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Microbiology Flashcards

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1
Q

What is antibiotic resistance driven by?

A

Use and misuse of antibiotics Transmission in community and healthcare setting Globalisation

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2
Q

Mechanisms of antibiotic resistance?

A

Intrinsic resistance Acquired resistance through horizontal gene transfer and chromosomal mutations

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3
Q

What percentage of S. aureus infections in NZ are caused by MRSA?

A

5-15%

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4
Q

What confers the resistance to beta-lactam antibiotics in MRSA?

A

Presence of mecA gene which produces an abnormal penicillin-binding protein

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5
Q

Treatment for MRSA?

A

Vancomycin

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6
Q

What is an ESBL?

A

Extended-spectrum beta-lactamases - hydrolyse penicillins, cephalosporins, monobactams - often resistant to gentamicin, ciprofloxacin and co-tramoxazole

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7
Q

How do you treat ESBLs?

A

Carbapenem such as meropenem

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8
Q

What populations are at high risk of developing an infection from vancomycin-resistant enterococci?

A

○ Dialysis patients ○ Transplants ○ Haematology patients ○ ICU patients

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9
Q

Are enterococci Gram +ve or Gram -ve?

A

Gram positive

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10
Q

Why are enterococci hard to eradicate and treat?

A

Relatively low virulence, but have many genes encoding adhesion proteins so can develop resistance quickly

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11
Q

What are the main organisms associated with healthcare associated infections? (9)

A

• Staphylococcus aureus • Escherichia coli (UTI) • CoNS (coagulase negative Staphylococcus infection) • Klebsiella pneumoniae • Enterococcus faecalis • Candida albicans • Viruses: ○ Influenza ○ Norovirus • Clostridium difficile

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12
Q

What is the commonest cause of nosocomial diarrhoea?

A

Clostridium difficile

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13
Q

Treatment for Clostridium difficile diarrhoea?

A

Metronidazole PO

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14
Q

What is impetigo?

A

High contagious skin infection restricted to the epidermis

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15
Q

Clinical presentation of impetigo?

A

Usually found on face, hands and neck and is generally mild and self-limiting disease that heals without scarring

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16
Q

Pathogens associated with impetigo?

A

Almost always caused by S. aureus. Occasionally associated with S. pyogenes

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17
Q

Treatment of impetigo?

A

No school 2-3 days Basic hygiene Topical antibiotics for localised rashes (fusidic acid 2% cream tds) Oral antibiotics for extensive lesions (flucloxaxillin or cephalexin)

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18
Q

What is an abscess?

A

Collection of pus within the dermis and deeper skin tissues that is tender and fluctuant

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19
Q

Pathogens associated with abscesses?

A

Most common is S.aureus. Rarely, can be polymicrobial

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20
Q

Difference between a furuncle and a carbuncle?

A

Furuncle involves one hair follicle, carbuncle involves several hair follicles

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21
Q

Treatment of abscess without systemic symptoms?

A

Incision and drainage + covering with dry dressing

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22
Q

Treatment of abscess )+/- MRSA) with systemic symptoms?

A

Incision and drainage + flucloxacillin PO (if MRSA treat with co-trimoxazole or clindamycin)

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23
Q

What is cellulitis?

A

Bacterial infection of the skin affecting the dermis and subcutaneous fat

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24
Q

Risk factors for cellulitis?

A

Obesity Diabetes Disrupted skin

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25
Q

Treatment of mild cellulitis (no systemic symptoms)?

A

Oral flucloxacillin Oral Co-trimoxazole or clindamycin if MRSA

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26
Q

Treatment of severe cellulitis?

A

IV fluclox or cephalexin IV vanc if MRSA

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27
Q

What is necrotising fasciitis?

A

Aggressive subcutaneous infection which tracks along the superficial fascia very quickly

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28
Q

How does NF evolve? When is NF suspected?

A

Almost always presents as an initial cellulitis that deterioates very quickly - suspect it in all patients that do not improve after first 24 hours

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29
Q

What is the mortality of NF?

A

>20%

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30
Q

Causative organisms for monomicrobial NF?

