Finals Flashcards

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1
Q

Pathogen, pathogenicity and virulence; determination of virulence

A

A pathogen is a microorganism (or virus) that is able to produce disease.
Pathogenicity is the ability of a microorganism to cause disease in a host organism.
Virulence is the degree of pathogenicity.
Dont forget the relationship of the host (degree of resistance to virulence factors) and the pathogen, which is dynamic.

Determination of virulence depends on the virulence factors of the pathogen: genetics, biochemical, or structures which enable it to produce a disease

Determination: lethal dose 50 or 90, meaning the dose/number it takes to kill 50 or 90% of the test subjects.

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2
Q

List up some virulence factors

A

Some virulence factors:
Capsule (K-antigene, anti-phagocytic: polysaccaride, poly-D-glutamate, hyaluronic acid)
Exotoxins
Pili ( adherance)
Flagella (H-antigene: movement)
O antigens (LPL)
Enzymes (coagulase, urease, IgA protease, M-protein (inhibit opsonization), protein A (binds to Fc-portion on Ig) ++)

Some special enzymes:

1: streptolysin O and hemolysin, these damage neutrophils and RBS, respectively, preventing destruction of the pathogen. This is common for S. pyogenes.
2: Leukocidin damage neutrophils. Common for staphylococci.

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3
Q

Define infection

A

inflammatory response to the presence of or invasion of normally sterile host tissue by microorganisms.

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4
Q

Molecular masking: what is it and give examples

A

Hide itself from phagocytes/immune system. Can do this by;

1: Coagulase on S. aureus coat itself with fibrin + protein A which binds to Fc portion on Ig.
2: Hyaluronic acid capsule in S. pyogenes
3: Treponema Pallidum binds fibronectin

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5
Q

Which organism have a capsule? What is its importance? which bacteria produces biofilms?

A

K-antigene

Importance:

1: prevent the phagocytosis of phagocytes
2: can be used as antigenes in vaccines
3: Quelling reaction or capsular swelling test
4: Latex agglutination + ELISA
5: Meningitis!

A common mnemonic used to remember some encapsulated pathogens is:

“Even Some Super Killers Have Pretty Nice Big Capsules”

Escherichia coli
Streptococcus pneumoniae
Salmonella
Klebsiella pneumoniae
Haemophilus influenzae
Pseudomonas aeruginosa
Neisseria meningitidis
Bacteroides fragilis
Cryptococcus neoformans (yeast)
Other encapsulated bacterias include:
Bacillus anthracis (poly-D-glutamate)
Streptococcus agalactiae
Streptococcus pyogenes (hyaloronic acid)
Staphylococcus epidermidis (not sure if it does have a real capsule, but makes a slime layer/biofilm)
Biofilms
Strep mutans (dental plaques!) + Staph. epidermidis (catheters!)
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6
Q

Some bacteria are resistant to phagolysosome fusion or inhibit this formation: what are common for them and name some bacterias

A

This is common for intracellular bacterias: typical with granuloma formation!

Inhibit formation: Salmonella, M. tuberculosis, Legionella, Chlamydia

Can survive in phagolysosome: bacillus anthracis, M. tuberculosis, S. aureus

Rickettsia produces phospholipases that lyses the phagosomes and by doing this can escape the phagosomes.

Listeria escape before fusion

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7
Q

Structure of the peptidoglycan layer, function, what attaches to it, and what antibiotics act on its synthesis?

Some differences between gram + and - ?

A

Cell walls are present in most prokaryotes (except mycoplasma bacteria)

The sugar component consists of alternating residues of β-(1,4) linked NAG and NAM . Attached to the N-acetylmuramic acid is a peptide chain of three to five amino acids. The peptide chain can be cross-linked to the peptide chain of another strand forming the 3D mesh-like layer. The amount and type of peptide varies: in e.g. E.coli -> L-alanine, D-glutamate, DAP, and D-alanine

NAG: N-acetylglucosamine
NAM: N-acetylmuramic acid
Transpeptidase: inhibited by penicillin, cephalosporin.
Please note that the enzyme lysozyme act on this peptidoglycan layer

Function: maintein shape and prevent osmotic lysis

Fimbria, pilli and flagella can bind to the cell wall
Cell wall is also important for bacteriphages at they attach to it.

