Week 3-UTI Flashcards

1
Q

Revise host microbe interactions and infection

A

Interactions can be:

Symbiotic –> close, often long term interaction between two different species (mutualistic/ commensal/ parasitic)

Commensal –> Symbiotic relationship between two different species where one derives some benefit and the other is unaffected

Colonisation –> when a microbe grows on or in another organism without causing any disease

Infection = invasion and multiplication of microbes in an area of the body where they are not normally present, usually leads to disease

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2
Q

List host risk factors for infection

A
  • extremes of age
  • stress
  • starvation
  • compromised barriers to infection:
    • physical (anatomical)
    • biochemical (physiological)
  • Immunocompromised host
    • primary immunodeficiency (from birth)
    • Secondary immunodeficiency (acquired after birth)
    • Immunosuppression (iatrogenic from immune suppressing treatment).
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3
Q

What are normal commensal bacteria?

A

Normal commensal bacteria = “normal flora” or “microbiota”

Occupy the majority of available body areas such as skin, mouth, upper airway/lower airway, GI tract, genital tract

They are at least commensal and probably mutualistic in preventing more pathogenic bacteria from occupying those areas.

Antibiotic tx eliminate normal flora and make infection more likely.

This is less relevant in “sterile site” infections (e.g. UTI)

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4
Q

Describe the stages of bacterial pathogenesis

A

A A Its MERDT

Access –> reach suitable site

Adherence –> bind to site

Invasion –> penetrate barriers

Multiplication –> replicate

Evasion –> avoid host immune sx

Resistance –> resist antimicrobial tx

Damage –> damage host cells

Transmission –> released to infect other hosts

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5
Q

What does the urinary tract include in men/ women?

How does urinary tract infections enter the body?

Where do most organisms that cause UTI come from?

Why is UTI more common in women vs men?

A

Urethra, bladder, ureters, kidneys (both)

prostate in men

UTI’s enter the body via the urethra –> male and female urinary tracts are normally sterile but can become colonised

Bacteria that cause UTI are most commonly from the anus

UTI’s are more common in women than men due to the shorter distance between the urethral opening and the anus, and the shorter length of the urethra.

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6
Q

What are the types/ sites of UTI?

A

Inflammation of the urethra = urethritis, often included in STI heading (gonorrohea etc)

Inflammation of prostate = prostatitis

Inflammation of the bladder = cystitis, most common (also called lower UTI)

Once infection reaches the kidneys (travels via the ureters) it is called pyelonephritis. Infection tends not to occur in the cortex (where it would be called nephritis) but in the pelvis region, essentially forms an abcess.

Pyelonephritis can be very severe, pts can become septic and may require surgical drainage.

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7
Q

What are the host risk factors for UTI?

A
  • Extremes of age –> younger children and older adults (post menopausal women)
  • Stress and starvation (not known to be specific to UTI)
  • Compromised barrier to infection:
    • Shorter urethra in women (esp. if sexually active / post menopausal)
    • Malformations (pKD, renal and ureteric malformations, strictures)
    • Internal obstructions (stones/ tumours)
    • Bladder outflow obstructions (pregancy, prostate enlargement)
    • Iatrogenic (urinary catheters, operations, post operative changes)
  • Immunocompromised host –> UTI more common with diabetes mellitus (increased sugar content of urine and mild immunosuppresive effect of DM)
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8
Q

Describe the bacterial pathogenesis in UTI

A

Access —> most bacteria causing UTI found in the colon (e.g. commensals)

Adherence –> Pili (fimbriae) and adhesin molecules

Invasion –> Haemolysin (breaks down RBC, same enzyme can break down tissue) increases invasive potential

Multiplication –> colonisation of urinary tract may precede infection

Evasion –> relatively few immune cells in urinary tract

Resistance –> many bacteria causing UTI’s have multi drug resistance

Damage —> causes urethritis, cystitis, pyelonephritis, nephritis and septicaemia

Transmission –> easily passed ou in urine (limited infection risk)

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9
Q

What are some of the common causitive agents of UTI?

