Presentation brochure
Main diseases in poultry farming VIRAL INFECTIONS Emmanuel Baraza Sasita
Main diseases in poultry farming viral infections
Main diseases in poultry farming VIRAL INFECTIONS Emmanuel Baraza Sasita
Author: Emmanuel Baraza Sasita Format: 22 x 28 cm. Number of pages: 128. Number of images: 112 Binding: Hardcover.
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Viral diseases entail great losses to poultry industry as they can reduce flock performance, productivity and profits without appearing as overt clinical diseases. Viruses can cause primary tissue damage and open the gates for other infectious agents (bacteria, mycoplasmas...). Therefore, effective biosecurity measures and vaccination programs are required to maintain a healthy immune status within the flock. This handy and rigorous book is focused on the main viral infections in poultry farming and includes the most updated information as well as numerous graphic resources (high quality images, graphs, flow charts) to better understand the content. The book has been written by an author with a wide experience in the study of these infections and their management and control in the field. Its format makes the contents more understandable and accessible to readers.
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Main diseases in poultry farming | viral infections
Presentation of the book It is well known that viral diseases cannot be treated with antibiotics, but vaccines can be effective for preventing some viral diseases. Viral diseases can reduce productivity, flock performance, and profits without appearing as overt clinical disease. Therefore, viruses are potentially more important than bacterial infections. Hence, this book is thought to be designed as a reference of the main viral poultry diseases in the world for the poultry health for development related courses. The book will also serve as a stand-alone disease diagnosis, prevention and recovery references for veterinarians working in the field. The major focus will be the description of the main viral diseases in poultry, that include Marek, Newcastle, Gumboro, fowlpox, influenza, etc., highlighting the aetiological and epidemiological features, clinical signs, diagnosis, treatment, where each of them will be depicted in a very visual and practical way for the veterinarians. In addition, vaccination is one of the most important points included in the book. In this case, vaccination failure and hatchery vaccination within each disease will be considered, bearing in mind that treatment and control (vaccination) are always two of the main objectives in poultry farming. Above all, pictures, graphs, flow charts and tables will be taken into account and will illustrate the topic in an interactive and graphic way for the veterinarian, who should understand how each disease works, lesions caused by each disease, etc.
Emmanuel Baraza Sasita
Main diseases in poultry farming | viral infections
The author Emmanuel Baraza Sasita
hkeita/shutterstock.com
Bachelor of Science in Biomedical Laboratory Technology and MSc in Molecular Biology and Biotechnology, both from the Faculty of Veterinary Medicine of Makerere University (Uganda). He is currently pursuing his PhD studies in virology. He has recently published an article on the prevalence of infectious bursal disease in local chickens in the area of Kampala (Uganda). In addition, he works as an academic writer, editor and reviewer. He works for academic and research writers based in the USA and the UK and reviews manuscripts for the journal Microbiology Research International (www.netjournals.org). He is also currently working on a project about contagious caprine pleuropneumonia at the International Livestock Research Institute.
Communication services Website Online visualisation of the sample chapter. Presentation brochure in PDF format. Author´s CV. Sample chapter compatible with iPad.
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Main diseases in poultry farming VIRAL INFECTIONS Emmanuel Baraza Sasita
Table of contents Introduction
8. Fowlpox
Viral infections
9. Infectious bronchitis
1. Avian encephalomyelitis
10. Infectious bursal disease
2. Avian influenza
11. Infectious laryngotracheitis
3. Avian leucosis
12. Marek’s disease
4. Duck viral hepatitis
13. Newcastle disease
5. Duck virus enteritis
14. Swollen head syndrome
6. Egg drop syndrome
15. Viral arthritis
7. Equine encephalomyelitis
References
8
Fowlpox
Introduction
a
Fowlpox is a common viral disease of domestic birds also referred to as bird pox, avian diphtheria or sore head. The disease has a worldwide distribution and is caused by the viruses of the family Poxviridae, genus Avipoxvirus. The viruses that cause pox in poultry are considered to be distinct from each other but antigenically similar (Fig. 1). Fowlpox is a relatively slow-spreading viral disease characterised by skin lesions and/or plaques in the pharynx. Chickens, turkeys (Fig. 2), pigeons and canaries have been b DNA genome
Outer membrane Inner membrane
Core Core wall
c
Lateral bodies Figure 1. Structure of the virus from the Poxviridae family.
