Micro Final Unit 3: Cumulative

  1. The Two ways To change bacterial genomes:
    • 1. Mutations
    • 2. Genetic recombination: thru horizontal gene transfer.
  2. Mutations:
    -Types of DNA mutations:
    -Ames Test?
    Permanent changes in DNA

    • Types of DNA mutation:
    • 1. Frameshift
    • 2. Point Mutation (silent mutation or nonsense mutation)
    • 3. Missense Mutation

    • Horizontal Gene Transfer:
    • --> two types: Recombiant?
    • --> Effects?

    Bacteria can pass their genes not only to their offspring but also LATERALLY to other microbes of the SAME generation.

    -transfer involves a DONOR cell that gives a portion of its total DNA to the RECIPIENT cell (aka "recombinant"-incorporation donor's dna into its own dna)

    1. Genetic exchange:
    DNA fragment/plasmi is transferred to bacteria

    2. Genetic (homologous) recombination: DNA fragment is integrated into the chromosome

    • Some effects of Horizontal gene transfer:
    • 1. Increased ability to cause disease
    • 2. Antibiotic resistance
  3. Three types of Horizontal gene transfer?? (pg 233-239)
    1. Transformation:
    2. Conjugation:
    3. Transduction:
    1. Transformation: gain DNA "naked" dna from environment; DNA fragment/plasmid is gained

    2. Conjugation: DNA transferred from donor to recipient through pillus (straight hair-like structure)

    3. Transduction:DNA carried from donor to recipient by bacteriophage (virus)
  4. Transformation (Horizontal Gene Transfer)
    - Griffith's role?
    -Avery's role?
    Gain DNA "naked" dna from environment; DNA fragment/plasmid is gained

    --> Recipient cell is "competent" (due to alternation in cell to make it permeable to large dna molecules) when it is in a physiological state to uptake the donor DNA.

    --> Frederick Griffith 1928: Streptococcus Pneumoniae; mixed dead encapsulated bacteria (non-virulent) with live non-encapsulated bacteria and injected into mice==>died. In blood: living encapsulated bacteia!! Found out that genes of dead bacteria entered the live cells; changing them genetically to become virulent.

    --> Avery and colleagues: discovered DNA is the hereditary material in 1944 (rather than previously thought protein)
  5. Conjugation (Horizontal Gene Transfer):

    -Transferred how?
    -what kind of dna?
    -compared to transformation?
    -F Factor & E.coli
    -Rolling Circle replication
    transferred from donor to recipient through pillus (straight hair-like structure)

    -->mediated by one kind of plasmid (a circular piece of dna that replicates independently from cell's chromosome); get transmitted during conjugation.

    -->unlike Transformation: Requires direct cell-to-cell contact; AND the donor cells must carry the plasmid while the recipient cell shouldn't (opposite mating type)

    -->E.Coli & F Factor : conjugative plasmid that carries genes for sex pili and for the transfer of the plasmid to another cell.

    --> Rolling circle replication: describes a process of unidirectional nucleic acid replication that can rapidly synthesize multiple copies of circular molecules of DNA or RNA, such as plasmids, the genomes of bacteriophages, and the circular RNA genome of viroids
  6. Transduction (Horizontal Gene Transfer)
    --> generalized?
    --> specialized?
    • DNA carried from donor to recipient by bacteriophage (virus)
    • --> generalized or specific transduction
    • --> accidental; transducing particle lacks viral genetic material

    -->bacterial DNA transferred from a donor cell to a recipient cell inside a virus that infect bacteria called a bacteriophage (generalized)

    -->Specialized transduction: The process of transferring a piece of cell DNA adjacent to a prophage to another cell.
  7. Plasmids (pg 234)
    --> F Plasmid
    --> R Plasmid & two groups of genes?
    --> Transposons
    self-replicating, gene-containing circular pieces of dina; found mainly in bacteria and sme eukaryotic microbes: saccharomyces cerevisiae.

    --> F Plasmids/ F Factor: conjugative plasmid that carries genes for sex pili and for the transfer of the plasmid to another cell.

