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A discussion of the aetiology, diagnosis and management of a fictitious tuberculosis infection in a health worker.

AEJNE Volume 4 - No.1 October, 1998.

Joanne Stuart
Undergraduate student,
Bachelor of Nursing Programme
Southern Cross University, Lismore.

Julia Roberts, a 30 year old nurse who works in an inner city hospital, presented to her GP complaining of a 2 month history of weight loss, cough, haemoptysis, low grade fever, and drenching night sweats. Her doctor suggests that she may have Tuberculosis (TB) and orders several tests to confirm the diagnosis.

According to Anderson, Anderson, and Glanze (1996:1599), 'TB' is the abbreviation for tuberculosis (formerly called consumption). Black (1996:591), Lee and Bishop (1997:388), Norris (1995:529) and Cook (1996:49) describe TB as an ancient worldwide bacterial disease, sometimes acute, more often chronic, caused by infection with the tubercle bacillus mycobacterium tuberculosis.

Benenson (1995:491) indicates the primary reservoir is humans, rarely primates, while Jensen and Wright (1993:369) add, in the human host TB may go unrecognised for many years, and is seen in different stages with progression of the disease depending on many subtle host and environmental factors. The American Lung Association (1995) and Hellman and Gram (1993:67) state the difference between TB infection and TB disease; while an infected person's immune defences are protecting them they are asymptomatic, but sometimes the body's defences can no longer control the bacteria, it starts to multiply and causes disease. Furthermore, Hamann (1994:102), Kumar, Kumzi and Stanley (1997:420) concur, defining TB as a communicable disease, primarily involving the lungs, sometimes invading the bloodstream, resulting in brain, liver, urogenital tract and bone infection and sometimes causing a generalised infection ('miliary' tuberculosis).

Although certain other agents referred to as atypical mycobacteria also cause TB, (eg., M. avium-intracellulare complex in AIDS patients), it is the organism Mycobacterium tuberculosis hominis, discovered by Robert Koch in 1882, that is responsible for the vast majority of cases (Black:1996:591, Stead and Bates 1983:1019). Kumar et al., (1997:421), and Gillies and Dodds, (1984:57), indicate the microscopy of mycobacterium TB reveals size variable 3 m x 0.3 m, non-motile, non-capsulate, straight or slightly curved rods with rounded or slightly expanded ends, acid fast organisms (ie., they have a high content of complex lipids that readily bind the Ziehl-Neelsen [carbol fuchsin] stain and subsequently resist decolourization). On culture it is strictly aerobic, grows very slowly (a generation time of 18 hours or more), even on rich media such as Lowenstein-Jensen (L-J) egg medium, macroscopic growth rarely appears until at least 2-4 weeks incubation at 37 C and the characters on L-J can be described as rough (dry and irregular surface), tough (hard and difficult to emulsify), and buff in colour (Mandell, Douglas and Bennett, 1990:1879). In addition, The NCGR Microbial Genome Site (7/8/1997), Cook (1996:49), and Lee et al., (1997:388) believe M. Tuberculosis is an obligate aerobe, having a waxy outer coat that allows it to resist chemical agents and drying, therefore making it possible for the organism to remain alive for long periods in sputum, rooms, bedding and similar environments.

Lee et al., (1997:388), Davey and McCance (1996:759), Black (1996:592), Kumar et al., (1997:420) and Mandell et al., (1990:1880), agree, describing the following pathophysiology in the symptomatic person (eg., Julia Roberts):

After organisms are inhaled, they lodge in the epithelial surface of the alveolus, and multiply inside white blood cells that have phagocytized them. The host response includes neutrophil infiltration and fluid accumulation within alveoli, then neutrophil destruction occurs due to the rupture of organisms. Lymphocytes move in, alveolar macrophages phagocytize living tubercle bacilli, which again multiply within, destroying their new host. Dead phagocytes continue to release infective organisms, an acute inflammatory response occurs and a large quantity of fluid is released, especially in the lungs.

