Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Microbio 13-15
| Question | Answer |
|---|---|
| Microbiota/Flora | The community of microbes found within a specific environment |
| Microbiome | The collection of microbial genomes in an environment |
| Digestion of Fibre | -Herbivores rely on gut microflora for fibre digestion via microbial enzymes - Mammals can digest starch but lack enzymes to break down beta glycosidic bonds in cellulose/hemicellulose - Microbes ferment fibres anaerobically |
| Foregut Fermenters | - Ruminants - Fermentation that occurs in the rumen |
| Hindgut Fermenters | - Horses - Fermentation occurs in caecum and colon |
| Rumen Microflora Components | - Bacteria - Fungi - Bacteriophages - Protozoa - Archaea |
| Bacteria (rumen microflora) | - Largest group, including cellulotic and not cellulotic types - Mostly gram negative on forage diets - Mostly gram positive on grain diets |
| Volatile Fatty Acids (in rumen) | Cellulose -> acetate, butyrate Starch/sugar -> propionate - Lactate can be converted to VFAs |
| Archaea (in rumen) | Methanogens eliminate H2 by producing methane (eructed) |
| Fungi (in rumen) | Degrade fibre, may improve feed digestibility |
| Protozoa (in rumen) | Ciliated; consume carbs and bacteria; reduce bacterial protein availability |
| Bacteriophages (in rumen) | Infect bacteria; role in rumen not well understood |
| Effect of Diet of Rumen Microflora | - High grain diets increase fermentable starch -> more lactic acid producing bacteria - Lactate lowers pH -> requires increase in lactate utilising microbes - Grain introduction should be gradual - Fibre should always be included in diet |
| Diet and Rumen Microflora (microbial adaptation times) | Lactic Acid Producers: 2-4 hours Starch Digesters: 4-5 days Fibre Digesters: 4-6 weeks |
| Lactic Acidosis | - Sudden grain increase leading to lactic acid surge - Rumen pH drops -> microbial imbalance, systemic metabolic acidosis Clinical Signs: dehydration, diarrhoea, death |
| Fungi and Phages in Gut | - Colonise plant walls, initiate feed breakdown - Produce cellulases, hemicellulases, xylanases - May be more important in low quality diets high in fibrous material |
| Methanogens | - Archaea 2-4% of population - Remove hydrogen produced during fermentation - Increase acetate and ATP production - Decreases lactate, propionate, ethanol |
| Approaches to Disease Control | - Eliminate pathogen - Reduce exposure to pathogen - Increase animal resistance - Control or eliminate factors - Treat infected/diseased animals |
| Eliminate Pathogen (disease control) | - Eradicate from population - Ensure pathogen is not reintroduced - Quarantine policies - Ensure introduced animals are free from infection |
| Reduce Exposure to Pathogen (disease control) | - Reduce transmission from animal to animal - Isolate diseased stock - Reduce stocking rates - Segregate different classes of stock (all-in-all-out production) |
| Increase Resistance to Pathogen (disease control) | - Vaccinate - Ensure young animals receive colostrum - Ensure animals are in optimal condition - Eliminate Stressors |
| Control or Eliminate Factors (disease control) | - Control exposure to or effects of other pathogens - Reduce exposure to adverse environmental conditions |
| Treatment (disease control) | - Only an option for some diseases - Generally least effective option - Can include targeted treatment (only treat diseased animals) or metaphylactic/blanket therapy (treatment of whole group) |
| Ovine Footrot | - Disease that occurs in warm, moist conditions - Severe effect on population due to lameness - Does not cause death |
| Ovine Footrot Pathogenesis | - Maceration of interdigital cleft - Infection by F.necrophorium - Enables colonisation by D.nodosus - Destruction of horn material and inflammation - Underrunning of hoof and separation from foot - Severe pain and reduced appetite |
| Ovine Footrot Epidemiology | - Temp need to be at least 10*C - 500mm of rainfall - seasonal distribution is important - D.nodosus survives less than 1 week off sheep - Can survive throughout the year in underpin hoof - Infects sheep and goats |
| Ovine Footrot Immunity | - Merinos especially susceptible - No natural acquired immunity but natural resistance in British breeds - 9 Pilus serotypes - Can be induced by very high levels of antibody against pili that D.nodosus uses to attach |
| Ovine Footrot Control | - Eliminate D.nodosus in underrun hooves - Footbathing - Hoof trimming - Penicillin injection |
