GENERAL PRINCIPLES OF INFECTIOUS DISEASES Department of Infectious Diseases, t he Third Affiliated Hospital Li Gang ( 李刚） 2009.2.
Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.
Introduction·Definition of infectious diseases and communicable diseases. · Distinction between infectious diseases and communicable diseases.
1. Infectious disease: any infection caused by microbes or parasites.
2. Communicable disease: infection transmitted from persons or animals to other persons.
The goal of studying infectious disease:1. To study etiology, epidemiology, pathogenesis, clinical manifestations, treatment and prevention of infectious diseases. 2. To control and eliminate these diseases. (occurrence, spreading, prevention)
Prion; virus; chlamydia; rickettsia; bacteria; fungus; spirochete.
Emerging pathogens and infectious diseases
1977 Hantaan virus
1977 Ebola virus
1982 E coli O157：H7
1992 Vibrio cholerae O139 strain
2003 SARS coronavirus
Three kinds of infection
⑵ Opportunistic infection:Pathogens within the host can induce pathologic changes if host immunity is suppressed by some factors.
⑶ Pathogenic infection: According to the severity of the pathologic changes, several degrees in clinical manifestation from mild, moderate to severe will occur.
1. Elimination: pathogens were excluded out by host nonspecific or specific immunity. Such as Candida albicans Escherichia coli
2. Covert (subclinical) infection:￭ Most frequently occurs in healthy individuals. ￭ The outcomes will be: A. Immunity acquired. B. Carrier state: healthy carriers.
4. Carrier state: Definition of different types of carriers: . incubation carrier . acute carrier . convalescent carrier . chronic carrier
5. Latent infection: After infection, pathogens remain latent inside the body. Develop clinical manifestations when the host immunity has been impaired. Pathogens usually will not be excreted by the host during period of latency.
The Role of Pathogens in the Infection Process:⑴ Invasiveness: adhesion, penetration ability. ⑵ Virulence: toxins, enzymes, and histolytic ability.⑶ Infection dose: minimal dose that can cause an infection.⑷Variability: change in structure of the pathogen to evade from host immunity.
The Role of Immune Response in Infection Process:Differentiation between protective immunity and allergy. . Protective immunity: beneficial . Allergy(anaphylactic reaction): harmful
⑴ Nonspecific immunity:A. Natural barriers:external (skin, mucous membrane, cilia), internal (blood-brain barrier).B. Phagocytosis:macrophages, monocytes, and granulocytes.C. Humoral factors: complements, interferons, lysozyme, cytokines.
⑵ Specific immunity: Immune respond to specific recognizable antigens. A. Cell-mediated immunity: Important in intracellular infections by viruses, fungi, protozoa and certain bacteria.B. Humoral immunity: Different kinds of antibodies (immune globulins) and their functions.
1.Portal of entry:Each pathogen has its specific portal of entry.Such as: Mycobacterium tuberculosis, Meningococcus via breath tract. Shigella via digestive tract.
2. Localization and Dissemination in the host:Specific for each pathogen.Such as: . Mumps virus in parotid gland. . Hepatitis C virus in the liver. . Shigella in the intestine.
3. Channels of excretion: Important factor for host infectivity. As the source of infection. Such as: . Hepatitis A in the stool. . Hepatitis B in the blood. . Measles virus in expiratory air.
Mechanism of Tissue Damages1. Direct invasion: Cytolysis, tissue necrosis, inflammation.2.The actions of toxins and cytokines: Resulting in septic shock, Disseminated intravascular coagulation, etc.
Mechanism of Tissue Damages3. Immunopathogenesis: Immunosuppression, T-cell destruction, immune complexes, antibody-mediated cytotoxicities.
1. Fever(pyrexia): Exogenous and endogenous pyrogens.. Exogenous pyrogens: virus etc. . Endogenous pyrogens: IL-1, TNF, IL-6, interferon etc.
2. Metabolismchanges:(1) Protein: higher proteins catabolism. “acute” proteins (C-reactive protein, sign of acute inflammation). (2) Carbohydrate: acceleration of glucolysis.
2. Metabolismchanges:(3) Water and electrolytes: dehydration, hypokalemia.(4) Endocrine disturbances: higher anabolism, stress, hyper-corticosteroidemia.
1. Sources of infection:Definition. Human, animal.⑴ Patients: acute, chronic; typical, atypical(mild, severe).⑵ Subclinical infection:no symptoms. poliomyelitis.⑶ Carriers:chronic, typhoid, shigellosis.⑷ Infected animals:(natural source)rabies, plague.
2. Routes of transmission⑴ Air, droplets, dusts. e.g. measles.⑵ Water, food, flies(fecal-oral infection).e.g. typhoid.⑶ Fingers, utensils(contact infection).e.g. shigellosis, influenza.
