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MCB 4203 Exam 1 2024/2025 COMPLETE Pathogenic Microbiology EXAM WITH ANSWERS GRADED A+, Exams of Microbiology

Florida State College at Jacksonville (FSCJ)Microbiology

A comprehensive review of key concepts in pathogenic microbiology, focusing on koch's postulates and their application in understanding disease causation. It delves into the historical development of germ theory, explores the limitations of koch's postulates, and introduces molecular koch postulates. The document also examines the role of physical barriers in host defense, particularly the skin and mucosal membranes, and discusses the mechanisms by which bacteria evade these barriers. It includes examples of specific pathogens, such as helicobacter pylori and staphylococcus epidermidis, and their interactions with the host.

Typology: Exams

2024/2025

Available from 12/16/2024

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MCB 4203 - Pathogenic Microbiology
MCB 4203 Exam 1 2024/2025 COMPLETE Pathogenic
Microbiology EXAM WITH ANSWERS GRADED A+
FSCJ
Pleomorphic theory of disease
Antoine Bechamp: microzymas ("little bodies") are fundamental building blocks of life;
can assume different forms
- in a healthy body, microzymas repair and nourish cells
- in a diseased body (i.e. acidic pH), microzymas morph to destructive bacteria, viruses
etc.
- disease is caused by poor environment/diet; can be prevented/treated by improved
air quality and nutrition
*** "germs" are the result of host disease, not the cause
Germ theory of disease
*** diseases are caused by living microorganisms
- Louis Pasteur: process of fermentation, food spoilage ("pasteurization"), and
silkworm disease were caused by the growth of microorganisms; "father of germ
theory disease"
- Friedrich Henle
Dr. Robert Koche
- improved pure-culture isolation and staining methods; animal models of disease
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Download MCB 4203 Exam 1 2024/2025 COMPLETE Pathogenic Microbiology EXAM WITH ANSWERS GRADED A+ and more Exams Microbiology in PDF only on Docsity!

MCB 4203 Exam 1 2024/2025 COMPLETE Pathogenic

Microbiology EXAM WITH ANSWERS GRADED A+

FSCJ

Pleomorphic theory of disease Antoine Bechamp: microzymas ("little bodies") are fundamental building blocks of life; can assume different forms

  • in a healthy body, microzymas repair and nourish cells
  • in a diseased body (i.e. acidic pH), microzymas morph to destructive bacteria, viruses etc.
  • disease is caused by poor environment/diet; can be prevented/treated by improved air quality and nutrition *** "germs" are the result of host disease, not the cause Germ theory of disease *** diseases are caused by living microorganisms
  • Louis Pasteur: process of fermentation, food spoilage ("pasteurization"), and silkworm disease were caused by the growth of microorganisms; "father of germ theory disease"
  • Friedrich Henle Dr. Robert Koche
  • improved pure-culture isolation and staining methods; animal models of disease
  • best known for his discovery of Mycobacterium tuberculosis Koch's 1st Postulate
  1. the microorganism should be found in all cases of the disease in question, and its distribution in the body should be in accordance with the lesions observed.
  • isolated from a dead animal Koch's 2nd Postulate
  1. the microorganism should be grown in pure culture in vitro (or outside the body of the host) for several generations and identified Koch's 3rd Postulate When such a pure culture is inoculated into susceptible animal species, the typical disease must result Koch's 4th Postulate
  2. the microorganisms must again be isolated from the lesions of such experimentally produced disease in pure culture and identified Is postulate 1 applicable to all disease-causing animals?
  • negative control: DNA from healthy uninfected tissue Immunohistochemistry
  • labeled antibodies or DNA probes (specific for the bacteria) are used to detect the presence of bacteria in tissue samples
  • +ve detection signal should be observed in diseased tissue but not healthy tissue Demonstrating the ability of isolated bacterium to cause disease in humans or animals (postulate 3)
  • can be difficult to satisfy this postulate for many pathogens
  • a "human model" of infection is usually not allowed
  • a "good" animal model may not be available (ex. H. pylori) Can the disease causing bacterium be re-isolated from intentionally infected animals? (postulate 4)
  • assuming postulates 1-3 have been met, postulate 4 demonstrates that the disease lesions of the intentionally-infected host contain the microbe Is a 5th postulate needed?
  • "information about the microbe should enable scientists to design effective therapeutic or preventative measure for eliminating the disease"
  • may provide more convincing evidence if other postulates are not "conclusive"

What are molecular Koch postulates used to demonstrate?

