Noble Desk

DISEASE
Disease is defined as a condition that impairs normal body functions. The severity of disease depends on the degree of impairment.
Various causes of poultry disease
1. Infectious: Bacterial such as salmonellosis, colibacilosis, pasteurellosis; viral such as Newcastle disease.
2. Parasitic: Endoparasite such as helminthiasis; Ectoparasite such as mite infestation.
3. Protozoan: Coccidiosis
4. Non-infectious: Nutritional such as deficiency diseases (vitamin deficiency); metabolic such as fatty liver syndrome.
Factors that influence occurrence of poultry disease
1. Host factor
-Age: Young birds are more susceptible to infectious agents than adult birds.
-Availability of various route of entry.
-Immune status of host
-Poor management condition
-Carrier status of birds
2. Environmental factor
-Wet litter
-Too hot or too cold conditions
-Dusty litter
-Poor ventilation
-High build up of chicken droppings
-Sharp wires in the cages.
3. Management practices
-High stocking density
-Chickens of mixed ages/varying species reared together
-Poor quality food and water
-Poor hygiene and inadequate cleaning program
-Leaking water bowls
-Rat and fly problems
-No security measures to prevent people and animals from entering the chicken house.
4. Causative agent
-Invasiveness
-Dose of causative agent
-Virulence of the causative agent
-Lifecycle of agents
Sources of infection to poultry flock
Spilled vaccines: Vaccine spillage is a source of infection because most live vaccines are live disease agents, so they should be properly handled.
Human beings: This involves farm manager, farm attendants, veterinarians, visitors and neighbors. They introduce infection and are potential disease transmitters to poultry flock.
Sick birds: These are birds that show clinical sign of disease but are not detected and removed.
Carriers: These are birds that have recovered from a clinical disease or did not show clinical signs of a disease but the causative organism is found in many parts of the body.
Vectors: These are animals that indirectly transfer infectious agents to the flock for example, rodents, flies, insects, pests and stray animals.
Live bird market: A lot of birds (healthy, sick and apparently healthy) are found in the live bird market which is a major source of poultry disease outbreaks thus the popular ALL-IN/ALL-OUT should be practiced.
Formites: These are inanimate objects that introduce infectious agents indirectly to a poultry flock. They include contaminated equipments, human shoes, clothing etc.
Laboratory exposure: Experimental animals and researchers are potential sources of infectious agent introduction in poultry flock in the absence of strict sanitary measure.
General signs of disease in poultry
Head held close to the body, tail and possibly wings droop, neck twisted with head held over back or between legs.
Combs and wattles are shrunken, pale or blue in color. Face parts are shrunken. Eyes are dull and may be held only partly open. Nostrils are caked and crusted. Eyes are watery. Sinus areas below the eyes are swollen or flutters with respiration.
Legs and feet are dehydrated with prominent tendons. Joints are enlarged and warm to the touch. Bottom of feet are cracked, crusted or discolored. Scales are enlarged and crusty.
There is loss of weight and strength. The muscle at the point of the keel and near crop cavity are shrunken resulting in a thin breast.
The manure or dropping is milky white, green, yellow or red. The droppings are very liquid or very sticky and not firm.
There is loss of appetite or excessive drinking.
Feathers are not preened. Feathers are fluffed out or broken. Staining is observed in areas of abdomen. Birds are generally ruff looking.
There is gurgling, rattling or snickering noise; gasping and obvious movement of abdominal wall.
There is reduced depth of colour. In adult hens, excess of yellow pigment may be associated with disease decreasing rate of lay.
Disease prevention
Healthy flock selection: Selection of viable and disease free chicks is necessary.
Adequate nutrition: Balanced nutrition should be given to poultry.
Adequate housing: Provide adequate housing for birds. The housing should be wild bird and insect proof, cross ventilation and foot dips at the entrance of the poultry house.
Adequate environment for the birds: This includes low humidity, good drainage system and adequate sunshine.
Sanitation: There should be regular cleaning and disinfection of housing, equipment, vehicles and people.
