This disease is a fatal toxaemia in lambs, sheep, goats, calves and seldom in adult cattle. The disease is manifested by diarrhoea, involuntary contraction of muscles, paralysis and sudden death. It occurs after a sudden change to a better, more nutritious diet. The disease is often noted in sheep that have been fed heavy grain, and in animals which graze on lush growing pastures. Clostridium perfringens multiplies in abomasum and intestine and produces toxin which paralyses the vital centres in brain and damages endothelium of blood vessels. The disease occurs extensively in particular in Southern Africa but is well controlled by vaccination.
Antemortem findings :
Short course of the illness (2 – 12 hours) in lambs and longer course (24 hours) in sheep Animal found dead without previous sign of the disease Dullness and depression Rapid shallow respiration Loss of appetite and frothing Muscular contractions Green pasty diarrhoea Grinding of the teeth and muscular tremor Logging behind the flock Staggering and recumbency.
Postmortem findings :
No lesions in peracute cases Large amount of clear, straw coloured pericardial fluid Petechial haemorrhages of the heart muscle Congestion of the abomasal and intestinal mucosa and liver Soft pulpy kidneys a few hours after death is characteristic of this disease Overload of the rumen and abomasum with concentrate Haemorrhage and edema in sheep brain Rapid decomposition of the carcass.
Judgement :
Carcass of an animal affected with enterotoxaemia is condemned.
Differential diagnosis :
Sudden death in lambs: pasteurellosis, hypocalcemia and hypomagnesemia (reduced blood calcium and magnesium), polioencephalomalatia (less acute form), acute rumen impaction (no convulsions are present and the course is longer) and other septicemias. Adult sheep: rabies, acute lead poisoning, pregnancy toxaemia and louping-ill.
Sunday, September 9, 2007
Foot and mouth disease (FMD)
FMD is an acute viral and extremely contagious disease of cloven footed animals such as cattle, sheep, goats, pigs and antelope. It is manifested by vesicles and erosions in the muzzle, nares, mouth, feet, teats, udder and pillar of the rumen. There are three main strains of viruses causing FMD, namely A, O and C. Three additional strains, SAT 1, SAT 2 and SAT 3 have been isolated from Africa and a further strain ASIA-1 from Asia and the Far East.
Transmission:
Direct and indirect contact with infected animals and their secretions including saliva, blood, urine, faeces, milk and semen, aerosol droplet dispersion, infected animal by-products, swill containing scraps of meat or other animal tissue and fomites and vaccines.
Antemortem findings:
Before vesicle formation:Incubation is 1 - 5 days or longer Morbidity: Nearly 100 % Mortality: variable depending on the strain of virus and its virulence and susceptibility of host; 50 % in young animals, 5 % in adults Fever up to 41.7°C Dullness Lack of appetite Drastic drop in milk production. Uneasiness and muscle tremors.
Vesicle formation:Smacking and quivering of lips Extensive salivation (Fig. 45) and drooling Shaking of feet and lameness The vesicles and later erosions are commonly found on the muzzle, tongue, oral cavity, teat and on the skin between and above the hoofs of the feet. In more chronic cases in cattle the hoof become loose and the animal may walk with characteristic “clicking” sound (Slippering).
Some strains of FMD, particularly in swine, sheep and goats cause erosions instead of vesicles.
Postmortem findings :Necrosis of heart muscle(tiger heart), usually only in young acutely infected animals.Ulcerative lesions on tongue, palate, gums, pillars of the rumen and feet.
Judgement :
In countries or in zones within a country free or nearly free of FMD diseased or suspect animals are prohibited to be admitted in an abattoir or slaughtered. If FMD is suspected on postmortem examination the carcass and viscera are condemned and appropriate action recommended by the regulatory authorities of the country must be taken. In countries where this disease is present, the judgement should be in accordance with the current animal health requirements, and consisted with effective public health protection. Particular attention should be paid to secondary bacterial infections and general findings. Sanitary measures should be taken to comply with national animal health policy.
Remarks : Latent infections with Salmonella organisms were reported in animals affected with FMD.
