MINAMATA DISEASE & WATER BORN DISEASE

- Minamata disease sometimes referred to as Chisso-Minamata disease is a neurological syndrome caused by severe mercury poisoning. Symptoms include ataxia, numbness in the hands and feet, general muscle weakness, narrowing of the field of vision, and damage to hearing and speech. In extreme cases, insanity, paralysis, coma, and death follow within weeks of the onset of symptoms. A congenital form of the disease can also affect fetuses in the womb.

- Minamata disease was first discovered in Minamata city in Kumamoto prefecture, Japan, in 1956. It was caused by the release ofmethylmercury in the industrial wastewater from the Chisso Corporation's chemical factory, which continued from 1932 to 1968. This highly toxic chemical bioaccumulated in shellfish and fish in Minamata Bay and the Shiranui Sea, which, when eaten by the local populace, resulted in mercury poisoning. While cat, dog, pig, and human deaths continued for 36 years, the government and company did little to prevent the pollution. The animal effects were severe enough in cats that they came to be called "dancing cat fever.

As of March 2001, 2,265 victims had been officially recognised as having Minamata disease (1,784 of whom had died) and over 10,000 had received financial compensation from Chisso. By 2004, Chisso Corporation had paid $86 million in compensation, and in the same year was ordered to clean up its contamination. On March 29, 2010, a settlement was reached to compensate as-yet uncertified victims.

A second outbreak of Minamata disease occurred in Niigata Prefecture in 1965. The original Minamata disease and Niigata Minamata disease are considered two of the Four Big Pollution Diseases of Japan.

Finding the cause

Researchers from Kumamoto University also began to focus on the cause of the strange disease. They found that the victims, often members of the same family, were clustered in fishing hamlets along the shore of Minamata Bay. The staple food of victims was invariably fish and shellfish from Minamata Bay. The cats in the local area, who tended to eat scraps from the family table, had died with symptoms similar to those now discovered in humans. This led the researchers to believe that the outbreak was caused by some kind of food poisoning, with contaminated fish and shellfish being the prime suspects.

On November 4 the research group announced its initial findings: "Minamata disease is rather considered to be poisoning by a heavy metal... presumably it enters the human body mainly through fish and shellfish.

Identification of mercury

• As soon as the investigation identified a heavy metal as the causal substance, the wastewater from the Chisso plant was immediately suspected as the origin. The company's own tests revealed that its wastewater contained many heavy metals in concentrations sufficiently high to bring about serious environmental degradation including lead, mercury, manganese, arsenic, thallium and copper plus the chalcogen selenium. Identifying which particular poison was responsible for the disease proved to be extremely difficult and time consuming. During the years 1957 and 1958, many different theories were proposed by different researchers. At first, manganese was thought to be the causal substance due to the high concentrations found in fish and the organs of the deceased. Thallium, selenium and a multiple contaminant theory were also proposed but it was not until March 1958, when visiting British neurologist Douglas McAlpine suggested that Minamata symptoms resembled those oforganic mercury poisoning, that the focus of the investigation centered on mercury.

• In February 1959, the mercury distribution in Minamata Bay was investigated. The results shocked the researchers involved. Large quantities of mercury were detected in fish, shellfish and sludge from the bay. The highest concentrations centred around the Chisso factory wastewater canal in Hyakken Harbour and decreased going out to sea, clearly identifying the plant as the source of contamination. Pollution was so heavy at the mouth of the wastewater canal that a figure of 2 kg of mercury per ton of sediment was measured: a level that would be economically viable to mine. Indeed, Chisso did later set up a subsidiary to reclaim and sell the mercury recovered from the sludge.

• Hair samples were taken from the victims of the disease and also from the Minamata population in general. In patients the maximum mercury level recorded was 705 ppm (parts per million), indicating very heavy exposure and in non-symptomatic Minamata residents the level was 191 ppm. This compared to an average level of 4 ppm for people living outside the Minamata area.

On November 12, 1959, the Ministry of Health and Welfare's Minamata Food Poisoning Subcommittee published its results:

"Minamata disease is a poisoning disease that affects mainly the central nervous system and is caused by the consumption of large quantities of fish and shellfish living in Minamata Bay and its surroundings, the major causative agent being some sort of organic mercury compound.

