Search term(s): submandibular       Displaying results for: submandibular, All Assets

   

Clinical Signs

Gross Lesions

Histopath

.

Normals

FirstPrevious 0 of 0 NextLast Larger image

Preview Image

Sort Results

This Image

Clinical Sign:

Tissue:

Etiology:

Species:

DESCRIPTION

DISEASE PROFILE

DIFFERENTIALS

...

3.6.08.bDSC_0199.JPG

Preview

View Asset

gross image

  • ecchymoses: skin
  • edema: subcutaneous
  • subcutaneous tissue

submandibular, wattles

Avian Influenza

chicken (Gallus gallus)

Morphologic Diagnosis

Subcutaneous tissue (ventral neck and head): Severe acute diffuse edema. Subcutaneous tissue (wattles): Moderate acute multifocal hemorrhage.

Clinical Description

This image was taken 4 days post experimental inoculation with highly pathogenic avian influenza. There is a severe accumulation of serous exudate in the wattles and intermandibular space. In HPAI, edema tends to be most pronounced in the face and neck regions.

Pathologic Description

The skin on the ventral neck and intramandibular space has been opened to reveal the subcutaneous structures. The subcutaneous tissues are gelatinous and expanded by clear, yellow tinged fluid. The edges of the wattles can be seen on the edges of the reflected skin. These tissues contain numerous, bright red hemorrhages.

VIT E-SELENIUM - 009A.jpg

Preview

View Asset

gross image

  • edema: subcutaneous
  • subcutaneous tissue

submandibular

Vitamin E and Selenium Deficiency

chicken (Gallus gallus)

Clinical Description

Subcutaneous edema tends to accumulate in ventrally dependent areas, such as the subcutaneous tissue located under the mandible, as shown here.

CORYZA-003A.jpg

Preview

View Asset

gross image

  • congestion: conjunctiva
  • edema: conjunctiva
  • suppurative exudate: infraorbital sinus
  • swelling: infraorbital sinus

conjunctiva, head, infraorbital sinus, periorbital region, submandibular

Infectious Coryza

chicken (Gallus gallus)

Morphologic Diagnosis

Head and face: Catarrhal and suppurative sinusitis with edema and conjunctivitis

Clinical Description

On post-mortem examination, chickens infected with the severe form of Infectious Coryza (Avibacterium paragallinarum), subcutaneous edema may be found in the face, wattles, and intermandibular region.

Pathologic Description

There is a small amount of clear mucoid nasal discharge and the eyelids and skin around the eye is swollen.

Avian Influenza

Avian Influenza

Avian Influenza

Etiology

Avian Influenza (AI) [also known as Fowl Plague] is a viral infection affecting wild and domestic birds. These influenza viruses occur naturally in the intestinal tract of many species of wild birds with no disease outcome. However, pathogenic forms of the Avian Influenza virus can result in a highly contagious respiratory infection. Many species of birds are susceptible to AI including chickens, turkeys, guinea fowl, and other domestic birds, as well as a some wild avian species. AI viruses are classified into two general types based on their pathogenicity for chickens: Low Pathogenic (LP) and Highly Pathogenic (HP) types.

AI is caused by viruses that are members of the family Orthomyxoviridae, and the genus Influenzavirus, Type A. Influenza viruses Type B and C are pathogenic for humans but not for birds. Virus classification is based on antigenic differences in the nucleoprotein (NP) and matrix proteins (M1). Further subtyping of the AI virus is made based on the presence of 2 glycoproteins on the surface of the virus, hemagglutinin (HA) and neuraminidase (NA). Each AI virus has 1 of 16 different HA subtype glycoproteins and 1 of 9 different NA subtype glycoproteins (e.g. H5N1).

The HA and NA protein subtypes confer differences in viral pathogenicity. In LP strains, the HA protein can be cleaved by proteases present only in the respiratory and digestive tracts. In HP strains, proteases in most cells of the body can cleave the protein, resulting in a much wider tissue tropism than mildly pathogenic strains.

The HA protein is the major antigen that elicits antibodies which protect against clinical signs and death. Such antibodies are HA subtype specific. The antigenicity of influenza viruses may change gradually by point mutation (antigenic drift) or drastically by genetic reassortment (antigenic shift). Immunological pressure on HA and NA is thought to drive antigenic drift.

