CHAPTER I

PRELIMINARY

A. Background
Tuberculosis is an infectious disease caused by Mycobacterium tuberculosis which usually
attacks the lungs and can infect organs or tissues in the body. Tuberculosis is the main cause in
the world which causes death from an infectious disease. This is due to inadequate programs to
control disease with poor supervision, multiple drug resistance (MDR), co-infection with HIV, a
rapid increase in the population of young adults in the world - the age group with the highest
mortality rate from tuberculosis, poor density and nutrition (Amin, 2009).
Tuberculosis is one of many diseases that are usually in someone infected with HIV. In patients
with M. Tuberculosis and HIV co-infection, it increases from 0.4% to 8% (20-fold). HIV-TB co-
infection has become a health threat to humanity, which if not taken seriously will cause both of
them to no longer be controlled. (Wulandari, 2010).
Between TB and HIV have a strong relationship due to HIV infection, the TB disease has
increased again. Pulmonary tuberculosis is the most common opportunistic infection in people
with HIV. HIV infection is a risk factor for the development of TB through a mechanism in the
form of reactivation of latent infection, rapid progression in primary infection or reinfection with
Mycobacterium tuberculosis (M. tuberculosis) (Fauci, 2008).
According to WHO in 2002 there were 8.8 million new cases of Tuberculosis (TB) and 3.9
million were cases that were accompanied by Human Immunodeficiency (HIV) infection. In
1992, WHO declared TB as a global emergency, every year around 4 million new cases of
infectious TB were added to non-communicable cases. At the same time throughout the world
there is daily HIV transmission to 2000 children under 15 years, HIV exacerbates TB infection
by increasing reactivation and accelerating TB progression. Increased HIV cases will increase
transmission and proliferation of MTB in patients who have had previous infections. (WHO
2009; Mulyadi & Fitrika, 2010)
From the description above, the author is interested in discussing more about the relationship
between HIV disease and TB disease.

A. Problem Formulation

The problem formulation of this paper is:

1. What is the basic concept of HIV disease?
2. What is the basic concept of TB disease?
3. What is the relationship between HIV disease and TB disease?
B. Purpose of the Paper
The purpose of making this paper is:
1. Understand about HIV disease
2. Understanding TB
3. Understand the relationship between HIV disease and TB disease.

1.1
 CHAPTER II
BASIC DISEASE CONCEPT

A. Basic Concepts of HIV Disease

1. Understanding
HIV (Human Immunodeficiency Virus) is a type of virus that attacks the human immune system
and can cause AIDS. HIV attacks one type of white blood cells which is responsible for warding
off infections. These white blood cells are mainly lymphocytes that have CD4 cells as a marker
on the surface of lymphocyte cells. Because the reduced CD4 value in the human body shows a
reduction in white blood cells or lymphocytes which should play a role in dealing with infections
that enter the human body. In people with a good immune system, CD4 values range from 1400-
1500. Whereas in people with impaired immune systems (for example in people infected with
HIV) CD4 values will increasingly decline (even in some cases can be up to Zero) (Djuanda,
2005).
AIDS stands for Acquired Immuno Deficiency Syndrome, which means a collection of
symptoms or syndromes due to decreased immunity caused by HIV virus infection. The human
body has immunity to protect itself from external attacks such as germs, viruses, and diseases.
AIDS weakens or damages the body's defense system, so that eventually a variety of other
diseases arrive (Yatim, 2006).

2. Pathogenesis
CD4 + lymphocytes are the main target of HIV infection because the virus has an affinity for
CD4 surface molecules. CD4 + lymphocytes function to coordinate a number of important
immunological functions. The loss of this function causes progressive impaired immune
response. The virus is lowered by antigen-presenting cells to regional lymph nodes. In this model
the virus is detected in the lymph nodes then within 5 days after inoculation. Individual cells in
lymph nodes that express SIV can be detected by in situ hybridization within 7 to 14 days after
inoculation. SIV Viremia is detected 7-21 days after infection. The peak number of cells that
express SIV in lymph nodes is related to the peak of antigenemia p26 SIV (Amin, 2009).
Antibodies appear in the circulation within a few weeks after infection, but in general can be
detected the first time after virus replication has decreased to the level of 'steady-state'. Even
though these antibodies generally have a strong neutralization activity against infection
viruses, but apparently can not kill the virus. Viruses can avoid neutralizing antibodies by
adapting the envelope. Including the ability to change the glycosylation site, consequently the 3
dimensional configuration changes so that neutralization mediated by antibodies cannot occur
(Amin, 2009).
HIV infection will not immediately show certain signs or symptoms. Some exhibit non-typical
symptoms of acute HIV infection, 3-6 weeks after infection. Symptoms that occur are fever,
painful swallowing, swollen lymph nodes, rashes, diarrhea, or cough after acute infection begins
asymptomatic (asymptomatic) HIV infection. This asymptomatic period generally lasts for 8-10
years. But there is a small group of people who travel very fast the disease can only be around 2
years, and some are slow (non-progressor) (Amin, 2009).
      As the immune system deteriorates, PLHAs begin to display symptoms due to opportunistic
infections such as weight loss, old fever, weakness, enlarged lymph nodes, diarrhea, tuberculosis,
fungal infections, herpes, etc. (Amin, 2009) .

