(ND), an influenza-like viral infection of birds that causes epidemics in domestic poultry, and which can spread to humans. The disease was first seen in the English city of Newcastle. It is caused by a single-stranded RNA virus belonging to the viral family Paramyxoviridae. The ND virus is quite stable and can remain infectious for long periods even at low temperature. Newcastle disease is sometimes called avian influenza, but should not be confused with the true influenza strains that infect poultry.
Both wild and pet birds may contract the ND virus. Chickens are among the most susceptible birds; their eggs may also be infected, but can be made safe by heating. The most dangerous strains of the virus, which are rare in the United States, may cause severe illness in birds, including pneumonia, gastrointestinal disease, or encephalitis (inflammation of the brain) leading to paralysis. In chickens and turkeys the disease may be so severe that nearly all those in an infected flock die within three days before any signs of illness have developed. In pet birds the disease ranges from very mild to severe.
Newcastle disease is transmitted by contact with infected birds themselves, which emit the virus when breathing, or with infected products, clothing, feed, and even farm equipment. Once ND is established it is essential to thoroughly disinfect all contaminated objects using strong chemicals.
Newcastle disease is a zoonosis, a disease normally occurring in animals that is communicable to humans. Illness in humans can result from close contact with infectious birds, but is most frequent in persons who work in laboratories where samples from infected birds are analyzed. Generally, headaches and flulike symptoms develop and last four to seven days. A mild, superficial inflammation of the eyes with reddening (conjunctivitis) is common. In humans infected by the virus serious illness or permanent vision impairment is rare. When a pet bird develops ND, the owner should be aware that it may continue to shed the virus, or be contagious, for several months.
Sunday, June 15, 2008
Tay-Sachs disease
a recessive disorder most common among persons of Middle and Eastern European Jewish origin, and detectable by prenatal tests. Infants appear normal at birth but become listless and inattentive during the first few months of life. An early sign is an exaggerated startle response to sound. Rapidly progressive symptoms include retardation, paralysis, blindness, seizures, and cherry-red retinal spots; death by age 3 is common. Tay-Sachs disease is caused by abnormally low activity of the enzyme hexosaminidase A, resulting in the formation of sphingolipids in the brain
Some diseases of Cats
A good veterinarian is of primary importance to any pet owner. Cat owners should choose a veterinarian who is interested in cats and has treated them successfully. Call a veterinarian at once for advice if a cat seems ill; never try to diagnose a disease or treat the animal yourself.
The most widespread and serious infectious disease of cats is panleucopenia—often called cat distemper, viral enteritis, or cat typhoid. Its onset is sudden and severe, with reduced activity, fever, loss of appetite, and vomiting of yellow fluid. Every cat should be immunized to protect against this disease. The first vaccination is usually given when the animal is about ten weeks old, and boosters should be given annually.
Upper respiratory infections are exceedingly common, and the best-known are pneumonitis and rhinotracheitis. Symptoms resemble those of the common cold in humans and distemper in dogs. The cat's “colds,” however, cannot be passed on to humans or dogs although they are highly infectious for other cats.
Rabies is an invariably fatal viral disease. It is transmitted by the bite of a rabid animal. Rabies has become established among the wild animals in many parts of the world. A cat that roams outdoors in an area where rabies occurs may be bitten by a rabid animal. It is therefore advisable that all cats in such areas be given preventive vaccinations.
A cat that swallows large amounts of fur while grooming may develop fur balls or hair balls. Occasionally these may cause ulcers or completely obstruct the digestive tract. Prevention, in the form of frequent combing and brushing, is best. If fur balls occur in spite of grooming, the animal may be given a teaspoonful of mineral oil in its food or a dab of petroleum jelly on its paws twice a week.
Bite wounds may become infected and cause serious problems. Contrary to popular belief, the cat cannot heal the wound by licking it. It is better to seek veterinary attention as soon as possible.
Many apparently normal cats have tiny mineral crystals in their urine. For reasons not yet fully understood, these crystals often clump together to form sandlike particles or small stones which may cause irritation or obstruction of the urinary passages. A urinary obstruction is a grave emergency and must be treated immediately by a veterinarian.