    • -->R Plasmids (resistance factors): medically significant' resistant to a different number of antibiotics; R factors carry genes that confer upon their host cell resistance to antibiotics, heavy mentals or cellular toxins.
    • -Have two groups of genes:
    • (1) Resistance transfer factor-RTF: includes genes for plasmid replication and conjugation.
    • (2) R-determinant: has resisstance genes that codes for enzyme production which inactivate certain drugs or toxin substances.

    -->Transposons: small dna segments that can move from one region of a dna molecule to another
  8. Q: An organism that acquires a plasmid does not need homologous recombination to pass the plasmid on to its daughter cells.
    What does the plasmid have that a typical fragment of DNA does not have?
    An origin of replication.
  9. Differences between transformation and conjugation?
    Transformation: DNA gained from environment; have "competent cells"-original cell is dead; fragments and plasmids

    Conjugation: DNA donated to recipients by pillus; donor cell is alive; the two cells must touch (direct contact); works with JUST plasmids.
  10. List some of the phenotypes that can be gained by bacteria when the bacteria gain new genes from other bacteria.
    Antibiotic resistance capsule (Griffith mice)
  11. How can a bacterium become antibiotic resistant? List several ways...
    Transformation OR conjugation
  12. Heat (Physical Control of Microbes):
    a. autoclave & monitoring
    b. Bacticinerator
    c. Boiling water.
    d. pasteurization: time and temp? goal?
    -Time and temp are inversely related.

    • a) autoclave: sterilize using moist heat; 121 degrees celsius at 15 Pounds Per Square Inch (PSI)==> Protein denaturing.-use for objects, some plastics, and liquids, metal objects... may corrode.
    • -steam must contact item
    • -two ways to monitor: (1) autoclave tape has strips that you put through a machine and if the strips get marked then it is sterile and (2)

    b) Bacticinerator: Incineration and flaming; loops and sterilizing trash?

    c) Boiling water: good disinfectant for drinking; not reliable way to sterilize.

    • d) Pasteurization: head liquid briefly w/ goal of killing pathogens
    • -Not sterile nor a disinfectant.
    • -30 mins at 62.9 deg C or 15 secs at 76 degs C
  13. Antimicrobial drugs
    -what are they made?
    -why effective?
    -Narrow vs. Broad Spectrum of activity: adv/disadv w/ examples
    • • Antibiotics- produced in nature
    • • Chemotherapeutic agents- synthetic, produced in lab

    • Why are antibiotics made in nature?
    • • Bacteria and fungi in soil
    • • Win competition with other microbes

    • Will an antimicrobial drug be effective?
    • -Target microbial metabolism
    • -Minimal side effects in host

    • Spectrum of activity
    • a. Narrow spectrum example: penicillin
    • -->advantage: not killing all the normal flora
    • --> disadvantage: May not be a good match for the pathogen, or possible resistance

    • b. Broad spectrum example: gentamicin (gram negative)
    • --> advantage: not sure of which bacteria causes something
    • --> disadvantage: kill all normal flora => oppurtunistic pathogenic microbes can grow
  14. Different modes of action of antimicrobial drugs:
    --> 6 ways??
    • Inhibit DNA synthesis

    • Inhibit RNA synthesis /transcription

    • Inhibit protein synthesis/ translation (drugs that act at the ribosome)

    • Inhibit cell wall synthesis ( penicillin, cephalosporins, vancomycin)

    • Inhibit enzyme--> inhibit metabolite synthesis by targeting enzymes (sulfanilamide, trimethoprim)

    • Damage cell membrane (polymyxin B)
    • 1. Beta lactam antibiotics:
    • Penicillins, Cephalosporins, Carbapenems
    • 2. Chloramphenicol-only one drug
    • 3. Aminoglycosides
    • 4. Tetracyclines
    --> what does it inhibit?
    --> three subgroups:
    1. Penicillins:
    --> discovery? Works against? Treats? Beta lactamase enzyme?
    2. Cephalosporins