2. Mode of Transmission
a. Sexual Transmission
Sexual transmission, both Homosexual and Heterosexual, is the most common transmission of
HIV infection. This transmission is related to semen and vaginal or seric fluid. Infection can be
transmitted from every person with HIV infection to their sex partners. The risk of HIV
transmission depends on the choice of sex partners, number of sex partners and the type of sex.
People who frequently have sexual relations by changing partners are a group of people who are
at high risk of being infected with the HIV virus.
1) Homosexual
In the western world, the United States and Europe have high rates of homosexual promiscuity
with AIDS, aged between 20-40 years of all russia groups. Anogenetal sexual intercourse is a
high-risk sexual behavior for HIV transmission, especially for sexual partners who passively
accept semen ejaculation from someone with HIV. This is related to the rectum mucosa which is
very thin and easily exchanged when anogenital contact.
2) Heterosexual
In Africa and Southeast Asia the main mode of transmission through heterosexual contact with
promiscuity and most sufferers is the active sexual age group of both men and women who have
multiple partners and change.
b. Non Sexual Transmission
1) Parenral Transmission
 That is due to the use of syringes and other piercing tools (piercing tools) that have been
contaminated, for example in the misuse of injecting narcotics that use contaminated syringes
together. Besides it can also occur through needles used by health workers without

sterilized beforehand. The risk of contracting this way of parental transmission is less than 1%.
 Blood / Blood Products
Transmissions via transfusions or blood products occurred in western countries before 1985.
After 1985 transmission through this route in western countries was very rare, because donor
blood was examined before being transfused. The risk of contracting an infection / HIV through
blood transfusion is more than 90%.
1) Transplacental Transmission
Transmission from HIV positive mothers to children carries a risk of 50%. Transmission can
occur during pregnancy, childbirth and while breastfeeding. Transmission through breast milk
including transmission with low risk.

A. Basic Concepts of TB Disease

1. Understanding
Tuberculosis is a direct infectious disease caused by TB bacteria, Mycobacterium tuberculosis.
The majority of TB germs will attack the lungs, but TB germs can also attack other organs
(MOH, 2007).
Tuberculosis is an infectious disease that attacks the lung parenchyma. The infectious agent is
Mycobacterium tuberculosis which is an aerobic rod that is acid resistant, grows slowly, and is
somewhat sensitive to heat and ultraviolet light. Tuberculosis can be transmitted to other parts of
the body such as meninges, bones, kidneys, and lymph nodes. (Brunner & SuddARVh, 2001)

2. Etiology and Mode of Transmission

The cause of tuberculosis is Mycobacterium tuberculosis, a type of rod-shaped bacteria with a
length of 1-4 / um and 0.3-0.6 / um thick. Which belongs to the Mycobacterium tuberculosae
complex is (Amin, 2009).
1. M. tuberculosae
2. Asian Variants
3. African Variant I
4. African Variant II
5. M. bovis
The process of infection with M. tuberculosis is usually inhaled, so that pulmonary TB is the
most frequent clinical manifestation compared to other organs. Transmission of this disease is
largely through inhalation of bacillus containing droplet nuclei, especially those obtained from
pulmonary TB patients with coughing up blood or phlegm containing acid-resistant bacilli
(AFB). Transmission of HIV is through heterosexual and homosexual contact, blood and blood
products and by infected mothers to infants either through intrapARVum, perinatal or breast
milk. Potential risk factors for tuberculosis are individuals who have HIV co-infection, where
suppression of cellular immunity occurs. (Amen, 2009)
 1. Pathogenesis of Tuberculosis
The pathogenesis of M. tuberculosis infection is divided into 2 major parts, namely primary
infection and post primary infection (Kumar, 2006).
a. Primary infection (primary infection)
The first infection of M. tuberculosis is known as a primary infection. Within an hour can reach
the lungs, bacilli can pass through the lymph nodes in the lungs hilum and some into the
bloodstream (Kumar, 2006).
Initial reactions include exudative responses and infiltration of neutrophil granulocytes. This is
quickly replaced by macrophages which digest the germ and transport it into the regional lymph
nodes. In general, there are 4 big possibilities for the fate of M. tuberculosis namely, (1) killed by
the immune system, (2) can be cultured and causes primary TB, (3) can become dormat and
asymptomatic, (4) can proliferate after the latent period (reactivation of disease). In addition,
there are 4 things that can occur, especially in primary infections, namely: (Innes, 2007)
1) Spread from the primary focus to the hilum and mediastinal lymph glands to form a primary
complex, in many cases heal spontaneously.
2) Instantly extends from primary focus to progressive primary tuberculosis.
3) Spread to the pleura becomes pleural tuberculosis and pleural effusion.
4) Spread in the bloodstream: slight bacilli in the lungs, bones, renal, urogenital infections often
in months or years, spread massively to miliary TB and meningitis.
Interaction with T lymphocytes, with the development of cellular immunity can be demonstrated
3-8 weeks after initial infection by a positive reaction to the skin on intradermal injection of
protein from bacilli (PPD). Late type hypersensitivity reactions occur, resulting in tissue necrosis
and at this level the classical pathology of tuberculosis can be seen. Granulomatous lesions
consisting of white mass like cheese in the central part of the necrosis area are called caseous
necrosis, surrounded by epithelioid cells and giant cells of langhans, both cells originating from
macrophages. Lymphocytes are present and there are various degrees of fibrosis. After that, the
area of caseose necrosis is completely healed and hardened (Kumar, 2006).

a. Post primary tuberculosis (post primary tuberculosis)

