TUBERCULOSIS

INSTRUCTOR : DR. Varela

PRESENTED BY : TENZIN

ENAM

HASIM

GIA

CAHSU, Belize 2015

TUBECULOSIS

Tuberculosis is a communicable chronic granulomatous

disease caused by Mycobacterium tuberculosis. It usually

involves the lungs but may affect any organ or tissue in the

body.

Typically, the centers of

tubercular granulomas undergo

caseous necrosis.

Tuberculosis flourishes wherever there is poverty,

crowding, and chronic debilitating illness, elderly

persons, with their weakened defenses, are vulnerable.

Certain disease states also increase the risk: diabetes

mellitus, Hodgkin disease, chronic lung disease, chronic

renal failure, malnutrition, alcoholism, and

immunosuppression.

In areas of the world where HIV infection is prevalent, it

has become the single most important risk factor for the

development of tuberculosis.

It is important that infection be differentiated from

disease. Infection implies seeding of a focus with

organisms, which may or may not cause clinically

significant tissue damage (i.e., disease).

In most persons, an asymptomatic focus of pulmonary

infection appears that is self-limited.

Generally, the only evidence of infection, if any remains,

is a tiny, telltale fibrocalcific nodule at the site of the

infection.

Viable organisms may remain dormant in such loci for

decades, and possibly for the life of the host. Such

persons are infected but do not have active disease and

so cannot transmit organisms to others.

However when their defenses are lowered, the infection

may reactivate to produce communicable and potentially

life-threatening disease.

Primary tuberculosis

It is the form of disease that develops in a previously

unexposed, and therefore unsensitized, person. Elderly persons

and profoundly immunosuppressed persons may lose their

sensitivity to the tubercle bacillus and so may develop primary

tuberculosis more than once. With primary tuberculosis, the

source of the organism is exogenous. About 5% of those newly

infected develop significant disease.

The chief implications of primary tuberculosis are that (1) it

induces hypersensitivity and increased resistance; (2) the foci of

scarring may harbor viable bacilli for years, perhaps for life, and

thus be the nidus for reactivation at a later time when host

defenses are compromised; and (3) uncommonly, the disease

may develop without interruption into so-called progressive

primary tuberculosis.

Progressive primary tuberculosis occurs in individuals

who are immunocompromised such as AIDS( CD4+

counts <200 cells/mm3 ) or in malnourished children or

in the elderly. Certain racial groups, such as Inuit.

Immunosuppression results in an inability to mount a

CD4+ T cell-mediated immunologic reaction. The lack of

a tissue hypersensitivity reaction results in the absence

of the characteristic caseating granulomas (nonreactive

tuberculosis).

Progressive primary tuberculosis more often resembles

an acute bacterial pneumonia, with lower and middle

lobe consolidation.

Lymphohematogenous dissemination is a dreaded

complication and may result in the development of

tuberculous meningitis and miliary tuberculosis.

Symptoms-

nonproductive cough,

chest pain,

fever and

loss of appetite.

Secondary (or postprimary)

tuberculosis:

is the pattern of disease that arises in a previously

sensitized host.

commonly it arises from reactivation of dormant primary

lesions many decades after initial infection, particularly

when host resistance is weakened.

It may also result from exogenous reinfection because of

waning of the protection afforded by the primary disease

or because of a large inoculum of virulent bacilli.

Reactivation of endogenous tuberculosis is more common in low-prevalence areas.

Whatever the source of the organism, only a few individuals (less than 5%) with primary disease subsequently develop secondary tuberculosis.

Secondary pulmonary tuberculosis is classically localized to the apex of one or both upper lobes.

Because of the preexistence of hypersensitivity, the bacilli excite a prompt and marked tissue response that tends to wall off the focus. As a result of this localization, the regional lymph nodes are less prominently involved early in the developing disease than they are in primary tuberculosis.

On the other hand, cavitation occurs readily in the

secondary form, resulting in dissemination along the

airways. Indeed, cavitation is almost inevitable in

neglected secondary tuberculosis, and erosion into an

airway becomes an important source of infectivity,

because the person now raises sputum containing

bacilli.

Symptoms –

Productive cough

Hemoptysis

Fever

Loss of appetite

Night sweat

Localized secondary tuberculosis may be asymptomatic.

Systemic symptoms,often appear early in the course include malaise, anorexia, weight loss, and fever. Commonly, the fever is low grade and remittent (appearing late each afternoon and then subsiding), and night sweats occur.

With progressive pulmonary involvement, increasing amounts of sputum, at first mucoid and later purulent, appear. When cavitation is present, the sputum contains tubercle bacilli. Some degree of hemoptysis is present in about half of all cases of pulmonary tuberculosis. Pleuritic pain may result from extension of the infection to the pleural surfaces.

