Human bacterial diseases Essay Example
Human bacterial diseases Essay Example

Human bacterial diseases Essay Example

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Introduction

Leprosy (Hansen's Disease), sometimes called "Hanseniasis" or "H.D.," is a chronic my bacterial disease of man, caused by Mycobacterium leprae (infectious in some cases), primarily affecting the peripheral nerves and secondarily involving skin and certain other tissues/organs, in particular the eye, mucosa of the nasal and upper respiratory tract and also the testes.

In most cultures, HD still carries a strong stigma that sometimes makes more trouble for the patient than the actual leprosy itself. One of the main characteristics of Leprosy is its ability to affect the various nervous systems of the body, particularly the peripheral nerves. The key targets of M.leprae (Mycobacterium leprae) are the nerves' Schwann Cells.

Leprosy does not affect the Central Nervous System. Where the sensory nerves are damaged, in varying d

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egrees, they cannot register pain. Where those nerves supply the extremities of hands and feet, the latter are vulnerable to burns and other injuries that can often result in the loss of fingers and toes and sometimes hands and feet. Where the eye is affected, corneal anesthesia. Cranial Nerve involvement can often lead to blindness, where the lack of health education makes the sufferer unaware of the means to prevent injury due to dust or other irritants.

Where the motor nerves are involved, various forms of paralysis such as "Dropped Foot", "Dropped Wrist", "Clawed Hand", "Lagophthalmos" (eye cannot close due to nerve paralysis) can result.

Where the autonomic nerves are damaged, the hair follicle, particularly in the cooler areas such as the eye-brows, can often result in the loss of hair in the affected parts. Damage to the autonomic nerves also can result in poor or no

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function of the sweat and sebaceous glands. This causes a drying of the skin and consequent cracking, exposing the sufferer to secondary infection. Leprosy is not a curse from the gods or divine punishment for some sins committed in the past.

Leprosy is a disease like any other disease and it is TOTALLY CURABLE. Another myth that still prevails, even in "educated" societies, is that the disease causes flesh to rot and fingers and toes to "drop off". Nothing could be further from the truth. Tragically, limbs that are damaged, because the victim cannot feel pain, sometimes have to be amputated but, we can now detect the disease before the patient is conscious of any loss of sensation.

Even if the patient has experienced some measure of deformity, we are able, through chemotherapy, physiotherapy, and reconstructive surgery, to correct many of the disabilities. Ideally, we should detect the disease before there is any need for physiotherapy or reconstructive surgery.

In such cases, where only chemotherapy is required, treatment is very cheap. On average, it costs only $15.00 per month to provide drugs and services to cure one patient of leprosy. What other disease, of such horrendous magnitude, can be treated for a mere $180.00 per year? However, progress is being made. In 1951, there were 15 million leprosy sufferers worldwide.

Today, the W.H.O. (World Health Organization) estimates that 6 million people remain to be treated, either through chemotherapy, or physiotherapy/surgery, or both. It should also be remembered that even though many patients are being cured, thousands still suffer because of deformity and stigma. They may have become bacteriologically "negative" but a prejudiced, uneducated, and ill-informed society may

still reject them because of these disabilities that they had absolutely no control over.

We may be able to kill off their germs, but we cannot restore their sightless eyes or amputated limbs.

Incidentally, many of their insensitive, ulcerated fingers and toes are eaten off, not by the leprosy germ, but by rats and other animals. For this reason, early diagnosis, along with early treatment and health education, are of vital importance. Historical Although leprosy is widely regarded as one of the oldest diseases known to man, it has not accurately been described and distinguished from other diseases with similar appearances until 1847. Historically, the first full accounts of various forms of leprosy are from India (600 B.C.). They described different kinds of skin lesion as well as peripheral nerve damage and offered a unifying concept to embrace all these manifestations. The next records of leprosy are slightly later dated from China. In the Western world, no identifiable clinical descriptions of leprosy are known prior to the third century B.

