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Medical & General Microbiology > Mid Term Revision > Flashcards

Mid Term Revision Flashcards

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Biology 101 flashcards USMLE® Step 1 flashcards
1
Q

ILOs

A
  • Have knowledge of the human microbiome project
  • Have knowledge of the normal healthy human microbiota.
  • Discuss the potential role of the human microbiota in health and impact of disappearance of some microbiota in health and disease.
  • Evidence of microbiome causality of disease
  • Potential of synthetic microbiomes in medicine
  • Potential of metabolic approaches to microbiome manipulations and therapies
  • Understand the difference between disease and infection
  • Understand what constitutes an infection
  • Be able to discuss the concept of virulence and virulence factors
  • Have an appreciation of polymicrobial diseases
  • Have an appreciation of disease mechanisms – entry, establishment, evasion, damage
  • Have an understanding of the clinical significance of the anatomy of disease causing microorganisms
  • Understand classical approaches employed in the clinical microbiology laboratory
  • Be aware of current advancements in approaches to clinical microbiology
  • Be able to describe an example of a Gram negative pathogen
  • Be able to describe an example of a Gram positive pathogen
  • Understand the concept of zoonoses and emerging infections
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2
Q

Antigenic Drift

A

Point mutations in the genes encoding the virus glycoprotein envelope

Reduces antibody binding affinity

(hemagglutinin and or neuraminidase genes)

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3
Q

Antigenic Shift

A

Genetic reassortment of genome segments between human and animal viruses. These combine to form a new subtype

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4
Q

The human gut microbiome

A
  1. protects against disease by crowding out pathogenic organisms
  2. The co evoluton hypothesis
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5
Q

What do gut microbes do?

A
  1. Immune system regulation
  2. Removal of toxins
  3. Crowd out pathogens
  4. Improve intestine function
  5. Gut-brain links in communication
  6. Important as liver- metabolites in gut
  7. Considered a vital organ
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6
Q

The Human Microbiome Project

A

Highly parallel DNA sequencers + high throughput mass spectrometers enable characterisation of whole microbial communities :

  1. genomes
  2. proteins
  3. metabolic products
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7
Q

Human Microbiome Analysis

A

16S rRNA - component of the 30S subunit (prokaryotic ribosomes)

This is a highly conserved region with variable regions - it can be used to identify and distinguish between bacteria (taxonomic groups)

OR

culture independent sequencing techniques (for less common types of organisms)

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8
Q

VBNC

A

Viable non culturable (vast majority)

Genome sequencing allows analysis

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9
Q

The core human microbiome

A

the set of genes present in the human gut

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10
Q

The variable human microbiome

A

the set of genes present in a smaller subset of humans

Variables:

  1. host genotype
  2. physiological status (including: innate and adaptive immune systems)
  3. host pathobiology (disease)
  4. host lifestyle (inc, diet)
  5. host environment
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11
Q

The gut microbiome

A
  1. The most heavily colonised organ is the GI tract
  2. Contains approx 70% of all microbes in the body
  3. Strict anaerobes predominate over facultative aerobes and anaerobes
  4. Dominated by 2 phyla: Bacteriodetes (bacteriodes) and Firmicutes (clostridium)
  5. The human gut contains 500-1000 species
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12
Q

Evidence of microbiome in disease

A
  1. Intestinal microbiota is distinct in irritable bowel syndrome - host genetics play a part
  2. Association with microbiota and obesity in mice and humans
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13
Q

Helicobacter pylori

A
  1. 1st formally recognised bacterial carcinogen
  2. 4th cause of cancer related death globally
  3. Contains a urease enzyme that converts urea to ammonia which is alkaline, neutralises some of the stomach acid around it
  4. Microaerophilic, spiral shaped, gram negative bacteria
  5. Approx 50% human population is infected
  6. Induces gastritis, peptic ulcers, gastric cancer and mucosa-associated lymphoid tissue lymphoma
  7. Susceptibility is multifactorial (environment, genes, immune status, other microbiology)
  8. Difficult to eradicate
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14
Q