    3. Carbapenems
    --> example and what it treats?
    • Inhibit peptidoglycan crosslinking in tetrapeptides *NAM & NAG*
    • --> bacteriocidal: kills the bacterium;
    • -->Includes the subgroups:
    • A) penicillins:
    • Example: penicillin (the original)- Discovered by Alexander Fleming 1928 (an accident; mixing fungi, zone of inhibition around the growing mold)
    • • Produced by Penicillium notatum (now P. chrysogenum)
    • • Worked against Staphylococcus aureus
    • • First antibiotic; Narrow spectrum
    • • Treat strep throat (Streptococcus pyogenes)
    • -Organisms make Penicillinase: A type of beta lactamase: an enzyme that works against penicillin to become resistant to it. (another broader term: beta lactamase)

    B)cephalosporins -outdated and no longer works

    C)carbapenems ex: imipenem used to treat some Gram Negative bacterial infections
  17. Antifungal drugs that target ergosterol
    --Three Groups:
    1. Polyene: ex
    2. Azole: 2 ex's
    3. Allylamine: ex
    -sterol molecule in cell membrane; damages plasmid membrane (mode of action)

    • 1.Polyene group
    • - ex: amphotericin B: Treat systemic infections; Older drug like... two systemic infections: Valley Fever and Histoplasmosis.

    • 2. Azole group
    • - clotrimazole:
    • - treat some cutaneous infections (athlete's foot, jock itch) & yeast infections
    • -fluconazole: treat systemic infections. better than ampotericin b/c less side effects

    3. Allylamine group- ex: terbinafine: treat nail infection
  18. Antibiotic resistance genes & Mechanisms
    -->Acquiring antibiotic resistance genes
    -->Antibiotic resistance mechanisms; what do reistant organisms actually do:
    -From mutations or pre-existing genes

    • -->Acquiring antibiotic resistance genes:
    • • Natural selection - increases frequency b/c the well adapted cells are surviving & reproducing vs the ones that are not well-adapted
    • • Conjugation (DNA transferred from donor to recipient through pillus (straight hair-like structure)
    • • Transformation (in a lab); only certain bacteria can do this.

    • -->Antibiotic resistance mechanisms; what do reistant organisms actually do:
    • 1. Drug inactivation (penicillinase) to become resistant; cuts ring
    • 2. Drug efflux: drug pumped out of cell
    • 3. Alteration of drug target site shape (e.g. ribosome); so bacteria still works, but the drug can no longer bind.
  19. Problems with antibiotic resistant bacteria: MRSA
    --> aquired how? where did it start? carried where?
    --> how is it treated?!
    --> staph aureus: gram wut?
    --> how to prevent?
    • -->Methicillin resistant Staphylococcus aureus
    • • Community acquired MRSA: tends to be skin infections that can spread
    • • Healthcare associated MRSA in clinics, hospitals e.g. at surgical site infection -started in hospital settings;
    • • Treated with vancomycin and maybe surgery or amputation to get rid of infection; used to be treated with penicillin group related drugs (oxacillin, methicillin,etc) but became resistant so must be treated with a non-penicillin drug
    • -->Staphylococcus aureus: gram +

    • -->Prevent transmission of MRSA skin infections:
    • • Good hygiene
    • • Don’t share towels, sports equipment, clothes
    • • Get a “spider bite” checked
    • • Cover an infected area
    • **Note: healthy carriers can have MRSA in their noses; a third of people have S. aureus
  20. VISA & VRSA
    --> how did it originate?
    VISA - vancomycin intermediate Staph.aureus & VRSA - vancomycin resistant Staphylococcus aureus;

    • **KNOW: MRSA gained additional resistance to vancomycin, looking for additional drugs OTHER than vancomysin
    • • Problems in hospitals

    So far, other drugs still work…What drugs do NOT work? pencillin groups and vancomycin..
  21. VRE-- what microbe? found where? causes?
    Vancomycin resistant enterococcus

    • Enterococcus faecalis: Gram positive coccus
    • • Intestines or female genital tract (normal flora becomes resistant to vancomycin in hospitals which then spreads to other patients)