The colonies of bacilli, are sealed off by the neutrophils and macrophages, forming chronic granulomas, (the primary lesion or Ghon focus), that sometimes heals, but more often produces tissue necrosis or calcification. The central portion of the granuloma undergoes destruction, typically giving it a cheesy, or caseous appearance. Collagenous scar tissue grows around the tubercle, isolation of the bacilli is completed and further multiplication of the bacilli is prevented, due to completion of the immune response.

However, occasionally the host's immune system fails, allowing uncontrolled multiplication of tubercle bacilli in the lungs, resulting in formation of numerous tubercles. Subsequently, organisms are spread by blood-borne dissemination, resulting in milary tuberculosis. When the host has sufficient resistance, lesions can be walled off from the rest of the lung by encapsulation. While ever necrotic tissue is present, the inflammatory response will continue.

Vander, Sherman and Luciano (1994:641), Black (1996:457), and Ludwig-Beymer and Huether (1996:328) indicate the following; Julia's low grade fever is an adaptive systemic response to the infection caused by mycobacterium TB. Her body is raising it's temperature to kill microorganisms, and adversely affect their growth and replication, decrease levels of iron, zinc, and copper (minerals needed for bacterial proliferation). Fever causes lysosomal breakdown and autodestruction of cells, increases lymphocytic transformation and motility of polymorphonuclear neutrophils (facilitating the immune response) and enhances phagocytosis. Exogenous pyrogens (exotoxins and endotoxins from infectious agents) cause fever by stimulating release of an endogenous pyrogen from macrophages, resulting in an elevation of hypothalamic set point. Adaptive responses to infection include secretion of acute phase proteins, release of neutrophils, monocytes, amino acids, and also many other responses elicited by one or more cytokines released from stimulated macrophages. Thus, interleukin-1 (IL-1), tumour necrosis factor (TNF), and interleukin 6 (IL-6), all of which serve local roles in immune responses, also serve as hormones to elicit responses such as fever.

Stead et al., (1983:1021) suspect defervescence during sleep may explain Julia's drenching night sweats. Childs (1994:683) and Vander et al., (1994:641) briefly describe the process as, stimulation of sweat glands by Julia's sympathetic nervous system produces secretion of fluid onto her skin, causing her skin to cool when the thermal energy needed to transfer the fluid to a gas is absorbed by the surrounding air from her skin's surface.

Vander et al., (1994:726) and Closs (1994:749) suggest the following to explain Julia's weight loss; Secretion of IL-1, TNF, and IL-6 has increased plasma IL-1, TNF,and IL-6 resulting in decrease in appetite, greater demands upon the body due to infection or disease generally increase the basal metabolic rate (BMR), however when a person suffers wasting because of infection, the BMR may decrease below normal. Black (1996:458) argues, decreases in plasma concentrations of iron occur in response to infection, having adaptive value since bacteria require a high concentration of iron and other minerals to multiply. Julia's weight loss may also be associated with her condition worsening at night, difficulty in breathing, so less sleep, less appetite (vicious circle), anxiety, possibly depression, and maybe poor nutrition. Davey et al., (1996:741) concur with Vander et al., (1994:724) understanding Julia's cough reflexes originate in receptors located between airway epithelial cells, are stimulated by the medullary respiratory neurons and cause a deep inspiration and violent expiration. When Julia coughs, she produces haemoptysis (the expectoration of blood - stained sputum), often a sign of active TB. Haemoptysis is caused by the erosion of small pulmonary arteries in the wall of a cavity, in severe cases it may be massive and life-threatening (Daly, Holmes, Blake and Charnow, 1995:398). In sum, Julia's 2 month history of signs and symptoms suggest she is in the illness phase of active TB, indicating the need to commence tests immediately.

