In the tropical regions of Africa, the bloodsucking tsetse fly carries deadly diseases to humans and other animals. It is a brownish-colored insect, only a little larger than the common housefly. When it is at rest its wings close flat on the back and are completely overlapping, whereas those of the housefly are held somewhat erect and spread. There are 21 known species of the tsetse fly. Some carry the disease trypanosomiasis (African sleeping sickness) from one human victim to another. Others carry the disease nagana to cattle and other animals.
When the fly bites an infected victim, the insect draws into its own bloodstream a parasite called a trypanosome. After going through a stage of development in the fly, the parasite is transferred to the next victim. Thus the disease, caused by the parasite, is passed from person to person, from animal to animal, through the bite of the fly. The disease is so called because in the last stages of the illness the victim falls into a sleep, which often ends in death.
The tsetse fly breeds in brushy places in tropical forests and on the edges of rivers and lakes. The female, unlike most insects, does not lay eggs. Instead, she deposits on the ground a single full-grown larva at intervals of about two weeks. The larva hides in brush and immediately goes into the pupal stage, from which it emerges as a mature fly.
Tsetse flies belong to the genus Glossina of the family Glossinidae, which is related to the Muscidae. The scientific name of the commonest carrier of African sleeping sickness is G. palpalis. The principal carrier of nagana is G. morsitans.
Sunday, June 15, 2008
Kawasaki disease
rare disease of lymph nodes that causes acquired heart disease in children usually under age 5; characterized by prolonged fever, changes in lips and mouth, swelling of cervical lymph nodes, skin rash, reddening and swelling of hands and feet, and coronary artery damage; may be caused by virus; usually treated with high doses of aspirin; most children conquer fever and rash, but about 20 percent have weakened hearts after the disease.
Newcastle disease
(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.
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.
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.
Flesh-eating disease
(or necrotizing fasciitis), severe skin infection that causes necrosis, or death, of several layers of the skin. It can be caused by one form of or a combination of rare but extremely virulent strains of bacteria of the genus Streptococcus (group A). Milder forms of these bacteria cause strep throat and scarlet fever. Although these bacteria have probably existed since before the origins of humans, several small but harsh outbreaks of the virulent strains in Europe and North America during the spring and summer of 1994 focused attention on this so-called flesh-eating disease.
Any bacteria can enter the body and eventually the bloodstream through cuts, scrapes, or unhealed sores. Once the virulent strain of Streptococcus is in the bloodstream, it can multiply and quickly spread the infection, which can kill up to one square inch of body tissue per hour. Symptoms, which develop one to three days after exposure, include high fever, blistering of the skin, and muscle soreness. Most people in generally good health are able to withstand the initial infection and never develop the disease. The bacteria are spread only through direct contact with bodily secretions from an infected person. If caught in an early stage, the infection is treatable with antibiotics and replenishment of lost fluids. In severe cases, surgery and amputation may be necessary. About 30 percent of victims eventually die from the disease.
Any bacteria can enter the body and eventually the bloodstream through cuts, scrapes, or unhealed sores. Once the virulent strain of Streptococcus is in the bloodstream, it can multiply and quickly spread the infection, which can kill up to one square inch of body tissue per hour. Symptoms, which develop one to three days after exposure, include high fever, blistering of the skin, and muscle soreness. Most people in generally good health are able to withstand the initial infection and never develop the disease. The bacteria are spread only through direct contact with bodily secretions from an infected person. If caught in an early stage, the infection is treatable with antibiotics and replenishment of lost fluids. In severe cases, surgery and amputation may be necessary. About 30 percent of victims eventually die from the disease.
Catalepsy
a physical state in which muscles of the face, body, and limbs take on a condition of suspended animation; trancelike or unresponsive state of consciousness; also called anochlesia; may last for many hours; body position or expression does not alter and limbs remain in whatever position they are placed (known as flexibilitas cerea, or waxy flexibility); associated with hysteria, epilepsy, and schizophrenia in humans, and with organic nervous disease in animals; may also be caused by brain disease and some drugs.
Leprosy
Throughout the ages leprosy has been one of the most dreaded diseases and its victims the most shunned. Almost all cultures have believed that persons who contracted leprosy were spiritually unclean. In modern times the disease has still retained some of its mythical character, and many people do not realize that leprosy is a disease that is only mildly contagious and not fatal. In the early 1990s the World Health Organization estimated that about 5.5 million people had leprosy.
Cause and symptoms.
Leprosy is caused by a rod-shaped bacterium, Mycobacterium leprae, a relative of the tuberculosis bacillus. The organism was identified in 1874 by Armauer Hansen, a Norwegian physician, and an alternative name for leprosy is Hansen's disease. The infection is very slow to develop, ranging from six months to ten years, and children are much more susceptible than adults.
There are two main types of reaction to M. leprae in the body. In the milder form of the disease, tuberculoid leprosy, the body's cells crowd around the invading organisms in the deep skin layers, which are the first areas of infection. This response sometimes seals off the infection from the rest of the body or at least limits its spread. The reaction, however, destroys hair follicles, sweat glands, and nerve endings at the site of infection. The skin above the site becomes dry and discolored and loses its sense of touch. Fingers and toes that have no feeling are easily injured, and, if the patient has not been trained to take protective measures, they may in time become mutilated and fall off.
In the second and more contagious form of the disease, lepromatous leprosy, the body is not able to mount a resistance, and the M. leprae multiply freely in the skin. Large, soft bumps, or nodules, appear over the body and face. Mucous membranes of the eyes, nose, and throat may be invaded. In extreme cases the voice may change drastically, blindness may occur, or the nose may be destroyed.
Treatment and Research.
Until sulfa drugs were developed in the 1940s and were found to be helpful, there was no satisfactory treatment. Patients were merely isolated in an attempt to protect the larger community, and many victims hid. To avoid the undesirable side effects of sulfa drugs, a group of related drugs known as sulfones was developed. Many patients improve with these drugs, especially those with the tuberculoid form of the disease. In most cases treatment must continue for years. Research was long hampered by scientists' inability to induce leprosy in animals in order to study the disease. In 1960 it was found that M. leprae could be grown on the footpads of mice, but the yield was low. A search then began for an animal with a body temperature similar to that of the mouse footpad and the cooler parts of the human body on which the bacteria thrive. In 1971 it was discovered that leprosy could be established in the nine-banded armadillo and other animals. In 1976 it was found that armadillos get leprosy in the wild.
Cause and symptoms.
Leprosy is caused by a rod-shaped bacterium, Mycobacterium leprae, a relative of the tuberculosis bacillus. The organism was identified in 1874 by Armauer Hansen, a Norwegian physician, and an alternative name for leprosy is Hansen's disease. The infection is very slow to develop, ranging from six months to ten years, and children are much more susceptible than adults.
There are two main types of reaction to M. leprae in the body. In the milder form of the disease, tuberculoid leprosy, the body's cells crowd around the invading organisms in the deep skin layers, which are the first areas of infection. This response sometimes seals off the infection from the rest of the body or at least limits its spread. The reaction, however, destroys hair follicles, sweat glands, and nerve endings at the site of infection. The skin above the site becomes dry and discolored and loses its sense of touch. Fingers and toes that have no feeling are easily injured, and, if the patient has not been trained to take protective measures, they may in time become mutilated and fall off.
In the second and more contagious form of the disease, lepromatous leprosy, the body is not able to mount a resistance, and the M. leprae multiply freely in the skin. Large, soft bumps, or nodules, appear over the body and face. Mucous membranes of the eyes, nose, and throat may be invaded. In extreme cases the voice may change drastically, blindness may occur, or the nose may be destroyed.
Treatment and Research.
Until sulfa drugs were developed in the 1940s and were found to be helpful, there was no satisfactory treatment. Patients were merely isolated in an attempt to protect the larger community, and many victims hid. To avoid the undesirable side effects of sulfa drugs, a group of related drugs known as sulfones was developed. Many patients improve with these drugs, especially those with the tuberculoid form of the disease. In most cases treatment must continue for years. Research was long hampered by scientists' inability to induce leprosy in animals in order to study the disease. In 1960 it was found that M. leprae could be grown on the footpads of mice, but the yield was low. A search then began for an animal with a body temperature similar to that of the mouse footpad and the cooler parts of the human body on which the bacteria thrive. In 1971 it was discovered that leprosy could be established in the nine-banded armadillo and other animals. In 1976 it was found that armadillos get leprosy in the wild.
Coronary Artery Disease
Disease of the coronary arteries that supply oxygen and nutrients to the heart is the most common heart ailment. Coronary artery disease accounts for more than a third of all deaths among males in the United States between the ages of 35 and 55. It also strikes many women past the age of 50. Hypertension (high blood pressure), overweight, cigarette smoking, diabetes mellitus, excess cholesterol, triglycerides and other fats in the blood, and lack of regular exercise contribute to the chance of developing this disease.
Coronary artery disease is characterized by formation of one or more atheromas. These are fatty deposits of cholesterol that form beneath the inner lining of the artery and obstruct the passage of blood needed to nourish the heart muscle. This also sets up conditions for a blood clot in the coronary artery. Atheroma formation seems to run in families. However, eating foods rich in saturated animal fat and cholesterol are also contributing factors.
Many persons with coronary artery disease do not experience any symptoms. However, if the obstruction is bad enough, it may cause angina pectoris, myocardial infarction (heart attack), or heart enlargement and failure. Angina pectoris is a severe, squeezing chest pain that occurs when the coronary blockage prevents adequate oxygen from reaching the heart, especially during periods of exertion. Rest and medication often relieve the pain. Unlike a heart attack, angina is a temporary condition, and heart muscle is not destroyed.
Myocardial infarction is the medical term for a heart attack. When the coronary artery becomes so obstructed that the myocardium, or heart muscle, does not receive oxygen, the muscle tissue dies, or becomes infarcted. For many years doctors believed that the infarction was caused by a blood clot blocking the coronary artery. However, later studies revealed that most clots form in the artery after the infarction.
The first hours after a heart attack are critical because abnormal heart rhythms, or arrhythmias, may develop. Without swift medical intervention, death follows in three or four minutes after an attack. Patients are usually treated in the coronary care unit of a hospital for a few days to enable electronic monitoring of the heart rate and rhythm.
Repeated heart attacks can strain the remaining healthy heart muscle, leading to heart failure. As attacks destroy more and more heart muscle, the remaining muscle enlarges to compensate. Increased pressure in the weakened heart causes fluid to back up into the lungs. As a result, the heart output—that is, the volume of blood pumped out with each contraction—cannot keep pace with the body's oxygen demands.
Coronary artery disease is characterized by formation of one or more atheromas. These are fatty deposits of cholesterol that form beneath the inner lining of the artery and obstruct the passage of blood needed to nourish the heart muscle. This also sets up conditions for a blood clot in the coronary artery. Atheroma formation seems to run in families. However, eating foods rich in saturated animal fat and cholesterol are also contributing factors.
Many persons with coronary artery disease do not experience any symptoms. However, if the obstruction is bad enough, it may cause angina pectoris, myocardial infarction (heart attack), or heart enlargement and failure. Angina pectoris is a severe, squeezing chest pain that occurs when the coronary blockage prevents adequate oxygen from reaching the heart, especially during periods of exertion. Rest and medication often relieve the pain. Unlike a heart attack, angina is a temporary condition, and heart muscle is not destroyed.
Myocardial infarction is the medical term for a heart attack. When the coronary artery becomes so obstructed that the myocardium, or heart muscle, does not receive oxygen, the muscle tissue dies, or becomes infarcted. For many years doctors believed that the infarction was caused by a blood clot blocking the coronary artery. However, later studies revealed that most clots form in the artery after the infarction.
The first hours after a heart attack are critical because abnormal heart rhythms, or arrhythmias, may develop. Without swift medical intervention, death follows in three or four minutes after an attack. Patients are usually treated in the coronary care unit of a hospital for a few days to enable electronic monitoring of the heart rate and rhythm.
Repeated heart attacks can strain the remaining healthy heart muscle, leading to heart failure. As attacks destroy more and more heart muscle, the remaining muscle enlarges to compensate. Increased pressure in the weakened heart causes fluid to back up into the lungs. As a result, the heart output—that is, the volume of blood pumped out with each contraction—cannot keep pace with the body's oxygen demands.
Heart Diseases
Cardiovascular Disease
Cardiovascular disease—disease of the heart or blood vessels—can develop in any part of the circulatory system. Problems can occur with the valves, the sinoatrial node, the heart muscle, or the blood vessels.
Arteriosclerosis
commonly called hardening of the arteries, includes a variety of conditions in which artery walls thicken and lose elasticity. There is evidence that heredity and a high cholesterol level in the blood can lead to atherosclerosis, the most common form of arteriosclerosis. (See also Cholesterol; Food and Nutrition, “Fats and Oils.”)
Hypertension.
The force of the blood being pumped through the arteries exerts pressure on the arterial walls. When this pressure is too high it is an unhealthy condition called hypertension, or, simply, high blood pressure. If left untreated, it can lead to heart attack, stroke, kidney disease, or other illnesses.
Rheumatic fever
causes inflammation of the body tissues, joints, and heart. All heart tissues, including the pericardium, can be affected, but the heart's valves are most often damaged. Antibiotics can lessen the adverse effects and prevent serious heart damage.
Bacterial endocarditis
a bacterial infection of the inner lining of the heart muscle, leads to inflammation of the lining. More than half of the incidents of bacterial endocarditis are a result of rheumatic fever. Bacteria may also be introduced into the bloodstream during minor medical procedures, but this is rare.