    • Causes wound infections, UTI, blood infections in hospitals
  22. Clostridium difficile
    Gram Positive ROD; forms endospores and produces exotoxin (**can survive most antibiotics**)

    • Overgrowth due to broad spectrum antibiotic use
    • -can cause life-threatening (See nosocomial infection handout)
    • --causes endospores;
  23. Klebsiella pneumoniae
    -gram? shows up where?
    -resistant to? and what enzyme makes it resistant?
    Oct. 2010 new drug resistant bacteria:

    Gram negative bacteria, Opportunistic; show up in clinical settings

    • New strain is resistant to carbapenems (ibapenem used against gram neg; so now not many other drugs to treat)

    KPC or CRKP: Carbopenem resistant Klesiella pneumoniae

    • Has carbapenemase-makes it resistant to carbapenems
  24. Prevent the spread of antibiotic resistance in bacteria...
    • • Prevent infection
    • • Take a sample from the patient
    • • Test the microbe for antibiotic sensitivity
    • • Educate patients to take antibiotics correctly
    • • Avoid unnecessary antibiotics
  25. What is the definition of a broad spectrum antibiotic?
    Broad spectrum antibiotics are those which affect a large or broad range of gram-positive or gram-negative bacteria. It is valuable because it saves time but the main disadvantage is that it destroys a person's normal flora which allows opportunistic pathogens to grow.
  26. How is an antibiotic different from a synthetic antimicrobial drug?
    An antibiotic is a natural substance created by the microorganism in small amounts to inhibit another microorganism. But synthetic antimicrobial drugs like sulfa drugs are man-made in the lab when scientists performed a systematic survey of chemicals to look for a magic bullet against bacterial infections.
  27. Give an example of a drug that is inactivated by a Beta -lactamase?
  28. Is MRSA resistant to oxacillin?
    Methicillin-resistant Staphylococcus aureus (MRSA) have developed resistance to a wide range of penicillins, cephalosporins and other penicillinase-resistant antibiotics such as oxacillin.
  29. Name of broad spectrum antibacterial drug that is used to treat chlamydia and rickettsia infections.
  30. Five Stages of a disease:
    1. Incubation Period: no signs/symptoms; interval b/w initial infection and first appearance of symptoms; time of incubation depends on the specific microbe, it's virulence (degreee of pathogenicity) and the resistance of he host

    2. Prodromal period: mild signs/symptom; short period

    3. Period of Illness: Most severe signs/symptoms while generally the person overcomes the illness

    4. Period of decline: signs and symptoms subside; from 24 hours to a few days

    5. Period of convalescence: Body returns to prediseased state; still able to spread disease.
  31. Endemic:
    Disease always present in a population
  32. Epidemic
    Greater than expected number of cases of disease in a population in a short time.
  33. Pandemic
    Worldwide spread of disease; worldwide epidemic
  34. communicable vs. Noncommunicable diseases
    disease is passed from one host to another
  35. Signs vs. Symptoms
    • Signs: objective indications of disease
    • ex: fever, rash, hair/weight loss

    • Symptoms: Subjective indications of disease.
    • ex: pain
  36. Septicemia/Bacteremia:
    bacterial infection spread through the blood.
  37. pathogenicity:
    ability of microbe to cause disease
  38. vector:
    insect or other animal that moves pathogen from one host to another
  39. zoonosis:
    disease that a human gets from an animal
  40. Virulence:
    ability of microbe to cause severe disease
  41. Intro to nosocomial infections:
    --> aka? most common type?
    --> how does it occur?
    --> source of microbes?
    • -aka hospital acquired infections
    • -most common type: UTI's

    -->In hospitalized patients, catheters, open woulnds (trauma + surgery), needles, and breathing equipment aid microbial entry.

    -->Medical personnel/patients = sources of microbes that cause disease in vulnerable hospitalized patients; can also spread if proper infection control procedures are not followed.
  42. Escherichia coli:
    --> gram? found where?
    --> oxygen requirements?
    --> Causes?
    Gram Negative ROD; usually part of normal flora-in intestinal coliform.

