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MICI Module 2 > Uti, Endocarditis/meningitis & STIs > Flashcards

Uti, Endocarditis/meningitis & STIs Flashcards

1
Q

Describe gonorrhoea bacteria

A

Gram negative diplococcus (coffee bean shaped)

Fastidious and susceptible to drying, requires transport medium

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2
Q

How is gonorrhea transmitted

A

Through contact of mucous membranes sexually or perinatally

Typically spread in the 20-25 age group

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3
Q

What are the clinical manifestations of gonorrhea

A 
Pelvic inflammatory disease
Pharyngitis 
Conjunctivitis 
Joint infection 
Neonatal conjunctivitis
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4
Q

How is gonorrhea diagnosed

A

Nucleic acid amplification testing
Or
Culture of urethral/cervical swabs

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5
Q

Benefits of nucleic acid amplification test?

A

More sensitive than a culture as it can also detext dead organisms
Can defect from urine sample (more comfortable)

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6
Q

What are some issues with urethral/cervical swabs

A

Less sensitive but very soecific

Resistance becoming a problem

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7
Q

What are treatments for gonorrhea

A
  • Cefixime (oral beta lactam) or ceftriaxone (injection) combined with azithromycin incase of chlamydia co infection
  • ciprofloxacin (flouroquinolone) although increasung resistance
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8
Q

Describe chlamydia bacteria

A

Chlamydia trachomatis causative agent

Obligate intracellular bacteria devoid of cell wall, can not be gram stained

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9
Q

Why can’t chlamydia bacteria be gram stained

A

Obligate intracellular bacteria that has no cell wall

Must be detected by molecular amplification or cultured

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10
Q

Describe chlamydia lifecycle

A

2 alternating forms
Reticulate body: actively replicating then ruptures creating elementary bodies
Elementary body: transmitted infectious form that enters cells and develops reticulate body

Reticulate -> replicate -> rupture

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11
Q

What cells does chlamydia infect

A

Urethral, cervical and conjunctivial epithelial cells

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12
Q

Describe chlamydia epidemiology

A

One of the most common stis
15-25 age range
Asymptomatic carriers common

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13
Q

What are clinical manifestations of chlamydia

A 
Urethritis cervitis 
Pelvic inflammatory disease
Proctitis (rectum inflammation)
Reactive arthritis 
Conjunctivitis (esp in babies)
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14
Q

Describe chlamydia specimens

A

Men: urethral swabs and urine samples

Women: vaginal swabs, endocervical swabs, urine

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15
Q

How is chlamydia detected

A

Nucleic acid amplification test

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16
Q

How is chlamydia treated?

A

Tetracyclines ( doxycycline), azithromycin, erythromicin

No cell wall betalactam can not be used

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17
Q

Describe syphilis bacteria

A

Treponema pallidum
Tightly coiled spirochaete

Too fine to gram stain must use dark feild microscopy

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18
Q

What are the three stages of syphilis

A 
Primary (localized)
Secondary (systemic) 
Latent (asymptomatic)
Tertiary (late) 
Congenital
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19
Q

Describe primary syphilis

A

1-4 weeks following contact

Chancre (painless ulcer) heals spontaneously

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20
Q

Describe secondsry syphilis

A

Skin rash, flu like symptoms, lymphadenopathy

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21
Q

Describe tertiary syphilis

A

Cardiovascular and neurological symptoms

Gumma (masses that appear on skin)

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22
Q

Describe congenital syphilis

A

Bone, teeth and brain damage

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23
Q

What is unique about a syphilis rash

A

Does not spare soles and palms

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24
Q

How is syphilis diagnosed

A

Dark feild microscopy for primary disease only! ( chancre)
Serology is main route of diagnoses
Specific tests used

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25
Q

How is syphilis treated

A

Penicillin treatment if choice, doxycycline if allergy
Longer treatment required if CNS involved
Hiv common coinfection so test for that

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26
Q

Describe herpes bacteria

A

Linear double stranded DNA virus

Neurotopic: invades nerves and becomes dormant reactive if regrowth

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27
Q

What is the clinical presentation of herpes?

