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INFECTIOUS DISEASES 1 BY: DR (MRS) B.J.THANENTHIRAN (MBBS) INFECTION The presence and growth of a microorganism that produces tissue damage. The extent of the infection depends on the number and virulence of the organisms and the ability of the body to contain or destroy them. 2 Improved living conditions Appropriate vaccination Effective antibiotics Then why infectious diseases continue? 3 Because of Chronic diseases Treatment with immunosuppressive drugs AIDS But in developing countries due to Malnutrition Unsanitary living conditions 4 CATEGORIES OF INFECTIOUS AGENTS Prions – modified host proteins Viruses – obligate intracellular agents8 Bacteriophages, plasmids & transposan – mobile genetic elements Bacteria Chlamydiae, rickettsiae & mycoplasma Fungi Protozoa Helminths Ectoparasites 5 FACTORS INFLUENCING THE ESTABLISHMENT OF INFECTION A. In the host In addition to a good state of general health & nutrition the following mechanisms operate in preventing & limiting infection. 1. Skin – dense keratinized outer layer low pH presence of fatty acids 2. Urogenital tract – flushed many times/day long length of urethra in males 3. Respiratory tract – mucociliary blanket 6 4. Intestinal tract – acid gastric juice viscous mucus layer covering gut lytic pancreatic enzymes bile detergent secreted IgA commensal flora 7 A. B. In the microorganisms – factors potentiating invasive capacity 1. 2. Quantity of dose Virulence 8 EXAMPLES OF FAILURE OF PROTECTIVE 1. AND DEFENSE MECHANISM In skin 1. 2. 3. 4. 5. 2. Direct breach by wounding & burns Softening of the surface by exposure to water & sweat IV cannulation Needle prick Bites by arthropods / animals In respiratory tract 1. 2. 3. 4. Repeated smoking Patients with cystic fibrosis Intubated patients Aspiration of gastric acid damage to mucociliary defense 9 3. In intestinal tract 1. 2. 3. Low gastric acidity Antibiotics that unbalance normal bacterial flora Mechanical obstruction 4. Deficiency of the immunological system 5. Debilitating diseases 10 ROUTES OF ENTRY OF INFECTIOUS AGENTS 1. Through the skin or mucous membranes 1. 2. 3. 2. By ingestion 1. 3. By direct close contact By contamination of abrasions & wounds By inoculation Contaminated food & water By inhalation 1. By dust & droplets 11 SPREAD OF MICROBES THROUGHOUT THE BODY Microbes spread rapidly along the wet epithelial surfaces of intestine, lungs, genitourinary tract Many microbes don’t travel beyond epithelium, but others spread Tissue planes of least resistance Regional lymphatics Vascular system 12 In blood they spread Free in plasma By leucocytes – mycobacterium, HIV, CMV By RBC – plasmodium 13 RELEASE OF MICROBES FROM THE BODY Skin shedding Coughing & sneezing Urination & defecation Talking & singing Spitting Kissing 14 HOW INFECTIOUS AGENTS CAUSE DISEASE 1. Infectious agents can contact or enter host cells & directly cause cell death. 2. Pathogens can release endotoxins / exotoxins 3. That kill host cells at a distance Release enzymes that degrade tissue component Damage blood vessels & cause ischemic injury Pathogens can induce host cell responses that may cause additional tissue damage, usually by immune mediated mechanisms. 15 IMMUNE EVASION BY MICROBES Remaining inaccessible Cleaving antibody, resisting complement mediated lysis or surviving in phagocytic cells Varying / shedding antigens Causing specific/ nonspecific immunosuppression 16 DIAGNOSIS OF INFECTIOUS AGENTS Staining Gram stain Acid fast stain Silver stain PAS Culture PCR Antibody probes 17 INFLAMMATORY RESPONSE TO INFECTIOUS AGENTS Histologic patterns of host reaction induced by infectious agents are Suppurative polymorphonuclear inflammation 1. Mononuclear inflammation 2. Chronic inflammation, response to viruses, intracellular bacterias / intracellular parasites Cytopathic – cytoproliferative inflammation 3. Viruses Necrotizing inflammation 4. 