    -Facultatively anaerobic

    -In community settings, can cause: UTI, nosocomial pneumonia, and wound infections
  43. Staphylococcus aureus
    --> gram? found where?
    --> oxygen requirements?
    --> Causes
    --> MRSA?
    Gram Positive COCCUS; can be carried in healthy people's noses & end up on skin

    -->Community setting can cause: Toxic Shock Syndrome, food intoxication, skin infections (boils, impedigo) can spread to other organs.

    --> MRSA: community acquired Methicillin resistant Staph. aureus; BIG problem in hospitals

    --> can cause: nosocomial pneumonia
  44. Pseudomonas aeruginosa

    --> gram?
    --> oxygen requirements?
    --> Causes ? in what kind of patients?
    --> nosocomial?
    Gram Negative Rod; strict aerobe; Resistant to many antibiotics & resistants

    **NOTE: GENTAMICIN & Quat Ammonia...

    --> Causes wound infections (especially in burn victims who are missing a skin barrier)

    --> causes pneumonia (esp. in cystic fibrosis patients-forms a biofilm in CF air passages) and immunocompromised individuals.

    --> Can cause nosocomial UTI & wound infections
  45. Clostridium difficile
    --> gram?
    --> oxygen requirements?
    --> virulence factors:
    --> Causes and life-threatening how?
    --> Hospital issues?
    Gram Positive ROD; forms endospores and produces exotoxin (**can survive most antibiotics**)

    --> grows well when normal intestinal flora is eliminated (such as antibiotics)

    --> can be a life threatening diarrheal disease

    --> Big problem in hospitals, nursing homes and a serious risk for the elderly and NOW recent cases have occurred in healthy individuals D:
  46. Acinetobacter baumanii
    --> Gram?
    --> ICU issues?
    --> treat with with what drug group??
    • Gram Negative Rod
    • -->Can contaminate respiratory equipment in ICU: respirators with saline; opening up and closing tube breaks the sterility.
    • -->Big problem for injured soldiers overseas (Iraq)
    • --> treated with carbapenem; can become resistant.
  47. Three Factors that contribute to Nosocomial infections? How?
    1. Microbes in hospital environment: will always be there (normal flora)

    2. Compromised Host: the sick patient (can't change this either)

    3. Chain of Transmission: what we CAN change; "infection control" to stop microbe from traveling from patient to patient.
  48. Infection control methods used to prevent spread of nosocomial infections:

    **BEST/MOST Important way to prevent?
    Gowns, sterilization of equipment used, hand-washing, minimize invasive procedures, use aseptic techniques and hand sanitizer

  49. The 10 Virulence Factors (list)
    --> virulence:
    Virulence: More likely to cause severe disease; degree of pathogenicity of a microbe.

    • 1. Dose
    • 2. Adhesion/attachment to host cells
    • 3. Invasion of host cells
    • 4. Biofilms
    • 5. Capsules
    • 6. Enzymes
    • 7. Antigenic variation
    • 8. Cell to Cell Transmission
    • 9. Exotoxins
    • 10. Endotoxins
  50. Dose (virulence Factor)
    --> ex: poultry juice
    • ex: Campylobacter jejuni
    • --> only a small number of microbes needed to cause disease (in poultry-drop of juice)
  51. Adhesion/Attachment to Host Cell (virulence Factor)
    --> example of microbe:
    Microbes sticking to host cells; all viruses and some bacteria

    ex: E. coli : from petting zoos, raw spinach, lettuce, and hamburgers
  52. Invasion of Host Cells (virulence Factor)

    --> example:
    • -microbe enters/invades host cells
    • -all viruses but some bacteria

    • ex: Salmonella enterica serotype Typhimurium: attach to host cell, force it to swallow a bacterial cell and eventually spreads to other organs
    • --seen in poultry, eggs, inside tomatoes and reptiles
  53. Biofilms example (Virulence Factor)
    Steptococcus mutans: forms cavities

    any group of microorganisms in which cells stick to each other on a surface. These adherent cells are frequently embedded within a self-produced matrix of extracellular polymeric substance (EPS). Biofilm EPS, which is also referred to as slime (although not everything described as slime is a biofilm), is a polymeric conglomeration generally composed of extracellular DNA, proteins, and polysaccharides.
  54. Capsule example (Virulence Factor)