Ear irritations are most often caused by mites, which are tiny parasites about as large as the point of a pin. The insides of the ears look as though they are filled with a dry brown dirt. The cat shakes its head often and may scratch the outside of the ears and neck persistently. A few drops of any mild oil massaged into the ear canal suffocates the mites and loosens the dirt, which may then be removed with cotton-tipped sticks.
Any cat may get fleas. These small jumping insects live in the cat's fur and suck blood through the animal's skin. Products for treatment are readily available, but use only a preparation labeled safe for cats, and use it strictly as directed.
Worms are a common intestinal parasite of cats. An owner should never try to worm a cat without the advice of a veterinarian. There are several different types of worms, each requiring a different kind of drug for control.
Ringworm, a fungal skin disease, is probably the only infection that is clearly and commonly passed from cat to man. Simple sanitary measures such as keeping pets off the table and washing the hands after handling a cat eliminate most possible risks.
Cats may be poisoned by a variety of substances. They may eat poisonous plants—which include rhododendron, hyacinth, poinsettia, and ivy. Waxes, cleaning fluids, disinfectants, detergents, and mothballs may be toxic or irritating. Antifreeze, weed killers, insecticides, and rodent poisons are outdoor hazards. Cats react adversely to many chemicals and drugs, such as aspirin or iodine, that are safe for humans or other animals. They should never be given medicines not labeled safe for cats or prescribed by a veterinarian.
The most widespread and serious infectious disease of cats is panleucopenia—often called cat distemper, viral enteritis, or cat typhoid. Its onset is sudden and severe, with reduced activity, fever, loss of appetite, and vomiting of yellow fluid. Every cat should be immunized to protect against this disease. The first vaccination is usually given when the animal is about ten weeks old, and boosters should be given annually.
Upper respiratory infections are exceedingly common, and the best-known are pneumonitis and rhinotracheitis. Symptoms resemble those of the common cold in humans and distemper in dogs. The cat's “colds,” however, cannot be passed on to humans or dogs although they are highly infectious for other cats.
Rabies is an invariably fatal viral disease. It is transmitted by the bite of a rabid animal. Rabies has become established among the wild animals in many parts of the world. A cat that roams outdoors in an area where rabies occurs may be bitten by a rabid animal. It is therefore advisable that all cats in such areas be given preventive vaccinations.
A cat that swallows large amounts of fur while grooming may develop fur balls or hair balls. Occasionally these may cause ulcers or completely obstruct the digestive tract. Prevention, in the form of frequent combing and brushing, is best. If fur balls occur in spite of grooming, the animal may be given a teaspoonful of mineral oil in its food or a dab of petroleum jelly on its paws twice a week.
Bite wounds may become infected and cause serious problems. Contrary to popular belief, the cat cannot heal the wound by licking it. It is better to seek veterinary attention as soon as possible.
Many apparently normal cats have tiny mineral crystals in their urine. For reasons not yet fully understood, these crystals often clump together to form sandlike particles or small stones which may cause irritation or obstruction of the urinary passages. A urinary obstruction is a grave emergency and must be treated immediately by a veterinarian.
Ear irritations are most often caused by mites, which are tiny parasites about as large as the point of a pin. The insides of the ears look as though they are filled with a dry brown dirt. The cat shakes its head often and may scratch the outside of the ears and neck persistently. A few drops of any mild oil massaged into the ear canal suffocates the mites and loosens the dirt, which may then be removed with cotton-tipped sticks.
Any cat may get fleas. These small jumping insects live in the cat's fur and suck blood through the animal's skin. Products for treatment are readily available, but use only a preparation labeled safe for cats, and use it strictly as directed.
Worms are a common intestinal parasite of cats. An owner should never try to worm a cat without the advice of a veterinarian. There are several different types of worms, each requiring a different kind of drug for control.
Ringworm, a fungal skin disease, is probably the only infection that is clearly and commonly passed from cat to man. Simple sanitary measures such as keeping pets off the table and washing the hands after handling a cat eliminate most possible risks.