Differential diagnosis in bovine and ovine species : Vesicular stomatitis, allergic stomatitis, feedlot glossitis, photosensitization, bluetongue, rinderpest, infectious bovine rhinotracheitis, malignant catarrhal fever, bovine papular stomatitis, bovine viral diarrhoea, pseudocowpox, ovine pox, contagious ecthyma, footrot, mycotoxicosis and increased salt in concentrate.Discussion : In order to prevent the spread of the virus in the abattoir, the equipment and room should be disinfected with 2 % NaOH (caustic soda). In some countries sodium carbonate (Na2CO3) is used. The vehicle conveying diseased animals should also be disinfected and abattoir personnel leaving the abattoir should pass through a footbath with 1 % solution of NaOH.The virus of FMD can survive in meat and meat products for a considerable length of time. Outside the pH range of 6 – 9, viral infectivity is destroyed. A bovine carcass matured at above +2°C produces a drop in the pH of muscle tissue to between 5.3 – 5.7 within 24 hours of slaughter. This is caused by the formation of sarcolactic acid. Quick freezing of the meat arrests acid production and consequently the virus remains infective for about 6 months. In salted meat at 4°C, the virus is still infective in bone marrow and lymph nodes for 6 months. In blood clots in large vessels of cattle and swine, the virus is infective for 2 months. The virus is inactivated by ultraviolet rays, acetic acid, 2 % lye and ethylene oxide. At high temperatures, the virus is only active for a short period. 2 % NaOH solution inactivates the virus in 1 – 2 minutes. In dry refuse in stalls, the virus remains infective for 14 days, 3 days on soil surfaces in summer compared to 39 days in fall. It is also infective for 39 days in urine and for 20 weeks on hay dried at 22°C. The virus can be destroyed with 0.5 % citric or lactic acid, by cooking meat to an internal temperature of 69°C and by pasteurization processes of milk.
Transmission:
Direct and indirect contact with infected animals and their secretions including saliva, blood, urine, faeces, milk and semen, aerosol droplet dispersion, infected animal by-products, swill containing scraps of meat or other animal tissue and fomites and vaccines.
Antemortem findings:
Before vesicle formation:Incubation is 1 - 5 days or longer Morbidity: Nearly 100 % Mortality: variable depending on the strain of virus and its virulence and susceptibility of host; 50 % in young animals, 5 % in adults Fever up to 41.7°C Dullness Lack of appetite Drastic drop in milk production. Uneasiness and muscle tremors.
Vesicle formation:Smacking and quivering of lips Extensive salivation (Fig. 45) and drooling Shaking of feet and lameness The vesicles and later erosions are commonly found on the muzzle, tongue, oral cavity, teat and on the skin between and above the hoofs of the feet. In more chronic cases in cattle the hoof become loose and the animal may walk with characteristic “clicking” sound (Slippering).
Some strains of FMD, particularly in swine, sheep and goats cause erosions instead of vesicles.
Postmortem findings :Necrosis of heart muscle(tiger heart), usually only in young acutely infected animals.Ulcerative lesions on tongue, palate, gums, pillars of the rumen and feet.
Judgement :
In countries or in zones within a country free or nearly free of FMD diseased or suspect animals are prohibited to be admitted in an abattoir or slaughtered. If FMD is suspected on postmortem examination the carcass and viscera are condemned and appropriate action recommended by the regulatory authorities of the country must be taken. In countries where this disease is present, the judgement should be in accordance with the current animal health requirements, and consisted with effective public health protection. Particular attention should be paid to secondary bacterial infections and general findings. Sanitary measures should be taken to comply with national animal health policy.
Remarks : Latent infections with Salmonella organisms were reported in animals affected with FMD.
Differential diagnosis in bovine and ovine species : Vesicular stomatitis, allergic stomatitis, feedlot glossitis, photosensitization, bluetongue, rinderpest, infectious bovine rhinotracheitis, malignant catarrhal fever, bovine papular stomatitis, bovine viral diarrhoea, pseudocowpox, ovine pox, contagious ecthyma, footrot, mycotoxicosis and increased salt in concentrate.Discussion : In order to prevent the spread of the virus in the abattoir, the equipment and room should be disinfected with 2 % NaOH (caustic soda). In some countries sodium carbonate (Na2CO3) is used. The vehicle conveying diseased animals should also be disinfected and abattoir personnel leaving the abattoir should pass through a footbath with 1 % solution of NaOH.The virus of FMD can survive in meat and meat products for a considerable length of time. Outside the pH range of 6 – 9, viral infectivity is destroyed. A bovine carcass matured at above +2°C produces a drop in the pH of muscle tissue to between 5.3 – 5.7 within 24 hours of slaughter. This is caused by the formation of sarcolactic acid. Quick freezing of the meat arrests acid production and consequently the virus remains infective for about 6 months. In salted meat at 4°C, the virus is still infective in bone marrow and lymph nodes for 6 months. In blood clots in large vessels of cattle and swine, the virus is infective for 2 months. The virus is inactivated by ultraviolet rays, acetic acid, 2 % lye and ethylene oxide. At high temperatures, the virus is only active for a short period. 2 % NaOH solution inactivates the virus in 1 – 2 minutes. In dry refuse in stalls, the virus remains infective for 14 days, 3 days on soil surfaces in summer compared to 39 days in fall. It is also infective for 39 days in urine and for 20 weeks on hay dried at 22°C. The virus can be destroyed with 0.5 % citric or lactic acid, by cooking meat to an internal temperature of 69°C and by pasteurization processes of milk.