Crohns Disease

A
  1. Adhesive and invasive form of ecoli (AIEC) in CD patients
  2. Intracellular invasion by AIEC is associated with active CD and intestinal pathology
  3. The receptor that facilitates AIEC binding in epithelial cells is unregulated in CD
  4. Host genetics: Defects in innate immunity (eg. mucosal barrier, autophagy, phagocytosis)
  5. Microscopically (loss of barrier, inflammatory cytokines, lesions and fibrotic scarring)
  6. Microbiota (AIEC, dysbiosis, carcinogenic microbiota)
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15
Q

Obesity related shift in microbiota

A

A shift in the relative abundance of bacteriodetes and firmicutes has been observed in obese humans - more Firmicutes

Obesity associated microbiome has more capacity for energy harvest in mammalian cells

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16
Q

Human Microbiome Project Therapeutics

A

Potential strategies for therapeutic microbiome manipulation:

  1. Antibiotics
  2. Bacteriophage
  3. Probiotics
  4. Prebiotics
  5. Synbiotics
  6. Nutritional therapy
  7. Microbiota restoration
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17
Q

Example Microbiota Therapies 1
Lactobacillus jensii

A

Vaginal commensal Lactobacillus jensenii engineered to produce antiviral protein cyanovirin-N: colonisation by recombinant bacteria inhibits host infection by SHIV in simian model

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18
Q

Example Microbiota Therapies 2

Lactococcus lactis

A

Lactococcus lactis genetically modified to produce anti inflammatory cytokine interleukin-10 (IL10): administration in mice with colitis shown to reduce inflammation during gut transit

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19
Q

Example Microbiota Therapies 3

E.coli

A

Probiotic E coli engineered to synthesise N-acyl-phosphatidylethanolamines (NAPEs): host mediated conversion of NAPEs to N-acylethanolamides (NAEs) prevents obesity in mice (through inc. satiety)

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20
Q

Metabolic Therapies

A
  • Bacterial gut metagenome produces primary and secondary metabolites
  • Secondary metabolites are called ‘specialised metabolites’
  • Specialised metabolites can produce molecules that have effects in the body, e.g. GABA produced by bacteria can have neurological effects
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21
Q

Metabolic Therapies - Lactobacillus rhamnosus

A
  • Lactobacillus rhamnosus produces GABA
  • Probiotic treatment increases GABA receptor expression in the hippocampus
  • This reduces anxiety and depression behaviours in the mouse model
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22
Q

Disease definition

A

conditions that impair normal tissue function

Disease and infection are not synonymous

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23
Q

Infection definition

A

When a pathogen invades and begins growing within a host

Disease and infection are not synonymous

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24
Q

What is a ‘true pathogen’?

A

An infectious agent that causes disease in virtually any susceptible host

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25
Q

What is an opportunistic pathogen?

A

Opportunistic pathogens are potentially infectious agents that rarely cause disease in individuals with healthy immune systems

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26
Q

Pathogenicity definition

A

The capacity of a microbe to cause damage in a (susceptible) host

It is a discontinuous variable, that is, there is or is not pathogenicity

It is a microbial variable that can only be expressed in a susceptible host: it is dependent on host variables.

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27
Q

EEMSD - pathogenicity!

A

Encounter - Entry - Multiplication - Spread - Damage

Damage:
Tissue Pathology
Loss of organ function
Growth in normally sterile sites

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28
Q

Virulence definition

A

The amount of damage a pathogen is able to cause in a host

Virulence is a continuous variable, that is, it is defined
by the amount of damage or disease that is manifest

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29
Q

Discontinous vs. Continuous variables

A

Virulence: continous variable + experimentally determined

Pathogenicity: discontinous variable + host dependent

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30
Q

How is virulence measured?