Figure 2. (a) 2, (b) 3 and (c) 4 week-old turkey with skin pox exhibiting wart-like sores, which have eventually enlarged and formed masses of yellow, dirty crusts.
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found to be the most affected species worldwide. Morbidity is about 10-95 %, while mortality has been found to range between low to moderate (0-50 %). Infection can occur following skin abrasions and bites, or by the respiratory route. It is transmitted by birds, fomites and mosquitoes (infected for 6 weeks). The virus persists in the environment for months. The disease is more prevalent in males due to their tendency to fight, which results in skin damage (Fig. 3). The disease can last for about 14 days on an individual bird. Fowlpox is a common disease in backyard chickens that have not still been vaccinated. Most birds can survive the infection, although the young or weak ones can easily die.
There are many types of avian poxviruses. They tend to be specific to particular species of birds, and all age groups are at risk. The incidence varies based on climate, management, hygiene, biosecurity and use of a regular vaccination program. Avian pox may occur in two forms including cutaneous or diphtheritic form. The cutaneous form is characterised by the appearance of nodular lesions on the comb, wattle, eyelids and other non-feathered areas of the body. In the diphtheritic form (wet pox), yellowish lesions occur on the mucous membrane of the mouth, oesophagus or trachea accompanied by mild or severe respiratory signs. Historically, outbreaks of diphtheritic form (wet pox) have been associated with severe mortality losses in both vaccinated and unvaccinated flocks. Field isolates from severe wet pox cases have been studied and some have been found to contain intact reticuloendotheliosis virus (REV), provirus or long terminal repeats of REV. Most of these field strains have been reported to be highly pathogenic and induce an antibody response to both REV and fowlpox virus. REV is associated with immunosuppression, while the integrated sequences in the genome of fowlpox virus have been suggested to play a critical role in pathogenesis and prolonged persistence of wet pox. Wet pox alone can cause high mortality rates (up to 50-60 % in unvaccinated chickens). This disease can start out as wet
pox and spread to birds in the dry pox form and vice versa. It has been found to be related to both wet and dry pox at the same time. Infectious laryngotracheitis (ILT) can occur as a dual infection with wet pox.
Aetiology and epidemiology Fowlpox is considered to be a highly infectious disease caused by various host-specific pox virus strains. The virus can be directly transmitted by infected birds, or carried by mosquitoes or other blood-sucking insects. The elimination of the breeding areas of these insects can lead to the reduction of the virus spread. The fowlpox virus targets the skin and the surface of the mouth as well as the throat. Depending on its location, pox is referred to as either skin pox or wet pox. Skin pox forms wart-like sores, which eventually enlarge and form masses of yellow, dirty crusts (Fig. 4). In about a week, these scabs darken and fall off. Wet pox forms cheesy masses in the mouth, nose and throat, which interfere with eating and drinking (Fig. 5). Antibiotics may be administered to prevent bacterial infections, but vaccination based on the vaccine manufacturer’s instructions (e.g. 1-2 months before the start of egg production) is the best method of control and prevention. In this case, broilers may not be vaccinated. This virus is capable of surviving for a long time in infected material, and such material should therefore be incinerated. Fowlpox affects most species of poultry. Chickens, turkeys, pheasants, quail, ducks, psittacine and ratites of all ages (except newly-hatched chicks) are susceptible. It is transmitted by direct contact between infected and susceptible birds or by mosquitoes. Virus-containing scabs could also be sloughed from affected birds and hence acting as infection source. The virus is capable of entering the bloodstream through the eye, respiratory tract or skin wounds. Mosquitoes have been found to be infected following feeding on birds with fowlpox virus in their bloodstream. There is some evidence that the mosquito remains infective for life. Mosquitoes are the primary reservoir and spreaders of fowlpox on poultry ranges. For example, several species of mosquitoes have been reported to transmit fowlpox, being noted that
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8
mosquitoes were associated with outbreaks during winter and early spring. The virus present in the scabs has been reported to contaminate the environment and hence, to remain infectious for a couple of months. Mechanical transmission is considered the primary method to disseminate the virus, and the infection can occur through lacerated or injured skin.
