Pathogenesis of Infectious Diseases PDF

Chapter 14: PATHOGENESIS OF INFECTIOUS DISEASES FIRST SEMESTER I ACADEMIC YEAR 2024-2025 I PROF. JOHN LEONARD CHAN Pathogenesis Why Doesn't Infection Always Occur? ​ Pathos (Greek):Disease Emphasize the 1.​ Unsuitable Environment: con...

Chapter 14: PATHOGENESIS OF INFECTIOUS DISEASES FIRST SEMESTER I ACADEMIC YEAR 2024-2025 I PROF. JOHN LEONARD CHAN Pathogenesis Why Doesn't Infection Always Occur? ​ Pathos (Greek):Disease Emphasize the 1.​ Unsuitable Environment: connection between the Greek root and ​ Skin: Low pH, fatty acids, its implications for the study of disease. dryness create a barrier. ​ Pathogen: A microbe capable of ​ Other examples: Stomach causing disease. Briefly mention acidity, mucosal surfaces with examples (bacteria, viruses, fungi, protective secretions. parasites). 2.​ Lack of Receptors: Pathogens require ​ Pathology: The study of the structural specific receptors on host cells to attach and functional manifestations of and infect. disease. Briefly mention key areas ​ Briefly explain the concept of within pathology (e.g., anatomic host-pathogen specificity. pathology, clinical pathology). 3.​ Antimicrobial Factors: ​ Pathologist: Physician specializing in ​ Lysozyme: Present in tears, pathology. Highlight their role in saliva, and other secretions. diagnosing diseases through examining ​ Other examples:Antimicrobial tissues, cells, and body fluids. peptides, complement system. ​ Pathogenicity: The ability of a microbe 4.​ Microbial Antagonism: to cause disease. Briefly touch upon ​ Normal microbiota compete for virulence factors (e.g., toxins, capsules) resources and space. that contribute to pathogenicity. ​ Production of bacteriocins by ​ Pathogenesis: The steps involved in normal microbiota. the development of a disease. Briefly 5.​ Host Factors: outline the stages: entry, adherence, ​ Nutrition, overall health, stress, invasion, damage, and host response. age, and immune system status all play a significant role. Infection vs. Infectious Disease Stages of an Infectious Disease ​ Infectious Disease: A disease caused by ​ Incubation Period: Time between a microbe. Provide clear examples (e.g., exposure and the appearance of the first influenza, tuberculosis, HIV/AIDS). symptoms. Influenced by factors ​ Infection: like dose of pathogen, virulence, and ○​ Broad Definition: The presence host immunity. of a pathogen within the body. ​ Prodromal Period: Mild, nonspecific ○​ Microbiological Definition: symptoms (e.g., fatigue, malaise, Colonization of the body by a low-grade fever). May last from several hours to a few days. pathogen, regardless of disease ​ Period of Illness: Time of most severe development. symptoms. Disease is most ○​ Example: Carriers of communicable during this phase. asymptomatic infections (e.g., ​ Convalescent Period: Recovery phase. individuals carrying Salmonella Symptoms gradually subside. Possible without experiencing illness). complications: Long-term damage, chronic infection.  