Norris (1995:530) believes diagnostic tests include physical examination, chest x-ray, tuberculin skin test (purified protein derivative, 'PPD'), and sputum smears and cultures, pointing out diagnosis must be precise, since several other diseases may mimic TB. Bloom (1995:130) and Mandell et al.,(1990:1879) consider a chest x-ray or the tuberculin skin test maybe suggestive of diagnosis, but agree with Evans (1994:52), Pagana and Pagana (1997:823), Berkow and Fletcher (7/8/1997), and Fischbach (1995:285), stating confirmation of diagnosis must be made by isolation of organisms of the mycobacterium tuberculosis complex on culture of sputum or bronchial brushings by Zeihl-Neelsen staining, the fasting gastric washings (takes 6 to 8 weeks), or as Saab (1997:66) and Evans (1994:53) suggest, in a doubtful case of TB with a clear effusion where culture for tubercle is negative, some of the fluid can be sent for injection into a guinea-pig. Clearly, Bloom (1995:131), Kumar et al., (1997:425), Benenson (1995:490), Black (1996:593), and Lee et al., (1997:390) agree, a presumptive diagnosis of active disease is made by demonstration of acid-fast bacilli in stained smears from sputum or other body fluids; a positive sputum smear justifies initiation of antituberculosis therapy. Tilkion (1987:507) suggests biopsy of the liver, bone marrow, or lymph nodes may be diagnostic of miliary TB, while needle pleural biopsy revealing the typical granuloma with giant cells, showing caseous necrosis, is sufficiently diagnostic to initiate therapy.

Microbiology culture: Evans (1994:52) indicates, use of sterile containers for collection of 3 to 5 sputum specimens (early morning), from bronchi (antiseptic mouthwash to be withheld, postnasal secretions or saliva are unacceptable), or provide sputum via procedures such as laryngeal swab, ultrasonic nebulization, chest physiotherapy, nasotracheal or tracheal suctioning. Tilkion (1987:508), recommends biopsy specimens, laryngeal swabs, or gastric washings, should be transported to the laboratory immediately for preparation, since the bacillus die quickly. Collins, Lyne and Grange (1995:411) point out collection of sputum should not occur over a 24 hour period as it increases the frequency of contamination. Fischbach (1995:284) concurs, adding direct microscopy as unreliable, because environmental mycobacteria are frequently present in specimens. Pagana et al., (1997:828) advises standard (universal) specimen collection and handling, pointing out sputum can be viscous and difficult to manipulate, therefore requiring the use of plastic disposable loops, as ordinary bacteriological loops are unsafe and unsatisfactory. Evans (1994:52), reports antibiotics as possibly causing false-negative cultures or delayed growth of organisms, adding when a specimen is collected and TB is suspected, ?TB should be written on the request form.

Skin: The Richmond Area Health Service Infection Control Pamphlet (1997:1) and Peoples Plague : Facts about Tuberculosis, (1994:51) explain Mantoux skin testing for Julia involves PPD of tubercle bacillus to be injected intradermally, usually in the left arm; a positive reaction is measured by the size of the lump (induration) that develops at the injection site over the following 48 - 72 hours. Pagani et al., (1997:827) warns contraindications include;

* patients with known active TB.

* patients who have recieved bacille Calmette-Guerin (BCG) immunization against PPD, because these patients will demonstrate a positive reaction to the PPD. vaccination even though they have never had TB.

* precise injection site is imperative as deeper injections are apt to be washed out by vascular flow, making dosage uncertain.

* false-negative results can occur due to some viral diseases, anergic states such as Hodgkins disease, sarcoidosis, massive infection and pleural effusion.

Fischbach (1995:282) and Pagani et al.,(1997:827) conclude, although the PPD test is used to detect TB infection, it is unable to indicate whether the infection is active or dormant. Joyce, Lefever and Kee (1991:407) discuss additional tests such as the multipuncture test (Tine test or Mono - Vacc.) that involves PPD impregnation of the tines, and Vollmer's patch test involving the impregnation of a bandaid-like-patch with concentrated old tuberculin .

Pagana et al., (1997:828) and Kumar et al., (1997:425) comment on the recently developed Polymerase chain reaction culture methods, where organisms are identified in 36 to 48 hours. PCR amplification of M. tuberculosis DNA allows rapid diagnosis, by amplification of genomes, which then can be detected by genetic DNA probes. However, both authors note the average detection time is longer for extrapulmonary specimens than for sputum specimens, with culture remaining the gold standard because it also allows testing of drug susceptibility.

