Background Information On Tuberculosis And

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This chapter provides background information on tuberculosis (TB), human immunodeficiency virus and acquired immunodeficiency syndrome, and the interaction between them.

T^h tuberculosis

I.I.I H Basic facts about TB

Mycobacterium tuberculosis

TB is a bacterial disease caused by Mycobacterium tuberculosis (and occasionally by Mycobacterium bovis and Mycobacterium africanum).These organisms are also known as tubercle bacilli (because they cause lesions called tubercles) or as acid-fast bacilli (AFB).When sputum containing tubercle bacilli is stained with certain dyes and examined under the microscope, the bacilli look red.This is because they are acid-fast (they have kept the dye even after being washed with acid and alcohol). Tubercle bacilli can remain dormant in tissues and persist for many years.

Tuberculous infection and tuberculosis

Tuberculous infection occurs when a person carries the tubercle bacilli inside the body, but the bacteria are in small numbers and are dormant. These dormant bacteria are kept under control by the body's defences and do not cause disease. Many people have tuberculous infection and are well.Tuberculosis is a state in which one or more organs of the body become diseased as shown by clinical symptoms and signs. This is because the tubercle bacilli in the body have started to multiply and become numerous enough to overcome the body's defences.

Sources of infection

The most important source of infection is the patient with TB of the lung, or pulmonary TB (PTB),and who is coughing. This person is usually sputum smear-positive (see Chapter 3). Coughing produces tiny infectious droplet nuclei (infectious particles of respiratory secretions usually less than 5 ^m in diameter and containing tubercle bacilli). A single cough can produce 3000 droplet nuclei. Droplet nuclei can also be spread into the air by talking, sneezing, spitting and singing, and can remain suspended in the air for long periods. Direct sunlight kills tubercle bacilli in 5 minutes, but they can survive in the dark for long periods.Transmission therefore generally occurs indoors. Droplet nuclei are so small that they avoid the defences of the bronchi and penetrate into the terminal alveoli of the lungs, where multiplication and infection begin. Two factors determine an individual's risk of exposure: the concentration of droplet nuclei in contaminated air and the length of time he or she breathes that air.

TB of cattle (bovine TB) occurs in some countries. Milk-borne M. bovis may infect the tonsils presenting as scrofula (cervical lymphadenitis), or the intestinal tract, causing abdominal TB.

Routes by which TB is not transmitted

TB is not transmitted through food and water or by sexual intercourse, blood transfusion, or mosquitoes.

Risk of infection

An individual's risk of infection depends on the extent of exposure to droplet nuclei and his or her susceptibility to infection. The risk of infection of a susceptible individual is high with close, prolonged, indoor exposure to a person with sputum smear-positive PTB. The risk of transmission of infection from a person with sputum smear-negative PTB is low, and even lower from someone with extrapulmonary TB (EPTB).

Risk of progression of infection to disease

Infection with M. tuberculosis can occur at any age. Once infected with M. tuberculosis, a person can stay infected for many years, probably for life. The vast majority (90%) of people without HIV infection who are infected with M. tuberculosis do not develop TB. In these, asymptomatic but infected individuals, the only evidence of infection may be a positive tuberculin skin test.

Infected persons can develop TB at any time.The disease can affect most tissues and organs, but especially the lungs. The chance of developing disease is greatest shortly after infection and steadily lessens as time goes by. Infected infants and young children are at greater risk of developing disease than older people because they have an immature immune system.TB is also more likely to spread from the lungs to other parts of the body in this age group. Children who develop disease usually do so within two years following exposure and infection. Most do not develop disease in childhood but may do so later in life.Various physical or emotional stresses may trigger progression of infection to disease. The most important trigger is weakening of immune resistance, especially by HIV infection.

Natural history of untreated TB

Without treatment, by the end of 5 years 50% of PTB patients will be dead, 25% will be healthy (self-cured by a strong immune defence) and 25% will remain ill with chronic infectious TB.

Epidemiology

M. tuberculosis infects a third of the world's population. In 2000 there were an estimated 8.3 million new cases of TB worldwide. 95% of TB cases and 98% of TB deaths are in developing countries. 75% of TB cases in developing countries are in the economically productive age group (15-50 years). In 2000, Sub-Saharan Africa had the highest TB incidence rate (290/100000 per year) and the highest annual rate of increase of cases (6%).There were 1.8 million deaths from TB in 2000, with 226000 attributable to HIV (I2%).TB deaths comprise 25% of all avoidable adult deaths in developing countries.