Cats may be poisoned by a variety of substances. They may eat poisonous plants—which include rhododendron, hyacinth, poinsettia, and ivy. Waxes, cleaning fluids, disinfectants, detergents, and mothballs may be toxic or irritating. Antifreeze, weed killers, insecticides, and rodent poisons are outdoor hazards. Cats react adversely to many chemicals and drugs, such as aspirin or iodine, that are safe for humans or other animals. They should never be given medicines not labeled safe for cats or prescribed by a veterinarian.
Bacillary dysentery
(or shigellosis), an infectious disease of the digestive system. Its symptoms are diarrhea, fever, stomach pain, and vomiting. It is transmitted by the Shigella bacterium in contaminated food and water. The incubation period is from one to seven days. The disease is treated by drinking plenty of fluids and taking antibiotics, and preventive measures include improved sanitation and food-handling methods,
Lyme disease
tick-borne microbial disease first recognized in 1975 in Lyme, Conn. In that year two children in Lyme developed swollen and painful joints and were diagnosed as having juvenile rheumatoid arthritis. Their parents learned that many other children and adults in the area had been diagnosed with the same disease. Because rheumatoid arthritis does not usually manifest itself in clusters, the parents informed researchers at Yale University in New Haven, Conn., of the developing problem.
Ticks and Spirochetes
By the late 1970s researchers had traced the cause to a microorganism transmitted by the deer tick Ixodes dammini (now called I. scapularis), which is common in the wooded and grassy areas of Lyme, Conn. In 1982 the actual bacterium responsible for the disease was identified and named Borrelia burgdorferi, after Willy Burgdorfer of Rocky Mountain Laboratories in Hamilton, Mont., who isolated the spirochete, or spiral-shaped organism.
The disease has been identified in other continents of the world including Africa, Asia, Australia, and Europe. In the United States the disease occurs most often in the Northeast, Minnesota, and northern California. Between 15 and 30 percent of all I. scapularis ticks in the larval and nymph stages in the northeastern United States are infected with the B. burgdorferi microbe. About 50 percent of the adult ticks are infected. Between 1 and 3 percent of people in the Northeast who are bitten by an infected tick go on to develop Lyme disease. In northern California the bacterium is carried by the tick I. pacificus. The incidence of human infection with Lyme disease in California is much lower than that in the Northeast because the I. pacificus tick feeds more often on lizards and other animals that are more resistant to infection with the B. burgdorferi microbes.
I. scapularis ticks have a two-year life cycle that includes three feeding sessions. In the first summer, larva may feed on a bird, or on an infected or uninfected mouse. The following spring a nymph that fed as a larva on an infected mouse may feed on a bird, mouse, dog, or human, often transmitting the infection. In the fall an infected adult tick may feed on a deer, horse, dog or human, likewise transmitting the infection. Because the B. burgdorferi microbes are kept alive in part of the mouse population, tick larva become infected each summer if they feed on an infected mouse, thus continuing the cycle.
Course of the Disease
A person may contract the disease when an infected tick, usually in the nymph stage of development, attaches itself to the person's skin and stays attached for 36 to 48 hours. It takes that long for the B. burgdorferi microbes to start to multiply in the tick's gut and travel to its salivary glands. The microbes then have the opportunity to travel with the tick's saliva into the human host. Blood tests can be used to diagnose Lyme disease because human hosts begin to produce antibodies to fight the microbes; however, the antibodies are slow to appear, taking weeks or months after infection to reach detectable levels. Most cases of Lyme disease are easily treated by means of antibiotics if begun early enough. In about 10 percent of infected people who go untreated, the disease may progress to a chronic stage.
Of those who become infected, most will experience at least one symptom. Three to 30 days after the infection begins, most people will develop a round red rash at or near the site of the bite. The rash may expand to several inches in diameter, but it does not hurt or itch. As it expands it tends to clear up in the center so that it resembles a bull's-eye. Even without medical treatment the rash usually disappears within days or weeks, but this does not mean that the disease is cured.
Other symptoms may also occur in the early stages of the disease. These include the influenza-like symptoms of headaches, fatigue, chills, fever, loss of appetite, and backaches. There may also be some joint and muscle pain but no swelling. About one fifth of untreated sufferers may experience neurological symptoms. These can include Bell's palsy, meningitis, encephalitis, and radiculoneuropathy. The temporomandibular joint may also be affected.
