From Negative to Positive

MCP Hahnemann University
Philadelphia, Pennsylvania

Instructor(s): Bresnitz, Eddy A.; Palmarozza, Linda; Dash, Georgia; et.al.
Subject area: Health / Medicine
Department: Medicine
Level: Undergraduate Medical, Graduate Medical
Duration of exercise: 15 minute play, then discussion time
Cost/equipment needed: Video tape, VCR, discussion points, and curriculum
Learning objective: Develop Individual Skills, Provide Information
Teaching style: Group Activity, In-class Activity

Please note that the copyright for this course project is retained by the instructor.



"From Negative to Positive" is a dramatic presentation on video (with accompanying discussion points and curriculum) highlighting issues relating to the transmission and control of tuberculosis in a health care facility. Nosocomial tuberculosis frequently results from a failure to adhere to policies and procedures that reduce the risk of transmission. Misconceptions of disease risk, apathy, pressures of work, poor role modeling, and ignorance of policies all contribute to low adherence. Health worker education and implementation, and reinforcement of policies are important to maintaining a low risk workplace. This scenario reflects these issues. After the play, an informal debriefing session addresses play dynamics and content issues.


From Negative to Positive: A Play About Nosocomial Tuberculosis

Produced by: Plays About Living
Diane Steinbrink Coordinator

Written by:
Linda Palmarozza; Eddy A. Bresnitz, MD, MS; Georgia Dash, MS, CIC; Matthew Levison, MD; Bonnie O'Connor, Ph.D.; Grace Paranzino, MS, RN; Harriet Rubenstein, JD, MPH

Directed by:
Christopher Whelan

Cast:
Nurse Manager - Ruth DeCou
Infection Control Practitioner - Lawrence H. Geller
Resident - Peter Criswell

Cameras/Editing/Graphics:
Michael Bartolino; George Zeiset; Educational Media, Allegheny University of the Health Sciences

Division of Occupational and Environmental Health, Department of Community and Preventive Medicine
MCP/Hahnemann School of Medicine, Allegheny University of the Health Sciences 1998

This program was supported by a Public Health Service Environmental & Occupational Medicine Academic Award, 1-KO7-ES00293 to Eddy A. Bresnitz MD, MS from the National Institute of Environmental Health Sciences, National Institute of Health

Table of Contents

Objectives and Summary of Play

Bibliography

Potential Discussion Points

Tuberculosis Control Program in a Health Care Setting: An outline

Proposed OSHA TB Standard: A Summary

Tuberculosis Curriculum: A Summary

CDC Update on Status of the TB Epidemic in US

CDC Educational and Training Material order form

From Negative to Positive: Health Care Facility Control of Tuberculosis Transmission

Learning Objectives
At the end of this session, the participant will be able to:

1. Discuss risk factors for transmission of tuberculosis in a health care facility.

2. Outline the components of a tuberculosis control program in a health care facility.

3. Describe major reasons for non-adherence to recommendations and policies for tuberculosis prevention.

Summary
From Negative to Positive is a dramatic presentation (length 15 min.) highlighting issues relating to the transmission and control of tuberculosis in a health care facility. Nosocomial tuberculosis frequently results from a failure to adhere to policies and procedures that reduce the risk of transmission. Misconceptions of disease risk, apathy, pressures of work, poor role modeling, and ignorance of policies all contribute to low adherence. Health worker education and implementation, and reinforcement of policies are important to maintaining a low risk workplace. This scenario reflects these issues.

After the play, an informal debriefing session addresses play dynamics and content issues.

Bibilography
Barnhart S. Sheppard L, Beaudet N. Stover B. Balmes J. Tuberculosis in Health Care Settings and the Estimated Benefits of Engineering Controls and Respiratory Protection. JOEM. 1997; 39(9):849-854.

Bowden KM, McDiarmid MA. Occupationally Acquired Tuberculosis: What's Known. JOM. 1994; 36(3):320-325.

Camins BC, Bock N. Watkins DL., Blumberg HM. Acceptance of Isoniazid Preventive Therapy by Health Care Workers After Tuberculin Skin Test Conversion. JAMA. 1996; 275(13):10131015.

Glanz K and Yank H. Communicating About Risk of Infectious Disease. JAMA. 1996; 275 :253-256.