Haematology data that indicates the presence of an infection include the following:

Leukocytes: these white blood cells may be increased in number due to trying to remove debris, including dead or injured host cells of all kinds, defending Julia's body against the mycobacterium tuberculosis that cause infection and inflammation. Leucocytes are classified as either granulocytes (neutrophils, basophils, and eosinophils) or agranulocytes (monocytes/macrophages, lymphocytes). Julia's blood test may show in excess of 10,000 leucocytes/mm of blood.

Neutrophils (polymorphonuclear neutrophil, or PMN): these granulocytes are phagocytes and would be increased due to quickly migrating out of the capilliaries and into the inflamed lung tissue (neutrophils are usually first on the scene), where they ingest and destroy the bacilli, beginning the process by which the body's defence mechanisms isolate the bacilli, preventing their spread. The neutrophils and macrophages seal off the colonies of bacilli, forming a granulomatous lesion called a tubercle. Julia's blood test may show an increase greater than 50 - 60% of total white cell count.

Monocytes: these agranulocytes are immature macrophages formed and released by the bone marrow and may be increased in the blood test. When they move from blood into tissues, they go through a series of cellular changes, maturing into macrophages, destroying not only microorganisms but also larger particles, such as debris left from dead neutrophils. Although macrophages perform much the same job as neutrophils, they arrive second on the scene and in large numbers, can live for months or years (some migrate to fixed sites in lymphoid tissues), and have a nonspecific role in host defences, also being critical to specific host defences. Julia's blood test may show an increase in monocytes beyond the normal range of 2% - 6% of total leukocyte count.

Lymphocytes: derived from lymphoid stem cells in bone marrow, circulate in the blood and increase to perform specific host immune defences, ie., antibodies are produced to fight the bacilli that migrate through the lymphatics and lodge in Julia's lymph nodes. Julia's blood test may show in excess of 20 - 40% per microlitre.

Platelets: are disk-shaped cytoplasmic fragments essential for blood coagulation and control of bleeding. Julia's blood test may show a decrease in platelets, because of blood loss due to her haemoptysis. Julia's blood test would show less than 250,000 per microlitre.

Electrolytes: Julia may experience an electrolyte imbalance due to fluid loss (drenching night sweats), weight loss and other effects of her chronic lung disease.

Erythrocyte sedimentation rate (ESR): Byrne, Saxton, Pelikan and Nugent (1986:94) describe ESR as a measure of the speed with which red blood cells in anticoagulated whole blood settle to the bottom of a calibrated tube. This normally takes place slowly, but the rate is increased in infectious disease such as TB. A gradually increasing ESR is indicative of continuing or increasing problems, whereas the opposite reflects clinical improvement and a sign of an abating inflammatory condition. Therefore Julia's ESR may be elevated.

C-reactive protein (CRP): Byrne et al., (1986:612) is an abnormal plasma protein that appears in the serum, reflecting to some degree the extent and severity of the inflammatory condition or tissue necrosis. Julia may have an elevated level, as Dacie and Lewis (1995:127), note a persistently elevated CRP values may occur in active pulmonary TB.

It is worth noting, should Julia's system be or become immunodeficient, (ie., impaired function of one or more components of the immune or inflammatory response, including B cells, T cells, phagocytic cells, and complement), each of the abovementioned blood test results would alter, due to the disruption of lymphocytes (Rote, Huether and McCance, 1996:202 ). Bloom (1995:253) agrees, pointing out a reduction in WBCs below normal (leucopenia), occurs in TB probably due to a toxic effect on the marrow itself.

Benenson (1995:491) and Jensen et al., (1993:374) and Stead et al., (1983:1019) indicate TB may result from progression of a recent infection or much later from recrudescence of dormant infection, by inhalation of tubercle bacilli in airborne droplet nuclei during expiratory efforts such as coughing, singing, sneezing and even talking. Benenson (1995:491) informs the degree of communicability depends on the number of bacilli discharged, the virulence of the bacilli, adequacy of ventilation, exposure of the bacilli to the sun or UV light, and opportunities for their aerolization.