These symptoms usually subside even without treatment; however, approximately six months after the tick bite, about half of the people who receive no antibiotics will develop attacks of arthritis with swelling and pain in one or more joints, especially in the knee joint.
The chronic arthritis of Lyme disease is characterized by repeated swelling of one or more joints, which may remain swollen and painful for more than a year. In most other types of arthritis, paired joints on each side of the body are affected. The affected joints of a person suffering from Lyme disease, however, typically are asymmetrical, or unpaired.
The chronic arthritic form of the disease is rare in Europe; however, chronic skin and nervous disorders have been observed. Neurological problems include reduced cognitive ability and insanity. About 10 percent of Europeans who remain untreated go on to suffer a chronic skin disorder in which an area of the skin becomes extremely thin, wrinkled, and red. Untreated infections of B. burgdorferi can cause disorders in nearly every organ, though symptoms involving the joints, nervous system, skin, and heart are the most common. The differing symptoms found in the United States and Europe probably result from different strains of B. burgdorferi.
Mice, Moths, and Acorns
The results of a three-year study published in 1998 revealed that a chain of intricately woven relationships among forest species may control the incidence of Lyme disease. Ecologists studying the relationships among white-footed mice, gypsy moths, and acorns in eastern United States forests found that large crops of acorns support a massive increase in the white-footed mice population. By feeding on gypsy moth larvae, the mice protect oak trees, which then produce more acorns. Although the increased mouse population affords protection to oak trees, however, it also harbors increased numbers of the ticks that spread Lyme disease. This phenomenon is termed a self-perpetuating tiered relationship among species.
The overall abundance of acorns in a given year directly affects the population size of white-footed mice. The increased amount of acorns leads to a population explosion among the mice, who will also feed on gypsy moth larvae and pupae. Gypsy moths usually feed on the leaves of oaks, thereby causing much damage to the trees. By feeding on gypsy moth larvae and pupae, the mice exert an indirect positive effect on the oaks. During years of low or zero acorn production, white-footed mice populations decrease in size; this allows the gypsy moth population to thrive and to forage on oaks.
However, the periodic acorn masts—the seasons when oaks bear acorns, usually two to five years apart—also attract white-tailed deer. The deer serve as hosts to the ticks that carry the spirochete organism that transmits Lyme disease. White-footed mice are also known to serve as hosts for these ticks. This suggests that the periodic masting of acorns in eastern United States forests might indirectly determine the incidence of Lyme disease during mast years, and gypsy moth outbreaks in non-mast years.
By rigorously testing several hypotheses, ecologists out to tease apart the intricacies of the tangled web. First they trapped and removed white-footed mice from several experimental plots to demonstrate that decreased numbers of white-footed mice would result in increased survival of gypsy moth larvae. They then simulated an acorn mast by distributing more than 3 tons of acorns over the plots that had the decreased mouse populations. Mouse numbers increased greatly and gypsy moth populations showed drastically decreased survivorship. The studies conclusively demonstrated that gypsy moth population size depends on the relationship between white-footed mice and acorns.
The researchers also tracked the numbers of ticks and tick larvae during the experiments. White-footed mice are a known reservoir of Lyme disease—this means that the mice carry the ticks that carry the organism that causes the disease, but the mice are not affected by the organism. The researchers found eight times as many tick larvae in the acorn-enriched plots as in the control plots (plots that had the same numbers of mice but were not given acorns). The increased incidence of tick larvae was related to increased numbers of white-tailed deer that were also attracted by the simulated acorn mast. Deer also harbor the ticks that carry Lyme disease. The deer undoubtedly brought increased numbers of adult ticks into the area. Once in the area, the adult ticks could produce large numbers of larvae, which would eventually mature and infest the mice.
The results of the study strongly suggest that increased acorn production directly supports the increased abundance of white-footed mice and deer; an increased population of mice suppresses gypsy moth outbreaks; and mice and deer support tick populations, potentially increasing the risk of Lyme disease. Epidemiologists caution that the study itself does not have much predictive value because of the many other factors important in determining outbreaks of Lyme disease. Ecologists note that the results emphasize the importance of ecosystem management. Attempts to decrease the spread of Lyme disease by trapping white-footed mice would send gypsy moth populations soaring, which would ultimately result in the devastation of the oak population.