Preventing flock contact with reservoirs of infection: This involves removal of all animate and inanimate objects that transfer infection directly or indirectly to the flock. The inanimate objects that are reservoirs of infection include contaminated water, feed, dust, litter, soil, shoes and equipment including housing while animate reservoirs of infection include live reservoirs, sick birds, other domestic poultry, wild animals, feral birds, arthropods, snails, other domestic animals and humans.
Proper disposal of dead bird: This can be done through the following:
-Rendering: freshly dead poultry are rendered into fertilizer at a rendering temperature capable of sterilization.
-Incineration: smokeless and odorless incinerators are used for disposal of dead carcasses.
-Burying: deep hole dug and carcass buried so that animals cannot get to it.
-Pit disposal: well constructed hole in the ground were carcasses are dumped.
-Composting: compost mixtures of straw, whole poultry carcasses, manure and water in a definite ratio, compost heat rapidly and completely reduces soft tissue within 14 days.
Isolation or quarantine of sick birds: This can be done through providing separate housing for keeping sick birds pending recovery.
Vaccination: The process of injecting live attenuated or killed suspensions of an infectious agent in order to produce resistance against infectious agents on exposure.

RICKETS
Rickets is a condition characterized by increased bone flexibility and deformity resulting in lameness and seen in rapidly growing chicks. It is manifested as a thickened and poorly mineralized growth plate and poorly mineralized bone. It is caused by calcium, phosphorus and vitamin D deficiency or imbalance. In birds with severe rickets, the keels are crooked, the legs bowed, the long bones end are enlarged, the bones soft and rubbery and birds may show stiff legged gait.
Note that calcium and phosphorus ratios are central to rickets development and high dietary phosphorus content has a similar effect to low dietary calcium concentration.
Chondrodystrophy
Chondrodystrophy results in short thick and usually misshapen long bones and often apparent enlargement of hock joint. Displacement of gastrocnemius tendons may occur. Chondrodystrophy is a generalized disorder of the growth plate of long bones such that linear growth is impaired and appositional growth remains normal. It differs from rickets in that mineralization is not impaired. Manganese deficiency alone may result in chodrodystrophy. Deficiency of the following nutrients have been reported to contribute to chodrodystrophy. They are choline, niacin, vitamin E, biotin, folic acid and pyridoxine.
OSTEOPAENIA, OSTEOMALACIA AND OSTEOPOROSIS
Osteopaenia is a non-specified term used to describe a decrease in amount of bone tissue such as can result from osteomalacia and osteoporosis. In osteomalacia, there is defective mineralization while in osteoporosis, there is loss of bone substance associated with normal mineralization of bone matrix. Deficiency in mineralized bone or osteoporosis may be caused by bone loss due to estrogen activity associated with onset of lay, follicular activity and subsequent egg laying or may be precipitated by inadequate dietary calcium. Ostomalacia which is a defect in bone mineralization is a response to dietary insufficiency of calcium. Exercise and environmental factors such as increased cage size may result in small improvement in bone strength of laying hens.

This is a problem of mature laying birds characterized by fatty liver, mortalities and drop in egg production. In contrast to mammals where lipogenesis is in adipose tissues, it occurs in the liver in birds. As birds approach sexual maturity and lay, there is further increase in liver lipogenesis. It is this lipogenic liver function that forms the key stone for occurrence of condition involving excess accumulation of liver fat.
Aetiology
It is caused by too much amount of caloric dense which is high carbohydrate and low fat resulting in obesity especially in absence of lipotrophic nutritional factors like choline and  inositol.
High temperature and lack of exercise like in caged layers.
Housing and environmental problem which predispose birds to excessive heat and poor ventilation can be the cause.
Increased lipogenesis resulting from abnormal estrogen and thyroxine levels in blood can be the cause.
Some bird strains vary in amount of lipid or fat in which they contain in liver (25%-50%) depending on bird strain.
Clinical manifestation and effects of the disease
There are mortalities in actively laying birds.