AI subtype classification requires viral isolation and characterization. Further subtyping is based on the antigenicity of the two surface glycoproteins, HA and NA. Classification cannot be made through clinical observations alone because the severity of the infection depends not only on the subtype of the virus but also the host species, the age of the bird, the host's immune status, and the presence of any secondary infections or environmental stress.

Due to the significant economic and public health implications of an AI outbreak, the World Organization for Animal Health (OIE) requires notification of any bird that is diagnosed with low pathogenic notifiable AI (LPNAI) or highly pathogenic notifiable AI (HPNAI). For the purposes of international trade the OIE defines notifiable avian influenza (NAI) as an infection of poultry caused by any influenza A virus of the H5 or H7 subtypes or by any AI virus with an intravenous pathogenicity index (IVPI) greater than 1.2 or, as an alternative, if the virus produces at least 75% mortality after inoculation.

HPNAI viruses have an IVPI greater than 1.2 in 6-week-old chickens or, as an alternative, cause at least 75% mortality in 4 to 8-week-old chickens infected intravenously. H5 and H7 virus isolates that do not have an IVPI of 1.2 or greater, nor produce 75% mortality under experimental conditions, but have an amino acid sequence at the cleavage site of the hemagglutinin that is similar to that observed for other HPNAI isolates, should be considered as HPNAI. LPNAI are all influenza A viruses of H5 and H7 subtype that do not display features of HPNAI viruses.

To date, all highly pathogenic strains of AI have been of the H5 or H7 subtypes. Although most H5 and H7 subtypes are in fact low pathogenic strains, since AI is unstable, there is a potential for LPNAI to mutate into HPNAI. Therefore all H5 and H7 subtypes require reporting to the OIE in order to facilitate global virus control measures. Within the United States, these pathotypes are considered exotic diseases and, in addition to being reported to the OIE, they should also be reported to the State and Federal veterinary authorities.

Host range

The AI viruses have been shown to naturally infect a wide variety of wild and domestic birds. The viruses have been isolated from more than 90 avian species however, in free-living birds most natural infections do not produce recognizable disease. The practice of housing birds in captivity and the development of commercial poultry systems have altered the normal epidemiology of the virus, resulting in clinically significant disease within domestic poultry.

In chickens, AI is capable of producing significant disease and economic losses. Ducks and other waterfowl are susceptible to the Asian HPAI H5N1 currently circulating in Asia, but have innate resistance to most other strains of Avian Influenza. Migratory waterfowl can act as carriers and transport viruses between geographic areas, helping to spread AI viruses to other susceptible animals.
In general, mammals are poorly susceptible to AI. However, several infections of highly pathogenic notifiable Avian Influenza (HPNAI) viruses have been reported since 1997 in humans, pigs and other mammals. Most of these cases have been linked to close contact with infected poultry. Although chicken-to-human infections have been rare, the virus is highly unstable and can alter pathotypes by passage in various animal species. The recombination of avian and human influenza viruses in pigs may be a potential source for sporadic pandemics of human influenza.

Epidemiology

AI viruses are distributed worldwide and identified frequently from clinically normal migratory waterfowl, imported birds, and species in live-bird markets. Data shows migratory waterfowl are the reservoir for AI viruses. Migratory birds introduce LPNAI viruses into poultry and, once introduced, the virus adapts to poultry and spreads from flock-to-flock, mostly by human activity. Most outbreaks of HPNAI in poultry arise from mutations in a LPNAI strain.

AI is excreted from the nares, mouth, and cloaca of infected birds. Spread occurs rapidly among birds housed on the floor but is slower in caged birds. Spread is primarily through contaminated feces and aerosol from the respiratory tract. The ingestion of contaminated feed and drinking water is another common source of transmission. The virus may also be transmitted indirectly by fomites such as contaminated equipment, personnel, clothing, foot wear, artificial insemination, and other human activity.

The incubation for AI is usually 1-7 days and depends on the strain, the dose, the species, and the age of the bird. The typical incubation period for an individual bird is approximately 3 days. It may take up to 14 days for an entire flock to become ill.
The morbidity of LPNAI is variable and the mortality is usually low, unless secondary infections are present or the birds are housed under poor management conditions. The morbidity and mortality of HPNAI may be near 100% within 2-12 days after the onset of the first signs of illness.

Clinical Signs

The severity of clinical signs depends on factors such as age, sex, species, concurrent infections, environment, as well as the pathogenicity of the virus.

