Tuberculosis Overview Quiz

Infectious Diseases - Tuberculosis

• Tuberculosis (TB) is a chronic granulomatous inflammation caused by Mycobacterium tuberculosis.
• TB is a common, communicable, chronic infectious disease.
• Risk factors include poverty, crowding, malnutrition, chronic illnesses like diabetes and lung disease, alcoholism, and AIDS.

Causative Bacteria

• The causative bacteria are human tubercle bacilli (acquired by inhalation) and bovine tubercle bacilli (acquired by consuming infected milk).
• Mycobacteria are slender, aerobic, non-motile, gram-positive rods, stained with Ziehl-Neelsen stain.

Methods of Infection

• Inhalation of infected droplets coughed or sneezed from individuals with open pulmonary TB or dust contaminated with infected sputum.
• Ingestion of contaminated milk or self-swallowing of infected sputum from an open case of pulmonary TB.
• Skin inoculation with infected materials (very rare).
• Transplacental route (congenital TB, rare).

Host Response to TB Bacilli

• Proliferative reaction
• Exudative reaction

Proliferative Tissue Reaction (Tubercle Formation)

• Initial response involves neutrophil attraction, quickly destroyed by the organisms.
• Macrophages are attracted after the first day.
• Bacteria multiply inside macrophages, leading to rupture and release of more organisms.
• Macrophages modify to resemble epithelioid cells.
• Epithelioid cells aggregate to form granulomas.
• Some epithelioid cells fuse to form Langhan's giant cells.
• Lymphocutes and fibroblasts are found at the periphery of the granuloma.
• Caseation necrosis occurs at the centre of the granuloma.
• Tubercles fuse, forming small, rounded, visible grey follicles (1-2 mm), becoming grayish yellow and cheesy with caseation.

Exudative Reaction

• In serous membranes (lung and meninges), protein-rich, yellowish serous exudate is formed.
• Infiltration of large numbers of lymphocytes, a small number of epithelioid cells, and Langhans' giant cells with rapid caseation.

Fate of Tuberculosis Granuloma

• Dystrophic calcification in caseous material or hyalinized lesions.
• Enlargement of the lesion and fibrosis.
• Cold abscesses form if caseation increases, liquefying material accumulating in bones, joints, lymph nodes and epididymis.
• Sinus formation occurs when cold abscesses extend into surrounding tissue (e.g., discharging caseous material on the skin).

Immunization Against TB

• BCG vaccine (attenuated bovine TB bacilli) induces cell-mediated immunity and delayed hypersensitivity.
• Tuberculin (Mantoux) skin test: intradermal injection of PPD (purified protein derivative), inducing delayed hypersensitivity in infected or previously infected individuals. A positive test shows indurated area (≥5 mm) peaking in 48-72 hours.

Spread of TB Infection

• Local spread by macrophages carrying bacilli.
• Spread through natural passages:
  • Lung to pleura
  • Transbronchial spread to adjacent lung segments
  • Tuberculous salpingitis to peritoneal cavity
  • Infected sputum to larynx
  • Renal lesions to ureter and urinary bladder
• Lymphatic spread via lymphatic vessels to regional lymph nodes.
• Blood spread via lymphatic connections (thoracic duct) causing isolated organ TB or miliary TB (many organs affected).

Types of TB

• Primary TB
• Secondary TB (Reactivation)

Primary TB

• Initial infection by TB bacilli.
• Primarily affects non-immunized children.
• Most patients are asymptomatic or have a mild flu-like illness.
• Sites include lung, tonsils, intestines, and skin.
• Characteristic of a primary complex (small TB lesion at infection site, TB lymphangitis, TB lymphadenitis).

Secondary (Reactivation) TB

• Reactivation of a dormant primary lesion.
• Affects previously sensitized hosts, mostly adults.
• Often occurs decades after initial illness, especially with weakened host defenses.
• Can also be due to exogenous reinfection.
• Immunity due to increasing activity of macrophages, and a decrease in TB bacilli reaching lymph nodes.
• Hypersensitivity is increased, causing tissue damage with caseous necrosis.

Pulmonary Tuberculosis

• Type of TB developing in a previously unsensitized patient (first infection with TB bacilli), which occurs more commonly in children.
• Infection happens by inhalation of human TB bacilli.
• Bacilli commonly implant in distal air spaces of the lower part of upper lobe or upper part of lower lobe, often near the pleura ("subpleural").