Accelerated weight gain can be observed.
There is drop in flock egg production and egg bounding. Egg bounding is the blockage of oviduct by egg due to narrowing of lumen by fat.
Post-mortem findings
There is enlarged putty-like and friable liver which may contain up to 70% fat. The liver may show multiple haemorrhagic foci or hematoma or actual liver rupture with the presence of blood clot in peritoneum. There may be excessive fat deposit in abdominal wall which may attain 2-3cm in thickness. There is excessive perigastric and pericardial fat. There is egg bounding of fully formed eggs in oviduct.
Control
Control should be targeted as at alleviating as many are the causative factors as possible including:
Reduction in caloric intake during hot season, introduction of some additional fibre or use of more fibre raw materials, environmental control of heat stress through improved ventilation and supplementation with lipotrophic factor for example, addition of yeast in feed.

This is a metabolic disorder of young broilers and sometimes pullets commonly 10-30 days of age characterized by extensive fatty infiltration of body tissue with enlarged liver, kidneys and heart. It arises from a failure of hepatic gluconeogenesis due to marginal deficiency in biotin.
Aetiology
The condition involves interaction of nutritional, environmental stress and maternal factors such as marginal deficiency of dietary biotin and combination of fat and protein.
High levels of fat offer protection by depressing the need for lipogenesis making more biotin available for gluconeogenesis or pyruvate carboxylase.
Floor rearing makes fecal biotin available.
Starvation and stress which deplete the glycogen reserve can cause the condition.
Age and biotin status of the parent bird, other diseases which cause stress and depress intestinal absorption are also factors to consider.
Clinical signs
The signs are of sudden onset with affected birds depressed and recumbent. Mortality is between 5-20%
Post-mortem lesions
There is enlarged pale fat infiltrated liver and kidneys.
Pink adipose tissue and subcutaneous fat and blackish fluid in intestine and crop can be observed.
The parlour of liver and kidneys is due to excess amount of fat which is about 2-5 times the normal. Fatty infiltration is widespread but less marked in other times including cardiac and skeletal muscles and central nervous system.
Control
Alleviating as much as connective factor as possible can help in the control of this condition.

Vitamin B2/riboflavin
This is essential for normal growth and health. Deficiency results in condition in chicks 10-14 days old known as curled toe paralysis. Birds are unable to rise from their hocks but remain alert, the legs being outstretched with flaccid paralysis and frequent incoiling of the toes. Sciatic and brachial nerves are swollen and discoloured. Response to vitamin B2 is rapid. In newly hatched chicks, downfeathers are clubbed and glued together resulting in condition known as clubbed down.
Biotin
This is necessary for growth, food utilization, epidermal tissue sustenance, bone growth and development and reproduction. It is a cofactor for various carboxylation enzymes, two of the most relevant being pyruvate carboxylase (gluconeogenesis) and acetyl coenzyme A carboxylase (lipogenesis). In young birds deficiency signs include impaired feathering, periocular dermatitis, encrustations in beak and eyelid angles and on toes and footpads in early stages. Subsequently, there is depressed growth, heamorrhagic encrustation of the feet, poor feathering, parrot beak and abnormal bone formation. In adult breeder birds, severe deficiency results in reduced egg production and reduced hatchability. In young broilers, it may cause fatty liver kidney syndrome.
Choline
This is a lipotrophic factor involved in fat immobilization and it is a structural part of acetylcholine involved in nerve impulse transmission. Deficiency results in reduced growth, fatty liver, reduced hatchability and chondodystrophy.

This is an acute highly contagious viral disease of domestic fowl associated with upper respiratory disease manifested but is otherwise asymptomatic besides its effects in egg production in adult chicken.
Aetiology
It is a corona virus belonging to the family Coronaviridae. Infectious bronchitis virus has a number of antigenically distinct strains which include mass strain, conn strain, hohe and grey strain and Australian-T strain. Mass strain and conn strain are associated with respiratory tropism while Hohe and grey strain and Australian-T strain are associated with kidney tropism. Predisposing factors are intercurrent infections like Newcastle disease, infectious laryngotracheitis, mycoplasmosis, infectious coryza and E. coli. Cold air can predispose to the disease.