Low pathogenic AI in wild birds usually produces no clinical signs. In domestic poultry, clinical signs reflect abnormalities in the respiratory, digestive, urinary, and reproductive organs. Generalized signs include depression, decreased activity, huddling, ruffled feathers, decreased feed and water consumption and occasionally greenish diarrhea. Respiratory manifestations include mild to severe coughing, sneezing, rales, rattles, excessive lacrimation, matted eyelids, and nasal discharge. Increased broodiness and a 5-30% decrease in egg production are observed in laying hens and breeders. Turkeys, infected with swine flu, may experience a much larger drop in egg production. Eggs may be thin-shelled and misshapen, but production will usually return to near-normal levels following recovery. Some viral strains may be associated with egg yolk peritonitis.

Some strains of highly pathogenic AI replicate poorly in wild birds and domestic ducks, producing few clinical signs. Ducks, quail, and turkeys may have mild sinusitis. Recent HPAI Asian H5N1 strains have produced more severe clinical signs in ducks and some wild birds.

In chickens, highly pathogenic AI produces clinical signs that reflect widespread viral replication and damage to multiple body systems. The disease may be fulminate, with some birds found dead without exhibiting any clinical signs. Birds that survive 3-7 days post infection may exhibit depression, ruffled feathers, decreased feed and water consumption, and a precipitous drop or total cessation of egg production. Diarrhea is often present. Early in the course of the disease, the feces may be bright green and watery. As the disease progresses, the droppings may become totally white. Birds may show cyanosis and edema of the skin, particularly of the combs, wattles, and periocular areas. Occasionally, edema and ecchymoses of the shanks and feet may also be observed. In some cases neurologic disease develops. Nervous deficits can include head and neck tremor, inability to stand, torticollis, loss of perching reflex and opisthotonus. Respiratory signs are less prominent in HPNAI than with LPNAI but may include coughing, sneezing (with blood tinged discharge), and rales. Most birds will die within 1-2 days following the onset of illness but some birds may survive for as long as a week. Recovery is uncommon.

Post-mortem Lesions

Lesions are variable in distribution and severity, depending greatly on host species, pathogenicity, and secondary infections.
Domestic ducks with LPNAI may have sinusitis, conjunctivitis, and other mild respiratory lesions. In chickens, lesions are more pronounced and are distributed throughout the upper respiratory tract and include catarrhal, fibrinous, serofibrinous, mucopurulent, or fibrinopurulent exudates. The tracheal mucosa may be edematous with congestion and hemorrhages. The infraorbital sinuses may be swollen and mucoid to mucopurulent nasal discharge may be present. Catarrhal to fibrinous inflammation may be observed in the coelomic cavity. The ovaries may be hemorrhagic with ova involution and degeneration. Eggs may be misshapen and fragile. The coelomic cavity may contain ovules or be filled with egg yolk, from ruptured ova, resulting in egg yolk peritonitis. This peritonitis may cause air sacculitis and diffuse coelomic cavity inflammation in birds that survive for 7-10 days post infection. Catarrhal to fibrinous enteritis may also be observed in the ceca and in the intestines.

Birds infected with HPNAI that die peracutely may not show any gross lesions. In chickens infected with the acute to subacute form, significant gross lesions are usually observed. At gross necropsy, one of the most frequent external findings is edema, manifested by swelling of the head (combs, wattles and periocular regions), upper neck, and feet. This edema may be accompanied by petechial and ecchymotic hemorrhages. Additionally, areas of nonfeathered skin such as the wattles and combs, are commonly cyanotic and have dark areas, caused by ecchymotic hemorrhages and necrotic foci. Internally, generalized hemorrhages and edema can be found in the muscles, especially the pectoral muscles, as well as the tissues of the hocks and feet. With most strains of HPNAI, pinpoint petechial hemorrhages are frequently observed along the abdominal fat, pericardium, serosal surfaces and peritoneum. Visceral organs may also be marked by hemorrhages. The glands of the proventriculus may have hemorrhagic lesions, particularly at the junction with the ventriculus (gizzard). The lining of the ventriculus may peel easily, frequently revealing underlying hemorrhages, erosions, and ulcers. The intestinal mucosa may have hemorrhagic areas, especially in the lymphoid tissue of the cecal tonsils and Peyer's patches in the small intestine.

In laying birds, the ovary may be hemorrhagic or degenerated with darkened areas of necrosis. In birds that survive, the peritoneal cavity is frequently filled with yolk from ruptured ova, causing severe airsacculitis and inflammation. The eggs are frequently soft and fragile due to decreased calcium deposition.