5. Pyogenic bacterias C.perfringens Chronic inflammation & scarring 18 NOSOCOMIAL INFECTION / HOSPITAL INFECTION Infection acquired in a hospital. They can be exogenous in origin or endogenous in origin Exogenous in origin – source may be another person in hospital (cross infection) or a contaminated item of equipment / building service (environmental infection) Endogenous in origin – infecting organisms being derived from the patient’s own skin, GI / upper respiratory flora (self infection) 19 INANIMATE RESERVOIRS OF INFECTION Equipment & materials in use in hospital Organisms in air, dust & on surfaces Fluids 20 ROLE OF ANTIBIOTIC TREATMENT Use of antibiotics affect microbial flora in GIT which leads to antibiotic associated diarrhoea. Sensitive strains of microorganisms which normally maintain a protective function on the skin & other mucosal surfaces tend to be eliminated whereas those that are resistant survive. 21 SUSCEPTIBILITY TO NOSOCOMIAL INFECTION Low natural resistance – in infants & elderly Preexisting disease – Eg-DM Medical / surgical treatment – immunosuppressive drugs, radiotherapy, splenectomy Bypass of body’s natural resistance – injury / procedures ( indwelling catheter, tracheostomy) 22 MICROORGANISMS CAUSING HOSPITAL INFECTION Urinary tract infections Escherichia coli Klebsiella Pseudomonos aeruginosa Respiratory infections Haemophilus influenzae Streptococcus pneumonia Staphylococcus aureus Wounds & skin sepsis Staphylococcus aureus Streptococcus pyogenes Escherichia coli Gastrointestinal infections Salmonella serotypes Clostridium difficile Viruses 23 ROUTES OF TRANSMISSION Route Source Examples of diseases 1. Aerial (from persons) droplets skin scales Mouth Nose Skin exudates Measles, TB, Pneumonia Staphylococcus sepsis Stap & strep sepsis 2. Aerial (from inanimate source) particles Respiratory equipment Air conditioning plant Gram – negative respiatoy infection Legionnaires disease 3. Contact (from person) direct spread indirect via equipment Respiratory secretions Faeces ,urine, skin & wound exudates Stap & strep sepsis Enterococcal & viral diarrhoea Pseudomonas aeruginosa sepsis 4. Contact (environmental source) Equipment, food, fluids Enterobacterial sepsis Pseudomonas aeruginosa 5. Inoculation Sharp injury, blood products Hepatitis B, HIV, malaria 24 PREVENTION & CONTROL OF NOSOCOMIAL INFECTION Infection control policy Infection control committee Infection control team Sterilization Aseptic techniques Cleaning & disinfection 25 Skin disinfection & antiseptics Prophylactic antibiotics Protective clothing Isolation Source isolation Protective isolation Hospital building & design Personnel – screening of staff & immunization 26 HUMAN IMMUNODEFICIENCY VIRUS HIV is a lentivirus (a member of the retrovirus family) Acquired immunodeficiency syndrome is a collection of symptoms & infections resulting from the specific damage to the immune system caused by HIV. 27 28 Spherical & contains dense, cone – shaped core surrounded by a lipid envelope derived from the host cell membrane. The virus core contains The major capsid protein p24 Nucleocapsid protein 2 copies of genomic RNA 3 Viral enzymes Viral core is surrounded by a matrix protein p17 beneath viral envelope Viral envelope itself is studded by 2 viral proteins. 