It is known that at least 20% of the hardened primary lesions contain tubercle bacilli, which are
initially dormant but are able to be activated by a decrease in the host immune system.
Reactivation is typical of post primary tuberculosis with cavities, usually at the apex or upper
part of the lung. Post primary tuberculosis is associated with all forms of tuberculosis that occur
after at least one week in primary infection when immunity to mycobacterium is developing
(Kumar, 2006).
 4. Pathophysiology & Pathogenesis
Mycobacterium Tubeculosis found in the droplet nuclei in the air can be sucked in
healthy people and will be attached to the NAPA tract or lung tissue. These particles can
enter alveolar when the particle size < 5 micrometers. These germs will be faced first by
netrophiles, then macrophages and out of the Traceobronchial branch with a cilia
movement. If the sedentary germ is in the pulmonary tissue, it will multiply in the
cytoplasm of macrophages. Here it can be carried over to other organs. A nested germ
in the pulmonary tissues will be in the form of a nest tuberculosis small pneumonia and
is called the primary nest or the primary Aphek or the nest (focus) ghon. When
spreading to the pleural then it occurs pleural effusion. Germs can also enter through the
gastrointestinal tract, lymph tissues, oropharynx and skin, occurring regional
lymphadenopathy then bacteria enter into a vein and spread throughout the organs such
as the lungs, brain, kidneys, bones. When entering the pulmonary artery, there is a
connection throughout the lung to TB Milier. From the primary nest there will be
inflammation of the lymph tract towards the hilus (local lymphangitis), and also
followed by enlargement of the hilus lymph nodes (regional lymphadenitis).
Lymphadenit becomes a primary complex with a 3 – 8 week process. 1.2 This primary
complex can then be: • Cured completely without leaving any defects. This happens a
lot. • Cured by leaving a small amount of fibrotic line lines, the calcification of the
Dihilus, the condition is present in the lesions of pneumonia that is wide > 5 MM and ±
10% of which can occur again due to the dormant germs.
• Complicate and spread in a) the percontinuitatum, that is, spread to the
surrounding areas., b) in bronchically the corresponding lung or pulmonary next to it.
Germs can also be swallowed together with sputum and saliva so that it spreads to the
intestines, c) lymphogenous to other organs, d) in a hematogenic body to other organs. 2
 Table 1. Course of TB infection (Innes, 2007)
Time of infection Manifestation

3-8 weeks Primary complex, positive tuberculin skin

test
Meningeal, military and pleura
3-6 months to 3
years Gastrointestinal, bone and joint and
lymphatic nodes
Renal tract disease
Around 8 years
Post primary infections associated with
disease reactivation.
Next 3 years
PATHWAY PATHOPHYSIOLOGY HIV / AIDS

Transmission of HIV into the body through

the blood, breast milk / body fluids of
infectious mothers

The binding of HIV gp120 with the T Helper

+ CD4 membrane receptor

Fusion / fusion of viral membranes with

Helper + CD4 T cell membranes

Reverse transcriptase enzyme

HIV RNA  cDNA

Enzyme integrase
cDNA enters the T helper nucleus

MRNA transcription and translation produce

viral structural proteins

Protease enzymes
Arranging viral RNA with
newly formed proteins,

New HIV viruses are formed in the body

 Risk of Transmission of Replication and development of HIV
Infection in body fluids

HIV infects other Helper + CD4 T cells HIV attacks dendritic cells and
macrophages in lymphoid tissue

Blood flow Inflammatory Helper + CD4 T cell damage in

carries HIV to reaction large numbers Swollen lymph glands
peripheral blood
vessels Hipertermi Failure of B cell stimulation
in the intestines Damage
Antibody production decreases Social interactions
Impaired High Risk of
balance of Infection Decreased body immunity
normal flora in
the intestine
(E.coli) Oral infection Respiration Skin infections
(Candida
Absorption of albicans)
water in the Pneumonia TB
intestine is Intake  Pneumocystis Oral candidiation.
disrupted Herpes zozter,
carinii
Metabolism herpes simplex,
Diarrhea  sarcoma Kaposi,
School buildup dermatitis
Energy
No production
Nutrition  Airway obstruction
Lack of Weakness
Volume of balance
Less than Pain
Body Fluids Impaired
Need Clearing the airway is not
Activity intolerance Skin
effective Integrity
Decreased body immunity

Neurologic
infection

Ensefalopari
HIV

Changes in
mental status,
headaches,
psychomotor
slowdown,
seizures,
affective
disorders

Risk of
injury
A. HIV-TB
1. Epidemiology
HIV patients are 20-37 times more likely to have TB compared to people who don't have HIV infection. TB is one of the leading causes of death
in HIV patients globally. Of the 1.7 million people who died of TB in 2009, 400,000 were HIV patients. Of the 9.4 million new TB cases
discovered in 2009, 1.2 million were HIV patients. The higher the prevalence of HIV in an area, the higher the prevalence of HIV-TB
coinfection in HIV patients in the area (Wisharilla, 2012).
In areas with high HIV prevalence in populations with a possibility of TB-HIV coinfection, HIV counseling and testing is indicated for all TB
patients as part of routine management. 19,20 In areas with low HIV prevalence, HIV counseling and testing is only indicated in TB patients
with complaints and signs suspected of being related to HIV and in TB patients with a history of high risk of HIV exposure. Not all pulmonary
TB patients need to be tested for HIV. Only certain pulmonary TB patients require HIV testing, for example:
a. there is a history of high risk behavior for HIV infection
b. the results of OAT treatment are unsatisfactory
c. MDR TB / chronic TB

2. Diagnosis
TB diagnosis in patients with known CD4 levels. The minimum examination that needs to be done to confirm the diagnosis of pulmonary TB is
smear sputum examination, chest X-ray and if possible a CD4 examination is done. The description of TB-HIV sufferers can be seen in the table
below:

Early infection (CD4> 200 / Early infection (CD4> 200 /

mm3) mm3)

Microscopic phlegm Often positive Often negative

Extraparu TB Rarely General / many

Mycobacteremia There is no There is

 Tuberculin Positive negative

Chest X-ray Reactivation of Tb, cavity at Typical primary miliary /

peak interstitial TB

Hilar / mediastinal There is no There is

adenopathy

Pleural effusion There is no There is

Table 2. Clinical Manifestations of TB in HIV patients (Wisharilla, 2012)

There are differences in clinical manifestations between TB-HIV patients with early HIV infection and advanced infection. Therefore, different
clinical approaches are needed to diagnose it. In addition, when compared with non-HIV TB patients, smear results are more often negative,
plain photographs are more often atypical, and TB is more often extrapulmonary. This is caused by an impaired immune system so that the
immune reaction to TB is different from ordinary people. Therefore, it is important to know the characteristics of TB-HIV.