A direct consequence of increasing numbers of adults with TB is an increase in childhood TB. Neonatal BCG immunization has had limited effect in preventing childhood TB in developing countries. Infants and young children (less than 5 years) are at particular risk for infection and disease. Accurate definition of the burden of childhood TB is difficult because of difficulties with diagnosis, particularly in regions where childhood HIV infection is common. Chapter 4 deals with these issues in more detail.

1.1.2 3 Pathogenesis ofTB

Primary infection

Primary infection occurs in people who have not had any previous exposure to tubercle bacilli. Droplet nuclei, which are inhaled into the lungs, are so small that they avoid the mucociliary defences of the bronchi and lodge in the terminal alveoli of the lungs. Infection begins with multiplication of tubercle bacilli in the lungs.The resulting lesion is the Ghon focus. Lymphatics drain the bacilli to the hilar lymph nodes. The Ghon focus and related hilar lymphadenopathy form the primary complex. Bacilli may spread in the blood from the primary complex throughout the body. The immune response (delayed hypersensitivity and cellular immunity) develops about 4-6 weeks after the primary infection. The size of the infecting dose of bacilli and the strength of the immune response determine what happens next. In most cases, the immune response stops the multiplication of bacilli. However, a few dormant bacilli may persist.A positive tuberculin skin test would be the only evidence of infection. In a few cases the immune response is not strong enough to prevent multiplication of bacilli, and disease occurs within a few months.

Outcomes of primary infection

->-

no clinical disease positive tuberculin skin test

(usual outcome: 90% of cases)

-

hypersensitivity reactions e.g. erythema nodosum phlyctenular conjunctivitis dactylitis

primary complex

-

pulmonary and pleural complications e.g. tuberculous pneumonia hyperinflation and collapse/consolidation pleural effusion

disseminated disease lymphadenopathy (usually cervical)

meningitis pericarditis miliary disease

Following primary infection, rapid progression to intra-thoracic disease is more common in children less than 5 years of age. Chest X-Ray (CXR) may show intrathoracic lymphadenopathy and lung infiltrates.

Post-primary TB

Post-primary TB occurs after a latent period of months or years following primary infection. It may occur either by reactivation of the dormant tubercle bacilli acquired from a primary infection or by reinfection. Reactivation means that dormant bacilli persisting in tissues for months or years after primary infection start to multiply.This may be in response to a trigger, such as weakening of the immune system by HIV infection. Reinfection means a repeat infection in a person who has previously had a primary infection.

The immune response of the patient results in a pathological lesion that is characteristically localized, often with extensive tissue destruction and cavitation. Post-primary TB usually affects the lungs but can involve any part of the body.The characteristic features of post-primary PTB are the following: extensive lung destruction with cavitation; positive sputum smear; upper lobe involvement; usually no intrathoracic lymphadenopathy. Patients with these lesions are the main transmitters of infection in the commmunity.

Post-primary TB

Pulmonary TB

e.g. cavities upper lobe infiltrates fibrosis progressive pneumonia endobronchial

Extrapulmonary TB

Common

Less common

Pleural effusion

Empyema

Lymphadenopathy (usually cervical)

Male genital tract (epididymitis, orchitis)

Central nervous system (meningitis, cerebral tuberculoma)

Female genital tract (tubo-ovarian, endometrium)

Pericarditis (effusion/constrictive)

Gastrointestinal (ileocaecal, peritoneal)

Spine, other bone and joint

Kidney Adrenal gland Skin

(lupus vulgaris, tuberculids, miliary)

I PRACTICAL POINT I

Post-primary infection with pulmonary disease usually occurs in adults and leads to microscopy-positive sputum smears.

1.2 HUMAN IMMUNODEFICIENCY VIRUS 1.2.1 J Introduction: HIV and AIDS

Since the first description of AIDS in 1981, researchers have identified two types of HIV, the cause of AIDS. HIV-1 is the predominant type worldwide. HIV-2 occurs most commonly in West Africa, and occasional infections have occurred in East Africa, Europe, Asia and Latin America. Both types cause AIDS and the routes of transmission are the same. However, HIV-2 transmission is slightly less easy and the progression of HIV-2 infection to AIDS may be slower.