Gram +: much thicker. Contain teichoic acid (provide rigidity to the cell-wal)
Gram - : much thinner. They have a prominent periplasmic space in between the cytosolic membrane and the cell wall

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8
Q

Lipopolysaccharide: what is it, structure, where is it found, what function does it have? Does all bacteria have the same LPS?

A

LPS or endotoxin. Found on gram negative bacteria.

Consist of: Lipid A (endotoxin part), core polysaccaride, and an outer O-spesific polysaccharide (O-antigen)

LPS can:

1: activate macrophages
2: cause IL-1, TNFa, and IL-6 release
3: induce fever and shock
4: DIC (coagulation)
5: endothelial dysfunction

The outer O-antigen can differ. In neisseria meningitidis and H. influenzae this O-antigen is relative short (lipoologisaccharides). To be noted, these two bacterias can bind sialic acid to its LPS and by doing so makes it much more difficult for MAC complexes to lyse this bacterias

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9
Q

What ribosomal units does bacteria have and which antibiotics can act on it?

A

Prokaryotes have 30s + 50s forming 70s.

50s: macolides, chloramphenicols
30s: aminoglycosides, tetracyclins

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10
Q

What are the difference between pilli, fimbria and flagella?

A

Pili and fimbriae are cell surface appendages present in bacteria other than flagella. These are not for locomotion, which is the major function of flagella (flagellin proteins)

Flagella (H-antigen): one or several, and axial or terminal. Spirochetes have several axial flagellas. E.coli and Proteus mirabilis have flagella; important in UTI

There are som key differences between pili and fimbriae: Often, fimbriae are referred to as “common pili” involved in attachement, while pili are known as “sex-pili” which stabilizes mating bacteria durind DNA transfer by conjugation.

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11
Q

What are spores and what is is good for?

A

“Rest, and wait for better times”

Spores are highly resistant structures formed in response to adverse conditions, Bacillus and clostridium; both are gram positive spore forming bacterias.

Sporulation occurs when nutrients are depleted or the environment in general in not suitable. Spores form inside the cell.

Contains DNA, small amount of cytoplasm, cell membrane, peptidoglycan, very little water, and a thick keratinlike coat. The spore have no metabolic activity which allow it to remain dormant for years

Sporulate when the environment is good

Medical importance: highly resistant to heat, and chemicals. Can survive for years.

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12
Q

Bacterial genetics

A

DNA in the form on nucleotide. Only one chromosome. Haploid.
Plasmin: extrachromosomal DNA.

Methods of gene transfer
Transformation: Uptake of naked DNA from the environment by competent cells. Cells become competent under certain physiological conditions. DNA is taken up. DNA is linear HR (exchange of DNA). Need RecA

Conjugation (”bacterial mating”): Gene transfer from one bacteria to another involving direct cell-cell contact. Fertility factor control conjugation; Sex pili (genes of F) establish cell-cell contact. A single strand of donor DNA (male; have the F-factor) is transferred to recipient (female). Bacterial genes transferred by conjugation have to be stabilized by HR. Plasmid genes are stable without HR. Conjugation with recombination may produce new genetic combinations. All the recipient becomme F+ after conjugation with plasmids; does not become F+ with Hfr chromosome conjugation (use HR; exchange)!
Males: F+
Females: F-

Transduction: transfer of bacterial DNA by a phage vector. Phage picks up DNA through an error in phage production. Generalized and specialized types:
Generalized: Phage puts a piece of bacterial DNA into its head, and all genes have an equal chance of being transduced. “Phage mistake when packing”. Can occur in lytic and temperate infections.
Specialized: Dependent on integration of phage DNA into the bacterial chromosome at a specific site, and an excision error allows bacterial DNA to be excised and packaged with phage DNA. Only temperate phages (depend on excision errors)

Some information of Phage: bacterial viruses. Can be virulent, meaning it infects bacterial cells resulting in bacterial cell lysis, or temperate: often infects bacterial cells without lysing the cells. Integrates phage DNA into bacterium. Can also replicate lytically.