A

LD50 (lethal dose) or ID50 (infectious dose)

  • LD50: the amount of a toxic agent that is sufficient to kill 50% of a population within a certain time
  • ID50: the infective dose that will cause 50% of exposed individuals to become ill
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31
Q

What could influence the ID50 and LD50 values of a pathogen?

A
  1. route of infection - e.g. cutaneous anthrax vs. inhalation anthrax (latter is systemic - ‘cardinal’s cap’)
  2. host immune status
  3. genetic makeup of host
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32
Q

Virulence Factor definition

A

Molecules produced by bacteria, viruses, fungi, and protozoa that add to their effectiveness

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33
Q

Koch’s molecular postulates

A
  1. “The gene under investigation should be associated with pathogenic members of a genus or pathogenic strains of a species.” The gene should be found in all pathogenic strains of the genus or species but be absent from non-pathogenic strains
  2. “The gene, which causes virulence, must be expressed during infection.“
  3. “Specific inactivation of the gene(s) associated with the suspected virulence trait should lead to a measurable loss in pathogenicity or virulence.”
  4. “Reversion or allelic replacement of the mutated gene should lead to restoration of pathogenicity.”
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34
Q

Classic virulence factors

A

Toxins

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35
Q

Limitations of the virulence factor concept

A

Pathogenicity conferred by virulence factors is difficult to apply to many microbes whose pathogenicity is limited mostly to immunocompromised hosts

e.g. C. albicans and Aspergillus fumigatus

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36
Q

Biofilm definition

A

A syntrophic consortium of microorganisms

Cells stick to each other and often also to a surface

Adherent cells become embedded within a slimy extracellular matrix

Matrix is composed of extracellular polymeric substances (EPS)

In a biofilm, the physical nature of this entity protects the
bacteria

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37
Q

Requirements for disease

A

1. Point of entry

2. Establishment

3. Avoiding host defence mechanisms

4. Damaging the host

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38
Q

UTIs

A

Most common hospital infection is UTI

Normally a change in pH in urinary tract (normally acidic) causes UTI

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39
Q

Portals of entry - mucous membranes

A
  1. Mucous membranes need to be protected:
  • Washing with secretions, e.g. tears, saliva, mucous and urine
  • Filter hairs in nasal passages prevents entry of large particles.
  • Cilia in respiratory tract push mucous and microbes upward.
  1. Non-specific innate Mechanisms:
    * Mechanical Factors e.g. keratinised surface of skin (tough so acts as an

effective barrier against entry)

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40
Q

Mucous membranes

A
  • Form a protective covering that resists penetration and traps many microbes
  • are often bathed in antimicrobial secretions which contain a variety of antimicrobial substances
  • contain mucosal-associated lymphoid tissue (MALT) (part of the secondary lymphatic system)
41
Q

Antimicrobial secretions

A
  • Body fluids are not normally suitable for microbial growth due to the presence /absence of various factors (e.g. iron is not bioavailable in blood or breast milk, it is complexed in molecules (Transferrins or haemoglobin)) bacteria need iron to multiply
  • Long chains of fatty acids (e.g. oleic acid) occur in slightly acid secretion of the skin (pH 4-6) and these are lethal to many bacteria.
  • Lactenin - (nitrogenous protein) present in breast milk which are selectively bactericidal for Streptococcus pyogenes - protects against mastitis
42
Q

Antimicrobial Secretions - Lysozyme

A

Main mediator as protection against infection

  • Lysozyme hydrolyzes bond connecting sugars in peptidoglycan (cell wall)
  • Action of lysozyme is more effective on G+ve bacteria
43
Q

Antimicrobial secretions - GI tract

A

1. Stomach: ​

gastric acid

2. Intestines: ​

  • pancreatic enzymes– bile
  • intestinal enzymes, GALT (M cell patches, Peyers patch), peristalsis
  • shedding of columnar epithelial cells
  • sIgA
  • normal microbiota– Paneth cells
  • lysozyme
  • cryptins (defensins: peptides)