Black (1996:591) considers prolonged close exposure to an infectious case may be necessary for successful transmission of this disease. Also, Benenson (1995:491) suggests direct invasion through contaminated articles (fromites), mucous membranes or breaks in the skin may occur, but is extremely rare. Mid North Coast Health Service Infection Control Manual (MNCHSICM 1996:82) advises, extrapulmonary TB is not infectious if enclosed, although there is some slight risk of transmission in the presence of a tuberculosis discharge.

The MNCHSICM (1996:82-84) and Benenson (1995:492) suggest the following precautions;

* Active cases should be treated with appropriate anti-TB drugs in a single room for at least 2 weeks.

* In outpatient facilities where there may be active cases, if they are not on appropriate anti-drugs, isolate them in a single room.

* The direction of air flow in single rooms must be from the hallway into the room (negative pressure) and the air from the room should be filtered to the outside of the building and directed away from intake vents or windows.

* Doors of these rooms are to be kept closed wherever possible (to maintain air flow direction).

* Infectious patients should be isolated from immunocompromised persons (this includes immunocompromised staff not working on the same ward as the patient).

* Patients need to be instructed in the careful handling and disposal of their sputum and body fluids, and to wear recommended particulate mask (PCM2000 duckbill face mask) while in common shared areas of the hospital, as do all health care workers and visitors entering the room.

* Equipment:- specified equipment is needed outside and inside the room, an appropriate 'infection hazard' sign on the door (depending on Hospital Policy), and waste disposal guidelines must be adhered to.

* Laboratory specimens should be well sealed with no contamination of the outside of the container and transported immediately to the lab in a sealed bag.

The name of the vaccine is Bacillus Calmette-Guerin (BCG) and according to Mackett and Williamson (1995:135), it is an avirulent bovine tubercle bacillus that is the most widely used vaccine in the world.

Advantages and disadvantages of BCG according to Mackett et al., (1995:135), Altmann and Carnie (1996:521) and Connaught (1995:2):

Advantages

* BCG is one of only two vaccines the World Health Organisation (WHO) recommend to be given at birth to newborns in areas where TB is common. A single immunization with BCG can give long-lasting cell-mediated immunity to TB; it can be given repeatedly; complications are rare; and BCG is a highly potent adjuvant in it's own right.

* BCG vaccination is successful in at least 90% of people.

* BCG has been engineered as a vector to express antigens from other organisms, eg., the envelope glycoprotein of HIV.

* Vaccination is possible for children and adolescents under 16 who are in contact with a multi-drug resistant TB patient or the child or adolescent cannot take the appropriate antibiotic. Furthermore, Altmann and Carnie (1996:521) suggest the studies show high protection from systemic disease (miliary TB and tuberculous meningitis) in children.

Disadvantages

* Menzies, Fanning, Yuan and Fitzgerald (1995:41) argue against BCG vaccination because the efficacy of the vaccine is variable, ranging from 0 - 80% in controlled trials, and when given to adults the vaccine makes subsequent reactions to tuberculin uninterpretable.

* BCG provides partial protection to health workers and family members, however, Altmann et al., (1996:521) indicate inappropriate technique can lead to increased risk of abscess or lymphadenopathy, and administration to inappropriate persons (such as the immunosuppressed) can lead to disseminated BCG disease.

* BCG should not be given if you have or have ever had TB, have a fever, suffer from skin conditions such as eczema or dermatitis, have HIV disease or are in a high risk group but have not been tested for HIV, if you have received another live vaccine within 4 weeks, or you have a positive Mantoux test (Connaught 1995:3).

