have produced a comprehensive description of all aspects of

New castle disease vaccination. The live vaccines are produce from mild variuses

(Lantogenic strains eg. Hitchner B1, Lasota strains) while the inactivated vaccines are

from the mesogenic strains (eg. Mukteswar, Roakin and Komarav).

2.6 Administration

Just as important as the timing of vaccination is proper administration of vaccines.

With vaccinations, the most important consideration is to vaccinate the entire flock to

prevent diseases. In any vaccinated flock, a certain percentage of the birds may not be

adequately vaccinated and thus remain susceptible to disease. If a large percentage of the

17

birds are protected, then the pathogens shed from the infected bird are less likely to find

another susceptible bird to infect and eventually the threat of spread of disease is

drastically reduced (Butcher et al., 2003). Therefore, the fewer the birds that are

susceptible, the less likely that a field challenge will result in severe disease within the

flock.

Reputable vaccines manufacturers subject all batches of vaccines to stringent

quality control test, ensuring that the end user is supplied with a product containing

sufficient antigen to initiate an immune response in the target bird. Thus, assuming bird

health, vaccine administered the target bird in the prescribed dosage will induce

immunity to the specific disease (Cserep, 2002). Furthermore, a well planned vaccination

schedule will result in maximum immunity at the time when poultry are most susceptible

to infection or when disease would have the highest negative impact on economic

performance.

Extreme care must be taken to ensure that the vaccines are handled properly and

delivered appropriately so that each bird receives an immunizing dose. Strict attention to

detail can mean the difference between protected birds and those that remain susceptible.

It is important to read the information supplied with the vaccine vials, administer it

properly and pay close attention to withdrawal times (Jordan et al., 1996).

Vaccines administered properly, at the correct time and with the appropriate

antigen content do not guarantee 100 percent protection. However, a well designed, well

timed and soundly executed vaccination program coupled with good management,

nutrition and biosecurity will go a long way to helping maintain a healthy and productive

flock. Timing of vaccination of broiler chickens can be especially difficult due to the

18

presence of maternal antibodies. Because of their short life, broiler chickens are

sometimes not vaccinated in countries where there is a low risk for New castle disease.

Vaccination of laying hens always require more than one dose of vaccine to maintain

immunity throughout their lives (Allan et al., 1978).

Vaccination programmes are designed to prevent or reduce losses caused by

disease in either or both the vaccinated birds and their progeny. In devising a vaccination

programme, both immunological and commercial factor must be considered as well as

methods of administration. There are many methods of administration of vaccines, they

include through drinking water, spray, eye drop, injection and wing web (Butcher et al.,

2006). Of all the methods of administration of live vaccines, the eye drop or intranasal

route is probably the most effective, although they are time consuming. Accuracy is

important such that the vaccine must disappear after a blink (eye drop) or inhalation

(intranasal) before the bird is released.

2.7 Types of Vaccination Programmes

Vaccination programmes vary considerably from area to area and country to

country and according to the local pattern of disease (Bundy et al., 1975). The

vaccination programme for common diseases of poultry are presented in Table 1.

19

Table 1: The vaccination programme for the common diseases of poultry.

Schedule Type of vaccine Broiler layers Turkey

Day 1 NDV (i/o) + Mareks ” ” ”

Day 7-10 IBDV 1st Dose ,, ,,

Day 17-20 IBDV 2nd Dose ” ”

Day 21 NDV (L) ” ” ”

Week 6 NDV (K) 1st Dose ” ”

Week 8 Fowl Pox Vaccin ” ”

Week 16 NDV (K) 2nd Dose ” ”

NDV (i/o) = New Castle Disease Vaccine (intraocular)

IBDV = Infectious Bursal Disease Vaccine

NDV (L) = New Castle Disease Vaccine (Lasota)

NDV (K) = New Castle Disease Vaccine (Komorov)

It is important to note that prevention is by far better than cure. This is particularly

true of poultry diseases because every disease occurance is accompanied by economic

loss in excess of the cost of prophylaxis and vaccination (Obioha 1992).Vaccination

schedule slightly differs from one place to another. Therefore, local Veterinarian should

be contacted (Obori 2005).

According to Jordan (1990) vaccination programme are designed to prevent or reduce

losses caused by disease in either or both the vaccinated birds and their progeny. In

devising a vaccination programme, both immunological and commercial factors must be

considered, including the following:

20

1. The general health of the flock and the local pattern of disease. Vaccine must not

be administered to sick birds.

2. The genetic type and function of the bird.

3. The cost benefit of vaccination against potential loss.

4. The short or long-term protection required.

5. The vaccinations or diseases that occurred in the previous generation which

would influence maternal antibody status. Having decided on the types of

vaccine required, the route, method and frequency of administration must be

considered.