DISEASES OF THE NEWBORN
This includes the principles of diseases which occur during the first month of life in animals born alive at term.
1)Prenatal disease:
Fetal diseases: Diseases of the fetus during intrauterine life, e.g. prolonged gestation, congenital defects, abortion, fetal deaths with resorption or mummification.
2) Parturient diseases:
diseases associated with dystokia causing cerebral anoxia, injuries of skeleton and soft tissues.
3) Postnatal diseases:
(A) Early postnatal diseases: within 48 hours e.g. malnutrition due to poor mothering, hypothermia due to exposure to cold, low vigor in neonates due to malnutrition, special disease (Navil ill and Collibacillosis).
(B) delayed postnatal diseases: within 2 -7 days after parturition e.g. mammary incompetence resulting in starvation, increased susceptibility to infection due to hypoglobulinemia such as lamb dysentery, colibacillosis and foal septicemia.
(C) late postnatal disease: within 1 - 4 week of life e.g. white muscle disease, enetrotoxemia.In summary, the causes of mortality in newborn lambs are largely physical and environmental and occur immediately at birth or shortly thereafter.In calves, the major causes of mortality are with dystokia and with neonatal diarrhea in postnatal life. Meanwhile, lambs are susceptible to physical and environmental influences.
1)Prenatal disease:
Fetal diseases: Diseases of the fetus during intrauterine life, e.g. prolonged gestation, congenital defects, abortion, fetal deaths with resorption or mummification.
2) Parturient diseases:
diseases associated with dystokia causing cerebral anoxia, injuries of skeleton and soft tissues.
3) Postnatal diseases:
(A) Early postnatal diseases: within 48 hours e.g. malnutrition due to poor mothering, hypothermia due to exposure to cold, low vigor in neonates due to malnutrition, special disease (Navil ill and Collibacillosis).
(B) delayed postnatal diseases: within 2 -7 days after parturition e.g. mammary incompetence resulting in starvation, increased susceptibility to infection due to hypoglobulinemia such as lamb dysentery, colibacillosis and foal septicemia.
(C) late postnatal disease: within 1 - 4 week of life e.g. white muscle disease, enetrotoxemia.In summary, the causes of mortality in newborn lambs are largely physical and environmental and occur immediately at birth or shortly thereafter.In calves, the major causes of mortality are with dystokia and with neonatal diarrhea in postnatal life. Meanwhile, lambs are susceptible to physical and environmental influences.
Displaced Abomasum
The abomasum is the fourth, or "true," stomach in the cow. It normally lies low down in the right front quadrant of the abdomen, just inside the seventh through 11th ribs.
Adjacent to the abomasum, on the left side of the abdomen, is the large first stomach, or rumen.
The abomasum occasionally may be displaced to the left of the rumen and upwards when its muscular wall loses tone and the stomach becomes filled with gas. This condition is left abomasal displacement.
Abomasum displaced to the left of rumen. In another displacement, the abomasum rides up high on the right side underneath the last ribs and again is enlarged with gas and some fluid. Sometimes the right displaced abomasum turns into a much more serious and often fatal abomasal torsion.In either left or right abomasal displacement, the entrance and exit to the stomach are slightly kinked. The kinks, together with the gas and fluid distension, slow food passage to a slower-than-normal rate. The signs seen in the cow are usually dullness; a marked drop in feed intake, especially of concentrates; a drastic reduction in milk yield; and scanty feces either firm or diarrheic. Most left displacements occur within one month after calving. Heavy yielding and older dairy cows are usually affected. Right displacements are spread out more throughout the three months after calving.
Cause:
Abomasal displacement is seen almost exclusively in dairy breeds. Several theories attempt to explain the condition, but no definite single cause is known. Heavy concentrate and low roughage feeding programs produce an enlarged abomasum while rumen size decreases. Such diets in late pregnancy may play a role in producing the condition. Heavy grain feeding and sudden changes in levels of grain feeding are often suspected. Incidence of abomasal displacements has increased tremendously in the last two decades, a period of rapidly improving management and feeding practices. This condition seems to be a bad side-effect of otherwise good animal husbandry practices.