Ticks and Spirochetes
By the late 1970s researchers had traced the cause to a microorganism transmitted by the deer tick Ixodes dammini (now called I. scapularis), which is common in the wooded and grassy areas of Lyme, Conn. In 1982 the actual bacterium responsible for the disease was identified and named Borrelia burgdorferi, after Willy Burgdorfer of Rocky Mountain Laboratories in Hamilton, Mont., who isolated the spirochete, or spiral-shaped organism.
The disease has been identified in other continents of the world including Africa, Asia, Australia, and Europe. In the United States the disease occurs most often in the Northeast, Minnesota, and northern California. Between 15 and 30 percent of all I. scapularis ticks in the larval and nymph stages in the northeastern United States are infected with the B. burgdorferi microbe. About 50 percent of the adult ticks are infected. Between 1 and 3 percent of people in the Northeast who are bitten by an infected tick go on to develop Lyme disease. In northern California the bacterium is carried by the tick I. pacificus. The incidence of human infection with Lyme disease in California is much lower than that in the Northeast because the I. pacificus tick feeds more often on lizards and other animals that are more resistant to infection with the B. burgdorferi microbes.
I. scapularis ticks have a two-year life cycle that includes three feeding sessions. In the first summer, larva may feed on a bird, or on an infected or uninfected mouse. The following spring a nymph that fed as a larva on an infected mouse may feed on a bird, mouse, dog, or human, often transmitting the infection. In the fall an infected adult tick may feed on a deer, horse, dog or human, likewise transmitting the infection. Because the B. burgdorferi microbes are kept alive in part of the mouse population, tick larva become infected each summer if they feed on an infected mouse, thus continuing the cycle.
Course of the Disease
A person may contract the disease when an infected tick, usually in the nymph stage of development, attaches itself to the person's skin and stays attached for 36 to 48 hours. It takes that long for the B. burgdorferi microbes to start to multiply in the tick's gut and travel to its salivary glands. The microbes then have the opportunity to travel with the tick's saliva into the human host. Blood tests can be used to diagnose Lyme disease because human hosts begin to produce antibodies to fight the microbes; however, the antibodies are slow to appear, taking weeks or months after infection to reach detectable levels. Most cases of Lyme disease are easily treated by means of antibiotics if begun early enough. In about 10 percent of infected people who go untreated, the disease may progress to a chronic stage.
Of those who become infected, most will experience at least one symptom. Three to 30 days after the infection begins, most people will develop a round red rash at or near the site of the bite. The rash may expand to several inches in diameter, but it does not hurt or itch. As it expands it tends to clear up in the center so that it resembles a bull's-eye. Even without medical treatment the rash usually disappears within days or weeks, but this does not mean that the disease is cured.
Other symptoms may also occur in the early stages of the disease. These include the influenza-like symptoms of headaches, fatigue, chills, fever, loss of appetite, and backaches. There may also be some joint and muscle pain but no swelling. About one fifth of untreated sufferers may experience neurological symptoms. These can include Bell's palsy, meningitis, encephalitis, and radiculoneuropathy. The temporomandibular joint may also be affected.
These symptoms usually subside even without treatment; however, approximately six months after the tick bite, about half of the people who receive no antibiotics will develop attacks of arthritis with swelling and pain in one or more joints, especially in the knee joint.
The chronic arthritis of Lyme disease is characterized by repeated swelling of one or more joints, which may remain swollen and painful for more than a year. In most other types of arthritis, paired joints on each side of the body are affected. The affected joints of a person suffering from Lyme disease, however, typically are asymmetrical, or unpaired.
The chronic arthritic form of the disease is rare in Europe; however, chronic skin and nervous disorders have been observed. Neurological problems include reduced cognitive ability and insanity. About 10 percent of Europeans who remain untreated go on to suffer a chronic skin disorder in which an area of the skin becomes extremely thin, wrinkled, and red. Untreated infections of B. burgdorferi can cause disorders in nearly every organ, though symptoms involving the joints, nervous system, skin, and heart are the most common. The differing symptoms found in the United States and Europe probably result from different strains of B. burgdorferi.