2.8 Tips For Successful Vaccination

The facts indicated below are for successful vaccination

a. Vaccination of poultry younger than 10 days of age cannot be expected to produce

uniform or lasting immunity, even in the absence of parental immunity. An exception

is that vaccination for Marek's disease is ordinarily given on the day of hatch.

b. Each vaccine is designed for a specific route of administration. Use only the

recommended route.

c. Do not vaccinate sick birds (except in outbreaks of laryngotracheitis or fowl pox).

d. Protect vaccines from heat and direct sunlight.

e. Most vaccines are living, disease-producing agents. Handle them with care.

f. When using the drinking-water method of vaccination, be sure the water is free of

sanitizers and chlorine. Live-virus vaccines are readily destroyed by these

chemicals.

21

g. After vaccinating, burn or disinfect all opened containers to prevent accidental

spread to other poultry.

The quality of a vaccine cannot be guaranteed if the product is mishandled or

improperly used after it leaves the manufacturing plant. All vaccines are labeled with

instructions for use and dates of expiration (Jacob et al 2003).

2.9 Vaccine Distribution

Seventeen vaccines are currently being produced and sold to farmers by National

Veterinary Research Institute Vom. The southern part of Nigeria is the main market for

poultry vaccines with the south west being largest user of the vaccines. The northern part

of Nigeria is the largest market for large and small ruminant vaccine. The south east also

buys a large number of doses of TCRV for small ruminants. It has become obvious that

in general, many conventional vaccines are usually deficient in efficacy, potency or

safety.

2.10 Factors Which Interfere With Vaccine Efficacy

Factors which interfere with vaccination of commercial poultry can be divided

into three main groups. They are: factors associated with the vaccine itself, those of

vaccine administration, and factors which are endogenous to the bird (McMullin 1985).

The most serious problems occur when two or more of these factors are involved.

Specific examples can be given of how many of the factors affect vaccination under

practical conditions. Possible reasons for an incorrect diagnosis of low vaccine efficacy

should also be considered.

22

The flock may not have been vaccinated due to oversight, or deliberately because

of intercurrent disease and fear of vaccine reactions. Immunization requires a period

post-vaccination to reach peak resistance. The degree and nature (local/systemic) of

resistance and the length of this period differs among the different types of vaccine used

in poultry. If a vaccine fails to fully protect against a disease because the birds were

infected prior to or soon after vaccination this is only an apparent vaccine failure.

A. Factors associated with the vaccine itself

All of The factors associated with the vaccine itself tend to be closely inter-

related. A deficiency in one can be partially compensated by another. A vaccine of

moderate-to-poor titre may give satisfactory results if very carefully applied, while it may

be a disaster if poorly applied. Stability of live virus vaccines is affected by the success of

lyaphilization and the temperature under which it is stored. Period of validity must

strictly followed or the vaccine re-titrated (Beard and Brugh, 1975). It is possible to

encounter considerable variation among commercial vaccines in the type of virus used.

Nagi et al; 1980 studied three commercial vaccines against infectious bursal disease and

found marked difference, both in titre of antibody produced and in persistence of the

virus in the tissues. Muskett et al; (1979) in a similar study found one vaccine to be

highly pathogenic in young chicks.

B. Factors associated with administration of the vaccine to the bird.

The route by which the vaccine is administered can affect the outcome of

vaccination. The superior protection against New castle disease afforded by aerosol

administration of live virus vaccines is well documented (Beard and Easterday, 1967).

Winterfied et al (1980) had shown that aerosol vaccinated birds are also more resistant to

23

infection with virulent virus than those vaccinated only with inactivated vaccine by the

intra muscular route. In ultimate analysis it is essential that the antigen present in the

vaccine is uniformly distributed within the flock. The use of "mass vaccination" (drinking

water and aerosol) tends towards less uniformity in application than individual

application, and need considerable operator care in order to control this tendency. Even

with individual application, problems of uniformity of application can occur due to

poorly adjusted syringes, faulty droppers, etc. Administration of certain

combinations of live virus vaccines may affect the response to each virus, especially

when they contain viruses which have the same target tissues (Beard and Brugh, 1975).

The diluent used for live virus vaccines is very important to ensure that an adequate titre

of virus actually reaches the birds. The classical problem of administering live-virus

vaccine in chlorinated drinking water is well known, but less extreme. Immunization

against infectious disease is rarely dependent on a single inoculation. In the case of those

diseases for which only one or a few applications are made, efficacy usually relies on the

persistence of the vaccine agent for a long period in the bird (Wyeth and Cullen, 1979).

C. Factors endogenous to the bird

Factors endogenous to the bird that can interfere with efficacy of vaccine applied

include:-

Previous exposure: Repeated exposure over too short a period may not be advantageous.

Common practice dictates that the same vaccine should not be re-applied to a flock within 14

days.

