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Bacteriology

Kelly Scott Infectious disease English 139 cards

Cards in this deck (139)

  1. 1Koch's postulates1. Must find the same pathogen in each diseased pathogen
    2. Isolate pathogen in culture
    3. Infect healthy pathogens
    4. Re-culture the same pathogen in the newly diseased animals
    Exceptions: immuno-suppressed animals
  2. 2Bacterial classificationsProtists
    Usually unicellular
    Prokaryotes
  3. 3ProtistsAll bacteria, protozoa and fungi
  4. 4Higher vs lower protistsHigher: eukaryotic
    Lower: prokaryotic
  5. 5EukaryotesHave a true nucleus
    .
  6. 6ProkaryotesNo true nucleus, condensed chromatin
  7. 7Sub-division of bacteriaGenus and species
    Morphologt
    Stain
    Oxygen requirement
    spore formation
  8. 8Typical bacteria sizeMost extra-cellular
    1-5 microns by 0.2-2 microns
  9. 9Two principle morphologiescocci - round
    (diplo, strepto, staph, and sarcinae)
    bacilli - rod like
    (coccobacilli, vibrio, spirilla, spirochete)
  10. 10Bacterial structureCell wall: shape, protection and antigens
    -rigid
    -surrounds cytoplasmic membrane
    -anchors pili, flagella and capsule
    Gram - or +
  11. 11Gram +2 layers: cell membrane and pep.
    Thick peptidoglycan with teichoic and lipoteichoic acids
  12. 12Gram -3 layers
    cell membrane
    thin peptidoglycan later
    phospholipids, lipoproteins and lipopolysaccharide layer
  13. 13Space in gram + bacteria wallperiplasmic space
  14. 14LPSNon permeable structure
    In gram - bacteria
    Actively creates transmembrane pores for transport of substances
    Has lipid A molecules - cause septic shock. Don't lyse cells for treatment, prevent replication instead
  15. 15Gram stainingMake smear
    heat fix and dry
    Stain with crystal violet
    Fix stain with iodine
    Decolourise with alcohol (removes LPS)
    Counter stain with safranin red
    Most accurate in exponential growth phase
  16. 16Gram positive stained bacteriaPurple
    retain crystal violet
    PURPLE POSITIVE
  17. 17Gram negative stained bacteriaStain pink/red
  18. 18Cytoplasmic membraneLipid bilayer between the two protein laters
    Semi permeable
    Involves in cell processes
    Involved in endospore production!
  19. 19Cytoplasmic contentsDNA haploid chromosome
    Inclusion bodies: storage
    Ribosomes: protein synthesis
    Plasmids - circular non chromosomal DNA
    (used to exchange genes)
  20. 20Additional structures on bacteriaFlagellum: increase movement
    Capsule or slime layer: allows for adhesion
    Pilus / fimbria: stick between tight junctions of cells
    Conjugation pili: movement of plasmids
  21. 21CapsulesGlycocalyx
    Slime layer attached to cell wall that is gelatinous. Comprised of polysaccharides and polypeptides
    Allows for adhesion
    Protects against phagocytosis
    Present in biofilms (such as plaque)
  22. 22FlagellaWhip like structures for locomotion
    Can visualise motility in liquid or semi-solid medium
    Can have multiple flagella
  23. 23Pili/fimbriaeFine filamentous appendages to anchor between cell junctions
    Mostly in gram negative bacteria
    Long conjugation pilli for exchange of genetic material (plasmid)
  24. 24EndosporesResistant, dormant survival form of the bacteria produced in bacillus and clostridium species
    Highly resistant to high temperatures, boiling, disinfectants and drying
    Can stay in dormant spore for ages until a suitable environment is available
  25. 25AntigensProteins: exotoxins or enzymes
    Lipopolysaccharies on cell wall
    Carbohydrates on capsules
    Used for identification and for stimulating the host immune system (vaccines)
  26. 26ExotoxinsProtein secreted from a living bacterium released on lysis and injected into cells by the bacteria
    Damage the host by destroying cells and disrupting cell metabolism.