According to Dolin, Raviglione and Kochi (1994:215) one third of the world's population is infected with mycobacterium tuberculosis, the leading killer of adults in the world today, while Tomasz (1994:1247) claims global incidence is predicted to increase from 7.5 million new cases annually in 1990 to 10.2 million new cases by the year 2000, an increase of 36%. Current data suggest that between 5% and 10% of persons co-infected with HIV and mycobacterium TB will develop TB each year, compared with less than 0.2% of persons infected with M. TB but not HIV. Dolin et al., (1994:214) continues, estimating around 95% of HIV-infected TB cases are attributable to HIV infection, and the remaining 5% of co-infected cases would have developed TB regardless of their HIV status.

In Australia the notification rate of TB has not been increasing; less than 6 cases per 100 000 population per year, and with about 1000 cases of TB reported each year, this compares favourably with those from other countries (Benenson 1995:490). Although Lee et al., (1997:388) argue a high incidence of infection exists in Aboriginal and Islander populations in northern parts of Australia, while other high risk groups include people born overseas (especially those from China, Africa, some American regions, Cambodia, Vietnam, other South-East Asian countries and the Phillipines). Cook (1996:50) reports the number of cases in England and Wales, which had been declining until 1987, have risen by 12%, resulting in notification of over 5000 new cases per year.

Spence, Hochkiss, Williams and Davies (1993:760), The American Lung Association (1995:1), and Lee et al., (1997:388), accede factors increasing risk of becoming infected with TB include:

* people infected with the human immunodeficiency virus and AIDS ( this infection has become the single most important risk factor),

* people in close contact with those known to be TB infectious (high and medium risk Mantoux negative health care workers, patient's family members, coworkers or friends),

* contact with undiagnosed/untreated cases of pulmonary TB,

* people with medical conditions (silicosis, other chronic lung diseases, Hodgkins disease, elderly people with weakened immune systems),

* Immunosuppressed persons (long term use of corticosteroids),

* foreign born people from countries with high TB rates,

* people who work in or are residents of long term care facilities (nursing homes, prisons, some hospitals),

* a link is often cited between TB and poverty, overcrowding, malnutrition, the homeless, alcoholic and IV drug using individuals.

Treatment depends on whether a person has only TB infection or TB disease. An infected person may be given preventative antimicrobial therapy (1 x daily isoniazid (INH) for 6/12, or in some cases 12/12), that aims to kill germs not doing damage at that time, but may break out later (American Lung Association:1995, and Hellman and Gram 1993:68). However, before initiation of antitubercular treatment, appropriate biological specimens should be obtained from the patient to identify pathogens and determine drug susceptibility (Bloom 1995:134, Berkow and Fletcher 1992:143). Since the tubercule bacillus develops resistance to most of the antituberculous drugs given on their own, treatment for those with active disease involves a combination of INH plus 2, 3 or 4 others, usually for 6/12 to 9/12 (Benenson 1995:496).

The Food and Drug Administration (FDA) has 'granted marketing approval for fixed-dose tablets containing rifampin (RIF), INH and pyrazinamide (PZA) (Rifater/Marion Merrell Dow) for treatment of pulmonary TB during initial 2-month intensive treatment', with continuation therapy of RIF 450 or 600 mg and INH 300 mg for a further 4/12 (Medical Sciences Bulletin, 1994). The new triple-drug Rifater tablet was developed for convenience of administration, contains 120 mg RIF, 50 mg,INH, and 300 mg PZA, all 3 components are widely distributed throughout the body, including the CSF, and readily absorbed from the GIT tract after oral administration (Medical Sciences Bulletin, 1994).

Benenson (1995:496) and Desir (cited in Black 1996:595) suggest the currently accepted initial treatment regimen consists of 4 drugs: INH, RIF, PZA, and ethambutol (EMB) or streptomycin (SM). Benenson (1995:496) insists patients with organism susceptibility to INH and IRF should receive these 2 drugs for a full 6/12, supplemented by PZA during the first 2 /12, with regimens including only INH and RIF continued for 9/12. Treament also involves education about the drugs, possible side effects, the need for long term supervision; possibility of sputum reverting to positive after a series of negatives, drug-taking compliance and bacterial drug resistance (Benenson 1995:496, Bloom 1995:134 and Cook 1996:50).