A

S. pyogenes S. aureus Vibrio vulnificus Aeromans

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31
Q

Risk factors for monomicrobial NF?

A

Obesity Venous insufficiency IVDU

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32
Q

Risk factors for polymicrobial NF?

A

GU-related (perianal abscess, penetrating abdo wound, surgery) IVDU with contaminated needles

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33
Q

Treatment of NF?

A

Surgical debridement Empiric antibiotics: - Tazabactam + piperacillin - ceftriaxone + metronidazole

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34
Q

What do yeasts look like on microscopy?

A

Round or oval shaped

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35
Q

How do yeasts reproduce?

A

Budding

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36
Q

What are some common examples of infectious yeasts? (2)

A

Candida albicans Cryptococcus neoformans

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37
Q

What do moulds look like on microscopy?

A

Tubular hyphae

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38
Q

How do moulds reproduce?

A

Spores

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39
Q

What are 3 examples of infectious moulds?

A

Dermatophytes Aspergillus species (e.g. fumigatus) Zygomycetes

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40
Q

What is the main difference between human and fungal cells?

A

The cell membrane of fungi contains ergosterol rather than cholesterol (can target this for an antifungal)

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41
Q

Systemic antifungals?

A

Amphotericin B Oral azoles (e.g. fluconazole) Echinocandins

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42
Q

Systemic/mucocutaneous antifungal?

A

Terbinafine

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43
Q

Topical antifungals?

A

Nystatin Topical azoles Amphotericin B pastilles

44
Q

What is the most common fungal infection?

A

Candida albicans

45
Q

Where is candida albicans commensal?

A

Mouth, gut, vagina (approx. 80% of population)

46
Q

3 main clinical syndromes of candida infection?

A
  1. local overgrowth on mucous membranes 2. invasive focal infection 3. widespread visceral dissemination in the neutropenic host/severely ill patient
47
Q

What is this?

A

Candida albicans - dark budding yeasts with psuedohyphae on gram stain

48
Q

What isthe main species of candida?

A

Candida albicans

49
Q

Treatment for skin/mucosal candidiasis (no systemic involvement)?

A

Topical treatment:

  • Nystatin suspension or pastilles
  • Amphotericin B pastilles
  • Azole pessaries or cream
50
Q

Treatment of serious/systemic candidiasis?

A

Oral or IV antifungal (e.g. azole)

51
Q

What are the two variants of Cryptococcus?

A
  • C. neoformans
  • C. gatti
52
Q

What is the most common type of infection by Cryptococcus?

A

Aymptomatic pulmonary infection followed by haematogenous spread to CSF resulting in meningitis in the immunocompromised host

53
Q

What are some features of cryptococcal meningitis?

A

Slowly progressive, chronic lymphocytic meningitis

10-100 WBCs in CSF with lymphocyte predominance

High protein, low glucose in CSF

Positive cryptococcal antigen in CSF and serum

54
Q

What is this?

A

Cryptococcus species on India ink stain - encapsulated yeasts

55
Q

Treatment of cryptoccocal meningitis?

A

LP to reduce pressure in CSF

IV amphotericin B and IV or oral fluconazole for at least 6 weeks

56
Q

What are ‘tinea’ infections caused by?

A

Dermatophyte infection

57
Q

What are the most common dermatophyte species?

A

Trichophyton rubrum (70%)

Trichophyton mentagrophytes

Microsporum canis

Epidermophytons

58
Q

Are dermatophyte infections self-limiting?

A

No

59
Q

Treatment for dermatophyte infections?

A

Skin:

  • Topical azole (e.g. clotrimazole, miconazole)

Nails:

  • Oral terbinafine OR itraconazole
60
Q

What is pityriasis versiocolour caused by?

A

Malassezia furfur yeast

61
Q

Treatment of pityriasis versicolour?

A

Oral or topical azole for 2 weeks

62
Q

What is a greasy rash on face/dandruff called?

A

Seborrhoeic dermatitis (caused by pityrosporum species)

63
Q

Treatment of seborrhoeic dermatitis?

A

Topical azole

64
Q

What is a spore-bearing, branching mould that is common in rotting vegetation?

A

Aspergillus fumigatus

65
Q

What diseases does Aspergillus fumigatus cause?