3. Clinical Features of HIV in TB Patients

If a patient has been diagnosed with TB, then there is also a clinical picture of HIV sufferers, as can be seen in the table below.
History of risk factors Sign The symptoms

PMS Weight loss (> 10kg or> 20% Scar on herpes zoster
original weight)

Herpes zoster Diarrhea (> 1 month) Sarkoma Kaposi

Pneumonia Retrosternal pain when Candidiasis oral

swallowing (esophageal
(rekurens/no)
candidiasis)

Severe bacterial Burning sensation in the legs Limfadenopati

infection (peripheral sensory
generalisata simteris
neuropathy)

Newly managed TB Ulkus genital persisten

Table 3. Clinical features of HIV infection (Wisharilla, 2012)

3. PLHIV Therapy with TB Coinfection

Infection therapy and TB control are top priorities in the treatment of patients with HIV-TB coinfection. The management of TB HIV
coinfection is complicated because some ARV drugs produce unwanted interactions with anti-TB drugs and / or increase the toxicity of OAT
(Fauci, 2008).
A simplified standard ARV regimen is used to support HIV treatment programs so that it can reach many people living with HIV (WHO, 2010).
The principles in giving ARV are as follows (Ajmala, 2013).
a. ARV drug guidelines must use 3 types of drugs that are absorbed and are in therapeutic doses. The principle is to guarantee the effectiveness
of drug use.
b. Helping patients to be obedient to take medication, among others, by getting closer access to ARV services
c. Maintain continuity of ARV drug availability by implementing good logistics management.
WHO recommends that first-line ARV regimens contain two nucleoside reverse transcriptase inhibitors (NRTIs) plus one non-nucleoside
reverse transcriptase inhibitors (NNRTIs). This combination is good, relatively inexpensive, has generic formulations and FDC, and maintains a
powerful new class (Protease Inhibitor) for second-line regimens (WHO, 2010).

Target population Recommended choice Note

Adult and child AZT or TDV + 3TC (or Is the appropriate choice of
FTC) + EFV or NVP guidance for most patients.
 Use FDC if available

Pregnant woman AZT + 3TC + EFV or NVP Must not use EFV in the
first trimester
TDF bias is an option

HIV / TB co- AZT or TDF + 3TC (FTC) Start antiretroviral therapy

infection + EFV immediately after TB
therapy can be tolerated
(between 2 weeks to 8
weeks)
Use NVP or triple NRTI if
EFV cannot be used.

For chronic active TDF + 3TC (FTC) + EFV Consider HBsAg testing
HIV / Hepatitis B or NVP especially if TDF is the first
infection line guide. is required

Table 4. Recommended first-line guidelines for adults who have never received ARV therapy (Ajmala, 2013).

In patients who have received ARV if they have contracted TB, the regimen must be adjusted to match the chosen OAT. After complete TB
therapy, antiretroviral drugs can be continued or replaced depending on the clinical and immunological conditions of the patient. The optimal
time to start ARVs in relation to the start of TB therapy is unclear (Wulandari, 2010).
The main priority in patients with TB-HIV co-infection is to start TB therapy, followed by cotrimoxazole and ARVs (Ajmala, 2013).
a. Treatment of TB in people living with HIV who are not yet on ARV treatment
If not on ARV treatment, TB treatment can be started immediately. If the patient is on TB treatment then continue TB treatment until it can be
tolerated and after that given ARV treatment. The decision to treat antiretroviral drugs in patients with TB treatment should be made by a doctor
who has received TB-HIV patient management training.
b. Treatment in people living with HIV is currently on ARV treatment
If the patient is on antiretroviral treatment, TB treatment should be started at a minimum in hospitals where staff have been trained in TB-HIV,
to arrange TB treatment plans together with ARV treatment. This is important because there are possible problems that must be considered,
including drug interactions (rifampicin with several types of ARV drugs), failure of ARV treatment, IRIS or need for substitution of ARV drugs.

Information
CD4 Guidance recommended

Whatever the Start TB therapy Start antiretroviral

CD4 count therapy immediately
Use guidelines that contain (AZT or
after TB therapy can be
TDV) + 3TC + EFV (600 mg /
 day). tolerated (between 2
weeks to 8 weeks)
After the OAT is completed, EFV
can be replaced with NVP if
necessary.
In cases where NVP-based
guidelines are forced to be used in
conjunction with TB treatment,
NVP is given without palead-in
dose (NVP is given every 12 hours
since the start of therapy)

CD4 not Start antiretroviral

possible to Start therapy TB therapy immediately
check after TB therapy can be
tolerated (between 2
weeks to 8 weeks)

Table 5. ARV therapy for TB-HIV co-infected patients (Ajmala, 2013).

Guide ARV when TB Therapy Options

Guide ARV
appear ARV
First line 2 NRTI + EFV Continue with 2 NRTI + EFV
2 NRTI + NVP Replace with EFV or Forward with
2 NRTI + NVP. Triple NRTI can be
considered for 3 months if NVP and
 EFV cannot be used

Two line 2 NRTI + Pls Prefer rifampicin cannot be used in

conjunction with LPV / r, it is
recommended to use OAT
guidelines without rifampicin. If
rifampicin needs to be given then
another option is to use LPV / r at a
dose of 100 mg / 200 mg twice a
day. Need to monitor strict liver
function if using rifampicin and a
double dose of LPV / r

Table 6. Guidelines for ARVs for PLWHA who later appear active TB
(Ajmala, 2013).