C., when the Lepromatous type came to be known to the physicians of Alexandria under the name elephantiasis. Some scholars have suggested that Alexandria obtained leprosy when the troops of Alexander the Great returned from the Indian campaign in 327-326 B.C.

Italy is said to have acquired leprosy from Pompey's soldiers returning from Egypt (62 B.C.). The exact meaning of the word leprosy still varies widely in the Old and New Testaments. In Hebrew, tsaraath, scaly blemishes on skin, cloth, leather, or the walls of houses are associated with ritual defilement.

But still, nowhere is their mention of the characteristic signs of leprosy as we know

them today, even with all the confusing descriptions mentioned. In the Old Testament, references show that it may possibly have been to rue leprosy, and the lepra of the New Testament probably included the disease. Not until 1873, did Armauer Hansen of Norway, recognize that the disease was caused by M. Leprae. This new knowledge subsequently led to improved staining methods and better microscopes making possible a wealth of pathological studies. But until the 1940s, early diagnosis and isolation were the only possible methods for the control of HD.

By 1950, Dapsone became the standard treatment for HD, and the rapid improvement in patients led to hopes of the elimination of HD.

The number of leprosy sufferers in the world is not known with certainty. Estimates have been made by governments and other private organizations, but some countries are reluctant to acknowledge the seriousness of their leprosy problem or even that they have a problem. They may also lack reliable and complete statistics for leprosy and other endemic diseases. The majority of these cases are found in Africa, India, South America, and Southeast Asia.

There are about 4,000 cases in the United States, but about three-fourths of these patients have contracted the disease in other countries and brought it to the U.S. California, Florida, Louisiana, and Texas are the states where the disease is found most commonly. Today the spread of leprosy is subject to movements of population, for instance of Southerners in the U.S.

northwards, of Mexican farmhands seasonally to California, of Puerto Ricans to New York City. Leprosy may be introduced by immigrants into countries that have been free of original cases for many years;

such as southern Europeans into France, Switzerland, and Belgium, by North Africans into France. In these countries, however, the imported disease has not re-established itself, and secondary cases among contacts are extremely rare.

Types of Leprosy

There are two main types of leprosy.

Lepromatous, which affects mainly the skin, and Tuberculoid, mainly comprising of the nerves. The two other forms, Borderline and Indeterminate, eventually grow into one of the two principle types. Lepromatous Type This type is found in patients without an immune resistance to the Mycobacterium leprae organism and is the widespread, anergic form of the disease. The organisms can always be found in enormous numbers in the deep layers of the affected skin. The disease then spreads up the nerves but does not adhere to them as in the Tuberculoid form.

It very often spreads to the skin of the face, where it causes thickening and corrugation of the skin and a typical leonine appearance. Soft nodules appear on the ears, nose, and cheeks and sometimes break down into discharging sores. The nose often is teeming with bacilli, and this sometimes leads to the destruction of the septum of the nose and the palate. There are many varieties of Lepromatous leprosy: Macular, Diffuse, Infiltrated, Nodular, and Polyneuritic.

The Lepromatous skin lesions involve cooler parts of the body surface and are characterized by massive collections of macrophages containing large numbers of acid-fast bacilli.

Tuberculoid Type

This is the localized form of the disease and is due to a combination of bacterial proliferation and the immunologic responses of the host bacilli. The skin lesions are characterized as single or multiple; macular or

raised; either indolent or spread centrifugally with some rapidity, and show a variable loss of pigmentation, sweating and tactile sensitivity. These skin lesions consist of one or, at most, a few well-circumscribed skin lesions with profound anesthesia. Due to the body's immune system, which responds more intensely to the presence of leprosy bacilli, this form of the disease is the most resistant. The body immune system also contains or localizes the disease to either a skin patch or a nerve trunk. The patient is unable to feel pain and minor injuries pass unnoticed.

Large eroding ulcers can form, causing loss of fingers and toes; sometimes the condition of the limb is so bad that amputation is necessary.