A

Primary infection: fever, headache, myalgia, painful lesions, discharge, disuria, tender nodes

Latent: shedding virus without lesions

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28
Q

Describe recurrent herpes infections

A

Less severe than primary infection usually localized to genital area
Tingling/pain 50% of patients

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29
Q

Describe congenital herpes infection

A

Life threatening to baby if passed during birth

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30
Q

How is herpes diagnosed

A

Nuckeic acid amplification test
Swabs of local lesions
Culture on cells (less sensitive)

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31
Q

How is herpes treated

A

Antivirals

Long term prophylaxis if frequently recurrent

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32
Q

Describe UTI prevalance

A

50% of women have one before 30
Incidence decreases with age
About 25% of women experience a reinfection 6 months after first UTI

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33
Q

Define bacteriuria

A

Presence if bacteria in urine. Does not mean infection

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34
Q

Define asymptomatic bacteriauria

A

Prescence of bacteria and absence if symptoms

Usually clinically insignificant unless pregnant or undergoing unvasive procedures of urinary tract

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35
Q

What is an upper uti called

A

Pyelonephritis

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36
Q

What is a lower uti called

A

Cystitis and urethritis

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37
Q

How are utis classified

A

Location (upper/lower)
Condition of patient (complicated/uncomplicated)
Evolution (acute, chronic, recurrent)

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38
Q

Describe cystitis

A

Confined to bladder
Disuria, urinary frequency, urinary urgency
Absense of symptoms ir physical signs suggesting inflation at other sites withun urinary tract

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39
Q

What bacteria causes acute urethritis

A

Chlamydia trachomatis

Neisseria gonorrhea

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40
Q

What bacteria causes vulvitis

A

Contact dermatitis or allergic reaction

Candida albicans HSV infection

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41
Q

Define pyelonephritis

A

Clinical diagnosis that implies a more invasive infection INCLUDING THE KIDNEYS
Inflammation of kidney renal pelvis assumed as well as tenderness involving flank,nausea,chills,fever,headache

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42
Q

Define prostatistis

A

Inflammation or infection of the prostate gland

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43
Q

Define intrarenal abcess/perinephric abcess

A

Collection of pus in kidney or soft tissue surrounding kidney

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44
Q

Define uncomplicated UTIs

A

Patients with normal genitourinary tracts

Usually non pregnant premenopausal women

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45
Q

Describe complicated UTIs

A

Structural of functional abnormalities of the genitourinary tract
Pregnant women, elderly,men,children
Chronic symptoms, upper tract disease

46
Q

Describe UTI relapse

A

Recurrence of infection by same organism after discontinued treatment

47
Q

Describe UTI re infection

A

Recurrence of infection by different organisms after discontinued Treatment

48
Q

What causes UTIs

A

Usually due to patients own intestinal flora ascending route of infection

Organisms enter urinary tract in retrograde fashion via the urethra

Complicating factors such as catheters tubes, surgery, stones allow organisns to enter tract and alter typical spectrum of organisms

49
Q

What are risk factors for UTI

A 
Aging
Being female
In males inter course or prostatic hypertrophy
Urinary tract obstruction
Impaired bladder innervation 
Hematogenous spread (through blood)
50
Q

True or false a majority of UTIs are caused by a single pathogen

A

True

51
Q

What bacteria is responsible for 90% of all UTIs

A

Enteribacteriacea
Gram negative, facultative anerobic bacilli
Common intestinal flora

52
Q

What is the most commonly isolated pathogen in UTIs

A

Escherichia coli most commonly isolated 70% in all UTIs

53
Q

What bacteria is responsible for a majority of community acquired UTIs

A

E.Coli

54
Q

What is a major virulence factor in UTIs

A

Adherence

E.coli has fimbrae which bind to p blood group present on uro epithial cells in 99% of population

55
Q

Describe hemolysins, colicin V in UTIs

A

Aid in resistance to complement dependent bactericidal effect of serum

56
Q

Describe k antigen in UTI

A

Associated with uppee tract infections

57
Q

Describe type I finbrae and uti

A

Inter bacterial binding and biofilm production

58
Q

Describe proteus, morganella and providencia

A

Classical uti pathogens
Highly Motile, produce fimbrae
UREASE PRODUCING organisms
Increases urinary pH which leads to crystal formation and obstruct flow