Passive protection: Circulating antibody may affect the response to vaccination, even

independently from the previous factor, i.e. when it is not produced by the bird itself. The

24

commonest source of passive protection is that transmitted from the breeder bird to her chick

via the yolk (Mcmullin, 1985). The baby chick has circulating antibodies in similar

concentrations to those found in the breeder at 1-3 days of age. They fall to undetectable

titres by 14 - 30 days (depending on the method of detection used). There is no doubt that

maternal antibody can influence the response to vaccination during the first weeks of life

(Davdaar and Kouwenoven, 1977).

Immunosuppression: Stress of any sort is well known to reduce disease resistance and can

also be expected to affect response to vaccination (Sivanandan et al; 1980). Exceptionally

poor environmental conditions could contribute to vaccination failure under some

circumstances.

25

CHAPTER THREE

MATERIALS AND METHODS

The materials and methods used in this experiment are as follows:

3.1 Location and Duration of the study

This experiment was carried out at the poultry unit of the Department of Animal

Science farm, University of Nigeria Nsukka. The experiment lasted 10 weeks from 25th

of January to 4th of April 2008.

3.2 The Experimental animals.

A total of 90 birds of Anak strain were used and they were bought from reliable

suppliers at day old. The day old broilers were housed in pens that were cleaned and

disinfected two weeks earlier. The study was made up of three treatments with two

replicates per treatment consisting of 15 birds each ie. 30 birds per treatment. The birds in

each treatment were brooded differently. The treatments and allocation of birds are as

indicated in Table 2. The treatments are the extent of delay in weeks before the birds

were inoculated with the conventional vaccines used to protect against poultry diseases in

the tropics.

Treatment one is the control experiment with normal routine vaccination that is

recommended in the tropics where Newcastle disease is endemic. Treatment two is

delayed inoculation for one week while Treatment three is delayed inoculation for two

weeks.

26

Table 2: The days of vaccination and the treatments used were

Vaccine Treatment 1

(control)

Treatment 2 (1 week delay) Treatment 3 (2 week

delay)

NDV (i/o) 1st day 7th day 14th day

Gumboro

vaccine

14th day 21st day 28th day

NDV

(Lasota)

17th day 24th day 31st day

Gumboro

vaccine

19th day 26th day 33rd day

NDV

(Lasota)

26th day 33rd day 40th day

3.3 General sanitation and Health measures

Drinkers were washed everyday while the remnants of feed in feeding troughs

were removed and the troughs cleaned before another feed were introduced. There was an

outbreak of coccidiosis when the birds were six weeks of age. This was controlled by

giving them Embazine forte for three days, clean water for two days and then the

medication continued for another three days. The litter was raked from time to time and

27

topped with fresh litter material to ensure the comfort of the birds and reduce disease

build-up when litter cakes.

3.4 Experimental Design:

The study was a completely randomized design with linear model:-

Xij = µ + Ti +Eij

Where Xij = Individual observation

µ = Population mean

Ti = Treatment effect

Eij = Random error

3.5 Data Collection Analysis

Data was collected at weekly intervals as the birds grow based on the following

parameters:-

a. Weekly body weight was measured with a sensitive weighing scale and recorded

in kg.

b. Live weight gain/birds which was calculated as the difference between the

weight of the birds in one week and the weight in next week and thereafter

converted to daily weight gain by dividing with the number of days spanning the

measurements. The values were in kg

c. Shank length was measured with a meter-rule and recorded in cm

d. Mortality rate was measured by counting the number of birds each day and

noting the number that died.

28

e. Haematological values (PCV and WBC) and Haemagglutination inhibition

values were determined based on the procedures described below:

Procedures for the Haematological Examination

At the end of 10 weeks of the experiment, 5 broilers were randomly selected from

each replicate and blood samples were collected from the wing vein with a sterile needle

into sterile bijou bottles. The blood evaluations were carried out at Physiology and

Microbiology laboratory, Faculty of Veterinary medicine, University of Nigeria, Nsukka.

i. Packed cell volume (PCV) Determination

Five Heparizied micro capillary tubes were used to collect blood from the bijou

bottles. The capillary tubes were sealed at the end with plastacin and centrifuged. The

value of packed cell volume per blood sample was recorded.

ii. White blood cell count

The white cell count may be elevated in bacterial infections and may drop below

normal values in viral diseases (Brown 1976).

A 1ml pipette was used to aspirate 0.38mls of WBC diluting fluid (ie. 1% acetic acid)

into five different test tubes. Then using a WBC diluting fluid pipette 0.02mls of blood

was aspirated from the bijou bottle and transferred into the test tube. The suspension

(WBC count diluting fluid and blood) was mixed and sample was taken and used to

charge a Naubauer counting chamber which then was placed under a light microscope

and WBC counted using X 400 magnification. The WBC on the four large corner

squares that are marked “W” were counted, and then the result was multiplied by 2.5 and

20.