A

Escherichia coli --> gram negative bacilli from the colon

other “coliforms” (e.g. klebsiella, enterobacter) = gram -ve from colon

Staphylococcus saprophyticus = Gram +ve cocci from perineum and vagina

Enterococci spp. (faecal streptococci) = Gram =ve cocci from colon

Pseudomona spp. Gram -ve bacilii from the environment

Tuberculosis = variable gram staining bacilli from systemic infection

STI’s –> (neisseria gonorrhoeae, chlamydia spp.) –> urethritis

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10
Q

Describe the process of diagnosis of UTI?

A

1) symptoms –> dysuria, frequency, or urgency of micturition

haematuria, opaque or malodorous urine

Lower abdominal or loin pain

2) Risk factors –> age (young child/ elderly) compromised barrier to infection or immunocompromised (e.g. diabetes)?

3) Signs –> Lower abdominal or loin tenderness (sign its spread to kidneys), fever or septic shock

4) investigations –> urinalysis w dipstick for WBC’s, blood, nitrite (produced by bacteria), protein (inflammatory marker)

Mid stream specimen of urine for M + c + s (microscopy, culture and sensitivity)

blood investigations (FBC, Uand E, CRP)

Blood cultures (for bacteria, only in patients with fever)

Imaging (USS, CT, urogram (contrast within the urinary tract then CT done) (done if the infection is resistant, persistent, recurring).

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11
Q

What is required for microbiological urine sample?

A

Midstream urine sample to obtain uncontaminated urine sample

Clean with antiseptic wipe, then patient collects midstream to get good sample.

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12
Q

What are the microscopic markers of UTI?

What suggests infection? What suggests renal disease? What suggests contamination?

How could you use microscopy to target treatment?

A

1) microscopy –> WBCs > 100/ ul suggests infection

RBC suggest haemorrhage or infection

Casts (collections of cells stuck together, composition of WBC/ RBC, sign of inflammation) suggests renal disease

epithelial cells suggests contamination of sample

2) Culture –> CFUs (colony forming units) > 100/ ul suggests infection
3) Sensitivities –> tested with app. range of antibiotics

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13
Q

What cells can be seen on MS?

A

Large multinucleate cell = WBC

Smaller biconcave cell = RBC

Larger cell = epithelial cell suggesting some contamination

Tiny black marks = bacteria

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14
Q

Outline the approaches to antibiotic therapy in UTI tx?

A

MSSU sample and microscopy, culture and sensitivity to identify the organism and app. antibiotic.

This is targeted therapy -> specific therapy based on confirmed diagnosis

Empirical therapy approach –> best guess, therapy w/out confirmed diagnosis ( in emergency cases, cannot wait 24 hrs for culture)

Prophylactic –> preventative therapy to prevent UTI from occuring (rare as this breeds resistance).

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15
Q

Outline treatment approaches for UTI

A

1) only treat in cases when they meet the criteria for diagnosis –> WBC’s > 100/ ul + CFU > 100/ ul

Low epithelial cell count (avoided contaminants)

Good correlation with clinical features and other investigations

2) If there is colonisation but no features of infection (e.g. no white cells/ raised protein in urine/ no symptoms) then only treat in children and pregnant women (risks tx outweigh benefits otherwise)
3) If pt has urinary catheter only treat if there is evidence of infection (as urinary catheters always lead to colonisation). Catheter should be changes during treatment.

Any change of urinary catheter can make colonisation, leading to infection, give prophylactic antibiotics when doing this.

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16
Q

Why might empirical AB’s be used in UTI?

when is a narrow spectrum AB used?

Why is narrow spectrum used?

Whats the length of AB tx?

When is radiological intervention used?

A

Empirical AB’s may be require before diagnosis confirmed or if infection is shown but no organism required (follow local AB guidelines for the area).

Narrow spectrum used if organism is identified from culture and sensitivity. Narrow spectrum to prevent adverse effects and minimise risk of resistance developing.

Choose right drug, right dose, right frequency, right duration.

Radiological intervention required if UTI has developed a blockage –> hydronephritis

17
Q

What are some AB’s used in UTI?

In primary care?

A

Primary care –> nitrofurantoin and trimethoprim

secondary care –> co-amoxiclav or ciprofloxacin

For suspected Multidrugresistant organisms –> ertapenem (broad spectrum IV only)

18
Q

When should narrow spectrum AB be used?

When should broad spectrum be used?

A

Narrow spectrum –> if low risk and low severity

Broad spectrum –> if high risk and high severity

Choice always based on local laboratory data and clinical guidelines