Antibiotic drug resitance is ubiquitous and occurs when sensitive organisms have mutated, developing resistance to particular antimicrobials, by inactivation of the drug, alterations of the bacterial membrane so the antimicrobial is no longer taken up, or alterations of the target molecule (Rote et al., 1996:199). Antibiotics contribute to the survival of strains of bacteria that contain resistance plasmids (R plasmids or R factors), ie., when a population of organisms containing both resistant and nonresistant organisms is exposed to an antibiotic, the resistant organisms survive and multiply, while the nonresistant ones are killed (Black 1996:207). Black (1996:208) continues, outlining the process in the following way:

1. Resistance plasmids (small extrachromosomal DNA), generally contain a resistance transfer factor (RTF) and at least one resistance (R) gene.

2. Transfer of resistance from one organism to another occurs due to RTF conjugation of the whole resistance plasmid, while each R gene carries information that confers resistance to a specific antibiotic.

3. Alteration of the target leading to inadequate drug binding, or drug activation: as a result of mutations in chromosomal genes.

4. Large numbers of previously nonresistant organisms can acquire resistance quickly, due to the rapid transfer of resistance plasmids from resistant to nonresistant organisms.

'Transfer of resistance plasmids accounts for increasingly large populations of resistant organisms and reduces the effective use of antibiotics', as in the development of drug resistant mycobacterium TB (Black:208).

Due to increasing antibiotic use and misuse, over the past decades, the Centre for Disease Control (CDC) and Prevention (1996) insists resistance has emerged in all kinds of microorganisms - including M. tuberculosis - posing new challenges for both clinical management and control programmes.

Fujiwara (in Black 1996:594) and Rote et al., (1996:200) explain treatment with a single drug - due to irregular drug supply, inappropriate prescription, or poor drug compliance (due to many factors) - suppresses the growth of susceptible strains to that drug, but permits multiplication of drug resistance strains, resulting in aquired resistance. Fujiwara (in Black 1996:594) describes primary resistance as, subsequent transmission of such resistant strains from an infectious case to other persons leading to disease which is drug resistant from the outset. Therefore, before using any antibiotic to treat disease, it is imperative to identify the antibiotic to which an organism is most sensitive (Black 1996:208). Likewise, to minimize the development of resistance the world needs a breakthrough by people of power, influence and compassion who will educate all people (not only the patients), to see that medications are put to use effectively throughout the world (WHO Report 1996). Effective use of medication involves the right person taking an appropriate prescription of the right drug, right dosage, at the right time, taken by the right route, for the correct length of time, and correct monitoring of progress and further tests and treatments (Kozier et al., 1995:1311).

The WHO Report (1996) recommends Directly Observed Treatment, short-course (DOTS) to stop TB at the source by requiring health workers to watch patients swallow each dose of medicines until the patient is completely cured. If a patient receives DOTS, they will meet with a health care worker every day or several times per week at a place both parties agree on (eg., chest clinic, home, work or even on a street corner (Fujiwara, in Black 1996:596).

List of References

1. Altmann, A.E., and Carnie, J.A., 1996, 'BCG vaccination practices in Victoria', Australian and New Zealand Journal of Public Health, 20:5, pp.521-523.

2. Anderson, K.N., Anderson, L.E., and Glanze, W.D., 1996, Mosby's Medical, Nursing, and Allied Health Dictionary, Sydney, Mosby.

3. Anonymous, 1995, 'Peoples Plague: Facts About.... Tuberculosis', American Lung Association, http://www.pbs.org/ppol/tbfacts.html, 2/3/1998.

4. Anonymous, 1994, 'The TB Skin Test - Mantoux :Getting a rise out of tuberculosis with the PPD test', Nursing, 8, pp.51-53.

5. Benenson, A.S., 1995, Control of Communicable Diseases Manual, Washington, American Public Health Association.

6. Berkow, R. and Fletcher, A. J., 1992, The Merck Manual of Diagnosis and Therapy, New Jersey, Merck Research Laboratories.