29

Haemagglutination Inhibition Procedure

The haemagglutination inhibition was determined using the procedure outlined below:

Serum samples:

Collection of blood samples from five randomly selected chickens in each of the

replicate was done at the end of 10 weeks of age. The blood samples were collected by

venipuncture of the wing vein and discharged into clean sterile bottles for serum

formation. Clotted blood sample were kept at room temperature to enhance serum

formation. Sera were harvested into clean bottles and then stored at -20°C until used to

determine the humoral immune response to NDV (antibody titre), Haemagglutination

(HA) and Haemagglutination Inhibition (HI) tests.

Washing of Erythrocytes

2ml of ND antibody free blood was collected from adult birds in a test tube

containing EDTA as anticoagulant. 10ml phosphate buffered saline (PBS) was added and

the level of blood marked. Equal volume of ordinary tap water was added in a similar

tube and placed at the opposite side of the tube containing the blood sample in order to

counter balance the load. The blood was centrifuged 3000 rpm for 5 minutes and the

supernatant (plasma) and buffy coat were discarded. Packed RBC was re-suspended in

10ml of PBS. The process of RBC suspension in PBS and centrifugation was repeated

until a clear supernatant was obtained. The packed volume of RBC was re-suspended in a

measured volume of PBS solution to make 0.5% RBC suspension (Beard, 1989).

i. Haemagglutination (HA) Test.

30

The standard HA technique was used .The test was used to determine the titre of

the antigen before converting it to 10 HA units for running of HI test. 200 doses of Lasota

ND vaccine was suspended in 10ml of sterile PBS (PH 7.0). Clean, dry, microtitre plates

with v-bottom wells were labeled and 50μl of PBS (PH 7.0) was dispensed into two rows

of wells from left to right using a micropipette. 50μl of the suspended Lasota ND vaccine

was added to the first pair of wells and then thoroughly mixed. A 12 fold serial dilution

was then carried out using a multi channel micropipette from one to the twelfth well. The

content of the pipette after the twelfth well was discarded. 50μl of washed chicken RBC

suspension (0.5%) indicator was added into each well using the microtitre pipette. Each

of the plates was gently shaken and then allowed to stand for about 45 minutes at room

temperature after which the results were read. The reciprocal of the highest dilution that

gave complete or 100% HA was taken as the HA titre of the antigen. The titre was

adjusted to 10 HA unit for the HI test.

ii. Haemagglutination Inhibition (HI) Test.

96-well titretek microtitre plates which allow 8 samples to be titrated were used.

50μl of PBS were dispensed into each well using eight-channel micropipette. 50μl of

each serum sample was put in the first row and transferred from there to the last well thus

double diluting out each serum sample. After the 2-fold dilution of the serum sample,

50μl of 10 HA units of virus were dispensed into each well and plates were left

undisturbed at room temperature (25°C) for 45 minutes (Cooke, 1993). 50μl of 0.5%

washed chicken RBC was added into each well and the plates were gently tapped to

ensure even mixing. A 50μl of PBS and 50μl of 0.5% washed chicken RBC was added

into two wells of another plate to serve as positive control. Also, 50μl of the 10 HA

31

antigen and 50μl of 0.5% washed chicken RBC was added into another two wells of the

same plate to serve as negative control. The plates were kept undisturbed at room

temperature (25°C) for 45 minutes until a clear pattern of haemagglutination Inhibition

was seen. The HI titre was expressed as reciprocal of the highest dilution of serum at

which 100% positive erythrocyte haemagglutination Inhibition occurred. The GMT was

calculated using the tube number method as described by (villagas and Purchase, 1989).

3.6 Analysis of Data

The data collected were processed and analyzed using a stat-graphic computer

package. Significantly different means were separated using Duncan’s New Multiple

Range Test in the same package (software).

32

CHAPTER FOUR

RESULTS

The results obtained are presented in the Tables below. The analysis of variance

of weekly live body weight, weekly shank length and the haematological values are

shown in the appendices. The weekly live weight and daily gain weight of the birds in

the three treatments are presented in Tables 3 and 4.

Table 3: Weekly live body weight (kg) of broilers subjected to varying vaccination schedule.

Age Treatment 1 Treatment 2 Treatment 3 (wks)

1 0.090 0.084 0.085

2 0.260 0.254 0.243

3 0.392 0.373 0.354

4 0.533 0.504 0.481

5 0.676 0.630 0.622

6 0.759 0.738 0.694

7 0.989 0.968 0.916

8 1.217 1.167 1.026

9 1.454 1.427 1.389

10 1.744 1.716 1.685

Mean±SE 0.810±0.21a 0.786±0.32b 0.750±0.16b

33

From the analysis of variance there were significant difference (P<0.5) between

treatments in live body weight of birds at the end of 10 weeks. When comparison of

treatment means were carried out, it was discovered that mean body weight of birds in

treatment one(control) was significantly higher than body weight of birds in treatments

two(one week delay) and treatment three(two weeks delay). This tends to show that

vaccinating at normal timing helps in better performance of the birds. The weekly body

weights and daily gains in weight between the birds in the various treatments were

deliberately presented in order to pin point the exact stage of growth at which delay in

vaccination of the birds affected their performance.

