Noble Desk

Livestock production in Nigeria is faced by a number of problems, amongst which are malnutrition and gastrointestinal parasitic diseases. These problems are not without deleterious effects in man. In this piece, the afore-mentioned problems of livestock are examined concomitantly with their effects on human welfare and health care. The main objectives of any livestock or domestic animal farmer for setting up animal business is to make profit and boost production with a view of making animal protein available to the populace. Nevertheless a cursory view into the livestock or domestic animal industries in Nigeria has shown that malnutrition and gastrointestinal parasitic infection are some of the major problems normally confirmed that have been creeping the growth of the industry. Farm animals are normally confined under unnatural intensive or semi intensive conditions. Consequently, they depend entirely on the feed provided by man for their nutritional requirement. Livestock nutrition involves the physical feeding of the animals and adequate and proper monitoring of essential ingredients present in the feed. In other words, for livestock animals/poultry to meet slaughter weight at the appropriate age, properly balanced and high quality rations must be fed to them. This means that the nutritional needs of livestock for carbohydrate, fats, proteins, minerals, and vitamins must be met fully for efficient production. To do otherwise, will amount to malnutrition and consequent poor production, poor resistance to distresses and diseases, and general poor health of the animal. Thus, malnourished animals can easily be wiped out by excruciating weather and mild infections since their immunity is very low. In simple terms, malnutrition is the condition in which nutrition is defective qualitatively and or quantitatively. In a research and report sponsored by Smithking Beecham Nigeria Plc in 1992, Ikechukwu Nnadozie described malnutrition as a condition of the various constituents of the feed/diet and deficiencies of essential nutrients. Many times, malnutrition in livestock animals may occur as follows:-
(i)Non-availability of essential feeds stuff containing the required nutrients.
(ii) Faulty ration formulation
(iii) Wrong substitution of an essential feed ingredient with a less nutritive ingredient.
(iv) Drought and poor pasturage
(v) Cost consideration in isolation of quality consideration on the sides of feed manufacturers. Many manufacturers are often preoccupied with the interest of making mega profits and thus fail to strike a balance between feed quality and profitability. Some of them are unpatriotic to the extent of engaging in the mischievous or unorthodox practice of deceiving the farmers by compounding substandard or fake feed. It is not a surprise because of the economic situation of the country. In such feeds, most of the essential ingredients are purposely removed yet the labeled inscription on the feed always indicated that the feed is wholesomely fit qualitatively. Such practice has negatively affected the survival of livestock or domestic animal business to the detriment of the teeming populace. There is no doubt that optimum production can only be achieved if good feed is fed to the animals. But in a situation where the essential feed ingredients that are responsible for the healthy growth and development of livestock animals are deficient and those that are included in the feed are grossly insufficient, nutritional disorders, retarded growth, emaciation, loss of body condition and conformation, loss of height and production, abortions, infertility and death will be evident in most animals fed such and the consequence is a great economic loss due to gross under production of animal protein. This is a predicament in the pursuit of good health care for the Nigeria people. Little or no animal protein in the food of people constitutes a great health risk to them. This is so because protein is very essential in building up the immune status of any individual which is indispensable in protecting the body against infection. There are also protein deficiency related disease conditions such as kwashiorkor. Fatty infiltration of the liver arises and may cause cirrhosis. The effects is however fatal. Many other disease conditions can be induced in both animal and man by malnutrition. A diet is therefore regarded as badly balanced if it is lacking in total protein especially animal protein and deficient in many essential substances including minerals and vitamins. Now, from the view point of intestinal parasites in animals, mal-absorption and other complication detrimental to the health and wellbeing of animals may occur. Research and report sponsored by Smithkline Beecham Nigeria Plc. revealed that some nutritional disturbances may however be independent of the diet and originate from faulty intestinal absorption or from the effect of parasitic infections interfering with the intake, absorption or utilization of nutrients. Parasitic diseases are some of the major problems facing both veterinary and medical personnel today. There is no gain saying the fact that parasitic diseases have caused significant morbidity and mortality in our livestock and domestic animals as well as in man. These parasitic diseases affect the nutritional status of the host resulting in emaciation, loss of weight, body condition and conformation as well as loss of production, poor resistance to diseases and other serious debilitations and lastly death. Many gastrointestinal helminthes can have connection with intestinal discomfort and mal-absorption. For