Menzies D, Fanning A, Yuan L, Fitzgerald M. Tuberculosis Among Health Care Workers. N Engl J Med. 1995; 332(2):92-98.

Rubel AJ, Garro LC. Social and Cultural Factors in the Successful Control of Tuberculosis. Public Health Reports. 1992; 107(6):626-636.

Sumartojo E. When Tuberculosis Treatment Fails: A Social Behavioral Account of Patient Adherence. Am Rev Respir Dis. 1993; 147:1311-1320.



Potential Discussion Points
by Eddy A. Bresnitz, MD, MS Grace Paranzino, MS, RN

1. TB Program Guidelines
2. Role of employee health services
3. What are the existing policies/procedures
4. Testing contacts: ? Confidentiality
5. INH & pregnancy issues
6. Social stigma of TB
7. Public health issues
8. Use of respirators
9. PPD testing of employees
10. Exposed other pts/families: risk management
11. Adherence to meds by health professionals
12. Isolation and removal from job: workers' comp
13. Sick leave and co-workers picking up slack
14. Negative pressure rooms
15. Pressures of the job in following policy
16. Perception of low/no risk of HCP
17. Treatment of disease issues
18. Early recognition of disease
19. Transmission of infection to employees



Tuberculosis Control Program in a Health Care Setting: An Outline
by Georgia Dash, MS, CIC and Eddy A. Bresnitz, MD, MS

A. ASSIGNMENT OF RESPONSIBILITY
1. Multidisciplinary TB Control Committee

B. RISK ASSESSMENT AND PERIODIC REASSESSMENT OF THE PROGRAM
1. Employee / Student Health Tuberculin Testing Program
C. EARLY DETECTION AND TREATMENT OF PATENTS WITH TB
1. Identification/Evaluation/Initiation of Treatment
-maintain high index of suspicion for TB in admitted patients (see algorithm)
-place patient in room with "portable" HEPA filter (If negative pressure room unavailable)
-use up-to-date rapid identification techniques: DNA Gen-Probe: 5-6 days
-treat with 4 drugs where > 4% TB population have INH resistance
2. Tuberculosis Case Registry (Hospital-Based)
-admission information on previous treatment of TB in database file of all patients
-past history of TB: isolate first, even before you know TB is not the issue

D. ISOLATION OF PATENTS WITH INFECTIOUS TB
Principle: prevent spread and reduce number of droplet nuclei in general air circulation
1. Construction of Negative Pressure Rooms with W light2. "Portable" HEPA Filtration Units
-when negative pressure room unavailable (clinic, ED, no beds)
-need to test for efficacy when setting up
3. AFB Isolation Algorithm
-QA of Isolation (see attached)
-guidelines for who to isolate on admission

E. RESPIRATORY PROTECTION PROGRAM (Personal Protective Equipment)
1. Submicron Masks
-submicron masks for patients and visitors ($0.50)
2. Respirators: Fit Testing Required; Required and accepted by OSHA; reusable
-qualitative vs. quantitative
-positive pressure respirator required if fit test fails-easier to use than HEPA
3. Non-adherence issues with wearing a mask
-excuses: inconvenient, bulky to carry, forgetting, losing

F. MANAGEMENT OF PATENTS WITH ACTIVE TUBERCULOSIS
1. Reporting to Department of Health (by lab, MD, hospital epidemiologist)
-mandatory: see attached form
2. Directly Observed Therapy (meds provided at no cost)
-improve adherence 4 decreased organism resistance
-DOT Center or local health district center, physician's office or home visit
-outreach and/or legal action for noncompliers, e.g., incarceration (last resort)
3. Information for Physicians and other Health Care Providers
-updates on policy and treatment guidelines
-hospital policy setting by committee
4. Patient Education
-improve adherence
Information should include:
G. OUTPATENT INITIATIVES
1. Survey in Clinics
-assess community knowledge/plan community-based programs (e.g., religious organizations, health fairs, schools, community centers, residential communities)
2. Patient Education
-promote risk reduction behavior
-address myths/stigma
-improve surveillance

H. OTHER
1. Hazard communication and training, both at pre-placement and annually
2. Appropriate record keeping


HANDOUTS

Isolation Algorithm for Patients with Suspected Clinical Pulmonary TB (1 page)

ACOEM Report (November 1997) OSHA Proposes New TB Standard (2 pages)