    Highly potent and causes systemic disease
  27. 27EndotoxinsLPS in the cell wall of gram negative bacteria (Lipid A)
    Results in fever, leukopenia and DIC
    Stimulates macrophages, induces cytokines, TNF and IL-1 release
    C. tetani and C. botulinum
  28. 28EnterotoxinsHost cell dealth or damage from nacteria that bind the small intestine cells. Cause electyolyte loss and enzymes
    C. perfringens
  29. 29Hydrolytic enzymesActively destroy RBC membranes causing inflammation
    Strep pyogenes
    Staph. aureus
  30. 30Binary fissionCell elongates
    Transverse membrane formed
    New cell grows inward and nuclear material distributed
    Cell membrane constricts forming new cells or chains/clumps (partial or full cleavage)
  31. 31Bacterial growth in ideal conditionsGrowth is increase in numbers rather than size
    double every 20 minutes
    grow in liquid or semi-solid media
  32. 324 phases of bacterial growthLag: environmental suitability and prep for replication
    Log / exponential: active replication
    Stationary: equal number of cells replicating and dying
    Death: more bacteria dying then replicating
  33. 33Bacterial coloniesStart as a single organism and form a small heap of organisms
  34. 34Requirements for growthCarbon: carbs, lipids and peptides
    Nitrogen
    Growth Factors: coenzymes
    Inorganic salts: Phosphate, N, S, K, Mg, Fe, Ca
  35. 35Enrichment mediaBlood agar
    Additional growth factors have been added
    WIll grow most things
  36. 36Selective mediaDesigned to suppress the growth of some microbes and allowing others. Can add antimicrobials, salts and dyes.
    Eg. restrict gram - or gram +
  37. 37Differential mediaAllows growth of more than one microbe. Morphologically distinguishable colonies
  38. 38Physical conditions for growthOxygen required for aerobes
    Obligate anaerobes: grow only with no oxygen (gut and rumen)
    Facultative anaerobes: can grow with or without oxygen
  39. 39Temperature for growthMesophile: grow best at 25-45 degrees
    Thermophile: optimum growth between 45-70 degrees
  40. 40Methods of controlling infectionHeat (autoclaves)
    Moist cycles: can't kill capsuled organisms or spores. Use dry cycle for these.
  41. 41AntisepticNon selective chemical applied to skin or surfaces to kill micro-organisms
  42. 42Intrinsic resistanceProperty of the organism which involves chromosomal genes resulting in an impermeable cell wall or development of an alternative biochemical pathway
  43. 43Acquired resistanceOccurs after exposure to a drug and is due to a mutation in the bacterial DNA sequence or the acquisition of foreign DNA via plasmids
  44. 44Disc susceptibility testDiscs with different antibiotics and concentrations placed over plates with bacteria on them
    Antibiotic diffuses through the agar
    Measure the diameter of nil growth to measure the susceptibility
  45. 45Factors of normal skin that prevent unwanted colonisationDry
    Lactic acid produced in sweat and by normal skin flora
    Lipids, lysozymes and defensins
    Physical removal via sloughing dead keratinocytes
    Skin is normally cooler than inner body temp
  46. 46Role of normal skin floraSkin flora outcompetes pathogens and better at replicating
    Secrete chemicals against pathogens
    Stimulate the skin's immune system
  47. 47Important bacteria+: staphylococcus and streptococcus (resident)
    -: E. coli, pseudomonas (transient)
    Yeast: candida and malasezzia
  48. 48StaphylococciGram positive, In pairs or clumps
    Catalase positive
    Non motile and non spore forming
    Coagulase test correlates with pathogenicity