    Steptococcus pneumoniae

    --The capsule is considered a virulence factor because it enhances the ability of bacteria to cause disease (e.g. prevents phagocytosis). The capsule can protect cells from engulfment by eukaryotic cells, such as macrophages.[2] A capsule-specific antibody may be required for phagocytosis to occur. Capsules also contain water which protects bacteria against desiccation.
  55. Antigenic Variation (Virulence Factor)
    Proteins on microbe surface change, and becomes unrecognizable to immune system

    ex: influenza virus, HIV
    -virulence factor?
    -Found where?
    -Serious complications?
    Listeria monocytogenes causes Listeriosis

    **VIRULENCE FACTOR: Cell to Cell Transmission**

    in macrophages, phagocytosed==> don'[t kill but instead float through cytoplasm; travels from 1 macrophage to another

    -Gram positive rod; found in soil and animal intestines; soft french cheeses, deli meats and hot dogs

    -serious consequences: meningitis, Pregnancy: miscarriage, fetal brain damage, and fetal meningitis
  57. Exotoxins vs. Endotoxins (Virulence Factor)
    Exotoxins: are secreted proteins into the bloodstream, mostly gram positive; HIGHLY TOXIC; gets into bloodstream and causes effect at specific sites in the body.

    ex: Clostridium botulinum, Clostridium tetani, and Staph aureus

    • ENDOTOXINS: Lipid A portion of LPS (in cell wall of gram negative cells); weakly toxic; causes endotoxic shock--if microbes die and exotoxins released so person goes into shock D:
    • --> ex: any lysed gram negative organism
  58. Botulism
    -caused by? gram? found?
    - signs/symptoms?
    -how is it destroyed?
    -Infant botullism vs adult?
    Caused by: Clostridium botulinum (gram positive ROD;found in soil)

    • -exotoxin causes flaccid paralysis (flabby muscles); can be destroyed by heat (can of beans, cooking)
    • -Improperly canned foods (anaerobic conditions)
    • -Infant botulism: caused by ingesting endospores from honey and soil;
    • adults get botulism by ingestion of exotoxins --> blurry vision, difficulty swallowing and breathing
    • -Treatment: antitoxin and supportive care.
  59. Tetanus:
    -caused by? oxygen req, gram? found where?
    -signs and symptoms?
    Clostridium tentani: obligately anaerobic, endospore-forming, gram positive rod, common in soil contaminated with animial fecies.

    -exotoxin prevents muscle relaxation; constant contracted muscles

    -endospores enter wounds

    -->symptoms: lock jaw, muscle stiffness/spasms

    --> Treatments: antibiotic, antitoxin, and muscle relaxant. "Tetanus Toxoid Vaccine-TDaP"
  60. Staphylococcus aureus
    --> virulence factors? how is it produced?
    --> what growth conditions?
    • -exotoxin causes signs/symptoms of foodborne illness; we contaminate the food by cooking food high in protein...; good growth conditions: on a picnic table
    • --> food intoxication

  61. Meningitis
    --> Microbes for fungus, virus?
    --> signs/ symptoms: <2 years and >2 yrs?
    --> Diagnosis?
    --> Three major bacterial causes of meningitis:
    • Inflammation of the meninges (the membranes that surround the brain), occurs when a microbe enters the CSF from the blood.
    • **note: acute disease, communicable, not local infection

    • -->Microbes: Fungus (cryptococcus neoformans), viruses (west nile) and bacteria..
    • --> Signs/Symptoms: Under 2 yrs: inactivity, irritability, vomiting, maybe skin rash. Over 2 years: fever, stiff neck, headache, possible vomitting and nausea

    --> Diagnosis: detection of microbe from CSF or serum.