The trachea may appear normal, with the exception of excessive mucous accumulation, or it may be severely affected, with extensive hemorrhagic tracheitis. The lungs may be deep red in color, due to congestion and hemorrhage, and may exude edematous fluid when cut. The bursa of Fabricius and thymus are usually atrophic. The kidneys may be swollen, severely congested, and may by plugged with white urate deposits in the tubules. Necrotic foci may be present in the pancreas, spleen, heart, and occasionally the liver and kidneys.

Differential Diagnosis

AI should be differentiated from other respiratory diseases such as: Newcastle disease, infectious bronchitis, infectious laryngotracheitis, avian pneumovirus, and infectious coryza, among others. Other diseases that cause sudden death and septicemias, such as fowl cholera, should also be considered. Particular attention should be given to differentiating AI from mycoplasmosis, chlamydiosis and fowl cholera in young turkeys.

Diagnosis

In cases where HPAI is suspected, it is important to submit clinical samples to a recognized laboratory capable of carrying out AI diagnosis. Currently, there are a number of laboratories in the United States and around the world that have the capabilities to perform molecular testing, such as reverse transcriptase-polymerase chain reaction (RT-PCR) or a simplified faster real time reverse transcriptase polymerase chain reaction (rRT-PCR), to detect the presence of AI from clinical samples. The validated testing procedures performed at these laboratories are very sensitive, accurate, and rapid.

Cases involving respiratory signs and drop in egg production should be investigated for LPNAI. A presumptive diagnosis can be made in the field if compatible clinical signs and gross lesions are accompanied by a positive influenza type A test result, via commercial antigen capture immunoassay. However, because this test does not distinguish between LPAI and LPNAI, and may produce false-positive results, additional laboratory testing will be needed.

HPNAI should be suspected in any flock experiencing peracute death, high mortality, severe depression, inappetence, and a drastic decline in egg production. The presence of compatible gross lesions and the detection of Type A influenza antigen in oropharyngeal or tracheal swabs, supports a field diagnosis of HPNAI. However, these findings should be followed by more specific tests to identify and characterize the virus's antigenic and pathogenic type.

For HPNAI or LPNAI testing, collect and submit tracheal or cloacal swab samples as well as tissue samples taken from several internal organs such as the trachea, lung, spleen, cecal tonsils, or brain. Specimens should be collected from several birds, as it is not unusual for many specimens to fail to yield virus. If large numbers of birds are dead, you can submit up to 5 swab samples in one tube but do not mix swabs taken from different sites.

Blood for serum testing should be collected from several birds using standard serum tubes. If the specimens can be delivered to a laboratory within 24 hours, they should be placed on cold packs for shipping. If delivery will take longer, quick freeze the specimens in dry ice or liquid nitrogen, but do not allow the samples to thaw during transit. Freezing and storage at standard freezer temperature (-20 degrees C) is not recommended.

In the laboratory, virus isolation is usually performed by inoculation of embryonated chicken eggs with organ homogenizates or with tracheal or cloacal swabs. The AI virus is detected if the allantoic fluid of inoculated eggs hemagglutinates chicken red blood cells. The virus can be sub-typed using specific sera against all known HA and NA proteins. Specific hemagglutination inhibition is the basis of the serologic test for influenza antibodies. The ELISA (enzyme-linked immunosorbent assay) and AGID (agar gel immunodiffusion) tests can be used for determining the presence of antibody in the sera.

Any suspected case of Notifiable Avian Influenza (NAI) in the United States should be immediately reported to the State Veterinarian for the State where the case is suspected. A current list of animal health officials (State Veterinarians) contact information is available at http://www.usaha.org/members.shtml#agency . For suspected cases of NAI in other countries, notification should be given to the Chief Veterinary Officer (or OIE Country Delegate) of the country or territory where the case is suspected. A current list of Chief Veterinary Officers is available at http://www.oie.int/eng/OIE/PM/en_PM.htm?e1d1 .