instance, heavy infection of Ascaris (round worm) in animals could induce mal-absorption syndrome and affect the growth of the victims. The infection with Ascaria species is known as Ascariasis. It also includes infection with small intestinal parasites of the genera: Parascaris and Toxascaris. The Round worms feed by sucking the host’s digested food products leading to anaemia. Examples of Round worms in various animal species include Ascaris suum in pig, Ascaris Cumbricoides in man, Toxocara canis in dogs, Toxocara cati (cat) Parascaris equorum in Horse and Toxocara vitulorum in cattle. In heavy infections, these round worms can produce small intestinal blockage, ulceration, volvulus intussusception and intestinal perforation. The worms in their migratory form can occlude the bile ducts and thus cause icterus (Jaundice). The public health and economic significance of this is that of meat condemnation. Toxocara vitulorum larvae have extensive hepatic and parenchymatus migrations to precipitate hepatic intralobular necrosis and granulation reaction in the liver (milk spot liver) as well as pulmonary emphysema and consolidation. Again, the public health significance is that of meat condemnations. Oesophagostomum species in Ruminants is an important gastrointestinal parasite that is associated with protein-losing-enteropathy which is a pathologic effect of the parasite in the intestine due to resulting in the reduction in the plasma protein of the animal. Hypoproteinaemia and oedema may be the result. Another gastrointestinal parasite worthy of mentioning is strongloides stercoralis (threadworm). This parasite is associated with villous destruction and eventual mal-absorption with weight loss in the victim. Trichuris trichuria (Whipworm) is also among the group of gastrointestinal worms that can reduce significantly the nutritional status of the affected animal. In heavy infection they may cause inflamed intestinal mucosa, abdominal pain, distension and diarrhea. In summary, gastro intestinal parasitic infections have serious debilitating effects on livestock or domestic animals in terms of weight loss, blood loss, loss of condition, ill health and death. Their public health significance is evidence in meat condemnation in the affected animal.
                                              SUGGESTION 
To avoid being deceived by unpatriotic feed manufacturers, farmers are advised to analyze the feeds they intend to feed their stock at equipped laboratory to clarify the adequacies of individual constituents in the feed.
Improved techniques of crop cultivation and animal husbandry should be employed.
Crops should adequately be protected from pest and disease before and after harvest.
Livestock or domestic animals should be dewormed routinely.
Environmental hygiene is always necessary in the farm.
                                              CONCLUSION
Livestock or domestic animal production remains an essential factor and a major determinant in the economic position of any nation. Therefore, with good nutrition and proper management and diseases control, the livestock or domestic animal industries is as lucrative and profit yielding as any other business.

Aetiology
Egg drop syndrome virus is a naturally occurring adenovirus of ducks and geese which have infected and caused disease in chicken. It grows to very high titre in embryonated duck eggs but poorly in chicken embryo.
Transmission
Three patterns of Egg drop syndrome have become evident over time.
1. Classical egg drop syndrome: It follows introduction of virus into primary breeders stock most likely through a vaccine grown in duck cell. The main method of spread is vertically through the embryonated eggs. Such hatched chicks do not show clinical signs, spread virus or develop antibodies.
2. Endemic egg drop syndrome: it results from lateral spread between flocks. It is primarily due to contaminated eggs or egg trays and it is usually seen in commercial layers. Any age of laying flock may be affected and there is often association between flock and egg packing station.
3. Sporadic egg drop syndrome: It results from introduction from from duck, geese or any infected wild bird either through direct contact or indirectly through contaminated drinking water.
Clinical signs
The first signs are usually a loss of shell strength and pigmentation. This is quickly followed by thin shelled, soft shelled and shell less eggs. Eggs may show mineral deposits. The birds are apparently healthy but sometimes they appear slightly depressed for 48 hours or so.
Classical egg drop syndrome is manifested either by a sudden fall in egg production or around peak production or a failure to achieve or hold predicted production.
Diagnosis
A combination of a sudden fall in egg production associated with thin shelled, soft shelled and shell less eggs in a flock with apparently healthy birds is almost diagnostic. The easiest method to confirm diagnosis is by feeding affected eggs to susceptible hens which then produce affected eggs.
Also the pouch shell gland can be harvested and samples inoculated into embryonated duck eggs. Virus growth is detected by testing for haemagglutination. Detection of antibodies to Egg drop syndrome virus by the H1 test using fowl erythrocyte is sensitive and easy.
ELISA is also used to detect antibodies to Egg drop syndrome virus. Care must be taken to collect blood only from birds which have sero converted and are laying infected eggs.
Control
Since classic Egg drop syndrome is spread primarily by vertical transmission via the egg, birds should be derived from uninfected breeders stock.