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13
Q

Mechanism of antibiotic resistance

A

Drug resistance
Intrinsic, plasmid or chromosomal.
Intrinsic: e.g. mycoplasma is resistant to penicillin as it does not have a cell wall.
Chromosomal-mediated: resistance located on bacterial chromosome. Most common modification of drug receptor so that the drug can no longer bind (PBP: MRSA). Transporters/pumps.
Plasmid-mediated: resistance located on the plasmid. R-factor (carry genes for drug resistance). One section of DNA mediated conjugation (F+), other section carries genes for drug resistance. Plasmid-mediated resistance is created by variety of mechanism, but often genes coding for enzymes that modify the drug (e.g. B-lactamase). One plasmid can code for several drug resistances

How do multiple drug resistance plasmids arise? Via gene cassettes/intergrons/transposons: mobile genetic elements that can move themselves or a copy from one molecule of DNA to another (jumping genes). Found in eukaryotes, bacteria and viruses. Have indirect repeats on each end. Carry transposase enzyme create mutation with their insertions. Insertion produces direct repeats on either side of the mobile segment.

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14
Q

Sterilization: what is it, and give some methods

A

Sterilization = the process of killing or removal of all microorganism in a preparation (including bacterial spores)

Sterile = treated objects are free of all living organisms

Methods

1: Physical methods - heat (dry* or moist**), gamma-radiation. Flames
2: Chemical methods - ethylene oxide, plasma (H2O2; in vacum -> ROS)
3: Membrane filtration - used for temperature-sensitive fluids. Viruses can pass :( variable pore size

  • Dry heat: 3h with 140, 2 hour with 160, or 1 h with 180 degrees.
    • Moist - Autoclave: 121 at 1 atm for 30 min or 134 at 2 atm for 10 min.
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15
Q

Disinfection: what is it, give some methods, and what is the importance of the phenol coefficiant?

A

Disinfection = treatment which reduces the number of potentially pathogenic microorganism in an environment (this process do not destroy all pathogens)

Disinfectant = a chemical substance used to kill micro-organism on non-living surfaces (too toxic to be applied directly to tissue)

Antiseptic agent = chemical used to reduce the number of potentially pathogenic microorganisms on living tissue (skin, mucous membrane) - Ignaz Semmelweis

Phenol coefficient is used to compare disinfective agents. Takes the “highest dilution factor that kills bacteria after 10 min, but nor after 5 min” relative to the dilution factor of phenol.

Important to remember: the length of time the agent is applied and the concentration of the agent (think about scrubbing in surgery).

Methods:

1: Physical - pasteurization, boiling, UV-radiation
2: Chemical - isopropanol, alcohols (70%; bactericidal - disrups lipid membrane), phenols (protein denaturation), heavy metals (protein denaturation), oxidizing agents (iodine, chlorine (!)), alkylating agents (formaldehyde), detergents (surface active agent; cationic and anionic detergents)

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16
Q

What are the difference between antisepsis and asepsis?

A

Asepsis = is the state of being free from disease-causing micro-organisms (such as pathogenic bacteria, viruses, pathogenic fungi, and parasites). The term “asepsis” often refers to those practices used to promote or induce asepsis in an operative field in surgery or medicine to prevent infection
- Sterile is the absence of ALL microbs, Aseptic is just the absense of disease produceing microbs

Antisepsis = chemical used to reduce the number of potentially pathogenic microorganisms on living tissue (skin, mucous membrane) - Ignaz Semmelweis

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17
Q

Selective toxicity and chemotherapeutic index: give some examples

A

Selective toxicity = implies that a drug is harmful only to other organisms without harming the host: act on other biochemical structures not present on the host.

Chemotherapeutic index (Paul Ehrlich): the highest concentration of the antimicrobial agents that can be tolerated by the host, divided by the lowest concentration of the agent that inhibit or kills the microorganism
Chemotherapeutic index = maximal tolerated dose / minimal effective dose
- Penicillin have high range
- Aminoglycosides have low range which means it need to be monitored much more closely to prevent adverse effects.  

“The therapeutic index (TI) (also referred to as therapeutic ratio) is a comparison of the amount of a therapeutic agent that causes the therapeutic effect to the amount that causes toxicity. The related terms therapeutic window or safety window refer to a range of doses which optimize between efficacy and toxicity, achieving the greatest therapeutic benefit without resulting in unacceptable side-effects or toxicity”

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18
Q

Principles of antibacterial chemotherapy

What are bacteriostatic and bactericidal effect?