Congenital heart disease
is heart disease present at birth. It ranges from minor heart murmurs that require no treatment to fatal structural defects.
Fibrillation.
In a normal, healthy heart the muscles contract and relax in an orderly manner. This rhythmic pulsing can be disturbed, however, by faulty electrical impulses that cause the heart to beat abnormally or irregularly. Ventricular fibrillation—rapid, uncoordinated contractions of the heart—is one of the most serious disturbances of heart rate and rhythm and can lead to cardiac arrest and death. Other rhythm disorders, or arrythmias, include auricular fibrillation and flutter, tachycardia (rapid heartbeat), and bradycardia (slow heartbeat).
Congestive heart failure
occurs when engorgement of the veins serving the lungs or of those serving the rest of the body prevents the heart muscle from being able to pump forcefully enough to deliver an adequate supply of blood to the body. It can be caused by disease of either the heart muscle or the valves.
Heart attack
occurs when the flow of blood to the heart muscle itself is cut off or so severely impeded as to cause destruction of cardiac tissue. It is a life-threatening episode of heart disease and can result from a blood clot or advanced atherosclerosis in the coronary arteries.
Diagnosis and Treatment
A physician can detect many heart conditions before symptoms become apparent by using an instrument called an electrocardiograph, for example. It detects tiny electrical impulses from the contracting heart and records them on an electrocardiogram, or EKG or ECG. Normal hearts produce characteristic peak-and-valley tracings. These reflect the contractions of the auricles and ventricles. A tracing that varies from this pattern may indicate a disorder.
Heart conditions can also be diagnosed with the aid of various types of X rays, including X-ray films and fluoroscopy, which enable physicians to see the heart in action. More detailed examinations can be made using such techniques as angiocardiography, which tracks the passage of blood through the heart, coronary arteries, and larger vessels; computed tomography (CT), which provides a detailed cross-sectional image of the heart; and magnetic resonance imaging (MRI), which can show images of the heart in many planes.
Treatment of heart conditions may be possible with prescribed drugs that improve blood flow, reduce blood pressure, prevent blood clots from forming or enlarging, increase the heart's pumping ability, or regulate the heartbeat. Frequently prescribed drugs include anticoagulants that prevent unwanted clotting and vasodilators that widen the blood vessels.
Other treatments include pacemaker implantation and cardiac catheterization. A pacemaker is an electronic device that produces rhythmic electrical impulses to regulate the patient's heartbeat. In the process known as cardiac catheterization, physicians insert a catheter, or thin plastic tube, through an artery in the arm or leg to reach the coronary arteries. They then inject special enzymes through the tube to dissolve arterial blood clots. In some cases physicians use a small balloon on the end of the catheter. The balloon is inflated slightly in a narrowed artery to widen it.
Coronary bypass surgery may be necessary to provide a new path for blood flow around a blocked artery. In the most radical surgery the patient may undergo a heart transplant, in which the diseased heart is replaced with a healthy heart from a deceased donor.
Most physicians recommend changes or improvements in personal habits as the best way of avoiding the early onset of some types of heart disease. Some preventive measures include controlling obesity, hypertension, blood cholesterol levels, and diabetes; avoiding smoking; and fostering healthful habits such as good nutrition, exercise, stress management, and regular medical examinations.
Cardiovascular disease—disease of the heart or blood vessels—can develop in any part of the circulatory system. Problems can occur with the valves, the sinoatrial node, the heart muscle, or the blood vessels.
Arteriosclerosis
commonly called hardening of the arteries, includes a variety of conditions in which artery walls thicken and lose elasticity. There is evidence that heredity and a high cholesterol level in the blood can lead to atherosclerosis, the most common form of arteriosclerosis. (See also Cholesterol; Food and Nutrition, “Fats and Oils.”)
Hypertension.
The force of the blood being pumped through the arteries exerts pressure on the arterial walls. When this pressure is too high it is an unhealthy condition called hypertension, or, simply, high blood pressure. If left untreated, it can lead to heart attack, stroke, kidney disease, or other illnesses.
Rheumatic fever
causes inflammation of the body tissues, joints, and heart. All heart tissues, including the pericardium, can be affected, but the heart's valves are most often damaged. Antibiotics can lessen the adverse effects and prevent serious heart damage.
Bacterial endocarditis
a bacterial infection of the inner lining of the heart muscle, leads to inflammation of the lining. More than half of the incidents of bacterial endocarditis are a result of rheumatic fever. Bacteria may also be introduced into the bloodstream during minor medical procedures, but this is rare.
Congenital heart disease
is heart disease present at birth. It ranges from minor heart murmurs that require no treatment to fatal structural defects.
Fibrillation.
In a normal, healthy heart the muscles contract and relax in an orderly manner. This rhythmic pulsing can be disturbed, however, by faulty electrical impulses that cause the heart to beat abnormally or irregularly. Ventricular fibrillation—rapid, uncoordinated contractions of the heart—is one of the most serious disturbances of heart rate and rhythm and can lead to cardiac arrest and death. Other rhythm disorders, or arrythmias, include auricular fibrillation and flutter, tachycardia (rapid heartbeat), and bradycardia (slow heartbeat).
Congestive heart failure
occurs when engorgement of the veins serving the lungs or of those serving the rest of the body prevents the heart muscle from being able to pump forcefully enough to deliver an adequate supply of blood to the body. It can be caused by disease of either the heart muscle or the valves.
Heart attack
occurs when the flow of blood to the heart muscle itself is cut off or so severely impeded as to cause destruction of cardiac tissue. It is a life-threatening episode of heart disease and can result from a blood clot or advanced atherosclerosis in the coronary arteries.
Diagnosis and Treatment
A physician can detect many heart conditions before symptoms become apparent by using an instrument called an electrocardiograph, for example. It detects tiny electrical impulses from the contracting heart and records them on an electrocardiogram, or EKG or ECG. Normal hearts produce characteristic peak-and-valley tracings. These reflect the contractions of the auricles and ventricles. A tracing that varies from this pattern may indicate a disorder.
Heart conditions can also be diagnosed with the aid of various types of X rays, including X-ray films and fluoroscopy, which enable physicians to see the heart in action. More detailed examinations can be made using such techniques as angiocardiography, which tracks the passage of blood through the heart, coronary arteries, and larger vessels; computed tomography (CT), which provides a detailed cross-sectional image of the heart; and magnetic resonance imaging (MRI), which can show images of the heart in many planes.
Treatment of heart conditions may be possible with prescribed drugs that improve blood flow, reduce blood pressure, prevent blood clots from forming or enlarging, increase the heart's pumping ability, or regulate the heartbeat. Frequently prescribed drugs include anticoagulants that prevent unwanted clotting and vasodilators that widen the blood vessels.
Other treatments include pacemaker implantation and cardiac catheterization. A pacemaker is an electronic device that produces rhythmic electrical impulses to regulate the patient's heartbeat. In the process known as cardiac catheterization, physicians insert a catheter, or thin plastic tube, through an artery in the arm or leg to reach the coronary arteries. They then inject special enzymes through the tube to dissolve arterial blood clots. In some cases physicians use a small balloon on the end of the catheter. The balloon is inflated slightly in a narrowed artery to widen it.
Coronary bypass surgery may be necessary to provide a new path for blood flow around a blocked artery. In the most radical surgery the patient may undergo a heart transplant, in which the diseased heart is replaced with a healthy heart from a deceased donor.
Most physicians recommend changes or improvements in personal habits as the best way of avoiding the early onset of some types of heart disease. Some preventive measures include controlling obesity, hypertension, blood cholesterol levels, and diabetes; avoiding smoking; and fostering healthful habits such as good nutrition, exercise, stress management, and regular medical examinations.
Disease in Pigs
Pigs are subject to a number of diseases, and some of them can afflict humans as well. (See also Disease, Human.)
Anthrax is an acute, infectious, often fatal disease affecting all warm-blooded animals. In pigs the symptoms include swelling of the throat, weakness, and high temperature. Anthrax can be largely prevented by immunization.
Brucellosis causes infectious abortion in pigs. Its symptoms are not always evident; blood tests are the only reliable method of diagnosis. No known preventive medicinal agents or cures exist for this disease.
Hog cholera is a highly contagious virus that affects only pigs and is the most serious disease of domestic pigs in North America. The disease is marked by sudden onset, fever, loss of appetite, and weakness, though some pigs may die without showing symptoms. This disease has been largely controlled in most of the United States.
Foot-and-mouth disease , or aftosa, is a disease that affects cloven-hoofed animals. It is characterized by blisters and sores in the mouth and on the skin around the hooves. The disease is widespread in Europe, Asia, Africa, and South America.
Swine flu is an acute respiratory disease caused by the combined infection of a bacterium and a virus and can also affect humans. There is no known treatment.
African swine fever is a highly contagious, usually fatal, viral disease of pigs. Its symptoms and lesions resemble those of hog cholera. There is no known vaccine or treatment.
Leptospirosis is caused by a bacterium that is readily transmitted from one species to another and can affect both livestock and humans. Use of vaccines is an effective preventive measure.
Parasites affect pigs probably more often than any other species of livestock, with the possible exception of sheep. Internal parasites of pigs include large intestinal roundworms, coccidia, nodular worms, stomach worms, trichinae, thread worms, and whipworms. External parasites include hog lice, blowflies, mites, ringworms, and screwworms.
History
Wild pigs existed as far back as 36 million years ago. The hunting of wild pigs by early humans was often depicted in Western European cave and rock paintings dating back thousands of years.
Domestic pigs probably descended from one species—the Eurasian wild boar (Sus scrofa). Domestication of the pig coincided with the formation of the first permanent human settlements. The oldest known sites of pig domestication were established about 8,500 to 9,000 years ago in Iraq, Jordan, and Turkestan. The first domestic pigs in China existed about 6,900 years ago and in Great Britain as early as 2,800 years ago. The Vikings and, later, Spanish and English colonists brought swine to the Americas. Today wild or domestic pigs can be found on every continent except Antarctica.
Anthrax is an acute, infectious, often fatal disease affecting all warm-blooded animals. In pigs the symptoms include swelling of the throat, weakness, and high temperature. Anthrax can be largely prevented by immunization.
Brucellosis causes infectious abortion in pigs. Its symptoms are not always evident; blood tests are the only reliable method of diagnosis. No known preventive medicinal agents or cures exist for this disease.
Hog cholera is a highly contagious virus that affects only pigs and is the most serious disease of domestic pigs in North America. The disease is marked by sudden onset, fever, loss of appetite, and weakness, though some pigs may die without showing symptoms. This disease has been largely controlled in most of the United States.
Foot-and-mouth disease , or aftosa, is a disease that affects cloven-hoofed animals. It is characterized by blisters and sores in the mouth and on the skin around the hooves. The disease is widespread in Europe, Asia, Africa, and South America.
Swine flu is an acute respiratory disease caused by the combined infection of a bacterium and a virus and can also affect humans. There is no known treatment.
African swine fever is a highly contagious, usually fatal, viral disease of pigs. Its symptoms and lesions resemble those of hog cholera. There is no known vaccine or treatment.
Leptospirosis is caused by a bacterium that is readily transmitted from one species to another and can affect both livestock and humans. Use of vaccines is an effective preventive measure.
Parasites affect pigs probably more often than any other species of livestock, with the possible exception of sheep. Internal parasites of pigs include large intestinal roundworms, coccidia, nodular worms, stomach worms, trichinae, thread worms, and whipworms. External parasites include hog lice, blowflies, mites, ringworms, and screwworms.
History
Wild pigs existed as far back as 36 million years ago. The hunting of wild pigs by early humans was often depicted in Western European cave and rock paintings dating back thousands of years.
Domestic pigs probably descended from one species—the Eurasian wild boar (Sus scrofa). Domestication of the pig coincided with the formation of the first permanent human settlements. The oldest known sites of pig domestication were established about 8,500 to 9,000 years ago in Iraq, Jordan, and Turkestan. The first domestic pigs in China existed about 6,900 years ago and in Great Britain as early as 2,800 years ago. The Vikings and, later, Spanish and English colonists brought swine to the Americas. Today wild or domestic pigs can be found on every continent except Antarctica.
Notifiable diseases
medical conditions that must be reported to local health authorities by doctor who diagnoses patients with these conditions; include tuberculosis, hepatitis, malaria, food poisoning, scarlet fever, measles, dysentery, birth defects, cancers, lead poisoning, and anthrax; in case of infectious diseases, enables health officials to take necessary steps to control spread of diseases by isolating victims, improving sanitation, or offering immunization to those not yet affected; also provides valuable statistics on incidence and prevalence of medical conditions; practice first introduced in England and Wales in about 1900.
Heartworm disease
serious disease complex of dogs and cats in the United States and worldwide. Heartworm disease is caused by the parasitic filarial worm Dirofiliaria immitis, the adults of which colonize the right ventricle of the heart and the pulmonary artery. The disease, which is transmitted by mosquitoes, is potentially fatal, but it is also completely preventable by properly testing and medicating animals before they become infected. The disease is endemic in the southeastern United States, though the rate of incidence has risen dramatically across the United States; few states report no cases of heartworm.
In the host animal, adult heartworms live in the right ventricle of the heart, the vena cava, and the pulmonary arteries. The adult female worms produce microscopic larvae called microfilaria, which circulate throughout the bloodstream of the host animal, and are ingested by mosquitoes when the latter feed on the host. In the gut of the mosquito, the microfilaria develop into an infective larval form. When the insect bites an uninfected host animal, the infective larvae are injected into the host's tissue, then migrate to the blood, reaching the heart within about four months; in the heart, the larvae mature into adults during the next two to three months. The females produce microfilaria, which enter the circulation, and the cycle perpetuates when the infested blood is ingested by a mosquito.
