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Host-Microbe Interactions Chapter 14. Disease Etiology Pathogen –Primary vs. opportunistic Virulence.

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Presentation on theme: "Host-Microbe Interactions Chapter 14. Disease Etiology Pathogen –Primary vs. opportunistic Virulence."— Presentation transcript:

1 Host-Microbe Interactions Chapter 14

2 Disease Etiology Pathogen –Primary vs. opportunistic Virulence

3 Contamination Infection vs. Infestation Pathogenesis Pathology

4 Symptoms Signs Syndrome Sequelae

5 Anatomical Barriers as Ecosystem Skin and mucous membranes are physical barriers to infection –May supply foundation for microbial ecosystem

6 Humans are usually sterile in utero Soon after birth, microbial populations begin to establish Normal microbiota –Resident flora –Transient flora

7 Isolated colonies in specific body regions Factors that influence distribution: Nutrient availability, salinity, oxygen availability, host defenses, mechanical factors Dominant type of organism may change with age and situation

8 –Normal flora play a role in defenses protection from colonization by pathogens microbial antagonism »Competitive exclusion »Bacteriocins

9 Symbiotic relationships form between microbes and host –Relationships may change depending on state of host and attributes of microbes

10 –Mutualism (++) –Intestinal bacteria –Probiotics –Commensalism (+ neutral) –Flora on skin and conjunctiva –Parasitism (+-) –Pathogens

11 –State of host resistance usually determines extent of infection primary infection secondary infection (typically opportunistic) Sub-clinical (inapparent) infection Pathogenicity

12 Distribution of pathogens –Local infection –Systemic (generalized) infection Septicemia can result from: –Bacteremia –Toxemia –Viremia

13 Many people are carriers of pathogens –Viruses; Neisseria; Salmonella; Streptococcus Why are they less affected or not at all?

14 Predisposing factors: –gender –genetic background –climate and weather –inadequate nutrition –age –habits and lifestyle –chemotherapy –emotional disturbances

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16 Characteristics of infectious disease: –communicable contagious Often reflects ID 50 –non-communicable disease

17 Etiology of Infectious Diseases Robert Koch demonstrated that specific microbes caused specific diseases –experimented with grazing animals infected with anthrax

18 Koch’s postulates –Same pathogen must be present in each case of disease –Pathogen is isolated from diseased host and grown in pure culture –Pure culture must cause disease when inoculated into healthy animal –Pathogen must be re-isolated from inoculated animal

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20 Exceptions to Koch’s postulates –some bacteria have unique culture requirements –some diseases are caused by multiple pathogens Polymicrobial diseases (mixed infections) –Ethical considerations

21 Stages of an Infectious Disease

22 Duration of a Disease –acute diseases –chronic diseases –latent disease

23 Establishment of Infection In order to cause disease pathogen must follow a series of steps –Gain entrance to host –Adherence –Colonization –Avoid Host Defenses –Cause host damage

24 Portals of entry 1. Mucus membranes Respiratory tract Gastrointestinal tract Genitourinary tract Placenta 2. Skin 3. Parenteral route Bite, puncture, injection, wound

25 Most microbes have a preferred portal of entry –Streptococci when inhaled may cause pneumonia; when ingested they do not A few microbes cause illness no matter how they enter –May cause different illness based on portal –Plague has 2 forms; bubonic and pneumonic –Anthrax has three forms

26 Adherence –Critical Step –Binding of adhesins to host receptors is highly specific

27 Virulence factors –Capsules –Incomplete phagocytosis –Fimbrae –Components of cell wall

28 Extra-cellular enzymes (exoenzymes) –Coagulases & Kinases Form or dissolve blood clots –Hyaluronidase & Collagenase Dissolve hyaluronic acid and collagen fibers –IgA proteases & Leukocidins Destroy antibodies or WBCs

29 Damage to the Host Damage often facilitates dispersal of pathogen –Diarrhea or coughing Main sources of damage: –Steal nutrients –Binding to and invading host cells –Induce hypersensitivity reactions (allergies) –Production of toxins (Toxigenicity)

30 Exotoxins –G+ bacteria Produced as part of their metabolism Secreted externally or following cell lysis Among most lethal substances –Proteins Enzymatic nature Highly soluble Heat Liable

31 –Toxoids Inactivated exotoxins Induce antitoxins that provide immunity –Antibodies against a specific toxin Passive immunity in form of antitoxin can be given as treatment

32 –Grouped into functional categories Neurotoxins Enterotoxins Cytotoxins

33 Staphylococcus aureus –enterotoxin; exofoliatin toxin; Toxic Shock Syndrome toxin Vibrio cholera –cholera enterotoxin Clostridium species –botulinum neurotoxin; tetanus neurotoxin; gangrene toxin

34 Endotoxins –G- bacteria –Released when cells die and their cell walls lyse –Lipopolysaccharide (LPS) outer membrane The lipid portion (lipid A) is toxin –Heat stable; not suitable for use as toxoids Do not cause formation of antitoxins

35 –All endotoxins produce the same symptoms Chills, fever, weakness, aches May activate blood clotting proteins May cause septic shock that can be fatal –Salmonella, Proteus, Klebsiella and Neisseria

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37 Portals of Exit Mucus membranes –Respiratory & gastrointestinal are most common Skin/wounds Biting insects Contaminated needles and syringes


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