CAUSE STONES AND CRYSTALIZATION

Swarm agar plate

59
Q

What are biofilms

A

Colonization on catheter

Protects bacteria from hosts defenses and antibiotics

60
Q

Describe uro-pathogen staph saprophyticus

A

1-5% if cystitis

Typically associated with younger sexually active females

61
Q

Describe UTI dipstick testing

A

Interested in detection of nitrates and leukocytes produced by infection
Detection of nitrates: reasonably sensitive for gram negative bacteria but highly specific
Detection if leukocytes: sensitive but not specific

Need to find both

62
Q

What is significant bacteruria in a urine culture defined as

A

10^5 bacteria/ml (10^8/litre)

Lower numbers may be significant in children or catheter specimens

63
Q

Describe clean catch mid stream specimens

A

Most frequently used method
Urethra cleaned prior to collection
First void urine allowed to pass to clear urethra then mid stream collected in sterile containers

64
Q

Describe collection bag samples

A

Used in children
Often contaminated
Most meaningful result is a negative culture

65
Q

Describe indwelling catheter specimen collection

A

Urine obtained by inserting needle into catheter or through diaphragm
Preferably obtain through new catheter not old

66
Q

Describe suprapubic aspiration specimen collection

A

Invasive.

Specimen obtained directly from bladder

67
Q

How is a uti specimen transported

A

Bacteria grows rapidly in urine and sample must be sent as aoon as posible
If not in lab by 1-2 hours must be refrigerated
If not recieved in 24 hrs lab rejected
Unkess tranported by boric acid tube

68
Q

Describe boric acid tube

A

Preserves and maintain viability of organism w/o further bacterial growth

69
Q

Should all patients with UTI be cultured

A

No, we know what typically causes a UTI (e.coli) treat empirically

70
Q

What treatment is used in uncomplicated cystitis

A

Nitrofuratonin (not empiracle choice anymore bc resistance)
Fosfomycin
TMP/SMX

Ciprofloxacin/noroxaxin if no other choice

71
Q

What treatment is used in pyelonephritis

A

B lactam WITH amynoglycoside
Or
Ciprofloxcin (usually avoided)

72
Q

What is endocarditis

A

An infection of the endocardial surface of the heart

The wall of the heart may be involved as well as infection may occur at structural defects

73
Q

Who is particularly susceptible to endocarditis

A

Patients with artificial valves or other foreign materials

74
Q

Descrube acute endocarditis

A

Presenting within 6 weeks
More virulent organism that causes damage more quickly (fever chills)
S.aureus and S. Pyrogenes responsible

75
Q

Describe subacute and chronic endocarditis

A

Presenting from 6 weeks to 3 moths
Chronic after 3 months
Often caused by low virulence organisms with gradual destruction of valves
Viridians (alpha haemolytic) streptococci

76
Q

What bacteria typically infects normal valves

A

S. Aureus; highly virulent

77
Q

What bacteria are more likely to cause infection on abnormal valves

A

Low virulence, skin and oral microorganisms

Alpha haemolytic streptococci, enterococci and coagulase negative staphylococci

78
Q

What are commonest organisms to cause natuve valve IE

A

Alpha haemolytic “viridians” streptococci

79
Q

What organisms are commonest in PV IE

A

Coagulase negative staphylococci

80
Q

What is bacteremia

A

Bacteria circulating in the blood

81
Q

Describe endocarditis pathogenesis

A

Mucous membranes and skin colonized
Trauma = bacteremia
Adherence (promoted by fibrin, platelet aggregation and endothelial damage)
Further platelet fibrin deposition takes place
Vegetations develop after bacterial division
Vegetarions develop with dormant organisms
Vegetations fragment and embolize other organs

82
Q

What heart valve complications can arise from infection

A

Cauliflower shaped vegetations may develop of valves
Inflammation may destroy valve
Small emboli in arteries = myocardial infection
Abscessed may develop in the heart muscle = impair electrical conduction