29 ROUTE OF INFECTION 1. Sexual transmission 2. Parenteral transmission (IV drug abusers, hemophilics receiving blood concentrate) 3. Mother to infant transmission (transplacental spread, during delivery, ingestion of HIV contaminated breast milk) 30 Attachment of HIV to cells by the interaction of the external envelope glycoprotein gp120 with part of the CD4 molecule of T helper cells Attachment is followed by interaction of the HIV envelope with a second receptor(CCR5,CXCR4) Entry of virus with the fusion of the viral envelope with the cellular membrane Viral RNA released into cytoplasm Reverse transcriptase act to form dsDNA 31 DNA copy circularized, enters the nucleus & is spliced into the host DNA Viral mRNA production by host RNA polymerase RNA & protein synthesis Virion formation Virions are assembled at the membrane 32 33 34 Numerous organ systems are infected by HIV Brain: macrophages and glial cells Lymph nodes and thymus: lymphocytes and dendritic cells Blood, semen, vaginal fluids: macrophages Bone marrow: lymphocytes Skin: langerhans cells Colon, duodenum, rectum: chromaffin cells Lung: alveolar macriphages 35 GENERAL MECHANISMS OF HIV PATHOGENESIS Direct injury Nervous (encephalopathy and peripheral neuropathy) Kidney (HIVAN = HIV-Associated Nephropathy) Cardiac (HIV cardiomyopathy) Endocrine (hypogonadism in both sexes) GI tract (dysmotility and malabsorption) Indirect injury Opportunistic infections and tumors consequence of immunosuppression as a 36 STAGES OF INFECTION 1. Early acute phase 2. Short flu like illness No symptoms Infected persons can infect others Middle chronic phase Last for an average of 10yrs Free from symptoms There may be swollen glands Level of HIV in blood drops to very low levels HIV antibodies are detectable in the blood 37 3. Final crisis Symptoms are mild Immune system deteriorates Emergence of opportunistic infections Immune system weakens Illness become more severe leading to AIDS diagnosis 38 39 EXAMPLES OF AIDS INDICATOR DISEASES Candidiasis Coccidioidomycosis Pneumosystis carinii pneumonia Toxoplasmosis of brain Kaposi’s sarcoma 40 HIV RISK REDUCTION Avoid unprotected sex Use barriers such as condum Avoid multiple partners Don’t share needles used by others for drugs, tattoos, body piercing In pregnancy – antivirals in late pregnancy & consider on breast milk 41 Morphological features Anatomic changes in tissues (with exception of lesions in brain) are neither specific nor diagnostic. Changes in lymph nodes In early stages Marked follicular hyperplasia Intense plasmacytosis in medulla Increased cellularity in sinuses ( macrophages plasma cells, B cell lymphoblasts) HIV particles can be seen in germinal centers With disease progression Follicular involution & generalized lymphocyte depletion , organized net work of follicular dendritic cell is disrupted, follicle becomes hyalinized. 42 Changes in brain Bain is often atrophic. Morphological features are more pronounced within white matter & basal ganglia. Myelin pallor associated with the presence of macrophages, scanty perivascular mononuclear inflammatory infiltrates, microglial nodules & multinucleated giant cells. HIV encephalopathy often associated with vacuolar myelopathy, a condition characteized by vacuolation & myelin breakdown in dorsal & lateral columns of the spinal cord. 43 CLOSTRIDIUM INFECTIONS Gram positive, spore bearing, anaerobic bacilli. Most are saphrophytes normally occur in soil, decomposing plants & animal matters. Clostridium perfringens & Clostridium sporogens are commensals of animal & human gut. Pathogenic species of clostidia Clostridium perfringens Clostridium tetani Clostridium bolulinum Clostridium difficil 44 CLOSTRIDIUM PERFRINGENS Causing Gas gangrene Food poisoning Colitis Enteirtis necroticum 45 Gas gangrene Clostridium perfringens is the commonest cause of gas gangrene. Gas gangrene is almost always a polymicrobial infection involving anaerobes & facultative organisms. Main source of infection – animal & human excreta and spores. Infection usually derived from contamination of a wound with soil. It may derived from dirty clothing, street dust & air of an OT if ventilating system is poorly designed. 