Although the birds generally exhibited poor growth probably as a result of

breeding errors traceable to their source, it is apparent that the delay in vaccination

affected the growth performance of the birds in Treatment 2 and 3 from the third to the

5th week of age. The birds in Treatments 2 and 3 did not come down with observable

symptoms probably because of their immunity level couple with the high plane of

nutrition applied in effort to improve growth. The birds were fed ad libitum through the

study but gained very poorly as shown in the weight gains in Table 4 and final body

weight (at 10 weeks) shown in Table 3. The birds apparently picked up from the 6th week

and remained stable till the end of 10th week.

34

Table 4: Mean of daily live weight gain (kg) of broilers subjected to varying

vaccination schedules.

Age Treatment 1 Treatment 2 Treatment 3

(wks)

2 0.170 0.170 0.158

3 0.138 0.113 0.111

4 0.141 0.131 0.127

5 0.143 0.176 0.181

6 0.183 0.058 0.032

7 0.230 0.230 0.222

8 0.228 0.199 0.210

9 0.237 0.260 0.263

10 0.296 0.270 0.266

Mean± SE 0.177±0.12b 0.161±0.11a 0.157±0.11a

There were significant differences (P<0.05) in live weight gain of birds in the

various treatments. A comparison of the treatment means showed that treatment 1

(control) was superior to treatments two and three in their rates of growth especially at

the early stages of growth (weeks 1-5). This shows that birds gain weight better when

subjected to normal vaccination, while birds in treatments where vaccinations were

35

delayed probably failed to gain as expected due to physiological constraints arising form

efforts to combat disease pathogens in the system that could have been taken care of with

early vaccination programme.

Table 5: Weekly Shank length (cm) of broilers subjected to varying vaccination schedules.

Age (wks)

Treatment 1 Treatment 2 Treatment 3

1 1.55 1.45 1.50

2 2.05 1.90 1.85

3 2.80 2.55 2.35

4 3.60 3.01 2.90

5 4.45 3.90 4.75

6 5.25 5.25 5.10

7 6.50 6.25 6.20

8 7.35 7.10 7.05

8 7.90 7.75 7.80

10 8.20 8.20 8.15

Mean SE 4.96 0.53 4.74 0.54 4.77 0.54

Although the development of shank lengths of the birds (Tables 5 and 6) followed

the same trend as body weight, the birds in the various treatments did not differ

36

significantly (P>0.05). The delay in body growth of birds from weeks 3-5 was slightly

evident in their shank length development

Table 6: Mean daily shank length gain (cm) of broilers subjected to varying

vaccination schedule

Age Treatment 1 Treatment 2 Treatment 3

(wks)

2 0.55 0.50 0.35

3 0.65 0.55 0.40

4 0.85 0.60 0.55

5 0.80 0.75 0.65

6 0.95 0.80 0.75

7 0.95 0.85 0.80

8 0.85 0.85 0.85

9 0.65 0.55 0.75

10 0.45 0.30 0.35

Mean± SE 0.67± 0.07 0.58 ± 0.02 0.55±0.04

37

Table 7: Mortality rates of broilers subjected to different vaccination schedules.

Age

(week)

Treatment 1 Treatment 2 Treatment 3

R1 R2 R1 R2 R1 R2

1

2

3

4

5

6

7

8

9

10

-

-

-

-

-

-

-

-

-

-

-

-

-

-

-

-

-

-

-

-

-

-

-

-

-

-

-

-

1

-

-

-

-

-

-

-

-

-

-

-

-

-

-

-

-

-

-

-

1

-

-

-

-

-

-

-

-

-

2

-

Total mortality =4

The above table showed a total mortality of 4 birds in all the treatments with no

mortality in treatment 1, one mortality in treat 2 and three mortalities in treatment 3.

38

Table 8: Mean values for blood parameters of broilers subjected to different

vaccination schedules.

Parameters Treatment 1 Treatment 2 Treatment 3 SEM

PCV 27.00a 25.50a 12.50b 0.33**

WBC(mm³) 65.41×104b 95.23×104a 104.45×104a 2.52×104**

Haemaagglutination

test

26.75b 136.00b 832.00a 53.42**

a, b – Row means with different superscripts are statistically significant at 1% (P < 0.01)

The result of mean PCV levels showed that the percentage PCV level of treatment

one(normal routine vaccination programme) was significantly higher than those of other

treatments that were delayed by one week and two weeks. These differences were

statistically significant (P<0.01).