83
Q

What are brain consequences from endocarditis

A

Micro emboli = confusion or coma
Stroke
Abscesses
Memegiris may occur from ongoing bacteremia or emboli

84
Q

What are other consequences from endocarditis

A

Kidney: renal artery obstruction; inflammation and damage
Other:
Emboli in spleen, eyes, extremities or other organs
Blood vessels weakened stretched and burst

85
Q

What risk factors can be identified when diagnosing endocarditis

A 
Previous heart disease
Dental or other surgical procedures 
Intravenous drug use
Recent heart surgery
Long standing in dwelling lines
86
Q

What are tools for diagnosis for endocarditis

A 
Blood cultures (positive in 90% of cases) 
Echocardiography (recognition if vegetation’s)
87
Q

How long is endocarditis treated

A

At LEAST 4 weeks

88
Q

How is endocarditis treated

A

Combonation treatments, especially with penicillin and aminoglycoside combos

89
Q

Describe endocarditis prevention

A

Prophylactic antibiotics following at risk dental and surgical procedures

90
Q

Define meningitis

A

Inflammation of fhe membranes covering rhe brain and spinal cord

Can be acute or chronic

91
Q

What js encephalitis

A

Inflammation of brain tissue, not to be confused with meningitis

92
Q

What is acute meningitis

A

Severe and sudden onset
Headache
Neck stiffness
Confusion

93
Q

What causes acute meningitis

A 
Streptococcus pneumoniae (kids and adults)
Neisseris meningitidis (esp. young adults) 
Haemophilus influenzae (esp.children)
Listeria monocytogenes (esp, babies and elderly)
94
Q

What are other causes of acute meningitis

A

Viral causes (less severe)
Enteroviruses (summer/fall)
Arboviruses (vector transmission)
Herpes viruses

95
Q

What kind if menigitis does not cause outbreaks

A

Streptococcus pneumoniae

96
Q

True or false there is a vaccine for neisseria menjngitidis

A

True! Used during outbreaks

97
Q

What type of meningitis is virtually eliminated

A

Haemophilus influenzae thanks to vaccine!

98
Q

Describe intial pathogenesis for meningitis

A
  • nasopharyngeal colonization
  • local invasion
  • bacteriemia
  • meningeal invasion
  • bacterial replication in subarachnoid space
  • release if bacterial cell wall components
99
Q

Describe the development pathogenesis of meningitis

A
  • release if bacterial cell wall component
  • macrophages release cytokines
  • subarachnoid space inflammation
  • increase CSF outflow resistance
  • cerebral vasculitis
  • blood brain permiabilitt
  • brain edema
  • confusion and coma
100
Q

Do you treat meningitis empirically

A

Absolutely!! Rapidly progressing !!

101
Q

How is menigitis diagnosed

A

Cloudy cerebral spinal fluid jncreased white cells, high protein, low glucose

Can be seen on gram stain (may be negative is empirically treated)

Csf cukture for bacteria (pcr may be used)

102
Q

How is viral meningitis disgnosed

A

Using PCR

103
Q

How is chronic meningitis diagnosed

A

Test for specific agents

104
Q

How soon should a suspected meningitis case be treated

A

Less than an hour After arriving at ER

105
Q

How is menigitis treated

A

Ceftrixalone/vancomycin AND ampicillin for at risk groups when empiracally treated

Usually single antibiotic after cause determined

106
Q

How is S. Pneumoniae meningitis treated

A

Third generation cephalosporin (ceftriaxone) vancomycin if resistance

107
Q

How is neisseria menigitidis and haemophilus influenzae menigitis treated

A

Third generation cephalosporin CEFTRIAXONE

108
Q

How is listeria meningitis treated?

A

Ampicillin

Resistant to all cephalosporins

109
Q

Describe HPV

A

Caused by human papillomaviruses
Some serotypes are causative agents of cancers
Transmission by sexual contact

110
Q

What are some consequences of HPV

A

Cancers (cervical,anal,oral)

Skin growths on genitalia, perianal area (usually transient infection resolving in months)

111
Q

How are genital warts removed

A

Chemical means, freezing or surgery if necessary

MICI Module 2 (3 decks)

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