Infectious Diseases Выполнила: Шаймерденова Ш. Проверила: Кыдырмолдина Э.

Описание презентации Infectious Diseases Выполнила: Шаймерденова Ш. Проверила: Кыдырмолдина Э. по слайдам

Infectious Diseases Выполнила: Шаймерденова Ш. Проверила: Кыдырмолдина Э. Курс: 5 Группа: 59 -02 Infectious Diseases Выполнила: Шаймерденова Ш. Проверила: Кыдырмолдина Э. Курс: 5 Группа: 59 —

Infectious Disease Terms 1. Epidemiology 2. Epidemic 3. Endemic 4. Pandemic 5. Pathogen 6.Infectious Disease Terms 1. Epidemiology 2. Epidemic 3. Endemic 4. Pandemic 5. Pathogen 6. Opportunist 7. Nosocomial 8. virulence

Normal Micro flora & its importance 1. Prevent the growth of pathogens 2. StimulateNormal Micro flora & its importance 1. Prevent the growth of pathogens 2. Stimulate the immune system to produce antibodies that cross-react with invading pathogens 3. Aid in digestion of cellulose in ruminants. 4. Produce essential nutrients

Koch’s Postulates 1. The same pathogen must be present in every case of theKoch’s Postulates 1. The same pathogen must be present in every case of the disease; 2. The pathogen must be isolated from the diseased host and grown in pure culture; 3. The pathogen from the pure culture must cause the disease when it is introduced into a healthy but susceptible organism. 4. The pathogen must be isolated from the inoculated animal and be shown to be the original organism.

Modifications to Koch’s Postulates 1. Some infectious agents cannot be cultured e. g. prionsModifications to Koch’s Postulates 1. Some infectious agents cannot be cultured e. g. prions 2. Some pathogens have non-virulent strains whose presence does not link them to a disease. E. g. non encapsulated Diplococcus pneumoniae

Types of Pathogens 1. Bacteria 1. Gram positive 2. Gram negative 3. Acid-Fast e.Types of Pathogens 1. Bacteria 1. Gram positive 2. Gram negative 3. Acid-Fast e. g. Mycobacteria 1. Spherical described as cocci 2. Rod shaped described as bacilli

Gram Positives • Unique Features – Thick peptidoglycan wall – No periplasmic space –Gram Positives • Unique Features – Thick peptidoglycan wall – No periplasmic space – No outer membrane (capsule) – E. g. Streptococcus pyogenes, Staphylococcus aureus, Bacillus anthracis, Clostridium tetani

Gram Positive wall Gram Positive wall

Gram Negatives • Unique features – Thin peptidoglycan wall – Has periplasmic space containingGram Negatives • Unique features – Thin peptidoglycan wall – Has periplasmic space containing different degradative enzymes such as deoxyribonucleases, -lactamases and proteases – Outer membrane containing lipid A, an endotoxin – E. g. Neisseria , Salmonella typhi, E. coli, Yersinia pestis, Vibrio cholerae

Gram Negative wall Gram Negative wall

Types of pathogens 2. Parasites (Eukaryotic Pathogen) 1. Fungi e. g.  Candida, AspergillusTypes of pathogens 2. Parasites (Eukaryotic Pathogen) 1. Fungi e. g. Candida, Aspergillus 2. Protozoa e. g. Plasmodium , Schistosoma 3. Worms e. g. Ascaris, Taenia

Types of pathogens 3. Viruses 1. Are pieces of DNA or RNA surrounded byTypes of pathogens 3. Viruses 1. Are pieces of DNA or RNA surrounded by protein coat. The may be 2. Encapsulated e. g. HIV, HBV, measles, mumps, influenza, rabies 3. Non-encapsulated e. g. adenoviruses, HPV, Polio

Viruses Viruses

Modes of transmission 1. Direct contact e. g. touching,  handshaking, or sexual intercourseModes of transmission 1. Direct contact e. g. touching, handshaking, or sexual intercourse 2. Indirect contact e. g. food, water or droplets in air; 3. Animal vectors e. g. insect bites in malaria, plague and oncho, dog bite in rabies

Pathogenesis • Sequence of activities 1. Transmission of causative agent to susceptible host; 2.Pathogenesis • Sequence of activities 1. Transmission of causative agent to susceptible host; 2. Adherence of the agent to a target tissue; 3. Colonization and invasion; 4. Damage to host by toxins or other mechanisms; 5. Exit from host; 6. Survival outside host long enough for step 1 to occur.