⑷ Arthropods.A. Biologic:intermediate hosts. e.g. mosquitoes in malaria, chiggers in scrub typhus. B. Mechanical:passive transfer. e.g. flies in amebiasis.
3. Population susceptibility:
Proportion of susceptibles.
Basic characteristics:(1) Pathogens.(2) Infectivity. (3) Epidemiological features: age, sex, season; imported or endemic; sporadic, epidemic, pandemic, outbreaks.(4) Post-infection immunity.
2. Clinical Characteristics:(1) Development stage:A.Incubation period.B.Prodromal period.C.Symptomatic period. Apparent clinical manifestations.D.Convalescent period.E. Recrudescence or relapse.F.Sequelae.
Forms:A. Sustained fever:Difference of body temperature less than 1℃ within 24 hours, over 39℃. e.g. Second week of typhoid.
B. Remittent fever: Change of body temperature more than 1 ℃ within 24 hours, the base line higher than normal. e.g. Septicemia.
C. Intermittent fever:Fluctuation between normal temperature and high fever within 24 hours. e.g. Malaria.
D. Relapsing fever: Fever lasting 5~7 days with relapse after several days. e.g. Relapsing fever.
E. Undulent fever: Fever lasting several weeks with relapse after several weeks. e.g. brucellosis.
F. Irregular fever: Curve of body temperature is irregular. e.g. Brucellosis, septicemia.
G. Saddle-type fever: Fever for several days, then with normal temperature for 1 day, and then relapse. e.g. Dengue.
(3) Toxemic symptoms:A. General presentations: malaise; headache; anorexia; pain in muscles, joints and bones; disturbance in consciousness; meningeal irritation; septic shock; liver and kidney failure, etc.
4. Clinical forms:(1) development: Acute, subacute and chronic forms. (2) forms of clinical manifestation: mild, moderate (typical) or severe forms of the disease. ambulatory form in typhoid (without symptom and signs).
1. Clinical manifestations(1) Mode of onset(2) Type of fever(3) Accompanying symptoms:headache, myalgia, arthralgia etc.(4) Signs:Consciousness, jaundice, skin rash, buccal membrane, Koplik spot, eschar, subcutaneous hemorrhage, liver, spleen, lymph nodes.
Characteristic sign of scrub typhus
2. Epidemiological Data:(1) History of contact with similar cases.(2) Occupation, living environment and life style.(3) History of vaccination.(4) History of transfusion of blood or blood products.
3. Laboratory Examinations:(1) Routine examinations: blood, urine, stool. Leukocytosis, leukopenia, eosinopenia, eosinophilia. Biochemical analysis of the blood for liver functions and kidney functions, etc.
Infection with virus:
epidemic hemorrhagic fever,
Japanese B encephalitis,
Infection with bacteria, etc.
(2) Detection and isolation of pathogens:A. Adequate collection and transportation of specimens.
B.Direct examination: macroscopy: e.g. Ascaris lumbricoides, hook worm, Enterobius vermicularis, etc.microscopy:e.g.Plasmodium, Cryptococcus neoformans,Mycobacterium tuberculosis
C.Culture by artificial media or tissue culture. Media culture:Entamoeba histolytica, Shigella, Salmonella, etc. Tissue culture:dengue virus, poliovirus, etc.
D.Animal inoculation. Intraperitoneal inoculation: Rickettsia tsutsugamushi.Intracerebral inoculation:encephalitis virus.
E. Specific antigen detection: Methods: agglutination test, ELISA, EIA, FAT, RIA, flow cytometry, etc.
F. Molecular biologic assay: Using isotope or non-isotope probes; Polymerase chain reaction (PCR).Mycobacterium tuberculosis, hepatitis C virus, etc.
(3) Detection of specific antibodies: By means of : ELISA, RIA, etc. IgM, IgG antibodies.
Skin test:e.g. for tuberculosis, cysticercosis.
1. Aim of treatment: . Not only for alleviation of symptoms and signs, but also for isolation of patients to prevent propagation of infection to the community. . Comprehensive treatmentincludes drug therapy, nursing care and isolation. . Pay attention to both specific and symptomatic treatments.
2. Therapeutic methods:⑴General and supportive treatment. ⑵ Etiologic (specific) treatment.⑶ Symptomatic treatment.⑷ Rehabilitation therapy for sequelae.⑸ Traditional Chinese medicine and acupuncture.
Three kinds of case report:Kind A: plague, cholera, smallpox. <6hs.Kind B: AIDS, hepatitis, etc. <12hs.Kind C: influenza, mumps, etc.<48hs.
⑴ Immunological prophylaxis: . Active (vaccination): intracutaneous inoculation with smallpox vaccine. subcutaneous inoculation with hepatitis B vaccine. . passive (immunoglobulins): intramuscular injection with antibodies against tetanus bacillus.