46 Characters of gas gangrene Rapidly spreading edema Myositis Necrosis of tissue Gas production & profound toxemia 47 Pathogenesis of gas gangrene Impairment of normal blood supply of tissue with a consequent reduction in oxygen tension may allow an anaerobic focus to develop Circumstances & events that may lead to gas gangrene Tissue damage & contamination with clostridial spores & pyogenic organisms. 1. 2. Presence of foreign bodies, including soil with damaging salts 3. Inflammatory reaction 48 4. 5. Extravasation of fluid, oedema Impaired tissue perfusion; stasis 6. Impaired phagocytosis & intraleucocytic bactericidal mechanisms 7. 8. 9. 10. Poor oxygenation Multiplication of facultative bacteria Further reduction in oxygen & pH Germination & outgrowth of clostridial spores 49 Multiplication of obligate anaerobes with production of toxins, aggressins (hyaluronidase, collagenase, alpha toxin) & gas in affected tissues 11. 12. Further impairment in local blood supply & extension of area of tissue damage. 13. Profound toxemia & shock 50 Food poisoning Meat is often contaminated with heat resistance spores. Disease is mediated by enterotoxin production. Clinical features – abdominal cramps & diarrhoea 51 CLOSTRIDIUM TETANI The germination of spores & their outgrowth depend on reduced oxygen tension in devitalized tissue & non viable materials in a wound. Simultaneous present. growth of anaerobic organism is Tetanus bacilli remains strictly localized but tetanus toxin (tetanoplasmin – neurotoxin) is elaborated & diffuse. Toxin diffuses to affect the relevant level of spinal cord (local tetanus) & then to affect the entire system (generalized tetanus) 52 Toxins attach to gangliosides & the toxin is internalized Moved from the peripheral to the central nervous system by retrograde axonal transport & transsynaptic spread Once the entire toxin is internalized into presynaptic cells, they affect the membrane of synaptic vessicles Prevent the release of neurotransmitter gama aminobutric acid Motor neurones are left under no inhibitory control & undergo sustained excitatory discharge 53 Sites of infection Infection in superficial abrasion, thron prick, contaminated splinter. Otogenic tetanus Cryptogenic tetanus Tetanus neonatorum Postoperative tetanus 54 Clinical features IP – 10-14 days but there is a considerable range Stiffness & pain in or near a recent wound Stiffness of jaw – lock jaw Pain & stiffness in neck & back Stiffness spread to involve all muscle groups Sympathetic stimulation – sweating, tachycardia, arrythmias & swings in BP 55 56 Prevention & control Prompt & adequate wound toilet & proper surgical debridement of wounds. Immunization (active &passive) 57 CLOSTRIDIUM BOTULINUM Factors make it as a formidable pathogen Wide spread occurrence in nature Ability to produce potent neurotoxin in food Resistance of its spores to inactivation 58 Food poisoning Botulism is a severe often fatal form of food poisoning. The preformed toxin in the food is absorbed from the intestinal tract. Although it is a protein, it is not inactivated by the intestinal proteolytic enzymes. After absorption into the blood stream, botulinum toxin binds irreversibly to the presynaptic nerve endings of the peripheral nervous system & cranial nerves. Inhibits acetylcholine release. 59 Clinical features IP – 1-2days, but it may be much long. Nausea & vomiting. Diplopia & drooping eyelids with squint Vertigo & blurred vision. Progressive descending motor loss with flaccid paralysis. Weakness. Sleepiness. Thirsty with dry mouth & tongue. Difficulty in speech & swallowing. Difficulty in breathing. 60 Control & prevention Great care in canning factories. Immunization (active & passive) 61 CLOSTRIDIUM DIFFICILE Commonly occurs in faeces of neonates & babies until the age of weaning. Not generally found in adults. Produce an enterotoxin & cytotoxin. Causea antibiotic associaded pseudomembranous colitis. diarrhoea & 62 THANK YOU 63