Genitourinary tract

  • low pH of urine and vaginal epithelia
  • urea and other toxic metabolic end products in urine hypertonic nature of kidney medulla
  • flushing with urine and mucus
44
Q

Antimicrobial Peptides - Defensins

A

Defensins:

  1. Defend from pathogens
  2. Shape Microbiota
  3. Protect stem cells
  • peptides that are open- ended, rich in arginine and cysteine, and disulfide linked
  • Found in neutrophils, intestinal Paneth cells and intestinal and respiratory epithelial cells
45
Q

Antimicrobial Peptides - Cationic

A

Cationic peptides:

  • cathelicidin produced by a variety of cells
  • neutrophils and respiratory epithelial cells
  • LL37 (leucine leucine 37 a.a.) proteolytic product of a cathelicidin (amphipathic)
46
Q

Antimicrobial Peptides - Bacteriocins

A

Bacteriocins

  1. Peptides produced by bacteria including normal microbiota
  2. Lethal to closely related species

e. g., colicins produced by E. coli
e. g., sakacins produced by lactobacilli

47
Q

Antimicrobial Peptides - Selectivity

A
  • host amphipathic antimicrobial peptides selectively bind to the differential membranes
  • host secretions are amphipathic so really good at binding to bacterial membranes (cholesterol molecule in host membrane decreases charge on the membrane, bacteriamore negatively charged as no cholesterol)
  • damage the integrity of the cell they bind to
48
Q

Establishment of Infection

Adherence Factors

A

Adherence mediation: nearly always proteins

49
Q

Adherence factors

N. meningiditis

A
  • interactions are multi-adhesion, multi-molcule
  • proteins are predominantly involved in attachment
  • through pili and pores
50
Q

Evading host defences

A
  1. Leukocidins
  • Kill white blood cells including neutrophils and macrophages!
  • Produced by Staphylococcal and Streptococcal spp.
  1. Coagulase
  • Causes fibrin clots to form in the blood of a host
  • Advantageous to the bacteria in evasion
51
Q

Damage (exotoxins)

A
  1. Neurotoxins – cause paralysis
  2. Enterotoxins – cause sickness and diarrhoea
  3. Cytotoxins – cause cell death

TB has no obvious virulence factor (toxin that causes damage in absence of the bacterial cell)

52
Q

Endotoxin: LPS

A
  1. On the surface of Gram negative bactera
  2. part of the cell
  3. Highly toxic
53
Q

Bacterial anatomy

A

Certain bacterial structures satisfy several of the requirements for infection.

  1. Structures outside the bacterial cell wall - cause the most disease
  2. The bacterial cell wall
  3. Inside the cell wall
54
Q

Bacterial anatomy: G+ve vs G-ve

A

+ve = cell wall (thick peptidoglycan) plasma membrane, stains purple

-ve = LPS, outer membrane, cell wall (thin peptidoglycan), plasma membrane

55
Q

Clinical significance of the bacterial cell wall: G+ve

A
  • Teichoic acid is being considered as a vaccine target for both S. aureus and C. difficile due to the high levels of antibiotic resistance.
  • M protein from Strep. pyogenesis highly variable but important in infection- protrudes from cell wall
  • Mycolic acid from Mycobacterium tuberculosis prevents the action of many antibiotics and host effects (‘myco’ = Greek for slimy, slimy because of mycolic acid) unique to actinomycetes
56
Q

Clinical significance of the bacterial cell wall: Gram Negative

A
  • Lipid A anchors LPS to the outer phosholipid bilayer, release of this leads to a heightened immune reaction
  • O-antigen highly variable and recognized by the immune system, can be used in typing (e.g. Ecoli 0157)
57
Q

Structures outside the cell wall: Glycocalyx

A

Polysaccharides and proteins:

loosely attached = slime layer

highly organized structure = capsule (poly-d-glutamic acid)