Given the changes in the zoonotic potential recently seen with the emergence of human infections with the HPAI Asian H5N1 strain, it is recommended to treat any future HPAI as a potentially zoonotic disease. Seek the advice of the Public Health authorities in dealing with any outbreak action. A current list of Public Health authorities in the US is available at: www.astho.org or at http://www.statepublichealth.org/. Information on Public Health authorities outside the US is available at: http://www.who.int/countries/en/

Prevention and Control

The recommended strategy for controlling NAI is eradication. This requires 5 components including: 1) inclusion and exclusion biosecurity practices, 2) increasing host resistance through vaccination, 3) diagnostics and surveillance, 4) elimination of infected animals from the flock, and 5) educating personnel in AI control strategies.
1) Implementing biosecurity practices includes controlling human traffic, quarantining birds before introduction, proper cleaning and disinfection of facilities, keeping healthy birds away from contact with sick birds and wild birds, and incubating eggs only from clean flocks. Strict quarantine measures not only reduce the possibility of introducing Avian Influenza to a farm but also to a region or country.
2) Inactivated vaccines have been shown to be effective but are fairly expensive. Recombinant fowl poxvirus, carrying an inserted H5 gene, have shown similar efficacy in chickens. However, no vaccine will provide absolute prevention against infections or control environmental contamination. Other major drawbacks to current vaccines for controlling NAI include the labor associated with administering vaccine injections to individual birds and the need to match the vaccine to the field hemagglutination subtype in order to confer protection.
3) Diagnostics and surveillance play a critical role in controlling NAI. In the field, appropriate diagnostic samples should be collected and submitted to an accredited laboratory, capable of carrying out AI diagnosis. If NAI is suspected, field samples are inoculated into embryonated eggs, and after incubation for several days, allantoic fluid from inoculated eggs are tested for hemagglutinating activity. Upon detection of any hemaglutinating virus, a presumptive diagnosis of NAI is made and an immediate quarantine of the farms under testing should be made. This quarantine is designed to limit the movement of birds, equipment, and personnel to prevent potential viral dissemination. Agents that show hemagglutinating activity are then further identified in the laboratory by a number of techniques including the newer rapid rRT-PCR .
4) If NAI infection is confirmed by laboratory testing, all birds within the flock should be culled, utilizing humane euthanasia techniques, and disposed of properly. This depopulation effort requires the use of proper personal protective equipment (PPE) in accordance with national or international standards.
5) Finally, it is important to have personnel trained in animal disease control measures before a potential outbreak event. The success of disease control activities requires advanced preparation and familiarity with proper biosecurity and emergency management protocols
Due to the significant economic and public health implications of an AI outbreak, all cases of LPNAI and HPNAI must be reported to the State and federal veterinary authorities in order to facilitate global virus control measures.

Selected References

  1. Charlton, B. R. (ed). 2006. Avian Disease Manual, 6th ed. American Association of Avian Pathologists (AAAP), 953 College Station Road, Athens, Georgia 30602-4875.
  2. Swayne, D.E. 2008. Avian Influenza. In Foreign Animal Diseases, 7th ed. United States Animal Health Association. C. Brown and A. Torres (ed.).. Boca Publications Group, Inc. Boca Raton, FL. (http://www.usaha.org/pubs/fad.pdf)
  3. Swayne, D.E. and D.A. Halvorson. 2008. Influenza. In Diseases of Poultry, 12th ed. Y.M. Saif. et al. (ed.). Blackwell Publishing, Ames, Iowa.
  4. World Organization for Animal Health (OIE) website. 2008. www.oie.int

Thank you to the following individuals for reviewing these materials:

Dennis Senne
Alfonso Torres
Alejandro Banda
Benjamin Lucio-Martinez
Jose Bruzual
Jaime Ruiz
John Coakley

Printable View

Infectious Coryza

Infectious Coryza

Infectious Coryza

Etiology

Infectious coryza (IC) is a respiratory disease primarily affecting chickens and occasionally pheasants and guinea-fowl. The disease is caused by Avibacterium paragallinarum, a gram-negative nonmotile bacterium.

Host Range

IC primarily affects chickens. Turkeys, ducks, and other wild avian species appear to be refractory to the infection. The disease has no public health significance for humans.

Epidemiology

IC is primarily spread through chronically infected carrier birds. Airborne transmission and contaminated drinking water may help spread the infection to susceptible birds. Chickens of all ages are susceptible; however the disease is usually less severe in immature birds. In the absence of concurrent infection, infected birds typically recover in 2-3 weeks. Hens in lay typically have a shorter incubation period and the course of the disease tends to be longer. Birds that recover frequently become chronic carriers.