In the host, the adult worms cause significant damage to the walls of the heart as well as the blood vessels. The vessels become inflamed, and the ventricle of the heart enlarges, causing the right side of the heart to work harder and resulting in enlargement of the right ventricle. The presence of worms in the ventricle and the pulmonary artery further impede blood flow to the lungs, leading to pulmonary hypertension and pulmonary emboli, or blood clots. If the animal is not treated for the disease, death due to right-sided heart failure is usually inevitable.
The pathogenesis of the disease is similar in dogs and cats, though there are important differences. In the dog, as many as 250 adult worms may be present at one time. This is a considerable number, especially if one takes into consideration the size of the adult worms: females average 11 inches (27 centimeters), and males 7 inches (17 centimeters), in length. The number of worms infecting cats is much lower, usually two to three adult worms per cat. The worms live from five to seven years in dogs, but only one to two years in cats. In dogs, the clinical signs of the disease are usually coughing, respiratory distress (labored breathing) and exercise intolerance. Symptoms of the disease in cats vary considerably. Some cats never show any significant signs, appearing normal one day and suffering acute heart failure the next. Other cats develop a chronic form of the disease, with vomiting and respiratory difficulties as the only clinical signs. Regardless of the clinical signs, the disease is usually more severe in cats and more difficult to detect and treat.
Treatment, though effective, is a challenge. For many years, heartworm disease in dogs was treated with arsenamide, a form of arsenic. This drug, though effective at resolving the disease, had serious side effects, including kidney and liver toxicity. New drugs with a higher margin of safety have been developed to treat heartworm disease in dogs. These adulticides kill the adult worms, which must then be cleared by the body. The risk of post-treatment lung inflammation and blood clots is high, hence the dog must be confined for a month after treatment. Other drugs are given to kill the microfilaria circulating in the dog's blood. In cats, treatment is more difficult. Some cats are able to clear the worms without treatment, though monitoring the animal for complications is essential. Supportive therapy, such as fluids and occasionally steroids, are indicated in some cases. The adulticides used to treat the disease in dogs are very risky to use in treating cats because there is a strong chance that the cat will develop pulmonary emboli after receiving the drugs.
The disease is diagnosed by a blood test that reveals the presence of the microfilaria in the blood. In some cases, no microfilaria are present in the blood though the animal is infected and may have adult worms in the heart. These cases, known as occult infection, may be diagnosed based on clinical history of symptoms and chest x-rays.
Heartworm disease is easily preventable. The animal must first be tested to determine if microfilaria are present in the circulation. This is essential, because if preventive medication is given to an animal that is already infected, the results could be fatal. Once the animal tests negative, a monthly medication is administered. This preventive treatment should begin in early spring and should continue for two months after the mosquito season ends. Because of the increasing prevalence of heartworm in the United States, many veterinarians now recommend preventive treatment year-round; however, a yearly test in the spring is still advisable.
In the host animal, adult heartworms live in the right ventricle of the heart, the vena cava, and the pulmonary arteries. The adult female worms produce microscopic larvae called microfilaria, which circulate throughout the bloodstream of the host animal, and are ingested by mosquitoes when the latter feed on the host. In the gut of the mosquito, the microfilaria develop into an infective larval form. When the insect bites an uninfected host animal, the infective larvae are injected into the host's tissue, then migrate to the blood, reaching the heart within about four months; in the heart, the larvae mature into adults during the next two to three months. The females produce microfilaria, which enter the circulation, and the cycle perpetuates when the infested blood is ingested by a mosquito.
In the host, the adult worms cause significant damage to the walls of the heart as well as the blood vessels. The vessels become inflamed, and the ventricle of the heart enlarges, causing the right side of the heart to work harder and resulting in enlargement of the right ventricle. The presence of worms in the ventricle and the pulmonary artery further impede blood flow to the lungs, leading to pulmonary hypertension and pulmonary emboli, or blood clots. If the animal is not treated for the disease, death due to right-sided heart failure is usually inevitable.
The pathogenesis of the disease is similar in dogs and cats, though there are important differences. In the dog, as many as 250 adult worms may be present at one time. This is a considerable number, especially if one takes into consideration the size of the adult worms: females average 11 inches (27 centimeters), and males 7 inches (17 centimeters), in length. The number of worms infecting cats is much lower, usually two to three adult worms per cat. The worms live from five to seven years in dogs, but only one to two years in cats. In dogs, the clinical signs of the disease are usually coughing, respiratory distress (labored breathing) and exercise intolerance. Symptoms of the disease in cats vary considerably. Some cats never show any significant signs, appearing normal one day and suffering acute heart failure the next. Other cats develop a chronic form of the disease, with vomiting and respiratory difficulties as the only clinical signs. Regardless of the clinical signs, the disease is usually more severe in cats and more difficult to detect and treat.
Treatment, though effective, is a challenge. For many years, heartworm disease in dogs was treated with arsenamide, a form of arsenic. This drug, though effective at resolving the disease, had serious side effects, including kidney and liver toxicity. New drugs with a higher margin of safety have been developed to treat heartworm disease in dogs. These adulticides kill the adult worms, which must then be cleared by the body. The risk of post-treatment lung inflammation and blood clots is high, hence the dog must be confined for a month after treatment. Other drugs are given to kill the microfilaria circulating in the dog's blood. In cats, treatment is more difficult. Some cats are able to clear the worms without treatment, though monitoring the animal for complications is essential. Supportive therapy, such as fluids and occasionally steroids, are indicated in some cases. The adulticides used to treat the disease in dogs are very risky to use in treating cats because there is a strong chance that the cat will develop pulmonary emboli after receiving the drugs.
The disease is diagnosed by a blood test that reveals the presence of the microfilaria in the blood. In some cases, no microfilaria are present in the blood though the animal is infected and may have adult worms in the heart. These cases, known as occult infection, may be diagnosed based on clinical history of symptoms and chest x-rays.
Heartworm disease is easily preventable. The animal must first be tested to determine if microfilaria are present in the circulation. This is essential, because if preventive medication is given to an animal that is already infected, the results could be fatal. Once the animal tests negative, a monthly medication is administered. This preventive treatment should begin in early spring and should continue for two months after the mosquito season ends. Because of the increasing prevalence of heartworm in the United States, many veterinarians now recommend preventive treatment year-round; however, a yearly test in the spring is still advisable.
Fifth disease
a mild but contagious viral disease of children that causes a very characteristic facial rash. The formal name for the disease is erythema infectiosum, which means “infectious redness.” The name fifth disease was applied to the condition because it was the fifth pink-red infectious rash of childhood to be described. The others are scarlet fever, measles, rubella, which is often called German measles, and roseola.
Although persons of any age may contract fifth disease, children attending elementary school are the major group at risk. The virus causing this condition, human parvovirus B19, is spread by exposure to airborne droplets exhaled by an infected person. The disease is seen mainly in the spring months, and often occurs as a small outbreak in a geographically limited region.
More than half of the children who are exposed to fifth disease will contract the illness. After an incubation period ranging from four days to two weeks, an infected child usually has a fever of less than 101° F (38° C), may feel slightly ill or tired, and develops the most characteristic sign of fifth disease: a bright red or rosy rash on both cheeks, making them look as if they have been slapped. In fact, the infection has been called “slapped cheeks disease.” The rash does not itch, and may extend to the upper arms, thighs, and buttocks, where it is more pink than bright red and has a lacy or netlike appearance.
Children usually are no longer ill after five to ten days, but the rash often recurs a number of times over a period of several weeks. It seems to be triggered by exposure to direct sunlight, exercising, or emotional stress. The child may continue in school or day care at this stage because once the rash appears, there is no longer any risk of giving the disease to others. The only treatment for the patient during the acute illness phase is bed rest. Drinking plenty of fluids is also important.
Fifth disease generally is diagnosed from the appearance of the rash. A specific blood test will confirm the diagnosis, but it is not necessary in an otherwise healthy child. In some cases, however, it is hard to distinguish the rash characteristic of fifth disease from that of rubella. A blood test is needed to diagnose rubella. Anyone who contracts fifth disease becomes immune to the virus for many years or possibly for life. In fact, more than half of all adults are immune to parvovirus B19.
Most adults who develop fifth disease have only mildly pink cheeks, and some lack a rash altogether. They do tend to develop joint pain and swelling, especially in the knees, which may last as long as three months.
Fifth disease does pose two special risks. If a pregnant woman is exposed, the virus—which damages red blood cells—can produce severe anemia in the developing fetus. (Anemia is a disorder in which an individual has too few red blood cells.) Out of every ten infants who are infected with fifth disease before birth, about one has this complication, which in rare cases proves fatal. The fetus also may develop edema, or swelling, from fluid accumulating in the tissues. There is some indication that exposure to the virus increases the chance of a miscarriage. However, the virus does not cause birth defects, as occur in babies whose mothers had rubella in early pregnancy. The other risk is that some persons with chronic disorders of the red blood cells, such as sickle-cell anemia, may become severely anemic if they contract fifth disease. In patients with a weak immune system, the infection may last much longer than usual and cause marked anemia.
Although persons of any age may contract fifth disease, children attending elementary school are the major group at risk. The virus causing this condition, human parvovirus B19, is spread by exposure to airborne droplets exhaled by an infected person. The disease is seen mainly in the spring months, and often occurs as a small outbreak in a geographically limited region.
More than half of the children who are exposed to fifth disease will contract the illness. After an incubation period ranging from four days to two weeks, an infected child usually has a fever of less than 101° F (38° C), may feel slightly ill or tired, and develops the most characteristic sign of fifth disease: a bright red or rosy rash on both cheeks, making them look as if they have been slapped. In fact, the infection has been called “slapped cheeks disease.” The rash does not itch, and may extend to the upper arms, thighs, and buttocks, where it is more pink than bright red and has a lacy or netlike appearance.
Children usually are no longer ill after five to ten days, but the rash often recurs a number of times over a period of several weeks. It seems to be triggered by exposure to direct sunlight, exercising, or emotional stress. The child may continue in school or day care at this stage because once the rash appears, there is no longer any risk of giving the disease to others. The only treatment for the patient during the acute illness phase is bed rest. Drinking plenty of fluids is also important.
Fifth disease generally is diagnosed from the appearance of the rash. A specific blood test will confirm the diagnosis, but it is not necessary in an otherwise healthy child. In some cases, however, it is hard to distinguish the rash characteristic of fifth disease from that of rubella. A blood test is needed to diagnose rubella. Anyone who contracts fifth disease becomes immune to the virus for many years or possibly for life. In fact, more than half of all adults are immune to parvovirus B19.
Most adults who develop fifth disease have only mildly pink cheeks, and some lack a rash altogether. They do tend to develop joint pain and swelling, especially in the knees, which may last as long as three months.
Fifth disease does pose two special risks. If a pregnant woman is exposed, the virus—which damages red blood cells—can produce severe anemia in the developing fetus. (Anemia is a disorder in which an individual has too few red blood cells.) Out of every ten infants who are infected with fifth disease before birth, about one has this complication, which in rare cases proves fatal. The fetus also may develop edema, or swelling, from fluid accumulating in the tissues. There is some indication that exposure to the virus increases the chance of a miscarriage. However, the virus does not cause birth defects, as occur in babies whose mothers had rubella in early pregnancy. The other risk is that some persons with chronic disorders of the red blood cells, such as sickle-cell anemia, may become severely anemic if they contract fifth disease. In patients with a weak immune system, the infection may last much longer than usual and cause marked anemia.
Plant Diseases
There are more than 80,000 plant diseases known worldwide. In fact, all plants are vulnerable to attack by disease. Crop plants are frequent victims, and crop diseases can result in enormous agricultural and economic losses.
Some plant diseases can actually be beneficial in natural ecosystems because they balance the growth of plant populations. Though epidemics may occur in nature, they are rare because the diversity of wild plants slows the spread of most plant disease. Crops are grown as single species in large numbers and diseases can spread easily under these conditions.
Types of Plant Diseases
Plant diseases are classified as noninfectious if they are caused by some environmental factor and are not transmitted from one plant to another. Infectious diseases are those that are caused by a disease organism such as a virus, fungus, or nematode.
Noninfectious diseases
are probably the major causes of poor health in plants and are most frequently the result of adverse environmental conditions. Low concentrations of soil minerals such as nitrogen, phosphorus, or iron can result in abnormal plant growth. Symptoms of such nutrient deficiencies often include yellow or abnormally formed leaves and slow plant growth. Another frequent cause of poor plant health is too much water, which results in low amounts of oxygen in the soil and poor root growth. Plants may also become diseased if soil acidity is too low or too high.
Plants are also damaged by toxic chemicals. For example, pesticides applied to crops may have adverse effects on plant growth. Poor health in plants may result from pollutants in the air. Ozone (O3) is released into the air in large quantities by automobiles and factories. This chemical has been shown to damage the growth of a number of major forest trees. Sulfur dioxide and nitrous oxide are also added to the air by auto exhaust and smoke. These chemicals dissolve in rain water and make it acidic. In many parts of the world this acid rain causes crop plants and forest trees to become diseased and sometimes die. (See also Acid Rain; Pollution, Environmental.)
Physical injury—as from lightning, ice storms, machinery, or animals and insects that eat foliage and stems—adversely affects plant growth. In many cases, however, physical injury does not kill plants directly, but it creates wounds through which infectious diseases can enter the plants.
Infectious diseases.
