Introduction To Infectious Diseases By Dr Gaikwad Sir 2

INTRODUCTION TO INFECTIOUS DISEASES

DR ANU GAIKWAD, Assoc.Professor , Dept.of Gen.Medicine.

Why? • Infectious diseases remain a major cause of death and debility • Responsible for worsening the living conditions of many millions of people around the world. • Frequently challenge the physician's diagnostic skill

Changing Epidemiology • Antibiotic resistance Pneumococci -Penicillin Enterococci -Vancomycin • Old diseases rebounded with renewed ferocity. • Discovery of infectious agents in recent decades • Resurgence of Infectious diseases • Non infectious diseases have infectious agents in their etiology

• Helicobacter pylori-In peptic ulcer disease &gastric malignancy • Human papillomavirus-Causes invasive Ca.Cervix • Human herpesvirus type 8 - Kaposi's sarcoma. • Epstein-Barr virus – Lymphomas &Hodgkin's disease. • Other diseases with infectious etiology Rheumatoid arthritis Sarcoidosis Inflammatory bowel disease Atherosclerosis • Changes in pt. populations hindered

Host Factors in Infection • Knowledge of the relationship between specific risk factors and disease is essential • Factors influencing the likelihood of infection Geography Environment Behavior Age & Comorbid conditions Immunization history Prior illnesses Level of nutrition

IATROGENIC INFECTIONS Acquired in several ways: (2)Through contact with pathogens during hospitalization. (3)Through breaching of the skin& mucosal surfaces (with endotracheal tubes or bladder catheters) (4)Through introduction of foreign bodies (5)Through alteration of the natural flora with antibiotics (6)Through treatment with immunosuppressive drugs.

Innate Immunity • Innate immune mechanisms exploit molecular patterns found specifically in pathogenic microorganisms. • Serves to protect the host without prior exposure to an infectious agent • Protects before specific or adaptive immunity has had a chance to develop • Functions as a warning system that activates components of adaptive immunity early in the course of infection.

Adaptive Immunity • Cellular immunity comprises of Tlymphocytes, macrophages, and natural killer cells • Primarily recognizes and combats pathogens that proliferate intracellularly • T lymphocytes are activated by macrophages and B lymphocytes • Cytotoxic T cells may directly attack and lyse host cells that express foreign antigens • Helper T cells stimulate the proliferation of B cells and the production of immunoglobulins • T cells elaborate cytokines (e.g.,

• Cytokines also augment the host's immunity by stimulating the inflammatory response (fever, the production of acute-phase serum components, and the proliferation of leukocytes • The immune system has also developed cells that specialize in controlling or downregulating immune responses. For example, Treg cells, a subgroup of CD4+ T cells, prevent autoimmune responses by other T cells

Reticuloendothelial system • Comprises monocyte-derived phagocytic cells • Located in the liver (Kupffer cells), lung (alveolar macrophages), Spleen (macrophages&dendritic cells) kidney (mesangial cells), Brain (microglia) Lymph nodes(macrophages&dendritic) that clear circulating microorganisms

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Antibodies

Complex glycoproteins Produced by mature B lymphocytes Circulate in body fluids Secreted on mucosal surfaces Specifically recognize and bind to foreign Ag’s Directly impede the function of an invading organism Neutralize secreted toxins and enzymes Facilitate the removal of the antigen (invading organism) by phagocytic cells. Promote the deposition of complement

The complement system • Group of serum proteins functioning as a cooperative, self-regulating cascade of enzymes • Adhere & disrupt surface of invading organisms. • Surface-adherent proteins (e.g., C3b) can then act as opsonins for destruction of microbes by phagocytes • C5a, act as chemoattractants for PMNs • “Terminal" components (C7, C8, and C9) can directly kill some bacterial invaders by forming a membrane attack complex and disrupting the

• Complement activation and deposition occur by either or both of two pathways: • The classic pathway is activated primarily by immune complexes (i.e., antibody bound to antigen), • The alternative pathway is activated by microbial components, frequently in the absence of antibody

PolyMorphicNeutrophils. • Short-lived white blood cells that engulf and kill invading microbes • Attracted to inflammatory sites by chemoattractants • Localize to the site of infection through selectins • Enter into the extravascular compartment through diapedesis • Arachidonic acids further enhance the inflammatory process after the diapedesis.

Approach to the Patient • A careful history is essential . • details on underlying chronic diseases, medications, occupation, and travel. • Emphasize on A sexual history history of contact with animals Blood transfusions A history of exposure to insect vectors

The physical examination • Be thorough, and pay attention to seemingly minor details Fever- common manifestation of infection soft heart murmur- bacterial endocarditis retinal lesion – candidiasis/CMV infection Rashes are extremely important clues childhood exanthems (measles, rubella) Target lesion of erythema migrans

Laboratory Investigations • Carefully consider and direct toward establishing an etiologic diagnosis in the shortest possible time, at the lowest possible cost, and with the least possible discomfort to the patient. • Pay special emphasise on specimen collection. • A good lab with efficient technician is essential • Store serum during acute phase of the illness • Bacterial and fungal Ag’s can be

Treatment • Based on broad knowledge of medicine and careful clinical judgment • Life-threatening infections must be treated immediately. • Choose broad spectrum AMAs empirically. • withhold AMAs in a self-limited process. • Beware of DRUG TOXICITY. ALLLERGIC REACTIONS

• Abscesses require surgical or percutaneous drainage for cure • Foreign bodies, removed in order to eliminate an infection of the device or of the adjacent tissue. • Immunomodulators are newer drugs Glucocorticoids Activated protein C Prostaglandin inhibitors Specific lymphokines Tumor necrosis factor inhibitors

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