Mice, Moths, and Acorns
The results of a three-year study published in 1998 revealed that a chain of intricately woven relationships among forest species may control the incidence of Lyme disease. Ecologists studying the relationships among white-footed mice, gypsy moths, and acorns in eastern United States forests found that large crops of acorns support a massive increase in the white-footed mice population. By feeding on gypsy moth larvae, the mice protect oak trees, which then produce more acorns. Although the increased mouse population affords protection to oak trees, however, it also harbors increased numbers of the ticks that spread Lyme disease. This phenomenon is termed a self-perpetuating tiered relationship among species.
The overall abundance of acorns in a given year directly affects the population size of white-footed mice. The increased amount of acorns leads to a population explosion among the mice, who will also feed on gypsy moth larvae and pupae. Gypsy moths usually feed on the leaves of oaks, thereby causing much damage to the trees. By feeding on gypsy moth larvae and pupae, the mice exert an indirect positive effect on the oaks. During years of low or zero acorn production, white-footed mice populations decrease in size; this allows the gypsy moth population to thrive and to forage on oaks.
However, the periodic acorn masts—the seasons when oaks bear acorns, usually two to five years apart—also attract white-tailed deer. The deer serve as hosts to the ticks that carry the spirochete organism that transmits Lyme disease. White-footed mice are also known to serve as hosts for these ticks. This suggests that the periodic masting of acorns in eastern United States forests might indirectly determine the incidence of Lyme disease during mast years, and gypsy moth outbreaks in non-mast years.
By rigorously testing several hypotheses, ecologists out to tease apart the intricacies of the tangled web. First they trapped and removed white-footed mice from several experimental plots to demonstrate that decreased numbers of white-footed mice would result in increased survival of gypsy moth larvae. They then simulated an acorn mast by distributing more than 3 tons of acorns over the plots that had the decreased mouse populations. Mouse numbers increased greatly and gypsy moth populations showed drastically decreased survivorship. The studies conclusively demonstrated that gypsy moth population size depends on the relationship between white-footed mice and acorns.
The researchers also tracked the numbers of ticks and tick larvae during the experiments. White-footed mice are a known reservoir of Lyme disease—this means that the mice carry the ticks that carry the organism that causes the disease, but the mice are not affected by the organism. The researchers found eight times as many tick larvae in the acorn-enriched plots as in the control plots (plots that had the same numbers of mice but were not given acorns). The increased incidence of tick larvae was related to increased numbers of white-tailed deer that were also attracted by the simulated acorn mast. Deer also harbor the ticks that carry Lyme disease. The deer undoubtedly brought increased numbers of adult ticks into the area. Once in the area, the adult ticks could produce large numbers of larvae, which would eventually mature and infest the mice.
The results of the study strongly suggest that increased acorn production directly supports the increased abundance of white-footed mice and deer; an increased population of mice suppresses gypsy moth outbreaks; and mice and deer support tick populations, potentially increasing the risk of Lyme disease. Epidemiologists caution that the study itself does not have much predictive value because of the many other factors important in determining outbreaks of Lyme disease. Ecologists note that the results emphasize the importance of ecosystem management. Attempts to decrease the spread of Lyme disease by trapping white-footed mice would send gypsy moth populations soaring, which would ultimately result in the devastation of the oak population.
Mad cow disease
or bovine spongiform encephalopathy (BSE), a neurological disease that primarily affects mature cattle. The first suspected case of BSE occurred in Great Britain in April 1985. A specific diagnosis was arrived at in 1986. By June of 1990 there were 14,324 confirmed cases out of an estimated population of 10 million cattle in Great Britain.
Cases of BSE in British cattle in 1995 totaled more than 146,000. Additional cases were reported in other countries including Switzerland (about 200 cases), Ireland (about 120 cases), and Portugal (about 30 cases). BSE is one of a group of transmissible and fatal spongiform encephalopathies (TSEs) affecting both animals and humans. This has raised concern regarding possible risks to human health. The disease has crossed the species barrier to infect at least 18 other species. Some researchers suggested a possible link between scrapie or BSE and Creutzfeldt-Jakob disease (CJD) in humans.