The result on WBC count showed that the percentage WBC count of broilers that

were delayed by two weeks were higher than broilers subjected to one week delay and

normal routine programme. There differences were statistically significant (P<0.01).

The result of the haemaagglutination test (HI) showed that there was a higher

increase in treatment three (two weeks delay) compared to other treatment from the

analysis of variance at HI values of treatment one (control) had significantly better values

(P<0.01) than treatment three (two weeks delay) and treatment two (one week delay).

39

CHAPTER FIVE

DISCUSSION

The parameters considered in this study were weekly live body weight, daily live

weight gain, shank length, daily gain in shank length, PCV, WBC, and

haemaagglutination inhibition test. These were studied in order to determine the effect of

delayed routine vaccination programme on growth performance and mortality rate of

broilers. From the result statistically significant differences (P<0.05) were noticed in all

the growth parameters except in weekly shank length and mean daily gain in shank

length.

The results also revealed that birds that were vaccinated accordingly did

significantly better in their growth performance than those that their vaccination were

delayed. These results agreed with those of Jordon (1990) which indicate that well

designed, well timed and soundly executed vaccination programme coupled with good

management, nutrition and biosecurity will go a long way to maintain a healthy and

productive flock.

It was observed from the result that there were no significant differences in

weekly shank length and mean daily gain in shank length, which suggests that delay in

vaccination schedule did not really affect the growth of there body components.

The results also showed an increase in the PCV values of the birds vaccinated

accordingly but decreased among the other birds that had their vaccination schedules

delayed. Furthermore the result indicate a very high level of WBC among the birds that

were subjected to one week and two weeks delay in the normal routine vaccination

programme. Brown (1976) had earlier reported their the WBC may be elevated in

40

bacterial infections and may drop below normal values in viral disease. It follows from

these results that in treatments where vaccination programme were delayed the birds were

more exposed to bacteria infections which now made their WBC to be above normal.

There were however no visible indications of viral infections among the treatments with

delayed vaccination schedules to warrant a drop in WBC levels below normal values.

It was observed from the result that there were significant differences (P<0.01)

among treatments in haemaagglutination inhibition test (HI). Mcmullin (1985) had

observed that the passive protection which is transmitted from the breeder bird to her

chick via the yolk fell to undetectable titers by 14-30 days. While Thayer et al (1988)

also reported that poor performance in some broiler birds was related to low antibody

titers against IBDV in the source breeder flocks. The result of mean HI test showed that

the maternal antibody of New castle disease decreased especially in broilers that are

subjected to two weeks delay compared to birds subjected to normal routine vaccination

programme and broilers subjected to one week delay in normal timing of vaccination.

The results imply that delays in vaccination schedules used in this study, resulted in

reduced growth performance and reductions in immunity levels, they were not prolonged

enough to cause drastic effects on body growth and total collapse in immunity response

of the birds body system as to result in observable symptoms of New Castle disease,

Gumboro and other bacterial infections of poultry.

41

CHAPTER SIX

SUMMARY Conclusion AND RECOMMENDATION

In this study the performance of broiler birds that were vaccinated according to

the local vaccination programme and birds that there vaccination schedule were delayed

by one week and two weeks were compared to know the effects of the delay on their

growth rate, blood parameters and mortality rate. Based on the findings, birds that were

subjected to the normal routine vaccination schedule excelled over those that their

vaccination schedule were delayed in all parameters measured except in weekly shank

length and daily gain in shank length which were similar in all treatments.

In conclusion, therefore, just as the timing of vaccination and proper

administration are equally important (Jordon 1990), extreme care must be taken to ensure

that the vaccines are handled properly and delivered appropriately so that each bird

receives an effective immunizing dose. Birds in the control treatment had normal routine

vaccination programme and performance better than birds in other treatments.

Recommendation

It is important to note that prevention is by far better than cure. This is particularly

true of poultry diseases because every disease occurence is accompanied by economic

loss in excess of the cost of prophylaxis and vaccination (Obioha 1992). Unfortunately

vaccination is seldom practiced by small flock owners. There may be several reasons for

this, which include the fact that they rarely have disease problems, or may not know

where to purchase vaccines, non availability of vaccines at the purchasing centers. It is

recommended that broiler produces should do all within their reach to procure and

administer vaccines to their flock at the appropriate times ensure better performance.

42

Small poultry flocks do suffer from many diseases which could be controlled

through appropriate vaccination (Butcher et al 2003). If a vaccine fails to fully protect

against a disease because the birds were infected prior to or soon after vaccination this is

only an apparent vaccine failure (Mcmullin 1985). Vaccination is no substitute for

effective management. It must be understood that vaccines may be effective in reducing

clinical disease but exposed birds, in most cases still become infected and shed disease

organisms (Jacob et al 2003). So control of viral diseases is dependent upon prevention

through sanitation, biosecurity and by vaccination.