IC is distributed worldwide. Both commercial chickens as well as village chickens appear to be equally at risk. The disease can cause significant economic losses in intensive poultry operations, especially in multi-age farms. In developing countries, stress factors and the presence of concurrent infections frequently exacerbate losses.

Clinical Signs

The incubation period for IC is approximately 1-3 days. The severity of infection varies depending on the age, breed, environmental stress, and presence of concurrent infections.

In the mild form, typically seen in young chickens, birds may become depressed and have nasal discharge and mild swelling of the face.

In the severe form, typically seen in young adults, there is an acute infection of the upper respiratory tract. Signs may include serous to mucoid nasal discharge, swelling of the infraorbital sinuses, facial edema including swollen eyelids that do not open, swollen wattles and intermandibular space, and conjunctivitis. If the lower respiratory tract becomes involved, rales may be observed. Signs usually persist for only a few weeks, however, if secondary infection occurs, the swelling can persist for months. Feed consumption, egg production, and growth are often severely reduced.

Post-mortem Lesions

On post-mortem examination, gross lesions may be found on the mucous membranes of the nasal passages, sinuses, and ocular conjunctiva. Findings may include inflammation and catarrhal lesions. Subcutaneous edema may be found in the face, wattles, and intermandibular region. Rarely, pneumonia and airsacculitis may be present.

Differential Diagnosis

Swelling of the face and wattles must be differentiated from chronic fowl cholera, Newcastle disease, infectious bronchitis, avian influenza, avian metapneumovirus (swollen head syndrome), mycoplasmosis, and infectious laryngotracheitis. A nonpathogenic species, Avibacterium avium, may be cultured from the sinus of chickens, either alone or in combination with A. paragallinarum. A. paragallinarum is catalase negative, while nonpathogenic species are catalase positive.

Diagnosis

A smear of sinus exudate can be made and Gram stained, which will reveal Gram-negative, bipolar-staining rods with a tendency toward filament formation. The sinus exudate should be cultured on a blood agar plate, previously streaked with Staphylococcus aureus. This will serve as a feeder colony by providing V-factor. The plate should be incubated in a candle jar or CO2 incubator. Tiny dewdrop-like colonies of A. paragallinarumc will develop adjacent to the feeder colony. The organism can be further identified by biochemical tests or polymerase chain reaction (PCR). Serologic tests include agar gel precipitation and hemagglutination-inhibition.

Prevention and Control

Management practices that include all in, all out of flocks, help to prevent and control the disease. Antimicrobial therapy is very effective but it should be used according to specific residue regulations in birds producing eggs for human consumption.

Commercially available IC vaccines are inactivated whole cell bacterins. They may contain one or several isolates representing various serogroups. In severe outbreaks, autogenous vaccines are commonly used. Broilers are not commonly vaccinated against IC. In many countries, replacement layers and breeders receive two vaccinations subcutaneously or intramuscularly, at least four weeks apart, before twenty weeks of age.

Selected References

  1. Blackall, P.J. 2008. Infectious Coryza. In A Laboratory Manual for the Isolation and Identification of Avian Pathogens, 5th edition. L. Dufour-Zavala Louise et al. (ed.) OmniPress, Inc., Madison, Wisconsin.
  2. Blackall, P.J. and E.V. Soriano. 2008. In Diseases of Poultry, 12th ed. Y.M. Saif. et al. (ed.). Blackwell Publishing, Ames, Iowa.
  3. Blackall, P.J. 1999. Infectious Coryza: overview of the disease and new diagnostic options. Clin Microbiol Rev Oct;12(4):627-32. Review.
  4. Charlton, B. R. (ed). 2006. Avian Disease Manual, 6th ed. American Association of Avian Pathologists (AAAP), 953 College Station Road, Athens, Georgia 30602-4875.
  5. Glisson, J.R. 1998. Bacterial respiratory disease of poultry. Poult Sci Aug;77(8):1139-42. Review.
  6. World Organization for Animal Health (OIE) website. 2008. www.oie.int

Thank you to the following individuals for reviewing these materials:

Richard Chin
Jose Bruzual
Morella DeRosa

Printable View

Vitamin E and Selenium Deficiency

Vitamin E and Selenium Deficiency

Vitamin E and Selenium Deficiency

Etiology

Vitamin E plays multiple roles in poultry nutrition and is an essential dietary vitamin required for the normal embryonic development of birds. Diets deficient in vitamin E can lead to a variety of disorders in poultry including encephalomalacia, exudative diathesis, and muscular dystrophy.