Endemic Egg drop syndrome can be controlled by vaccination with inactivated oil-adjuvanted vaccine given at 14-18 weeks of age. As the main method of horizontal spread is via the infected egg and egg trays, plastic trays should be washed and sterilized before returning to the farm.
Sporadic Egg drop syndrome can be controlled by segregation of chicken from ducks and geese and other wild birds. If surface water is given to birds, the water should be chlorinated and replaced with borehole derived water.

This disorder is a lympho-propagative neoplasm of domestic fowl caused by the same subgroup of RNA viruses that are pluripotential in their pathological manifestation. Oncogenic spectrum is influenced by origin of the virus, virus dose, route of inoculation, age and genotypes of the host.
Aetiology
It is caused by leucosis sarcoma virus which belong to the family Retroviridae. These viruses are pluripotential in the causation of the pathological type of tumor. Some may produce lymphoid leucosis, others myeloid leucosis and some erythroid leucosis. Lymphoid leucosis is the most prevalent of the three manifestations of the leucosis. The virus is ubiquitous in most commercial flocks and their presence is not necessarily resulting in disease.
Host
It is a disease of domestic fowl. The disease is rare before 25 weeks of age and usually occurs after 40 weeks of age.
Transmission
Avian leucosis is transmitted vertically from parent to progeny and horizontally by direct or indirect contact.
Clinical signs
Incubation period from infection to development and death is long and variable about 4 months or more. The birds may be anorexic, weak and emaciated. Diarrhea may occur and wattles may peel. In lymphoid leucosis, enlarged liver may be palpable.
Post-mortem lesions
There are 3 post-mortem forms of Avian leucosis. They are erythroid, lymphoid, myeloid and lymphoid leucosis.
Lymphoid leucosis(big liver disease)
It is the most prevalent manifestation caused by avian leucosis sarcoma virus. It is usually characterized by enlargement of the liver by infiltrating lymphoblast and the pattern of involvement is diffused but occasionally it can be nodular. Other organs like the spleen, kidney, heart and ovaries are also involved. Nodular tumors can be found in the bursa of fabricius in nearly all cases.
Erythroid leucosis(erythroblastosis)
It is a rare and sporadic disease. There is anaemia which is associated with large number of immature red blood cell in the blood. The liver and spleen are moderately enlarged and are cherry red in colour. The disease originate from the bone marrow and leukaemia is present.
Myeloid leucosis
This involves an extravascular proliferation of cells of the granulocyte series with a sporadic disease. It may occur as a myeloblastosis or a myelocytomatosis . the liver and spleen are diffusely and greatly enlarged and the liver has a granular morocco death appearance. The tumours of myelocytomatosis are nodular and discrete and thus a yellowish white colour and affect a wide range of organs including the liver, spleen and have a predilection of the visceral surface of flat bones such as ribs. Solid tumor caused by avian leucosis sarcoma virus include fibrosarcoma, endothelioma, chondroma, haemangioma, nephroblastoma and  hepatocarcinoma.
Diagnosis
It is based on combination of clinical signs, post-mortem lesions, age at infection and histology. Cytological examination of may grumwald giemsa stained impression smears of fresh tumor tissues is a useful aid in diagnosis.
Control
No treatment or vaccine is available. Control must be based on a high standard of vaccine to reduce infection from the environment and using birds from a disease free sources and genetically resistant stocks.

This is an infectious and highly contagious viral lympho-proliferative disease which may be readily transmitted to young susceptible chicks with the inoculation of blood or tumor cells of the affected cells.
Aetiology
The causative agent is a cell associated DNA herpes virus. Isolates of marek’s disease virus vary greatly in pathogenicity. A herpes virus antigenically related to marek’s disease virus is present in commercial turkey. This virus which is not able to cause disease in turkey and chicken is now extensively used as  vaccine for marek’s disease.
Host
Marek’s disease affect chicks of about 6 weeks of age although it occur most frequently in 12-24 weeks of age. Chicken may rarely be affected later in life. Affected flock remains so throughout its life and continue to shed virus throughout its commercial life. The virus is an ubiquitous infection of poultry worldwide.
Transmission
The source of the infection include oral, nasal, tracheal discharge and cloacal excrements. These materials may retain infectivity for over one year. Poultry house dust and litter may also remain infectious for one year. The route of infection is mainly by airborne route. Fowl ticks have also been incriminative in transmission of the disease following blood meal.