Fate of Primary Pulmonary Complex

• Healing: Complete fibrosis in small lesions
• Fibrous capsulation and central calcification in larger lesions.
• Spread: Direct spread causing TB pneumonia and pleurisy/pericarditis.
• Blood spread: Small no. of bacilli destroyed by RES; Moderate no. of bacilli isolate organ TB, Large no. of bacilli causes miliary TB.
• Bronchial spread causes TB bronchopneumonia.

Secondary Pulmonary TB (Reactivation)

• Arises in a previously sensitized host.
• Common in adults.
• Primarily from reactivation of dormant primary lesions decades after initial infection; particularly when host resistance is less.
• Also possible from exogenous reinfection.

Secondary Pulmonary TB (Localization)

• Classically localized to the apex of one or both upper lobes, due to less resistance in these areas, including less blood supply and greater aeration compared to other lung regions.
• Right lung bronchus in alignment with trachea more so than left lung.
• Cavities occur rapidly in secondary TB, causing erosion into airways and dissemination.
• This leads to the patient producing sputum containing bacilli—an important source of infectivity.

Course of TB Disease

• Depends on the infecting bacilli dose and host immunity/hypersensitivity state.
• Regression: Low bacilli count and strong immunity; lesion heals through fibrosis (fibrotic TB).
• Progression: Moderate bacilli count and moderate immunity: chronic, fibrocaseous pulmonary TB. Large bacilli count and low immunity: acute tuberculous bronchopneumonia.

Complications of Secondary Pulmonary Tuberculosis

• Hemoptysis
• Rupture of cavity into pleural sac → pneumothorax or pyopneumothorax.
• Right-sided heart failure due to extensive lung fibrosis
• Secondary amyloidosis
• Other lung, larynx, tonsils or tongue infections from infected sputum
• Intestinal TB from swallowing infected sputum.

Clinical Picture of TB

• Weight loss, sweating, night fever
• Chest pain (pleurisy), dyspnea (due to pleural effusion)
• Hemoptysis

Parasitic Infections - Schistosomiasis (Bilharziasis)

• Chronic granulomatous disease caused by schistosoma infection.
• Endemic in Egypt.
• Caused by two species:
  • Schistosoma hematobium: affects the genitourinary system.
  • Schistosoma mansoni: affects the digestive system..

Sites of Bilharzial Lesions

• Schistosoma hematobium ova produce lesions in the urinary bladder, ureters, urethra, seminal vesicles, prostate, spermatic cord, epididymis, vulva, vagina, and fallopian tubes; ova can spread to other tissues, including the lungs.
• Schistosoma mansoni ova produce lesions mainly in the intestine; ova fail to engage in vascular wall and are carried by blood to the liver as emboli.

Bilharziasis of the Urinary Bladder (Bilharzial Cystitis)

• Pathological lesions are most marked in the trigone, around ureteric orifices, and in the posterior wall of the urinary bladder.
• Lesions frequently include sandy patches (calcified ova deposits), billharzial polyps (sessile, pedunculated, or branched), and bilharzial ulcers (single or multiple, small or large).

Epithelial Changes in Urinary Bladder Bilharziasis

• Hyperplasia: Thickening of transitional epithelium due to inflammation.
• Brunn's nests: Masses of transitional cells in the submucosa due to transitional epithelium dipping into lamina propria.
• Cystitis cystica: Cysts lined by transitional epithelium due to Brunn's nests.
• Cystitis glandularis: Cysts lined with mucin-secreting columnar cells (metaplasia of transitional epithelium)
• Squamous metaplasia and leukoplakia: Thick white patches (leukoplakia) due to keratinization, premalignant.
• Dysplasia and carcinoma in situ: Transitional or metaplastic squamous epithelium affected. Premalignant lesions that can progress to invasive cancer.

Complications of Bilharzial Cystitis

• Hematuria
• Secondary bacterial infections (e.g., calcium phosphate stones, fistulae).
• Bladder neck obstruction due to fibrosis.
• Bilateral hydroureter and hydronephrosis may occur.
• Chronic renal failure due to bilateral hydronephrosis.
• Carcinoma of the urinary bladder
• Pulmonary bilharziasis
• Contracted urinary bladder