7. Black, J. G., 1996, Microbiology Principles and Applications, New Jersey, Prentice Hall.

8. Bloom, S.R., 1995, Toohey's Medicine: A Textbook for Students in the Health Care Professions, Melbourne, Churchill Livingstone.

9. Byrne, C., Saxton, G. I., Pelikan, R. M., and Nugent, J., 1986, Laboratory Tests: Implications for Nursing Care, Sydney, Addison - Wesley Publishing Company.

10. U.S. Department of Health and Human Services Public Health Service, Centres for Disease Control and Prevention, National Centre for Prevention Services Division of Tuberculosis Elimination, 'Questions and Answers About TB', CDC/Division of Tuberculosis Elimination - FAQ, http://www.cdc.gov/nchstp/tb/faq.htm, 5/11/1995.

11. Childs, C., 1994, 'Temperature control', in Alexander, M.F., Fawcett, J.N., and Runciman, P.J., eds., Nursing Practice: Hospital and Home, The Adult, Melbourne, Churchill Livingstone, pp. 679-695.

12. Closs, S.J., 1994, 'Sleep' in Alexander, M.F., Fawcett, J.N., and Runciman, P.J., eds., Nursng Practice: Hospital and Home, The Adult, Melbourne, Churchill Livingstone, pp. 743-756.

13. Collins, C., Lyne, P., and Grange, J., 1995, Microbiological Methods, Great Britain, Butterworth Heinmann.

14. Connaught, 1995, BCG Vaccine Consumer Product Inforrmation, Canada, Connaught Laboratories Limited, A Pasteur Merieux Company.

15. Cook, R., 1996, 'Tuberculosis', Nursing Standard, 10:48, pp. 49-52.

16. Dacie,J.V., and Lewis, S.M., 1995, Practical Haematology, Melbourne, Churchill Livingstone.

17. Daly, S., Holmes, P.A., Blake, G. J., and Charnow, J.A., 1993, Professional Guide to Signs and Symptoms, Pennsylvania, Springhouse Corporation.

18. Davey, S.S., and McCance, K.L., 1996, 'Alterations of Pulmonary Function', in Huether, S.E., and McCance, K.L., eds., Understanding Pathophysiology, Sydney, Mosby, pp.739-772.

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21. Evans, D.M.D., 1994, Special Tests: The procedure and meaning of the commoner tests in hospital, Melbourne, Mosby.

22. Fischbach, F., 1995, Quick Reference to Common Laboratory and Diagnostic Tests, Philadelphia, Lippincott Company.

23. Fujiwara, P.I., 1996, 'Microbiologist's Notebook': Multidrug-Resistant Tuberculosis', in Black, J.G., ed., Microbiology Principles and Applications, New Jersey, Prentice Hall, pp.594-595.

24. Gillies, F., and Dodds, D., 1984, Bacteriology Illustrated, New York, Churchill Livingstone.

25. Hamann, B., 1995, Disease:Identification, Prevention, and Control, Sydney, Mosby.

26. Hellman, Major S.L., and Gram, M.C., 1993, 'The Resurgence of Tuberculosis: Risk in Health Care Settings', American Association of Occupational Health Nurses, 41:2, pp.66-72.

27. Jensen, M.M., and Wright, D.N., 1993, Introduction to Microbiology for the Health Sciences, New Jersey, Prentice Hall.

28. Joyce, D., Lefever, C.M., and Kee, J.L., 1991, Laboratory and Diagnostic Tests with Nursing Implications, California, Appleton and Cange.

29. Kozier, B., Erb, G., Blais, K., and Wilkinson, J.M., 1995, Fundamentals of Nursing: Concepts, Process, and Practice, Sydney, Addison-Wesley Publishing Company, Inc.

30. Kumar, V., Kumzi, C., and Stanley, L., 1997, Basic Physiology, Philadelphia, WB Saunders Company.

31. Lee, G., and Bishop, P., 1997, Microbiology and Infection Control for Health Professionals, Sydney, Prentice Hall Australia Pty. Ltd.

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