11.2.2 I HIV/AIDS epidemiology

By the end of 2002, there were an estimated 42 million adults and children living with HIV or AIDS. Of these, 28.5 million (68%) were living in sub-Saharan Africa, and 6 million (14%) in South and South-East Asia. In 2002, an estimated 5 million adults and children became infected with HIV, and an estimated 3.1 million adults and children died from HIV/AIDS. 2.4 million (77%) of these deaths occurred in sub-Saharan Africa. Sub-Saharan Africa is the region with the highest overall HIV seroprevalence rate in the general adult (15-49 years) population (9% as of end 2002).

Of 25 countries with an adult HIV seroprevalence rate above 5% in 2001, 24 are in sub-Saharan Africa. The only other country with an adult HIV seroprevalence greater than 5% is Haiti. In 9 countries (all in Southern Africa), the adult HIV seroprevalence rate is 15% or above. Sub-Saharan Africa thus bears the largest burden of the HIV/AIDS epidemic. However, certain countries in other regions are also badly affected by HIV, with an adult HIV seroprevalence of 1-5%, e.g. Cambodia, Myanmar and Thailand (South-East Asia) and Belize, Guatemala, Guyana, Haiti, Honduras, Panama, and Suriname (the Americas). HIV seroprevalence appears to be stabilizing in sub-Saharan Africa but is still increasing in some other large populations, e.g. in the Russian Federation.

11.2.3 I HIV transmission

Worldwide the most common route of HIV transmission is through sexual intercourse. Other sexually transmitted infections (especially those that cause genital ulcers) increase the risk of HIV transmission. The main routes of HIV transmission vary between regions. The main routes of transmission of HIV in sub-Saharan Africa are through sexual intercourse, blood and from mother to infant. In most low-income countries roughly equal numbers of men and women are HIV-infected. Bloodborne HIV transmission occurs through contaminated blood transfusion, injections with contaminated needles and syringes, and the use of non-sterile skin-piercing instruments. The commonest route of HIV transmission in the fast-growing HIV epidemics in the Russian Federation and Ukraine is through injecting drug use.

About one-third of children born to HIV-infected mothers are also HIV-infected, with infection occurring mainly around the time of birth.There is a smaller risk of HIV transmission through breastfeeding. However, in many low-income countries breastfeeding is still safer than bottle feeding.

There is no evidence that HIV transmission occurs through everyday contact, hugging or kissing, food or drink, or the bites of mosquitoes or other insects.

1.2.4 I Prevention of HIV transmission in health units Transmission to patients

Patients may potentially be at risk of HIV infection from HIV-positive staff and HIV-positive patients. Known HIV-positive staff should not perform surgery or invasive diagnostic or therapeutic procedures on patients. Cross-infection between patients can occur from contaminated medical, surgical or dental equipment. It is vital to follow recommended sterilization procedures. When and where possible, reducing injections helps to decrease the risk of cross-infection.

Transmission to staff

Most HIV-positive health workers acquire HIV infection outside the workplace, by sexual transmission from an HIV-positive partner or spouse.The risk of HIV transmission from patients to staff is small if staff observe standard infection control procedures.The risk is less than that of hepatitis B transmission. Less than 0.5% of health workers exposed by a needle-stick injury to the blood of an HIV-positive patient have acquired HIV infection. Contaminated "sharps" pose a risk of HIV transmission to health staff. Therefore handle all "sharps" carefully and follow local guidelines for their disposal. If you have a needle-stick injury, squeeze the wound to encourage blood flow and wash well with soap and water. In areas of high HIV prevalence, assume that all blood and body fluids are potentially infectious. The table on page 30 indicates measures to prevent transmission of HIV to health workers. Where available, start postexposure prophylaxis with antiretroviral drugs as soon as possible (within 24 hours) after a needle-stick injury.