  • that specific bacterial gene(s) contribute to virulence Molecular Koch postulates
  1. gene (or its product) should only be found in bacterial strains that cause disease
  2. gene should be "isolated" by molecular cloning
  3. mutation/disruption of the gene should reduce virulence in vivo (or introduction of gene into avirulent strain should confer virulence)
  4. gene is expressed by bacterium in vivo during the infective process Caveats to Koch's molecular postulates
  5. not easy to demonstrate for pathogens that have an "arsenal" of virulence factors
  6. genetic manipulation of some pathogens difficult or impossible
  7. cannot be applied to polymicrobial/microbiota shift disease Molecular cloning plasmid DNA - insert new DNA (amplified from pathogen by PCR) - replicate inside bacteria - bacterial colony forms containing many copies of DNA

Skin

  • stratified squamous cells (**keratinocytes) --keratin protein --desquamation --inhospitable environment for many pathogens (low pH & low temperature)
  • hair follicles and glands --simple epithelial cells w/ potential breach areas** --protected by lysozyme, toxic lipids resident microbiota (microflora)
  • 1 gram-positive rods/cocci
  • physical, metabolic competition
  • production of toxins/growth inhibitors
  • transient and permanent colonizer are reservoirs for opportunistic pathogens** Skin (...continued)
  • physical barriers "backed up" by immune system (ex. Langerhans cell**) --process invading bacteria' activate immune cells of the Skin Associated Lymphoid Tissue (SALT)
  • breaches in skin can often lead to opportunistic infections caused by skin bacteria --cuts/abrasion, surgery

--implanted medical devices can cat as conduits to the bloodstream and provide protection from host defenses Staphylococcus epidermidis

  • gram-positive cocci; non hemolytic, coagulase negative
  • normal resident of skin microflora
  • can colonize various implanted medical devices
  • biofilm growth; produces protective EPS (exopolysaccharide) matrix
  • difficult to treat with antibiotics (genetic resistance & biofilm/EPS)
  • best treatment is prevention Defenses of the skin dry, acidic environment --prevents growth of many bacteria dead, keratinized cells --keratin is hard to degrade, and dead cells discourage colonization sloughing of surface cells --removes bacteria that adhere toxic lipids, lysozyme
  • 1 active against gram +ve bacteria
  • can also act on gram - ve bacteria if outer membrane is disrupted (detergents, bile salts) lactoferrin - binds iron; makes it unavailable to bacteria lactoperoxidase - heme-containing peroxidase antimicrobial peptides (AMPs) - highly catatonic regions enable them to insert and/or depolarize bacterial cell membranes --form channels.holes, collapse proton motive force -- ex) defensins, cathelicidins, histatins --are not functional in all body sites specialized defenses of the GI tract stomach lumen - acidic (pH ~ 2) --DNA found from 128 species of bacteria occupying the stomach --food-borne pathogens (e. coli, Salmonella) have acid-tolerance response** (pH ~ 4); ingestion with foods also provides them protection --H. pylori lives in the mucin layer (near normal pH) that covers and protects stomach lining & has the ability to protect itself from high stomach acidity long enough to reach the mucin H. pylori survival in the stomach

urease - generates ammonia from urea; localized raise in pH -- urease activity facilitates flagellar motility through the mucous layer by changing the properties of gastric mucins (gel -- viscoelastic solution) chemotaxis and cell shape --cell shape mutants have lost helical twist and/or curvature exhibit attenuated colonization --chemotaxis mutants have altered localization, including lower numbers of bacteria that are in close association with gastric epithelial cells specialized defenses of the GI tract (...continued)

  • bile salts (intestine & colon) - steroids with detergent-like properties --produced in liver, stored in gall bladder, released into GI tract via bile duct --neutralize stomach acid, aid in fat digestion --disrupt bacterial membranes
  • rapid flow of contents (intestine)
  • normal resident microbiota (not present in uterus, upper genital tract, urinary tract)
  • mucosal defense systems (MALT, GALT) --secretory IgA (apical side of epithelium) increases stickiness of mucin by attaching to mucin sugars at one end and trapping bacteria at antigen-binding ends

checks for the presence of C14 - urea

  • a tablet containing urea (a chemical made of nitrogen and a minimally radioactive carbon) is swallowed and the amount of exhaled carbon dioxide is measured -- this indicates the presence of H. pylori in the stomach H. pylori colonization lumen --> mucous layer via flagella, chemotaxis, urease, and helical shape H. pylori colonization & persistence factors
  • resistant to DNA damaging molecules produced by innate immune cells
  • constitutively expresses DNA repair proteins (RecA); lacks classic SOS response
  • natural competence up-regulated in response to DNA damage; may promote chronic persistence via enhanced deversification H. pylori colonization mucus ----> cell-associated adhesins (BabA, SabA) - shifts balance from mucus-associated --- cell-associated by interacting with epithelial cell surface

once H. pylori is cell associated, it secretes two toxins through special secretion systems which help it survive -- VacA & CagA -- elicit changes in the cell physiology meant to promote the release of iron VacA (vacuolating cytotoxin)