    Normally in skin and mucus membranes, opportunistic infections
  49. 49Staphylococci infectionsMastitis
    UTIs
    Greasy pig
    Septic arthritis
    Toxaemia due to enterotoxins: severe diarrhoea, nausea and vomiting
  50. 50Diagnosis of staphylococcus infectionSample
    Gram stain
    Catalyse test
    coagulase: positive is pathogenic
    Haemolysis of blood agar indicates a pathogenic staphylococci
  51. 51Treatment of staphylococcusMethicillin or B-lactam
    MRSA is common - needs Vancomycin
  52. 52StreptococcusColonise mucus membrane in nose and throat
    Gram positive chains
    Catalase negative
    Haemolysis in blood agar: partial, complete or non
  53. 53Streptococcus habitatsLactic - in cheese
    Viridans: resident of resp and GI tract
    Pyogenic: pathogenic
  54. 54Streptococcus infectionsMastitis
    Stangles
    Septicaemia and respiratory infection
    Meningitis
  55. 55Diagnosis of streptococcusGram stain
    Catalase negative
    Biochemical tests
    Haemolysis: indicates pathogenic
  56. 56Treatment of sreptococcusLess resistant than staph
    Use penicillin or B lactams
    Isolate sick animals
    Decontaminate the environment
  57. 57Common gram negative bacteriaSalmonella and E.coli
    Enterobacteriaceae
    Live in the gut
  58. 58Enterobacteriaceae characteristicsGram negative
    Rods,Facultative anaerobes
    Motile via flagella, Non spore forming
    +/- capsules and pili (pathogenicity traits)
    Resistant in environment susceptible to disinfectants, grow at 37 degrees
    Oxidase negative
    Ferment glucose -> acid and gas (TSI slants)
  59. 59Transmission of disease in enterobacteriaceaeIngestion of contaminated food and water
    Endogenous UTI
    Environmental - mastitis
  60. 60Selective and differential mediaMacConkey - will grow gram -ve
    Selective: inhibits gram positive
    Differential: lactose fermenters are pink and non lactose fermenters are creamy
    XLD - black colonies are salmonella
  61. 61EndotoxinsLPS (Lipid A) component of cell wall stimulates immune system and causes septic shock, DIC and fever
  62. 62EnterotoxinsCytotonic and cytotoxic
  63. 63Cytotonic enterotoxinsDo not damage cell integrity
    Secreted into the intestinal lumen and absorbed by cells resulting in severe fluid loss
  64. 64Cytotoxic enterotoxinsDamages cell and vascular endothelium resulting in oedema, haemorrhage and thrombosis
    Bloody diarrhoea
  65. 65Virulence factorsCapsules
    Attachment pilli (overcome peristalsis)
    Iron uptake systems - lyses RBCs to use iron
  66. 66Antibiotics, management and treatmentResistance from plasmids
    Use antibiotics that do not cause lysis - prevents excess release of Lipid A and shock
    Improve husbandry, reduce stress and improve immunity via colostrum and vaccines
  67. 67Host immunity to gram negative bacteriaBacteriostatic antibiotics best, allows host immune system to remove the infection
    Humoral immunity - IgA
  68. 68E. coliGram - rids
    Ferment lactose
    Pink on XLD
    Commensal in intestines and rumen
    Found in the environment and soil
    opportunistic infections from faecal contamination. Mastitis, septicaemia and UTI
  69. 69ETECTrue E.coli pathogens
    Neonatal diarrhoea - calf scours
  70. 70VTECE.coli
    Food borne disease and bloody diarrhoea
  71. 71Calf ETEC diarrhoeaCalf scours: Watery diarrhoea caused by E.coli K99, Usually in first 5 days of life
    - milk reduces stomach pH, allows establishment of bacteria in the gut
    -Immature intestinal flora
    -Enterocytes have K99 receptor when immature
    Diagnosis via ELISA or post mortem
  72. 72E.coli diagnosisGram stain
    Oxidase negative