OFFICIAL REPORT OF TB SUSPECT OR CASE FORM from Philadelphia Department of Health (2 pages)



Tuberculosis Curriculum: A Summary
MCP/Hahnemann School of Medicine
by Matthew E. Levison, MD

Supported by a grant from the NHLBI Tuberculosis Academic
Award (#HL03013)

TUBERCULOSIS COMPETENCIES
1. Initiate TB clinical risk assessment
2. Initiate a diagnostic work-up for possible active pulmonary tuberculosis
3. Institute an institutional TB control program
4. Plan an individual TB therapeutic program
5. Plan an individual TB chemoprophylaxis program

REFERENCES
· Haas and Des Prez. Mycobacterium tuberculosis. in Mandell, Douglas and Bennett: Principles And Practice Of Infectious Diseases (4th Ed). pg 2213-42.
· Iseman. Tuberculosis. in Cecil Textbook of Medicine (20th ed .), pg 1683-91.

LEARNING OBJECTIVES

Describe the characteristics for an aerosol that is involved in transmission of certain infectious agents of the respiratory tract?
Aerosolized particles are <5µ, and because of their light weight, remain suspended in air for prolonged periods, unless removed by venlilation.

Describe the significance on the mode of transmission of an infectious agent and on its initial pathogenesis, if the infectious agent is in the form of an aerosol?
Ventilation is the main measure to clear the ambient air of an aerosol.

Surgical masks, which do not fit the contours of the face tightly, allow entrance of inhaled aerosol particles into the respiratory tract. Special high efficiency filtering, tightly fitting masks are required to prevent aerosol-transmitted infections.

Aerosolized particles <5µ bypass the mucociliary barrier in upper respiratory tract and tracheobronchial tree.

As a result, inhalation of very dilute suspensions of aerosolized particles is sufficient to penetrate the airways as far as the alveoli, whereas inhalation of much denser suspensions of larger particles is necessary to penetrate as far as the alveoli, because most larger particles will be trapped by the mucociliary barrier in the nasopharynx and larger airways.

Inhaled aerosols are distributed to all alveoli with the inspired air. As a result the initial focus of an aerosol-transmitted infection is usually in the midlung zones (the upper part of the lower and middle lobes and the lower part of the upper lobes), which receive a relatively greater distribution of inspired air.

Name infections that are typically transmitted by aerosols?
TB is a classic aerosol-transmitted infection. Others include coccidioidomycosis, now epidemic on the West coast and SW desert regions of US (see enclosed recent publication), histoplasmosis, influenza. pulmonary anthrax, and Q fever. The pathogenesis of TB (see below) is also a paradigm for that of some of these diseases (e.g., histoplasmosis and coccidioidomycosis).

Describe characteristics of a good producer of an infectious TB aerosol?
Person with pulmonary or laryngeal TB who is untreated, was just started on treatment (<2 weeks), or treated with inappropriate drugs, especially if the pulmonary lesion is cavitary TB.

Contagiousness is related to bacterial density in the respiratory secretions. Cases with positive acid-fast smears of sputum (>106 /ml sputum) will be more contagious than those with negative AFB smears and only positive cultures (<106 CFU/ml sputum). Cavitary pulmonary TB, because of the high mycobacterial density in the cavity, is the usual form of TB that is most contagious.

Describe the public health consequences if an infection is transmitted by an aerosol ?
A contagious patient may quickly contaminate the ambient air in a closed room. Contamination may then persist for prolonged periods of time in the absence of effective ventilation. Infection is unlikely to occur out of doors. Larger droplets of respiratory secretions >5µ are unimportant in TB transmission since they fall by gravity to the floor. Also if particles ≥5µ are inhaled, these particles tend to be removed by mucociliary action and coughing, and are unlikely to reach the alveoli. Fomites are also unimportant, and no special housekeeping measures for dishes and bedclothes are necessary. Proximity to a contagious case is also important: One case of cavitary TB in a submarine infected 45% of the crew, and 80% of those who slept in same compartment.

Special masks (respirators) are required for the prevention of TB; routine loose-fitting surgical masks are mainly used to prevent contamination of a patient's open wound during surgery from the healthcare worker' s respiratory organisms, but will not prevent the healthcare worker' s inhalation of infectious aerosols generated by a contagious patient because of the relatively large pore size of the surgical mask and gaps between the mask and the wearer's face.