| Ovine Footrot Prevention | - Quarantine incoming sheep - treat if doubtful - Only buy from safe suppliers (avoid saleyards) - Ensure fences are secure to stop introduction of stray sheep - Be careful of transporters |
| Bovine Respiratory Disease (BRD) | - Most common in feedlots but can occur in grazing cattle - Typically occurs within first 4 weeks of being at feedlot - Signs of depression, lethargy, reluctance to move, extended head, droopy ears, eye, nose and mouth discharge, rapid shallow breathing |
| BRD Aetiology | Many pathogens involved Viruses: - Bovine herpesvirus 1 - Bovine parainfluenza 3 - many others Bacteria: - Pasteurella multocida - Mycoplasma bovis |
| BRD Epidemiology | Contributing Factors: - Stress of transport - Mixing of cattle from multiple sources - Close contact - Dust impairing the respiratory clearance mechanism Cows are exposed to everything all at once while in feedlots |
| BRD Pathogenesis | - Some bacteria involved are part of the cows normal flora so they are always present - Other bacteria survives in small numbers - Aggregation of large number of compromised animals in confined space - Compromised immune mechanisms |
| BRD consequences | - Death - Reduced weight gain - Reduced feed conversion efficiency - Compromised animal welfare and profitability |
| BRD Control | - Reduce stress and mixing of animals - Purchase direct from farm (avoid saleyards) - Limit mixing of animals from different farms - Avoid sudden changes (grouping, feed, water) once in feedlot |
| What are Antimicrobials? | Chemicals that selectively inhibit the growth or kill organisms without affecting the host eukaryote - Most effective against bacteria but there are other kinds (antifungals etc) - Most were originally derived from other microorganisms |
| Why are antimicrobials used? | - To treat disease - To prevent disease - To improve production - growth promotion (not legal now) Used in humans, domestic animals and sometimes plants |
| Inherent Resistance | - Natural resistance - Lacks a transport mechanism that the antimicrobial relies on to enter the cell - Lacks the target of an antimicrobial molecule - Innate production of enzymes that inactivate the drug |
| Intrinsic Resistance | Some bacteria lack a target for, or are impermeable to some antibiotics |
| Acquired Resistance | Bacteria that are normally susceptible become resistant to the drug |
| Transferability | Some resistance genes can readily spread from one bacteria to another, other cannot |
| Multiple Resistance | Resistance genes can be accumulated by some bacteria, generating multiple resistant organisms - Can include resistance to heavy metals and disinfectants |
| Approaches to Disease Control | - Eliminate pathogen - Reduce exposure to pathogen - Increase animal resistance - Control or eliminate factors - Treat infected/diseased animals |
| Eliminate Pathogen (disease control) | - Eradicate from population - Ensure pathogen is not reintroduced - Quarantine policies - Ensure introduced animals are free from infection |
| Reduce Exposure to Pathogen (disease control) | - Reduce transmission from animal to animal - Isolate diseased stock - Reduce stocking rates - Segregate different classes of stock (all-in-all-out production) |
| Increase Resistance to Pathogen (disease control) | - Vaccinate - Ensure young animals receive colostrum - Ensure animals are in optimal condition - Eliminate Stressors |
| Control or Eliminate Factors (disease control) | - Control exposure to or effects of other pathogens - Reduce exposure to adverse environmental conditions |
| Treatment (disease control) | - Only an option for some diseases - Generally least effective option - Can include targeted treatment (only treat diseased animals) or metaphylactic/blanket therapy (treatment of whole group) |
| Ovine Footrot | - Disease that occurs in warm, moist conditions - Severe effect on population due to lameness - Does not cause death |
| Ovine Footrot Pathogenesis | - Maceration of interdigital cleft - Infection by F.necrophorium - Enables colonisation by D.nodosus - Destruction of horn material and inflammation - Underrunning of hoof and separation from foot - Severe pain and reduced appetite |
| Ovine Footrot Epidemiology | - Temp need to be at least 10*C - 500mm of rainfall - seasonal distribution is important - D.nodosus survives less than 1 week off sheep - Can survive throughout the year in underpin hoof - Infects sheep and goats |