I therefore recommend that all poultry farmers whether small scale farmers or

large scale farmers should vaccinate their flocks according to that recommended routine

vaccination schedule for their area. This helps in ensuring the growth and production

performance of the birds, with reduced rates of morbidity and mortality which could be

encountered if the birds are not vaccinated.

43

REFERENCES

Abdu. P.A. (2005) Evolution of the pathogenicity of New Castle disease voms and its implications for Diagnosis and control. Veterinary teaching Hospital Ahmadu Billo University, Zaria)

Allan, W.H., J.C. Lancaster, and B.Toth (1978). New Castle disease vaccines-their production and use. FAO, Rome, Italy.

Beard, C.W. 1989. Serologic Procedures. In a laboratory mannal for the Isolation and

identification of Avian Pathegens. 3rd H.G. Purchase, LH. Arp. CH H Domermuth, and J.C Pearson (eds) Kennett Square. PA: Amer. Assoc. Avian Pathologist. Pp 192-200

Beard, C.W. and Brught, M. (1975) Immunity to New Castle Disease. Am. J.Vet. Res, 36(4): 509-512,

Beard, C.W. and Easteraday, B.C. (1967). The influence of the route of administration of New Castle disease virus on host response. J. Infect. Dis., 117:55-61.

Benton, W.J., Cover, M.S, Rosenberger J.K. (1967). Studies on the transmission of the infections bursal agent (IBA) of chickens. Avian Diseases 11:430-438.

Box, P.G, Helliwell, B.I, Helliwell, P.H. (1970). New Castle disease in turkeys. Vet Rev 86:524-527.

Brown, A. Barbara (1976). Hematology: Principles and Procedures. Henry Kimpton publishers, London.

Butcher, G. D. and Miles, Richard D. (2008). Vaccine failure in poultry. University of Florida IFAS Extension.

Calnek, B.W, Barnes, H.J, McDougald. L.R, Salf, Y.M. (1997) Diseases of pultry. Iowa state university press, Ames, Iowa 50014. Pp541-562

Clarence, E. Bundy, Ronald, V. Diggins and Virgil, W. Christensen. (1975). Livestock and Poultry Production.

Cross, G.M. (1988). New Castle disease-vaccine production. In D.J. Alexander (ed). New Castle Disease. Kluwer Academic publishers, boston, MA, Pp. 333-346.

Cserep, T. (2002) “Intervet Poultry Division Datafile-Drinking Water Vaccination”. intervet UK Limited.

44

Davelaar, F.G., and Kouwenhoven, B. (1977) Influence of material antibodies on vaccination of chicks of different ages against infectious bronchitis. Avian Path.., 6:41-50.

Doyle, T.M. (1935). New Castle., disease of fowls. Journal of comp. Pathol. Their 48:1-20

Dozier, A.W, Lacy, P.M, and Vest, R.L. (2001). Broiler Production and Management. Department of Poultry Science, Cooperative Extension Service. The University of Georgia College of Agricultural and Environmental Sciences Attens, GA 30602. 229/386-3442.

Erah Pat, Hauwa Keri and Emmanuel Ehizibolo (Editors) 1999. Proceedings of the National workshop on vaccine and Biologicals. Organised by NAFDAC, WHO, UNICEF and National Programme on Immunization (NPI).

Ganiyu Obori (2005). Poultry care. Published by Ganob and Associates Limited.

Gary, D. Butcher and Richard, D. Miles. (2003). Infectious Bursal Disease (Gumboro) in commercial Broilers. Institution of Food and Agricultural Science, University of Florida, Gainnesville, 32611.

Gentry, R.F,M.O. Branue (1972). Prevention of virus inactivation during drinking water vaccination of poultry. Poult SC. 51:1450-1456

Gillespie R. James. (1997). Modern livestock and pultry production. Diseases and

parasites of pultry. By Delma publishers a division of international Thomson publishing inc.

Helmboldt, C. F., E. Garner. (1964). Experimentally include Gumboro disease (IBA).

Avian Disease 8: 561-575.

Hofstad, M.S. (1953). Immunization of chickens against New Castle disease by formation inactivated vaccine. Am. J. Vet. Res. 14: 586-589 Okye J.O.A and Shoyinka S.V.O (1984). New Castle Disease in a vaccinated flock which has experienced Subclincal intentions bursal disease. Trop. Anim. Health Prod. 15:221-225.

Jacob, J.P, Butcher, G.D and Mather, F.B. (2003). Vaccination of small poultry flocks. Cooperative Extension service, Institute of Food and Agricultural Sciences, University of Florida, Gainesville, 32611.