Describe the initial events in the body before the onset of the cellular immune response to TB, and describe the consequences that these events have on the subsequent manifestations of TB?
The inhaled bacteria are ingested by alveolar macrophages, which are unable to control intracellular bacterial multiplication, eventually destroying the macrophage. The released viable mycobacteria are again ingested by new macrophages and the cycle is repeated.

Blood-borne monocytes and lymphocytes are attracted to the site, which also ingest the tubercle bacilli released from degenerating macrophages. Infected macrophages are carried to regional lymph nodes via the Iymphatics. In the nonimmune host the infected macrophages are not retained in these regional nodes; they spread randomly to tissues throughout the body via the bloodstream (primary Iymphohematogenous dissemination).

Intracellular multiplication and survival of M. tb, an obligate aerobe, in certain tissues is favored by high tissue oxygen tension, e.g., apices of lung, kidneys, bone. Unimpeded bacterial growth before the development of delayed cellular immunity, results in relatively large populations of M. tb at these sites, and provides a tissue nidus for subsequent evolution of progressive disease in lung apices and elsewhere. Progressive disease can occur either promptly atter initial infection in certain patients or after latent periods of up to many years.

Describe what happens with the development of an adequate cellular immune response?
With development of the cellular immune response in 2-10 weeks, specifically sensitized T lymphocytes elaborate Iymphokines and macrophages show increased capacity tor phagocytosis and intracellular kiting of M. tb. If at this time the number of M. tb is small, the sites of M. tb implantation may resolve and heal completely

However, with onset of cellular immunity, the number of bacilli killed may be sufficiently large as to result in tissue necrosis and subsequent fibrosis and calcification and produce a recognizable reaction on chest X ray in the primary focus (Ghon) and in the draining regional lymph nodes. Much less commonly, with the onset of the cellular immune response, pulmonary apical metastatic (hematogenous) foci contain sufficient numbers of bacilli at that point that necrosis ensues, producing tiny calcific deposits called Simon foci, in which viable bacilli may persist in 50 % of cases.

Granuloma formation. Histologically, the inflammatory response in TB is characterized by the formation of granulomas. Granulomas form in the immune host as an organized microscopic aggregation of rounded histiocytes (macrophages) that vaguely resemble epithelial cells, hence the name, epithelioid cells, and may contain ingested microorganisms. In the margins of the cluster of epithelioid cells, and sometimes in the center. are multinucleated giant cells, formed by the fusion of macrophages. About the periphery of the granuloma are plump fibroblasts interspersed with macwophages and lymphocytes. A special type of necrosis (caseous) may occur in the centers of some granulomas that may subsequently calcify and is characteristic of TB .

In the lung apices and kidneys, discharge of liquified caseous material into a bronchus or ureter, respectively, may result in a residual cavity. During the process of caseation the disease may spread by local extension or by the intrabronchial or ureteral route to other sites in the lower respiratory tract (e.g., other bronchopulmonary segements or larynx) or urinary tract (e.g., ureters, bladder, or prostate), respectively.

In >90% of TB infected persons, the infection then remains latent throughout life.

What is the differential diagnosis of pulmonary granulomas (of extra-pulmonary granulomas)?
Pulmonary: TB, Histoplasmosis, Coccidioidomycosis, Blastomycosis, Cryptococcosis, Sarcoidosis, Berylliosis, Silicosis, Asbestosis, Schistosomiasis (with eosinophils), Paragonomiasis (with eosinophils), Nocardiosis and Actinomycosis (mixed inflammatory reaction, i.e., polys, macrophages, fibrosis), Melioidosis (Pseudomonas pseudomallei) certain vasculitic syndromes, e.g., Wegener's granulomatosis.

Extra-pulmonary: The above, plus Cat-scratch Disease, Syphilis, Tuberculoid leprosy, Tularemia, Brucellosis, Typhoid fever (Salmonella typhi), Glanders (Pseudomonas mallei), Lymphogranuloma venereum (LGV).

Describe what happens if the initial cellular immune response is deficient?
The initial infection progresses and results in primary progressive disease and extra-pulmonary involvement. Intensity and duration of exposure increases risks for development of disease as well as tor infection. The risk for development of clinical tuberculosis diseases is greatest during the six months atter infection and remains high for the next 2 years.