| Ovine Footrot Immunity | - Merinos especially susceptible - No natural acquired immunity but natural resistance in British breeds - 9 Pilus serotypes - Can be induced by very high levels of antibody against pili that D.nodosus uses to attach |
| Ovine Footrot Control | - Eliminate D.nodosus in underrun hooves - Footbathing - Hoof trimming - Penicillin injection |
| Ovine Footrot Prevention | - Quarantine incoming sheep - treat if doubtful - Only buy from safe suppliers (avoid saleyards) - Ensure fences are secure to stop introduction of stray sheep - Be careful of transporters |
| Bovine Respiratory Disease (BRD) | - Most common in feedlots but can occur in grazing cattle - Typically occurs within first 4 weeks of being at feedlot - Signs of depression, lethargy, reluctance to move, extended head, droopy ears, eye, nose and mouth discharge, rapid shallow breathing |
| BRD Aetiology | Many pathogens involved Viruses: - Bovine herpesvirus 1 - Bovine parainfluenza 3 - many others Bacteria: - Pasteurella multocida - Mycoplasma bovis |
| BRD Epidemiology | Contributing Factors: - Stress of transport - Mixing of cattle from multiple sources - Close contact - Dust impairing the respiratory clearance mechanism Cows are exposed to everything all at once while in feedlots |
| BRD Pathogenesis | - Some bacteria involved are part of the cows normal flora so they are always present - Other bacteria survives in small numbers - Aggregation of large number of compromised animals in confined space - Compromised immune mechanisms |
| BRD consequences | - Death - Reduced weight gain - Reduced feed conversion efficiency - Compromised animal welfare and profitability |
| BRD Control | - Reduce stress and mixing of animals - Purchase direct from farm (avoid saleyards) - Limit mixing of animals from different farms - Avoid sudden changes (grouping, feed, water) once in feedlot |
| What are Antimicrobials? | Chemicals that selectively inhibit the growth or kill organisms without affecting the host eukaryote - Most effective against bacteria but there are other kinds (antifungals etc) - Most were originally derived from other microorganisms |
| Why are antimicrobials used? | - To treat disease - To prevent disease - To improve production - growth promotion (not legal now) Used in humans, domestic animals and sometimes plants |
| Inherent Resistance | - Natural resistance - Lacks a transport mechanism that the antimicrobial relies on to enter the cell - Lacks the target of an antimicrobial molecule - Innate production of enzymes that inactivate the drug |
| Intrinsic Resistance | Some bacteria lack a target for, or are impermeable to some antibiotics |
| Acquired Resistance | Bacteria that are normally susceptible become resistant to the drug |
| Transferability | Some resistance genes can readily spread from one bacteria to another, other cannot |
| Multiple Resistance | Resistance genes can be accumulated by some bacteria, generating multiple resistant organisms - Can include resistance to heavy metals and disinfectants |
| Why does resistance arise? | - Absence of antibiotics - Presence of antibiotics - Removal of antibiotics |
| Absence of Antibiotics | - Do not dominate population (there is not enough antibiotic) Usually displaced eventually |
| Presence of Antibiotics | - Susceptible bacterial growth inhibited - Ecological opportunity for antimicrobial bacteria - Resistance phenotype functions as colonising factor - Resistant bacteria dominate |
| Why does resistance arise? | Exposure of bacterial populations will allow resistant bacteria to replace susceptible ones - Any use can select for resistance - More use and longer term will select for resistance - More likely if lower concentrations of the antibiotic is used |
| Responsibility for resistance | - Controlling the problem depends on understanding how resistance arises and spreads - Complex issue with complex problems - Integrated approach needed for control |
| Consequences of Resistance | - Reduced efficacy of antimicrobials - Limitations on veterinary and medical use - Food safety and environmental concerns - Animal ownership concerns |
| Critical Control Points in Antibiotic Resistance | 1. Origin of resistance genes 2. Spread of resistance genes 3. Development of multiple resistance 4. Spread of resistant bacteria 5. Selection of resistant bacteria 6. Reservoirs of resistant bacteria 7. Infection with resistant bacteria |
| Origins of Resistance | - Random mutations in the gene that reduce susceptibility - Acquisition of genes from other organisms - Acquired genes more likely to be transferrable to other bacteria |