Preventive therapy with cotrimoxazole

All TB patients are HIV positive, cotrimoxazole preventive therapy should be started as soon as possible. Cotrimoxazole preventive therapy
substantially reduces mortality in HIV-positive TB patients. Cotrimoxazole is known to prevent Pneumocystis jirovecii and malaria and is likely
to have an impact on various bacterial infections in HIV-positive TB patients (WHO, 2010).

Patient Monitoring during therapy

Drug side effects that often occur in HIV-positive TB patients, and some toxicity that is usually for ARVs and TB drugs. Overlaps between ARV
toxicity, TB therapy and cotrimoxazole including rashes and liver dysfunction, and monitoring of other side effects (WHO, 2010).

3. Interaction of HIV and TB

HIV and M. tuberculosis are both intracellular pathogens that interact with each other at the population, clinical and cellular levels. PLWHA are
susceptible to TB. The progression of TB becomes active since the beginning of exposure is greater in PLWHA (40%) compared to non-PLHIV
who are less than 0.1% per year (Wulandari, 2010).
TB has also been shown to accelerate the course of HIV infection. The annual mortality rate of HIV-related TB being treated ranges between
20.35%. The mortality rate of HIV - TB is four times higher than the mortality rate of TB without HIV. The high mortality rate among TB
sufferers is caused mainly by progressive HIV infection, although early mortality (within the first 3 months) is mostly due to the TB itself.
Tuberculosis can occur at any stage of HIV infection and with varying presentations (Wulandari, 2010).

1. Signs and Symptoms

The main symptom of pulmonary TB patients is coughing up phlegm for 2 weeks or more. In addition, additional symptoms can also be
followed by phlegm mixed with blood, night sweats without activity, decreased appetite, decreased body weight, malaise and the body feels
weak. Symptoms of shortness of breath and chest pain can be found if there are complications (pleural effusion, pneumothorax and pneumonia).
The clinical symptoms of pulmonary TB in PLWHA are often not specific. Clinical symptoms that are often found are fever and significant
weight loss (more than 10%). In addition, other symptoms associated with extrapulmonary TB (pleural TB, pericardial TB, miliary TB, central
nervous system and abdominal TB) can be found such as diarrhea for more than one month, enlargement of lymph nodes in the neck, shortness
of breath, etc. .4,5

1. Sputum laboratory examination

Microscopic
In PLWHA, although it is difficult to find pulmonary TB cases only by relying on sputum microscopic examination because the sputum of
PLWHA suffering from pulmonary TB is usually smear negative, sputum microscopic examination is still necessary. Sputum microscopic
examination is sufficient to do with two sputum specimens (During and Morning = SP) and if at least one sputum specimen results in smear is
positive then the diagnosis of TB can be established.
Culture
Sputum culture examination is the gold standard for diagnosing TB. There are two types of media used in the examination of culture, namely
solid media and liquid media. The examination time with liquid media is shorter compared to solid media. However, TB germs are slow-growing
germs so culture takes about 6-8 weeks. 6
Examination of culture requires a long time so that if the enforcement of TB diagnosis in PLWHA only relies on culture testing it can cause TB
mortality rates in PLWHA to increase. In PLWHA, which results from microscopic examination of sputum smear is negative, it is highly
recommended to have sputum culture examination because this can help establish TB diagnosis if the results of other supporting examinations
are negative. Sputum culture examination is carried out at laboratories that have met the standards set by the Directorate of Medical Support
Services and Health Facilities (BPPM and SK). 1,3,4

1. Radiological investigations
Chest X-ray examination of PLWHA plays an important role in establishing the diagnosis of pulmonary TB, especially BTA negative.
Indications of chest X-ray examination in people living with HIV:
BTA positive
Chest X-ray required on:
• the patient is short of breath (pneumothorax, pericardial effusion or pleural effusion).
• hemoptysis patients.
• patients with other suspected lung infections.

BTA is negative
Perform chest X-ray of smear negative pulmonary TB patients.
Radiological abnormalities found in pulmonary TB
1. Diagnosis flow
Diagnosis of Pulmonary TB in PLWHA
There are several things that need to be considered in the flow of TB diagnosis in PLWHA, including: Provision of antibiotics as a diagnostic aid
is no longer recommended. The use of antibiotics with the intention of being a diagnostic tool such as the flow of TB diagnosis in adults can
cause diagnosis and treatment of TB so late that it can be 8