Indeterminate Type

This form of the disease effects people who are unable to resist infection of M. Leprae. The first sign of the disease is one or a few of hypopigmented skin macules with little sensory loss confined to the lesion. The development of these lesions can take anywhere from two to four years.

However, due to its variable course, in three-fourths of all patients, the disease heals spontaneously and in some cases, remains Indeterminate and eventually progresses to one of the forms of Tuberculoid or Lepromatous leprosy. Borderline Type As the name suggests, it includes those types of disease between Lepromatous and Tuberculoid leprosy. When a patient has this form of the disease they can go either two ways: Upgrading, which is when the patient develops more clinical, bacteriological, and histopathologic features of the Tuberculoid type. Downgrading, which is when the patient develops more features of the Lepromatous type. Borderline Tuberculoid leprosy (BT) resembles Tuberculoid disease except

that the number of skin lesions is usually greater, the edges of the skin lesions are less well defined, there is a tendency for satellite lesions to develop near the edges of the larger lesions, and individual lesion tend to be larger.

BT tends to damage peripheral nerves more widespread and severe than in TT.

Borderline Lepromatous leprosy (BL) resembles Lepromatous disease except that at least some of the skin lesions are selectively anesthetic and show varying degrees of distinctness in their borders. BL can develop (upgrade) from Indeterminate leprosy or by downgrading from BT. In Borderline leprosy (BB), the skin lesions are few to numerous in number, red or brown in color, rounded or oval in shape. The lesions are infiltrated throughout or with a central clear area or areas producing a punched-out appearance. Classification The method of classifying leprosy has been around for some time now.

The method was established in Madrid at the sixth International Congress of Leprosy in 1953. It was agreed that the basic criteria of classification should be clinical, depending on the examination of smears from skin lesions and nasal mucosa.

The congress also agreed that there should be two distinct forms of leprosy, Lepromatous and Tuberculoid. These two would be the poles of the immunological spectrum.

This form of classification did present some problems though, the International Classification System was much too complicated for the use of Indian leprologists. The Indian leprologists thought that the classification should be simple enough for use by field workers, but advanced enough for research done by workers with special investigative techniques.  This means that the LL and BL forms are Multibacillary leprosies.

justify;">Transmission Hansens disease is a communicable disease and the human-being is the only known source for infecting other human-beings. It is thought that the bacilli are passed from one person to another through the skin and upper respiratory tract. Persons with untreated Multibacillary types of the disease (Lepromatous and Borderline) are the main sources of infection. The theory of transmission through the respiratory tract, which may house millions of leprosy bacilli, is based on:

  1. The inability of the organisms to be found on the surface of the skin.
  2.  The demonstration of a large number of organisms in the nasal discharge.
  3.  The high proportion of intact bacilli in the nasal secretion.
  4.  The evidence that M. Leprae can survive outside the human host for several days or even weeks. Also, with each cough or sneeze, the bacilli are discharged on droplets or dust particles that healthy individuals can then inhale.

However, the transmission of skin contact can not also be ruled out. This is based upon the results of individuals who are in close association with leprosy patients.

These people that work with leprosy patients have by far, a much greater chance of acquiring the disease. There still remains a small amount of evidence that we can acquire the disease through insects. A large number of experiments have been conducted in the past showing how insects have bitten people and transmitted the disease. The question of whether insects actually transmitted infection has remained unanswered.

There however, is absolutely no evidence that transmission can be accomplished through sex. Diagnosis Leprosy is a disease of the nervous system, but not all nerves are affected.

The central nervous system is spared, but the peripheral and cutaneous nervous systems can be infiltrated by M. Leprae bacilli and then, secondarily, the skin is affected.

NERVES:

  1. There may be an area of anesthesia or numbness with/or "pins and needles, "ants crawling" or tingling in any area.
  2.  In the hands or feet, there may be a weakening of the small muscles and/or the presence of disability in those areas.
  3. Thickening and/or tenderness of the peripheral and cutaneous nerves.
  4. Weakening or loss of function of the sweating mechanism in those areas. SKIN: 1. Erythematous or hypopigmented patch of skin with loss of sensation to either/or/and touch, pain, temperature. 2. Smooth, oily, shiny and oedematous appearance of the skin.
  5. Diffuse erythema of the skin.
  6.  On a shiny, erythematous and oedematous skin, there may be nodules or papules.
  7.  There may be a sudden onset of painful erythematous nodules as above.
  8.  There may be a thickening of the earlobes.
  9.  The eyebrows may become thin or even disappear, beginning from the outside.