Exposure to risk

Precautions for prevention of transmission of HIV

venepuncture

wear gloves use a closed vacuum system if available discard needle and syringe into "sharps" box discard gloves and swabs into leakproof plastic bag for incineration label blood bottle and request form "inoculation risk"

invasive procedure, surgery, delivery of a baby

wear gloves and apron protect your eyes (glasses or protective goggles) discard sharps into "sharps" box

spilled blood or other body fluids

clear up as soon as possible using available disinfectant (e.g. glutaraldehyde, phenol, sodium hypochlorite)

resuscitation

avoid mouth-to-mouth resuscitation (use bag and mask)

laundry disposal

wear gloves and apron dispose into leakproof plastic bags wash laundry at high temperatures or with appropriate chemical disinfectant

1.2.5 I] Immunopathogenesis of HIV infection How HIV infects cells

HIV infects cells that have the CD4 antigen molecules on their surface. These cells are principally the helper subset of T-lymphocytes, which are central to cell-mediated immunity.They are called CD4+ T-lymphocytes. In recent years it has also been discovered that HIV needs other molecules, called chemokines, on the cell surface to gain entry into the cell. Patients who do not have some of these specific chemokines (for example, CCR5) are more resistant to HIV infection. Others, who have molecular changes in these chemokine receptors, progress more slowly to AIDS.

How HIV destroys the immune system

The critical abnormality resulting from HIV infection is a progressive decline in the number of CD4+ T-lymphocytes.These cells are the most important cells in the cell-mediated immune response. In addition the surviving CD4+ T-lymphocytes do not perform their functions as well as they did before infection. Progressive HIV infection therefore causes progressive decline in immunity.

1.2.6 ] Natural history of HIV infection

Acute HIV infection

Acute HIV infection is also called "primary HIV infection" or "acute seroconversion syndrome". Between 40% and 90% of new HIV infections are associated with symptomatic illness. The time from exposure to onset of symptoms is usually 2-4 weeks. Some people present with a glandular-fever -like illness (fever, rash, arthralgia and lymphadenopathy). Occasionally acute neurological syndromes may occur, which are often self-limiting. These include aseptic meningitis, peripheral neuropathy, encephalitis and myelitis. A severe illness may predict a worse long-term outcome. Most symptomatic patients seek medical help. However, the diagnosis is infrequently made, for several possible reasons. First, the clinician may not consider HIV infection. Secondly, the nonspecific clinical features may be mistaken for another cause, e.g. malaria. Thirdly, standard serological tests at this stage are usually negative. Serological tests first become positive about 4-12 weeks after infection, with over 95% of patients "seroconverting" within 6 months of HIV transmission. The diagnosis of acute HIV infection is best established by demonstration of HIV RNA in plasma.

Asymptomatic HIV infection

In adults, there is a long, variable, latent period from HIV infection to the onset of HIV-related disease and AIDS.A person infected with HIV may be asymptomatic for 10 years or more.The vast majority of HIV-infected children are infected in the perinatal period.The period of asymptomatic infection is shorter in children than in adults.A few infants become ill in the first few weeks of life. Most children start to become ill before 2 years of age.A few children remain well for several years.

Persistent generalized lymphadenopathy (PGL)

PGL is defined as enlarged lymph nodes involving at least two sites other than inguinal nodes. At this time, the lymph tissue serves as the major reservoir for HIV. PGL occurs in about one-third of otherwise healthy HIV-infected people. The enlarged lymph nodes are persistent, generalized, symmetrical, and non-tender. PGL has no particular prognostic significance.

Progression from HIV infection to HIV-related disease and AIDS

Almost all (if not all) HIV-infected people, if untreated, will ultimately develop HIV-related disease and AIDS. Some HIV-infected individuals progress more quickly than others to HIV-related disease and AIDS.The rate of progression depends on virus and host characteristics. Virus characteristics include type and subtype: HIV-1 and certain HIV-1 subtypes may cause faster progression. Host characteristics that may cause faster progression include: age less than 5 years; age more than 40 years; concurrent infections; and genetic factors.

Advancing immunosuppression

As HIV infection progresses and immunity declines, patients become more susceptible to infections. These include TB, pneumonia, recurrent fungal infections of the skin and oropharynx, and herpes zoster. These infections can occur at any stage of progression of HIV infection and immunosuppression. Some patients may develop constitutional symptoms (unexplained fever and weight loss), previously known as "AIDS-related complex" (ARC). Some patients develop chronic diarrhoea with weight loss, often known as "slim disease".

Certain specific HIV-related diseases occur predominantly with severe immunosuppression. These include certain opportunistic infections (e.g. cryptococcal meningitis) and certain tumours (e.g. Kaposi sarcoma). At this late stage, unless patients receive specific therapy for HIV infection, they usually die in less than 2 years.This late stage is sometimes known as "full-blown AIDS".

I PRACTICAL POINT I

TB can occur at any point in the course of progression of HIV infection.

