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HISTORY:
Earliest description of this disease can be found from the
records on tablets of Babylo-Assyrian (668-626 BC), writings of
Rig Veda, Old testament of Hebrews, Writings in Greek form days
of Homer, Ossuary relics of Tuberculous lesions in neolithic man
and egyptian mummies.
The disease description with cough, fever, blood spitting and
emaciation was called as Leo ping in China, Rajyakshma in India,
Pthisis by Hippocrates (460 – 377BC).
Development of Anatomy led to observation of small, rounded,
whitish gray bodies called tubercles by Sylvius (1614 – 1672).
The pathological alterations in the lung was described by
Morgagni (1682 – 1771). Schoelein was the person who coined the
term ‘tuberculosis’ in the year 1839. Robert Koch in the year
1882, established that tuberculosis in man and animals are
caused by tiny, slender, rod shaped bacilli and called them
‘tubercle bacilli’. The discovery of X-ray by Roengten in 1895
revolutionised the method of diagnosis of the disease.
Sanatorium for treatment this disease was first established in
Germany by Brehmer (1853). In India started at Ajmer (1906),
Almora (1908), Madanapalle (1908).
Calmette and Guerin accidentally found that the cultures of
bovine Tuberculosis growing in glycerine potato medium altering
their characters by addition of ox bile. They showed loss of
virulence after 231 subcultures in glycerol ox bile potato
medium
EPIDEMIOLOGY:
The incidence and mortality were high when the disease
affected susceptible groups as they offered favourable condition
for the spread of disease. Industrial revolution, overcrowding,
poor sanitation, poor housing, poor nutrition, over work,
stressful condition in cities lowered natural resistance and the
incidence of the disease was more. Improved standards of living,
better housing, less crowding, better sanitation, good
nutrition, shorter working hours reduced the incidence of the
disease.
MORTALITY DATA:
England and Wales:
346 / 1,00,000 in mid 19th century
126 / 1,00,000 at beginning of this century
31 / 1,00,000 in 1951
6.7/ 1,00,000 in 1960
United states of America
250 / 1,00,000 before the discovery of bacilli
100 / 1,00,000 at beginning of the century
33 / 1,00,000 by 1946
12 / 1,00,000 by 1951
1.5 / 1,00,000 by 1975
India:
800 / 1,00,000 hospital death early part of century
400 / 1,00,000 – Calcutta and Madras – early part of century
200 / 1,00,000 by 1949
64.1 / 1,00,000 by 1953
WHO studies reveal a global incidence of 3.5 to 4 million cases
per year ( 90% from the developing countries – late 1990), which
is only a fraction of the actual fact. Estimated 8 million new
cases of which 97% belongs to developing countries in 1997 (Asia
– 5 million, Africa – 1.6 million, middle east – 0.6 million,
Latin America – 0.4 million.
It is estimated that 2 million deaths shall occur due to
tuberculosis with 98% from the developing countries. It is
predicted that the annual incidence rate shall increase by 40%
by 2020.
Till 1985, in industrialised world records were reliable and
predictable, there was decline of cases except during war years,
from first half of the century. After 1985, the rate of decline
ceased and there was increase in number of cases in USA, UK and
other countries. In developed countries the affected population
include elderly, immigrants from third world countries, members
of ethnic communities and immuno-compromised individuals. In
developing counties it mainly affects adults.
PATHOGENESIS AND IMMUNITY:
Infection begin when mycobacterium tuberculosis enters the
host through droplet nuclei. Majority are trapped in upper
airways and expelled by ciliated mucosal cells. Usually fewer
than 10% of agent reaches the alveoli. Non specifically
activated macrophages ingest the bacilli. Invasion of
macrophages by mycobacterium leads to association of C2a with
bacterial cell wall and C3b opsonisation of bacteria and
recognition by macrophages. The balance between bactericidal
activity of macrophage and the virulence of the bacillus (linked
to bacterium’s lipid rich cell wall and to its glycolipid
capsule, both confer resistance to complement and free radicals
of phagocyte) determines the events following phagocytosis. The
number of invading bacilli also has a role.
The genes that confer virulence to Mycobacterium tuberculosis
have been identified. Kat-G encode for catalase which is
protective against oxidative stress. RpoV main stigma factor.
Defect in these two genes result in loss of virulence.
