Symbionts and Pathogens Flashcards
Symbionts colonisation of Animals
- What each partner called
- Healthy animal characteristics
- Host & microbes exist over long period of time in dynamic co-operation
- larger partner = host
- smaller partner = symbiont
- in healthy animal; internal tissues normally free of microorganisms (i.e. brain, muscle)
- body surface colonised by complex community of microorganisms
Types of Symbiosis (3)
- Commensalism: Symbiont benefits, no harm/benefit to host
- Mutualism: both host & symbiont benefit - obligatory relationship
- Parasitism: Symbionts benefit at expense of host
Benefits of symbiosis w/ bacteria
- Benefits may involve nutrient exchange b/w animal and bact. symbiont
- animals cannot syn. some a.a. & vitamins
- break down some complex molecules
- bacterial partner may add value by doing some of these things
- together both partners have advantages over single species
Bacteria in large intestine
-16S rRNA
- More than 800 bact species est. to inhabit colon - most anaerobic
- majority can’t be cultured by traditional methods
- done by extracting DNA and looking at 16S rRNA sequence variation
- is a component of prokaryote ribosomes
- is a highly conserved gene
Coevolution w/ microbiota
- Microbes often only thought of as cause of disease - actually contribute large amount to human genome
- contributes approx 8 million unique protein coding genes
(i. e. there are lots of microbes w/in us)
- contributes approx 8 million unique protein coding genes
Infectious Diseases
-What it results from
- Is the change from the state of health due to the presence of an organism of its products
- results from:
- disturbance in the balance b/w bacterial virulence and host resistance
*primary goal of microorganism is to acquire nutrients and multiply, rather than to harm the host
Bacterial action upon exposure to cell
- How cell responds
- Ways bacteria can protect themselves from host immune system
- First attach to cell surface & set up a population of organisms
- Cells respond by activating innate immune response
- pathogenic bacteria then invade superficial layer
- virulent bacterial may be protected from death by number of survival factors;
- polysaccharide capsule
- secretion of molecules that specifically inhibit the innate host response
3 Factors that determine pathogenicity of an organism
- Invasiveness or invading host tissues
- Infectivity or evading host defences
- Virulence or toxigenicity (actively damaging host cells or processes)
Number of invading microbes
- LD50
- ID50
-Virulence of a microbe or potency of its toxin is epressed as the LD50
LD50 (Lethal dose for 50% of hosts) is no. of microbes in a dose that will kill 50% of inoculated test animals
ID50 (Infectious dose for 50% of hosts): is dose required to produce a demonstrable infection in 50% of test animals
Virulence of the pathogen
- what virulence is directly related to
- 4 Variables that affect virulence
- Degree of virulence related directly to the ability of the organism to cause disease despite host resistance mechanisms
- Affected by;
1. Number of infecting bacteria
2. Route of entry into the body
3. Specific and nonspecific host defense mechanisms
4. Virulence factors of the bacterium (produced by a microorganism and cause disease)
*no. of bacteria required to cause disease changes - depends on the species
Overview of process of infection by pathogen (6 steps)
- Enter the host
- Adhere to cell surfaces
- Colonise cell surfaces
- Invade tissues
- Evade host defenses
- Produce toxins and other harmful products
Innate immunity (of host)
- What it is
- Features of it
- Is first line of defence by a mammalian host during period after initial exposure
- If invader eludes the first, non-specific line of defence, then specific immune system is triggered
- is dependent on macrophages and dendritic cells (DCs)
- these cells can sense pathogens & respond promptly by producing a variety of cytokines (cellular messengers that enhance response)
- is non-specific
- is no memory of lasting protective immunity
- majority of microorganisms destroyed w/in minutes or hours by innate defenses
Pathogen-Associated molecular patterns (PAMPs)
