Tuberculosis and Homoeopathy

D Beenadas
Lecturer, Department of MM
Govt. Homeopathic Medical College. Calicut

Tuberculosis
Tuberculosis  is a  bacterial infection caused by  Mycobacterium tuberculosis. The bacteria usually attack the lungs, but they can also  affect the central nervous system, the  lymphatic system, the circulatory system, the genitourinary system, bones, joints and even skin.

Other mycobacteria such as  Mycobacterum bovis, My.africanum,  My. Canetti and My. Mycroti  also cause tuberculosis, but these species are less common.

Other names

In the past, tuberculosis has been called consumption, because it seemed to consume people from within and long relentless wasting.

Phthisis  – (Greek for consumption) and phthisis pulmonalis;

Scrofula –  affecting the lymphatic system and resulting in swollen neck glands

• wasting disease
• white plague, because sufferers appear markedly pale
• king’s evil, because it was believed that a king’s touch would heal scrofula.
• Koch’s disease after the scientist , Robert Koch

INCIDENCE :- Has worldwide distribution, more common in poorer countries.

CONTRIBUTING FACTORS:- Malnutrition, inadequate medical care, poverty, crowding, chronic debilitating conditions like uncontrolled diabetes, alcoholism and immuno compromised states like AIDS.

MODES OF TRANSMISSION 

1. Inhalation:– Inhalation of organism present in fresh cough droplets or in dried sputum from an open case of pulmonary tuberculosis.
2. Ingestion:– Ingestions of organisms lead to development of tonsilar or intestinal tuberculosis. This can be either from self-swallowing of ingested sputum of an open case of pulmonary tuberculosis or ingestion of bovine tubercle bacilli from milk of diseased cows.
3. Inoculation:- Inoculation of organism into skin may rarely occur from infected postmortem tissues.
4. Transplacental route :- This results in development of congenital tuberculosis in foetus ,which is rare.

SPREAD OF TUBERCULOSIS :-

1. Local spread:- By macrophages carrying the bacilli into surrounding tissues.
2. Lymphatic spread :- Tuberculosis is primarly an infection of lymphoid tissue. The bacilli may pass into the lymphoid follicles of pharynx, bronchi, intestine or regional lymph nodes resulting in regional tuberculous -lymphadenitis which is typical of childhood infections. Primary complex is primary focus with lymphangitis and lymphadenitis.
3. Haematogenous spread :- This occur either as a result of tuberculous bacillaemia because of drainage of lymphatics into the venous system or due to caseous material escaping through intestinal wall of a vein. This produce millet-sized lesions in different organs of body- lungs, liver, kidney, bones and other tissues called miliary tuberculosis.
4. By natural passages:- Infection may spread from
   1. Lung lesions into pleura-  tubercular pleurisy.
   2. Transbronchial spread into the adjacent lung segment.
   3. Tuberculous salpingitis into peritoneal cavity- Tubercular peritonitis.
   4. Infected sputum into larynx- Tubercular laryngitis.
   5. Swallowing of infected sputum-  Ilieocaecal tuberculosis.
   6. Renal lesions into ureter and down to trigone of bladder.

Hypersensitivity and immunity in tuberculosis.
Hypersensitivity or allergy and immunity or resistance play a major role in development of tuberculosis. Tubercle bacillus as such do not produce any toxins ; and the tissue changes are due to host response to the organism, in the form of cell-mediated hypersensitivity and immunity (Type1V hypersensitivity ). This two host responses develop as a consequences of several lipids present in the micro organisms which are –

1. Mycosides- such as ‘cord factor’ which are essential for growth and virulence of organism in the animals.
2. Glycolipids- present in mycobacterial cell wall like ‘wax-D’ which acts as an adjuvant acting along with tuberculoprotein.

The tissue reaction to tubercle bacilli is different in healthy animals not previously infected –Primary infection – from animals which are previously infected – secondary infection. In primary infection, intradermal injection of tubercle bacilli into skin of healthy guinea pig evokes no visible reaction for 10-14 days. After this period, a nodule develop at the site of inoculation, which subsequently ulcerates and heals poorly , as the guinea pig unlike human beings, does not posses any natural resistance. The regional lymph nodes also develops tubercles. This            process is a manifestation of delayed type of hypersensitivity and is comparable to primary tuberculosis in children although healing invariably occurs in children.