In children and elderly, and in HIV-intected patients, the primary pulmonary focus in the midlung field may become an area of advancing pneumonia, which may cavitate and spread to other alveoli via the bronchi. Apical posterior seeding during primary Iymphohematogenous dissemination may progress within weeks without interruption in adolescents and young adults, or after a short latent period of months, resulting in pulmonary TB of the reactivation type. Progressive hematogenous dissemination is often followed within weeks by TB meningitis in children or AIDS patients.

Describe the clinical syndrome produced by pulmonary tuberculosis?
Pulmonary TB is a chronic (weeks-months), wasting (weight loss, generalized weakness, easy fatigue), febrile (fever and night sweats) illness with respiratory symptoms (productive cough, hemoptysis, pleuritic chest pain, shortness of breath).

What is the differential diagnosis of chronic, wasting febrile illness with respiratory symtoms?
Malignancy, AIDS, Vasculitic syndromes, e.g., Wegener's granulomatosis, TB, Histoplasmosis, Coccidioidomycosis, Blastomycosis, Cryptococcosis, Sarcoidosis, Chronic Berylliosis, Glanders, Melioidosis, Paragonomiasis, Nocardiosis, Actinomycosis, Anaerobic lung abscess.

Name TB risk factors.
HIV infection, diabetes mellitus, silicosis, cancer of the head and neck, endstage renal disease, prolonged conicosteroid or immunosuppressive Rx, malnutrition (>10% below ideal body weight), hematology/RES malignancy, intestinal bypass, malabsorption, gastrectomy.

Describe what happens if the cellular immune response subsequently wanes?
With fall in immunity as a result of the development of certain risk factors at a later point in life, e.g., AIDS, diabetes mellitus, cancer of the head and neck, endstage renal disease, immunosuppressive and conicosteroid Rx, silicosis, malnutrition. etc. the few surviving organisms can begin multiplying again, uncontrolled by host defenses and result in reactivation TB and possibly secondary hematogenous dissemination.

Episodes of secondary hematogenous dissemination may become progressively more frequent and eventually continuous, producing an often fatal clinical syndrome of progressive generalized hematogenous tuberculosis, i.e., miliary TB.

The risk of developing active TB after tuberculin conversion, i.e., development of cellular immunity, is ~5% in first 1-2 years and -5% during the rest of the person's lifetime. Three periods of life during which intection is most likely to produce disease is infancy, 15-25 years of age, and old age. Other factors that favor progression to disease include malnutrition, alcoholism, homelessness, incarceration, renal failure, immunosupression due to underlying diseases or medication, and AIDS. In HIV-intected persons, progression of latent TB infection to TB disease is 8%/year.

Name the risk factors for an inadequate immune response?
See above

Describe the effect that age of the patient has on the pathogenesis of TB?
See above

Describe the clinical microbiologic laboratory investigation of respiratory secretions required to make a diagnosis of TB.
A minimum of 3 sputum specimens obtained on consecutive davs is required for smear and culture. Processing specimens for identification of mycobacteria should be performed in a hood to prevent inhalation of infectious aerosols that may be generated by these processes. Mycobacteria are identified on smears processed with Kinyoun stain as redsolored bacilli or fluorescent bacilli processed with a fluorochrome stain. All specimens, including those that are smear-negative, should be cultured for mycobacteria as smear-negative specimens may contain mycobacteria in numbers below the level of detection by microscopy (i.e., ≤10 5-6/ml). Smear-positive specimens may contain M. tb or an atypical mycobacteria; further identification requires cultivation of the organisms or use of species-specific DNA probes.

If a patient cannot spontaneously expectorate, specimens may be obtained for culture by stimulation of coughing by inhalation of nebulized 3% saline, by bronchoscopy, or by aspiration of fasting gastric secretions. Cough-inducing procedures should be performed in a negative-pressure room to prevent inhalation of infectious aerosols by the healthcare worker. Culture for mycobacteria in special liquid media requires at least 2-3 weeks and up to 6 weeks of incubation to yield growth; use of specific DNA probes on smear-poisitive respiratory secretions requires several hours. All M. tb-containing specimens should be tested for drug-susceptibility. At the present time, this requires several more weeks of incubation, but specific DNA probes may rapidly detect the presence of drug-resistant genes in the future. DNA-fingerprinting (restriction fragment length polymorphism, RFLP) analyisis can be used to identify clones in epidemiologic investigtions.