    • Three major bacterial causes of meningitis:
    • 1. Streptococcus pneumoniae:
    • 2. Haemophilus influenzae type b:
    • 3. Neisseria meningitidis:
  62. Three major bacterial causes of meningitis:
    1. Streptococcus pneumoniae:
    2. Haemophilus influenzae type b:
    3. Neisseria meningitidis:

    **Characteristics of Bacterial meningitis:
    1. Streptococcus pneumoniae: Gram positive diplococcus; also causes pneumonia.

    • --> vaccines:
    • -Younger than 2 yrs:polysaccharide vaccine(PPSV)
    • -pneumococcal conjugated vaccine (PCV12): children <5 yrs

    • 2. Haemophilus influenzae type b: aerobic, gram negative rod.
    • --> vaccines: conjugated vaccine (<5 yrs); polysaccharide + protein

    • 3. Neisseria meningitidis: gram negative diplococcus (aka meningococcus)
    • --> vaccines: effective against 4 out of 5 strains, can't be used in children <2 yrs; "MCV4" (conjugated), "MPSV4" (polysaccharide vaccine)
    • --> other signs: low blow pressure, rash ("meningococcemia": when bacteria enter blood stream)

    • **Characteristics of Bacterial meningitis: Has a capsule, transmitted by respiratory secretions, found in noses/throats of seemingly healthy carriers, college dorm students/young children/military are mostly at risk, and it's a life threatening disease.
    • --> Treatment: usually antibiotics
  63. Anthrax (Basics)
    --> Microbe info: gram, virulence factors, oxygen?
    --> affected animals?
    --> prevent?
    --> four types of human anthrax:
    --> diagnosis and treatments?
    --> vaccines
    • Microbe: Bacillus anthracis
    • --> endospore forming, gram postive rod, found in soil, non-motile & aerobic, has capsule and exotoxins (virulence factors); obligate parasite.
    • --> affected animals: sheep, cattle, goats.
    • --> Signs/symptoms: "sudden death"
    • --> Prevent: annual vaccination boosters.

    • 1. Cutaneous skin: skin contact w/ endospores; 95% of anthrax cases in people, can get into bloodstream; treatable w/ antibiotics
    • 2. Gastrointestinal: by ingesting endospores in meat; nausea, vomiting, fever, bloody diahhrea, collapse/death; 80% mortality for untreated cases.
    • 3. Injectional: by injected drugs; fatal
    • 4. Pulmonary: inhaling endospores; flu-like symptoms; sudden shock/death (MOST DANGEROUS FORM) and bacteria can enter bloodstream

    --> Diagnosis: gram stain, PCR: detect bacteria in blood/skin/resp secretions

    --> Treatments: Doxycycline (tetra) or Ciprofloxacin (fluoroquinolone); must be started in beginning stages of disease.

    **Vaccines: attenuated (weakened) B. anthracis (animals), AVA-Anthrax vaccine absorbed (humans that work w/ animals since they can get spores from them.)
  64. Schistosoma mansoni EGG
    --worm type/phylum
    --life cycle
    • Image Upload 1
    • Flatworm (Phylum Platyhelminthes)--Blood FLUKE (Termatodes)
    • -causes schistosomiasis

    -Life cycle: Ova in stool/urine --> larvae (miracidia) reach water--> infect snails (intermediate host) & develop into cercariae--> infects humans in water (definitive host; site of parasite reproduction; travels to intestines thru blood vessels)

    --signs/symptoms: itchy skins, fever, rash, no death
  65. Taenia Pistiformis scolex
    -worm type/ phylum?
    -lifecycle: intermediate and definitive host?
    Image Upload 2

    • Flatworm (Phylum Platyhelminthes)
    • Tapeworm/Cestodes--> causes taeniasis

    • Body parts:
    • 1. Scolex: head w/ suckers
    • 2. Proglottids: tapeworm sections (egg production)
    • 3. cuticle: covering; absorb nutrients
    • 4. Hermaphroditic...

