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Pathology of Infectious Diseases PowerPoint Presentation

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This medical PowerPoint presentation is about the Pathology of infectious diseases, the study of the structural and functional changes in tissues and organs that result from infections caused by microorganisms such as bacteria, viruses, fungi, and parasites.

When microorganisms infect the body, they can cause a range of pathological changes, including inflammation, necrosis (cell death), granuloma formation, and fibrosis (scar formation). The type and severity of the pathological changes depend on the virulence of the microorganism, the host immune response, and the location of the infection.

In some cases, the immune response can be so strong that it causes tissue damage, as seen in autoimmune diseases like rheumatoid arthritis. In other cases, the immune response may be inadequate, resulting in chronic or recurrent infections.

The study of infectious disease pathology is important for understanding the mechanisms of disease progression, developing diagnostic tests, and designing effective treatments and preventive measures. Pathological examination of infected tissues is often used to confirm a diagnosis, determine the extent of disease, and monitor the effectiveness of treatment.

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Published on : Jun 23, 2023 | Views : 4260 | Downloads : 1

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Pathology of infectious diseases د.ايمان سعود خليفة LEC1
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Learning objectives You should: Know what infectious diseases are and identify infectious agents. Understand host barriers to infection and causes of failure of these barriers. Able to explain types of inflammatory responses to infection.
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Infectious diseases are disorders in which tissue damage or dysfunction is produced by microorganisms. Despite the availability and use of effective vaccines and antibiotics, infectious diseases remain an important health problem worldwide. Infectious disease= transmissible disease = communicable disease. Definition :
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Contagious mean person to person transmission. Non contagious acquired from sources such as animals, insects , soil, air or originating from normal microbial flora of the body.
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Infectious agents belong to a wide range of classes, they include; 1- Prions: which are modified host proteins lacking genetic molecules. 2- Viruses: obligate intracellular parasites which only replicate intracellularly. 3- Bacteriophage and plasmid. 4- Bacteria: prokaryotes lacking nucleic acid and endoplasmic reticulum. Infectious agents:
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5-Mycoplasma, rickettsiae, Chlamydia. 6-Fungi: non-motile filamentous, branching strands of connected cells. 7-Protozoa: single cell organisms with a well defined nucleus. 8-Helminthes: multicellular parasites with complicated life cycles often involving several hosts.
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Skin: Respiratory system: GIT: Urogenital tract: Host barrier to infection:
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Skin: normal defense in skin include epidermal barrier: The intact keratinized epidermis protects against infection by serving as a strong Mechanical barrier and by its low PH and producing antimicrobial fatty acids and defensins ( small peptides that are toxic to bacteria).
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Failure of local defense in skin occurs when there is; Mechanical defects (puncture, burn, ulcer). Needle sticks (e.g. may transmit hepatitis B or C). Arthropods and animal bites. Direct penetration.
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Respiratory system: Normal defenses including : The mucous layer secreted by the goblet cells in the nose &upper respiratory tract. The mucociliary clearance of the respiratory epithelium. Alveolar macrophages &neutrophils recruited to the lung by cytokines.
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The distance that infectious agents travel into the respiratory system is inversely proportional to their size, large particles are trapped in the mucociliary blanket that lines the nose and the upper respiratory tract , particles smaller than 5 microns are carried into the alveoli, where they are phagocytosed by alveolar macrophages or by neutrophils .
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Breakdown of these barriers is by followings: 1. Smoking (damage the mucociliary action). 2. Cystic fibrosis (increased viscosity of mucus secretion which result in obstruction of bronchial tree & thus increased the risk of infection). 3. Damage to epithelial cells of respiratory tract (like in viral infections which result in secondary bacterial infection). .
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4. Damage to alveolar macrophages (tuberculosis). 5. Lowering of cellular immunity (fungal infection this is called opportunistic infection).
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GIT: Normal defenses against infected pathogens are: Epithelial barriers. Acidic gastric secretions. Viscous mucous secretions. Bile and pancreatic enzymes.
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Immunoglobulin A (IgA) antibodies, secreted by B cells located in the mucosa associated lymphoid tissues. The normal protective gut flora. Most gastrointestinal pathogens are transmitted by food or drink contaminated with fecal material.
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Break down of these barriers is by followings: 1. Low gastric acidity (by drugs). 2. Killing the bacterial flora (by antibiotics). 3. Damage of intestinal lining epithelium (Rotavirus, salmonella, shigella…. Bloody diarrhea). 4. Secretion of enterotoxins (like food poisoning by staph. bacteria) or secretion of exotoxins which result in severe diarrhea (vibrio cholera).
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5. Lower immunity (opportunistic fungal infection). 6. Resist gastric acidity (cysts of intestinal amoeba).
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Urogenital tract: Normal defenses against infected pathogens are: Urination. Normal vaginal flora. Intact epidermal / epithelial barrier.