Figure 3. Cock (male) with warty, spreading eruptions and scabs on comb.
Mechanical vectors, such as insects, can easily carry pox virus and may deposit the virus on susceptible birds. Flies may walk on the eyes of the birds, leaving the virus behind, and mosquito bites can result in rapid spread of pox throughout the farm. Airborne transmission has also been suspected to be associated with several wet pox cases. The mucous membranes of both the mouth and trachea have been suspected to be highly susceptible to the virus. The infection could take place in the absence of apparent injury or trauma. In a contaminated house, the infection can easily be spread from bird to bird, cage to cage, and by the stagnated water in drinking cups.
Clinical signs and lesions
Figure 4. 2 month-old chicken with skin pox form that had wart-like sores, which eventually enlarged and formed masses of yellow, dirty crusts. In about a week, these scabs darken and fall off as seen here.
Lesions resulting from dry form always heal in approximately 2 weeks. If the scab is removed before the healing is complete, it will result in bleeding. On the other hand, the wet form is characterised by canker-like lesions in the trachea, larynx, mouth and pharynx. This wet form could lead to respiratory distress due to the obstruction of the upper air passages. Generally speaking, chickens could be affected by either or both forms of fowlpox at a point in time. Retarded growth is known to be the major symptom of fowlpox. Infections in laying hens can lead to transient decline in the production of eggs (Fig. 6).
Figure 5. 4 week-old chicken with wet pox exhibiting cheesy masses in the mouth, nose and throat, which interfered with eating and drinking.
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Clinical signs • Warty, spreading eruptions and scabs on comb and wattles (Figs. 7 and 8). • Caseous deposits in the mouth, throat and sometimes trachea (Fig. 9). • Depression. • Inappetence. • Poor growth. • Poor egg production (Fig. 6).
Figure 6. Decline in egg production.
a
b
Figure 7. Warty, spreading eruptions and scabs on comb and wattles.
Figure 8. 3 week-old chicken with warty, spreading eruptions and scabs on comb and wattles.
Figure 9. 3 week-old chicken with caseous deposits (cheesy-like deposits) in the mouth lining. This extends to the throat and sometimes to the trachea.
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8
Post-mortem lesions • • • •
Papules. Vesicles. Pustules (Fig. 10). Scabs.
Less commonly, caseous plaques in the mouth, pharynx, trachea and/or nasal cavities (in the diphtheritic form) may be found. Histopathologically, intracytoplasmic inclusions (Bollinger bodies) with elementary bodies (Borrel bodies) may be observed.
Diagnosis • A presumptive diagnosis may be made based on history, clinical signs and post-mortem lesions. The disease is confirmed by intracytoplasmic inclusions in scrapings/ sections, reproduction in the susceptible birds, isolation of the causative agent (pox virus) and polymerase chain reaction (PCR). • Fowlpox is often diagnosed by clinical signs, but lesion material containing fowlpox particles could lead to pocks on the dropped chorioallantoic membrane of embryonated chicken eggs. • Histopathological sections: intracytoplasmic inclusion bodies could be observed in stained sections or in scrapings of the lesions in chickens, but might not be visible in turkeys.
Differential diagnosis • • • • • •
Figure 10. 2 month-old hen with lumps on the face.
a
b
Stick tight fleas. Vitamin A deficiency. Favus. Trichomoniasis or physical damage to skin (in dry pox). Biotin or pantothenic acid deficiency. Respiratory signs mistaken for ILT.
Dry pox Dry pox can be visually identified by the characteristic scabs on the featherless areas of the bird (Fig. 11). Histopathology may be required for conclusive diagnosis.