Clinical signs and post-mortem lesions
There are two major forms of marek’s disease and more than one form can occur together.
1. Classical  marek’s disease: This is the neural form affecting the peripheral nerves especially the celiac, mesenteric, vagus, intercostal, brachial and sciatic nerves. The cardinal signs in affected nerves include diffused or nodular enlargement which is usually 2-3 times its normal size which is unilateral. There is discoloration or loss of whiteness or loss of cross striations. Mortality in classical marek’s disease is variable but is varies above 10-15%. The signs observed depends on the peripheral nerve involvement. Involvement of brachial and sciatic nerve is common and results in progressive paralysis of wing and leg. Involvement of cervical nerve results in torticolis while involvement of vagus and intercostals nerve result in dyspnea. When celiac and mesenteric nerve are involved, diarrhea is observed.
2. Acute mareks disease: This is the visceral form affecting the soft tissues like the liver, spleen, kidney, bursa, heart, gonads and occasionally proventriculus and lungs. Mortality is higher usually 10-30% or even as high as 70% in some cases. Many birds die suddenly without preceding clinical signs and others appear depressed before death and some show paralytic signs similar to those of classical marek’s disease. Affected organs are enlarged to several times than normal and show greyish discoloration.
3. Other forms: These include the ocular and cutaneous forms. Gross ocular changes include loss of pigmentation in the iris(grey eye) and irregularity of the pupils. In the cutaneous form, whitish nodules are seen in the feather follicle. Transient paralysis which is an uncommon encephalitic manifestation of the infection of marek’s disease virus occurring between 5-18 weeks of age. Birds suddenly develop varying degrees of paralysis of the legs, wing and neck and is characterized by recovery andsigns disappear after 24-48 hours.
Histopathology
In the peripheral nerve, marek’s disease is both neoplastic in nature with proliferation of lymphoblastic cells and inflammatory in nature with diffused light to moderately infiltration with small lymphocytes and plasma cells normally with edema. These are referred to as A and B response respectively. Lymphomatous lesions in the visceral organs are most uniformly proliferative in nature.
Diagnosis
This is based on a combination of clinical signs, post-mortem lesions, age at infection and histology. Because of the ubiquitous nature of marek’s disease virus, diagnosis is not based on isolation and recognition of the virus alone. Marek’s disease virus is present in most flocks.
Control
It is based on breeding and stocking resistant breeds of chicken.
Vaccination using 3 different types of vaccines which are: attenuated pathogenic, example rispeus strain; A-pathogenic, example 3B-1 strain; Herpes virus of turkey, example HV5. These vaccines are given at day old by intramuscular or subcutaneous route. They come in two forms: the cell associated form stored in liquid nitrogen AND lyophilized/freeze dried form.

This is the viral disease of domestic birds characterized by the development of nodular proliferative skin lesion on the non-feathered part of the body.
Aetiology
It is caused by fowl/ turkey/ pigeon virus belonging to the genus Avipox. The virus grow in the chorioallantoic membrane of embryonated chicken egg forming pocks which can be stained and seen using a light microscope. The virus may also be observed in cytoplasm of the affected bird. They form intracytoplasmic inclusion body known as Bollinger bodies. Fowl pox virus is the largest known virus and can be seen using light microscope.
Host
It can be seen in fowl, turkey, pigeons etc. infection can occur in susceptible host of all ages.
Transmission
It occurs through mechanical transmission of the virus to the injured or lacerated skin. Biting insects can also infect birds.
Clinical signs and post-mortem lesions
Incubation period varied from 4-10 days in chicken and turkey.
The disease may occur in two or more forms: cutaneous, diphtheritic or both.
The cutaneous or dry form is characterized by appearance of cutaneous nodular lesions on the comb, wattle, eyelids and other non-feathered part of the body.
Diphtheritic or wet form is characterized by diphtheritic yellow lesion in mucous membrane of the mouth, esophagus and trachea.
The cutaneous form however is the most common form seen in most disease outbreaks. Sometimes, the disease may show mild reduction in the rate of weight gain or lack of vigor. Fowl pox can cause reduction in laying bird. The cutaneous lesion vary in appearance. There is a papule which progress to vesicle which result in pustle and finally to scab stage. After about 2 weeks, the scab will fall off and the lesion is healed which may or may not leave a scar on the bird.
In the diphtheritic form, most lesions are formed in the mouth but others are present in the larynx, trachea and esophagus. These lesions can give rise to inappetence and difficulty in breathing. Lesions in the nares give rise to nasal discharge while those in conjunctiva give rise to ocular discharge and rarely, it may result to blindness. Mortality in chicken is always low while it may be high in turkey.