Studies and observations suggest that genetic factors play a key
role in innate non immune resistance to infection with
mycobacterium tuberculosis. The existance of this resistance is
suggested by the differing degrees of susceptibility to
tuberculosis in different populations
Initial stages of host-bacterial interaction:
Either the host’s macrophages contain bacillary
multiplication by producing proteolytic enzymes and cytokines or
the bacilli begin to multiply. If bacteria begin to multiply
then the macrophages are killed by lysis. Non activated
monocytes attracted from blood stream to the site by various
chemotactic factors ingest the bacilli released from lysed
macrophages. These phases are usually symptomless.
2-4 weeks after infection:
There develops two additional host response to infection,
namely,
1) tissue damaging response
2) macrophage activation response.
Tissue damaging response is the result of delayed type
hypersensitivity reaction to various bacillary antigens. It
destroys non activated macrophages that contain multiplying
bacilli.
Macrophage activating response is a cell mediated phenomenon
resulting in the activation of macrophages that are capable of
killing and digesting tubercle bacilli. Although both of these
response can inhibit mycobacterial growth, the balance between
these 2 determining the form of tuberculosis to be developed.
With the development of specific immunity between the
accumulation of large numbers of activated macrophages at the
site of primary lesion, granulomatous lesions (tubercles) are
formed, consisting of lymphocytes, activated macrophages like
epitheloid cells, giant cells. Initially the newly developed
tissue damaging response is the only event capable of limiting
mycobacterial growth with in the macrophages. The response
mediated by bacterial products not only destroys macrophages but
also produces early solid necrosis in the center of the
tubercle.
Although Mycobacterium tuberculosis can survive, its growth is
inhibited within this necrotic environment by low oxygen tension
and low pH. At this point some lesion may heal by fibrosis and
calcification, while other undergo further evolution.
Cell mediated immunity develop and is critical when bacillary
antigens processed by macrophages stimulate T-lymphocytes to
release a variety of lymphokines, which activates local
macrophages. These activated macrophages aggregate around the
lesions center and effectively neutralize tuberculosis bacilli
without causing further cell destruction. The central part of
lesion, the necrotic material resemble soft cheese (caseous
necrosis). Viable bacilli may remain dormant inside macrophages
or in necrotic material for years or throughout patients life
time. Healed lesions in lung parenchyma and hilar lymph nodes
may later be calcified and called as Ranke complex.
In minority of cases the macrophage activating response is weak,
and mycobacterial growth can be inhibited only by intensified
DTH reactions, which lead to tissue destruction. Lesions tend to
enlarge further leading to liquefaction of caseous material and
destruction of bronchial wall and blood vessels, which lead to
formation of CAVITIES. Liquefied caseous material with large
number of Bacilli drained through bronchi within the cavity
spread to the environment and facilitate the spread of bacilli.
CLINICAL
MANIFESTATIONS
PULMONARY
TUBERCULOSIS:
Primary disease:
It occurs as a result of initial infection with
Mycobacterium tuberculosis. In areas of high prevalence,
children are usually affected and the infection is localized to
middle and lower zones of lungs. It is accompanied by hilar and
para tracheal lymphadenopathy. In majority of cases the lesions
heals spontaneously and later may be evident as a small
calcified nodule (Ghons Lesion).
In children and persons with impaired immunity i.e. affected
with HIV or malnourished individuals primary pulmonary
tuberculosis may develop clinical illness.
The initial lesion increases in size and can evolve in different
ways:
1. Penetration of bacilli to pleural space leading to Pleural
Effusion.
2. Primary site enlarges and central portion undergoes
cavitation
3. Segmental or lobar collapse due to compression by enlarged
lymph node
4. Obstruction emphysema and bronchiectasis from partial
collapse.
5. Haematogenous spread leading to miliary tuberculosis.
6. Granulomatous lesions in multiple organs.
POST PRIMARY DISEASE:
Also called as adult type or reactivation or
secondary tuberculosis. It results from endogenous reactivation
of latent infection or is usually localized to the apical or
posterior segments of upper lobes, where high oxygen
concentration favours the growth of mycobacterial tuberculosis.
Signs and symptoms:
It starts as non specific or insidious symptoms like fever and
night sweats, weight loss, anorexia, general malaise and
weakness. Cough eventually develops initially as non productive
and later productive sputum. Blood streaking of sputum is
frequently documented associated with massive hemoptysis due to
erosion of a fully patent vessel.