Wastewater treatment

On October 21, 1959, Chisso was ordered by the Ministry of International Trade and Industry to switch back its wastewater drainage from the Minamata River to Hyakken Harbour and to speed up the installation of wastewater treatment systems at the factory. Chisso installed a Cyclator purification system on December 19, 1959, and opened it with a special ceremony. Chisso's president Kiichi Yoshioka drank a glass of water supposedly treated through the Cyclator to demonstrate that it was safe. In fact, the wastewater from the acetaldehyde plant, which the company knew still contained mercury and led to Minamata disease when fed to cats, was not treated through the Cyclator at the time. Testimony at a later Niigata Minamata disease trial proved that Chisso knew the Cyclator to be completely ineffective the purification tank was installed as a social solution and did nothing to remove organic mercury.

The deception was successful and almost all parties involved in Minamata disease were duped into believing that the factory's wastewater had been made safe from December 1959 onward. This widespread assumption meant that doctors were not expecting new patients to appear, resulting in numerous problems in the years to follow, as the pollution continued. In most people's minds, the issue of Minamata disease had been resolved.

WATERBORNE DISEASE

DEFINITION

Waterborne diseases are caused by pathogenic microorganisms that most commonly are transmitted in contaminated fresh water. Infection commonly results during bathing, washing, drinking, in the preparation of food, or the consumption of food thus infected. Various forms of waterborne diarrheal disease probably are the most prominent examples, and affect mainly children in developing countries; according to the World Health Organization, such diseases account for an estimated 4.1% of the total DALY global burden of disease, and cause about 1.8 million human deaths annually. The World Health Organization estimates that 88% of that burden is attributable to unsafe water supply, sanitation and hygiene.

- The term "waterborne disease" is reserved largely for infections that predominantly are transmitted through contact with or consumption of infected water. Trivially, many infections may be transmitted by microbes or parasites that accidentally, possibly as a result of exceptional circumstances, have entered the water, but the fact that there might be an occasional freak infection need not mean that it is useful to categorise the resulting disease as "waterborne". Nor is it common practice to refer to diseases such as malariaas "waterborne" just because mosquitoes have aquatic phases in their life cycles, or because treating the water they inhabit happens to be an effective strategy in control of the mosquitoes that are the vectors.

- Microorganisms causing diseases that characteristically are waterborne prominently include protozoa and bacteria, many of which are intestinal parasites, or invade the tissues or circulatory system through walls of the digestive tract. Various other waterborne diseases are caused by viruses. (In spite of philosophical difficulties associated with defining viruses as "organisms", it is practical and convenient to regard them as microorganisms in this connection.)

- Yet other important classes of water-borne diseases are caused by metazoan parasites. Typical examples include certain Nematoda, that is to say "roundworms". As an example of water-borne Nematode infections, one important waterborne nematodal disease is Dracunculiasis. It is acquired by swallowing water in which certain copepoda occur that act as vectors for the Nematoda. Anyone swallowing a copepod that happens to be infected with Nematode larvae in the genus Dracunculus, becomes liable to infection. The larvae cause guinea worm disease.

SOURCE:

- http://en.wikipedia.org/wiki/Minamata_disease

- http://en.wikipedia.org/wiki/Waterborne_diseases

MUSCLE ATROPHY

MUSCLE ATROPHY

- Muscle atrophy is defined as a decrease in the mass of the muscle it can be a partial or complete wasting away of muscle, and is most commonly experienced when persons suffer temporary disabling circumstances such as being restricted in movement and/or confined to bed as when hospitalized. When a muscle atrophies, this leads to muscle weakness, since the ability to exert force is related to mass. Modern medicine's understanding of the quick onset of muscle atrophy is a major factor behind the practice of getting hospitalized patients out of bed and moving about as active as possible as soon as is feasible, despite sutures, wounds, broken bones and pain.

- Muscle atrophy results from a co-morbidity of several common diseases, including cancer, AIDS, congestive heart failure, COPD (chronic obstructive pulmonary disease), renal failure, and severe burns patients who have "cachexia" in these disease settings have a poor prognosis. Moreover, starvation eventually leads to muscle atrophy.