Figure 11. (a) 2 month-old hen and (b) 3 month-old chicken with lesions on the featherless skin.
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a
Figure 12. 5 day-old chick with cheesy masses in the mouth, nose and throat.
Figure 13. 7 week-old chicken with both forms of fowlpox (canker-like lesions in the trachea, larynx, mouth and pharynx; warty, spreading eruptions and scabs on comb and wattles).
b
Figure 14. 3 week-old chicken with canker-like lesions in the trachea, larynx, mouth and pharynx; typical of wet pox.
Wet pox Diagnosis of wet pox can be complicated by lesions, which seem to be similar to those of other respiratory diseases. The only conclusive way to confirm wet pox is by using histopathology on suspect lesion tissue fixed in formalin. The presence of eosinophilic intracytoplasmic inclusion bodies (Bollinger bodies) is diagnostic for pox virus infection.
Cutaneous infections usually produce characteristic gross and microscopic lesions. Small cutaneous lesions are hardly distinguished from abrasions caused by fighting. Microscopic examination of the infected tissues stained with haematoxylin-eosin stain can reveal eosinophilic cytoplasmic inclusion bodies.
Wet pox lesions can also be found in the mouth or conjunctiva of the eye (Figs. 12-14). Other upper respiratory diseases, such as avian influenza, Newcastle disease, cholera, Mycoplasma gallisepticum, Mycoplasma synoviae and coryza may complicate the initial diagnosis of wet pox as they cause similar respiratory lesions.
The detection of cytoplasmic inclusions can also be undertaken by fluorescent antibody and immunohistochemical methods (antibodies against fowlpox virus antigens can be used). The elementary bodies in the inclusion bodies can be detected in smears from lesions stained by the Gimenez method.
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Fowlpox
Viral particles with typical pox virus morphology could be demonstrated using negative-staining electron microscopy as well as in ultrathin sections of the lesions. Virus isolation can be achieved by inoculating the chorioallantoic membrane of cell cultures of avian origin, developing chicken embryos or susceptible birds. Chicken embryos (9-12 days old) from a specific pathogen free (SPF) flock are the preferred and appropriate host for virus isolation.
(Figs. 15 and 16), while turkeys older than 8 weeks may be vaccinated using the thigh-stick method. Vaccination should be completed prior to expected exposure to the fowlpox virus. Areas that have mosquitoes throughout the year often use two vaccinations, one early and one later (at the start of egg production) for “permanent” protection.
Fowlpox outbreaks in poultry confined houses can be controlled by spraying to kill mosquitoes. However, if fowlpox is endemic in the area, vaccination is recommended. Vaccination is not recommended unless the disease becomes a problem on a farm or in the area. Chickens may be vaccinated at 4-6 weeks of age or according to the vaccine manufacturer’s instructions using the wing-web stick method
Since the effective cure for fowlpox is currently unavailable, prevention and cure are very critical for keeping flocks healthy. The recommendations below can help to reduce the effect of fowlpox on a flock: • Virus particles and debris could be found in the environment and poultry houses. Therefore, dust control and disinfection of the environment are critical. • An effective insect control program should be done. • A biosecurity program should be established to prevent the movement of equipment that may be contaminated with pox. • Vaccination is practiced based on history of exposurerevaccination. If necessary, it can be done in the face of an outbreak. • In the event of an outbreak, liquid iodine disinfectant (used for disinfecting water lines) added to water has been reported to reduce mortality: • Stock solution can be prepared by adding 30-45 ml/l of iodine disinfectant to water. • The stock solution can later be added to the water line through a medicator at a concentration of 8 ml/l drinking water. • The house can then be fogged with the prepared disinfectant to reduce exposure.
Figure 15. Vaccination of a 4 week-old chicken using the wing-web stick method.
Figure 16. Vaccination of a 3 week-old chick (coloured blue).