Host range
Domestic chicken is the natural host. All ages of chicken are susceptible to the disease but the clinical respiratory disease occurs in chicks and growers especially between 4 and 10 weeks of age.
Transmission
The virus is excreted in nasal exudates such that spread from bird to bird or flock to flock which is airborne.
Clinical signs
Incubation period is short between 18-24 hours.
Clinical signs of the disease in chicks are rales, dyspnea, sneezing, watery nasal discharge which may be accompanied by excessive lacrimation causing matting of the face feathers and facial swelling. Uncomplicated disease runs the course of about 10-14 days with low mortality. The renal form presents few clinical signs but may be accompanied by excessive urate deposits in the faeces leading to pasting on the vent.
The disease in adults affects egg production but occasionally present respiratory signs. The effects on  in egg production depends on fowl age at infection and include delay onset of laying, delay onset of peak production, reduction to percentage peak and sudden reduction in laying. Reduction in egg production may be as low as 5% or as high as 50%. Apart from this quantitative aspect, there are qualitative defects in egg production which are loss of shell pigmentation, thin shelled eggs and loss of shell formation. Others are watery albumen and broken chalaza.
Post-mortem lesions
In respiratory form, there is catarrhal inflammation of the tracheal mucosae and sinuses. In severe cases, mucoid plugs cause asphyxiation in young chicks.
In reproductive form, there is reduction in size and weight of the oviduct. When infection occurs in chicks or growers, there is agenesis of the oviduct which may be reduced to vestiges and is non-patent.
In uric or kidney form, the kidneys are swollen and inflamed in early stages or pale in advanced stages. Renal tubules are distended with whitish crystals of urate and there may be visceral gout with deposits of urates in liver, heart and kidneys.
Diagnosis
Tentative diagnosis can be reached by a combination of epizootiological signs like age at infection, clinical signs and post=mortem lesions. Confirmation is reached by isolation and recognition of the virus. It causes dwarfing and curling in embryo. Diagnosis can be done using ELISA and agar gel precipitation test.
Prevention and control
This is based on management and hygiene practices and the control of intercurrent diseases like Newcastle disease, chronic respiratory disease, infectious laryngotracheitis and vaccination using attenuated vaccines applied in drinking water and sprays or eyedrops according to manufacturer’s direction. Birds are vaccinated at first week of age and booster doses given at 4-6 weeks. Plurality of strains implies that a given vaccine may not be preventive against challenge from heterologous strain.

This is an infectious disease syndrome caused by any type A influenza virus.
Aetiology
Avian influenza virus belongs to the family Orthomyxoviridae. Viruses are typed into influenza A, B or C on basis of nucleocapsid or matrix antigens which are common for all viruses of same type. Influenza A viruses are subtyped on the basis of haemagglutination antigen and neuraminidase antigen found on envelop. At present, there are 14 recognized 5 H-types and 9N-types. Each virus possesses one H-type and one N-type.
Host
Many avian species domestic or wild can be infected with influenza viruses that may or may not cause disease. Among domestic avian species, turkeys have been most frequently involved in the disease outbreak of influenza whereas chickens are least frequently involved. Isolation rate for wild duck congregating on lakes prior to migration has been very high usually in range of 25%-60%and this indicates the potential for the spread of influenza virus throughout the world but especially along migratory routes. The viruses responsible for reported epidemic of highly pathogenic avian influenza HPAI up till now have been H5 and H7 subtypes. In some area such as Minnesota, USA and England, disease outbreaks due to low virulence influenza viruses have been reported every year since the 1960s and have represented a serious economic burden to turkey producers. Commercial ducks have also been shown to be frequently infected with avian influenza virus but geese have been rarely associated with the because of the marked resistance these birds show even to strains highly virulent for chicken and turkey.