increase the risk of death of people living with HIV. Therefore, the administration of antibiotics as a diagnostic aid is no longer recommended.
However, antibiotics need to be given to people living with HIV who may be caused by other bacterial infections together or without M.
tuberculosis. So, the purpose of giving antibiotics is not as a tool for TB diagnosis but as a treatment for other bacterial infections. Avoid using
fluoroquinolone antibiotics because it responds to M. tuberculosis and can cause resistance to the drug.
Chest X-ray examination plays an important role in diagnosing TB in PLHIV with negative smear. However, it should be noted that the thoracic
image in PLWHA is generally not specific, especially in advanced stages
If sputum culture testing facilities are available, then people with BTA who are smear negative, it is highly recommended to do sputum culture
examination because this can help to confirm the diagnosis of TB.
The flow of negative smear pulmonary TB diagnosis in PLWHA below is an activity step that must be carried out in the enforcement of TB
diagnosis in areas with high HIV prevalence with limited means. The flow of this diagnosis is only for PLWHA who are suspected of having
TB. It should be noted, the flow of TB diagnosis in outpatient PLWHA (without danger signs) is different from in-patient PLWHA (with danger
signs).
1. Differential Diagnosis
Pulmonary TB and extrapulmonary TB in people living with HIV have similarities with other diseases that have symptoms such as coughing,
fever and sometimes chest pain and similarity of chest X-ray images. Pneumonia can occur as a TB co-infection. In each case a careful clinical
examination must be performed. Perform smear microscopic examination on patients who cough for 2 weeks or more.
The following are some lung diseases that are often found in people living with HIV:
a. Bacterial Pneumonia
This pneumonia can affect infants, elderly people, alcohol dependence, patients with mental retardation, postoperative patients,
immunocompromised patients who suffer from other respiratory diseases or viral infections are very susceptible to bacterial pneumonia. The
bacteria that cause pneumonia are normal flora in the upper airway. When the immune system decreases, the bacteria will multiply and damage
the lung parenchyma.
If an infection occurs, most of the lung parenchyma is filled with fluid and the infection can quickly spread throughout the body through blood
circulation. Pneumococcus is the most common cause of bacterial pneumonia. Bacterial pneumonia is preceded by infection of the upper airway
and aspiration of mucus into the lower airway causes the upper respiratory tract bacteria to infect the lung parenchyma.
Clinical symptoms in pneumonia include productive cough, fever that can be accompanied by chills, tachycardia, tachypnea until cyanosis. In an
immunocompetent state, the body is able to fight but not the immunocompromised state so that the clinical symptoms that occur are not specific.
Bacterial pneumonia is often the cause of secondary infections in TB-HIV co-infection. Secondary infections that are not treated properly will
cause sepsis. This is often found but difficult to diagnose.
b. Kaposi's Sarcoma
Kaposi's sarcoma is characterized by typical lesions of the skin and black-blue mucous membranes. Kaposi's sarcoma in the mucous membranes
of the airways causes cough symptoms, 11

fever, hemoptysis and dyspnea accompanied by skin lesions elsewhere. Chest radiograph shows diffuse nodular infiltrates spread from the hilum
or a picture of pleural effusion. Pleural fluid cytology can help diagnose Kaposi's sarcoma.
a. Pneumocystis jirovecii pneumonia (PCP)
Pneumocystis jirovecii pneumonia in adults often occurs in PLHIV with clinical stage 4 (AIDS). Clinical symptoms include unproductive cough,
fever and progressive shortness of breath.
b. Mycobacterium Avium Complex (MAC)
Clinical manifestations of MAC generally include fever, night sweats, weight loss, weakness / fatigue and abdominal pain. Localized
manifestations include cervical or mesenteric lymphadenitis symptoms, pneumonitis, pericarditis, osteomyelitis and CNS infection.
On physical examination can be found hepatomegaly, splenomegaly or lymphadenopathy (in paratracheal, retroperitoneal and paraaorta). On
laboratory examination can be found anemia, increased alkaline phosphatase.
c. Parasitic infection
Parasitic infections that are often found in people living with Cryptococcus sp. and Nocardia sp. Clinical symptoms of cryptococcosis are
difficult to distinguish from clinical symptoms of pulmonary TB. The diagnosis of pulmonary cryptococcosis is established by the discovery of
fungal spores on phlegm smears.
Clinical symptoms of pulmonary TB-like nocardiosis such as productive cough can be accompanied by blood, fever, nausea, malaise, shortness
of breath, night sweats without activity, decreased appetite and weight, joint pain and chest pain. On physical examination can be found wet
crackles, weak breath sounds, lymphadenopathy, skin rash and hepatosplenomegaly.
Abnormalities in the chest X-ray are often found in the upper lobes in the form of cavities. The causative organism can be found to be positively
weak in acid-resistant staining. Clinical suspicion increases with the discovery of brain abscesses. The diagnosis is made by finding stems in
preparations with gram-positive staining. 1,6 12

Differential diagnosis based on chest radiograph

b. Chest X-ray images of diseases other than TB can also provide chest X-ray images like TB.
1. Management
Principles of Treatment
TB treatment category is not affected by HIV status in TB patients. In principle the treatment of TB in patients co-infectious TB
HIV should be administered immediately while the treatment of ARV begins after the treatment of TB can be well tolerated, it is
recommended to be administered at most quickly 2 weeks and no later than 8 weeks. 13
 A. Treatment of TB in ODHA that has not been in the treatment ARV
If the patient has not been in ARV treatment, TB treatment can begin immediately. If the patient is in the treatment of TB then
proceed with his TB treatment until it can be tolerated and thereafter given ARV treatment. The decision to start ARV treatment in
patients with TB treatment should be done by doctors who have received training in TB-HIV patients.

B. Treatment of TB in ODHA is in the treatment ARV

If the patient is in the treatment of ARV, it is recommended that the treatment of TB begins at least in the HOSPITAL whose
duties have been trained TB-HIV, to be regulated treatment plan TB along with the treatment of ARV (treatment of TB-HIV infection).
This is important because there are many possible problems that should be considered, among other things: drug interactions
(rifampicin with some types of ARV medications), failed treatment ARV, IRIS or need substitution ARV drugs. 1, 2, 3, 4, 5 14 15 16
Category Patient TB Treatment Regimen

Initial Phase Advanced Phase

1 New sputum smear positive 2 SHRZ ( EHRZ ) 6 HE

TB forms severe TBP, 2 SHRZ ( EHRZ ) 4 HR
extra-pulmonary TB
(severe), smear-negative 2 SHRZ ( EHRZ ) 4H3R3
TBP