Narrow vs. broad-spectrum antibiotics

Also explain what an antibiotic, semisynthetic antibiotic, and chemotherapeutic agent are.

A

Bacteriostatic effect: inhibit the growth of microorganisms but is unable to kill them within a short period, rely on host defenses to remove the pathogens.
- MIC = minimun inhibitory concentration: E-test, agar dilution or broth microdilution

Bactericidal effect: kill growing microorganisms within a short period. This is determined in vitro.
- The lowest concentration which kills 99.9% of the population is referred to as minimal bactericidal concentration (MBC)

Use narrow spectrum if possible; prevent side effects and large alterations in normal flora - dysbacteriosis (pseudomembranous colitis from C. difficile)

Dont forget - chemotherapeutic index and selective toxicity principle

Antibiotic = natural occurring agent produced by an organism to inhibit the growth or kill other microorganisms.

Semisynthetic antibiotic = natural synthetic agent which is modified chemically in order to have advantageous and pharmacokinetic properties

Chemotherapeutic agent = an antimicrobial synthesized chemically.

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19
Q

Antimicrobial drugs in combination: why is it sometimes useful?

A

Synergism: 1+1 = 3 (e.g. penicillin + aminoglycosides for enterococcus faecalis)
Antagonism: 1+1 = 0,1
Indifference: 1+1 = 1
Additive: 1+1 = 2

e.g. give penicillin together with a B-lacatamase inhibitor

You should always be aware of interactions with different drugs!

Antibiotics in combinations is used when:

  • mixed infection is present with different antibiotic sensitivity
  • pathogens hardly affected by drugs (M. tuberculosis)
  • pathogen is multiple resistant (pseudomonas)
  • it is difficult to achieve high enough dose at the infection site
  • prevent emergence of resistant organism during therapy
  • the immune system of the patient is week
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20
Q

Which tests can be used to determine antibiotics susceptibility?

A

Diffusion method: E-test, disc diffusion

Dilution method: agar, broth microdilution and tube dilution

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21
Q

Risks and side effects of antibacterial chemotherapy

A

Some risks and side effects

  • Allergy: type 1 hypersensitivity -> anaphylaxis. E.g. to penicillin and cephalosporins (rash and urticaria)
  • Dysbacteriosis: diarrhea and C. difficile (pseudomembranous colitis) from broad-spectrum antibiotics.
  • Candidiases infection as normal flora is altered
  • Direct toxic effect
    1: Tetracyclins - because of depositions in developing teeth, its use should be avoided in children up to 8 years and in pregnant and lactating woman
    2: Antifungal drugs are toxic to liver
    3: Aminoglycosides are toxic to kidney and nerves
    4: Chloramphenicol toxic to bone marrow
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22
Q

Antibiotics altering the peptidoglycan synthesis

A

Beta-lactams (inhibit peptidoglycan synthesis): penicillin, cephalosporins, carbapenems, and monobactams (used is someone has penicillin allergy)

Beta-lactams bind to PBP (penicillin binding proteins which is a transpeptidase) because they can be bound to beta-lactams. MRSA have altered PBP.

Beta-lactamase can destroy beta-lactams: this is why we can give beta-lactamase inhibitors to prevent this inactivation.

Bactericidal effect

Glycopeptides: Vancomycin (cross-linkage) and bacitracin (inhibit bacterial cell wall and movement of cell wall)

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23
Q

Antibiotics altering protein synthesis

A

Bacteria have 70s, which consist of 30s and 50s subunits:

50s: chloramphenicols, macrolides, linezolid, clindamycin, streptogramins.
30s: tetracyclins, aminoglycosides

mRNA synthesis: rifampin

24
Q

Antibiotics acting at the level of nucleic acid

A

Inhibitors of nucleic acid synthesis;

  • Sulphonamides: folate synthesis
  • Trimethoprim: folate synthesis

DNA gyrase (topoisomerase 2): fluorquinolones, quinolones

mRNA synthesis: rifampin

25
Q

Glycopeptides and antimicrobial drugs altering the membrane function: Antibiotics altering membrane function

A

Glycopeptides: Vancomycin (peptidoglycan synthesis)

Polypeptides: bacitracin and polymyxins (increase permability)

Lipopeptides: daptomycin (membrane depolarization)

26
Q

Exotoxins: parts and properties. Toxoid vaccine

A

Bacterial toxins are proteins, denaturete with head, acid and proteolytic enzymes, have high biological activity, and exhibit specificity of action.