Rhonchi due to partial bronchial obstruction and classic
amphoric breath sounds in areas with large cavities may be
heard. Low grade intermittent fever with wasting associated with
pallor and finger clubbing in certain cases. Haematoloty shows
mild anaemia and leucocytosis.
EXTRA PULMONARY TUBERCULOSIS:
1. Lymph node tuberculosis or tuberculosis
lymphadenitis:
It is the commonest extra pulmonary presentation frequently
among the HIV patients. It is presented as a painless swelling
of lymph node commonly at cervical and supraclavicular sites.
Usually discrete at early phase but later become inflamed and
caseous with a fistulous tract draining caseous material.
Systemic symptoms are limited to HIV infected persons and
concomitant lung disease may or may not be present. The
diagnosis is by FNABC or surgical biopsy. AFB are seen in 50% of
cases. Sputum culture is positive in 70-80%of cases. The
histologic examination shows granulomatous lesion.
2. Pleural tuberculosis:
Common in primary tuberculosis due to penetration by
tuberculosis bacilli. Depending on extent of reactivity the
lesion can be small, or become sufficiently large in order to
produce symptoms. The symptoms include fever, pleuritic chest
pain and dyspnoea. The physical findings of pleural effusion
like dullness on percussion absence of breath sounds are seen.
X-ray chest reveals effusion. Thoracocentesis establishes final
diagnosis and is also used as a therapeutic measure. FNABC
reveals tuberculous bacteria. Tuberculous empyema is a less
common complication.
3. Tuberculosis of upper air way:
Complication of advanced pulmonary cavitatory tuberculosis may
involve larynx, pharynx and epiglottis. The symptoms include
hoarseness and dysphagia and chronic productive cough. Carcinoma
can have similar features but usually painless.
4. Genito urinary tuberculosis:
It occurs in 15% of all cases of extra pulmonary tuberculosis
due to Haematogenous spread from the primary lesion and may
involve any part of Genito urinary tract. The local symptoms
like urinary frequency, dysuria, haematuria and flank pain
predominate. It may be asymptomatic and may be discovered only
after disease has developed. Urine examination reveals pyuria,
haematuria. IVP helps in diagnosis. Calcification and urethral
stricture are suggestive findings and lead to hydronephrosis and
renal damage. Culture of three morning samples yields a
definitve diagnosis.
5. Skeletal tuberculosis:
It is facilitated by reactivation of hematogenous foci or spread
from adjacent paravertebral lymph nodes. The weight bearing
nodes (spine, hip and knees in this order are affected most
commonly. The spinal tuberculosis (Pott’s disease or tuberculous
spondylitis) often involve two or more adjacent vertebral
bodies. In children the upper thoracic spine is the commonest
site and in adults the lower thoracic spine and lumbar
vertebrae.
Pathogenesis: from anterior superior or inferior angle of
vertebral body, the lesions reaches the adjacent body, also
destroying the intervertebral disc. With advanced disease
collapse of vertebral bodies results in Kyphosis (GIBBUS). A
paraverebral cold absess may also form and in thoracic region
this may attach to the chest wall as a mass. Lower spine may
reach inguinal or present as psoas abscess.
MRI or CT scan helps in diagnosis. Aspiration or bone biopsy
confirms diagnosis by culture and histologic findings.
The complication include paraplegia. Para paresis due to
large abscess is a medical emergency and require drainage.
Tuberculosis of hip joint causes pan and limping. Tuberculosis
of knee joint causes pain and swelling and sometimes after a
trauma. If the disease goes unrecognized it may lead to joint
deformity.
The treatment include chemotherapy and surgery
6. Tuberculous
meningitis and tuberculoma
Tuberculosis of
central nervous system accounts for 5% of extra pulmonary cases.
Usually seen in young children and in patients infected with
HIV. It occurs due to hematogenous spread to subarachnoid space
and due to old lesion in miliary patern found.
The case may present as head ache, confusion, lethargy, altered
Sensorium and neck rigidity. The disease evolves over 1-2 weeks,
a course longer than bacterial meningitis. Paresis of cranial
nerves (ocular nerves in particular) and involvement of cerebral
arteries may produce focal ischaemia. Hydrocephalus is common.
Lumbar puncture is the corner stone of diagnosis. The CSF shows
high leucoctyic count, protein content, and low glucose
concentration.
THE CONTROL OF TUBERCULOSIS:
Tuberculosis control means reduction in prevalence and
incidence of disease in the community. The WHO defines that
tuberculosis control is said to be achieved when the prevalence
of natural infection in the age group 0-14 years is of the order
of 1 per cent. This is abut 40% in India.