  73. 73Treatment of calf scoursIsolation of sick animals
    Rehydration
    Appropriate antibiotics
  74. 74Prevention of calf scoursVaccinate Dams
    Ensure adequate passive transfer via colostrum
  75. 75Coliform mastitisRapid onset acute systemic illness
    Environmental cause of mastitis
    Common for indoor housed cattle
    Common during calving and drying off
    Udder swelling, watery milk and white flakes in the milk
    High fever, endotoxaemia and diarrhoea
  76. 76Diagnosis of coliform mastitisMastitis score +3
    Coliform culture from milk
    SCC
  77. 77Treatment of coliform mastitisBroad spectrum IV antibiotics
    NSAIDs
    Fluids
    Strip infected quarter
    teat seal
    Improve environment hygiene
  78. 78SalmonellaGram negative, facultative anaerobes
    Do not ferment lactose
    Motile and non spore forming
    ZOONOTIC
    Colonises the intestinal tract
    Sub-clinical animals are carriers and reservoirs of salmonella
    Persist in the environment for 9 months
  79. 79Transmission of salmonellaCalves: from other calves in poor hygiene
    Contaminated feed via rodents, birds and insects
    Humans, equipment and vehicles can introduce salmonella to animals
  80. 80Salmonella diseaseEnteritis and foul smelling watery diarrhoea. Death from dehydration
    Meningitis and polyarthritis
    Septicaemia: fever inappetence, depression and rapid death
    Abortion in pregnant animals that develop septicaemia
  81. 81DiagnosisFaecal material or tissue
    Gram stain
    Oxidase negative
    TSI
    XLD media: black colonies
  82. 82VISERTherapy control method
    Vaccination of dams
    Isolation of sick
    Stress to be reduced
    Eliminate infection sources
    Reduce exposure to faecal contamination (feed and water soures)
  83. 83Salmonella treatmentBroad spectrum antibiotics - culture and sensitivity
    Fluid therapy
    Leave calves on milk but supplement electrolytes
  84. 84VaccinationsVaccinate dams 2-4 weeks pre parturition
    Vaccinate neonates for E.coli if desperate
  85. 85Leptospira characteristicsHelical, coiled bacteria
    Gram negative but doesn't stain well
    Visualised by antibodies and fluorescence
    Aerobic, facultative and obligate anaerobes
    Complex nutrition requirements so hard to culture
  86. 86Leptospira structureInternal flagella that run the length of the organism
    Movement and coiling via contraction and relaxation of flagella
  87. 87Where are leptospira foundZoonotic: in humans and animals
    Common in pigs, cattle, sheep, horse, goats and dogs
    Maintains in host adapted environment: each lepto has a specific host and will only cause mild disease.
    Non-host adapted serovar: significant clinical disease in unintended host
  88. 88Non-host adapted acute diseaseSEVERE
    Septicaemia, organ failure, abortion, hepatitis, meningitis
  89. 89Chronic diseaseAn issue in host adapted serovars
    Abortion and stillbirth
    Acute disease symptoms not present
  90. 90Epidemiology of leptospiraEach serovar has a host-adapted maintenance host that it causes limited disease in (nephritis and fertility)
    Maintenance host transmission to accidental host causes significant, acute disease
  91. 91HardjoCattle
  92. 92PomonaPigs
  93. 93CopenhageniRats
  94. 94Lepto in dogsCopenhageni
    Accidental host, pick it up from rats
    Acute interstitial nephritis and liver damage
  95. 95Diagnosis of leptoClinical signs
    Microscopy - multiple sections
    Serology: agglutination and increasing titre across multiple samples
  96. 96TreatmentStreptomycin to clear maintenance animals and reduce lesions + clinical signs
    Penicillin in humans
  97. 97PreventionPPE!