Diagnosis
This is based on clinical sign and post-mortem lesions.
Histological examination of the skin section for fowl pox lesion will reveal intracytoplasmic inclusion body or Bollinger bodies. Materials can be scraped from the lesions and smear made on glass slide and using appropriate stain and the virus can be seen using a light microscope.
Also, ground up scab inoculated into the chorioallantoic membrane of 9-12 days old embryonated egg has produced a characteristic pock lesion. Ground up scab may also be inoculated into a known susceptible chicken by scarification of comb and wattle. Characteristic pock lesion should be present at 5-7 days post inoculation.
Control
There is no satisfactory treatment. However, some workers remove the scab and dress the wound surface with a tincture of iodine.
Heavy pox can be prevented by vaccination with live vaccine. Two main routes are employed: wing web and thigh muscle. In wing web method, a bifurcated needle with a vaccine in central route is used to introduce the vaccine. In the thigh method, the feathers are removed and the vaccine brushed into the follicles.
Birds can be vaccinated at 3 weeks of age but preferable age is 6 weeks. Turkeys should not be vaccinated by wing web because they sleep with head under their wings which could lead to head lesion.
Vaccination of chicken is done using chicken pox vaccine or pigeon pox vaccine. Pigeon should not be vaccinated by fowl pox vaccine.

This disease is a very acute and contagious viral disease of chicken characterized by extensive damage of B lymphocytes in bursa of fabricius and other lymphoid tissue including the spleen, thymus and caecal tonsil. It is worldwide in distribution.
Synonyms
Infectious bursitis, Avian nephrosis, gumboro disease.
Economic importance of the disease
This disease is illustrated in two ways:
Clinical disease and mortality occur in chicken 3 weeks of age and older.
Severe and prolonged immune suppression of chicken at early stage which can lead to increase susceptibility to Newcastle disease, infectious bronchitis, E. coli infection and vaccine failures.
Aetiology
The disease is caused by infectious bursa disease virus which is a Birnavirus belonging to family Birnaviridae. It is a very stable virus capable of withstanding high temperature for extended period. It has two distinct serotypes: IBD serotype 1 and IBD serotype 2.
Serotype 1 is pathogenic whereas serotype 2 is non-virulent or apathogenic. In the serotype 1 group, there is considerable antigenic variation with variation in virulence or pathogenicity. In the serotype 1 group, there can be a pathogenic strain to very virulent strain that cause up to 50% mortality.
Host
The clinical disease is seen in chicken of ages 3-6 weeks of age. It causes subclinical infection of bird less than 3 weeks of age resulting in severe immunosuppression.
Transmission
This viral disease is very contagious and the virus persist in an environment for long period in time. Their appearance in this disease in successive of chicken in a farm once it has appeared is one of the traits of the infection.
Feral birds, meal worms, litter mites, rodents and humans could act as mechanical vectors of the disease. The virus presence in the faeces is the main source of the virus. The disease may also be spread by inhalation and cutaneous lesions.
Clinical signs
The severity of signs is dependent on age, breed of chicken as well as virus virulence. The incubation period is short about 2-3 days. One of the earliest sign of the infection in the flock is tendency of the bird to peck at their own vent. Other signs observed are trembling, soiled vent feathers, depression, whitish and watery diarrhea, anorexia, ruffled feathers, severe prostration and death. In fully susceptible flock, there is high morbidity usually approaching 100%. Mortality usually begins at 3 days post infection and will peak within a period of 5-7 days. The striking feature of this disease is a sudden high rate of morbidity, spiking mortality curve and rapid flock recovery. Most outbreaks are associated with about 30% mortality occasionally reaching 50%. Morbidity ranges from 10-100%
Post-mortem lesions
Dehydration result in darkening/ discoloration of the pectoral muscle. Haemorrhage is observed in muscle and thigh. There is excess mucous in the intestine. Renal changes include enlargement of the kidney, distention of renal tubules and ureters with accumulated urates leading to nephrosis.
The bursa is enlarged, inflamed and edematous and cream coloured and after about 3-8 days, it atrophies. Haemorrhages may be seen in the internal and serosal surface of the bursa. Haemorrhages is also present in thigh muscles.