Treatment No treatment is available. Fowlpox has been reported to be spread at a low rate and vaccination can be made to stop its spread to other birds. In this case, unaffected flocks may be vaccinated, often using wing-web puncture method. If there is any evidence of secondary bacterial infection, broad-spectrum antibiotics may be of some benefit. Appropriate vaccination program should be put in place to enable a proper management of the disease.
Prevention and control
8
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Acute and immunosuppressive forms reported. Immunosuppressive form reported.
Figure 3. Worldwide geographical distribution of IBDV (Van Den Berg, 2000).
Pathogenesis
Clinical signs
A basic knowledge of the early development of the immune system is critical to understand how IBDV adversely affects the immune system of chickens.
The viral incubation period is approximately 2 to 3 days, while the infection itself lasts f o r 5 to 7 days. Vent picking is one of the earliest signs of IBD.
During the course of embryonic development, up until about 10 weeks of age, immune system cells (lymphocytes) migrate to the bursa of Fabricius, where they are programmed to become antibody-producing cells (Hitchner, 1970). In young chickens, damage to the bursa of Fabricius caused by IBDV infection impairs this organ’s ability to program lymphocytes. Thus, in addition to the immunosuppressive effects of IBDV infection, the capacity of the immune system is reduced in affected chickens.
Clinical signs include: • Acute onset of depression. • Trembling. • White, watery diarrhoea. • Anorexia. • Prostration. • Ruffled feathers. • Soiling of vent feathers with urates. • Dehydration in severe cases, sometimes followed in later stages by subnormal temperatures and ultimately death (Fig. 4).
The earlier the bursa of Fabricius is damaged, the smaller the number of programmed lymphocytes with antibody-producing ability. As such, the aim of any IBDV control program should be to protect the bursa of Fabricius as early as possible. If the bursa of Fabricius is protected against the disease up to at least 3 weeks of age, an adequate number of lymphocytes should be programmed and the immunosuppressive effects of an IBD outbreak should be minimal.
The chickens most affected by clinical IBD are naive birds from 3 to 6 weeks of age. The clinical form of IBD can lead to mortality, immunosuppression and impaired growth. Clinical signs are associated with classic strains of IBDV serotype I.
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InfectIous bursal dIsease
Mortality caused by classic strains in fully susceptible flocks ranges from 1 % to 60 %, with morbidity reaching 100 % in some cases.
result of the destruction of the bursa of Fabricius. Most field infections are considered subclinical (the most economically important form of the disease).
Variant IBD strains are known not to cause overt clinical signs, but can cause immunosuppression and mortality linked to secondary opportunistic infections in immunocompromised birds. Mortality caused by vvIBDV strains ranges from 90 % to 100 % in susceptible leghorns, 25 % to 30 % in broilers, and 50 % to 60 % in laying hens. Susceptible chickens of less than 3 weeks of age may show clinical signs, but can also develop subclinical infections, which lead to a reduced humoral antibody response due to B lymphocyte depletion in the cloacal bursa accompanied by severe, prolonged immunosuppression.
Broiler integrations often include farms referred to as problem farms. Broilers in these farms usually have poor body weights and feed conversion rates, high mortality, excessive reactions to respiratory vaccines, and high condemnation rates at processing. In many cases, these farms are highly contaminated with IBDV, and the poor performance of broilers is due to factors associated with the immunosuppressive effect of subclinical IBD.
Subclinical infections cause the most significant economic losses. These infections can enhance the susceptibility of affected chickens to other conditions such as inclusion body hepatitis, gangrenous dermatitis, bacterial infections, respiratory diseases, and chicken anaemia virus.
Subclinical and clinical IBD
The clinical form of IBD tends to affect chickens from 3 to 6 weeks of age (Fig. 5), and is characterised by its sudden onset, with a rapid spike in the flock’s mortality rate (Fig. 6).
Post-mortem lesions Gross lesions
It remains unclear why young chickens show no clinical signs of disease. However, immunosuppression is induced as a
• Dehydration and haemorrhages in breast (pectoral) and leg (thigh) musculature (Figs. 7 and 8). • Discolouration of pectoral muscles (Fig. 7). • Increased mucus production in intestine. • The gross appearance of the kidneys can appear normal in birds that are necropsied during the course of the infection. • In advanced stages and in dead birds, the kidneys may be swollen and pale, with urate accumulation evident in the ureters and tubules (Figs. 9 and 10).