Chapter 14: PATHOGENESIS OF INFECTIOUS DISEASES FIRST SEMESTER I ACADEMIC YEAR 2024-2025 I PROF. JOHN LEONARD CHAN Symptoms vs. Signs of Disease Symptoms: Subjective, experienced by the patient. ​ Examples: Pain, fever, headache, fatigue, nausea. Signs: Objective, observed by others or measured. ​ Examples: Rash, fever, swollen lymph nodes, abnormal heart sounds, elevated blood pressure. ​ Laboratory test results are also considered signs. Latent Infections/Dormant Infections Herpesvirus Infections: ​ Cold sores (HSV-1): Recurrent outbreaks triggered by stress, sunlight, fever. ​ Genital herpes (HSV-2): Similar pattern of recurrent outbreaks. Localized vs. Systemic Infections ​ Shingles (Varicella-zoster virus): Localized Infection: Confined to a specific Reactivation of the chickenpox virus. area. Syphilis: ​ Examples: Boils, abscesses, urinary ​ A chronic disease caused by the tract infections (may initially be spirochete Treponema pallidum. localized). ​ Progresses through distinct stages. Systemic/Generalized Infection: Spread throughout the body. Stages of Syphilis ​ Mechanisms: Bloodstream, lymphatic system, nerves. 1.​ Primary Syphilis: ​ Examples: Septicemia, measles, ​ Appearance of a painless disseminated tuberculosis. chancre at the site of infection. ​ Highly infectious. Types of Disease Duration 2.​ Secondary Syphilis: 1.​ Acute: Rapid onset, short duration. ​ Rash, fever, swollen lymph Examples: Influenza, measles, common nodes, mucous membrane cold. lesions. Systemic spread of the 2.​ Subacute: Slower onset than acute, infection. less sudden than chronic. 3.​ Latent Syphilis: Examples: Subacute bacterial ​ No or few symptoms. endocarditis. ​ May last for years or even 3.​ Chronic: Slow onset, long duration. decades. May persist for months or years. ​ Bacteria remain dormant in the Examples: Tuberculosis, hepatitis B, body. HIV/AIDS. 4.​ Tertiary Syphilis:  Chapter 14: PATHOGENESIS OF INFECTIOUS DISEASES FIRST SEMESTER I ACADEMIC YEAR 2024-2025 I PROF. JOHN LEONARD CHAN ​ Severe complications affecting Multiplication: Pathogens replicate within the the heart, brain, and other host. organs. ​ Can occur years after the initial Invasion: Spread of the pathogen to other infection. tissues. Evasion of Host Defenses: Mechanisms to avoid immune system recognition and destruction (e.g., capsules, toxins). Damage to Host Tissues: Can occur through various mechanisms (e.g., toxin production, inflammation, immune response). Primary vs. Secondary Infections Primary Infection: ​ The initial infection. ​ Often weakens the host's defenses. Secondary Infection: ​ Caused by a different pathogen. ​ Occurs as a consequence of the primary infection. Example: Viral respiratory infection (primary) can damage the respiratory epithelium, allowing bacteria like Streptococcus pneumoniae to colonize and cause pneumonia (secondary). Virulence Factors Bullet Points: Steps in Pathogenesis ​ Virulence: The degree of pathogenicity. Entry: Pathogens enter through various portals ​ Virulence Factors: (e.g., skin, respiratory tract, gastrointestinal ○​ Traits that enable a pathogen to tract, urogenital tract). cause disease. ○​ Examples: Toxins, capsules, Attachment: Pathogens adhere to host cells adhesins, pili, enzymes, evasion using specific receptors and adhesins. mechanisms.  Chapter 14: PATHOGENESIS OF INFECTIOUS DISEASES FIRST SEMESTER I ACADEMIC YEAR 2024-2025 I PROF. JOHN LEONARD CHAN ​ S. pyogenes adherence to pharyngeal cells. M-protein: A type of pilus in S. pyogenes that mediates adherence and inhibits phagocytosis. Obligate Intracellular Pathogens ​ Cannot survive or multiply outside of host cells. Rely on host cell machinery for essential functions. ○​ Examples: Bacteria: Rickettsia, Chlamydia, Ehrlichia, Anaplasma; Protozoa: Plasmodium (malaria), Babesia. Characteristics of Obligate Intracellular Attachment: Adhesins and Receptors Pathogens Receptors: Molecules on host cells that ​ Rickettsia: pathogens recognize and bind to. Examples: ○​ Invade endothelial and vascular Glycoproteins, glycolipids. smooth muscle cells. "Leaky membranes" – require host cell Adhesins/Ligands: Molecules on the pathogen environment for essential surface that bind to host receptors. Examples: functions. Pili, fimbriae, viral envelope proteins. ​ Chlamydia: ○​ Invade various cell types (e.g., Specificity: Pathogens typically only attach to epithelial cells). cells with specific receptors. ○​ "Energy parasites" – utilize host cell ATP. ​ Laboratory Cultivation: Require specialized culture methods (cell cultures, animal models, embryonated eggs). Intracellular Pathogens: Target Cells ​ Intraleukocytic Pathogens: ○​ Ehrlichia spp.: Infect monocytes. ○​ Anaplasma phagocytophilum: Infect granulocytes. Bacterial Fimbriae (Pili) Structure: Hair-like protein appendages on the bacterial surface. Function: Enable bacteria to ​ Intraerythrocytic Pathogens: adhere to host cells and surfaces. ○​ Plasmodium spp. (malaria): Examples: Infect red blood cells. ​ N. gonorrhoeae adherence to urethral ○​ Babesia spp. (babesiosis): epithelium. Infect red blood cells. ​ E. coli adherence to bladder cells. Facultative Intracellular Pathogens  Chapter 14: PATHOGENESIS OF INFECTIOUS DISEASES FIRST SEMESTER I ACADEMIC YEAR 2024-2025 I PROF. JOHN LEONARD CHAN ​ Can survive and multiply both inside and outside of host cells. Virulence Factors: Toxins ​ Examples: Mycobacterium tuberculosis, ​ Endotoxins: Salmonella, Listeria monocytogenes. ○​ Components of Gram-negative ​ Often reside within phagocytes bacterial cell walls (LPS). (macrophages, neutrophils). ○​ Cause fever, shock, and other Intracellular Survival Mechanisms systemic effects. ​ Resisting Digestion: Mycobacterium tuberculosis: Waxy cell wall resists ​ Exotoxins: digestion. ○​ Proteins secreted by bacteria. ​ Preventing Phagolysosome Fusion: ○​ Include neurotoxins, Toxoplasma gondii inhibits fusion of enterotoxins, cytotoxins, and phagosome with lysosome. others. ​ Escaping the Phagosome: Listeria ​ Examples: monocytogenes escapes the ○​ Neurotoxins: Tetanus toxin, phagosome and replicates in the host botulinum toxin. cell cytoplasm. ○​ Enterotoxins: Produced by E. Virulence Factors: Attachment coli, Salmonella, C. difficile. ​ Cytotoxins: Receptors and Adhesins: ○​ Damage host cells. ​ Pathogens bind to specific receptors on ○​ Examples: Diphtheria toxin, host cells. leukocidins. ​ Adhesins (e.g., pili, fimbriae) on pathogen surface mediate attachment. Importance: Evasion of Host Defenses ​ Essential for colonization and ​ Antigenic Variation: Pathogens subsequent infection. change their surface antigens to evade immune recognition. Virulence Factors: Enzymes ​ Examples: Influenza virus, Trypanosoma brucei. ​ Necrotizing Enzymes: Destroy host ​ Camouflage and Molecular Mimicry: tissues (e.g., proteases in Clostridium Pathogens mimic host molecules to perfringens). avoid detection. ​ Coagulase: Produced by ​ Destruction of Antibodies: Some Staphylococcus aureus to form a fibrin bacteria produce IgA proteases to clot around the bacteria. degrade antibodies. ​ Kinases: Dissolve fibrin clots, allowing for bacterial spread (e.g., streptokinase). ​ Hyaluronidase: Breaks down connective tissue, facilitating tissue invasion. ​ Collagenase: Degrades collagen, aiding in tissue invasion. ​ Hemolysins: Damage red blood cells, releasing iron for bacterial growth. ​ Lecithinase: causes destruction of host cell membranes of RBC and other tissues. Major cause of gas gangrene. Muscle tissue.