Transmission
Sources of infection include aerosol from nasal discharge, feed and water contaminated with faeces.
Route of infection is either airborne or most likely through the ingestion of infective material.
Primary introduction of avian viruses into an area is usually due to water fowl activity.
H1N1 viruses may also be readily transmitted between pigs, humans and turkeys.
Secondary spread of avian influenza virus has been considered to be by human where virus is carried from location to location on foot, clothing and equipment.
Clinical signs
These are influenced by several factors such as strain of virus, species and age of host, presence of concurrent infectious agents, nutritional deficiencies. Environmental factors such as excessive ammonia and dust. The disease caused by different viruses varies in severity from high mortality with sudden death proceeded by few unknown clinical signs to a very mild and inapparent form. Often the first sign of avian influenza in chicken and turkey is sudden onset of high mortality which may approach 100% within 2 days. Clinical signs which may be associated with high mortality are cessation of egg production, respiratory signs, rales, excessive lacrimation, sinusitis, edema of head and face, subcutaneous haemorrhage, cyanosis of comb and wattle and diarrhea. The less virulent viruses may cause considerable disease. In uncomplicated infection, these viruses may cause drop or cessation of egg laying, respiratory disease, anorexia, depression, sinusitis and low mortality while other concomitant infection present exacerbate infection on birds under stress due to advance environmental condition. Mortality may rise to 50% of the flock and clinical signs showed a marked increase in severity. Ducks and other water fowls tend to be refractive even to viruses that are highly pathogenic to chicken.
Post-mortem lesions
The most severe cases show congestion or haemorrhage of the skin, liver, spleen, heart, kidney and lung. Infection with viruses of low virulence is usually associated with lesions of respiratory tract including the nasal and tracheal passages and mostly notable sinusitis.
Diagnosis
A tentative diagnosis can be reached through clinical signs due to their variability. The definitive diagnosis of influenza virus A is reached by isolation and recognition of virus in 8-10 day virus embryonated hen’s egg.
Samples collected in live animal include tracheal and cloacal swabs. In dead animals, faeces, intestinal contents and cloacal samples are collected. Further characterization to determine the subtype is also important.
Haemagglutination activity in bacterial
The recommended method for demonstration of the presence of influenza virus is by immunodiffusion using specific antiserum.
Control
Most developed countries have policy for prevention of introduction of highly pathogenic avian influenza via trading with other countries and stamping policy and eradication policies at national level in eradication of the disease.
Vaccination is practiced in a place like Minnesota at significant losses due to low virulent influenza viruses. Vaccines are not aim at highly pathogenic avian influenza viruses.
Inactivated oil emulsion vaccine is used to protect against low virulent viruses that cause little disease in absence of predisposing factors like mutation.      
Management practices like situating farms away from migratory routes is necessary.
Birds should be reared in bird proof cages.
Prevent movement of people from farm to farm.
Equipment and vehicles should be disinfected.
When disease outbreak occurs, depopulation should be considered.
Restock only after two weeks following thorough cleaning and disinfection.

This is an infectious viral disease of domestic chicken and sometimes turkey characterized by ataxia and in some cases paralysis in chicks but it is mainly asymptomatic in adults.
Aetiology
This is caused by RNA virus commonly known as enterovirus belonging to picornaviridae.
Host range
The disease is mainly a disease of many fowls but may occur infrequently in turkey, pheasants and guinea fowls.
Transmission
The mode of transmission is primarily vertical through the egg but also horizontal by ingestion of contaminated feed and water.
Source of infection include carrier adult, egg and actively infected chickens. The faeces from carrier and clinically affected chicks served as source of infection.