The toxin get its name depending on the location it act on. E.g. neurotoxin, enterotoxin, leukocidin, hemolysisn

Toxiod vaccine: keep it antigenic properties while removing its virulence. E.g. in DTaP

A + B unit: for toxins working intracellularly
A = active part - toxins
B = binds to receptor and facilitates entry into cell

27
Q

Pathogen, virulence, obligate, facultative and opportunistic pathogens

A

Pathogen: microorganism that is able to produce disease
Pathogenicity: the ability to cause a disease in a host
Virulence: the degree of pathogenicity, depends on the set of virulence factors.

Obligate pathogen: those bacteria that must cause disease in order to be transmitted from one host to another. These bacteria must also infect a host in order to survive, in contrast to other bacteria that are capable of survival outside of a host.
- Examples include M. tuberculosis and T. pallidum

Facultative pathogen: Finally, some bacterial pathogens cause disease only accidentally if they get the opportunity. These can be a part of the normal flora.
- Examples: E.coli, H. influensa, S. pneumoniae, S. aureus.

Opportunistic pathogens: can be transmitted from one host to another without having to cause disease. However, in a host whose immune system is not functioning properly (immunocompromised), the bacteria can cause an infection that leads to a disease.
- Examples include exogenous sources from V. cholerae and P. aeruginosa, and from the bodies own flora, E. coli and S. Aureus (endogenous).

28
Q

Role of the host in disease

A

In the same way pathogens have a set of virulence factors, the host have protective mechanisms to resist these. All of this protective factors determine the hosts degrees of resistance to the parasite

Host defense mechanisms are divided into two groups:

1: Constitutive defense - defenses common to all healthy adults. These defenses provide general protection against invasion of by normal flora, or colonization, infection, and infections disease caused by pathogens.
- This is known as the “natural” or “INNATE” immunity
- Consists of anatomical barriers, phagocytes, complement

2: Inducible defenses - defense mechanisms that must be induced or turned on by the host exposure to a pathogen, e.g. after infection. This induction of protection takes some time to develop.
- Adaptive immune system: B- and T-cells

EXTRA
Species vs. individual resistance
- Species: some are can get the disease, other cannot.
Difference in body temperature, receptors ++
- Individual resistance: influenced by age (small children and elderly, sex (UTI), stress, diet (malnutrition, vitamins, protein def.), trama, and underlying diseases, genetic diseases,

29
Q

Active immunisation: vaccines and recombinant vaccines

List up active vaccines

Prophylactic versus therapeutic immunization

A

Immunization = providing specific protection against most common and damaging pathogens

  • Can be active or passive,
  • Active can be natural (exposed to pathogen) or artificial (we expose Ag to the host)
  • Called active because the immune system have to develop its own protection
  • Long protection
Immune = usually means the ability to resist infections disease
Immunity = refers to the relative state of resistance of the host to a specific pathogen brought on by the activities of the immunological system

Live vaccines

1: BCG - M. bovis. Protect against miliary TB. Should not be given to immunocompromised
2: Adenovirus

Killed vaccines

1: Plague, pertussis (DTaP)
2: Conjugated*: H. influenza (HiB), pneumococcus, meningococcus
3: Toxoid: cholera, DTaP
4: Viruses: MMR (measles, mumps, rubella), small pox, (polio), yellow fever, hepatitis A, B, varicella zoster, rotavirus
5: Additional: influenzae, thypoid, cholera

*Polysaccharides are weakly antigenic -> conjugated with protein to have a longer memory (HiB, meningococcus and pneumococcus).

Prophylactic = before exposure to antigen. E.g. when traveling to endemic area.

Therapeutic = post exposure. E.g. after rabies exposure.