Capsule is important in preventing phagocytosis and allowing the infection process to continue

58
Q

Structures outside the bacterial cell wall: Fimbriae and pili

A
  • Involved in adherence
  • Shorter than flagella and typically found on Gram negative bacteria
  • Also aids in motility such as gliding or twitching motility
  • Potential vaccine candidates
  • Pili also used in immune evasion - antigenic variation.
59
Q

Structures outside the cell wall: flagella and axial filaments

A
  • Flagella protrudes far beyond the cell wall and glycocalyx.
  • Several configurations - peretrichous (all over), polar (one end), lophotricous (many at one end), amphitrichous (one at either end)
  • Aids in movement to distal tissues
  • H. pylori uses flagella to penetrate through gastric mucous
  • Axial filaments like flagella can produce a rotational movement of the whole organism. B. burgdorferi
60
Q

Structures INSIDE the bacterial cell wall

A

1. Plasma membrane
– Target for therapeutic strategies, colistin and polymyxin B

2. DNA

– Spread of antibiotic resistance on plasmids. Target of antibiotic therapy

3. Ribosomes
– Target for antibiotics

61
Q

Leading types of HCAIs

A
  1. UTIs - 34%
  2. Surgical site infections - 22%
62
Q

Why study cause of infection?

A
  1. Prognosis
  2. Treatment
  3. Isolation
  4. Care
63
Q

Patient Specimin - immunoassays

A

Rapid tests and immunoassays

  • Bacteria and fungi:
  • biochemical identification
  • Protozoa and viruses:
  • ELISA, flow cytometry, complement fixation
64
Q

Patient Specimin: Microscopy

A

Microscopy

  • Light: bacteria, fungi, protozoa
  • Electron: viruses
65
Q

Patient Specimin: Culture

A
  • Bacteria and fungi: purify and amplify
  • Viruses: cytopathology
66
Q

Patient Specimin: Biochemical Tests

A
  • Biochemical Tests
  • Bacteria and fungi: identification and sensitivity
67
Q

Patient Specimin: Molecular Testing

A

Bacteria, fungi, protozoa, viruses:

  • nucleic acid amplification, sequencing, fingerprinting
68
Q

Historical workflow

A
  1. stain-based methodologies for classification of microscopic morphology to support early diagnostic and therapeutic decisions
  2. microbial culture for propagation of the offending organism on agar or in liquid medium
  3. biochemical or antigenic techniques for the subsequent metabolic and phenotypic analysis of the microorganism, ultimately leading to microbe identification
  4. antimicrobial susceptibility testing to confirm therapeutic choices or tailor therapy
69
Q

Stains for microscopy - Gram Stain

A

Classic stain for differentiating between Gram –ve and Gram +ve bacteria

70
Q

Stains for microscopy - Acid Fast Stain

A

• Acid fast stain for tuberculosis

– Also known as the Ziehl- Neelson stain

• Advantages

  1. Specific
  2. No need for culture
  3. Performed directly on sputum
71
Q

Stains for microscopy - PAS (periodic acid-Schiff)

A

• PAS (periodic acid-Schiff)

– Stains for glycoproteins, often used for fungi

• Disadvantages

  1. High background
72
Q

Microbial culture

A

Selective media

– E.g. Mannitol salt agar, used for the isolation of Staphylococci.

Differential media

– MacConkey agar, recovery of Enterobacteriaceae.