Viruses are common agents of infectious diseases in plants. When a virus enters a plant cell, it causes the cell to produce more viruses and often causes the death of the cell. The symptoms of viral disease vary. They often include leaf mottling or changes in leaf color, malformation of stems and leaves, dead spots, or stunted growth. Perhaps the best-understood plant virus is the tobacco mosaic virus. This virus infects tobacco, potato, pepper, and eggplants. Because it is a very simple virus, it has been intensively studied by scientists. (See also Virus.)
Mycoplasmas and bacteria infect a wide variety of crop plants. These tiny, single-celled organisms may damage the host plant by releasing toxic chemicals, or they may directly digest plant tissue. These disease agents are often transmitted by the wind, but they may also be carried by insects or on farm machinery. They usually enter the plant through wounds. Perhaps the best-known bacterial disease is crown gall, caused by the bacterium Agrobacterium tumefaciens. This bacterium produces distinctive growths at the base of the plant's stems and may infect members of more than 40 families of plants. (See also Bacteria.)
Seventy-five percent of the diseases in plants are caused by fungi, such as rusts, smuts, and mildews. When fungal spores germinate on a plant, they produce infectious filaments called hyphae. These hyphae invade the plant tissues, absorbing nutrients from plant cells and often causing abnormal growth and cell death. Late blight is a disease caused by a fungus (Phytophthora infestans). The organism attacks potato plants and was responsible for the Irish potato famines of the mid-1800s. The chestnut blight is caused by a fungus (Endothia parasitica) that originally grew naturally on chestnut trees in China. In about 1900 the fungus was introduced into North America on nursery stock and quickly spread to American chestnuts. Within 30 years the disease had killed all chestnut trees in the eastern United States. Dutch elm disease is also caused by a fungus. Rusts and smuts are fungal diseases that attack the stems and flowering stalks of major crops such as corn and wheat. In 1935, for example, the black stem rust (Puccinia graminis) was responsible for the loss of 60 percent of the wheat crop in Minnesota and the Dakotas. (See also Fungus.)
Nematodes, or roundworms, are among the most abundant animals found in soil. Many of these microscopic worms cause plant diseases. They obtain food by sucking the cytoplasm from root cells (see Cell). Plants infected by these animals are often stunted and may show symptoms of water or nutrient deficiency. Nematodes are responsible for root knot and other root diseases. (See also Worm, “Roundworms.”)
Parasitic plants may cause diseases in other plants. Dodder (genus Cuscuta) is a plant that is unable to make its own food. It attacks host plants and obtains food from their cells. Dodder seeds may contaminate the seed stocks of clover, alfalfa, and flax; thus, the parasite is sown with the crop it infests. Witchweed is a small parasitic plant that attaches to the roots of host plants such as corn, sorghum, rice, and sugarcane and interferes with the growth of the plants. The common mistletoe is a parasitic plant that causes abnormal growth in many trees and robs its host of water and minerals. (See also Mistletoe; Parasite.)
Disease Control
Perhaps the simplest approach to disease control is to keep the pathogen, or disease-causing agent, away from susceptible plants. Toward this end, many states have strict rules regarding the import of crop plants and fruits that might carry pathogens.
Once a disease is established, the main approach to its control is eradication. Diseases may be eradicated by crop rotation—that is, a farmer may decide to replace a diseased crop with another species of crop plant. This technique is effective against disease organisms that do not produce spores or cannot survive for long periods of time in the soil. Sometimes a disease can be eradicated by pruning the diseased portion of the plant.
Some diseases can be controlled by growing plants in climates that are unsuitable for the pathogen. Farmers try to avoid inflicting mechanical damage on plants in order to prevent the entry of disease-causing agents. Insecticides may be effective against plant diseases that are spread by insects
Using plant breeding and genetic engineering techniques, scientists have been able to develop strains of plants that are resistant to disease. This process of plant selection must go on continually, because soon after disease-resistant plants are developed, disease organisms evolve the ability to infect them.
Biological control—the use of natural processes to combat pathogens—has become increasingly common. This sort of control may involve introducing the pathogen's natural enemies into its environment. Plant diseases can also be controlled by interplanting, or growing several crop plants together. This sort of planting simulates the conditions in natural ecosystems, where the diversity of plants limits the spread of infectious diseases.
Some plant diseases can actually be beneficial in natural ecosystems because they balance the growth of plant populations. Though epidemics may occur in nature, they are rare because the diversity of wild plants slows the spread of most plant disease. Crops are grown as single species in large numbers and diseases can spread easily under these conditions.
Types of Plant Diseases
Plant diseases are classified as noninfectious if they are caused by some environmental factor and are not transmitted from one plant to another. Infectious diseases are those that are caused by a disease organism such as a virus, fungus, or nematode.
Noninfectious diseases
are probably the major causes of poor health in plants and are most frequently the result of adverse environmental conditions. Low concentrations of soil minerals such as nitrogen, phosphorus, or iron can result in abnormal plant growth. Symptoms of such nutrient deficiencies often include yellow or abnormally formed leaves and slow plant growth. Another frequent cause of poor plant health is too much water, which results in low amounts of oxygen in the soil and poor root growth. Plants may also become diseased if soil acidity is too low or too high.
Plants are also damaged by toxic chemicals. For example, pesticides applied to crops may have adverse effects on plant growth. Poor health in plants may result from pollutants in the air. Ozone (O3) is released into the air in large quantities by automobiles and factories. This chemical has been shown to damage the growth of a number of major forest trees. Sulfur dioxide and nitrous oxide are also added to the air by auto exhaust and smoke. These chemicals dissolve in rain water and make it acidic. In many parts of the world this acid rain causes crop plants and forest trees to become diseased and sometimes die. (See also Acid Rain; Pollution, Environmental.)
Physical injury—as from lightning, ice storms, machinery, or animals and insects that eat foliage and stems—adversely affects plant growth. In many cases, however, physical injury does not kill plants directly, but it creates wounds through which infectious diseases can enter the plants.
Infectious diseases.
Viruses are common agents of infectious diseases in plants. When a virus enters a plant cell, it causes the cell to produce more viruses and often causes the death of the cell. The symptoms of viral disease vary. They often include leaf mottling or changes in leaf color, malformation of stems and leaves, dead spots, or stunted growth. Perhaps the best-understood plant virus is the tobacco mosaic virus. This virus infects tobacco, potato, pepper, and eggplants. Because it is a very simple virus, it has been intensively studied by scientists. (See also Virus.)
Mycoplasmas and bacteria infect a wide variety of crop plants. These tiny, single-celled organisms may damage the host plant by releasing toxic chemicals, or they may directly digest plant tissue. These disease agents are often transmitted by the wind, but they may also be carried by insects or on farm machinery. They usually enter the plant through wounds. Perhaps the best-known bacterial disease is crown gall, caused by the bacterium Agrobacterium tumefaciens. This bacterium produces distinctive growths at the base of the plant's stems and may infect members of more than 40 families of plants. (See also Bacteria.)
Seventy-five percent of the diseases in plants are caused by fungi, such as rusts, smuts, and mildews. When fungal spores germinate on a plant, they produce infectious filaments called hyphae. These hyphae invade the plant tissues, absorbing nutrients from plant cells and often causing abnormal growth and cell death. Late blight is a disease caused by a fungus (Phytophthora infestans). The organism attacks potato plants and was responsible for the Irish potato famines of the mid-1800s. The chestnut blight is caused by a fungus (Endothia parasitica) that originally grew naturally on chestnut trees in China. In about 1900 the fungus was introduced into North America on nursery stock and quickly spread to American chestnuts. Within 30 years the disease had killed all chestnut trees in the eastern United States. Dutch elm disease is also caused by a fungus. Rusts and smuts are fungal diseases that attack the stems and flowering stalks of major crops such as corn and wheat. In 1935, for example, the black stem rust (Puccinia graminis) was responsible for the loss of 60 percent of the wheat crop in Minnesota and the Dakotas. (See also Fungus.)
Nematodes, or roundworms, are among the most abundant animals found in soil. Many of these microscopic worms cause plant diseases. They obtain food by sucking the cytoplasm from root cells (see Cell). Plants infected by these animals are often stunted and may show symptoms of water or nutrient deficiency. Nematodes are responsible for root knot and other root diseases. (See also Worm, “Roundworms.”)
Parasitic plants may cause diseases in other plants. Dodder (genus Cuscuta) is a plant that is unable to make its own food. It attacks host plants and obtains food from their cells. Dodder seeds may contaminate the seed stocks of clover, alfalfa, and flax; thus, the parasite is sown with the crop it infests. Witchweed is a small parasitic plant that attaches to the roots of host plants such as corn, sorghum, rice, and sugarcane and interferes with the growth of the plants. The common mistletoe is a parasitic plant that causes abnormal growth in many trees and robs its host of water and minerals. (See also Mistletoe; Parasite.)
Disease Control
Perhaps the simplest approach to disease control is to keep the pathogen, or disease-causing agent, away from susceptible plants. Toward this end, many states have strict rules regarding the import of crop plants and fruits that might carry pathogens.
Once a disease is established, the main approach to its control is eradication. Diseases may be eradicated by crop rotation—that is, a farmer may decide to replace a diseased crop with another species of crop plant. This technique is effective against disease organisms that do not produce spores or cannot survive for long periods of time in the soil. Sometimes a disease can be eradicated by pruning the diseased portion of the plant.
Some diseases can be controlled by growing plants in climates that are unsuitable for the pathogen. Farmers try to avoid inflicting mechanical damage on plants in order to prevent the entry of disease-causing agents. Insecticides may be effective against plant diseases that are spread by insects
Using plant breeding and genetic engineering techniques, scientists have been able to develop strains of plants that are resistant to disease. This process of plant selection must go on continually, because soon after disease-resistant plants are developed, disease organisms evolve the ability to infect them.
Biological control—the use of natural processes to combat pathogens—has become increasingly common. This sort of control may involve introducing the pathogen's natural enemies into its environment. Plant diseases can also be controlled by interplanting, or growing several crop plants together. This sort of planting simulates the conditions in natural ecosystems, where the diversity of plants limits the spread of infectious diseases.
Creutzfeldt-Jakob disease
(or Creutzfeld-Jacob disease), a rare, fatal disease occurring in middle age; caused by a slow, unidentified virus and marked by muscular deterioration and progressive loss of intellect and personality; signs of disease do not appear until months or years after original infection and may include blindness and loss of speech; unlikely to be transmitted between humans, but some cases have resulted from exposure to instruments used in the treatment of a patient with the disease; death usually follows within a year of onset.
Legionnaire's disease
(legionellosis), a type of pneumonia, infection of the lungs, caused by a bacterium of the genus Legionella. The disease was named after a 1976 outbreak that killed 29 members of the American Legion attending a convention in a Philadelphia hotel. After the 1976 incident, scientists identified the bacterium as a common contaminant in water systems that had caused earlier mysterious epidemics of pneumonia. More than 700 cases are reported each year, but the incidence is thought to be much higher.
Legionella thrives in a warm, moist environment, as is found in water or air-conditioning systems in large buildings. Chlorination disinfects the system. The disease is spread by inhalation of heavily contaminated water droplets. The incubation period is two to ten days. The first symptoms include appetite loss, headache, muscle and stomach ache, diarrhea, and a dry cough. After a few days, pneumonia follows with high fever, chills, sleepiness, and coughing up of phlegm. Left untreated, the pneumonia worsens and becomes life-threatening. Once an analysis of the phlegm or a lung biopsy verifies the Legionella pneumophila infection, the patient is treated with an antibiotic, usually erythromycin or rifampin. Once medication has begun, relief from symptoms is quick but total recovery is gradual. Irreversible lung damage in elderly or unhealthy individuals may lead to death,
Legionella thrives in a warm, moist environment, as is found in water or air-conditioning systems in large buildings. Chlorination disinfects the system. The disease is spread by inhalation of heavily contaminated water droplets. The incubation period is two to ten days. The first symptoms include appetite loss, headache, muscle and stomach ache, diarrhea, and a dry cough. After a few days, pneumonia follows with high fever, chills, sleepiness, and coughing up of phlegm. Left untreated, the pneumonia worsens and becomes life-threatening. Once an analysis of the phlegm or a lung biopsy verifies the Legionella pneumophila infection, the patient is treated with an antibiotic, usually erythromycin or rifampin. Once medication has begun, relief from symptoms is quick but total recovery is gradual. Irreversible lung damage in elderly or unhealthy individuals may lead to death,
Gaucher's disease
rare inherited disorder transmitted as autosomal recessive trait; characterized by anemia, yellowish skin pigmentation, mental and neurological impairment, and bone deterioration caused by deficiency of enzyme necessary for processing fatty acids; infantile Gaucher's usually causes death by the age of 1; its symptoms include enlarged liver and spleen and mental retardation; juvenile Gaucher's develops more slowly, with death occuring in early adolescence; adult Gaucher's usually lacks mental and neurological symptoms of younger patients, and death is usually from a complication of the disease, such as pneumonia.
Yaws
also called frambesia contagious disease occurring in moist tropical regions throughout the world. It is caused by a spirochete, Treponema pertenue, that is structurally indistinguishable from T. pallidum, which causes syphilis. Some syphilologists contend that yaws is merely a tropical rural form of syphilis, but yaws is not contracted primarily through sexual activity, and later systemic complications from the disease are much rarer than in syphilis. The Wassermann and Kahn tests for syphilis, however, often read positive with yaws, and there is some degree of cross-immunity. The spirochetes of yaws are present in the discharge from lesions on the skin and are transferred by direct contact to the abraded skin of an uninfected person; by contaminated clothing; and by flies that feed on the sores. The disease is most frequently contracted in early childhood, and considerable immunity to subsequent infection is acquired.