In secondary infection – the tubercular bacilli are injected into the skin of guinea pig that has been infected with tuberculosis 4-6 weeks earlier. In 1-2days, the site of inoculation is indurated and dark, attaining a diameter of about 1c.m. This skin lesion ulcerates which heals quickly and the regional lymph nodes are not affected. This is called Koch’s phenomenon and is indicative of hypersensitivity and immunity of host.

Similar changes are produced if injection of live tubercle bacilli is replaced with Old Tuberculin (O.T.). Hypersensitivity and immunity are closely related and are initiated through T-lymphocytes sensitised against specific antigens in tuberculin. Thus lymphokines are released from T-cells which induce increased microbicidal activity of macrophages. 

Tuberculin (mantoux) skin tests.
Intradermal injection of  0.1 ml  of tuberculoprotein., Purified Protein Derivative (P.P.D.) is used for this test. A positive test is indicative of cell-mediated hypersensitivity to tubercular antigens but does not distinguish between infection and disease. Tuberculin test become positive within 4-6 weeks of infection.

• Delayed type of hypersensitivity develops in individuals who are having or have been previously infected with tuberculous infection which is identified as an indurated area of more than 15 mm. in 72 hour.
•  Patient having disseminated tuberculosis may show negative test due to release of large amounts of tuberculoproteins from the endogenous lesions, masking the hypersensitivity test.
• The test may be false positive in atypical mycobacterial infection and
• false negative in sarcoidosis, some viral infections, Hodgkin’s disease and fulminant tuberculosis.

Diagnostic value of tuberculin test is in those individuals who are ‘recent converters’ that  suggests infection by mycobacteria. Tuberculin testing is widely employed to assess the prevalence of disease in community, thus help in planning tuberculous control programs.

Immunisation against tuberculosis
This is induced by injection of attenuated strains of  bovine type of tubercle bacilli, Bacilli Calmette Guerin (B.C.G.) . Cell-mediated immunity with consequent delayed hypersensitivity reaction develops with healing of the lesion, but the cell-mediated immunity persists, rendering the host tuberculin-positive and  hence immune.

CLASSIFICATION

Pulmonary tuberculosis   –  When the disease becomes active, 75% of the cases are  pulmonary tuberculosis

Extrapulmonary tuberculosis –  25% of active cases, the infection moves from the lungs, causing other kinds of TB, collectively denoted  as extrapulmonary tuberculosis. This occurs more commonly in  immunosuppressed persons and young children. . Although extrapulmonary TB is not contagious, it may co-exist with pulmonary TB.

TYPES OF PULMONARY  TUBERCULOSIS:-
Lung is the main organ affected in tuberculosis. Developing upon the type of tissue response and age, the infection with tubercle bacilli is of two main groups –

                 1)Primary tuberculosis   and   2) Secondary tuberculosis

(1) Primary Tuberculosis:-
The infection of an individual who has not been previously infected or immunized is called primary tuberculosis or Ghon’s complex or childhood tuberculosis

Parenchymal lesion is otherwise known as Ghon’s lesion.  Primary complex or Ghon complex is the lesion produced at the portal of entry with foci in the draining lymphatic vessels and lymph nodes. Most commonly involved tissues for primary complex are lungs and hilar lymph nodes. Others include- tonsils and cervical lymph nodes. In ingested bacilli the lesion may be found in small intestine and mesenteric lymph nodes.

The incidence of disseminated form of progressive primary tuberculosis is particularly high in immuno compromised host, like AID’s patient.

Pulmonary complex or Ghon’s complex in lungs consists of 3 components-

1) pulmonary component:-  Lesion in the lung is the primary focus or Ghon’s focus. It is 1-2c.m.solitary area of tuberculous pneumonia located under the pleura, in the lower part of upper lobe. Hilar lymph nodes enlarge progressively and undergo caseation. Compression of neighboring bronchi esp. middle lobe leads to collapse, constriction and bronchiectatic changes. This may present latter as ‘middle lobe syndrome’.

2) Lymphatic vessel component – The lymphatics draining the lung lesion contain phagocytes containing bacilli and may develop beaded , military tubercles along the path of hilar lymph nodes.

3) Lymph node component :- This consists of enlarged hilar and tracheo-bronchial lymph nodes in the area drained. The affected  lymph nodes are matted and show caseation necrosis.