Diagnosis
This is based on clinical signs and post-mortem lesions. Positive diagnosis is based on post-mortem lesion especially by examination of the bursa for the characteristic gross lesion. Confirmatory diagnosis can also be based on virus neutralization test and agar gel precipitation test in which masserated bursa is used as an antigen against a known positive and serum obtained from a reference laboratory for example NVRI Vom.
Control
There is no therapeutic or supportive treatment for this disease due to harden nature of the virus that causes the disease.
Good animal husbandry and hygiene should be practiced.
Disinfection of poultry house and equipment with formaldehyde and iodophores reduces the viral load.
Vaccination is the principal method used to control the disease in the chicken.
The parent stock are vaccinated at 4-10 weeks of age with live vaccine and boosted with oiled adjuvanted inactivated vaccine at age of 16 weeks (16 weeks is at age of laying birds to pass immunity to new chicks). In the progeny or chicks, the maternally derived antibody level wanes with time protecting against virulent challenge up to 2-3 weeks of age. These chicks are then vaccinated at 2-3 weeks of age.

This is a contagious viral disease of all avians characterized by varying pathogenicity and clinical and pathological lesions in two or more systems of the body including the digestive, respiratory and nervous system. It is capable of causing very heavy mortality and without adequate control, it is impossible to breed poultry.
Synonyms
Ranikhet disease, Avian pneumoencephalitis, fowl pest, Avian pest distemper.
Aetiology
The disease is caused by a Newcastle disease virus called paramyxovirus. There are several strains of Newcastle disease virus but all these strains are immunologically and serologically similar but differ in pathogenicity. Due to its varying pathogenicity, Newcastle disease virus are grouped into 3: Lentogenic strain, mesogenic strain and velogenic strain.
Lentogenic strains are mild and at times, avirulent while mesogenic strains are intermediate and velogenic strains are very virulent. Examples of lentogenic strains include Hitchner B1, lasota, V4 and F stains etc. Examples of mesogenic strain include komarov, Roakin and H strain etc. Examples of velogenic strains are GB texas, Milano, hertz and kudu strain etc.
Newcastle disease virus agglutinate amphibians, reptiles and avians red blood cells.
Host
It is reported virtually in all diseases of poultry. All ages are susceptible but younger birds are more severely. It may cause conjunctivitis in man.
Transmission
It is transmitted by inhalation of droplets from respiratory tract containing the virus and inhalation of dry faecal substance from digestive tract.
It is also transmitted by ingestion of faeces and faecal substance
Feral birds, other animals, humans, poultry products, fowl equipment and contaminated poultry feed also result in spread of disease.
Clinical signs
The symptoms of Newcastle diseases depend on ages and species of the affected birds, the immune status, presence of concurrent disease and the strain of the infecting virus. The highly virulent and pathogenic virus called the velogenic strain may produce peracute infections where the first indication of the disease is death.
Typically the disease signs such as depression, prostration, greenish diarrhea and edema of the head are observed. Mortality is 100% and nervous signs may occur. There may be total cessation of egg production following thin shell.
The moderately virulent or mesogenic strain usually cause severe respiratory disease followed by nervous signs. Mortality is 50% or more. The respiratory signs include severe dyspnea, coughing, gasping, nasal discharge and presence of stringy saliva from the beak. Nervous signs include paralysis of leg and wing, opisthotonus, ataxia and trembling. In laying birds, there is reduced hatchability and laying of soft shelled eggs. The virus of low virulence or lentogenic strain may cause no disease or mild respiratory distress and mild reduction in egg production in chicken and turkey. However, presence of other disease may result in more severe cases.
Post-mortem lesions
There is no pathognomonic lesion associated with Newcastle disease. Some lesions observed include haemorrhage and necrosis of proventriculus, caeca and small intestine.
There may be also haemorrhage and congestion of the trachea.
Airsacculitis is present.
Diagnosis
Newcastle disease should be suspected when there is respiratory sign, greenish diarrhea, paralysis or heavy mortality is seen in unvaccinated flock. For diagnosis of Newcastle disease to be made at present, the only certain method of diagnosis which also allow characterization of the infecting strain is virus isolation and recognition.
Isolation and recognition of Newcastle disease virus
Sample from live animal include tracheal and cloacal swabs and in dead bird tissue include intestine and trachea.
Samples are placed in phosphate buffer saline containing antibiotic then inoculated into 8-10 days embryonated hen’s egg and held at 37°c until death or dying for 5-7 days. Haemagglutination activity in bacteria free allantoic fluid may be due to any of the avain paramyxovirus or othormyxovirus. Newcastle disease virus is confirmed by haemagglutination inhibition test using specific Newcastle disease antiserum.