73
Q

Biochemical techniques - Gram positive/negative

A

Flow diagrams

74
Q

Biochemical techniques: API strips

A

API strips (Analytical profile index)

  1. 20 biochemical tests simultaneously
75
Q

Biochemical techniques: Agglutination assays

A
  1. Doesn’t require culture
  2. Used frequently for detection of viral infections
  3. Conversely lack of agglutination in some assays is the measure of infection
  4. Visualise as a change in turbidity of solution
76
Q

Biochemical techniques: ELISA – Enzyme Linked ImmunoSorbent Assay

A

Direct and indirect ELISA

Capture ELISA

77
Q

Direct ELISA

A

An ELISA in which only a labelled primary antibody is used

  1. A buffered solution of the antigen to be tested for is added to each well of a microtiter plate
  2. The primary antibody with an attached (conjugated) enzyme is added, which binds specifically to the test antigen coating the well
  3. A substrate for this enzyme is then added. Often, this substrate changes color upon reaction with the enzyme
  4. The higher the concentration of the primary antibody present in the serum, the stronger the color change
78
Q

Indirect ELISA

A

An ELISA in which the antigen is bound by the primary antibody which then is detected by a labeled secondary antibody

  1. Microtitre plates are incubated with antigens
  2. Samples with antibodies are added
  3. Enzyme linked secondary antibody are added
  4. A substrate is added, and enzymes on the antibody elicit a chromogenic or fluorescent signal
79
Q

Capture (sandwich) ELISA

A

Sandwich ELISA is a less common variant of ELISA, but is highly efficient in sample antigen detection

  1. Prepare a surface to which a known quantity of capture antibody is bound.
  2. Block any nonspecific binding sites on the surface.
  3. Apply the antigen-containing sample to the plate.
  4. Wash the plate, so that unbound antigen is removed.
  5. A specific antibody is added, and binds to antigen (hence the ‘sandwich’: the Ag is stuck between two antibodies);
  6. Apply enzyme-linked secondary antibodies as detection antibodies that also bind specifically to the antibody’s Fc region (non-specific).
  7. Wash the plate, so that the unbound antibody-enzyme conjugates are removed.
  8. Apply a chemical that is converted by the enzyme into a color
80
Q

Determining antibiotic resistance/susceptibility

A

Etest strips

  • Antibiotic present at a gradient of concentrations
  • Enables quantitative analysis of plates
81
Q

Modern Clinical microbiology

A

1. Molecular methods (Nucleic acid based)

– NAATs

– NGS

2. Mass spectrometric methods

– MALDI TOF

– ESI

82
Q

Modern Clinical microbiology - Molecular Methods

(Nucleic acid based)

A

Single and multiplex PCR
– Often no need for culture
– Doesn’t detect live or dead
– Cheap!
– Sensitive
– No gold standard for comparison

– Prone to error in set up

83
Q

Next gen sequencing

A

Whole bacterial genomes

  1. Culture dependent currently – Species identification
  2. Wealth of information
  3. Becoming cheaper

Metagenomics and community profiling

  1. Culture independent
  2. Total DNA isolated from a sample for metagenomics
  3. Certain regions such as 16s r RNA sequenced in community profiling
84
Q

Mass Spec

A

• Mass spectrometric methods

– MALDI TOF

– ESI

– Cheaper than sequencing

– Reliant on databases of known patterns

85
Q

Spread and control of infection

A
  1. Clinical infection can be either be endogenous or exogenous
  2. Endogenous: Staphylococcus aureus
  3. Exogenous: Clostridium spp.
86
Q

Spread and control of infection

A
  1. Social and environmental factors
  2. Health education
  3. Food safety
  4. Vector control Chemoprophylaxis
  5. Outbreak investigation
87
Q

Gram negative pathogens: Neisseria meningitidis – beta proteobacteria

A
  1. Carriage in the nasopharynx in 10-15% of the population
  2. Epidemics occur every 10-12 years
  3. Meningitidis belt in Africa where rates of infection can be 1 in 100
  4. Classified by serogroup – reactivity to a bacterial polysaccharide capsule
88
Q

Neisseria meningitidis

A
  1. Carriage is facilitated by downregulation or loss of capsule expression, as this sterically inhibits adherence and biofilm formation.
  2. However, survival in the bloodstream and in epithelial cells is enhanced by capsule expression
  3. There are 12 serogroups of N. meningitidis that have been identified, 6 of which (A, B, C, W, X and Y) can cause epidemics.
89
Q