These various manifestations are not seen in all cases, so it is essential to know the salient points.

Without knowledge of these, it is possible to confuse leprosy with about 30 other conditions that may appear to be leprosy. If a person has one of these other conditions such as Carpal Tunnel Syndrome, Diabetic Ulcers, Bell's Palsy, Syphilis, Vitiligo, etc., and is "diagnosed" as having leprosy, the psychological damage (because of the stigma) can be devastating.

The two important diagnostic clinical signs are:

  1. Thickening/tenderness of the peripheral nerve trunks and/or cutaneous branches.
  2.  The majority of H.D.

cases can be diagnosed on the basis of these above

two signs. These forms are the "Paucibacillary" types and generally non-infectious. However, there are a few cases (Multibacillary or infectious) that do not display any of these signs. Their skin may be oily, shiny, smooth, and erythematous with or without nerve thickening/tenderness. Although, this is the more serious form of H. D., in the early stages there may not be any serious nerve involvement or damage.

This is because damage to the nerves is not due directly to the leprosy bacillus, but rather to the body's immune system violently reacting to the antigens liberated from the dying and dead M.leprae. To make a proper diagnosis, therefore, the patient must be examined bacteriologically by taking skin smears (not of the blood but rather the skin tissue and serum).

A proper diagnosis, therefore, will require the presence of the following three cardinal signs:

  1.  Loss or impairment of sensations.
  2.  Nerve enlargement at the sites of predilection.
  3.  The presence of acid-fast M.leprosy bacilli in smears from skin and/or nasal mucosa.

In some of the very early lesions suggestive of leprosy, where none of the above-mentioned cardinal signs are present, it may be necessary to conduct three other tests:

  1.  Skin Examination by Histo-Pathology. If the tissue is stained for acid-alcohol-fast M.leprae, the bacilli may be seen in the nerve. The need for such an examination is rare.
  2. Histamine Test: This also is rarely needed. Histamine Phosphate in one drop (1:1000) is placed on an area of normal skin of the patient and pricked with a needle. If the nerve is intact, there will be a weal and an erythematous flare showing that the nerve is intact. This same test is then

performed on the area of skin suspected of being leprous. There will be a weal as in the first test, but no erythematous flare if the nerve is damaged, indicating H.D.This test is rarely needed and is performed only as a "last resort".

  •  Sweat Test: In most cases, this is done by feeling with the back of the fingers for coolness of the normal, moist skin, in comparison with the warmness of dry skin affected by M.leprae. In some rare cases, it may be necessary to inject Pilocarpine Nitrate (1:1000) intradermally both in normal skin and skin with a suspected lesion of H.D. If the lesion is affected by M.leprae, sweating is absent.
  • This can be determined by applying Tr. Iodine on the skin, allowing to dry and then covering the area with starch before injecting. A positive sweat response will turn the starch blue, indicating that the sweating mechanism is intact.

    After a diagnosis has been made, classification is necessary to determine the type of leprosy and this will vary according to the patient's degree of Cell-Mediated Immunity. The course and duration of treatment will vary, depending on the degree of Immunity. Treatment MDT (Multidrug Therapy) uses three main drugs used in the treatment of leprosy: Dapsone (DDS), Rifampicin, and Clofazamine for Multibacillary leprosy patients and Rifampicin and Dapsone for Paucibacillary leprosy patients.

    Rifampicin is the most important drug used in the treatment, therefore, it is used in both types of leprosy treatment.