Jordan, F.T.W. (1990). Poultry Diseases. Third Edition.

45

Jorden F.T.W.Pattison. M. Alexender. D.J. (1996). Poultry Diseases. Typoset by phoenix photosetting, chatham, kent. Priated in the united kingdom at the university press, (ambridge) fourth edition.

Kirkby, M.W. (1951) Report to Assistant. Director of veterinary laboratory services veterinary department, Barnoda.

Knono, R; Akao. Y: Sasagawa A. and Nomnra, 1. (1979). Japan. Med. Sc. Riol 22;235-252;

Kraneveld, F.C. (1926). A PULTRY Disease in the Duch East Indies. Ned Indisch BI

Dietgeneeskd 38:448-450. Lancaster, J.E. and D.J. Alexander. (1975). New Costle diseas; Nirus and spread.

Monograph No. 11, Canadian Department of Agriculture, Ottawa. Loosli, J.K, Oyenuga, V.A and Babatunde, G.M (1973). Animal production in the

tropics. McMullin Paul (1985). Factors which interfere with vaccine efficacy. Proceedings of 1st

sta. Catarina Poultry Symposium pp 10-20.

MECreaten, R.M, Denny, G.O and MacDonald, S.C. (1992) New Castle Disease. Recent txperiences during an outbreak in Northern freland. Denary proceedings of society for vet. Epidemiology and preventive medicine 1-3 April 1992. Edimbough Pp. 40-46.

Muelenans, G.C.L eteller D.; Espoin, Lelong and Burny, A. (1988). Importance de la protene and Pimmunite an virus de la maladie de New Castle Bull Acad Vet France (61:51) 62.

Musket, J.C., Hopkins, I.G., Edwards, K.R. and Thornton, D.H. (1979). Comparison of two infectious bursal disease vaccine strains: Efficacy and potential hazards in susceptible and maternally immune birds. Vet. Rec., 104:332-334.

Naqi, S.A., Millar, D.L. and Grumbles. L.C. An evaluation of the three commercially

available infectious bursal disease vaccines. Avian Dis., 24(1):233-240. Obioha, F.C (1992). A guide to poultry production in the tropics. Avena publishers

Enugu.

46

Rautenschlein S, Kraemer C, Montiel E, Vanmarcke J, and Haase C. (2006). Bilateral Effects of Vaccination Against IBD and ND in Sific-pathogen-free Layers and Commercial Broiler Chickens. Avian Disease: vol. 51, no. 1, pp. 14-20.

Ritz, W.C. (2004). Mortality Management Options. University of Georgia. Siddique Muhammad and Ullah, Muhammad Sami (2004). Causes of vaccine failure in

poultry. University of Agriculture, Faisalabada, Pakistan Sivanandan, S. and Maeheswaran, S.K. (1980). Immune profile of infectious burals

disease. Avian Dis., 24(3):715-742 Thayer, S.G, Little, K.S, Fletcher, O.J, and Riddell, C. (1988). A study of Breeder

Vaccination Programs and Problems in the Broiler Progeny in Saskatchewan Utilizing Enzyme-linked Immunosorbent Assay. Avian Disease: Vol.32, No. 1, pp. 114-120.

Tom W. Smith, Jr. (2004). Poultry Disease Diagnosis. Extension Service of Mississippi

State University. Villegas, P. and Purchase, H.G. (1989). Titration of biological suspension. In a laboratory

mannal for the Isolation and identification af Avian pathorgens. Iowa. USA. Kendal Hunt. America Association of Avian Parthologists: 186-190.

Winterfield, R.W., Dhillon , A.S. and Alby, L.J. (1980) Vaccination of chickens against

New Castle disease with live and inactivated New Castle disease virus. Poult. Sc.,59:240-246.

Wyeth, P.J. and Cullen, G.A (1979). The use of an inactivated infectious bursal disease

oil emulsion vaccine in commercial broiler parent chickens. Vet. Rec., 104:188-193.

APPENDIX 1

Appendix 1: The ANOVA Procedure for Dependent variable of PCV

Source DF Sum of Squares

Mean Square

F Value Pr>F

Model 2 254.33 127.17 381.50 0.0002

Error 3 1.00 0.33

Corrected total

5 255.33

Appendix 3: The ANOVA Table for WBC

Source DF Sum of square Mean square F value Pr>F

Model 2 166568482×10³ 83284241×10³ 59.90 0.0038

Error 3 4171366×10³ 1390455×10³

Corrected total

5 170739848×10³

Appendix 4: The ANOVA Table for Haemaagglutination Inhibition test

Source DF Sum of Square Mean Square F value Pr>F

Model 2 763186.08 381593.04 33.61 0.0088

Error 3 34056.13 11352.04

Corrected total

5 797242.21