Yaws has three stages. The symptoms are an initial papule on the skin at the site of inoculation, followed by multiple cauliflower eruptions, and later, in some cases, by mutilating destruction of the skin, mucous membranes, and bones. The primary yaws sore is characterized by a wartlike thickening of the epidermis, which becomes fibrous, cracks open, bleeds easily, and discharges a serous fluid.
A month or more later, when the first lesion may have disappeared except for a scar, multiple eruptions of the same type characteristically develop, often at junctions of the skin and mucous membranes, as around the mouth, nose, and anus, or on the skin of the crotch, neck, arms, legs, and buttocks. These lesions, whether initial or secondary, are yellowish-red and look somewhat like a raspberry (hence the name frambesia, latinized from the French framboise: “raspberry”). Later, the disease may subside, leaving only superficial scarring, but in some instances there may be deforming tertiary yaws involving the nose, long bones (“boomerang leg” of Australia), and, rarely, the spleen, brain, and great blood vessels.
Penicillin is rapidly effective in killing the spirochete and in curing yaws except in the tertiary stage, when oxophenarsine with bismuth subsalicylate is used. Prevention centres on isolating and promptly treating cases to reduce exposure and on maintaining personal and group hygiene. All abrasions and sores of the skin and mucous membranes should be treated with appropriate antiseptics and covered with clean dressings, and all clothing in contact with yaws lesions should be sterilized or destroyed.
Yaws has three stages. The symptoms are an initial papule on the skin at the site of inoculation, followed by multiple cauliflower eruptions, and later, in some cases, by mutilating destruction of the skin, mucous membranes, and bones. The primary yaws sore is characterized by a wartlike thickening of the epidermis, which becomes fibrous, cracks open, bleeds easily, and discharges a serous fluid.
A month or more later, when the first lesion may have disappeared except for a scar, multiple eruptions of the same type characteristically develop, often at junctions of the skin and mucous membranes, as around the mouth, nose, and anus, or on the skin of the crotch, neck, arms, legs, and buttocks. These lesions, whether initial or secondary, are yellowish-red and look somewhat like a raspberry (hence the name frambesia, latinized from the French framboise: “raspberry”). Later, the disease may subside, leaving only superficial scarring, but in some instances there may be deforming tertiary yaws involving the nose, long bones (“boomerang leg” of Australia), and, rarely, the spleen, brain, and great blood vessels.
Penicillin is rapidly effective in killing the spirochete and in curing yaws except in the tertiary stage, when oxophenarsine with bismuth subsalicylate is used. Prevention centres on isolating and promptly treating cases to reduce exposure and on maintaining personal and group hygiene. All abrasions and sores of the skin and mucous membranes should be treated with appropriate antiseptics and covered with clean dressings, and all clothing in contact with yaws lesions should be sterilized or destroyed.
Mumps
also called epidemic parotitis, acute contagious disease caused by a virus and characterized by inflammatory swelling of the salivary glands. It frequently occurs as an epidemic and most commonly affects young persons who are between 5 and 15 years old.
The incubation period is about 17–21 days after contact; danger of transfer begins one week before the affected person feels sick and lasts about two weeks. Mumps generally sets in with symptoms of a slightly feverish cold, soon followed by swelling and stiffening in the region of the parotid salivary gland in front of the ear. The swelling rapidly increases and spreads toward the neck and under the jaw, involving the numerous glands there. The condition is often found on both sides. Pain is seldom severe, nor is there much redness or any tendency to discharge pus; there is, however, interference with chewing and swallowing. After four or five days the parts return to their normal condition.
During convalescence in patients past puberty, there occasionally occur swelling and tenderness in other glands, such as the testicles in males (orchitis) and the breasts (mastitis) or ovaries (oophoritis) in females, and, rarely, involvement of the pancreas, but these are of short duration and usually of no serious significance. The testicles may become atrophied, but sterility from this cause is very rare. Meningoencephalitis (inflammation of the brain and its membranous covering) is a fairly common concomitant of mumps, but the outlook for recovery is favourable.
Mumps itself requires no special treatment; a single attack usually confers lifelong immunity. Prevention can be attained through immunization with a vaccine made from attenuated (weakened) live mumps virus. This vaccine is administered after the age of one year, often in combination with measles and rubella vaccines.
The incubation period is about 17–21 days after contact; danger of transfer begins one week before the affected person feels sick and lasts about two weeks. Mumps generally sets in with symptoms of a slightly feverish cold, soon followed by swelling and stiffening in the region of the parotid salivary gland in front of the ear. The swelling rapidly increases and spreads toward the neck and under the jaw, involving the numerous glands there. The condition is often found on both sides. Pain is seldom severe, nor is there much redness or any tendency to discharge pus; there is, however, interference with chewing and swallowing. After four or five days the parts return to their normal condition.
During convalescence in patients past puberty, there occasionally occur swelling and tenderness in other glands, such as the testicles in males (orchitis) and the breasts (mastitis) or ovaries (oophoritis) in females, and, rarely, involvement of the pancreas, but these are of short duration and usually of no serious significance. The testicles may become atrophied, but sterility from this cause is very rare. Meningoencephalitis (inflammation of the brain and its membranous covering) is a fairly common concomitant of mumps, but the outlook for recovery is favourable.
Mumps itself requires no special treatment; a single attack usually confers lifelong immunity. Prevention can be attained through immunization with a vaccine made from attenuated (weakened) live mumps virus. This vaccine is administered after the age of one year, often in combination with measles and rubella vaccines.
Conjunctivitis
inflammation of the conjunctiva, the delicate mucous membrane that lines the eyelids and covers the front part of the white of the eye—the sclera. The inflammation may be caused by an infection or by a chemical burn or mechanical injury, or it may be part of an allergic reaction. Often both the conjunctiva and the cornea are inflamed, a condition called keratoconjunctivitis. (The cornea is the transparent part of the eyeball in front of the iris and the pupil.)
A variety of infectious agents can give rise to conjunctivitis. The microorganism Chlamydia trachomatis is responsible for trachoma, a disease in which the conjunctiva and cornea become scarred, leading to blindness. Trachoma is the most common cause of blindness in the world and is especially prevalent in the Middle East, Asia, and parts of Africa. Inclusion conjunctivitis, so called because of the small bodies that have been observed within (“included in”) the infected cells, is also caused by C. trachomatis. This disease occurs primarily in newborns who become infected when passing through the birth canal. The viruses of smallpox, chicken pox, and measles also may invade the conjunctiva. Adenoviruses, a group of viruses whose disease-causing members may cause respiratory infections or may survive for long periods in lymphoid tissue (e.g., in the tonsils), may attack the conjunctiva and cornea; the disease is called epidemic keratoconjunctivitis.
Bacterial conjunctivitis, also known as pinkeye, is a highly contagious disease of humans and of various domestic animals. The organisms most commonly responsible for bacterial conjunctivitis in humans are staphylococci; pneumococci (Diplococcus pneumoniae organisms); and Haemophilus influenzae organisms, which may invade the respiratory tract or the brain coverings. Gonococcal conjunctivitis, invasion of the conjunctivas by gonorrhea organisms, was once common among newborn infants, who became infected during delivery. This infection can cause blindness if not treated promptly. It is prevented by routine application of a drop of weak silver nitrate solution into each eye of an infant after delivery.
Conjunctivitis also may result from an allergic reaction. Phlyctenular keratoconjunctivitis, so called because of the presence of one or more phlyctenules—ulcerated, inflamed nodules—on the outer part of the cornea, is common among Eskimos. It usually occurs in association with malnutrition or tuberculosis and is thought to be an allergic response to bacteria. Vernal conjunctivitis, or vernal catarrh, is an allergic inflammation that tends to recur in the conjunctivas of susceptible children each year during the summer months and to depart with the coming of cold weather. There are two types of vernal conjunctivitis. In one, the lining of the upper eyelid is affected, with a characteristic red, pebbled appearance. Between the pebbly elevations there is a stringy white substance that has exuded from the mucous membrane. In the second type of vernal conjunctivitis the inflammation, manifested by separate yellowish-pink elevations, is in that part of the conjunctiva that is next to the cornea.
A severe form of conjunctivitis that may culminate in blindness occasionally accompanies erythema multiforme, an eruption on the skin and mucous membranes that sometimes occurs in association with a systemic infection, after drug poisoning or the injection of an antitoxin, or during pregnancy.
A variety of infectious agents can give rise to conjunctivitis. The microorganism Chlamydia trachomatis is responsible for trachoma, a disease in which the conjunctiva and cornea become scarred, leading to blindness. Trachoma is the most common cause of blindness in the world and is especially prevalent in the Middle East, Asia, and parts of Africa. Inclusion conjunctivitis, so called because of the small bodies that have been observed within (“included in”) the infected cells, is also caused by C. trachomatis. This disease occurs primarily in newborns who become infected when passing through the birth canal. The viruses of smallpox, chicken pox, and measles also may invade the conjunctiva. Adenoviruses, a group of viruses whose disease-causing members may cause respiratory infections or may survive for long periods in lymphoid tissue (e.g., in the tonsils), may attack the conjunctiva and cornea; the disease is called epidemic keratoconjunctivitis.
Bacterial conjunctivitis, also known as pinkeye, is a highly contagious disease of humans and of various domestic animals. The organisms most commonly responsible for bacterial conjunctivitis in humans are staphylococci; pneumococci (Diplococcus pneumoniae organisms); and Haemophilus influenzae organisms, which may invade the respiratory tract or the brain coverings. Gonococcal conjunctivitis, invasion of the conjunctivas by gonorrhea organisms, was once common among newborn infants, who became infected during delivery. This infection can cause blindness if not treated promptly. It is prevented by routine application of a drop of weak silver nitrate solution into each eye of an infant after delivery.
Conjunctivitis also may result from an allergic reaction. Phlyctenular keratoconjunctivitis, so called because of the presence of one or more phlyctenules—ulcerated, inflamed nodules—on the outer part of the cornea, is common among Eskimos. It usually occurs in association with malnutrition or tuberculosis and is thought to be an allergic response to bacteria. Vernal conjunctivitis, or vernal catarrh, is an allergic inflammation that tends to recur in the conjunctivas of susceptible children each year during the summer months and to depart with the coming of cold weather. There are two types of vernal conjunctivitis. In one, the lining of the upper eyelid is affected, with a characteristic red, pebbled appearance. Between the pebbly elevations there is a stringy white substance that has exuded from the mucous membrane. In the second type of vernal conjunctivitis the inflammation, manifested by separate yellowish-pink elevations, is in that part of the conjunctiva that is next to the cornea.
A severe form of conjunctivitis that may culminate in blindness occasionally accompanies erythema multiforme, an eruption on the skin and mucous membranes that sometimes occurs in association with a systemic infection, after drug poisoning or the injection of an antitoxin, or during pregnancy.
Glanders
also called Farcy, specific infectious and contagious disease of solipeds (the horse, ass, and mule); secondarily, humans may become infected through contact with diseased animals or by inoculation while handling diseased tissues and making laboratory cultures of the causal bacillus. In 1882 the bacteriologists Friedrich Löffler and Wilhelm Schütz in Germany isolated and identified the causal agent, which they named the Bacillus mallei, now designated technically as the Pfeifferella mallei or Malleomyces mallei. After infection, the disease usually follows a chronic course with a variable period of incubation extending from several weeks to several months.
Clinical cases in solipeds are manifested by a chronic nasal discharge from one or both nostrils, with or without visible ulceration of the nasal septum; chronic enlargement and hardening of the submaxillary lymph glands without outward discharge of pus; or the presence of pustules and ulcers (farcy buds) on the skin of the hindlegs or other parts of the body. Nonclinical, or latent, cases are essentially pulmonary in type, and the lesions remain in a concealed state (occult) in the lungs as tubercle-like nodules and suppurating foci. In many latent cases, the affected animal shows slight signs of lung trouble (altered breathing).
The only effective policy for the control of the disease is slaughter of infected animals and proper cleaning and disinfection of the affected premises. Under this policy, glanders was almost completely eradicated in the U.S., Great Britain, and Canada. The disease is still known to prevail in some parts of Europe, Asia, and Africa.
Glanders in man most frequently occurs through occupational contact with diseased horses, from making an autopsy on a diseased animal, or from making laboratory cultures of the bacteria. The treatment of human glanders has included the use of many drugs, largely tonic and palliative, combined with surgical treatment. In selected cases, the use of certain antibiotics has shown promising results.
Clinical cases in solipeds are manifested by a chronic nasal discharge from one or both nostrils, with or without visible ulceration of the nasal septum; chronic enlargement and hardening of the submaxillary lymph glands without outward discharge of pus; or the presence of pustules and ulcers (farcy buds) on the skin of the hindlegs or other parts of the body. Nonclinical, or latent, cases are essentially pulmonary in type, and the lesions remain in a concealed state (occult) in the lungs as tubercle-like nodules and suppurating foci. In many latent cases, the affected animal shows slight signs of lung trouble (altered breathing).
The only effective policy for the control of the disease is slaughter of infected animals and proper cleaning and disinfection of the affected premises. Under this policy, glanders was almost completely eradicated in the U.S., Great Britain, and Canada. The disease is still known to prevail in some parts of Europe, Asia, and Africa.
Glanders in man most frequently occurs through occupational contact with diseased horses, from making an autopsy on a diseased animal, or from making laboratory cultures of the bacteria. The treatment of human glanders has included the use of many drugs, largely tonic and palliative, combined with surgical treatment. In selected cases, the use of certain antibiotics has shown promising results.