(2)  Secondary Tuberculosis :-

The infection of an individual who has been previously infected or sensitized is called secondary or post-primary or reinfection or chronic tuberculosis. The infection may be acquired from  –

1. Endogenous source such as reactivation of dormant primary complex  or

2. Exogenous source such as fresh dose of reinfection by the tubercle bacilli.

Secondary tuberculosis occur most commonly in lungs, in the region of apex. Other sites and tissues which can be involved are  tonsils, pharynx, larynx, small intestine and skin.

HIV patient with  previous tuberculous infection have high incidence of reactivation of primary tuberculosis and the pattern of lesion is similar to that of primary tuberculosis, that is with involment of hilar lymph nodes than cavitation and atypical lesion in lung. Opportunistic infection with My. Avium-intracellulare can occur in AIDs patient.

Clinical features of tuberculosis. 

Clinical feature vary depending upon the location, extent and type of lesion. In secondary pulmonary tuberculosis, which is the common type includes :-

Pulmonary TB:– Productive cough, may be with haemoptysis, pleural effusion, dyspnoea orthopenia etc. In few cases the onset may be acute with high fever ,cough & haemoptysis and lesion may resemble lobar pneumonia. Nodular  type is  generally silent and detected radiologocally. Sputum is mucoid or mucopurulent, initially scanty, later copious. Mild streaky haemoptysis may occur initially, later progress due to erosion of blood vessels. Haemorrhage can occur from rupture of dilated vessel in a cavity – Rasmussen’s aneurysm. Laryngeal affection results in hoarseness. Extensive disease may produce dyspnoea and ARDS.  Chest x-rays shows typical apical changes like pleural effusion, nodularity and  miliary or diffuse infiltrates in lung parenchyma.

Extra pulmonary Tuberculosis :-
Skeletal Tuberculosis: Tuberculous osteomyelitis involves mainly the thoracic and lumbar vertebrae (known as Pott’s disease) followed by knee and hip. There is extensive necrosis and bony destruction with compressed fractures (with kyphosis or gibbus) and extension to soft tissues, including psoas “cold” abscess.Diagnosis

• CT
• MRI
• Aspiration of abscess
• Bone biopsy

Tuberculosis of upper airways :– involve larynx, pharynx, epiglottis, as complication of advanced cavitory  pul.TB. diagnosis by –

• AFB positive of sputum
• biopsy

Genital Tract Tuberculosis:  Accounts for 15% of EP Tuberculous. Tuberculous salpingitis and endometritis result from dissemination of tuberculosis to the fallopian tube that leads to granulomatous salpingitis, which can drain into the endometrial cavity and cause a granulomatous endometritis with irregular menstrual bleeding and infertility. In the male, tuberculosis involves prostate and epididymis most often with non-tender induration and infertility.Diagnosis by biopsy and culture.

pleural Tuberculosis :– due to penetration of tubercle bacilli into the pleural space.if effusion is small, remains unnoticed  and resolve spontaneously. If large, causes fever, chestpain , dyspnoea.Diagnosis include :-

• CXR – reveals effusion
• Thoracocentesis – culture is positive for Mycobacteria.
• Biopsy of pleura – reveals granuloma

Urinary Tract Tuberculosis: A “sterile pyuria” with WBC’s present in urine but a negative routine bacterial culture may suggest the diagnosis of renal tuberculosis. Progressive destruction of renal parenchyma occurs if not treated. Drainage to the ureters can lead to inflammation with ureteral stricture.

CNS Tuberculosis: A meningeal pattern of spread can occur, and the cerebrospinal fluid typically shows a high protein, low glucose, and lymphocytosis. The base of the brain is often involved, so that various cranial nerve signs may be present. Rarely, a solitary granuloma, or “tuberculoma”, may form and manifest with seizures. Symptoms are headache, mental changes – confusion, lethargy, altered sensorium and neck rigidity. Focal ischaemia due to cerebral artery involvement. Hydrocephalus present. Diagnosis by –

• CSF examination – lymphocyte predominate, AFB seen
• Culture of CSF
• CT and MRI  shows hydrocephalus

Gastrointestinal Tuberculosis: This is uncommon today because routine pasteurization of milk has eliminated Mycobacterium bovis infections. However, M. tuberculosis organisms coughed up in sputum may be swallowed into the GI tract. The classic lesions are circumferential ulcerations with stricture of the small intestine. There is a predilection for ileocecal involvement because of the abundant lymphoid tissue and slower rate of passage of lumenal contents. Symptoms are abdominal pain, diarrhea, obstructionpalpable mass, ulcerations and fistulae. Diagnosis –

Histological examination

Culture of specimen obtained intraopratively.