Clinical signs
In vertical infected chicks, incubation period is 2-3 days or longer but when there is horizontal transmission between chicks, incubation period is about 2 weeks. The early stage of the disease starts with dullness of the eyes followed by progressive ataxia and muscular incordination. In severely affected birds, there is reluctance to move or when forced to move, they present a shaky gait or crawl on their hocks and shanks. In advanced cases, tremor occurs in affected chicks. Mortality may occur for two reasons such as starvation due to inability to reach feed and water and trampling over by other chicks. In the later stages when most of the clinical signs are subsided, survivors may present with corneal opacity and blindness. The disease is in-apparent in adult birds except for a temporary drop in egg production. The disease is much milder in chicks than turkeys.
Post-mortem lesions
There is no gross detective lesion in avian encephalomyelitis. In the brain and spinal cord, lesions observed are disseminated non-purulent encephalomyelitis and ganglionitis.
Diagnosis
A tentative diagnosis is reached by considering the age of birds, clinical signs, absence of appreciable gross lesions which can be strengthened by histology.
A definitive diagnosis is based on isolation and recognition of the virus.
Control
The control can be achieved by management and hygienic practice which minimize infections by horizontal means.
Ensure that chicks are sourced from disease free breeder flocks.
Vaccines are available but usually targeted at breeder stock on which they are applied before the onset of egg production usually at 12-16 weeks of age.
Progeny from vaccinated birds or naturally infected flocks retain antibodies for about 8 weeks and should not be vaccinated before 10 weeks of age.

The cutting of hair is one of the most important of all the hair dressing skills. A good hair cut, skillfully executed can transform the most mediocre head of hair into something special. To cut hair proficiently, the hair dresser must be aware of where and how the length and bulk need to be removed from the hair in order to create a fascinating shape with good line and balance. Each head of hair differs in some way and each haircut should be carefully cut to emphasize good points and minimize defects. A good haircut is the basis for all good hair dressing and for good health.
These can be employed to produce particular effects on the various types of hair. Blow-drying and the movement towards natural and healthy looking hair has helped to encourage a greater obligation on the part of the hairdresser to produce better haircutting. To this end, it is necessary to become skilled in the different methods of cutting to enable the hairdresser to adapt these methods to any fashion changes.
The basic techniques are tapering, thinning and clubbing. Tapering is the method of removing bulk and length from the hair. Specifically, it will thin the hair at the same time as removing the length. By thinning the hair, a lot of the hair bulk is also removed, thus it will allow the hair to curl more easily. Obviously, this type of cutting will not make straight hair curly although it can influence any natural curl or wave movement already present in the hair. The hair can be tapered either dry or wet. The scissors are used in the slithering movement to taper dry hair. Taper cutting wet hair with the scissors can shred the hair and may also cause steps because of the hair’s tendency to stick together when wet. The excess of tapering is to remove excess length and bulk(thickness) from thick hair. To encourage natural and wave movement is by removing the weight from the points of the hair. Before a basic permanent wave, to aid winding hair which has finer, tape points will bend much more easily around a perm curler than thicker, clubbed hair. It produces a lighter, feathered effect to the hair style.
Thinning removes unwanted bulk but not length from the hair. It may be done with the razor or scissors although it must be called to mind that the scissors should only be used to thin out dry hair and the razor to thin out wet hair. Check the hair carefully to decide where on the head the bulk needs to be reduced, as it is not mandatory to thin out the whole head. Thinning removes excess bulk from the hair to give a finer, feathered effect to certain areas of the hair style and remove the weight from over-clubbed hair.
Club-cutting is a technique of cutting the hair straight across, by that removing the length from the hair although retaining the bulk. Since the weight is left on the points of the hair, it tends to depress any natural predisposition of the hair to curl. Hair can be club cut or dry either using the scissors or a razor. Though, club cutting with a razor demands enough practice and should only be tried when the operator is fully skilled in razor cutting. Club cutting allows the hair to be cut very precisely but it must always be called to mind that the head is a curved object and despite the fact that the hair may be cut in a linear manner, the slant at which the head is held away from the scalp is very important to produce the exact shape for the completed hair cut. Club cutting on fine hair is to retain as much bulk and weight in the hair that promote good or healthy hair. It discourages curl on over-curly hair for fashion cutting, where bulk needs to be retained.