Sexually transmitted disease
any disease (such as syphilis, gonorrhea, AIDS, or a genital form of herpes simplex) that is usually or often transmitted from person to person by direct sexual contact. It may also be transmitted from a mother to her child before or at birth or, less frequently, may be passed from person to person in nonsexual contact (such as in kissing, in tainted blood transfusions, or in the use of unsanitized hypodermic syringes). Sexually transmitted diseases usually affect initially the genitals, the reproductive tract, the urinary tract, the oral cavity, the anus, or the rectum but may mature in the body to attack various organs and systems. Tertiary syphilis, or paresis, for example, may affect skin, bones, the central nervous system, the heart, the liver, or other organs. Persons infected by an AIDS virus may remain outwardly healthy for years before the disease takes hold within the immune system (or, often, the disease may never arise at all).
The term venereal disease (VD), denoting any disease transmitted by sexual intercourse, lost favour in the late 20th century and was largely supplanted by the more comprehensive term sexually transmitted disease.
Sexually transmitted diseases have a long history. The best known of these diseases, syphilis (q.v.), is caused by the bacterium Treponema pallidum. Syphilis was first widely reported by European writers in the 16th century, and some medical historians assume that it was imported into Europe by explorers returning from the New World. Other authorities believe that syphilis is of ancient origin and may at one time have been mistakenly identified as leprosy. At any rate, syphilis first became widely recognized and reported about the year 1500, when a virtual epidemic swept Europe.
Urethritis is the infection and inflammation of the urethra (the passage that transmits urine from the bladder to the exterior of the body). Most cases of urethritis are in fact sexually transmitted. Urethritis that is caused by the gonococcus bacterium (Neisseria gonorrhoeae) is called gonorrhea (q.v.) and is one of the best-known sexually transmitted diseases. Gonorrhea was named by the Greek physician Galen and is thought to have been known to the ancient Chinese and Egyptians.
Syphilis and gonorrhea were long thought to be one disease. Real progress in characterizing them did not occur until the early 20th century, when their different causative microorganisms were identified and reliable diagnostic tests were developed. Effective treatment in the form of sulfa drugs and penicillin was introduced in the 1930s and '40s, and the eradication of such diseases seemed imminent. By the end of the 1950s, however, the frequency index had begun to rise again; among the many reasons cited were the tapering off of active “anti-VD” campaigns, the causative microorganisms' growing immunity to the antibiotics used in treatment, and a variety of sociological factors influencing sexual behaviour. The widespread acceptance of oral contraceptives and their supplantation of other methods of birth control were possibly linked, for a variety of reasons, to the spread of sexually transmitted diseases. Not only had the lack of oral contraceptives tended to discourage sexual promiscuity but also the older methods of condom and diaphragm had provided some protection against disease. Only with the outbreak of the AIDS epidemic did a return to the condom and “safe sex” receive new encouragement.
A disease that became especially widespread beginning in the 1960s and '70s was genital herpes (see herpes simplex). Herpes infections are significant not only in terms of the discomfort they cause but also for the potentially serious illness that might occur in infants born to mothers with genital herpes infections. A variety of treatments have been used for genital herpes, but none have been entirely satisfactory.
The sexually transmitted disease that caused perhaps the greatest alarm in the late 20th century was acquired immune deficiency syndrome, or AIDS (q.v.). From the time of its first clear identification in 1981, AIDS spread rapidly, with reported cases rising at a high rate, especially among homosexuals and intravenous drug users in the United States and western Europe and among heterosexuals in tropical Africa. The high mortality rate from AIDS and the absence of a cure or vaccine against the disease had a sobering effect on sexually permissive societies. Promiscuity tended to be more widely discouraged, and the adoption of practices presumed to constitute “safe sex” (or, rather, safer sex)—such as the use of condoms or avoiding anal intercourse—tended to be encouraged.
Nearly a score of other sexually transmitted diseases are known. All have reasonably effective drug cures. About half of all cases of urethritis that are not gonorrhea are chlamydia (q.v.), which is caused by an infection with Chlamydia trachomatis. The latter bacterium is also the infecting agent in pelvic inflammatory disease (q.v.) and in still another sexually transmitted disease, lymphogranuloma venereum (q.v.). The cause for the remaining 50 percent of nongonococcal urethral infections is not known; no organism has been definitely related.
Trichomoniasis is an infection of the urogenital tract caused by a protozoan, Trichomonas vaginalis; males usually have no symptoms with this infection, and only a portion of infected females have a vaginal discharge.
Candidiasis (yeast infection) is caused by Candida albicans (sometimes called Monilia albicans), which produces in women a thick, whitish vaginal discharge and causes irritation and itching in the genital area. Males may have irritation of the glans or skin of the penis. Because this yeast is ubiquitous in the environment, these infections are not always sexually acquired.
Warts occurring in the genital areas are caused by certain types of papilloma viruses, and these types of warts can be transmitted to other people by sexual contact. Most often, genital warts are nothing more than a nuisance, but occasionally they can become so numerous or so large as to interfere with urination, bowel movements, or vaginal delivery. There is also mounting evidence that papilloma viral infections of the genital tract are a factor in the development of cancer of the cervix and possibly of the genitals themselves.
Chancroid, granuloma inguinale, and lymphogranuloma venereum are three diseases that have their highest incidence in the tropics. Chancroid, also called soft chancre, is caused by the bacterium Haemophilus ducreyi and resembles in appearance the primary chancre of syphilis. Granuloma inguinale is thought to be caused by a bacterium, Calymmatobacterium (Donovania) granulomatis; the lesion begins as a small sore but may spread to involve large areas, usually in the genital region, in a destructive, ulcerating lesion. Lymphogranuloma venereum is caused by Chlamydia trachomatis and begins with a frequently unnoticed bump on the genitals. Later, lymph glands in the groin enlarge and may proceed to rupture and drain purulent material. Swelling of the genitals may develop much later.
All of the aforementioned diseases are spread primarily by sexual contact, but there are other diseases that are transmitted sexually only in a minority of cases. Chief among such diseases are cytomegalovirus, a viral infection that is ubiquitous in humans and is spread by various means, including sex, and the hepatitis B virus, which is spread primarily through intravenous injections and blood transfusions but which can also be transmitted sexually.
Finally, a common infestation is pediculosis pubis. The crab louse, Phthirus pubis, infests the hair of the pubic region, where louse eggs, or nits, are attached to the hairs. After about one week the larvae hatch, and in about two weeks they develop into mature crab lice. The lice attach themselves to the base of the hair and feed on the blood of the host. Persons become aware of the infection because they see the lice or the eggs or because intense itching develops after two or three weeks.
The term venereal disease (VD), denoting any disease transmitted by sexual intercourse, lost favour in the late 20th century and was largely supplanted by the more comprehensive term sexually transmitted disease.
Sexually transmitted diseases have a long history. The best known of these diseases, syphilis (q.v.), is caused by the bacterium Treponema pallidum. Syphilis was first widely reported by European writers in the 16th century, and some medical historians assume that it was imported into Europe by explorers returning from the New World. Other authorities believe that syphilis is of ancient origin and may at one time have been mistakenly identified as leprosy. At any rate, syphilis first became widely recognized and reported about the year 1500, when a virtual epidemic swept Europe.
Urethritis is the infection and inflammation of the urethra (the passage that transmits urine from the bladder to the exterior of the body). Most cases of urethritis are in fact sexually transmitted. Urethritis that is caused by the gonococcus bacterium (Neisseria gonorrhoeae) is called gonorrhea (q.v.) and is one of the best-known sexually transmitted diseases. Gonorrhea was named by the Greek physician Galen and is thought to have been known to the ancient Chinese and Egyptians.
Syphilis and gonorrhea were long thought to be one disease. Real progress in characterizing them did not occur until the early 20th century, when their different causative microorganisms were identified and reliable diagnostic tests were developed. Effective treatment in the form of sulfa drugs and penicillin was introduced in the 1930s and '40s, and the eradication of such diseases seemed imminent. By the end of the 1950s, however, the frequency index had begun to rise again; among the many reasons cited were the tapering off of active “anti-VD” campaigns, the causative microorganisms' growing immunity to the antibiotics used in treatment, and a variety of sociological factors influencing sexual behaviour. The widespread acceptance of oral contraceptives and their supplantation of other methods of birth control were possibly linked, for a variety of reasons, to the spread of sexually transmitted diseases. Not only had the lack of oral contraceptives tended to discourage sexual promiscuity but also the older methods of condom and diaphragm had provided some protection against disease. Only with the outbreak of the AIDS epidemic did a return to the condom and “safe sex” receive new encouragement.
A disease that became especially widespread beginning in the 1960s and '70s was genital herpes (see herpes simplex). Herpes infections are significant not only in terms of the discomfort they cause but also for the potentially serious illness that might occur in infants born to mothers with genital herpes infections. A variety of treatments have been used for genital herpes, but none have been entirely satisfactory.
The sexually transmitted disease that caused perhaps the greatest alarm in the late 20th century was acquired immune deficiency syndrome, or AIDS (q.v.). From the time of its first clear identification in 1981, AIDS spread rapidly, with reported cases rising at a high rate, especially among homosexuals and intravenous drug users in the United States and western Europe and among heterosexuals in tropical Africa. The high mortality rate from AIDS and the absence of a cure or vaccine against the disease had a sobering effect on sexually permissive societies. Promiscuity tended to be more widely discouraged, and the adoption of practices presumed to constitute “safe sex” (or, rather, safer sex)—such as the use of condoms or avoiding anal intercourse—tended to be encouraged.
Nearly a score of other sexually transmitted diseases are known. All have reasonably effective drug cures. About half of all cases of urethritis that are not gonorrhea are chlamydia (q.v.), which is caused by an infection with Chlamydia trachomatis. The latter bacterium is also the infecting agent in pelvic inflammatory disease (q.v.) and in still another sexually transmitted disease, lymphogranuloma venereum (q.v.). The cause for the remaining 50 percent of nongonococcal urethral infections is not known; no organism has been definitely related.
Trichomoniasis is an infection of the urogenital tract caused by a protozoan, Trichomonas vaginalis; males usually have no symptoms with this infection, and only a portion of infected females have a vaginal discharge.
Candidiasis (yeast infection) is caused by Candida albicans (sometimes called Monilia albicans), which produces in women a thick, whitish vaginal discharge and causes irritation and itching in the genital area. Males may have irritation of the glans or skin of the penis. Because this yeast is ubiquitous in the environment, these infections are not always sexually acquired.
Warts occurring in the genital areas are caused by certain types of papilloma viruses, and these types of warts can be transmitted to other people by sexual contact. Most often, genital warts are nothing more than a nuisance, but occasionally they can become so numerous or so large as to interfere with urination, bowel movements, or vaginal delivery. There is also mounting evidence that papilloma viral infections of the genital tract are a factor in the development of cancer of the cervix and possibly of the genitals themselves.
Chancroid, granuloma inguinale, and lymphogranuloma venereum are three diseases that have their highest incidence in the tropics. Chancroid, also called soft chancre, is caused by the bacterium Haemophilus ducreyi and resembles in appearance the primary chancre of syphilis. Granuloma inguinale is thought to be caused by a bacterium, Calymmatobacterium (Donovania) granulomatis; the lesion begins as a small sore but may spread to involve large areas, usually in the genital region, in a destructive, ulcerating lesion. Lymphogranuloma venereum is caused by Chlamydia trachomatis and begins with a frequently unnoticed bump on the genitals. Later, lymph glands in the groin enlarge and may proceed to rupture and drain purulent material. Swelling of the genitals may develop much later.
All of the aforementioned diseases are spread primarily by sexual contact, but there are other diseases that are transmitted sexually only in a minority of cases. Chief among such diseases are cytomegalovirus, a viral infection that is ubiquitous in humans and is spread by various means, including sex, and the hepatitis B virus, which is spread primarily through intravenous injections and blood transfusions but which can also be transmitted sexually.
Finally, a common infestation is pediculosis pubis. The crab louse, Phthirus pubis, infests the hair of the pubic region, where louse eggs, or nits, are attached to the hairs. After about one week the larvae hatch, and in about two weeks they develop into mature crab lice. The lice attach themselves to the base of the hair and feed on the blood of the host. Persons become aware of the infection because they see the lice or the eggs or because intense itching develops after two or three weeks.
Leptospirosis
also called Weil's disease, infectious jaundice, pea picker's disease , or swineherd's disease contagious disease of animals, occasionally communicable to humans, caused by a pathogenic spirochete of the genus Leptospira.
The reservoir of leptospires includes rodents and certain domestic animals. These animals excrete live, fully virulent organisms in their urine and contaminate the environment. Outside the animal body, leptospires can live for several weeks in fresh water. Thus infection takes place by direct contact with urine of infected animals or by indirect contact with contaminated food or water. Leptospires can readily penetrate mucous membranes but probably cannot gain entrance to the body through intact skin. A scratch or abrasion, as well as the nasal mucosa and eye, are excellent portals of entry; thus the origin of many infections can be traced to wading, swimming, or other contact with water containing virulent leptospires. The incidence in humans depends upon the opportunity for exposure in swimming, the harvesting of rice, and contact with animals.
Clinical evidence of disease in humans varies depending upon the infecting type of leptospire. Usually after an incubation period of about a week, fever, weakness, and pains in the legs, back, and abdominal muscles are noted. Nausea, vomiting, and diarrhea are not uncommon. One characteristic symptom is congestion of the conjunctival blood vessels around the corneas of the eyes. Jaundice may occur after the first week of illness. The death rate is approximately 30 percent of the severely ill and jaundiced patients.