11.2.7 I Clinical staging

WHO clinical staging system for HIV infection and HIV-related disease.

WHO has developed a clinical staging system (originally for prognosis), based on clinical criteria.The definition of symptoms, signs and diseases is according to clinical judgement. Clinical condition or performance score, whichever is the higher, determines whether a patient is at clinical stage 1, 2, 3 or 4 (see table on page 33). Clinical stage is important as a criterion for starting antiretroviral (ARV) therapy.

Adults

WHO clinical staging system for HIV infection and related disease in adults (13 years or older)

Stage 1: ° Asymptomatic

° Persistent generalized lymphadenopathy

Performance scale 1: asymptomatic, normal activity

° Minor mucocutaneous manifestations

(e.g. oral ulcerations, fungal nail infections) ° Herpes zoster within the last 5 years ° Recurrent upper respiratory tract infections (e.g. bacterial sinusitis)

and/or Performance scale 2: symptomatic, normal activity

° Unexplained chronic diarrhoea for more than 1 month

° Unexplained prolonged fever for more than 1 month ° Oral candidiasis (thrush) ° Oral hairy leukoplakia ° Pulmonary TB

° Severe bacterial infections (pneumonia, pyomyositis)

and/or Performance scale 3: bedridden < 50% of the day during the last month

Stage 4: ° HIV wasting syndrome, as defined by CDCa ° Pneumocystis carinii pneumonia ° Toxoplasmosis of the brain

° Cryptosporidiosis with diarrhoea, for more than 1 month ° Cryptococcosis, extrapulmonary

° Cytomegalovirus (CMV) disease of an organ other than liver, spleen, lymph nodes ° Herpesvirus infection, mucocutaneous for more than 1

month, or visceral any duration ° Progressive multifocal leukoencephalopathy (PML) ° Any disseminated endemic fungal infection (e.g. histoplasmosis)

° Candidiasis of the oesophagus, trachea, bronchi or lungs

° Atypical mycobacteriosis, disseminated

° Non-typhoid salmonella septicaemia

° Extrapulmonary TB

° Lymphoma

° Kaposi sarcoma

° HIV encephalopathy, defined by CDCb and/or Performance scale 4: bedridden > 50% of the day during the last month

(Note: both definitive and presumptive diagnoses are acceptable)

a HIV wasting syndrome = weight loss > 10% of body weight, plus either unexplained diarrhoea for more than one month or chronic weakness and unexplained fever for more than one month.

b HIV encephalopathy = clinical findings of disabling mental or motor dysfunction, interfering with activities of daily living, progressing over weeks and months, in the absence of a concurrent illness or condition other than HIV infection which could explain the findings.

Children

WHO clinical staging system for HIV infection and related disease in children

Stage 1: ° Asymptomatic

° Persistent generalised lymphadenopathy

Stage 2: ° Unexplained chronic diarrhoea

° Severe persistent or recurrent candidiasis outside the neonatal period

° Weight loss or failure to thrive

° Persistent fever

° Recurrent severe bacterial infections

Stage 3: ° AIDS-defining opportunistic infections

° Severe failure to thrive

° Progressive encephalopathy

° Malignancy

° Recurrent septicaemia or meningitis

1.2.8 ] Epidemiological surveillance of AIDS

AIDS is a term with an official definition used for epidemiological surveillance.This means that systematic reporting of AIDS cases is useful in helping to monitor the HIV pandemic and to plan public health responses.The term AIDS is not useful in the clinical care of individual patients. In managing patients with HIV-related disease, the aim is to identify and treat whichever HIV-related diseases are present.WHO has recommended case definitions for AIDS surveillance in adults and children where HIV testing facilities are not available.

I PRACTICAL POINT I

The term AIDS is used for epidemiological surveillance, not for clinical care.

WHO case definitions for AIDS surveillance in adults and children where HIV testing facilities are not available

Adults

The case definition for AIDS is fulfilled if at least 2 major signs and at least 1 minor sign are present.

Major signs

° weight loss > 10% of body weight ° chronic diarrhoea for more than 1 month ° prolonged fever for more than 1 month

Minor signs

° persistent cough for more than 1 montha ° generalized pruritic dermatitis ° history of herpes zoster ° oropharyngeal candidiasis

° chronic progressive or disseminated herpes simplex infection ° generalized lymphadenopathy

The presence of either generalized Kaposi sarcoma or cryptococcal meningitis is sufficient for the case definition of AIDS.