2 Relapse, Treatment Failure, 2 SHZE/ 1 HRZE 5 H3R3E3

 return to default 2 SHZE/ 1 HRZE 5 HRE
3 BTA sputum TBP - negative 2HRZ atau 2 6 HE
Extra-pulmonary TB H3R3Z3 2 HR/4H
(medium weight) 2HRZ atau 2 2H3R3/4H
H3R3Z3
2HRZ atau 2
H3R3Z3
4 Chronic case (still smear Uses second-line
positive after supervised re- drugs
treatment)
 CHAPTER III
BASIC NURSING CONCEPTS
A. Assessment
1. Client identity
Name, age, sex, place of residence (address), occupation, education and economic status of the middle-low and health sanitation which is not
supported by dense population and have had a history of contact with other pulmonary TB sufferers.
2. Current disease history
Includes complaints or disorders related to the disease felt at this time. With shortness of breath, coughing, chest pain, skin lesions, diarrhea,
night sweats, abdominal pain, weakness, decreased appetite and increased body temperature (fever) encourage sufferers to seek treatment.
3. Past medical history
History: HIV positive test, history of high-risk behavior, use of medications. Circumstances or diseases that have been suffered by sufferers that
may be related to pulmonary tuberculosis include ISPA pleural effusion and pulmonary tuberculosis which is again active.
4. Family history
Look for among family members who have HIV or pulmonary tuberculosis who suffer from the disease so that transmission continues.
5. Psychosocial history
Social history, drug abuse, free sex, depression due to family or social problems, loss of work and income, changes in lifestyle, express feelings
of fear, anxiety, grimace, had a history of contact with other pulmonary tuberculosis sufferers

1. Mental and spiritual status

Conditions of anger or resignation, denial, depression, ideas of suicide, apathy, withdrawal, loss of interest in the surrounding environment,
impaired thought processes, lost memory, impaired attention and concentration, hallucinations and delusions. Belief in God, motivation, worship
and coping mechanisms.
2. Patterns of health function
a) Patterns of perception and governance of healthy living
Clients with pulmonary TB usually live in crowded areas, lack of sunlight, lack of air ventilation and live in a crowded house. HIV sufferers are
often found to have a history of consuming alcohol, using drugs, promiscuity.
b) Nutrition and metabolic patterns
In patients with HIV with pulmonary TB there is usually a decrease in absorption of nutrients, an increase in the body's metabolic needs,
complaining of anorexia, decreased appetite, weight loss, digestive disorders.
c) Pattern of elimination
HIV clients with pulmonary TB are prone to diarrhea and urinary tract infections.
d) Patterns of activity and training
With physical weakness due to decreased immunity, coughing, shortness of breath and chest pain will disrupt activity. Sleep and rest patterns
With the shortness of breath and chest pain in patients with pulmonary TB resulting in disruption of sleep and rest comfort relationship patterns
and roles
e) Sensory and cognitive patterns
The senses (smell, touch, taste, vision, and hearing) can become distracted due to a viral infection.
f) Patterns of perception and self-concept
HIV sufferers often have low self-esteem because of social isolation coupled with pain and shortness of breath caused by symptoms of
pulmonary TB usually will increase the emotions and anxiety of clients about the disease to cause depression and allow increased risk of suicide.
HIV clients with pulmonary TB will experience feelings of isolation due to infectious diseases.
g) Reproductive and sexual patterns
HIV sufferers with pulmonary TB will experience changes in sexual and reproductive patterns will change due to sexually transmitted diseases
they suffer and the physical weakness they experience.
h) Patterns for dealing with stress

HIV sufferers with pulmonary TB are increasingly increasing stressors. the process of treatment that is> 6 months long can even increase.
Decreased adherence to therapy can occur with the saturation of therapy a) Values and belief patterns Due to shortness of breath, chest pain and
coughing disrupt client worship activities.
1. Physical examination
Based on body systems
a) Integumentary system
Cyanosis occurs in the skin, cold and damp, skin tugor decreases dry, itchy, rash or lesions, positive petechiae, facial edema, lesions on the
integument.
b) Respiratory system
In the respiratory system during physical examination found
Inspection: signs of pulmonary withdrawal, diaphragm, movement of the breath that is left behind, weak breath sounds, epsytaxis.
Palpation: Increased voice fremitus
Percussion: Dullness sounds
Auscultation: Brokial breath sounds with or without wet, rough and loud crackles.
Spuntum: green / purulent, yellowish, pink.
c) sensing system
HIV clients with pulmonary TB for sensing can develop disorders caused by viral infections: periorbital pain, photophobia
d) Cordiovascular system
The presence of tachypnea, tachycardia, cyanosis, hardened P2 sound, hypotension, peripheral edema, dizziness.
e) Gastrointestinal system
Lip or mouth ulcer, dry mouth, decreased appetite / dysphagia, anorexia, weight loss accompanied by chronic diarrhea.
f) Musculoskeletal system
There are limited activities due to weakness, lack of sleep and unpleasant daily conditions: focal motor de fi cient, weak, unable to do ADL.

A. Nursing Diagnosis
1. High risk of infection associated with decreased immunity (immunosuppression)
2. Activity intolerance is related to weakness, oxygen exchange, malnutrition, fatigue.
3. Changes in nutrition less than the body's needs related to lack of intake, increased metabolic needs, and decreased absorption of nutrients.
4. Low self-esteem is associated with social isolation.
5. The ineffectiveness of family coping has to do with anxiety about the condition of a loved one.
6. Ineffective individual coping: depression is associated with anxiety about the disease, low self-esteem
7. Ineffective breath patterns associated with gas can not diffuse properly, tightness (pain)
8. Acute pain associated with fluid infiltration into the pleural space, tightness
 9. Disruption of gas exchange associated with damage to capillary alveolar membrane
10. Lack of knowledge related to the disease process and adherence to therapy

A. Nursing Plan

Perencanaan Keperawatan
Nursing
Goals and results
No diagnoses
criteria Intervensi Rasional