Figure 4. 3 month-old chicken with acute onset of depression.
Figure 5. 6 week-old chickens (most susceptible) infected with IBDV.
IBD can follow one of two courses depending on the age of the affected bird. The subclinical form affects chickens of less than 3 weeks of age. No clinical signs are observed in these cases, but severe, permanent immunosuppression can occur.
10
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Figure 4. Sinusitis (swelling of the infraorbital sinuses).
Figure 5. Conjunctivitis with severe lacrimation and swelling of the periorbital region and infraorbital sinuses.
Mild or chronic form
ILTV can be isolated and identified in chicken embryos or tissue culture from embryonic liver, or kidney cells, or in kidney cells from adult chickens. Chicken embryos are considered appropriate for virus isolation.
• Affected birds may be drowsy with signs of conjunctivitis, squinting and bronchitis combined with a cough. • Low morbidity (≈5 %). • Egg production can drop by 10 %. • Concurrent coryza infection is common. • Post-mortem analysis reveals false membranes or plugs in the upper respiratory tract, which can cause death.
Diagnosis The characteristic signs of acute disease include the presence of mucus, blood, yellow caseous exudates, or a hollow caseous cast in the trachea. Microscopic examination reveals a desquamative, necrotising tracheitis. The subacute form is characterised by the presence of punctiform haemorrhagic areas in the larynx and trachea. Mild conjunctivitis with lacrimation may also be observed. A diagnosis can be rapidly established based on detection of intranuclear inclusion bodies in the tracheal epithelium in early disease stages. Detection of viral DNA using virus-specific polymerase chain reaction (PCR) assays allows confirmation of the results of microscopic examination.
The isolated specimen is used to inoculate the chorioallantoic membrane of developing chicken embryos (9-12 days old). Subsequent microscopic examination of the developing lesions in the chorioallantoic membrane reveals intranuclear inclusions. Microscopic examination of the trachea allows differentiation between the intranuclear inclusion lesions caused by ILTV and the intracytoplasmic inclusions produced by the diphtheritic form of fowlpox infection. Field isolates and vaccine strains of ILTV can be differentiated by PCR amplification of multiple or single ILTV genome areas, followed by the sequencing of PCR products and comparative analysis of the resulting sequences. Recent studies indicate that full genome sequencing analysis allows more accurate differentiation between vaccine strains and field isolates. While severe acute ILT can be diagnosed based on high mortality together with blood expectoration, milder forms of the disease can resemble respiratory diseases caused by other
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InfectIous laryngotracheItIs
agents such as infectious bronchitis and Newcastle disease. Accordingly, laboratory methods are required to confirm diagnosis (Table 1). Currently used methods include: • Trachea histology. • Detection of antibodies. • Detection of virus.
Prevention and control • ILT can be controlled by implementing vaccination and biosecurity measures in endemic areas and on farms in which a specific diagnosis is established. • Viral vector recombinant vaccines and live attenuated vaccines are used to vaccinate against ILTV. Live vaccines can be produced using virulent isolates attenuated after consecutive passages in tissue culture or embryos. • Vaccines are administered by eye drop or through mass vaccination in water or sprays.
11
• Viral vector recombinant vaccines against herpesvirus and fowlpox of turkeys have been engineered to express ILTV immunogenic proteins and are administered to individual birds by wing-web puncture. • Disease control primarily focuses on management practices, with an emphasis on strict biosecurity measures. Given the possibility that the vaccine may cause disease, veterinary supervision is highly recommended when establishing and implementing these practices. • Because carrier birds can be produced through both vaccination and natural infection, it is crucial that susceptible chicken flocks are not exposed to vaccinated or previously infected chickens. • Birds should only be mixed when their complete histories are available, and the presence of potential ILT carriers has been ruled out. • Sanitation procedures, including the disinfection of equipment, boots and clothing, as well as adequate disposal of litter and carcasses, are essential components of ILT control.
