Infectious Diseases Lecture -1- PDF

Infectious diseases Lecture -1- Dr. Abeer Waleed Saeed C.A.B.H.S (Pathology), Department of Pathology / Ninevah Medical College  Intended learning outcome 1. Definition of Infection 2. Types of infectious micro-organisms 3. Fa...

Infectious diseases Lecture -1- Dr. Abeer Waleed Saeed C.A.B.H.S (Pathology), Department of Pathology / Ninevah Medical College  Intended learning outcome 1. Definition of Infection 2. Types of infectious micro-organisms 3. Factors influencing infection 4. Modes of transmission and dissemination of micro-organisms 5. Mechanism of bacterial infection 6. Presence of bacteria in blood 7. Gas Gangrene 8. Diphtheria  Aim of the lecture By the end of this lecture the student should be able to: 1. Understand the types of micro-organisms and its relation to human body 2. Recognize the factors that determine occurrence and severity of infection 3. Discuss and enumerate modes of transmission and dissemination of the infectious micro-organisms 4. Explain the pathological types of bacterial infection 5. Compare between bacteremia and septicemia 6. Understand the basic pathological changes and pathogenesis of certain bacterial infections (Gas gangrene and diphtheria)  Infectious diseases Infection: is defined as the invasion of living tissue by micro-organism or its products followed by local reaction which may be associated with general reaction.  Infectious diseases Commensals microorganisms: are those can infect human body and be harmless to the body ( some are present normally within the human body ). When commensal microorganisms cause disease at that time they are called opportunistic infections. The microorganisms cause diseases called pathogens may be Bacterial, viral , fungal , parasite ,….etc.  Factors influencing the infection The outcome of infection depends on the complex balance between the aggressive mechanisms of the micro-organism and the defense mechanisms of the host  Factors influencing the infection 1- Micro-organism factors : 1. Dose: number of m.o entering the body 2. virulence: their capacity to cause diseases. 3. Invasiveness: ability of m.o to multiply & spread in the body. 4. Transmission: ability of m.o to pass to another suitable host.  Factors influencing the infection 2-Host Factors: (defense mechanisms) A- Nonspecific defense mechanism: 1. Mechanical barriers: e.g. intact skin. 2. Glandular secretion: acidity of gastric juices. 3. Secretion currents: flow of tear, diarrhea..etc. 4. Phagocytosis: by macrophages & neutrophils. B- Specific defense (Immune response): by cell-mediated & humeral immunity.  Factors influencing the infection 3- Other factors: Local factors: e.g. ischemia promote infection. Systemic factors: e.g., malnutrition. Age: both very young & very old have increasing risk of infection.  TRANSMISSION OF MICROBES Transmission of infections can occur via: 1- Contact: such as S. aureus and dermatophytes (fungi). 2- Respiratory droplets: Viruses and bacteria can be shed in respiratory secretions during talking, coughing, and sneezing. Most respiratory pathogens, including influenza viruses, spread in large respiratory droplets, which travel no more than 3 feet. 3- Fecal-oral route: as in Cholera, Typhoid fever, hepatitis A and others.  TRANSMISSION OF MICROBES Transmission of infections can occur via: 4- Sexual transmission: As in AIDS, Hepatitis B, Syphilis. 5- Vertical transmission from mother to fetus or newborn: As in Rubella 6- Insect/arthropod vectors. As in malaria.  Dissemination inside the body Routes of dissemination of micro-organism inside the body: 1- Through out the nervous system, as in rabies. 2- Spread within inflammatory cells, as in M. Tb within macrophages 3- Spread through lymphatic vessels 4- Spread through blood vessels Bacterial Infections  Mechanism of Bacterial injury Bacteria damage the tissue through several mechanisms: 1- Release toxins that kill cells. 2- Release lytic enzymes, includes proteases, coagulase & fibrinolysins that destroy the tissue & facilitate the spread of bacteria 3- Elicit an inflammatory reaction that may destroy not only the bacteria but also the infected tissue. 