Diagnosis:
The veterinarian diagnoses displacement of the abomasum by compiling an accurate history of the animal, assessing clinical signs and listening with a stethoscope to the abdominal sounds. Abnormal sounds are produced when the abomasum becomes trapped high up on the left or right side and enlarged with gas. The veterinarian must rule out several other conditions that cause obstruction of the gut before he or she can make an accurate diagnosis. Sometimes the veterinarian must surgically enter the abdomen to arrive at the diagnosis.Many times, hauling the animal in a truck produces sufficient movement of the abdominal organs to partially correct the condition. The stockman may bring an affected cow to the veterinarian only to find that she is normal upon arrival at the veterinary hospital. In these instances, however, the condition usually recurs in a few days.
Treatment:
Treatment requires replacing the abomasum in its normal position. Preferably, the veterinarian also prevents recurrence by tacking the abomasum to the body wall. Often the cow gets temporary relief if she is cast on her right side and then rolled onto her back, permitting the abomasum to "float" back into its normal position. In nearly all such cases, however, the problem recurs within a few days. Permanent correction is best achieved by surgically entering the abdomen, emptying the gas, replacing the abomasum and suturing it down to the body wall.
The results of surgery are usually excellent. Complications are seen if the diagnosis is made several weeks after the displacement occurs. During that time, body condition is lost and abomasal ulcers may develop and sometimes perforate to produce a peritonitis.
Prevention:
To prevent the development of displaced abomasum, ensure that calculated total crude fiber in the ration exceeds 17 percent. Make all feed changes near calving time slowly, especially any increase in grain or other concentrates. Give cows plenty of time to reach peak production. Encourage exercise. Any case of ketosis in a newly calved cow could be a possible abomasal displacement. Seek veterinary help if you suspect a problem.
When chicks can't stand the heat
When chicks can't stand the heatBy Ron Meijerhof, Senior Technical Specialist, Hybro B.V. - Modern, fast growing, high yield broiler lines produce a lot of heat during incubation.If we measure the embryo (egg shell) temperature at the end of incubation with an infra-red ear thermometer, we often observe values of 103-104°F, when we are actually looking for 100-100.5°F as optimum.
The typical effects of these high embryo temperatures are easily observed at hatch and during take off, including: Increased levels of dead in shells, late deathsHigh temperatures at the end of incubation are a risk to the survival of the embryo, resulting in an increase in the number of late deads and embryos that are too weak to hatch. When late mortality (> 15 days) is over 3-4 per cent, high embryo temperature is often the cause.
Weak chicks, difficulty standingChicks that do survive high temperatures are weak because they almost died. Especially during take off, when the chicks are transported - eg. on a moving belt, weak chicks sit or even lie down, and when tipped over onto their side or back, will take a long time to get up again. This is bad sign, as good quality chicks tend to stand and try to balance on the moving floor. Small, pale, underdeveloped chicksAt high temperature, embryos utilise less yolk for development and stay smaller. As the pigment for the feathers is stored in the yolk, this means that the feathers stay more pale.
Poor yolk uptake, unhealed navelsReduced yolk utilisation leaves a bigger yolk in the chick. This means that the small, less developed embryo has to close the navel over a large yolk residue, causing more navel problems. Overly high temperatures cause black navels (button navels), while too low a temperature is usually associated with string navels. Blood in and on the shells, navel/yolk sac mortalityDue to difficulties in closing the navel properly, the chick’s navel is still unhealed on hatching. This bleeding navel shows as blood in and on the shells, and allows bacteria to penetrate the body cavity after hatching, causing navel/yolk sac mortality. Full bellies, hard yolk sacsLarge yolk residues can be measured by opening the chick, or by gently squeezing the chick’s belly. A plump, full belly indicates a large yolk residue and is associated with high embryo temperatures at the end of incubation. Malposition “head over wing”, skew heads, cross beaksThe normal position of an embryo in the shell just before hatch is with its head under the right wing. In this position, the head is protected from the shell by the wing and the bird uses the wing to move through the shell. At high temperatures, the embryo’s head remains on the wing and a high number with this malposition will be observed when breaking out. When the head is not protected by the wing, its right side is pushed against the shell. As the hatchling’s bones are very soft, the skull will form in the shape of the shell and the head will be skew, with its left side rounder then the right. This can be observed during a break out, but also just after hatch, as not all chicks in this malposition will be unable to hatch. When the pressure is too severe, the upper beak will also be pushed away by the shell, resulting in a cross beak. The embryo uses its wing to move through the shell, in order to pip it open. When the head is blocking the wing, the chick can’t move and is stuck in one position. As it is then unable to open the shell properly, it has to pip a hole and force the shell to break from that single hole. This results in an increased number of pips, and not every chick will make it. Red spots on beak, dirty nostrils, red hocksIf the embryo can’t move easily, it breaks the shell by forcing it with its beak. This will irritate the beak, creating a little red spot on the top, just there where the comb starts. The nostrils will also become dirty due to the difficult hatching process. As the chick uses it legs to free itself from the shell, and because the weakened, overheated chick will sit down more, the hocks will be irritated and red. Recognising these symptoms as indicative of overly high embryo temperature at the end of incubation is a very good start to solving the problem.