The advantages of this case definition are that it is simple to use and inexpensive. The disadvantages are its relatively low sensitivity and specificity. For example, HIV-negative TB cases could be counted as AIDS cases because of their similarity in clinical presentation.

a For patients- with TB, persistent cough for more than I month should not be considered as a minor sign. TB/HIV:A CLINICAL MANUAL

Children

The case definition for AIDS is fulfilled if at least 2 major signs and 2 minor signs are present (if there is no other known cause of immunosuppression).

Major signs

° weight loss or abnormally slow growth ° chronic diarrhoea for more than 1 month ° prolonged fever for more than 1 month

Minor signs

° generalized lymph node enlargement ° oropharyngeal candidiasis

° recurrent common infections, e.g. ear infection, pharyngitis ° persistent cough ° generalized rash

Confirmed HIV infection in the mother counts as a minor criterion.

The definition for children is not very specific, particularly in poor regions where childhood malnutrition and TB are common. Further, many children present with acute HIV-related illness such as PCP without any clinical evidence of AIDS.

1.3 HIV-RELATED TB

1.3.1 ] Epidemiology of coinfection of HIV and M. tuberculosis

By the end of 2000, about 11.5 million HIV-infected people worldwide were coinfected with M. tuberculosis. 70% of coinfected people were in sub-Saharan Africa, 20% in South-East Asia and 4% in Latin America and the Caribbean.

Numbers of coinfected adults (15-49 years) in WHO regions by end 2000

WHO Region

Number of people coinfected with TB & HIV (thousands)

% of global total

Africa

7979

70

Americas

468

4

Eastern Mediterranean

163

1

Europe

133

1

South-East Asia

2269

20

Western Pacific

427

4

Total

11440

100

HIV probably increases susceptibility to infection with M. tuberculosis. HIV increases the risk of progression of M. tuberculosis infection to TB disease. This risk increases with increasing immunosuppression. HIV increases not only the risk but also the rate of progression of recent or latent M. tuberculosis infection to disease. The table below shows the effect of HIV infection on lifetime risk of an M. tuberculosis-infected individual developing TB.

HIV status

Lifetime risk of developing TB

negative positive

5-10% 50%

HIV is the most powerful factor known to increase the risk of TB.

1.3.3 ] TB in the course of HIV progression

TB can occur at any point in the course of progression of HIV infection. The risk of developing TB rises sharply with worsening immune status.

1.3.4 ] Consequence of HIV/M. tuberculosis coinfection

Compared with an individual who is not infected with HIV, a person infected with HIV has a 10 times increased risk of developing TB. TB notifications have increased in populations where both HIV infection and M. tuberculosis infection are common. For example, some parts of sub-Saharan Africa have seen a 3-5 fold increase in the number of TB case notifications over the past decade. HIV seroprevalence in these TB patients is up to 75%. In sub-Saharan Africa, one-third or more of HIV-infected people may develop TB.

1.3.5 J Impact of HIV on TB control

The principles of TB control are the same even when there are many HIV/TB patients. However, in populations where HIV/TB is common, health services struggle to cope with the large and rising numbers of TB patients.

The consequences include the following:

° overdiagnosis of sputum smear-negative PTB (due to difficulties in diagnosis);

° underdiagnosis of sputum smear-positive PTB (due to excess laboratory workload); ° inadequate supervision of anti-TB chemotherapy; ° low cure rates;

° high morbidity during treatment; ° high mortality rates during treatment; ° high default rates because of adverse drug reactions; ° high rates of TB recurrence;

° increased transmission of drug-resistant strains among HIV-infected patients in congregate settings.

11.3.6 I Patterns of HIV-related TB

As HIV infection progresses, CD4+ T-lymphocytes decline in number and function. These cells play an important role in the body's defence against tubercle bacilli. Thus, the immune system becomes less able to prevent the growth and local spread of M. tuberculosis. Disseminated and extrapulmonary disease is more common.

Pulmonary TB

Even in HIV-infected patients, PTB is still the commonest form of TB.The presentation depends on the degree of immunosuppression. The table below shows how the clinical picture, sputum smear result and CXR appearance often differ in early and late HIV infection.