4- Elicit an immune reaction that may damage the tissues carrying the same antigen as the bacterium (“cross reactivity”).  Bacterial infection Bacterial infection is divided into: 1- Acute. 2- Chronic.  Bacterial infection Acute bacterial infection can be further subdivided into: 1-Catarrhal: affect mucus membrane. 2-Serous: Affect serous cavities and produce serous fluid 3-Pseudomembranous: Characterized by formation of pseudo-membrane as in diphtheria. 4-Pyogenic or suppurative (Pus producing) e.g. abscess. M.O stimulate the secretion of IL 1 & TNF which stimulate complement, this attract neutrophil which secrets lytic enzyme, destroy tissue & form abscess.  Bacterial infection Localization of pus leads to abscess formation which appear here as red congested Swelling at the side of the neck  Bacterial infection This is an example of pseudomembranous colitis. The mucosal surface is hyperemic and is partially covered by a thick membrane like yellow-green exudate.  Bacterial infection in blood Bacterial infection of the blood is classified into:Bacteraemia and Septicemia. 1-Bacteraemia Presence of small numbers of bacteria in the blood without multiplication. Patients have sub clinical or minor symptoms & lesion.  Bacterial infection in blood Bacterial infection of the blood is classified into: 1-Bacteraemia E.g., S. Viridans in blood after vigorous brushing of teeth with dental sepsis. These bacteria are destroyed rapidly in blood by immune system It is important because it may settle in various parts of the body & cause localized lesion e.g. infective endocarditis.  Bacterial infection in blood Bacterial infection of the blood is classified into: 2- Septicemia Multiplication in the blood of highly pathogenic bacteria. It is a serious infection with profound toxemia in which bacteria have overwhelmed the host defenses. It results in serious consequences which may end in death. Clinically: Tachycardia, hypotension, & shock. Gangrene  Gangrene Digestion of dead tissue by saprophytic bacteria in living body (necrosis with putrefaction (Greek term gangarina)). Types of gangrene : Gas gangrene Dry gangrene Wet gangrene  Gas gangrene Caused by infection with Clostridia species (Cl. perfringes) Gain entry into the tissues through open contaminated wounds. They kill the tissue by secreting potent exotoxins & then invade & digest the dead tissue. Cl. perfringes ferments sugar producing H2 & CO2 which collect as bubbles in the dead tissue and can easily be detected by palpation ( gas gangrene). Clinically a black discoloration and bad odor at the affected site like the skin and subcutaneous tissue , intestine ……etc Gas gangrene of the uterus, note the gas within the.necrotic tissue produced by clostridia species  Diphtheria Diphtheria is an acute, communicable disease caused by Corynebacterium diphtheriae. Transmission: respiratory droplets The disease is generally characterized by local growth of the bacterium in the pharynx with membrane formation; systemic dissemination of toxin then invokes lesions in distant organs.  Diphtheria After it is inhaled, C. diphtheriae implants on the mucosa of the upper airways, Then it elaborates a powerful exotoxin that causes necrosis of the mucosal epithelium, accompanied by a dense fibrino-purulent exudate This creates the classic superficial, dirty-gray pseudomembrane of diphtheria.  :Diphtheria The major hazards of this infection are: 1. Sloughing and aspiration of pseudomembrane >> Suffocation and death 2. Absorption of bacterial exotoxins: I. Myocarditis and myocardial fatty change II. Polyneuritis  Tuberculosis.Tuberculosis is a serious chronic pulmonary and systemic disease According to (WHO), affect more than a billion individuals worldwide, with * *8.7 million new cases and 1.4 million deaths each year.Caused by Mycobacterium tuberculosis & Mycobacterium bovis Aerobic bacilli The bacilli have waxy coat that cause them to retain red dye when treated with acid, that is why they are called Acid fast bacilli. ( Ziehl Neelsen stain) This is an acid fast stain of Mycobacterium tuberculosis.Which appear as red rods  Transmission of TB ◻ Possible entry sites exist: 1) Respiratory tract by inhalation (Mycobacterium tuberculosis) 2) Alimentary tract, through a milk of diseased cows. (Mycobacterium bovis). Mycobacterium avium & mycobacterium intracellulare cause infection in AIDS patients.  