1 High risk of Patients will be a. Observation of vital a. To find out the body's
infection free of signs vital functions
associated with opportunistic
decreased infections and b. Monitor for signs of b. For early treatment
immunity their new infection.
(immunosuppr complications.
ession) Result criteria: c. Use aseptic c. Prevent patients from
a. There are no techniques in every being exposed to pathogenic
signs of new invasive procedure. germs obtained in the
infection Wash hands before hospital.
b. The lab has no giving action.
opportunistic
infection, d. Instruct patient d. Prevents infection
c. Vital signs are methods to prevent
within normal exposure to pathogenic
limits, environments.
d. There are no
wounds or e. Collect specimens for e. Ensuring accurate
exudates. lab tests as ordered. diagnosis and treatment

f. Collaboration of
 antibiotics f. Maintain therapeutic
blood levels

2 Activity Patients a. Monitor a. The response varies from

intolerance is participate in physiological responses day to day
related to activities to activity
weakness, Result criteria: b. Reducing energy
oxygen free dyspnea and b. Provide treatment requirements
exchange, tachycardia assistance that patients
malnutrition, during activity. themselves cannot
fatigue. afford
c. Extra rest is necessary if
c. Schedule patient care it increases metabolic needs
so it doesn't interfere
with rest.

3 Changes in Patients have a. Monitor the ability to a. Decreased intake is

nutrition less adequate calorie chew and swallow. associated with sore throat
than the body's and protein and mouth
needs related intakes to meet
to lack of their metabolic b. BB monitor, intake b. Determine basic data
intake, needs. and output
increased Result criteria:
metabolic a. Nausea and c. Set anti-emetics to c. Reducing vomiting
needs, and vomiting are order
decreased controlled
absorption of b. Patients eat
nutrients. TKTP d. Plan a diet with d. Make sure that food is in
c. Serum albumin patients and other accordance with the wishes
and protein are important people. of the patient
within normal
limits,
 d. BB approaches
like before it
hurts.

4 Low self- The patient a. BHSP a. Clients can trust nurses

esteem is expresses feelings
associated with related to self- b. Help the patient b. Explore client feelings
social isolation esteem and express his feelings of
expresses self- inferiority
acceptance
Result criteria: c. Help the patient c. Clients can identify their
a. Positive coping identify feelings of feelings
b. Self-esteem inferiority
increases
d. Help clients motivate d. Increase client confidence
themselves and
generate positive
feeling

5 The Families or other a. BHSP a. The family trusts the

ineffectiveness important people nurse
b. Help the family
of family maintain support discuss the effects of
coping has to systems and b. Help families find out the
the patient's illness and
do with adapt to changes worrying impact
their feelings
anxiety about in their needs
the condition Result criteria: c. provide clear and
of a loved one. c. Straighten family
patients and concise information to
perceptions of the client's
families interact the family about the
condition and assumptions
in a constructive client's condition
that are burdensome to the
way client
d. provide emotional
support to the family
 e. provide adequate d. Nurse empathy as a form
information about how of sincerity of care
to take care of clients e. Help families how to care
for clients properly and
avoid the risk of contracting

6 Ineffective Clients can a. Review coping a. Knowing the client's

individual develop positive developed by the client coping status
coping: coping
depression is Criteria results: b. Identification of b. Assess the level of client
associated with The anxiety scale client anxiety anxiety
anxiety about is reduced
the disease, c. Help clients find c. Look for adaptive coping
low self- adaptive coping that can alternatives that fit the
esteem be developed client's character

d. Give credit for the d. Increase client confidence

client's efforts

e. Give suggestions that e. Give clients choice and

can reduce client knowledge
anxiety

f. Collaboration on the f. Reduce client anxiety

use of variety when medically
needed

7 Ineffective Clients can a. Assess client's a. Assess the adequacy of

breath patterns breathe breathing pattern the client's breathing
associated with adequately patterns
 gas can not Result criteria: b. Perform chest
diffuse Pain decreased physiotherapy to help b. Increases airway
properly, Crowded (-) mobilize and cleanse clearance and breathing
tightness RR within normal the secret effort
(pain) limits c. Give clients the
                               opportunity to rest c. To facilitate breathing
between actions and avoid fatigue
                              
                               d. Give o2 according to
the program d. Increase O2 intake
                              
                                        
e. Teach appropriate
relaxation techniques e. Reduce anxiety and pain
hypnotically
f. Collaboration of
analgesics f. Pharmacologically
reduce / eliminate pain

8 Acute pain The client reports a. Assess client's pain a. Know the client's pain
associated with reduced pain scale
fluid b. Give the position as b. Increase client comfort
infiltration into comfortable as possible
the pleural
space, c. Collaborative c. Reduce / eliminate pain
tightness analytic giving pharmacologically
9 Disruption of The client can a. Monitor the client's a. Knowing the client's
gas exchange maintain adequate vital signs condition
associated with ventilation
damage to Result criteria: b. Pulmonary b. Detects crepitations
capillary RR <25x / minute auscultation every 4
alveolar Sianosi (-) hours
membrane Hypoxia (-) c. Collaboration on c. Increase O2 intake
giving o2

10 Lack of Client knowledge a. Assess the client's a. Knowing the client's

knowledge increases knowledge of his illness perception
related to the Result criteria: and therapeutic
disease process The client can compliance
and adherence explain the
to therapy importance of b. Explain the b. Increase client knowledge
adherence to importance of
therapy and its adherence to therapy,
effects if it is not the benefits and effects
compliant of non-compliance
Clients adhere to
the programmed c. Give the client a c. Know the cause of non-
therapy chance to reveal the compliance
reasons for non-
compliance

d. Involve the family in d. Increasing the role of

monitoring the family in client care
implementation of
client therapy

REFERENCES
Https://www.Academia.Edu.com
https://www.laporanpendahuluanHIV-TB.com