30
Q

Passive immunity: risks and side-effects

A

Passive = given immunity, no “active” process. Host receives antibodies and/or immuno-reactive lymphocytes from another host.
Short life-time. E.g. protection form mother the first 6 months, in people given plasma Ig,

Passive immunity can be given in;

  • Against toxins: tetani, diphteria, botulinum
  • Viruses: rabies, measels, CMV, Variacella

Risks and side-effects: serum-sickness (type 3 hypersensitivity) and type 1 hypersensitivity (anaphylaxis). Transmission of serum can also have HIV and HepC in some cases

31
Q

Normal flora: skin, eyes, oral cavity, respiratory tract (nose, upper + lower tract), urogenital, GI-tract

What are the benefits on GI-flora?

A

Skin: staphylococci, cornyebacteria, propionibacterium acnes

Eye: Staphylococci epidermidis and propionibacterium acnes.

Oral cavity: streptococci (bovis! and sanguis), staphylococci, lactobacilli, cornynebacteria, some anaerobes (actinomyces and bacteriodes)

Respiratory tract

  • Upper respiratory tract: streptococci and various gram-negative rods. S. pneumonia, H. influenzae, N. meningitidis
  • Lower respiratory tract (trachea and down): virtually free of microorganisms
  • Nose: staphylococcus epidermidis and aureus, and cornyebacterium

Urogenital tract

  • Normally sterile
  • Vagina -> lactobacillus acidophilus

GI-tract: bacterioides, lactobacilli, enterococci, clostridium, E.coli, bifidobacterium

Benifits:

1: protect against pathogens
2: Vitamin B12 and vitamin K
3: stimulate the immune system in the development
4: SCFA

32
Q

Give examples of some spreading factors and enzymes causing hemolysis and leucolysis

A

Spreading factors

1: Hyaluroniase
2: Collagenase
3: Neuroamidase
4: Streptokinase and staphylokinase

Hemolysis and leucolysis

1: Phospholipase and lecithinase
2: Hemolysin
3: Streptolysin
4: Leukocidin

33
Q

Endotoxin: characteristic and mode of action

A

Part of the outer cell wall of gram negative bacteria. Essential for bacterial growth and survival, especially in the context of host-parasite interaction

Heat resistant and not suitable for toxoid. No enzymatic activity

Some bacterias can secrete LPS in periods of rapid growth.

Toxicity is associated with the lipid A part of LPS.

LPS consist of 3 parts: Lipid A - Core polysaccaride - O polysaccaride

Endotoxemia contribute to symptoms of gram-negative bacteremia and sepsis.

Endotoxin cause:

1: fever
2: DIC
3: shock (hypotension)
4: changes in WBC cell count

34
Q

Sepsis (definition, pathomechanism, microbiological diagnosis)

Start with defining infection, bacteriemia, SIRS, sepsis

A

Infection = inflammatory response to the presence of or invasion of normally sterile host tissue by microorganisms.

Bacteremia = the presence of live bacteria in the blood.

Sepsis = SIRS + infection in blood, or systemic response to infection with the same manifestations as SIRS

SIRS = Systemic inflammatory response syndrome (SIRS) is an inflammatory state affecting the whole body, frequently a response of the immune system to infection.. It have its own criterial:

1: HR over 90 BPM
2: Temperature over 38 degrees celcius
3: RR over 20 or PaCO2 below 32 mmHg
4: WBC over 12 000 or below 4000

Septic shock = sepsis + hypotension despite adequate fluid resuscitation

SIRS -> Sepsis -> Septic shock -> MODS (multiple organ dysfunction syndrome)

Diagnosis by blood culture (bottles) from venous system. 2-3 bottles (aerobic and anaerobic) x 3 blood cultures/day at spaced intervalls. Volume should be between 10 and 30ml.

35
Q

What types of fungal diseases can we have (groups) and which one are dimorphic?

A

Superficial: Malassezia furfur (pityriasis or tinea versicolor) and exophiala werneckii (tinea nigra)
Cutaneous: dermatophytes (trichophyton, epidermophyton, microsporium), candida, sporothrix
Systemic: histoplasma, blastomyces, paracoccidioides, coccidioides.
Opportunistic: candidia, pneumocystis jirovecii, cryptococcus neoformans

"Body Heat Probably Changes Shape"
B = Blastomyces dermatitidis
H = Histoplasma capsulatum
P = Paracoccidioides brasiliensis
C = Coccidioides immitis
S = Sporothrix schenckii
36
Q

What are the special sterol found in fungi? what antibiotic act on it?