Adrenal Tuberculosis: Spread of tuberculosis to adrenals is usually bilateral, so that both adrenals are markedly enlarged. Destruction of cortex leads to Addison’s disease.

Scrofula: Tuberculous lymphadenitis  presents as painless swelling esp. of the cervical and supra clavicular. Nodes are discreate in early disease, but may be inflamed may produce a mass of firm, matted nodes just under the mandible. There can be chronic draining fistulous tracts to overlying skin. This complication may appear in children.

Diagnosis :- Mycobacterium  may be cultured and positive in 70-80%

FNAC or surgical biopsy

Hitological examination shows granulomatous lesion.

Cardiac Tuberculosis: The pericardium is the usual site for tuberculous infection of heart. The result is a granulomatous pericarditis that can be hemorrhagic. If extensive and chronic, there can be fibrosis with calcification, leading to a constrictive pericarditis. Symptoms are  fever, dull retrosternal pain, and a friction rub.effusion and cardiac tamponade appear. Diagnosis by –

Pericardiocentesis – leukocyte count increased

Culture of fluid reveals mycobacteria

Lupus vulgaris:- is a manifestation of tuberculosis of skin esp. of hand and neck. Jelly like nodules appear first , which ulcerates with excessive scarring

Miliary or disseminated TB :-due to hematogenous spread of tubercle bacilli.symptoms are fever, night sweats, anorexia, weakness and weight loss. Diagnosis by –

CXR – military reticulonodular pattern

Tuberculosis in HIV patient :-  HIV accelerates the progression of infection by reducing host’s cell-mediated immunity. Non-respiratory disease esp. lymph node disease is common in HIV patient. Pulmonary disease is less likely to be cavitating and smear positive, so difficult to diagnose.

Multidrug- resistant tuberculosis :- It differs from other types that they spread rapidly, involved larger number of patients and occurred in institutions. Associated with previous treatment, HIV seropositivity, homelessness and drug abuse.

Systemic features – Fever, mid-night sweats, fatigue, loss of weight and appetite. Long standing and untreated cases of tuberculosis may develop systemic secondary amyloidosis. 

Complications of  pulmonary tuberculosis 

1. Early:-within months-

• a)      mild haemoptysis.
• b)      Pneumothorax
• c)      Pleural effusion

2        Intermediate:- occurring within several months or a few years-

• a)      massive haemoptysis
• b)      secondary infection of cavities.
• c)      Pneumothorax, pleural effusion, empyaema
• d)     Progressive fibrosis with dyspnoea
• e)      Spread to other organs-larynx, pericardium , etc.

f)       Non-healing of lesion due to drug resistance of organism.

      3  Late :- occurring after several years-

• a)  Pulmonary fibrosis with compensatory emphysema , cor pulmonale,        pleuro-pulmonary fibrosis.
• b)  Bronchiectasis
• c)  Persistence of open cavities with out healing
• d)  Aspergillomas in cavities
• e)  Co-existence of apical tuberculosis with carcinoma.
• f)  secondary amyloidosis.

Cause of death– due to pulmonary insufficiency, pulmonary haemorrhage, sepsis due to disseminated military tuberculosis, corpulmonale or secondary amyloidosis 

DIAGNOSIS:-

1. Clinical features

2 .Acidfast bacilli demonstrated by Zeil-Neelson’s method – is the most important diagnostic investigation. While examining a sputum smear, at least 100 fields should be seen for 10 minutes, before declaring it as negative. At least 3 bacilli should be seen before the smear is declared positive. Concentration method  are available using 24 hour collection of sputum to detect AFB when direct smear is negative.

3. Sputum culture- for identification of Mycobacteria.

4. Increased ESR , mild Lymphocytosis.

5.Mantoux test.

6.Chest x-ray- early cases shows infiltration in upper zones, later coalesce to form consolidation.

7. Nuclic acid amplification – test system based on amplification of mycobacterial nucleic acid.

8.Polymerase chain reaction  detection of bacterial DNA, and assays to detect the release of  interferon gamma in response to mycobacterial proteins such as ESAT-6   These are not affected by immunization or environmental mycobacteria,  so generate fewer false positive result