The typical effects of these high embryo temperatures are easily observed at hatch and during take off, including: Increased levels of dead in shells, late deathsHigh temperatures at the end of incubation are a risk to the survival of the embryo, resulting in an increase in the number of late deads and embryos that are too weak to hatch. When late mortality (> 15 days) is over 3-4 per cent, high embryo temperature is often the cause.
Weak chicks, difficulty standingChicks that do survive high temperatures are weak because they almost died. Especially during take off, when the chicks are transported - eg. on a moving belt, weak chicks sit or even lie down, and when tipped over onto their side or back, will take a long time to get up again. This is bad sign, as good quality chicks tend to stand and try to balance on the moving floor. Small, pale, underdeveloped chicksAt high temperature, embryos utilise less yolk for development and stay smaller. As the pigment for the feathers is stored in the yolk, this means that the feathers stay more pale.
Poor yolk uptake, unhealed navelsReduced yolk utilisation leaves a bigger yolk in the chick. This means that the small, less developed embryo has to close the navel over a large yolk residue, causing more navel problems. Overly high temperatures cause black navels (button navels), while too low a temperature is usually associated with string navels. Blood in and on the shells, navel/yolk sac mortalityDue to difficulties in closing the navel properly, the chick’s navel is still unhealed on hatching. This bleeding navel shows as blood in and on the shells, and allows bacteria to penetrate the body cavity after hatching, causing navel/yolk sac mortality. Full bellies, hard yolk sacsLarge yolk residues can be measured by opening the chick, or by gently squeezing the chick’s belly. A plump, full belly indicates a large yolk residue and is associated with high embryo temperatures at the end of incubation. Malposition “head over wing”, skew heads, cross beaksThe normal position of an embryo in the shell just before hatch is with its head under the right wing. In this position, the head is protected from the shell by the wing and the bird uses the wing to move through the shell. At high temperatures, the embryo’s head remains on the wing and a high number with this malposition will be observed when breaking out. When the head is not protected by the wing, its right side is pushed against the shell. As the hatchling’s bones are very soft, the skull will form in the shape of the shell and the head will be skew, with its left side rounder then the right. This can be observed during a break out, but also just after hatch, as not all chicks in this malposition will be unable to hatch. When the pressure is too severe, the upper beak will also be pushed away by the shell, resulting in a cross beak. The embryo uses its wing to move through the shell, in order to pip it open. When the head is blocking the wing, the chick can’t move and is stuck in one position. As it is then unable to open the shell properly, it has to pip a hole and force the shell to break from that single hole. This results in an increased number of pips, and not every chick will make it. Red spots on beak, dirty nostrils, red hocksIf the embryo can’t move easily, it breaks the shell by forcing it with its beak. This will irritate the beak, creating a little red spot on the top, just there where the comb starts. The nostrils will also become dirty due to the difficult hatching process. As the chick uses it legs to free itself from the shell, and because the weakened, overheated chick will sit down more, the hocks will be irritated and red. Recognising these symptoms as indicative of overly high embryo temperature at the end of incubation is a very good start to solving the problem.
Coccidiosis of Turkeys
Introduction:
Infection of turkeys with Eimeria spp. This disease is not very common in commercially reared turkeys though most turkey growers receive preventative medication for at least part of their lives. Five species of Eimeria have been identified that cause lesions in turkeys, of which two are associated with significant disease effects. E. meleagrimitis affects the upper small intestine, while E. adenoides affects the caecae and rectum. E. gallopavonis and E. meleagridis affect the lower small intestine rectum and caecae, while E. dispersa is found in the small intestine.