    Reduce contact with urine
  98. 98ControlIdentify and eliminate maintenance hosts of non host adapted
    Increase herd immunity and reduce transmission of host adapted
    Good hygiene to prevent environment contamination
    Isolate infected animals and prevent mixing
    Rodent control
  99. 99Campylobacter characteristicsGram negative, helical, motile, micro-aerophilic
    Pathogenic or a commensal of the reproductive, oral and intestinal tract
    Zoonotic! common in birds
  100. 100C. jejuniChickens are a reservoir, common in companion animals who eat raw chicken
    Diarrhoea that is watery, can last 15 days and also become chronic. May also contain blood and mucus
    Also test for giardia (dogs) and toxoplasma (cats)
    May cause immunosuppression
  101. 101C. fetus fetusSheep
    Causes abortion storms in late pregnancy
    Oral transmission from pasture and water
    Also from contact with the foetus, membranes and placenta
    Can survive in the environment for 20 days
  102. 102C. fetus and infertilityCan be C. fetus fetus or C. fetus veneralis
    Bulls are the carriers and transmit via semen. Treat the bulls!!
    Established infection is most common in bulls 3-4YO
    Vagina of cows can become chronically infected over pregnancy and abort
    Will clear infection if not pregnant
  103. 103Affects on cow fertility from C fetus infectionEndometritis and late return to service
    Further fertility issues from irregular cycling and a prolonged luteal phase
    Most common in replacement heifers who are naive
    Bulls appear normal clinically and produce normal semen
  104. 104Diagnosis of Campylobacter foetusStrawberry lesions of the uterus, foetus and liver
    Excessive fluid in the peritoneum and chest of the foetus on necropsy
  105. 105Samples for diagnosis of campylobacterEnteritis - faeces
    Abortion - placenta, foetal stomach contents, liver and lung
    Infertility - semen, sheath lavage, vag mucus
  106. 106Diagnostic tests for campylobacterGram stain (negative)
    Fluorescent antibody test
    Vag mucus agglutination
  107. 107Campylobacter treatmentC. fetus: antibiotics for bulls only
    C. jejuni: self limiting in humans but treat other animals
  108. 108Campylobacter control (7)Avoid contaminated pasture
    Reduce stock density
    Remove aborted material
    Segregate affected ewes
    Hygiene to avoid transmission
    Vaccination
    Screen AI semen before use
  109. 109Clostridium characteristicsGram positive
    Obligate anaerobe
    Spore forming
    Drumstick shape
    Normally in soil, putrefaction. Disease is not contagious! Opportunistic infection
    Can be in GI tract
  110. 110Groups of clostridium sp.Histotoxic: gas gangrene
    Infection introduced to tissue, actively repliates and invades. Toxins produced. (Blackleg, malignant oedema, black disease).
    Neurotoxic and enterotoxic
    Endogenous infections, imbalance of commensal bacteria that are producing toxins: absorption via the GI tract causing illness. (Tetanus and botulinum).
  111. 111TetanusTetanospasmin is the neurotoxin, released when bacteria lyse
    Blocks inhibitory impulses and interferes with release of neurotransmitter release
    Causes muscle spasms and seizures
    "Sawhorse" presentation
  112. 112Phase 1 of clinical diseaseConstricted pupils
    Tight lips
    erect ears
    can't open jaw
    Photosensitivity
  113. 113Phase 2Same as phase 1 plus erect tail
    Sawhorse stance
    trouble swallowing
    Stiff walking
  114. 114Phase 3Same as phase 2 plus
    Muscle tremors
    Inability to walk
    Seizures
  115. 115Phase 4Bradycardia or tachycardia
    Hypertension or hypotension
    Respiratory arrest
  116. 116Risk factors cor C.tetani infectionContamination of deep, penetrating wounds like after castration or tail docking
    10-20 day incubation period (must be anaerobic - wound must heal first)
  117. 117Treatment of C.tetaniDepends on stage
    Administer antitoxin/antibodies to neutralise the toxins
    Control muscle spasms
    Large dose of antibiotics - non lysing e. doxycycline
    Vaccinate for prevention!