| Spread of resistance genes | - Many resistance genes carried on mobile DNA elements - Even resistance genes not on transferrable elements can be transferred by: Transformation Transduction Conjugation |
| Transformation (in antibiotic resistance) | Importing DNA from dead bacterial cells |
| Transduction (in antibiotic resistance) | Transduction by bacterial viruses |
| Conjugation (in antibiotic resistance) | Sexual transfer |
| Development of Multiple Resistance | Mobile elements can be accumulated by bacterial cells - Results in clusters of resistance genes on chromosome, in plasmids and integrons - Clusters can be transferred as a block |
| Spread of Resistant Bacteria | -Typically travel within bacteria - Environmental: wind, water - Movement of contaminated soil, food, and water - Resistant human pathogens have most rapid and greatest dispersal (due to human movement) |
| Selection of Resistant Bacteria | - Exposure provides selective advantage to resistant bacteria - Allows resistant strains to increase and can enhance transfer to non-resistant strain - Multi-resistant strains can be selected by any of the antimicrobials they are resistant to |
| Antimicrobial Resistance Control | - Can't be stopped - only delayed - Use can be limited to delay and possibly prevent spread |
| Biosecurity (controlling resistance) | - Disemmination of resistant clones of bacteria - Transfer across both bacterial and animal species - Reservoirs in environment and other animals |
| Antimicrobial Usage (controlling resistance) | - Selection of resistance genes - Co-selection of resistance genes - Transfer across both bacterial and animal species |
| Responsible use of Antimicrobials | - Use only when necessary - Use most appropriate antimicrobial for the case - Use correct dose and only as long as needed - No justification for growth promotion use - Implement control measures to reduce need |
| What is an Antigen? | Anything that stimulates an immune response |
| Innate immunity | -Non antigen specific - No memory Includes - Physical barriers - Immune cells - Enzymes Influences adaptive immune system |
| Adaptive Immunity | Humoral (antibody-mediated) immunity B cells -> Plasma cells -> Antibody |
| Antibody Function | Prevent pathogen binding and entering cell, neutralising antibody Neutralise toxins Assist other immune cells/enzymes in killing pathogen |
| Cell mediated immunity | - T-cell mediated immunity - Cytotoxic T cells: kill infected cells, viruses |
| How does a vaccine work? | - Induces adaptive immune response - Acquired immunity - Immune memory |
| Aims of vaccination | -Prevent infection - Prevent disease - Reduce severity/duration of disease |
| Types of vaccines | -Live/attenuated -Killed/inactivated -Toxoids - Recombinant/sub-unit -Direct DNA |
| Live/attenuated vaccines | - Attenuated agent or non pathogenic strains - Less boosters (replicates in host) - Longer immunity duration - Antibody and CMI response |
| Safety issues of LAV | - Immunocompromised or pregnant animals - Reversion to virulence - Deletion mutants |
| Killed/inactivated vaccines | - Safe and successful - Antibody mediated response |
| Disadvantages of Killed/inactivated vaccines | - Reduced immunogenicity - Boosters required - Adjuvants required |
| Toxoids | - Detoxified bacterial toxins - Highly immunogenic - Circulating IgG is protective eg, tetanus and botulinum toxins |
| Non-living vaccines | Subunit vaccines - Recombinant proteins, synthetic peptide - Adjuvants |
| DIVA vaccines | Differentiate infected and vaccinated animals - marker vaccines - useful in disease eradication |
| Routes of administration | - subcutaneous or intramuscular |
| Adverse effects of vaccines | - Poor pregnancy outcomes - local site reactions - illness in immunosuppressed animals - allergic reactions - under-attenuation - neoplasia (cancer) - not common |
| Herd immunity | Not all population needs to be vaccinated/immune to limit spread of disease |
| Passive Immunity | - Passive transfer of immunity (natural) - Antitoxins (artificial) |
| Maternal Immunity | - Passive transfer in colostrum of ing in first 24-36 hours - absorbed systemically - persist in neonate circulation for week to months |
| Lactogenic immunity | Antibody in milk not taken up systemically provides local protection in suckling animals intestinal tract ceases upon weaning |
Created by:
sakelleher29
Popular Agriculture sets