A

Ergosterol

Synthesis: Azoles
Makes holes: Amphotericin B, Nystatin

Echinocandins inhibit the synthesis of glucans

37
Q

Fungal antibiotics: cell wall synthesis, ergosterol, RNA and DNA synthesis

A

Cell wall synthesis: Echinocandins (glucan)

Ergosterol formation: Azoles

Cell wall permeability (makes holes): Amphotericin B + Nystatin

DNA and RNA synthesis: 5-Flucytosine

Cell membrane synthesis: Terbinafine

38
Q

List up GI-protazoa

A

Ameba: Entamoeba histolytica
Flagellata: Giardia lamblia + Trichomonas vaginalis
Sporozoa: Isospora bellii + Cryptosporium parvum
Cilliata: Balantidium coli

39
Q

List up GI-helminths

A

da

40
Q

List up blood and tissue protazoa

A

Ameba: Naegleria fowleri + Acanthamoeba castellani
Flagellata: Leishmania, Trypanosoma

41
Q

List up blood and tissue helminths

A

jj

42
Q

General characterisation and taxonomy of protozoa

A

Protazoa are

  • Unicellular
  • Heterotrophic, can be aerob and anaerob
  • 2-80 uM in size
  • Complex life cycle: asexual (binary fission) and sexual (fusion of 2 cell, exchange DNA and division into 2 cells)
  • Cyst (survivor-protevtice membrane with thick wall
  • Trophozoite (vegetative, active, multiplying)

Sexual: fertilisation -> zygote -> encystation -> oocyst (infective sporozoite inside) -> trophozoite

GI-, and tissue and blood protazoa

Simplified morphological classification (classis, genus, species)

  • Lobosea (amoebae): Entamoeba, Naegleria, Acanthamoeba
  • Flagellata: Giardia, Trichomonas, Leishmania, Trypanosoma
  • Sporozoa (apicomplexa): Cryptosporium, Toxoplasma, Plasmodium
  • Ciliata: Balantidium coli
43
Q

General characterisation and taxonomy of helminthes

A

Multicellular
Heterotrophic
Eosinophilia!

Trematodes = flukes (leaf shapes, pair of suckers)
Cestodes = tapeworms (have segments; complete female and male parts)
Nematodes = roundworms (unsegmented body, adult worms can be either female or male - separated sexes, full intestinal tract)

E.g. Nematode life cycles ++

  • Some have only intestinal phases: Enterobius vermicularis and Trichuris trichuria.
  • Other can also have extraintestinal phases
44
Q

Which helminth (nematodes) can be transmitted to a human by;

1: ingestion of eggs
2: penetration of skin by filariform larva
3: with uncooked meat

A

Eggs: Enteriobius vermicularis, Trichuris trichuria, Ascaris lumbricoides, Toxocarna canis and cati

Skin: strongyloides stercoralis, ancylostoma duodenale, necator americanus

Undercooked meat: Taenia saginatum and solium, Trichinella spiralis

45
Q

List up nematodes (and filariasis/microfilariae)

A

Nematodes (roundworms)

  • Ancylostoma duodenale
  • Necator americanus
  • Strongyloides stercoralis
  • Ascaris lumbricoides
  • Enterobius vermicularis
  • Trichuristrichiura
  • Trichinella spiralis

Filariasis/microfilariae

  • Loa loa
  • Onchocerca volvulus
  • Wuchereia bancrofti
  • Dracunculus medinesis
  • Tococarna canis/cati
46
Q

General description and classification of viruses

A
  • Infectious genetic information
  • Intracellular
  • Size from 20 nm (parvovirus) to 300 nm (poxviruses)
  • Can be DNA or RNA (+ or + stranded)
  • Single or dobbel stranded
  • Capsid = protein coat
  • Viron = the entire viral particle
  • Cubital (icosahedral), helical, complex (poxviruses)
47
Q

List up DNA viruses - which one is the only single stranded DNA virus

A
7 viruses
Remember: 4 "P", 2 "H", 1 "A"
Parvovirus (ssDNA)
Pox
Herpes
Hepatitis B virus
Polyomavirus
Papillomavirus
Adenovirus

Envelope: 2 “H” viruses + 1 “P” -> Hepatitis B virus, herpesvirus, poxvirus

48
Q

List up RNA viruses. Which one is dsRNA?