Gram positive pathogens: Diphtheria (Corynebacterium diphtheriae)

A
  • Disease reports from 4th century B.C.
  • Corynebacterium diphtheriae
  • Gram positive, immotile rod
  • Colonises upper respiratory tract
  • Route of infection: Airborne droplet
  • Person to person: coughs, sneezes etc
90
Q

Diptheria

A
  1. Produces exotoxin
  2. Kills surrounding host cells
  3. Toxin spreads systemically
  4. Principally affects: Heart and Lungs
  5. Main cause of mortality
91
Q

Diptheria

A
  1. Classic AB toxin - the main virulence factor
  2. Controlled by immunisation (DTaB)
  3. All babies are offered vaccination against diphtheria as part of the 5-in-1 vaccine that is given when they’re two, three and four months old
92
Q

Emerging infections

A

Emerging infections are infections that are rapidly increasing in incidence and/or geographic range

While many pathogens periodically infect humans, few become adept at transmitting or propagating themselves

Human activity, however, is making this transition increasingly easy by creating efficient pathways for pathogen transmission around the globe

93
Q

Emerging infections - criteria

A

There are several possible reasons for a pathogen to appear in the list of “new” species.

  1. Both the pathogen and the disease it causes did not occur before 1980.
  2. The disease was already recognised but the pathogen was not identified as the etiological agent before 1980.
  3. The pathogen was already recognised but had not been associated with human disease before 1980.
  4. Neither the pathogen nor the disease it causes were recognised or reported before 1980, but they did occur.
  5. What was considered to be a single pathogen before 1980 was subsequently recognised as comprising two or more species.
94
Q

Emerging infections

Not all bad news!

A

The process of disease emergence can be divided into two steps

(1) Introduction - where these “Andromeda-like” infections come from
(2) Establishment and dissemination - which is much harder for most of these agents to achieve.

The basic lesson there is that many may be called, but few are chosen

95
Q

Zoonotic diseases

A
  1. Relatively few human pathogens are known solely as human pathogens.
  2. Many more pathogens—over 800 species—are capable of infecting animal hosts other than humans
  3. Escalated need for food production to meet demand has led to the intrusion of agriculture into previously untouched areas of the native environment
  4. Climate change has resulted in disturbances in ecosystems and a re-distribution of disease reservoirs and vectors
  5. Increased globalisation and travel has increased the chance, extent and spread at which disease transmission occurs
96
Q

Zoonotic diseases - animal to human

A
  • Many zoonotic agents cause little or no signs of disease in their natural hosts, such as wild birds and bats
  • Transmission hosts might present with disease symptoms ranging from moderate (for example, pigs infected with avian influenza virus) to severe (for example, horses infected with Hendra virus)
  • The terminal or spill over host can present with severe symptoms and high mortality rates (for example, in the case of humans infected with H5N1 influenza)
97
Q

Zoonotic diseases - human to animal transmission

A
  • Research regarding zoonotic diseases often focuses on infectious diseases animals have given to humans
  • Increasing number of reports indicate that humans are transmitting pathogens to animals
  • Recent examples include MRSA
98
Q

Zoonotic diseases – Streptococcus suis

A
  • Streptococcus suis (S. suis) is a family of pathogenic Gram positive bacterial strains that represents a primary health problem in the swine industry worldwide
  • S. suis is also an emerging zoonotic pathogen that causes severe human infections clinically featuring with varied diseases/syndromes
  • such as meningitis, septicemia, and arthritis
99
Q

Streptococcus suis

A

Massive variability in genomic content between serogroup 2 strains

The Chinese serogroup 2 strain 05ZYH33 has a pathogenicity island (PAI89K)

Contains a system similar to a Type 4 secretion system which is thought to stimulate the host immune reaction observed with streptococcal toxic shock-like syndrome (STSLS)

Medical & General Microbiology (24 decks)

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