- what it is (characteristics of RAMPs)
- Importance in innate immune system
- Pathogens, esp. bacteria, have molecular structures that;
- are not shared w/ hosts
- shared by many related pathogens
- relatively invariant (i.e. don’t evolve rapidly)
- they are what our innate immune system recognizes
5 examples of PAMPs (pathogen-associated molecular patterns)
- Flagellin protein of bacterial flagella
- Peptidoglycan layer of gram-pos. bacteria
- Lipopolysaccharide of gram-neg. bacteria
- Double stranded RNA
- Unmethylated DNA (DNA bases in eukaryotes have methyl groups attached)
Toll - like receptors
- what it is
- where they are found
- what do they promote
- Macrophages, dendritic cells & epithelial cells have set of receptors that recognize different types of RAMPs
- Toll-like receptors = transmembrane proteins involved in detection of microbes upon infection
- activation promotes the production of pro-inflammatory cytokines and molecules of the innate immune system
Non-specific immunity;
-4 types of defensive barriers to infection
- are present all the time*
1. Anatomical
2. Physiological
3. Phagocytic
4. Inflammatory
Non-specific immunity; Anatomical Defenses
- prevent ENTRY of pathogen
- e.g. skin acts as a barrier to infection
- oil & sweat make skin surface acidic (pH 3-5)
- sweat contains enzyme lysozyme that digests bacterial cell walls
- mucosal membranes line respiratory, digestive and urogenital tracts
- saliva, tears & mucous wash away potential invaders (contain antibacterial/antiviral substances)
- Normal flora outcompetes pathogens for attachment sites & nutrients
Non-specific Immunity; Physiological defenses
-Complement system
e.g. low stomach pH, lysozyme (cleaves peptidogycan layer of bacterial cell wall), interferon (induces an antiviral state in uninfected cells), complement system (lyses microorganisms or facilitates phagocytosis)
Complement system: Group of serum proteins that circulate in an inactive state - once activated able to damage membranes of pathogenic organisms
-complement proteins form membrane attack complex (MAC) that forms hole in cell membrane
Non-specific Immunity: Phagocytic defences
-Phagocytic cells actively ingest and destroy microbes Cells that phagocytose are; -Blood monocytes -Neutrophils -Macrophages -Dendritic cells
How Bacteria survive phagocytosis
- Create antiphagocytic capsule (e.g. Haemophilus influenzae)
- iving bacteria stays w/in phagosome (contents undigested) (e.g. Mycobacerium tuberculosis)
Non-specific Immunity: Inflammatory Defenses
- Characteristics
- 3 actions of inflammation
- Inflammation characterized by redness, swelling, heat, pain & loss of function
- tissue damage caused by an injury or invading pathogen
Inflammation;
- kills invading microbes
- clears away tissue debris
- repairs injured tissue
Events of inflammation (3)
- Dilation of blood vessels: increase local blood flow & temp
- Increase permeability of capillaries: fluid accumulates which may dilute harmful substances
- Phagocytes migrate from blood to tissue: they release lytic enzymes, make a killing and produce pus
Non-specific resistance to Infectious organisms (9)
- Skin (phys & chem barrier)
- Lyzozomes (break down peptidoglycan)
- Cilia (clear organisms out of tracts)
- Gastric acidity
- Motility, flow of intestinal contents, urine, mammary secretions, respiratory secretions (reduced motility can lead to microorganism build up)
- Iron binding proteins: compete w/ bacteria for iron, which they need to grow
- Mucus - acts as physical barrier, traps organisms
- Antimicrobial peptides in gut and other sites
- Normal microflora: competitively inhibits growth of potential pathogens
Natural genetic factors that assist in resistance to infectious organisms (4)
- Species
- Breed (some breeds have developed increased resistance to organisms)
- Strain
- Individual tissue type
Natural physiological factors (7)
- Nutrition
- age (usu. young & old more susceptible)
- Physiological stress (leads to depression of immune system)
- Environmental temp
- Concurrent disease
- Pregnancy (due to hormonal effects)
- Management stress (esp. in intensive animal industries)