Table 1. Techniques used for the diagnosis of avian ILT diagnosis (OIE, 2014). PuRPose MeThoD
Population freedom from infection
Animal freedom from infection before movement
Contribution to eradication policies
Confirmation of clinical cases
AgeNT IDeNTIFICATIoN
Prevalence of infectionsurveillance
Immune status in individual animals or populations post-vaccination
1
Virus isolation
–
–
–
++
–
–
Immunofluorescence for antigen
–
+
–
++
–
–
ELISA – antigen detection
+
++
+
+++
+
–
++
+++
++
++
++
–
–
–
–
++
–
–
PCR Histopathology
DeTeCTIoN oF IMMuNe ResPoNse VN ELISA – antibody detection
2
+
–
+
–
–
+
++
+
+++
+
+++
+++
Key: • +++ = recommended technique; ++ = suitable method; + = may be used in some situations, but use severely limited by cost, reliability, or other factors; – = not suitable for this purpose. • Although not all tests listed as category +++ or ++ have been formally standardised and validated, they are considered acceptable given their routine nature and the fact that they have been widely used without dubious results. • ELISA = enzyme-linked immunosorbent assay; VN = virus neutralisation. • 1 = a combination of agent identification methods applied on the same clinical sample is recommended; 2 = one of the listed serological tests is sufficient. 77
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Aetiology and epidemiology MD is caused by a herpesvirus, and can be differentiated from other lymphoid neoplastic diseases (Fig. 2). There are three serotypes of MD; these have many common antigens and are distinguished by serological tests (Table 1). Marek’s disease virus (MDV) is known to be transmitted by air within the poultry house. It can be found in the chicken-house dust, feather dander, saliva and faeces. The virus can be carried in the infected birds’ blood for life and it is considered to be the source of infection for susceptible birds.
MD is considered to be highly contagious and spreads by bird-to-bird contact, by contact with infected dust and dander, as well as by darkling beetles and mealworms that live in the chicken house, although the virus has no effect on them. Other organisms common to chicken houses such as freeliving mites, mosquitoes and coccidia do not transmit the disease. Chickens are most commonly exposed to MD by contact with residual dust and dander in previously infected houses by aerosol (air) contamination from a nearby house, or by virus particles carried by personnel and equipment. The virus does not survive the incubation process well and is not spread by hatching eggs. Immune transfer from the hen to the chick provides some protection to the chick for the first few days of life.
Clinical signs and lesions
Lipid envelop Nucleopcapsid
MD is considered to be a type of avian cancer, and chickens between 12 to 25 weeks of age are known to be the most susceptible. Game fowl, pheasants, turkeys and quail can be occasionally infected. Nerve tumours cause both paralysis and lameness, while eye tumours may lead to irregularly shaped pupils as well as blindness. Tumours of the kidney, liver, spleen, pancreas, gonads, proventriculus, muscles, lungs and skin can cause retarded growth; weak, laboured breathing; incoordination; enlarged feather follicles and paleness. In terminal stages, birds are emaciated with pale, scaly combs as well as greenish diarrhoea. MD signs vary from bird to bird based on the form of the disease and the type of nerve affected.
Cutaneous form Glycoproteins
It is characterised by enlarged reddened feather follicles and white bumps on the skin that form brown crusty scabs (Fig. 3).
DNA core
Figure 2. Enveloped MDV particle.
Table 1. Serotypes of MD (adapted from Jordan and Pattison, 1996). SeroType 1 viruSeS • Viruses grow best in duck embryo fibroblasts or chicken kidney cells. • Viruses grow slowly. • Produce small plaques.
SeroType 2 viruSeS • Viruses grow best in chicken embryo fibroblasts. • Viruses grow slowly. • Produce medium-size plaques.
SeroType 3 viruSeS (HvT) • Viruses grow best in chicken embryo fibroblasts. • Viruses grow rapidly. • Produce large plaques.
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