  118. 118C.botulinum characteristicsFoodborne but not zoonotic
    Causes irreversible flaccid paralysis
  119. 119Clinical presentation of botulism in cattleAcute: sudden death
    Sub-acute: Stiff gait, rumen atony, ataxia, dropped head, sternal recumbency, lolling tongue and salivating
  120. 120Clinical presentation of botulism in birdsTwisted necks and dropped heads
  121. 121Prevention of botulism infectionPrevent contamination of feed from dead birds or rodents
    Immunise with type specific toxoid
    Add nitrates to preserved food to prevent germination of spores
  122. 122Clostridial histologic diseasesBlack leg: C. chauvoei
    Malignant oedema: C. novyi and C sordelli
    Black disease: C. novyi type B
  123. 123Blackleg (C. Chauvoei)Acute infection causing gangrenous myositis
    Spores are ingested then in macrophages via latent infection
    Injury to muscle causes toxaemia and death
  124. 124Malignant oedemaC.novyi, C.sordelli
    Necrosis, thrombosis, bloody oedema and gas in connective tissue
    Puncture wounds resulting in oedema within hours.
    Pyrexia, inappetence, dullness, discolouration and coldness
  125. 125Black diseaseC.nobyi type B, also associated with liver fluke as it causes an anaerobic environment
    Causes necrotic hepatitis and toxaemia
    Rapid onset with depression and reluctance to move, white/yellow lesions
    Death within 48 hours
  126. 126Enterotoxic clostridial diseaseC.perfringens: Pulpy kidney and gas gangrene
  127. 127Enterotoxaemia type DPulpy kidney: Overeating disease
    C.perfringens normal in GI tract
    Sudden change in feeds imbalances gut flora causing C.perfringens to grow uncontrolled, causing toxaemia
  128. 128Presentation of enterotoxaemiaSudden death
    Pericardial effusion
    Gelatinous clots
    Autolysis of kidneys
    Haemorrhagic enteritis
    Grain in rumen
  129. 129Control of clostridial diseaseVaccination
    Prophylactic antibiotics
    Prevent contamination of wounds
  130. 130Antibiotic mechanism of actions (5)1. Inhibition of cell wall synthesis in replicating bacteria (B lactams)
    2. Disrupt cell membranes (Polymixins)
    3. Inhibit protein synthesis (Streptomycin [30s], Erythromycin [50s], Tetracycline [30s]).
    4. Inhibition of nucleic acid synthesis (Ciprofloxacin)
    5.Inhibition of metabolism - sulfonamides
  131. 131Causes for antibiotic resistanceRaised MIC compared to normal strain
    MIC too high for clinical use
    Expressing a resistance mechanism or gene
  132. 132Intrinsic resistanceInherent property of the organism, such as a cell wall impermeable to the drug
  133. 133Acquired resistanceOccurs after exposure to the drug such as mutation in DNA or acquisition of foreign DNA
  134. 134Mechanisms of antibiotic resistance (6)1. Drug alteration or inactivation
    2. Target site is insensitive
    3. Decreased drug accumulation
    4. Bypassing drug sensitive step
    5. Overproduction of target
    6. Absence of target metabolic pathway
  135. 135Beta lactam resistanceAntibiotic inactivation
    Bacteria hydrolyse the drug so it can't bind to the target
  136. 136Tetracycline resistanceDecreased accumulation of drug via Enhanced efflux: porins
    Target site insensitive due to protection proteins
  137. 137Resistance in sulfonamidesBy-passing antibiotic sensitive step
    Modified version of the enzyme binds antibiotic 1000x less well than the typical enzyme.
    Overproduction of target: hyperproduction of enzyme to overcome drug effectiveness
  138. 138Resistance to IsoniazidAbsence of metabolic pathway
    Gene lacking to produce enzyme that activates the antibiotic.
  139. 139Why is resistance an issue?Treatment failure
    Repeated or prolonged courses needed
    Use of broad spectrum drugs promotes resistance
    Expensive
    Cross infection resulting in superbugs

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Infectious disease Flashcards on Bacteriology , created by Kelly Scott on 13/07/2020.
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