This suggestion gained more support in 1996 when British scientists reported a series of related findings. A new variant of Creutzfeldt-Jakob disease (nvCJD) was identified as causing a form of CJD that affects younger people. In another finding, the brain proteins most affected by BSE in cows and CJD in humans are much more similar than was previously thought, given the evolutionary distance between the two species. A third report in 1996 announced research showing that not only is nvCJD different from CJD, but also that nvCJD is probably associated with BSE.
Clinical signs of mad cow disease include abnormally stilted gaits, high stepping, heightened sensory perception, itching, anorexia, and excessive licking, ending in death. Abnormal motor nerve control coupled with aggressiveness have earned the disease the common name of mad, or raging, cow disease. Although all types of cattle are susceptible, most cases have been reported in the Holstein-Friesian breed. The first clinical signs, or onset, of the disease has been observed in cattle at an age of 1 year 10 months to 15 years. From onset, the disease course varies from less than 2 weeks to 14 months usually resulting in death or humane destruction within 4 months.
The causative agent of BSE is not known, however, histopathological studies and clinical signs indicate a strong resemblance to that of scrapie, a neurologic disease of sheep. Brain extracts of suspect cattle have produced disease-specific structures known as scrapie-associated fibrils (SAF). SAF are attributed to infectious type agents called prions. Prions are associated with a unique protein found in brain tissue called prion protein (PrP).
In 1979 studies were conducted by the United States Department of Agriculture (USDA) to attempt experimental transmission of scrapie to cattle. Approximately 30 percent of the inoculated cattle developed progressive neurological signs of the disease. Upon initial histological examination scrapie could not be confirmed. However, a more recent examination of the same tissues, coupled with new information, have shown PrP structures to be present.
As of the mid-1990s there was no evidence of animal-to-animal transmission of BSE. BSE is considered a “common source” epidemic, meaning that animals contract the disease from a common element in their environment. Evidence has ruled out such possible sources of the disease as semen, chemicals, inheritance, chemicals, and pharmaceuticals. The primary suspected sources of the disease are diets fed to cattle containing ruminant-based meat and bone protein. Scrapie- or BSE-contaminated carcasses that are rendered for ruminant diets may account for the presence of SAF in the brains of affected cattle. The feeding of animal protein specifically derived from ruminants was ceased in the United Kingdom as of July 1988.
As of 1996, there were no reported cases of BSE in the United States, but scrapie and other forms of spongiform encephalopathy were present, hence the intense interest in BSE. A transmissible form of spongiform encephalopathy found in ranched mink, transmissible mink encephalopathy (TME), in the United States has been primarily attributed to the feeding of scrapie-infected sheep and goat carcasses to minks.
To prevent BSE from entering the United States, USDA's Animal and Plant Health Inspection Service (APHIS) has taken the following steps:
Beginning in July 1989, APHIS banned the importation of live ruminants and ruminant products from countries where BSE is known to exist.
Since 1991, there has been a voluntary ban in place on using products rendered from adult sheep in animal feeds.
In 1986, APHIS established a program for BSE surveillance in the United States and provided specialized training for 250 APHIS veterinarians who conduct field investigations involving animals with any suspicious symptoms.
APHIS veterinary pathologists and field investigators have received training from British counterparts for diagnosing BSE.
More than 60 veterinary diagnostic laboratories throughout the United States are participating in the BSE Surveillance Program, along with the National Veterinary Services Laboratories in Ames, Iowa.
APHIS veterinarians are tracing 499 head of cattle imported from Great Britain between 1981 and 1989 (before the ban on imports went into effect) to check their health status. As of Jan. 22, 1996, no signs of BSE have been found.
Between 1986 and Dec. 31, 1995, approximately 2,660 brain specimens from cattle exhibiting possible neurological problems had been studied by APHIS. All samples submitted were negative.
Cases of BSE in British cattle in 1995 totaled more than 146,000. Additional cases were reported in other countries including Switzerland (about 200 cases), Ireland (about 120 cases), and Portugal (about 30 cases). BSE is one of a group of transmissible and fatal spongiform encephalopathies (TSEs) affecting both animals and humans. This has raised concern regarding possible risks to human health. The disease has crossed the species barrier to infect at least 18 other species. Some researchers suggested a possible link between scrapie or BSE and Creutzfeldt-Jakob disease (CJD) in humans.