  • pore-forming toxin, all strains --disrupts cell polarity, promotes apoptosis of epithelial cells --inhibits T cell proliferation and effector functions --apoptosis of mononuclear cells (immune cells) ** dampening of immune response --> persistence in host **found in all H. pylori CagA (cytotoxin-associated gene A) encoded by the cag pathogenicity island --interacts with host cell signaling pathways --> altered cell polarity, proliferation, pro-inflammation --> bacterial nutrient and iron acquisition --not required for colonization --strains expressing CagA associated with increases cancer risk (bacterial oncoprotein) H. pylori morphologies
  • bacteria outnumber human cells 10:
  • smells: sweat odor and flatus are products of bacterial metabolism
  • intestinal microbiota aid in digestion & synthesize vitamins (K, B vitamins)
  • protect us from pathogen colonization (competition for food and real estate)
  • aid in development of immune system
  • disruption or elimination of normal microbiota can have pathological consequences (ex. antibiotic treatment --> yeast infection, diarrhea, etc.)
  • maintaining microbiota "health" --probiotics **do not colonize the colon --prebiotics foster the growth of "good" gut bacteria Skin staphylococcus epidermidis staphylococcus aureus
  • 1 gram positive
  • aerobic, facultative anaerobes Nasopharynx
  • S. aureus
  • S. pneumoniae
  • oral streptococci

gastrointestinal tract and rectum

  • of microbes in colon >> intestine

  • 1 anaerobic
  • reservoir for opportunistic infections
  • shift from "good" to "bad" microbiota may be responsible for diseases such as diabetes, obesity, asthma Genitalia
  • subject to hormone and nutrient flux
  • 'healthy" microbiota 1 Lactobacillus (low pH)
  • vaginosis - Gram +ve to Gram - ve shift (ex. Gardernella vaginalis) body sites normally considered sterile
  • brain-CNS
  • blood, tissues, organ systems
  • inner and middle ear
  • lower respiratory tract: larynx, trachea, bronchioles, lungs, alveoli
  • kidneys, bladder, posterior urethra
  • uterus, endometrium, fallopian tubes, cervix

16S microbial census - general strategy

  1. obtain bacterial DNA sample(s) for comparison (ex. healthy vs diseased, antibiotic vs no antibiotic)
  2. 16S PCR with CONSERVED region primers (amplifies ALL bacterial DNA present) --direct sequencing of PCR products ("Next-Gen" sequencing) --> bioinformatics analysis/species identification --16S gene clone library --> Sanger sequencing --> bioinformatics --denaturing gradient gel electrophoresis (DGGE) --> detection of population changes (no species identification) sequence PCR products directly by "massively parallel DNA sequencing" ("Next-Gen" or "high-throughput" sequencing)
  • can be quantitative
  • requires bioinformatics and statistical software to assemble reads, analyze data
  • many different technologies available --454 pyrosequencing, Illumina, Ion Torrent, PacBio, others --in general, a tradeoff between length of sequencing "read" and accuracy
  • identification of point mutations, new species, metabolic potential, etc.
  • can be adopted to transcriptome analysis ("RNAseq")
  • advances in sequencing technologies, robotics, bioinformatics methods --> reduced cost, ability to bypass need for culturing and/or molecular cloning 16S rRNA gene cloning library
  1. extract genomic DNA from samples
  2. amplify 16S rRNA genes by PCR with primers 8F and 1525R targeting the domain Bacteria
  3. combine PCR reactions starting with different amount of template and gel; purify products of correct size
  4. clone PCR products of 16S rRNA genes into the plasmid vector; transform competent E. coli cells with plasmids
  5. make clone libraries
  6. extract plasmids from transformed E. coli cells
  7. sequence plasmid inserts
  8. align library sequences with references from 16S rRNA gene database to determine phylogenic affiliations for each sequence
  9. generate phylogenetic trees using neighbor-joining and maximum-likelihood algorithms Advantages of 16S rRNA gene cloning library
  • 16S genes are large enough (1.5 kb) to contain enough sequence information for identification, but small enough to sequence by standard methods