- Disuse of the muscles, such as when muscle tissue is immobilized for even a few days of unuse such as when the patient has a primary injury such as an immobilized broken bone (set in a cast or immobilized in traction) will also lead rapidly to disuse atrophy and minimizing such occurrences as soon as possible is a primary mission of occupational & physical therapists employed within hospitals working in co-ordination with orthopedic surgeons.

- The similar in effect neurogenic atrophy is muscle atrophy that results from damage to the nerve that stimulates the muscle causing a shriveling about otherwise healthy limbs. Also, time in a circa zero g environment without exercise will lead to atrophy. This is partially due to the smaller amount of exertion needed to move about, and that muscles are not used to maintain posture. In a similar effect, patients with a broken leg joint undergoing as little as three weeks of traction can lose enough back and buttocks muscle mass and strength as to have difficulty sitting without assistance and experience pain, stress and burning even after a very short ten minute exposure when such positioning is contrived during recovery.

CLINICAL SETTINGS

- There are many diseases and conditions which cause a decrease in muscle mass, known as atrophy, including inactivity, as seen when a cast is put on a limb, or upon extended bedrest (which can occur during a prolonged illness); cachexia - which is a syndrome that is a co-morbidity of cancer and congestive heart failure; chronic obstructive pulmonary disease; burns, liver failure, etc., and the wasting Dejerine Sottas syndrome (HSMN Type III). Other syndromes or conditions which can induce skeletal muscle atrophy are liver disease, and starvation.

QUALITY OF LIFE

- Muscular atrophy decreases qualities of life as the sufferer becomes unable to perform certain tasks or worsen the risks of accidents while performing those (like walking). Muscular atrophy increases the risks of falling in conditions such as IBM (inclusion body myositis). Muscular atrophy affects a high number of the elderly.

OTHER MUSCLE DISEASES, DISTINCT FROM ATROPHY

- During aging, there is a gradual decrease in the ability to maintain skeletal muscle function and mass. This condition is called "sarcopenia". The exact cause of sarcopenia is unknown, but it may be due to a combination of the gradual failure in the "satellite cells" which help to regenerate skeletal muscle fibers, and a decrease in sensitivity to or the availability of critical secreted growth factors which are necessary to maintain muscle mass and satellite cell survival.

In addition to the simple loss of muscle mass (atrophy), or the age-related decrease in muscle function (sarcopenia), there are other diseases which may be caused by structural defects in the muscle (muscular dystrophy), or by inflammatory reactions in the body directed against muscle (the myopathies).

PATHOPHYSIOLOGY

Muscle atrophy occurs by a change in the normal balance between protein synthesis and protein degradation. During atrophy, there is a down-regulation of protein synthesis pathways, and an activation protein degradation. The particular protein degradation pathway which seems to be responsible for much of the muscle loss seen in a muscle undergoing atrophy is the ATP-dependent ubiquitin/proteasome pathway. In this system, particular proteins are targeted for destruction by the ligation of at least four copies of a small peptide calledubiquitin onto a substrate protein. When a substrate is thus "poly-ubiquitinated", it is targeted for destruction by the proteasome. Particular enzymes in the ubiquitin/proteasome pathway allow ubiquitination to be directed to some proteins but not others - specificity is gained by coupling targeted proteins to an "E3 ubiquitin ligase". Each E3 ubiquitin ligase binds to a particular set of substrates, causing their ubiquitination.

POTENTIAL TREATMENT

- Muscle atrophy can be opposed by the signaling pathways which induce muscle hypertrophy, or an increase in muscle size. Therefore one way in which exercise induces an increase in muscle mass is to downregulate the pathways which have the opposite effect.

- One important rehabilitation tool for muscle atrophy includes the use of functional electrical stimulation to stimulate the muscles. This has seen a large amount of success in the rehabilitation of paraplegic patients. 

SOURCE:

- http://en.wikipedia.org/wiki/Muscle_atrophy

SCOLIOSIS

DEFINE SCOLIOSIS

- Scoliosis is a medical condition in which a person's spinal axis has a three-dimensional deviation. Although it is a complex three-dimensional deformity, on an X-ray, viewed from the rear, the spine of an individual with scoliosis can resemble an "S" or a "?", rather than a straight line.