This suggestion gained more support in 1996 when British scientists reported a series of related findings. A new variant of Creutzfeldt-Jakob disease (nvCJD) was identified as causing a form of CJD that affects younger people. In another finding, the brain proteins most affected by BSE in cows and CJD in humans are much more similar than was previously thought, given the evolutionary distance between the two species. A third report in 1996 announced research showing that not only is nvCJD different from CJD, but also that nvCJD is probably associated with BSE.
Clinical signs of mad cow disease include abnormally stilted gaits, high stepping, heightened sensory perception, itching, anorexia, and excessive licking, ending in death. Abnormal motor nerve control coupled with aggressiveness have earned the disease the common name of mad, or raging, cow disease. Although all types of cattle are susceptible, most cases have been reported in the Holstein-Friesian breed. The first clinical signs, or onset, of the disease has been observed in cattle at an age of 1 year 10 months to 15 years. From onset, the disease course varies from less than 2 weeks to 14 months usually resulting in death or humane destruction within 4 months.
The causative agent of BSE is not known, however, histopathological studies and clinical signs indicate a strong resemblance to that of scrapie, a neurologic disease of sheep. Brain extracts of suspect cattle have produced disease-specific structures known as scrapie-associated fibrils (SAF). SAF are attributed to infectious type agents called prions. Prions are associated with a unique protein found in brain tissue called prion protein (PrP).
In 1979 studies were conducted by the United States Department of Agriculture (USDA) to attempt experimental transmission of scrapie to cattle. Approximately 30 percent of the inoculated cattle developed progressive neurological signs of the disease. Upon initial histological examination scrapie could not be confirmed. However, a more recent examination of the same tissues, coupled with new information, have shown PrP structures to be present.
As of the mid-1990s there was no evidence of animal-to-animal transmission of BSE. BSE is considered a “common source” epidemic, meaning that animals contract the disease from a common element in their environment. Evidence has ruled out such possible sources of the disease as semen, chemicals, inheritance, chemicals, and pharmaceuticals. The primary suspected sources of the disease are diets fed to cattle containing ruminant-based meat and bone protein. Scrapie- or BSE-contaminated carcasses that are rendered for ruminant diets may account for the presence of SAF in the brains of affected cattle. The feeding of animal protein specifically derived from ruminants was ceased in the United Kingdom as of July 1988.
As of 1996, there were no reported cases of BSE in the United States, but scrapie and other forms of spongiform encephalopathy were present, hence the intense interest in BSE. A transmissible form of spongiform encephalopathy found in ranched mink, transmissible mink encephalopathy (TME), in the United States has been primarily attributed to the feeding of scrapie-infected sheep and goat carcasses to minks.
To prevent BSE from entering the United States, USDA's Animal and Plant Health Inspection Service (APHIS) has taken the following steps:
Beginning in July 1989, APHIS banned the importation of live ruminants and ruminant products from countries where BSE is known to exist.
Since 1991, there has been a voluntary ban in place on using products rendered from adult sheep in animal feeds.
In 1986, APHIS established a program for BSE surveillance in the United States and provided specialized training for 250 APHIS veterinarians who conduct field investigations involving animals with any suspicious symptoms.
APHIS veterinary pathologists and field investigators have received training from British counterparts for diagnosing BSE.
More than 60 veterinary diagnostic laboratories throughout the United States are participating in the BSE Surveillance Program, along with the National Veterinary Services Laboratories in Ames, Iowa.
APHIS veterinarians are tracing 499 head of cattle imported from Great Britain between 1981 and 1989 (before the ban on imports went into effect) to check their health status. As of Jan. 22, 1996, no signs of BSE have been found.
Between 1986 and Dec. 31, 1995, approximately 2,660 brain specimens from cattle exhibiting possible neurological problems had been studied by APHIS. All samples submitted were negative.
Hirschsprung's disease
(or congenital megacolon), a disease characterized by the absence of nerves in the bowel wall. This prevents the normal movement of waste products through the colon, resulting in blockage. In infants, the disease is eventually treated with a colostomy, the removal of the diseased parts of the colon.
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