Characterization
There are 3 main pathogenicity tests used to characterize Newcastle disease virus:
Mean death time in egg
Intracerebral pathogenicity index in chicks
Intravenous pathogenicity index in chicks.
Control 
There are two main control methods of Newcastle disease:
Hygiene and sanitary precaution and good management practice.
Vaccination, both live and inactivated vaccine are recommended.
3 vaccines available for control are produced in Nigerian veterinary research institute(NVRI) vom and are administered as follows:
Age of chicken                                     Type of vaccine                                         Route of Administration
0-1 week                                               NDV- I/O(B1 STRAIN)                                Intraocular
3-4 weeks                                             NDV- Lasota(lasota strain)                       drinking water/intraocular
6-8 weeks                                             NDV-Komarov(komarov strain)               Intramuscular
Every 6 months thereafter                NDV-Komarov                                             Intramuscular

The federal government has been blamed long ago for the chaotic situation of things in the country and most especially in the teaching and general hospitals.
Somehow, it looks ridiculous having two counters selling drugs in the same hospital. One counter designated for the sale of Petroleum (special) Trust Fund(PTF) drugs and the other for the hospital’s pharmacy department. While one PTF is cheap, at the other counter, it is slightly expensive.
Patients mainly civil servants who avail themselves of medical treatment in the hospital have complained of the drugs not being able to retain its tablet form if not delicately handled.
The healthcare gathered that some of the drugs scattered inside the nylon if not well kept before the patient gets home. With peoples reaction to the same goods that are cheap and expensive respectively, there is already an apathy concerning PTF drugs.
To an average patient, once prices differ, it means there is trouble and confusion somewhere, that psychological make-up alone will prolong an illness and the patient may not get relief after taking those drugs.
Can PTF sustain this effort?
This is a million naira question bothering pharmacists and well meaning Nigerians. Why should PTF go into drug distribution and not production which should give permanent solution to the drug problem in the country and reduced the prices of finished products generally? However, there is no doubt that this PTF effort has provided incomes and open avenues for some pharmaceutical companies and importers to survive.
In an interview, the then managing director and chief executive of alliance chemist limited, Chief Bayo Ogunyemi said that the government was putting the cart before the horse, instead of encouraging drug distribution in the hospitals, government has taken over through PTF. He noted that it is the work of pharmacists to supply drugs to the hospitals and not government, and he lamented that the gesture has taken business from wholesale pharmacists and they are out of job as government has taken over through the PTF.
Ogunyemi said that the outcome of these prevailing situation was that PTF might not run the scheme properly while it had become unprofessional, noting as always with the government project, the end result might be mismanagement of finance and embezzlement.
Lamenting, the pharmacists wondered why PTF should go into drug distribution. According to him, PTF could help in drug production as there is no enough capital to set up factories and import raw materials for pharmaceutical companies to ensure low prices for finished products.
The managing director observed that there was vast difference between the practice of pharmacy and drug distribution in the early days and now, adding that in the 40s and 50s, drug distribution was done according to law, all pharmaceutical companies were manned by qualified pharmacists. No drugs according to him was issued out without the signature of qualified and registered pharmacists.
He stated that it was obvious then that doctors prescribe and pharmacists dispense, the situation was as it was done outside the country.
The West African Drug Company, the first big expatriate drug company in the country, well into drug distribution system, upheld the method to the letter and there was no branch that was not manned and supervised by a pharmacist.
He noted that drug distribution now is a free-fall-all affair regretting that traders who can hardly write their names sell drugs now, adding that it would appear there is official conspiracy to continue with the system.
Ogunyemi confirmed that the country has one of the best pharmacy laws and that the officials should be able to control drug distribution if the will power is there.
The government allows drug distribution to be what it is by not regulating the law and without inspection, everybody can do what they like.
With the introduction of import license for pharmaceutical products since 1986, faking and adulteration of drugs entered the industry as non  drug experts were issued licenses to import drugs into the country. As a result, traders(non-pharmacists) or businessmen travel overseas and negotiate with drug manufacturers who are feeding fast on the negligence of Nigerians.
Ogunyemi confirmed that the pharmaceutical society of Nigerian(PSN) has been doing quite a bit to call pharmacists to order, adding that sermon could only help to moderate the actions of people but cannot take the process of the law. He said that only effective inspection and punishment would stop the situation and warned that drug is not like buying clothes. It is only when it gets to the body system that it starts causing havoc.