The reservoir of leptospires includes rodents and certain domestic animals. These animals excrete live, fully virulent organisms in their urine and contaminate the environment. Outside the animal body, leptospires can live for several weeks in fresh water. Thus infection takes place by direct contact with urine of infected animals or by indirect contact with contaminated food or water. Leptospires can readily penetrate mucous membranes but probably cannot gain entrance to the body through intact skin. A scratch or abrasion, as well as the nasal mucosa and eye, are excellent portals of entry; thus the origin of many infections can be traced to wading, swimming, or other contact with water containing virulent leptospires. The incidence in humans depends upon the opportunity for exposure in swimming, the harvesting of rice, and contact with animals.
Clinical evidence of disease in humans varies depending upon the infecting type of leptospire. Usually after an incubation period of about a week, fever, weakness, and pains in the legs, back, and abdominal muscles are noted. Nausea, vomiting, and diarrhea are not uncommon. One characteristic symptom is congestion of the conjunctival blood vessels around the corneas of the eyes. Jaundice may occur after the first week of illness. The death rate is approximately 30 percent of the severely ill and jaundiced patients.
Saturday, June 14, 2008
Forms
Forms of motor neurone disease include:
* amyotrophic lateral sclerosis (ALS) (sometimes called Lou Gehrig's disease)
* primary lateral sclerosis (PLS)
* progressive muscular atrophy (PMA)
* bulbar[1]
o pseudobulbar palsy - spastic
o progressive bulbar palsy - spastic and flaccid
Spinal muscular atrophy (SMA) is sometimes (but not always) considered a form of MND.
Terminology
In this article, MND refers to a group of diseases which affect the motor neurones. In the United States, the term ALS is more commonly used, where it is also known as Lou Gehrig's disease, after the baseball player. Although previously described by other neurologists of the 19th century, it was Jean-Martin Charcot, a French neurologist, who suggested grouping together a number of disparate conditions all affecting the lateral horn of the spinal cord in 1869. In France the disease is sometimes known as Maladie de Charcot (Charcot's disease), although it may also be referred to by the direct translation of ALS, Sclerose Laterale Amyotrophique (SLA). To help prevent confusion, the annual scientific research conference dedicated to the study of MND is called the International ALS/MND Symposium.
Signs and symptoms
Symptoms usually present between the ages of 50-70, and include progressive weakness, muscle wasting, and muscle fasciculations; spasticity or stiffness in the arms and legs; and overactive tendon reflexes. Patients may present with symptoms as diverse as a dragging foot, unilateral muscle wasting in the hands, or slurred speech.
Neurological examination presents specific signs associated with upper and lower motor neurone degeneration. Signs of upper motor neurone damage include spasticity, brisk reflexes and the Babinski sign. Signs of lower motor neurone damage include weakness and muscle atrophy.
Note that every muscle group in the body requires both upper and lower motor neurones to function. The signs described above can occur in any muscle group, including the arms, legs, torso, and bulbar region.
The symptoms described above may resemble a number of other rare diseases, known as "MND Mimic Disorders". These include, but are not limited to multifocal motor neuropathy, Kennedy's disease, hereditary spastic paraplegia, spinal muscular atrophy and monomelic amyotrophy. A small subset of familial MND cases occur in children, such as "juvenile ALS", Madras syndrome, and individuals who have inherited the ALS2 gene. However, these are not typically referred to as MND, but by their specific names.
Diagnosis
The diagnosis of MND is a clinical one, established by a neurologist on the basis of history and neurological examination. There is no diagnostic test for MND. Investigations such as blood tests, electromyography (EMG), magnetic resonance imaging (MRI), and sometimes genetic testing are useful to rule out other disorders that may mimic MND. However, the diagnosis of MND remains a clinical one. Having excluded other diseases, a relatively rapid progression of symptoms is a strong diagnostic factor. Although an individual's progression may sometimes "plateau", it will not improve.
A set of diagnostic criteria called the El Escorial criteria[2][3] have been defined by the World Federation of Neurologists for use in research, particularly as inclusion/exclusion criteria for clinical trials. Owing to a lack of clinical diagnostic criteria, some neurologists use the El Escorial criteria during the diagnostic process, although strictly speaking this is functionality creep, and some have questioned the appropriateness of the criteria in a clinical setting.[4]
* MND in the presence of both upper and lower motor neurone degeneration is ALS.
* Where the illness affects only the upper motor neurones it is PLS.
* Where the illness affects only the lower motor neurones it is PMA.
* Progressive bulbar palsy is degeneration of the lower motor neurones innervating the bulbar region (mouth, face, and throat).
* Pseudobulbar palsy refers to degeneration of the upper motor neurones to the same region.
It it possible that Transcranial Magnetic Stimulation can be used to diagnose MND.[5]
Prognosis
Most cases of MND progress quite quickly, with noticeable decline occurring over the course of months. Although symptoms may present in one region, they will typically spread. If restricted to one side of the body they are more likely to progress to the same region on the other side of the body before progressing to a new region. After several years, most patients require help to carry out activities of daily living such as self care, feeding, and transportation.
MND is typically fatal within 2-5 years. Around 50% die within 14 months of diagnosis. The remaining 50% will not necessarily die within the next 14 months as the distribution is significantly skewed. As a rough estimate, 1 in 5 patients survive for 5 years, and 1 in 10 patients survive 10 years.[citation needed] Professor Stephen Hawking is a well-known example of a person with MND, and has lived for more than 40 years with the disease.
Mortality normally results when control of the diaphragm is impaired and the ability to breathe is lost. One exception is PLS, which may last for upwards of 25 years. Given the typical age of onset, this effectively leaves most PLS patients with a normal life span. PLS can progress to ALS, decades later.
PATHOLOGY
Causes
About 90% of cases of MND are "sporadic", meaning that the patient has no family history of ALS and the case appears to have occurred with no known cause. Genetic factors are suspected to be important in determining an individual's susceptibility to disease, and there is some weak evidence to suggest that onset can be "triggered" by as yet unknown environmental factors (see 'Epidemiology' below).
Approximately 10% of cases are "familial MND", defined either by a family history of MND or by testing positive for a known genetic mutation associated with the disease. The following genes are known to be linked to ALS: Cu/Zn superoxide dismutase SOD1, ALS2, NEFH (a small number of cases), senataxin (SETX) and vesicle associated protein B (VAPB).
Of these, SOD1 mutations account for some 20% of familial MND cases. The SOD1 gene codes for the enzyme superoxide dismutase, a free radical scavenger that reduces the oxidative stress of cells throughout the body. So far over 100 different mutations in the SOD1 gene have been found, all of which cause some form of ALS(ALSOD database). In North America, the most commonly occurring mutation is known as A4V and occurs in up to 50% of SOD1 cases. In people of Scandinavian extraction there is a relatively benign mutation called D90A which is associated with a slow progression. Future research is concentrating on identifying new genetic mutations and the clinical syndrome associated with them. Familial MND may also confer a higher risk of developing cognitive changes such as frontotemporal dementia or executive dysfunction (see 'extra-motor change in MND' below).
It is thought that SOD1 mutations confer a toxic gain, rather than a loss, of function to the enzyme. SOD1 mutations may increase the propensity for the enzyme to form protein aggregates which are toxic to nerve cells.
Pathophysiology
Skeletal muscles are innervated by a group of neurones (lower motor neurones) located in the ventral horns of the spinal cord which project out the ventral roots to the muscle cells. These nerve cells are themselves innervated by the corticospinal tract or upper motor neurones that project from the motor cortex of the brain. On macroscopic pathology, there is a degeneration of the ventral horns of the spinal cord, as well as atrophy of the ventral roots. In the brain, atrophy may be present in the frontal and temporal lobes. On microscopic examination, neurones may show spongiosis, the presence of astrocytes, and a number of inclusions including characteristic "skein-like" inclusions, bunina bodies, and vacuolisation.
There is a role in excitotoxicity and oxidative stress, presumably secondary to mitochondrial dysfunction. In animal models, death by apoptosis has also been identified.
Emotional lability / pseudobulbar affect
Around a third of all MND patients experience labile affect, also known as emotional lability, pseudobulbar affect, or pathological laughter and crying. Patients with pseudobulbar palsy are particularly likely to be affected, as are patients with PLS.
Extra-motor change in MND
Cognitive change can and does occur in between 33–50% of patients. A small proportion exhibit a form of frontotemporal dementia characterised by behavioural abnormalities such as disinhibition, apathy, and personality changes. A small proportion of patients may also suffer from an aphasia, which causes difficulty in naming specific objects. A larger proportion (up to 50%) suffer from a milder version of cognitive change which primarily affects what is known as executive function. Briefly, this is the ability of an individual to initiate, inhibit, sustain, and switch attention and is involved in the organisation of complex tasks down to smaller components. Often patients with such changes find themselves unable to do the family finances or drive a car. Depression is surprisingly rare in MND (around 5–20%) relative to the frequency with which it is found in other, less severe, neurological disorders e.g. ~50% in multiple sclerosis and Parkinson's disease, ~20% in Epilepsy. Depression does not necessarily increase as the symptoms progress, and in fact many patients report being happy with their quality of life despite profound disability. This may reflect the use of coping strategies such as reevaluating what is important in life.
Although traditionally thought only to affect the motor system, sensory abnormalities are not necessarily absent, with some patients finding altered sensation to touch and heat, found in around 10% of patients. Patients with a predominantly upper motor neurone syndrome, and particularly PLS, often report an enhanced startle reflex to loud noises.
Neuroimaging and neuropathology has demonstrated extra-motor changes in the frontal lobes including the inferior frontal gyrus, superior frontal gyrus, anterior cingulate cortex, and superior temporal gyrus. The degree of pathology in these areas has been directly related to the degree of cognitive change experienced by the patient, if any. Patients with MND and dementia have been shown to exhibit marked frontotemporal lobe atrophy as revealed by MRI or SPECT neuroimaging.
Epidemiology
The incidence of MND is approximately 1–5 out of 100,000 people. Men have a slightly higher incidence rate than women. Approximately 5,600 cases are diagnosed in the U.S. every year. By far the greatest risk factor is age, with symptoms typically presenting between the ages of 50-70. Cases under the age of 50 years are called "young onset MND", whilst incidence rates appear to tail off after the age of 85.
Tentative environmental risk factors identified so far include: exposure to severe electrical shock leading to coma, having served in the first Gulf War, and playing professional Association football. However, these findings have not been firmly identified and more research is needed.
There are three "hot spots" of MND in the world. One is in the Kii peninsula of Japan, one amongst a tribal population in Papua New Guinea. Chamorro inhabitants from the island of Guam in the Pacific Ocean have an increased risk of developing a form of MND known as Guamanian ALS-PD-dementia complex or "lytico bodig", although the incidence rate has declined over the last 50 years and the average age of onset has increased.[6] Putative theories involve neurotoxins in the traditional diet including cycad nut flour and bats that have eaten cycad nuts.[7][8]
Treatment
Currently there is no cure for ALS. The only drug that affects the course of the disease is riluzole. The drug functions by blocking the effects of the neurotransmitter glutamate, and is thought to extend the lifespan of an ALS patient by only a few months.
The lack of effective medications to slow the progression of ALS does not mean that patients with ALS cannot be medically cared for. Instead, treatment of patients with ALS focuses on the relief of symptoms associated with the disease. This involves a variety of health professionals including neurologists, speech-language pathologists, physical therapists, occupational therapists, dieticians, respiratory therapists, social workers, palliative care specialists, specialist nurses and psychologists.
Research efforts
The search for a drug that will slow MND progression is under way. For example, recent research using mouse models suggests that minocycline, a common antibiotic, may also be effective in extending the lifespan of MND sufferers.[9][10][11] This drug must pass clinical trials with ALS patients before it may be used as a general treatment for MND.
Minocycline extends the lifespan of MND mice with SOD1 mutations, but it does not prevent their eventual death. Other agents that are currently in trials include ceftriaxone, arimoclomol, IGF-1 and coenzyme Q10 to name but a few.
Etymology
Amyotrophic comes from the Greek language: A- means "no", myo refers to "muscle", and trophic means "nourishment"; amyotrophic therefore means "no muscle nourishment," which describes the characteristic atrophication of the sufferer's disused muscle tissue. Lateral identifies the areas in a person's spinal cord where portions of the nerve cells that are affected are located. As this area degenerates it leads to scarring or hardening ("sclerosis") in the region.
Forms of motor neurone disease include:
* amyotrophic lateral sclerosis (ALS) (sometimes called Lou Gehrig's disease)
* primary lateral sclerosis (PLS)
* progressive muscular atrophy (PMA)
* bulbar[1]
o pseudobulbar palsy - spastic
o progressive bulbar palsy - spastic and flaccid
Spinal muscular atrophy (SMA) is sometimes (but not always) considered a form of MND.
Terminology
In this article, MND refers to a group of diseases which affect the motor neurones. In the United States, the term ALS is more commonly used, where it is also known as Lou Gehrig's disease, after the baseball player. Although previously described by other neurologists of the 19th century, it was Jean-Martin Charcot, a French neurologist, who suggested grouping together a number of disparate conditions all affecting the lateral horn of the spinal cord in 1869. In France the disease is sometimes known as Maladie de Charcot (Charcot's disease), although it may also be referred to by the direct translation of ALS, Sclerose Laterale Amyotrophique (SLA). To help prevent confusion, the annual scientific research conference dedicated to the study of MND is called the International ALS/MND Symposium.