How PTB differs in early and late HIV infection

Features of PTB

Stage of HIV infection

Early

Late

Clinical picture

Often resembles post-primary PTB

Often resembles primary PTB

Sputum smear result

Often positive

Often negative

CXR appearance

Often cavities

Often infiltrates with no cavities

Extrapulmonary TB

The commonest forms extrapulmonary TB are: pleural effusion, lymphadenopathy, pericardial disease, miliary disease, meningitis, disseminated TB (with mycobacteraemia).

HIV-related TB in children

As in adults, the natural history of TB in a child infected with HIV depends on the stage of HIV disease. Early in HIV infection, when immunity is good, the signs of TB are similar to those in a child without HIV infection. As HIV infection progresses and immunity declines, dissemination of TB becomes more common. Tuberculous meningitis, miliary TB, and widespread tuberculous lymphadenopathy occur.

In an individual infected with HIV, the presence of other infections, including TB, may allow HIV to multiply more quickly.This may result in more rapid progression of HIV disease.

I I SUGGESTIONS FOR FURTHER READING I I TUBERCULOSIS

Crofton J, Horne N, Miller F. Clinical tuberculosis. Second edition. London, MacMillan Press Limited, 1999.

Schlossberg D, ed: Tuberculosis and nontuberculous mycobacterial infections. Fourth edition. Philadelphia,WB Saunders, 1998.

International Union Against Tuberculosis and Lung Disease. Tuberculosis guide for low income countries. Fifth edition. Paris, 2000.

Reider HL. Epidemiologic basis of tuberculosis control. Paris, International Union Against Tuberculosis and Lung Disease, 1999.

World Health Organization. Tuberculosis handbook. Geneva, 1998 (WHO/TB/98.253).

World Health Organization. Global tuberculosis control: surveillance, planning, financing. WHO report 2003. Geneva, 2003 (WHO/CDS/TB/2003.316).

HIV/AIDS

Fauci AS.The AIDS epidemic. Considerations for the 21st century. New England Journal of Medicine, 1999,341:1046-1050.

Royce RA, Sena A, Cates Jr W Cohen, MS. Sexual transmission of HIV. New England Journal of Medicine, 1997, 336: 1072-1078.

World AIDS series. Lancet, 2000, 355:WAI-WA40.

Joint United Nations Programme on HIV/AIDS (UNAIDS). Report on the global HIV/AIDS epidemic:July 2002. Geneva, (contains country-specific estimates).

Joint United Nations Programme on HIV/AIDS (UNAIDS). AIDS epidemic update: December 2002. Geneva, 2002.

CLINICAL STAGING SYSTEM FOR HIV AND HIV-RELATED DISEASE

World Health Organization. Scaling up antiretroviral therapy in resource-limited settings. Guidelines for a public health approach. Geneva, 2002.

AIDS CASE DEFINITIONS FOR SURVEILLANCE

Acquired immunodeficiency syndrome (AIDS).WHO/CDC case definition for AIDS. Weekly epidemiological record, 1986, 61: 69-73. (WHO clinical case definitions for AIDS in children where HIV testing is not available).

Centers for Disease Control and Prevention. 1994 revised classification system for human immunodeficiency virus infection in children less than 13 years of age. Morbidity and mortality weekly report, 1994; 43 (No. RR-12): 1-10. (Case definition for AIDS in children where HIV testing is available).

WHO case definitions for AIDS surveillance in adults and adolescents. Weekly epidemiological record 1994, 69: 273-275.

HIV-RELATED TUBERCULOSIS

Corbett EL, Watt CJ, Walker N, Maher D, Williams BG, Raviglione MC, Dye C. The growing burden of tuberculosis: global trends and interactions with the HIV epidemic. Archives of internal medicine, 2003, 163: 1009-1021.

Raviglione MC, Harries AD, Msiska R, Wilkinson D, Nunn P Tuberculosis and HIV: current status in Africa. AIDS, 1997, II (suppl B): SII5 - SI23.

Ya Diul M, Maher D, Harries A.Tuberculosis case fatality rates in high HIV prevalence populations in sub-Saharan Africa. AIDS, 200I, I5: I43-I52.

World Health Organization. A strategic framework to decrease the burden of TB/HIV. Geneva, 2002 (WHO/CDS/TB/2002.296; WHO/HIV_AIDS/2002.2).

World Health Organization. Guidelines for collaborative TB and HIV programme activities. Geneva, 2003, (WHO/CDS/TB/2003.3I9; WHO/HIV/2003.0I).

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