Infectious Diseases - Tuberculosis PDF

Infectious diseases I- Tuberculosis  Tuberculosis (T.B) Definition: A chronic granulomatous inflammation caused by mycobacterium tuberculosis Incidence: TB is a common communicable chronic infective disease Etiology: Risk factors: Poverty, crowding, malnutrition, chronic...

Infectious diseases I- Tuberculosis  Tuberculosis (T.B) Definition: A chronic granulomatous inflammation caused by mycobacterium tuberculosis Incidence: TB is a common communicable chronic infective disease Etiology: Risk factors: Poverty, crowding, malnutrition, chronic debilitating illness as diabetes, chronic lung disease, alcoholism and AIDS Causative bacteria: Human tubercle bacilli (acquired by inhalation) Bovine tubercle bacilli (acquired by consumption of infected milk) Mycobacteria are slender aerobic non motile gram +ve rods that are acid-fast stained with Ziehl-Neelsen stain. Methods of infection Inhalation (infected droplets coughed or sneezed from patients with open pulmonary TB, or dust contaminated with sputum of infected person). Ingestion (contaminated milk or self swallowing of infected sputum of an open case of pulmonary TB). Skin inoculation (infected materials), very rare. Tranplacental route: (congenital TB of the fetus), rare. Host response to TB bacilli Proliferative reaction Exudative reaction  Proliferative tissue reaction (The tubercle formation): Initial response is attraction of neutrophils within few hours which are rapidly destroyed by the organisms. Attracts the macrophages after the first day. The bacteria multiply inside the macrophages → rupture with release of numerous organisms. Macrophages undergo structural modification resembling →epithelioid cells. Aggregation of epithelioid cells → granuloma formation. Fusion of some epithelioid cells → Langhan’s giant cells. Lymphocytes and fibroblasts are found at the periphery of granuloma. Caseation necrosis at the center of granuloma.  Grossly; numbers of tubercles fuse with one another forming small rounded visible grey follicles 1-2 mm, become grayish yellow and cheesy with caseation.  Exudative reaction: In the serous membranes, lung, and meninges protein-rich clear yellowish serous exudate with moderate amount of fibrinogen is formed, and infiltration of large number of lymphocytes, small number of epithelioid cells and Langhans’s giant cells with rapid caseation occurs. Fate of tuberculosis granuloma Dystrophic calcification: in caseous material or hyalinized lesions. Enlargement of the lesion and fibrosis. Cold abscess: If caseation is increased → it accumulates and liquefied, as occurs in bones, joints, lymph nodes and epididymis Sinus: if cold abscess extend into surrounding tissue → discharges the caseous material on the surface e.g., skin.  Immunization against TB Induced by injection of attenuated strains of bovine TB bacilli, Bacille Calmette- Guerin (BCG) leading to development of cell mediated immunity and delayed hypersensitivity reaction. Tuberculin (Mantoux) skin test Intradermal injection of 0.1 ml of purified protein derivative (PPD) leading to development of delayed hypersensitivity in infected or previously infected individuals Positive test is identified as an indurated area of at least 5 mm in diameter that peaks in 48-72 hours  Spread of T.B infection occurs through: Local spread: by macrophages carrying the bacilli Spread through the natural passages: – Spread from lung into pleura – Transbronchial spread into adjacent lung segments – Tuberculous salpingitis spread into peritoneal cavity – Infected sputum into larynx – Renal lesions into ureter and down to the urinary bladder Lymphatic spread: via lymphatic vessels to regional lymph nodes. Blood spread: through – Lymphatic connections through thoracic duct – Caseous focus in the lung erodes vessels causing isolated organ or miliary TB in the lung, and in many organs all over the body Types of T.B Primary Secondary  Primary TB: Definition: Means infection by TB bacilli for the first time Main features: Non immunized persons Commonly occurs in children Exogenous infection 5% develop a significant disease, the rest are asymptomatic or have a mild flu like illness Sites: lung, tonsils, intestine, and skin Characterized by primary complex Primary complex; Consists of: Small TB lesion at site of infection TB lymphangitis TB lymphadenitis (many bacilli carried to draining LN)  Secondary (reactivation) TB Arises in previously sensitized host Mode of infection: Endogenous: from reactivation of a dormant primary lesion. Exogenous re-infection: when TB bacilli enter the body for the second time after the patient has overcome a primary infection or previously immunized by BCG vaccine Patient in secondary TB has developed type IV hypersensitivity reaction which results in: Immunity: due to increased phagocytic activity of macrophages causing decreased number of TB bacilli carried to LN which are rarely severely affected. Hypersensitivity: causing tissue damage with extensive caseous necrosis. Complications of tuberculosis: Spread Hemorrhage Destruction of the organ and fibrosis Amyloidosis Re-activation  Pulmonary tuberculosis Primary Pulmonary TB It is characterized by: Develops in a previously unexposed and therefore unsensitized patient (first infection with tubercle bacilli). This type occurs mainly in children. Infection is by inhalation of human T.B. bacilli. Typically, the inhaled bacilli implant in distal air spaces of the lower part of upper lobe or upper part of the lower lobe, usually close to the pleura (subpleural). Fate of Primary pulmonary complex Healing: Complete fibrosis in small lesion. Fibrous capsulation and central dystrophic calcification in bigger lesion. Spread: Direct spread: causing T.B pneumonia and T.B pleurisy and pericarditis. Blood spread: Small number of bacilli → destroyed by cells of RES, moderate number → isolated organ T.B, while large number of bacilli → miliary T.B. Bronchial spread: causing T.B bronchopneumonia. Encapsulation and reactivation.  