Signs and symptoms
Symptoms usually present between the ages of 50-70, and include progressive weakness, muscle wasting, and muscle fasciculations; spasticity or stiffness in the arms and legs; and overactive tendon reflexes. Patients may present with symptoms as diverse as a dragging foot, unilateral muscle wasting in the hands, or slurred speech.
Neurological examination presents specific signs associated with upper and lower motor neurone degeneration. Signs of upper motor neurone damage include spasticity, brisk reflexes and the Babinski sign. Signs of lower motor neurone damage include weakness and muscle atrophy.
Note that every muscle group in the body requires both upper and lower motor neurones to function. The signs described above can occur in any muscle group, including the arms, legs, torso, and bulbar region.
The symptoms described above may resemble a number of other rare diseases, known as "MND Mimic Disorders". These include, but are not limited to multifocal motor neuropathy, Kennedy's disease, hereditary spastic paraplegia, spinal muscular atrophy and monomelic amyotrophy. A small subset of familial MND cases occur in children, such as "juvenile ALS", Madras syndrome, and individuals who have inherited the ALS2 gene. However, these are not typically referred to as MND, but by their specific names.
Diagnosis
The diagnosis of MND is a clinical one, established by a neurologist on the basis of history and neurological examination. There is no diagnostic test for MND. Investigations such as blood tests, electromyography (EMG), magnetic resonance imaging (MRI), and sometimes genetic testing are useful to rule out other disorders that may mimic MND. However, the diagnosis of MND remains a clinical one. Having excluded other diseases, a relatively rapid progression of symptoms is a strong diagnostic factor. Although an individual's progression may sometimes "plateau", it will not improve.
A set of diagnostic criteria called the El Escorial criteria[2][3] have been defined by the World Federation of Neurologists for use in research, particularly as inclusion/exclusion criteria for clinical trials. Owing to a lack of clinical diagnostic criteria, some neurologists use the El Escorial criteria during the diagnostic process, although strictly speaking this is functionality creep, and some have questioned the appropriateness of the criteria in a clinical setting.[4]
* MND in the presence of both upper and lower motor neurone degeneration is ALS.
* Where the illness affects only the upper motor neurones it is PLS.
* Where the illness affects only the lower motor neurones it is PMA.
* Progressive bulbar palsy is degeneration of the lower motor neurones innervating the bulbar region (mouth, face, and throat).
* Pseudobulbar palsy refers to degeneration of the upper motor neurones to the same region.
It it possible that Transcranial Magnetic Stimulation can be used to diagnose MND.[5]
Prognosis
Most cases of MND progress quite quickly, with noticeable decline occurring over the course of months. Although symptoms may present in one region, they will typically spread. If restricted to one side of the body they are more likely to progress to the same region on the other side of the body before progressing to a new region. After several years, most patients require help to carry out activities of daily living such as self care, feeding, and transportation.
MND is typically fatal within 2-5 years. Around 50% die within 14 months of diagnosis. The remaining 50% will not necessarily die within the next 14 months as the distribution is significantly skewed. As a rough estimate, 1 in 5 patients survive for 5 years, and 1 in 10 patients survive 10 years.[citation needed] Professor Stephen Hawking is a well-known example of a person with MND, and has lived for more than 40 years with the disease.
Mortality normally results when control of the diaphragm is impaired and the ability to breathe is lost. One exception is PLS, which may last for upwards of 25 years. Given the typical age of onset, this effectively leaves most PLS patients with a normal life span. PLS can progress to ALS, decades later.
PATHOLOGY
Causes
About 90% of cases of MND are "sporadic", meaning that the patient has no family history of ALS and the case appears to have occurred with no known cause. Genetic factors are suspected to be important in determining an individual's susceptibility to disease, and there is some weak evidence to suggest that onset can be "triggered" by as yet unknown environmental factors (see 'Epidemiology' below).
Approximately 10% of cases are "familial MND", defined either by a family history of MND or by testing positive for a known genetic mutation associated with the disease. The following genes are known to be linked to ALS: Cu/Zn superoxide dismutase SOD1, ALS2, NEFH (a small number of cases), senataxin (SETX) and vesicle associated protein B (VAPB).
Of these, SOD1 mutations account for some 20% of familial MND cases. The SOD1 gene codes for the enzyme superoxide dismutase, a free radical scavenger that reduces the oxidative stress of cells throughout the body. So far over 100 different mutations in the SOD1 gene have been found, all of which cause some form of ALS(ALSOD database). In North America, the most commonly occurring mutation is known as A4V and occurs in up to 50% of SOD1 cases. In people of Scandinavian extraction there is a relatively benign mutation called D90A which is associated with a slow progression. Future research is concentrating on identifying new genetic mutations and the clinical syndrome associated with them. Familial MND may also confer a higher risk of developing cognitive changes such as frontotemporal dementia or executive dysfunction (see 'extra-motor change in MND' below).
It is thought that SOD1 mutations confer a toxic gain, rather than a loss, of function to the enzyme. SOD1 mutations may increase the propensity for the enzyme to form protein aggregates which are toxic to nerve cells.
Pathophysiology
Skeletal muscles are innervated by a group of neurones (lower motor neurones) located in the ventral horns of the spinal cord which project out the ventral roots to the muscle cells. These nerve cells are themselves innervated by the corticospinal tract or upper motor neurones that project from the motor cortex of the brain. On macroscopic pathology, there is a degeneration of the ventral horns of the spinal cord, as well as atrophy of the ventral roots. In the brain, atrophy may be present in the frontal and temporal lobes. On microscopic examination, neurones may show spongiosis, the presence of astrocytes, and a number of inclusions including characteristic "skein-like" inclusions, bunina bodies, and vacuolisation.
There is a role in excitotoxicity and oxidative stress, presumably secondary to mitochondrial dysfunction. In animal models, death by apoptosis has also been identified.
Emotional lability / pseudobulbar affect
Around a third of all MND patients experience labile affect, also known as emotional lability, pseudobulbar affect, or pathological laughter and crying. Patients with pseudobulbar palsy are particularly likely to be affected, as are patients with PLS.
Extra-motor change in MND
Cognitive change can and does occur in between 33–50% of patients. A small proportion exhibit a form of frontotemporal dementia characterised by behavioural abnormalities such as disinhibition, apathy, and personality changes. A small proportion of patients may also suffer from an aphasia, which causes difficulty in naming specific objects. A larger proportion (up to 50%) suffer from a milder version of cognitive change which primarily affects what is known as executive function. Briefly, this is the ability of an individual to initiate, inhibit, sustain, and switch attention and is involved in the organisation of complex tasks down to smaller components. Often patients with such changes find themselves unable to do the family finances or drive a car. Depression is surprisingly rare in MND (around 5–20%) relative to the frequency with which it is found in other, less severe, neurological disorders e.g. ~50% in multiple sclerosis and Parkinson's disease, ~20% in Epilepsy. Depression does not necessarily increase as the symptoms progress, and in fact many patients report being happy with their quality of life despite profound disability. This may reflect the use of coping strategies such as reevaluating what is important in life.
Although traditionally thought only to affect the motor system, sensory abnormalities are not necessarily absent, with some patients finding altered sensation to touch and heat, found in around 10% of patients. Patients with a predominantly upper motor neurone syndrome, and particularly PLS, often report an enhanced startle reflex to loud noises.
Neuroimaging and neuropathology has demonstrated extra-motor changes in the frontal lobes including the inferior frontal gyrus, superior frontal gyrus, anterior cingulate cortex, and superior temporal gyrus. The degree of pathology in these areas has been directly related to the degree of cognitive change experienced by the patient, if any. Patients with MND and dementia have been shown to exhibit marked frontotemporal lobe atrophy as revealed by MRI or SPECT neuroimaging.
Epidemiology
The incidence of MND is approximately 1–5 out of 100,000 people. Men have a slightly higher incidence rate than women. Approximately 5,600 cases are diagnosed in the U.S. every year. By far the greatest risk factor is age, with symptoms typically presenting between the ages of 50-70. Cases under the age of 50 years are called "young onset MND", whilst incidence rates appear to tail off after the age of 85.
Tentative environmental risk factors identified so far include: exposure to severe electrical shock leading to coma, having served in the first Gulf War, and playing professional Association football. However, these findings have not been firmly identified and more research is needed.
There are three "hot spots" of MND in the world. One is in the Kii peninsula of Japan, one amongst a tribal population in Papua New Guinea. Chamorro inhabitants from the island of Guam in the Pacific Ocean have an increased risk of developing a form of MND known as Guamanian ALS-PD-dementia complex or "lytico bodig", although the incidence rate has declined over the last 50 years and the average age of onset has increased.[6] Putative theories involve neurotoxins in the traditional diet including cycad nut flour and bats that have eaten cycad nuts.[7][8]
Treatment
Currently there is no cure for ALS. The only drug that affects the course of the disease is riluzole. The drug functions by blocking the effects of the neurotransmitter glutamate, and is thought to extend the lifespan of an ALS patient by only a few months.
The lack of effective medications to slow the progression of ALS does not mean that patients with ALS cannot be medically cared for. Instead, treatment of patients with ALS focuses on the relief of symptoms associated with the disease. This involves a variety of health professionals including neurologists, speech-language pathologists, physical therapists, occupational therapists, dieticians, respiratory therapists, social workers, palliative care specialists, specialist nurses and psychologists.
Research efforts
The search for a drug that will slow MND progression is under way. For example, recent research using mouse models suggests that minocycline, a common antibiotic, may also be effective in extending the lifespan of MND sufferers.[9][10][11] This drug must pass clinical trials with ALS patients before it may be used as a general treatment for MND.
Minocycline extends the lifespan of MND mice with SOD1 mutations, but it does not prevent their eventual death. Other agents that are currently in trials include ceftriaxone, arimoclomol, IGF-1 and coenzyme Q10 to name but a few.
Etymology
Amyotrophic comes from the Greek language: A- means "no", myo refers to "muscle", and trophic means "nourishment"; amyotrophic therefore means "no muscle nourishment," which describes the characteristic atrophication of the sufferer's disused muscle tissue. Lateral identifies the areas in a person's spinal cord where portions of the nerve cells that are affected are located. As this area degenerates it leads to scarring or hardening ("sclerosis") in the region.
An introduction to Mesothelioma
Mesothelioma is one of the deadliest diseases known to man; the average life span of an inflicted person from the time of diagnosis until death is less than 24 months. It’s a disease that strikes approximately 3,000 United States citizens each and every year; hard working people who have labored for a lifetime to provide for their families, doing the work that keeps this country running and a great place to live. They worked in factories, at shipyards, in mines, for the US military, as engineers, as pipefitters, as steel workers, as auto mechanics, and in so many other professions. They came home to their loved ones exhausted and covered in dirt and dust; tired, but content that they had a job and were providing for their family. Content that they were putting food on the table and a house over their loved one’s heads. Content that they were working to make a better life for their families in this generation and the next...
But what they didn’t know was that while they were working so hard, they were not only slowly killing themselves, but those that they were working so hard to help; their family, their loved ones.
Mesothelioma is a disease that is almost 100% preventable; the only known cause is via exposure to the deadly mineral Asbestos. It comes from inhaling the particles of dust as the asbestos degrades; eating away at the lining of your lungs and developing into a deadly cancer. Dust that was inhaled in clouds of white powder, dust that was carried home on the clothes of the men who built this country, dust that was cleaned from the clothes by the wives and children who supported their sole provider at home, dust that was packed around the heating systems in houses and offices and schools, dust that carried a deadly price; and dust made a fortune in blood money for the companies that produced it.
Unfortunately, the effects of asbestos on the human body were known to be deadly for years by the companies who employed the ‘greatest generation’ and made hundreds of millions, if not billions, of dollars off of their backs. But instead of taking simple steps to alleviate the problem and save the lives of thousands of their workers, they choose to do nothing and continue to make a “healthy” profit with a “deadly” product. Many even went so far as to hide the truth from their workers and their families. And because the normal latency period for Mesothelioma (The time from exposure until the patient falls ill) is 20 to 30 years, many got away with this for years. We are only now beginning to see the full effects of the disease, and feel the terrible outcry of the people against those who put profits before human lives to a degree that is simply unfathomable.
But what they didn’t know was that while they were working so hard, they were not only slowly killing themselves, but those that they were working so hard to help; their family, their loved ones.
Mesothelioma is a disease that is almost 100% preventable; the only known cause is via exposure to the deadly mineral Asbestos. It comes from inhaling the particles of dust as the asbestos degrades; eating away at the lining of your lungs and developing into a deadly cancer. Dust that was inhaled in clouds of white powder, dust that was carried home on the clothes of the men who built this country, dust that was cleaned from the clothes by the wives and children who supported their sole provider at home, dust that was packed around the heating systems in houses and offices and schools, dust that carried a deadly price; and dust made a fortune in blood money for the companies that produced it.
Unfortunately, the effects of asbestos on the human body were known to be deadly for years by the companies who employed the ‘greatest generation’ and made hundreds of millions, if not billions, of dollars off of their backs. But instead of taking simple steps to alleviate the problem and save the lives of thousands of their workers, they choose to do nothing and continue to make a “healthy” profit with a “deadly” product. Many even went so far as to hide the truth from their workers and their families. And because the normal latency period for Mesothelioma (The time from exposure until the patient falls ill) is 20 to 30 years, many got away with this for years. We are only now beginning to see the full effects of the disease, and feel the terrible outcry of the people against those who put profits before human lives to a degree that is simply unfathomable.
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