Host Range

Vitamin E deficiency may cause clinical disease in young chickens and turkeys raised in confinement. Clinical signs usually manifest in the first few weeks of life. In adults, no outward signs of illness occur. However, the hatchability of eggs from vitamin E-deficient chickens and turkeys is reduced.

Epidemiology

Most cases of vitamin E deficiency occur in birds that are fed rations high in polyunsaturated fats (e.g. cod liver oil and soy bean oil). When vitamin E in these diets becomes oxidized (rancid), the vitamin is no longer bio-available.

Clinical Signs

In encephalomalacia, nervous signs typically begin between 15-30 days of age. However, the onset of clinical signs has been observed in chicks as young as 7 days old and as late as 56 days old. Signs may include ataxia (loss of balance and falling backward), opisthotonus, torticollis, myoclonus (repeated muscle contractions of the legs), paresis, and prostration. Birds showing neurologic signs often continue to eat.

In exudative diathesis in chicks, capillary walls become abnormally permeable and subcutaneous edema develops. This edema is often located along the ventrum of the thorax, abdomen, and under the mandible. The edema may appear to have a slightly greenish-blue color, due to the hemoglobin breakdown of the leaking red blood cells. If extensive edema develops, birds may have difficulty walking and may stand with their legs spread apart.

In turkeys fed vitamin E deficient diets, abnormalities may develop in their legs. Enlarged hocks and bowing may develop at 2-3 weeks of age. The signs may disappear by 6 weeks of age. However if the deficiency is not corrected, the disorder will reappear in a more severe form by 14-16 weeks of age.

Post-mortem Lesions

On post-mortem examination, vitamin E deficiency associated with the encephalomalacia form may produce grossly visible lesions in the central nervous system. The most common lesions that are visible occur in the cerebellum. The cerebellum may appear softened and swollen and may extend into the foramen magnum. Hemorrhages, ranging from petichiae to ecchymotic, may be visible on the surface of the cerebellum. Lesions in the cerebrum are less common. One to two days after the onset of clinical signs, necrosis may be observed grossly within the brain tissue. Areas of necrosis appear as green to yellow opaque lesions. As the condition progresses, the cerebellum may become pale and small.

In the exudative diathesis form of the disease, subcutaneous edema is usually present under the ventral skin region.

In the muscular dystrophy form of the disease, muscle fibers can undergo degeneration, resulting in pale areas or streaks that may be found within smooth muscles (e.g., gizzard), skeletal muscles (e.g. pectoral/breast), and cardiac muscles. These lesions are more commonly observed in turkeys.

Differential Diagnosis

Nutritional encephalomalacia must be differentiated from avian encephalomyelitis, Newcastle disease, and vitamin B1 deficiency. Exudative diathesis should be differentiated from gangrenous dermatitis.

Diagnosis

Analysis of the feed ration may indicate rancidity or deficiency of vitamin E and/or selenium. Care should be taken to submit truly representative feed samples. Microscopic examination of tissue lesions can be used to confirm suspected cases of vitamin E deficiency, especially for encephalomalacia and exudative diathesis.

Prevention and Control

The relationship between vitamin E and selenium is not fully understood, however selenium appears to play a critical role in protecting capillary membranes from oxidative damage. The prevention and treatment of vitamin E deficiency disorders therefore is closely tied to selenium.

If clinical signs are identified early in the course of exudative diathesis and nutritional myopathy, they are often treated successfully by administering vitamin E and selenium in the feed. Encephalomalacia does not always respond to therapy.

Each of these disorders can be prevented by proper dietary supplementation with vitamin E and selenium. Synthetic antioxidants can prevent encephalomalacia, inorganic selenium can prevent exudative diathesis, and cystine can help in the prevention of muscular dystrophy.

Selected References

  1. Charlton, B. R. (ed). 2006. Avian Disease Manual, 6th ed. American Association of Avian Pathologists (AAAP), 953 College Station Road, Athens, Georgia 30602-4875.
  2. Klasing, K.C. 2008. Nutritional diseases. In Diseases of Poultry, 12th ed. Y.M. Saif. et al. (ed.). Blackwell Publishing, Ames, Iowa.
  3. World Organization for Animal Health (OIE) website. 2008. www.oie.int

Thank you to the following individuals for reviewing these materials:

Richard Chin
Jaime Ruiz
Jose Bruzual

Printable View