Virulent Factors • For all pathogens there is an infective dose and a lethalVirulent Factors • For all pathogens there is an infective dose and a lethal dose. • Virulent factors that confer pathogenicity include; 1. Pili that facilitate attachment; 2. Capsules that interfere with phagocytosis 3. Exotoxins 4. Endotoxins 5. Proteases that break down antibodies 6. Ability to vary antigens to evade antibodies

Bacterial Pathogenesis 1. Toxin production. Toxins fall into two categories;  exotoxins and endotoxins.Bacterial Pathogenesis 1. Toxin production. Toxins fall into two categories; exotoxins and endotoxins. 2. Invasiveness, where bacteria grow to large numbers locally and produce enzymes that damage host tissues.

exotoxins 1. Heat labile (60 -100 degrees for 30 mins) proteins produced and releasedexotoxins 1. Heat labile (60 -100 degrees for 30 mins) proteins produced and released by both gram positive and gram negative bacteria. 2. Produced by bacteria such as Clostridium (neurotoxins) and Bacillus (enterotoxin) (+) and E. coli and Vibrio (enterotoxin) (-)

endotoxins 1. Are heat stable (100 degrees for 1 hr) lipopolysaccharide produced only byendotoxins 1. Are heat stable (100 degrees for 1 hr) lipopolysaccharide produced only by gram –ve bacteria. They remain attached to cell wall. 2. Cause fever and shock and is of lower toxicity compared to exotoxins. 3. Produced by bacteria such as Salmonella

cholera 1. Causative Agent: Vibrio cholerae 2. Symptoms: severe diarrhoea up to 20 literscholera 1. Causative Agent: Vibrio cholerae 2. Symptoms: severe diarrhoea up to 20 liters a day of “rice water stool”, vomiting, muscle cramps caused by loss fluid and electrolytes. 3. Pathogenesis: Vibrio adheres to the small intestinal lining, multiply and produce the enterotoxin choleragen which causes the accumulation of c. AMP. An increased secretion of water and electrolyte from the cells results

Cholera 4. Epidemiology: Feacally contaminated water, crabs and vegetables fertilized with human faeces. HasCholera 4. Epidemiology: Feacally contaminated water, crabs and vegetables fertilized with human faeces. Has been eradicated most developed countries but a new strain discovered in 1992 is threatening another pandemic.

Cholera 5.  Incubation period: 12 -48 hours 6. Lab diagnosis: Microscopy, culture ofCholera 5. Incubation period: 12 -48 hours 6. Lab diagnosis: Microscopy, culture of sample from faeces or vomit. 7. Prevention: Purification of water, washing of hands. 8. Treatment: administration of solution of glucose and electrolyte orally or intravenously; tetracycline antibiotic orally

malaria 1. Causative Agent:  Plasmodium ( 4 species) 2. Symptoms (Clinical features): fever,malaria 1. Causative Agent: Plasmodium ( 4 species) 2. Symptoms (Clinical features): fever, chills, anaemia, headache, nausea, shivering, convulsions (esp. in under 5 yr olds) enlarged spleen. 3. Pathogenesis: site of action of pathogen include: liver, RBC, brain. The vector, female Anopheles mosquito, transfer pathogen during feeding.

malaria 4. Epidemiology: Endemic in 91 tropical and subtropical countries. Invade the liver 1malaria 4. Epidemiology: Endemic in 91 tropical and subtropical countries. Invade the liver 1 st and move to reproduce in RBCs resulting in their rupture and the associated chills. 5. Incubation Period: 1 – 2 weeks. 6. Lab diagnosis: Microscopy.

An Infected RBC An Infected R

Malaria - Prevention 1. Reduce the number of mosquitoes;  destruction of larvae andMalaria — Prevention 1. Reduce the number of mosquitoes; destruction of larvae and adult mosquitoes by biological and chemical control methods 2. Avoid being bitten; protective clothing and creams, treated bed nets 3. Use of drugs to prevent infection; chemoprophylaxis

Malaria -Treatment • Combination therapy: Artesunate Amodiaquine Malaria -Treatment • Combination therapy: Artesunate Amodiaquine

Tuberculosis 1. Pathogen: M. tuberculosis (pulmonary TB);  M. bovis(GI TB) 2. Transmission: airborneTuberculosis 1. Pathogen: M. tuberculosis (pulmonary TB); M. bovis(GI TB) 2. Transmission: airborne droplets (NB MTB is dessication resistant and survives in dried sputum); unpasteurized milk. 3. Clinical features: prolonged coughing sometimes with bloody sputum, shortness of breath, fever, sweating , weight loss

Tuberculosis 4. No toxin production. Pathogenicty is by invasiveness that produce characteristic lesions inTuberculosis 4. No toxin production. Pathogenicty is by invasiveness that produce characteristic lesions in the lungs. 5. Epidemiology: pathogen triggers acute inflammatory response + forms tubercle – giant cells containing MTB and surrounded by epithelial cells. Tubercles heals by fibrosis and calcification. Can desseminate via bloodstream to other internal organs