    There is a new drug, Ofloxacin. This drug however has some unpleasant side-effects: diarrhea, nausea, gastrointestinal disturbances, insomnia, dizziness, hallucinations, and nervousness. MDT does not work when only one drug is used because

    of the development of drug resistance to that drug. This is why Rifampicin, Clofazimine, and Dapsone are used together. Rifampicin is used once a month and has no toxic effects, however, urine will be slightly colored red after the first treatment.

    Clofazimine is most active when given daily and is well tolerated and virtually nontoxic in the correct dosage for MDT. This has a side-effect though, it causes brownish, black discoloration and dryness of the skin. Dapsone, given orally, is the safest drug and has very few side effects, except for allergic reactions. It was introduced in 1941, but not until 1946 was it successfully experimented with leprosy patients. Dapsone was the main antileprosy drug, but in the 1960s Clofazamine became available.

    This duo of Dapsone and Clofazimine proved to be invaluable in the treatment of leprosy patients.

    Once again a new drug was introduced, this time it was Rifampicin, in the 1970s. Rifampicin is now the main bacterial drug used in MDT. MDT kills bacilli, which interrupts the chain of transmission, and cures the disease before any serious nerve damage happens. Because of the danger of the emergence of drug-resistant leprosy bacilli, treatment must be given regularly. And though MDT sounds very expensive, it is the most cost-effective form for preventing disabilities due to leprosy. MDT works so well and fast that 70-80% of those who have Paucibacillary leprosy and are noninfectious can be cured in six months.

    The remaining 20-30% who have Multibacillary leprosy can be cured in two years.

    The fast action of MDT shows immediate improvement, encouraging the patient to go on with the treatment. MDT was introduced in the 1980s with

    Dapsone being the only drug at the time. Dapsone was bacteriostatic and could only prevent the multiplication of bacillus, but with the introduction of Rifampicin, a bacteriocidal drug, leprosy is now curable. Since then, MDT has cured over 4.

    2 million cases, and right now, 2.4 million are in need of effective MDT chemotherapy. Scientists hypothesize that between now and the year 2000, a total of 7 million. Immunity In fighting a disease, the body is capable of identifying any foreign organism and the defense mechanism recognizes the invading germs as "Antigens.

    " In the case of Leprosy, M.leprae is the Antigen. The body's defense mechanism starts with the skin that is a good, protective covering. Healthy skin inhibits the entry of germs except when it is cut. The body's fluids are mildly antiseptic with tears, sweat, and gastric juices putting up a first-line of resistance to any germs that could bring on the disease.

    However, if the invading germs manage to break through this first line of defense, there are several types of "Defense Cells" that are specifically designed to ingest and digest these foreign invaders.

    In actual fact, a battle takes place within the body as the defense cells fight against the bacteria to drive them away and this is called "Inflammation", which may be likened to the body's second line of defense. The body's protective mechanism has two aspects, Non-Specific and Specific. In the case of the Non-specific, the large defense cells called Macrophages, through their action of "phagocytosis" (engulfing) sweep through the body's bloodstream to ingest and digest any foreign bodies they encounter. The macrophage then dissolves the germ by certain chemicals or

    enzymes.

    The second type of protective mechanism is specific and the body's defense system can only "recognize" a foreign invader if it has experience in this identification of certain antigens. In Lepromatous patients, their macrophages can ingest the M. leprae but cannot digest (kill) because there are no "T-Type" ("T" for Thymus, the gland that programs these cells) lymphocytes to assist the macrophages to produce the needful digestive juices or enzymes. So, in the case of Lepromatous leprosy, the very cells that are meant to kill off the bacilli, are actually transporting them around the body and providing an environment in which they may even be able to multiply. At the present time though, leprosy cannot be prevented. Research on a preventive vaccine, however, is slowly progressing. This vaccine will be used the same way we use vaccines of Smallpox, Typhoid, Cholera, Plaque, and etc.

    A vaccine of killed or weakened leprosy bacilli will be used to immunize everyone from the disease. Already, a vaccine of killed leprosy bacilli has been used to immunize mice and armadillos against leprosy. Millions of people will need to receive MDT.

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