CASE FINDING:
A case is defined by WHO as a patient whose sputum is
positive for tubercle bacilli, and such cases are the target of
case finding.
CASE FINDING TOOLS:
1. SPUTUM EXAMINATION: sputum smear examination by direct
microscopy is now considered the method of choice. The
reliability, cheapness, and ease of direct microscopic
examination has made it number one case finding method all over
the world. Studies have shown that examination of two
consecutive specimens is sufficient to detect a large number of
infectious cases in the community. Under India’s District
Tuberculosis Programme (DTP), the first priority is given to
direct smear examination of sputum of patients, who, of their
volition, attend hospitals and health centres with the following
persistent chest symptoms
a. Persistent cough of about 3 or 4 weeks duration
b. Continous fever
c. Chest pain
d. Haemoptysis
2. Sputum culture: culture of sputum is only second in
importance in a case finding programme. It is not only
difficult, tedious, lengthy and expensive but also needs special
training and expertise. This method of examination is offered
only to patients presenting themselves with chest symptoms whose
sputum smear is negative by direct microscopic examination.
3. Mass miniature radiography: This method has been stopped as a
general measure of case finding, because of high cost, lack of
definitiveness, high proportion of erroneous interpretation and
very low yield of cases commensurate with the effort involved
4. Tuberculin test: As the diagnostic value of tuberculin test
is invalidated, this test has little value as a case finding
tool.
DIRECTLY OBSERVED TREATMENT, SHORT COURSE (DOTS)
Compliance with tuberculosis treatment regimens is limited
by their complexity and duration, a lack of symptoms in some
patients and medication side effects. In 1993, at least 20
percent of patients with pulmonary tuberculosis did not complete
therapy. Noncompliant patients are 10 times more likely than
compliant patients to transmit multidrug-resistant tuberculosis,
to require prolonged treatment and to experience disease
progression or relapse; they are also more likely to die as a
result of their infection. Noncompliance is more likely to be a
factor in men, homeless persons, drug addicts, alcoholics,
HIV-infected patients, patients with mental and physical
disabilities, and patients who have previously failed treatment.
Predicting noncompliance in advance is notoriously unreliable.
Thus, directly observed therapy, in which patients are observed
swallowing each dose of medication, should be strongly
considered in patients with latent tuberculosis infection who
are being treated with twice- or thrice-weekly regimens and in
all patients who are being treated for active tuberculosis.
When directly observed therapy is used, treatment completion
rates range from 85 to 96.5 percent. In the first two years
after directly observed therapy became more widely used, there
was a 21 percent decrease in all tuberculosis cases and a 39
percent decrease in multidrug-resistant tuberculosis cases.
Local public health departments offer directly observed therapy
services at minimal or no cost. Community health care providers
are responsible for identifying and referring appropriate
candidates for these services.
HOMOEOPATHIC MANAGEMENT:
The case has to be individualized and proper
similimum has to be selected
The following medicines have been given in the synthesis
repertory for this condition.
1. GENERALS -
TUBERCULOSIS
aven.; bac.; bell.; brom.; calc.; chinin-ar.; ferr-i.; hippoz.;
iodof.; lap-a.; led.; myrt-c.; nat-ar.; phos.; pyrog.; spong.;
teucr-s.; tub.; urea;