A

All except the DNA viruses are RNA, and every RNA virus except Reovirus (dsRNA) is ssRNA. Much easier to remember

Only reovirus, picornavirus, and calicivirus are not enveloped

49
Q

Principles of virus structures. Sub-viral agents: viroid, prion

A
  • Outer capsid protect the genetic material
  • Proteins on its surface is important for attachment to receptors (organ specificity)
  • RNA negative viruses bring its own RNA polymerase-
  • Can be enveloped or not*
  • DNA or RNA, ss or ds
  • Envelope = lipid-containing membrane formed when budding of a previous cell. Surrounds the virus particle. In general, the presence of an envelope confers instability of the virus -> more sensitive to heat, detergents, lipid solvents (such as alcohol). Virus encoded glycoproteins on its surface (peplomers)

Viroids: infectious RNA particle, formed of only ssRNA, with NO protein coat or capsid. Viroid infects mostly plants; no human pathogen until now.

Prions: an infectious protein particle formed only of proteins. RNA and DNA are absent. Prions infects animals causing neurological degenerative disease. Mad cow disease, Creutzfeldt-Jakob disease

50
Q

Propagation of viruses. Molecular bases of the biosynthesis of viruses: productive infection

A

Attachment (1): Virion have to bind tissue specific receptors. Receptor structures differ for different viruses -> this is why virion infection is tissue specific

Penetration (2): receptor-mediated endocytosis, envelope fusion with PM, or bacteriophage mode (pump virion material into cell)

Uncoating (3): physical separation of virus coat and genetic core

Synthetic period (4): intense formation of new material.

Assembly (5): newly synthesized viral genome and capsid assemble to form viruses. Virus specific glycoproteins are inserted into cellular membrane

Budding off or lysis of cell (6)

Replication strategies of viruses

  • ssDNA: replication in nucleus. Negative sense strand serves as a template. Host-cell polymerases are used. Only replicate in dividing cells. First form dsDNA -> mRNA + DNA.
  • dsDNA: nuclear replication
  • dsRNA: virion bring its own polymerase. Replication in cytoplasm.
  • ssRNA +: form mRNA directly in cytoplasm. Viral polymerase formed in cytoplasm.
  • ssRNA -: carries its own RNA-dependent RNA polymerase. Form + ssRNA first. Occurs in the cytoplasm, except with orthomyxoviruses.
  • retroviruses: ssRNA (+) -> dsDNA by the RNA-dependent DNA polymerase (reverse transcriptase) carried by the virion.
51
Q

Latent and persistent viral infections

A

Range of virus-cell interactions

  • Cytolytic (productive infection): host cell are termed permissive
  • Non-cytolytic (productive infection): viruses are released by budding. May lead to persistent infection.
  • Abortive (non-productive infection): the virus do not complete its replication cycle. Cells are infected but the virus are not produced by the cell -> the cell are termed non-permissive. No effect, no viral replication, no latency.
  • The virus enter the cell but are not produced by the infected cell: the cell are termed non-permissie. Latency = the cell remain its normal properties. Malignant formation.
52
Q

Serological reactions in the diagnosis of viral diseases

A
IgM
IgG
ELISA
complement
RIA
HA (hemoagglutinin
HA inhibition
Paul-Bunnel test for EBV (sheep RBC)
Latex agglutination
53
Q

What kind of viruses can use GI-tract?

A

Only naked viruses (fecal-oral route)! Gastric acid destroy the enveloped viruses.

54
Q

Explain “BOAR”

A

segmented viruses;

B: bnonya
O: orthomyxovirus
A: arenavirus
R: reovirus

55
Q

CHEAP TORCHES

A
C – Chickenpox and shingles
H – Hepatitis, C, (D), E
E – Enteroviruses
A – AIDS (HIV infection)
P – Parvovirus B19 (produces Hydrops faetalis secondary to aplastic anemia)
T – Toxoplasmosis
O – Other (Group B Streptococcus, Listeria, Candida, Lyme disease)
R – Rubella
C – Cytomegalovirus
H – Herpes simplex
E – Everything else sexually transmitted (gonorrhea, Chlamydia infection, Ureaplasma urealyticum, human papillomavirus)
S – Syphilis