Signs:
Huddling. Weight loss. Depression. Watery diarrhoea that may occasionally be blood stained or contain clumps of mucus or shed mucosa. Tucked appearance, ruffled feathers. Post-mortem lesions.
The affected area of intestine shows thickening of the wall and dilation. The contents may be haemorrhagic or be watery with white material shed from the mucosa.
Diagnosis:
Signs, lesions, microscopic exam of scrapings (oocysts, gamonts). Differentiate from necrotic enteritis.
Treatment:
Toltrazuril, Sulphonamides (e.g. Sulphaquinoxaline), Amprolium.
Prevention:
The ionophore coccidiostats lasalocid and monensin are routinely used in turkey growers, typically to 12 weeks of age. Diclazuril is also used for this purpose. Dosage levels of ionophores may be critical to efficacy and safety. Exposure of previously unmedicated birds to these compounds can cause toxicity. Salinomycin is toxic for turkeys even at very low doses. Avoid use of tiamulin in ionophore treated birds.
Sunday, September 2, 2007
Chicken Anaemia
A viral disease of chickens caused by Chicken Anaemia Virus or CAV. Prior to confirmation that it is in fact a virus it was known as Chicken Anaemia Agent or CAA.
Mortality is typically 5-10% but may be up to 60% if there are predisposing factors present such as intercurrent disease (Aspergillosis, Gumboro, Inclusion body heptatitis etc.) or poor management (e.g. poor litter quality).
Transmission is usually vertical during sero-conversion of a flock in lay, lateral transmission may result in poor productivity in broilers.
The virus is resistant to pH 2, ether, chloroform, heat (70°C for 1 hour, 80°C for 5 minutes) and many disinfectants even for 2 hours at 37°C. Hypochlorite appears most effective in vitro.
Signs:
Poor growth. Pale birds. Sudden rise in mortality (usually at 13-16 days of age). No clinical signs or effect on egg production or fertility in parent flock during sero-conversion. Post-mortem lesionsPale bone marrow. PCV of 5-15% (normal 27-36%). Atrophy of thymus and bursa. Discoloured liver and kidney. Gangrenous dermatitis on feet, legs wings or neck. Acute mycotic pneumonia
Diagnosis:
Gross lesions, demonstration of ongoing sero-conversion in parent flock, virus may be isolated in lymphoblastoid cell line (MDCC-MSB1).
Treatment:
Good hygiene and management, and control of other diseases as appropriate, may be beneficial. If gangrenous dermatitis is a problem then periodic medication may be required.
Prevention:
Live vaccines are available for parents, their degree of attenuation is variable. They should be used at least 6 weeks prior to collecting eggs for incubation. Their use may be restricted to those flocks that have not sero-converted by, say, 15 weeks.
Immunity:
there is a good response to field challenge (in birds over 4 weeks of age) and to attenuated live vaccines.
Mortality is typically 5-10% but may be up to 60% if there are predisposing factors present such as intercurrent disease (Aspergillosis, Gumboro, Inclusion body heptatitis etc.) or poor management (e.g. poor litter quality).
Transmission is usually vertical during sero-conversion of a flock in lay, lateral transmission may result in poor productivity in broilers.
The virus is resistant to pH 2, ether, chloroform, heat (70°C for 1 hour, 80°C for 5 minutes) and many disinfectants even for 2 hours at 37°C. Hypochlorite appears most effective in vitro.
Signs:
Poor growth. Pale birds. Sudden rise in mortality (usually at 13-16 days of age). No clinical signs or effect on egg production or fertility in parent flock during sero-conversion. Post-mortem lesionsPale bone marrow. PCV of 5-15% (normal 27-36%). Atrophy of thymus and bursa. Discoloured liver and kidney. Gangrenous dermatitis on feet, legs wings or neck. Acute mycotic pneumonia
Diagnosis:
Gross lesions, demonstration of ongoing sero-conversion in parent flock, virus may be isolated in lymphoblastoid cell line (MDCC-MSB1).
Treatment:
Good hygiene and management, and control of other diseases as appropriate, may be beneficial. If gangrenous dermatitis is a problem then periodic medication may be required.
Prevention:
Live vaccines are available for parents, their degree of attenuation is variable. They should be used at least 6 weeks prior to collecting eggs for incubation. Their use may be restricted to those flocks that have not sero-converted by, say, 15 weeks.
Immunity:
there is a good response to field challenge (in birds over 4 weeks of age) and to attenuated live vaccines.
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