2. GENERALS - INFLAMMATION - Glands; of – tubercular ; merc-k-i
(merc-k-i.;mercurius biniodatus cum kali iodatum) – grimmer
collected works
3. GENERALS - HISTORY; personal - tuberculosis; of bac.;tub.;
4. GENERALS - FAMILY HISTORY of - tuberculosis bac.; carc.; tub
5. GENERALS - CANCEROUS affections - tubercular base; on kali-i.
6. FEVER - INTERMITTENT - tuberculosis, in bapt.;
7. FEVER - CONSTANTLY HIGH TEMPERATURE - accompanied by -
diarrhea - children; in tuberculous lob-e.;lobelia erinus
(Clarke)
8. FEVER - AFTERNOON - tuberculosis, early ars-i.;
9. SLEEP - SLEEPLESSNESS - tuberculosis, in iod.; sang.;
10. EXTREMITIES - PAIN - Joints - tubercular family history dros.;
11. CHEST - PHTHISIS pulmonalis
acet-ac.; acet-ac.; agar.; agar.; aloe; alumn.; am-c.; am-m.;
ant-ar.; ant-t.; arg-met.; arg-met.; arn.; ars.; ars-i.; ars-s-f.;
arum-t.; aur.; aur-ar.; aur-m.; aur-m-n.; bac.; bac-t.; bals-p.;
bar-m.; berb.; beta; blatta-o.; brom.; bufo; calag.; calc.;
calc.; calc-i.; calc-p.; calc-s.; calc-sil.; carb-an.; carb-v.;
carbn-s.; carc.; card-m.; card-m.; cetr.; chinin-ar.; chlor.;
chlor.; coc-c.; con.; con.; cur.; dros.; dros.; dulc.; elaps;
elaps; erio.; eupi.; ferr.; ferr-ar.; ferr-i.; ferr-p.; fl-ac.;
gad.; gal-ac.;b gal-ac.; graph.; guaj.; guaj.; guajol.; ham.;
helx.; hep.; hippoz.; ichth.; iod.; kali-ar.; kali-bi.; kali-c.;
kali-n.; kali-n.; kali-p.; kali-s.; kali-sil.; kreos.; lac-d.;
lach.; lachn.;b lachn.; lec.;b led.; lyc.; lycps-v.; mag-c.;
mang.; med.; merc.; mill.; myrt-c.; naphtin.; nat-ar.; nat-cac.;
nat-m.; nat-p.; nat-s.; nit-ac.; ol-j.; ol-j.; ox-ac.; petr.;
ph-ac.; phel.; phel.; phos.; pix; plb.; psor.; ptel.;h puls.;
pyrog.; pyrog.; rumx.; rumx.; sabal; salv.; samb.; samb.; sang.;
sarr.; senec.; senec.; seneg.; sep.; sil.; slag; spong.; stann.;
stann-i.; stict.; still.; sul-ac.; sul-ac.; sul-i.; sulph.;
tarent-c.; teucr-s.;gm1 teucr-s.; ther.; thyr.; tub.; tub.;
tub-a.; tub-d.;al verb.; zinc.; zinc-i.; zinc-p.;
12. CHEST - CANCER - Mammae - accompanied by - ulcers -
tubercular ulcers; bell-p.
13. EXPECTORATION - TUBERCLES hep.; mag-c.; phos.; sil.; spong.;
14. EXPECTORATION - CALCAREOUS tubercles sars.;
15. COUGH - TUBERCULOUS persons, in phos.;
16. COUGH - TALL, slender, tuberculous subjects; in phos.;
17. RESPIRATION - ASTHMATIC - tuberculosis family history dros.;
18. LARYNX AND TRACHEA - INFLAMMATION - Larynx - tubercular sel.;
19. FEMALE GENITALIA/SEX - MENSES - suppressed - tuberculosis,
in lob.; lyc.; senec.; solid.; solid.; ust.;
20. FEMALE GENITALIA/SEX - LEUKORRHEA - tuberculous women; in
ferr.;
21. MALE GENITALIA/SEX - POLLUTIONS - tuberculosis, in calc.;
22. RECTUM - DIARRHEA - tuberculosis; during arg-n.; ars.;
chin.; chin.; coto; ferr.; phos.;
23. ABDOMEN - INFLAMMATION - tuberculosis abrot.;b
24. EXTERNAL THROAT - GOITRE - exophthalmic - tuberculosis in
family; with dros.;
25. FACE - ERUPTIONS - acne - tubercular children; in tub.;
26. EYE - INFLAMMATION - Iris - tubercular bar-i.; tub.;
27. HEAD - INFLAMMATION - meninges - tubercular apis; calc.; iod.;
lyc.; merc.; nat-m.; sil.; sulph.; tub.; zinc.; zinc.;
28. MIND - FEAR - tuberculosis; of calc.
References:
1. Harrison’s Principles
of internal medicine 15th edition
2. The oxford text book of medicine 3rd edition
3. Davidson’s Principles and practice of medicine
4. Clinical medicine – K.V.Krishnadas
5. Text book of medicine – K.V. Krishnadas
6. Repertory of homoeopathic materia medica – J.T.Kent
7. Synthesis Repertorium Homoeopathicum syntheticum – Frederick
schroyens
8. Park’s text book of Preventive and Social Medicine – K.Park
9. websites of WHO and Centre for Disease Control United States
of America
10. Text book on microbiology – Ananthanarayanan and Jayaram
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