Secondary Pulmonary T.B (Reactivation Tuberculosis) It is characterized by: Arises in a previously sensitized host. It occurs mainly in adults. Commonly it arises from: Reactivation of dormant primary lesions many decades after initial infection, particularly when host resistance is weakened. Exogenous re-infection  Secondary pulmonary T.B is classically localized to the apex of one or both upper lobes and more in right lung due to: less local resistance (less blood supply) and more areation, right bronchus is more in line with the trachea than the left bronchus Cavitations occur rapidly in secondary pulmonary TB, leading to erosion into and dissemination along airways. Such changes become an important source of infectivity, because the patient now produces sputum containing bacilli.  Course of the disease depends on: The dose of infecting bacilli, and the state of immunity and hypersensitivity. The disease goes through either: Regression: occurs with small number of bacilli and high immunity. The lesion heals by fibrosis → fibrotic tuberculosis. Progression: – Moderate number of bacilli and moderate immunity → Chronic fibrocaseous pulmonary tuberculosis. – Large number of bacilli and low immunity → Acute tuberculous bronchopneumonia.  Complications of secondary pulmonary T.B. Hemoptysis Rupture of cavity into pleural sac → pneumothorax or pyopneumothorax Spread Right sided heart failure due to extensive lung fibrosis. Secondary amyloidosis Infected sputum may cause TB of the other lung, larynx, tonsils or tongue Swallowing infected sputum causes intestinal TB  Clinical picture: – Loss of weight, sweating, and night fever. – Chest pain (pleurisy) and dyspnea due to pleural effusion. – Hemoptysis.  II- Parasitic infections Schistosomiasis (Bilharziasis) Definition: Bilharziasis is a chronic granulomatous disease caused by schistosoma infection. Incidence and causative organism: The disease is endemic in Egypt and is caused by one of the following two species: Schistcsoma hematobium: It affects the genitourinary system. Schistosoma mansoni: It affects the digestive system. Sites of bilharzial lesions Ova of Schistosoma hematobium: produce lesions mainly in the urinary bladder, ureters,, urethra, seminal vesicles, prostate, spermatic cord, epididymis, vulva, vagina, fallopian tubes, ovaries, or pass to the lungs and then to any tissue of the body. Ova of Schistosoma mansoni: produce lesions mainly in the intestine. Ova fail to engage in vascular wall are carried by blood as emboli to the liver  Bilharziasis of the urinary bladder (Bilharzial cystitis) Etiology: infection with Schistosoma hematobium. Gross features: Pathological lesions are most marked in the trigone, around ureteric orifices and in the posterior wall of the urinary bladder. The common lesions are: Sandy patches: irregular dirty yellowish patches due to shining of heavy deposits of calcified ova surrounded by dense fibrosis through thinned or atrophied mucosa. Billharzial polyps: single or multiple polyps which may be sessile, pedunculated, and simple or branched are formed. They may slough leading to bilharzial ulcer. Bilharzial ulcers: These are common bladder lesions (20%). Single or multiple, small or large ulcers, with irregular outline are formed.  Epithelial changes in urinary bladder bilharziasis: – Hyperplasia: Leads to thickening of transitional epithelium – Brunn’s nests: Solid masses of transitional cells present in the submucosa due to focal dipping of the hyperplastic urothelium into the lamina propria. – Cystitis cystica: Cysts lined by transitional epithelium. They are due to central degenerative changes in Brunn’s nests. They are usually of microscopic size, but may enlarge and become grossly visible as pale mucosal vesicles, few millimeter in diameter. – Cystitis glandularis: Cysts lined by mucin secreting columnar cells (similar to colonic epithelium). This is due to metaplasia of transitional epithelium lining the cystitis cystica. The lesion is precancerous → in adenocarcinoma. – Squamous metaplasia and leukoplakia: Very common. It may be associated with extensive keratinization and appear as thick white patches (leukoplakia). These lesions are precancerous. – Dysplasia and carcinoma in situ: Affect transitional or metaplastic squamous epithelium and may progress to carcinoma in situ or invasive carcinoma.  Complications of bilharzial cystitis:  Hematuria  Secondary bacterial infection. This may lead to: – Calcium phosphate stone due to alkaline change of pH of urine, ova and bacteria act as nidi for stone formation). – Fistulae with rectum or vagina.  Bladder neck obstruction due to fibrosis (causing obstruction to urine flow and urine retention). This leads to:  Hypertrophy, diverticulosis and dilatation of the bladder.  Bilateral hydroureter and bilateral hydronephrosis, if complicated by secondary bacterial infection, bilateral pyoureter and pyonephrosis occur.  Chronic renal failure due to bilateral hydronephrosis.  Carcinoma of the urinary bladder.  Spread of bilharziasis leads to Pulmonary bilharziasis.  Contracted urinary bladder. Thank you