Describe the principles of anti-mycobacterial therapy and its underlying concepts.
It is estimated that to maintain tuberculosis in the population one case of active cavitary pulmonary tuberculosis (usually it is the cavitary form o f tuberculosis where large numbers of aerosolized tubercle bacilli are generated) must infect at least 20 other individuals, because 10% of these TB-infected individuals (i.e., 2 individuals) will develop active pulmonary disease during their lifetime and 50% of these (one individual) will develop the cavitary form of the disease. To decrease the prevalence of TB, the chances of activation must be diminished by INH chemoprophylaxis o f latent infection and by early isolation and early, effective treatment o f active pulmonary disease.

· Always use at least 2 drugs to which the organism is susceptible to treat clinically active infection. The risk for emergence of drug resistance under selective pressure of drug therapy is dependent on the rate of mutation for drug resistance and the size of the microbial population. In latent infection population size is thought to be low and the risk for emergence of resistant mutants on therapy is low so that use of a single drug is adequate; whereas in clinically active disease the population size is much greater and the risk for emergence of mutation to resistance on therapy is much greater. If the mutation rate for drug resistance is 1 in 108 organism for each drug, the risk for a mutant resistant to 2 drugs would be 108 x 108 or 1016. Since the usual population size in infected tissues is much smaller than this, the likelihood is that a doubly resistant mutant will not be present, so that at least 2 drugs are always used for the treatment of clinically active disease.

· To shorten the course of therapy, drugs the rapidly reduce the size of the bacterial population is required: INH, Rifampin and PZA are bactericidal and are essential components of short-course therapy.
SiteSizeMetabolism/GrowthpHEffective Drugs
macrophage104-6/gmvery slowacidPZA, INH, Rifampin closed
caseous lesions105-7/gmslow and intermittentneutralINH, Rifampin
cavity 107-9/gmactive and rapidneutral INH, Rifampin, Strep

Describe the 6-month course of therapy for tuberculosis and how is therapy monitored for clinically efficacy and drug-side effects.
· INH, Rifampin, PZA + (if INH-resistance >4%) either Ethambutol or streptomycin daily for 2 weeks (INH 5 mg/kg/d, max 300 mg/d; Rifampin 10mg/kg/d, max 600 mg; PZA 25 mg/kg/d, max 2g/d; Ethambutol 15-25 mg/kg/d, max 2.5g/d; streptomycin 15 mg/kg/d, max I g/d in adults), then 2x weekly by Directly Observed Therapy (DOT) (INH 15 mg/kgd, max 900 mg/d: Rifampin 10mg/kg/d, max 600 mg; PZA 50-70 mg/kg/d, max 4g/d: Ethambutol 50 mg/kg/d, max 2.5g/d; streptomycin 20-40 mg/kg/d, max l.5g in adults) for 6 weeks, then
· INH, Rifampin twice weekly x 4 months (12 months for TB meningitis, bone and joint TB or miliary TB in children and 6-12 mos in some adults with suboptimal response) by DOT, if possible. Relapse rate about ≤5%.
· Sputum AFB smear and culture every I month until negative. With INH/Rifampin, >85% negative after 2 months. If after 3 months, AFB smear/culture positive or symptomatic, consult specialist. If organisms is INH and Rifampin-sensitive, dlc PZA, Ethambutol or streptomycin after 2 month. If MultiDrug Resistant TB (MDRTB), daily Rx throughout 18m course with at least drug drugs to which he organism is susceptible. Possible Rx agents include ethionamide, cycloserine, cipro or ofloxacin, amikacin, capreomycin, kanamycin, and rifabutin.
· Monitor for drug toxicity: INH, Rifampin, and PZA- Pre-therapy liver function tests and monthly for symptoms of jaundice, dark urine, nausea, vomiting, anorexia, weakness, malaise (d/c if SGOT 3-5x
ormal); PZA - pre-therapy serum uric acid and repeat if gouty attack occurs: Streptomycin - pre-therapy and monthly audiograms and weekly serum creatinine; Ethambutol - monthly visual acuity and red-green if dose >10 mg/kg/d.