SIGN AND SYMPTOMS

- The signs of scoliosis can include:

• Uneven musculature on one side of the spine
• A rib prominence or a prominent shoulder blade, caused by rotation of the ribcage in thoracic scoliosis
• Uneven hips, arms or leg lengths
• Slow nerve action (in some cases)

CAUSES

- An estimated 65% of scoliosis cases are idiopathic, about 15% are congenital and about 10% are secondary to a neuromuscular disease.

- Adolescent idiopathic scoliosis (AIS) has no clear causal agent, and is generally believed to be multifactorial, although genetics are believed to play a role.The prevalence of scoliosis is 1% to 2% among adolescents, however the likelihood of progression among adolescents with a Cobb angle of less than 20° is about 10% to 20%

- At least one gene, CHD7, has been associated with the idiopathic form of scoliosis. Studies in 2006 showed evidence of a linkage between idiopathic scoliosis and threemicrosatellite polymorphisms in the MATN1 gene (encoding for Matrilin 1, cartilage matrix protein), respectively consisting of 103, 101 and 99 base pairs.

- Congenital scoliosis can be attributed to a malformation of the spine during weeks three to six in utero. It is a result of either a failure of formation, a failure of segmentation, or a combination of stimuli.This incomplete and abnormal segmentation results in an abnormally shaped vertebra, at times fused to a normal vertebra or unilaterally fused vertebrae, leading to the abnormal lateral curvature of the spine.

- Secondary scoliosis due to neuropathic and myopathic conditions can result in a loss of muscular support for the spinal column which results in the spinal column being pulled in abnormal directions. Some conditions which may cause secondary scoliosis include muscular dystrophy, spinal muscular atrophy, poliomyelitis, cerebral palsy, spinal cord trauma, and myotonia. Scoliosis often presents itself, or worsens, during the adolescence growth spurt and is more often diagnosed in females than males.

MANAGEMENT

- The traditional medical management of scoliosis is complex and is determined by the severity of the curvature and skeletal maturity, which together help predict the likelihood of progression. The conventional options for children and adolescents are.

1. Observation
2. Bracing
3. Surgery

- For adults, treatment usually focuses on relieving any pain.

1. Painkilling medication
2. Bracing
3. Exercise
4. Surgery

PHYSICAL THERAPY

- Exercise

- Self care

- Productivity

- Leisure

- Bracing

- Casting

- Surgery

SOURCE:

- http://en.wikipedia.org/wiki/Scoliosis

BASIC SKELETAL SYSTEM AND IT FUNCTION

BASIC SKELETAL

KRYSA-SKELETAL-UNISEL-JPEG

FUNCTION OF SKELETAL SYSTEM

- SHAPE

Bone structure gives shape to the body. This shape changes as you grow, and your skeletal system determines your height, width and other factors, such as the size of your hands and feet. Body shape or type is genetically inherited. There are three main body shapes -- ectomorphs (tall and thin), mesomorphs (shorter and muscular) and endormorphs (apple or pear-shaped).

- SUPPORT

The skeleton provides support to the body and keeps your internal organs in their proper place. The vertebral column allows you to stand erect, while cavities -- hollow spaces in the skeleton are designed to hold your organs. For example, the skull holds the brain, the chest cavity holds your lungs and heart while the abdominal cavity holds your gastrointestinal organs. Additionally, the pelvis and leg bones are strong and thick to support the weight of the entire skeleton.

- MOVEMENT

The skeletal bones are held together by ligaments. Tendons attach your muscles to the bones of your skeleton. The muscular and skeletal systems work together to carry out bodily movement, and together they are called the musculoskeletal system. When muscles contract, the skeleton moves.

The shape of the skeletal system also impacts movement. The small bones of the foot allow for adaptation to all sorts of terrain, while the small bones in the hands allow for precise and detailed movement.

- PROTECTION

The skeleton protects vital organs from damage, encasing them within hard bones. The cranium bone --skull -- houses the brain, while the vertebral, or spinal, column protects the delicate spinal cord, which controls all bodily functions through communication with your brain. The bony thorax, comprised of the ribs and sternum, protects your heart and lungs.