He therefore enjoined the National Agency for Food and Drug Adminitration(NAFDAC) to make their inspection unit effective to assist in the eradication of the evil preverence of drugs in every nook and cranny of the country.
The managing director condemned the transfer of the issuance of patentt and proprietary medicine vendors licence from federal to state ministries of health, as it would encourage drug distribution by lay men. He said in the constitution of the country, drug is a federal matter and that PSN should be made to issue any licence pertaining to drugs in the country.
Patent and proprietary medicine vendors licence scheme was evolved to enable rural people and other areas where there are no pharmacist to get simple medication but with so many unemployed pharmacists scattered all over the federation, the licences should be scrapped or issued to qualified pharmacists.

Almost all diseases are hinged on stress. Some authorities estimate that at least one and half of general medical practice is for such stress induced diseases. These diseases are considered by some medical experts as to be protective measures taken by the individual against threat or symbol of danger which the early experience of the individual unconsciously interpretes as actual fearful dangers. People have been aware that emotions affect the body before science proved it experimentally. Emotions are however more far-reaching than such visible evidence indicates. Any emotion mild or severe registers in every cell and tissue of the body. With a strong emotion such as fear, the entire body tone changes, blood pressure rises, heart and breathing are faster, the adrenal glands, a small organ on top of the kidneys- become more active and changes in the gastrointestinal tract and shifting of blood supply take place.
WHAT IS STRESS?
Stress, a state of tension or pressure is caused by difficulties in life which may be physical such as results from accident or injury or emotional such as stress caused by an impending threat or other difficult situation.
In medicine today, stress is used in the psychological sense. In his definition of stress, the vicar of Archbishop vinning memorial church ikeja, Venerable Dr Olusegun Adeyemi noted that medically, stress is adjustment physically. Speaking on stress and its management, the Vicar said that there were in-built chemicals produced by the body which serve to defend oneself but when the secretions intensify, the chemicals accumulate and destroy the body it was meant to protect. Adeyemi stated that when this happens, it could affect the central nervous system, the brain and the spinal cord, adding that almost all the diseases are traceable to stress. He noted that when more blood is trafficking into the brain, one become irritable and over-react to things. The outcome may be headache, taking irrational decisions, being confused, disoriented and the catastrophic end may be stroke. According to him, the brain is loosely packed with blood vessels and when the force of breathing is too much, it would rupture and the body will paralyse at the right or left side.
The person may not be able to speak if it affect the speech center or becomes mute if the speech center dies, he added. Inadequate supply of blood to the heart works on the muscles and causes the heart to beat faster. The vicar noted that stress could lead to hypertension which is forceful beating from the heart  and results in destroying oneself from inside and could lead to heart attack. It could also lead to intestines not being able to digest food as the stomach weeps out acid which destroys the lining of the stomach and one develop peptic ulcer if not treated.
Stress could also affect genital system. In women, menstruation ceases while men becomes impotent- not having erection which could lead to marital problems. It affects the bladder resulting in bedwetting. It also affects the immunological system. The body on its own fights the multiplying organisms like cancer for many years. The body defense mechanism when stressed could disturb this.
Stress could also lead to mental problem and disorder. There may be fearbouts like inferiority complex or aggression and most men when stressed chew their teeth. Arthritis has a share of stress. The brain produces endorphins in reaction to stress which irritates the nerves. Also diabetes and asthma could be precedated prematurely by stress. Minor stresses may find expression in a variety of ways. It may be seen in an individual who drives recklessly and violently almost obviously in pursuit of an accident.
MANAGEMENT OF STRESS
Venerable Dr Adeyemi stated categorically that there is no cure for stress in the hospital, only advice on how to cope with the situation. He said as a man of God and medical practitioner(surgeon), he has come to realize that knowing the importance of the word of God is the most effective way of overcoming stress. The vicar pointed out that one should always realize that what kills one is inside one’s body and knowing ones character and disposition, body chemistry and positive thinking- as a man thinks himself, so will he be.
Talking right as by one’s word, one will be condemned, according to him, knowing and obeying the word of God, thinking of what to rejoice about the word of God, praying always, knowing the will of God and obeying the word of God and having faith in God always and dealing honestly with your fellow human beings are all known cure for stress, and eradicating diseases from the body.
Adeyemi stated that optimally, an average human being spends 8 hours at work and 8 hours for rest. If the 8 hours is manipulated for gossiping and the rest periods falls under 8 hours, it could be stress related.
Therefore, adequate rest is advocated to ensure the body mechanism functions properly.