TABLE: Describing the pharmacodynamics and use of the major anti-mycobacterial drugs

Which patients should be screened for TB?
See risk groups above

What is the usual method used for TB screening?
Hx, CXR, Tuberculin Skin Test (TST). If TST is to be repeated e.g., in healthcare workers, use 2- stage TST if age >55y.

How can clinical TB be prevented in appropriate persons with latent TB?
INH chemoprophylaxis: 5TU PPD (+)
≤5mm, any age if HIV + and anergic: 1. Household contact of active TB
≤5mm, any age if HIV + and not anergic: 1. Household contact of active TB (d/c/ if TST negative at 10 weeks after last exposure
≤5mm, child/adolescent: 1. Household contact of active TB (d/c/ if TST negative at 10 weeks after last exposure
≥5mm induration, regardless of age: 1. suspected or known HIV (+), 2. Household contact of active TB, 3. Untreated (+)CXR
≥10mm induration, regardless of age: 1. IVDU, 2. Medical conditions that I risk, ≥10mm induration, age <35y: 1. Foreign-born in high-prevalence country, 2. Residents of long-temm care facilities, e.g., pnsons 3. Medically underrserved. 4. Occupational exposure
≥10mm induration, age <35y: 1. Recent PPD Conversion
≥15mm induration, age ≥35y: 1. Recent PPD Conversion
≥15 mm induration, <35y: 1. Others with no known risk Pregnancy, no risk factors: delay INH until after delivery.

Name fctors that influence the response rates to chemotherapy?
Types of drugs and combinations used, Duration of therapy, Adherence to treatment regimen, Immunocompetence of patient

What patient characteristics influence adherence to treatment regimens?
None

Name other factors that influence adherence?
Patient's perception of the seriousness of the disease
Patient's perception of the efficacy of the treatment regimen
Duration of the treatment
Complexity of the treatment regimen
Relationship to the physician

How can adherence can be improved?
Demonstrate compassion and personal concern for the patient's future well-being Engage the patient in a cooperative effort when recommending a treatment regimen
Assume that the patient has their own explanation for the cause of the illness, why it happened to them and how it can be cured ("How does my explanation fit with what you have been thinking?")
Write out the regimen and explain it to patient
Keep the regimen as simple as possible Prepare the patient for possible side effects
Ask about any anticipated obstacles to adherence
Enlist the patient to suggest ways to overcome these obstacles
Amend regimen if possible
Get feedback at each return visit about barriers to adherence that have developed in interim and ask about ways to overcome these barriers.

Name methods of making the diagnosis of clinical TB?
Hx, Px, CXR, AFB stain/culture, DNA analysis

Name elements of a hospital TB control program?

Administrative Controls (organizational structure, personnel, budget and policy statements for TB control program)
Designate TB Control officer/committee
Conduct institutional (inpatient, outpatient, bronchoscopy suite, laboratory and ER facilities) TB Risk assessment: Incidence/Prevalence of TB and drug-resistance in community and in the institution. Evaluate TB conversions among healthcare workers in the facility. Review current institutional TB control policies. Institutional engineering controls (e.g., adequacy of numbers and maintenance of TB isolation facilities). Review of patient-charts for TB risk assessment, initiation and discontinuation of TB isolation, diagnosis, management, and discharge-planning for TB. Health Department-reporting. Adequacy of TB laboratory facilities. Adequacy of respiratory protection equipment. Education and counseling of healthcare workers.
Periodic reassessment of institutional risk, including periodic counseling and screening of healthcare workers, investigation of PPD conversions and active TB in healthcare workers, or possible patient-to-patient transmission.
Develop written TB Control Plan that includes all above.

Source Controls (Screening, early detection, prompt isolation and treatment)

Environmental Controls (Construction and maintenance of adequate number of respiratory isolation rooms in inpatient. ERs outpatient and bronchoscopy suite facilities. Availability and use of personal protection equipment).


HANDOUTS

CDC Update
Status of Tuberculosis Epidemic in United States:1997
Data Point to Number of Warning Signals
(April 9, 1998)
(1 page)

CDC Division of Tuberculosis Elimination
Educational Training Materials and Guidelines
(2 pages)

CDC Update
Status of Tuberculosis Epidemic in United States:1997
Data Point to Number of Warning Signals
(April 9, 1998)
(1 page)

CDC Division of Tuberculosis Elimination
Educational Training Materials and Guidelines
(2 pages)





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