Tissue Reaction to T.B. bacilli ◻ TB bacilli produce no Exotoxin, Endotoxin or enzymes. ◻ The Lesion of T.B is mainly due to the delayed hypersensitivity reaction (Type IV) to an antigenic protein component of the organism. ◻ This will result in granulomatous inflammation with central necrosis.  Tuberculosis Pathogenesis: 1- Entrance of MTB to macrophages 2- Replication of the microorganism inside macrophages 3- Stimulation Cell mediated immunity (Th1 response) after 3 weeks (by IL-12 and IL-18) 4- Th1 cells activated macrophages via release of INF-Y 5- Formation of Granuloma with central caseous necrosis Tuberculosis  Tuberculosis So the final lesion of TB (microscopically) consist of : Central area of caseous necrosis Surrounded by activated macrophages (epithelioid macrophages), some macrophages fuse to from multinucleated giant cells ( Langhans giant cells) Surrounded by rim of chronic inflammatory cells rich in lymphocytes. At the periphery there is fibrosis. Tuberculosis Characteristic tubercle at low magnification (A) and high magnification (B) shows central granular caseation surrounded by epithelioid and multinucleate giant cells. Tuberculosis ◻ Primary TB ◻ Secondary TB ◻ Progressive TB  Primary tuberculosis ◻ It follows initial exposure to TB bacilli in non immunized individuals of any age. ◻ Grossly: it forms a small sub pleural parenchymal lesion in the mid zone of the lung (Ghon focus) and spread to the hilar lymph nodes. Both lesions are called primary complex.(cheesy like material) ◻ 95% of cases healed by fibrosis. ◻ Some may enter into dormant state & few may spread into the body forming progressive primary T.B.  Secondary T.B. ◻ Either occurs as a reinfection or reactivation of dormant bacilli from primary infection when there is impairment in the immunity of the patient. ◻ Macroscopically : occurs at the apex of the lung with marked damage in the lung parenchyma with cavity formation ◻ Healing by fibrosis or may spread forming progressive secondary T.B.  Systemic miliary tuberculosis It is a form of progressive tuberculosis occurs when bacteria disseminate through the systemic arterial system. Individual lesions are either microscopic or small, visible (2-mm) foci of yellow-white lesion scattered through the involved organ parenchyma (the adjective “miliary” is derived from the resemblance of these foci to millet seeds) Miliary lesions may expand and coalesce, resulting in larger lesions Miliary tuberculosis is most prominent in the liver, bone marrow, spleen, and adrenals, but can involve any organ  Systemic miliary tuberculosis Millet seeds ◻ Miliary TB in spleen The natural history and spectrum of tuberculosis Clinical Features: ◻ ◻ According to organ involved. ◻ ◻ Fever, cough, night sweating , hemoptysis and weight loss Diagnosis:. I-History ll- Clinical examination. III- Investigation include : ** X- raySpinal tuberculosis (TB) is the most common extrapulmonary form of tuberculosis. In both developing and developed countries, TB has been on the rising trend due to factors such as increasing HIV coinfection, multidrug resistance of the organism, and global migration. Spinal TB, which most often affects the lower thoracic and thoracolumbar area, accounts for 50% of all musculoskeletal tuberculosis.***2 ** Detection of the m.o. in the specimen (sputum, in biopsy) by the use of Ziehl-Neelsen staining. ** Biopsy of the infected tissue. ** PCR amplification of T.B. bacilli Thank you References.Pathology outlines.1.2 ◻ REFERENCES: ◻ **Tuberculosis mortality rate worldwide 2010-2022 | Statista ◻ ***2 [HTML] sciencedirect.com ◻ [HTML] Active tuberculosis of spine: Current updates ◻ R Shanmuganathan, K Ramachandran… - North American Spine …, 2023 - Elsevier ◻ …Robbins and Cotran 11th edition ◻ Pathology outline.