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Failure of local defense in urogenital system occurs when there is; Obstruction, microbial attachment and local proliferation. Antibiotic use. Microbial attachment and local proliferation . Direct infection/local invasion . Local trauma (e.g. sexually transmitted diseases)
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Immune evasion by microbes: After bypassing host tissue barriers, infectious microorganisms must also evade host innate and adaptive immunity to successfully proliferate and be transmitted to the next host. Strategies include:
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Antigenic variation Inactivating antibodies or complement. Resisting phagocytosis, e.g. by producing a capsule Suppressing the host adaptive immune response, e.g. by interfering with cytokines or inhibiting MHC expression and antigen presentation. Establishing latency, during which viruses survive in a silent state in infected cells.
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The transmission can be: 1- Direct from person to person by aerosols, direct contact as in chicken pox, measles, (contagious). 2- It may need prolonged intimate or mucosal contact e.g sexually transmitted diseases Chlamydia , syphilis. 3- Some respiratory bacteria and fungi are transmitted only when the lesion is opened to the airways e.g in T.B.
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4- Other may take the feco-oral route for transmission (ingestion of stool contaminated food or water) as in cholera , rotavirus. 5- Other microbes need a reservoir host and transmitted from animal to human. 6- Others may be transmitted by human agency as in HBV, HIV that can be transmitted by sharing needles by addicts or viral contaminated blood transfusion.
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7. By blood sucking arthropods (malaria, leishmania). 8. By kissing, talking, spitting (mumps).
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Routes of entry, release and dissemination of microorg.
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How can the microorganism cause a disease? Infectious diseases involve interplay between microbial virulence factors and host responses. The infectious agents damage the tissue in 3 ways: 1- Enter the cell and cause death or dysfunction directly.
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2- Injury may be due to local or systemic release of microbial products including endotoxin , exotoxins or superantigens. 3- Induce host cellular responses which may cause additional damage to the surrounding tissues e.g suppuration, scarring, hypersensitivity reactions.
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Spectrum of Inflammatory Responses to Infection: Microbes produce 5 types of tissue reaction : Suppurative (Purulent) Inflammation: 2)Mononuclear &granulomatous inflammation: 3) Cytopathic-cytoproliferative response: 4) Necrotizing inflammation: 5 ) Chronic inflammation and scarring:
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1) Suppurative (Purulent) Inflammation: This pattern is characterized by increased vascular permeability and leukocytic infiltration, predominantly of neutrophils. The neutrophils are attracted to the site of infection by release of chemoattractants from the “pyogenic” (pus-forming) bacteria.
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Masses of dying and dead neutrophils and liquefactive necrosis of the tissue form pus. Abscesses(local collection of pus) differ in size from tiny to large according to the site and sequelae e.g pyogenic pharyngitis will heal completely while acute bact. Infection of the joint can destroy it within few days.
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focal abscess in the lung
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2) Mononuclear &granulomatous inflammation: a)Diffuse, predominantly mononuclear, interstitial infiltrates are a common feature of all chronic inflammatory processes,but when develop acutely, they often are response to viruses, intracellular bacteria, or intracellular parasites. For example: plasma cells are abundant in syphilis . lymphocytes predominate in HBV infection or viral infections of the brain.
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b) Granulomatous inflammation which is characterized by aggregates of activated macrophages which are called epitheloid cells that may accumulate around an area of necrosis, some of which may fuse together forming a giant cells.
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DDX of chronic granulaomatous infections: T.B Leprosy. Syphilis. Schistomiasis. Leishmaniasis.
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Causes of granulomatous inflammation: 1) Slowly dividing infectious agents (T.B bacilli). 2) Large size agents (schistosomiasis egg).
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3- Cytopathic-cytoproliferative response: These reactions are characteristic of viral mediated damage to the host cell &these include: Virus may replicate inside the cell  formation of viral aggregate which may be visible as inclusion bodies e.g Cytomegalovirus. Virus may induce cells to fuse and form multinucleated cells (e.g., measles virus or herpes-viruses).
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May cause focal cell damage  discohesion of the epithelial cells  blister formation. May cause proliferation of the epithelial cells, e.g warts that are caused by HPV. May cause dysplastic changes and cancer formation.
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inclusion bodies in Cytomegalovirus
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4) Necrotizing inflammation: Microbes who secrete powerful toxins cause rapid and severe necrosis that tissue damag is the dominant feature with few inflammatory cells ,e.g: Entamoeba histolytica which may cause liver abscess (necrosis) Clostridium perfringins that cause severe cell death just like coagulative necrosis.
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Necrotizing soft tissue infection inflammation:
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5 ) Chronic inflammation and scarring: Many infections may end in chronic inflammation which can lead to either: Complete healing, or: extensive scarring e.g chronic HBV infection may cause cirrhosis of the liver.
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Thanks for attention