Extrapulmonary manifestations of tuberculosis depend

on the organ system involved (for example, tuberculous

salpingitis may present as infertility, tuberculous

meningitis with headache and neurologic deficits, Pott

disease with paraplegia).

Dx. The diagnosis of pulmonary disease is based in part

on the history and on physical and radiographic findings

of consolidation or cavitation in the apices of the lungs.

Ultimately, however, tubercle bacilli must be identified.

Diagnostic discoveries

24th March 1882 (Robert Koch)TB Day

Discovery of staining technique that identified Tuberculosis bacillus

Definite diagnosis made possible and thus treatment could begin

1890 (Robert Koch) Tuberculin discoveredDiagnostic use when injected into

skin

1895 (Roentgen)Discovery of X-raysEarly diagnosis of pulmonary

disease

Diagnostics of Mycobacterium

Initial screening:-TB skin test (Purified Protein Derivative).Drawbacks: BCG injected subjects are positive, 3 days delay for result- QFT-G test (measures INF- response to TB specific antigen)

TB tests Active, depending on the suspected location of bacterium:-3-5 samples of sputum- multiple gastric aspirate- urine (UTI)- CSF (meningeal)2

Cultures

Samples are processed for fast acid stain (FAS smear positive indicates Mycobacterium) and cultured after alkali decontamination (30s in 1-2% NaOH)

Molecular methods use species-specific genes, including light and heave ribosomal RNA3

Clinical specimen/decontamination

culture Direct detection:- Microscopy- PCR- MTB rifampin resistance

Species identification:- 16S rRNA hybridization (MTB and MAC)-16S rRNA gene PCR sequencing (NTM)- restriction fragment length polymorphism

Susceptibility testingRifampin resistance(PCR oligohybridization sequencing)

18

Dr.T.V.Rao MD

Diagnosis of tuberculosis

Physical Examination

Microscopy (Ziehl Neelson Method)

Culture

oIdentification of cultural properties

Animal inoculation

Typing

oto trace the source of infection

Tuberculin tests

Chest X-rays

Lung biopsy

diagnosis

• Physical Examination : lymph nodes for swelling and use a

stethoscope to listen carefully to the sounds your lungs make while

you breathe.

• Blood tests : confirm or rule out latent or active tuberculosis. These

tests use sophisticated technology to measure your immune

system's reaction to TB bacteria.

Imaging tests : If a positive skin test, then doctor is likely to order a

chest X-ray or a CT scan. This may show white spots in your lungs.

Sputum tests : If chest X-ray shows signs of tuberculosis, then

doctor may take samples of your sputum — the mucus that comes

up when you cough. The samples are tested for TB bacteria.

Treatment

1st line treatment – ethambutol

(or streptomycin), isoniazid, pyrazinamide and

rifamycins.(rifampin, rifabutin, rifapentine)

2nd line – aminoglycoside, macrolides, cycloserine,

flouroquinolones.

Vaccine – bcg(not in US)

Reserve drugs which may be used when first line

drugs have failed are:

Ethionamide

Prothionamide

Amikacin

Kanamycin

Capreomycin

Viomycin

Cycloserine

Quinolones (ofloxacin, ciprofloxacin, sparfloxacin)

New cases – 4 drugs

Isoniazid

Rifampin

Pyrazinamide

Ethambutol/streptomycin

02000

month

4 month of isoniazid and rifampin.

The prognosis of tuberculosis is generally favorable if infections are

localized to the lungs, but it worsens significantly when the disease

occurs in the setting of aged, debilitated, or immunosuppressed

persons, who are at high risk for developing miliary tuberculosis,

and in those with MDR-TB.

Amyloidosis may appear in persistent cases.

Medication side effects

Serious side effects of TB drugs aren't common but can be

dangerous when they do occur. All tuberculosis medications

can be highly toxic to your liver. When taking these

medications, call your doctor immediately if you experience

any of the following:

Nausea or vomiting

Loss of appetite

A yellow color to your skin (jaundice)

Dark urine

A fever that lasts three or more days and has no obvious

cause

Prevention Protect your family and friends

Stay home. Don't go to work or school or sleep in a room with

other people during the first few weeks of treatment for active

tuberculosis.

Ventilate the room. Tuberculosis germs spread more easily in

small closed spaces where air doesn't move. If it's not too cold

outdoors, open the windows and use a fan to blow indoor air

outside.

Cover your mouth. Use a tissue to cover your mouth anytime

you laugh, sneeze or cough. Put the dirty tissue in a bag, seal it

and throw it away.

Wear a mask. Wearing a surgical mask when you're around other

people during the first three weeks of treatment may help lessen

the risk of transmission.

THANK YOU