- BLOOD CELL PRODUCTION AND STORAGE

The spongy tissue inside long bones, such as the femur, or thigh bone, have two types of marrow responsible for blood cell production. On average, 2.6 million red blood cells are produced each second by the bone marrow. Red bone marrow gives rise to blood cells while yellow bone marrow stores fat, which turns into red bone marrow in case of severe red blood cell depletion or anemia.

Skeletal bones also function as a storage bank for minerals, such as calcium and phosphorus. These minerals are necessary for vital body functions, such as nerve transmission and metabolism.

SOURCE:

-http://www.livestrong.com/article/115165-functions-skeleton/

ENVIRONMENTAL EPIDEMIOLOGY

                        DEFINE EPIDEMIOLOGY

Epidemiology is the study of how often diseases occur in different groups of people and why. Epidemiological information is used to plan and evaluate strategies to prevent illness and as a guide to the management of patients in whom disease has already developed.

                  FUNCTION OF EPIDEMIOLOGY

• Health surveillance, monitoring and analysis
• Investigation of disease outbreaks, epidemics and risk to health
• Establishing, designing and managing health promotion and disease prevention programmes
• Enabling and empowering communities to promote health and reduce inequalities
• Creating and sustaining cross-Government and intersectoral partnerships to improve health and reduce inequalities
• Ensuring compliance with regulations and laws to protect and promote health
• Developing and maintaining a well-educated and trained, multi-disciplinary public health workforce
• Ensuring the effective performance of health services to meet goals in improving health, preventing disease and reducing inequalities
• Research, development, evaluation and innovation
• Quality assuring the public health function     

                 JOHN SNOW & EPIDEMIOLOGY

- John Snow was a British physician, born on the 15th of March, 1813. Born in one of the poorest regions of York in the United Kingdom. John Snow apprenticed as a surgeon, before becoming a physician in 1850 and moving to London.

- As the summer of 1854 wound down, a major cholera outbreak struck Soho, a neighbourhood in London, England. From August 31st to September 3rd, 127 people died of Cholera. Within a week, 500 people had died and around one in seven people who developed cholera eventually died from it. This all occurred within 250 yards of the Cambridge Street and Broad Street intersection.

- He examined the neighbourhood, and talked to everyone he could. He was looking for an underlying theme that linked these people together. He suspected some contamination of the water, but couldn’t find any organic matter in it, which you would expect under the Miasma theory. However, the more he looked, the more it seemed like the pump was responsible. Almost all the cases of cholera occurred close to the Broad Street Pump. There were only 10 cases that were closer to another pump. Of these, 5 preferred the water from the Broad Street Pump (and got their water from the Broad Street Pump) and 3 were children who went to school near the Broad Street Pump. The last two were unrelated, and likely just background levels of cholera in the population. This was pretty convincing, but Snow mapped it out to make sure that he was on the right track. You might recognize the map – it’s what we use for our blog banner here on Public Health Perspectives.

- Snow provided more evidence for his theory that the pump was responsible for the cholera outbreak. For example, there was a brewery on Poland Street where 535 people worked, that had a pump on the premises. However, while cholera raged outside, only 5 of these people developed it. He explained this by pointing out that those who worked at the brewery were allowed to drink some of the malt liquor they made – and the foreman suspected that they didn’t drink any water at all. And even if they did, they used the pump on site.

- The evidence Snow presented in favour of his findings were too compelling for the local council to ignore, and while there was resistance to this finding, Snow had said enough for the local council to remove the pump handle, halting the spread of the disease. But, as Snow later pointed out, he couldn’t be sure that this stopped the disease, and the incidence of the disease might have been declining. But the end result was the same – cholera cases went down.

- That is not to say that everyone believed him. The council may have taken the pump down, but it wasn’t until 1885, when Robert Koch identified V. cholerae as the bacillus causing the disease that he had proof of his theory. He was right, but wasn’t around to see this discovery himself.

- John Snow died on the 16th of June 1858, at the age of 45. His legacy still lives on, over a 150 years later.

SOURCE:

- http://blogs.plos.org/publichealth/2013/03/11/john-snow-the-first-epidemiologist/

- http://en.wikiversity.org/wiki/Epidemiology_and_Public_Health

- http://www.bmj.com/about-bmj/resources-readers/publications/epidemiology-uninitiated/1-what-epidemiology