Infectious Diseases Flashcards

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1
Q

2 types of UTIs

A
Bladder infection (cystitis, confined to bladder/urethra).
Pyelonephritis (kidney).
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2
Q

Major pathogen of pyelonepritis

A

E.coli (ambulant patients)
> UPEC (uropathogenic)

> > ascending infections

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3
Q

Pyelonephritis course of infection

A

Contamination of periutheral area with UPEC that has colonized bowel > ascension into bladder > adherence to uroepithelial cells by type 1 and P fimbriae > some can invade epithelial cells

  • Some strains further ascend up urether into kidney (P fimbriae strains) > inflammation
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4
Q

Pathogenicity factors of E.coli

A
LPS (O-ag), 
capsule (K-ag), flagella (H-ag), 
pili/non-fimbriae 
adhesins, 
hemolyins
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5
Q

Causes of diarrhea?

A

viruses (noro/rota),
bacteria (campylobacter, salmonella, e.coli),
parasites (giardia)

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6
Q

Which enterobacteriacae cause diarrhea?

A

Salmonella, Shigella, Yersinia, E.coli

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7
Q

Characteristics of enterobacteriacae?

A

Gram-neg rods, facultatively anaerobic ( intestine), carbohydrate catabolism, catalase-pos, often motile (flagella),
cause diarrhea but also UTIs, sepsis etc

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8
Q

3 types of parthenogenesis of infectious diarrhea

A
  1. Enterotoxin-mediated
  2. Cytotoxin-mediated
  3. Invasion-mediated
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9
Q

Example for cytotoxin-mediated diarrhea

A

E.coli (EHEC: obligatory pathogenic, Shiga toxin)

and Shigella (Shiga toxin, enters M cells, survival in phagocytes)

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10
Q

Example for Enterotoxin-mediated diarrhea?

A

Vibrio cholerae.

AB-toxin cholera toxin (activates adenylate cyclase > electrolyte and water loss into intestine).

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11
Q

Comparison Enterotoxin and Cytotoxin.

A

Entero: alters physiology of cell, loss of electrolytes/water but no damage/fever, watery stool
Cytotoxin: destroys host cell, inflammation/fever/loss of electrolytes and water, stooly mostly with mucus and blood

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12
Q

Example invasion-mediated diarrhea

A

Salmonella: uptake into enterocytes > into macrophages > inflammatory responce, diarrhea

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13
Q

Transmission of skin/wound infections

A

Contamination with bacteria from environment or endogenous smear infection with transient skin flora or smear infection wiht pathogens from other body sites.
Then: locally confined or dissemination

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14
Q

Common cause of abscesses and wound infections?

A

Staphylococcus aureus (gram-pos cocci, transient skin/mucose flora, mostly endogenous infections, often resistant to antibiotics)

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15
Q

Virulence factors of S.aureus

A

cell-surface ass.: Protein A (binds Fc receptors of ab), clumping factor
secreted: plasmakoagulases, staphylokinase, hemolysins, exfoliative toxins, TSST-1, etc

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16
Q

Abscess formation by S.aureus

A

coagulases convert prothrombin to staphylothrombin > cleaves off fibrinopeptides from fibrinogen > fibrin dimers associate to fibrin threads > fibrin wall around skin is formed > are isolated from immune cells

(SSL10 peptides inhibit Thrombin formation that would attract neutrophils)

17
Q

Syndrome caused by S.aureus

A

Staphylococcal scalded skin syndrome (SSSS)

Exfoliative toxins: serine proteases that cleave desmoglein (required for association of skin cells > cleavage disrupts intergrity of skin) > destruction of epidermis

18
Q

Types of infections of respiratory tract

A
  1. upper tract (S.pyogenes, H.influenzae)

2. lower tract (S.pneumoniae, C.pneumoniae)

19
Q

VFs of Streptococcus pyogenes

A

adhesion/colonization: lipoteichonic acid, hyaluronic acid

invasion/spread: capsule, streptokinase, streptolysins,

immune evasion: M proteins, capsule, pyrogenic exotoxins

20
Q

Pneumonia types

A
  1. alveolar pneumiae/bronchopneuminae

2. atypical pneumoniae (infection of connective tissue of the lungs)

21
Q

Most common pathogen of pneumoniae in ambulant patients

alveolar/broncho-p.

A

Streptococcus pneumoniae (40-70% healthy carriers)

22
Q

VF of Streptococcus pneumoniae

A

Adhesion/colonization: phosphorylcholine, pili, CbpA
Invasion/dissemination to lungs: hyaluronidase, PavA
Growth/replication: lipoproteins PiaA and PiuA
Immunevasion: capsule, pneumolysin, IgA-protease

23
Q

Cause of atypical pneumoniae

A

Chlamydia pneumoniae: elementary bodies are taken up by host cells > transform to primary reticulate bodies (metabolically active) > diff into elementary bodies, can infect new cells

24
Q

Characteristics of meningitis, transmission

A

Infection of meninges (membranes that envelop brain/spinal cord) and liquor cerebrospinales

air-borne transmission > colonization of nasopharyngeal tract > translocation across epithelial layer > dissemination via blood stream > translocation across BBB > replication in cerebrospinal fluid > inflammation

pathogens alter spinal fluid

25
Q

Cause of meningitis, clinical signs

A

Neisseria meningitides

Stiff neck, fever, headache

26
Q

Signs of inflammation

A

fever, vasodilation and tissue perfusion (elevated haert beat and breath frequency), edema (damaged epithelial walls), pain, loss of function

27
Q

septiceamia

A

disseminated generalised inflamamtion (not locally confined) > overwhelm in inflammatory response

28
Q

Cause of septicaemia

A
Staphylococcus epidermidis (normal skin flora, adheres to plastic > catheters)
Recognition via TLR4
29
Q

Common themes of virulence factors

A

adhesion, invasion, spread, growth, immune evasion, toxins, (host response)

30
Q

What can appearance of spinal fluid tell you about the pathogens leading to meningitidis?

A

Bacteria: many cells (neutrophils), high protein and lactate concentration
Virus: fewer cells (granulocytes), low protein and lactate content, high glc levels