    • Live in human's small intestines (definitive host) & mate; eggs released into feces--> pigs/cows (enter larval stage; cysts found in muscle)--> undercooked meat infects ppl.
  66. Trichinella spiralis
    -worm type/phylum
    -Life cycle
    -Diagnosis & Prevention
    • Image Upload 3
    • -Cause trichinosis

    • Human eats larvae in uncooked meat; grow into adult worm,mate, produce larvae--> encyst in human muscle (now rare in us)

    Diagnosis: serology (look for antibodies; past resistance) & muscle biopsy

    Prevent: cook meat well, avoid pork..
  67. Enterobius vermicularis egg
    -worm type/phylum
    -Life cycle
    -Diagnosis & Prevention
    • Image Upload 4
    • -causes: enterobiasis; world wide disease

    • Life Cycle:
    • eggs layed in anal area-> fingers -> ingested & hatch in small intestine & adult worms infect large intestine (living there for 2 months)
    • **doesn't need intermediate host**

    • Diagnose: sticky clear tape to collect eggs
    • -drug treatment
    • Prevent: good hygiene/sanitation
  68. Enterobius vermicularis Adult Worm

    -worm type/phylum
    -Life cycle
    -Diagnosis & Prevention
    • Image Upload 5
    • -causes: enterobiasis; world wide disease

    • Life Cycle:
    • eggs layed in anal area-> fingers -> ingested & hatch in small intestine & adult worms infect large intestine (living there for 2 months)
    • **doesn't need intermediate host**

    Diagnose: sticky clear tape to collect eggs-drug treatment

    Prevent: good hygiene/sanitation
  69. Staphylococcus epidermidis
    • -Gram positive
    • -Facultative anaerobic; on human skin
    • -white..

    Image Upload 6
  70. Staphylococcus aureus
    • -coagulase: causes plaasma to clot (coagulae test)
    • -found on noses, yellow
    • -causes common infections: skin, toxic shock, and pneumonia
    • -enterotoxin (exotoxin): causes food poisioning
    • -MRSA

    Image Upload 7
  71. Streptococci:
    • gram positive; forms in chains; mouth/throat;
    • --lacks catalase
    • -strict or facultative anaerobes
    • -grouped by hemolysis or lancefield groups (based on detecting carb antigents thru serological methods)
    • a. Streptococcus pyogenes:
    • b. Streptococcus pneumonia:
  72. Streptococcus pyogenes:
    -aka "Group A Strep" or "beta hemolytic strep"

    • -causes mild infections: ear, impetigo, pharyngitis (strep throat--> scarlet fever)
    • -can be carriers; in throat
    • -Invasive GAS: necrotiziing fascitis ("flesh eating bacteria") and strep toxic shock.
    • -Diagnosis: agglutination test

    • --> Related infections:
    • 1. strep throat: fever, painful sore throate, swollen lymph nodes
    • 2. scarlet fever: rash, red/strawberry tongue
    • 3.Rheumatic fever: immune response against strep==> damage heart valves; multiple rounds of strep
    • 4. necrotizing fasciitis: rapid destruction; need skin grafts
    • 5. Strep toxic shock: drop in blood pressure/organ failure
  73. Streptococcus pneumonia:
    • -aka pneumococcus;
    • major cause of pneumonia and bacterial meningitis
    • -virulence: uses capsule
  74. Streptococcus LAB:
    -blood agar...what kind of mediums?
    -alpha vs. beta?
    • -blood agar: TSA + RBC
    • -enrichment medium: good for "picky organisms"
    • -differential medium: different microbes appear on diff mediums
    • -throat swab and use for first streak on an isolation plate

    • --> observations around colonies...
    • a. Alpha: greenish brown; partial lysing of RBC; strep pneumonia and strep mutans

    b. beta: clear areas; complete lysing, strep pyogenes & staph aureus

    Image Upload 8
  75. Ascaris lumbricoides
    -giant roundworm of humans, belonging to the phylum Nematoda. An ascarid nematode, it is responsible for the disease ascariasis in humans

    -There they break into the alveoli and pass up the trachea where they are coughed up and swallowed. The larvae pass through the stomach for a second time into the intestine where they mature into adult worms. They maintain their position by swimming against the intestinal flow caused by peristalsis.
Card Set
Micro Final Unit 3: Cumulative
Micro Final Unit 3: Cumulative