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Infectious Diseases PowerPoint Presentation

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Infectious Diseases Presentation Transcript

Slide 1 - Infectious Diseases By Andoh Wilson
Slide 2 - Infectious Disease Terms Epidemiology Epidemic Endemic Pandemic Pathogen Opportunist Nosocomial virulence
Slide 3 - Normal Micro flora & its importance Prevent the growth of pathogens Stimulate the immune system to produce antibodies that cross-react with invading pathogens Aid in digestion of cellulose in ruminants. Produce essential nutrients
Slide 4 - Koch’s Postulates The same pathogen must be present in every case of the disease; The pathogen must be isolated from the diseased host and grown in pure culture; The pathogen from the pure culture must cause the disease when it is introduced into a healthy but susceptible organism. The pathogen must be isolated from the inoculated animal and be shown to be the original organism.
Slide 5 - Modifications to Koch’s Postulates Some infectious agents cannot be cultured e.g. prions Some pathogens have non-virulent strains whose presence does not link them to a disease. E.g. non encapsulated Diplococcus pneumoniae
Slide 6 - Types of Pathogens Bacteria Gram positive Gram negative Acid-Fast e.g. Mycobacteria Spherical described as cocci Rod shaped described as bacilli
Slide 7 - Gram Positives Unique Features Thick peptidoglycan wall No periplasmic space No outer membrane (capsule) E.g. Streptococcus pyogenes, Staphylococcus aureus, Bacillus anthracis, Clostridium tetani
Slide 8 - Gram Positive wall
Slide 9 - Gram 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
Slide 10 - Gram Negative wall
Slide 11 - Types of pathogens Parasites (Eukaryotic Pathogen) Fungi e.g. Candida, Aspergillus Protozoa e.g. Plasmodium, Schistosoma Worms e.g. Ascaris, Taenia
Slide 12 - Types of pathogens Viruses Are pieces of DNA or RNA surrounded by protein coat. The may be Encapsulated e.g. HIV, HBV, measles, mumps, influenza, rabies Non-encapsulated e.g.adenoviruses, HPV, Polio
Slide 13 - Viruses
Slide 14 - Modes of transmission Direct contact e.g. touching, handshaking, or sexual intercourse Indirect contact e.g. food, water or droplets in air; Animal vectors e.g. insect bites in malaria, plague and oncho, dog bite in rabies
Slide 15 - Pathogenesis Sequence of activities Transmission of causative agent to susceptible host; Adherence of the agent to a target tissue; Colonization and invasion; Damage to host by toxins or other mechanisms; Exit from host; Survival outside host long enough for step 1 to occur.
Slide 16 - Virulent Factors For all pathogens there is an infective dose and a lethal dose. Virulent factors that confer pathogenicity include; Pili that facilitate attachment; Capsules that interfere with phagocytosis Exotoxins Endotoxins Proteases that break down antibodies Ability to vary antigens to evade antibodies
Slide 17 - Bacterial Pathogenesis Toxin production. Toxins fall into two categories; exotoxins and endotoxins. Invasiveness, where bacteria grow to large numbers locally and produce enzymes that damage host tissues.
Slide 18 - exotoxins Heat labile (60-100 degrees for 30 mins) proteins produced and released by both gram positive and gram negative bacteria. Produced by bacteria such as Clostridium (neurotoxins) and Bacillus (enterotoxin) (+) and E. coli and Vibrio (enterotoxin) (-)
Slide 19 - endotoxins Are heat stable (100 degrees for 1 hr) lipopolysaccharide produced only by gram –ve bacteria. They remain attached to cell wall. Cause fever and shock and is of lower toxicity compared to exotoxins. Produced by bacteria such as Salmonella
Slide 20 - cholera Causative Agent: Vibrio cholerae Symptoms: severe diarrhoea up to 20 liters a day of “rice water stool”, vomiting, muscle cramps caused by loss fluid and electrolytes. Pathogenesis: Vibrio adheres to the small intestinal lining, multiply and produce the enterotoxin choleragen which causes the accumulation of cAMP. An increased secretion of water and electrolyte from the cells results
Slide 21 - Cholera 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.
Slide 22 - Cholera 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
Slide 23 - malaria Causative Agent: Plasmodium (4 species) Symptoms (Clinical features): fever, chills, anaemia, headache, nausea, shivering, convulsions (esp. in under 5 yr olds) enlarged spleen. Pathogenesis: site of action of pathogen include: liver, RBC, brain. The vector, female Anopheles mosquito, transfer pathogen during feeding.
Slide 24 - malaria 4. Epidemiology: Endemic in 91 tropical and subtropical countries. Invade the liver 1st and move to reproduce in RBCs resulting in their rupture and the associated chills. 5. Incubation Period: 1 – 2 weeks. 6. Lab diagnosis: Microscopy.
Slide 25 - An Infected RBC
Slide 26 - Malaria - Prevention Reduce the number of mosquitoes; destruction of larvae and adult mosquitoes by biological and chemical control methods Avoid being bitten; protective clothing and creams, treated bed nets Use of drugs to prevent infection; chemoprophylaxis
Slide 27 - Malaria -Treatment Combination therapy: Artesunate Amodiaquine
Slide 28 - Tuberculosis Pathogen: M. tuberculosis (pulmonary TB); M. bovis(GI TB) Transmission: airborne droplets (NB MTB is dessication resistant and survives in dried sputum); unpasteurized milk. Clinical features: prolonged coughing sometimes with bloody sputum, shortness of breath, fever, sweating , weight loss
Slide 29 - Tuberculosis 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
 

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