A
  • Cavitating pneumonia with multiple lesions (in immunocompromised hosts)
  • Allergic bronchopulmonary aspergillosis (ABPA)
66
Q

What is this?

A

Aspergillus species - silver stain

67
Q

Treatment of Aspergillus pneumonia?

A

Amphotericin B IV for weeks

?liposomal amphotericin B (less nephrotoxic)

Voriconazole or other azoles

Surgery

68
Q

2 examples of endoparasites?

A

Tapeworms, roundworms

69
Q

Two examples of ectoparasites?

A

Lice, scabies

70
Q

Definition of a parasite

A

Life forms, larger than bacteria or viruses, that benefit at the expense of another life form (the host)

71
Q

What are protozoa?

A

Unicellular eukaryotes that may be motile due to the presence of flagellae or cilia

72
Q

4 important protozoal diseases?

A
  • Plasmodium falciparum* - malaria
  • Toxoplasma gondii -* toxoplasmosis
  • Giardia lamblia -* giardiasis
  • Trichomonas vaginalis -* trichomoniasis
73
Q

What is the most common mode of transmission of giardia? How does it survive?

A

Water contamination - can form a cyst that protects the cell from chlorine disinfection etc. so it can survive for a long time outside the body

74
Q

What is this?

A

Cysts and trophozoites of Giardia lamblia (in faeces)

75
Q

Treatment for giardiasis?

A

Metronidazole 500mg PO tds for 7 days

76
Q

What are the 3 main routes of transmission of Toxoplasma gondii?

A
  1. Food-borne
  2. Zoonotic (esp. cats)
  3. Congenital (mother to child infection)
77
Q

What does infection with T. gondii cause?

A
  • Normally a self-limiting mild illness that is acquired in childhood
  • Childhood illness results in persistent asymptomatic infection that may reactivate if immunocompromised resulting in serious disease (e.g. brain abscess)
  • Primary maternal infection during pregnancy may result in serious ocular and neurological infection in the foetus
78
Q

What are the two most common organisms that cause malaria?

A
  • Plasmodium falciparum* - severe disease
  • Plasmodium vivax* - benign disease
79
Q

What is the vector for malaria?

A

Anopheles mosquito (females)

80
Q

Where does the malaria parasite reside inside the host?

A

RBCs and liver

81
Q

Classic symptoms of malaria include?

A

Attacks of cyclical fevers (cold stage, hot stage, sweating stage) that last for 6-10 hours and occur every 2 days (or every 3 days with more rare strains)

82
Q

What is this?

A

Blood smear showing RBCs infected with Plasmodium falciparum in ring form (delicate rings with 1 or 2 chromatin dots)

83
Q

How does P. falciparum cause disease?

A

Infects any RBC leading to a high parasite load, and inserts an abnormal protein into RBC membrane causing them to adhere to the endothelium in capillaries, resulting in sequestration, particularly in the brain and kidneys.

84
Q

Why is P. vivax more benign than P. falciparum?

A

Low parasite load as it only infects young RBCs, and does not cause sequestration in capillaries so there is no risk of severe disease

85
Q

Treatment of P. falciparum?

A

Quinine and doxycycline to kill merozoites in erythrocytes

86
Q

Treatment of P. vivax?

A

Chloroquine (to kill merozoites in RBCs) and primaquine (to kill hypnozoites in liver that can reactivate later on in life)

87
Q

Malaria prevention includes?

A
  • Avoid malaria regions
  • Mosquito control
  • prophylactic treatment with doxycycline or mefloquine
88
Q

Most common cause of pharyngitis?

A

Viruses - adenovirus, coronavirus, enterovirus, rhinovirus

89
Q

Most common bacterial cause of pharyngitis?

A

Streptococcus pyogenes (GAS)

90
Q

When would you want to take a swab for pharyngitis?

A

In Maori and Pacific Island populations, to treat GAS and prevent rheumatic fever

91
Q

What is rheumatic fever?

A

Inflammatory disease involving heart joints, skin and brain that typically develops about 2-4 weeks after a throat infection

92
Q

What are the criteria used for diagnosis of ARF? What are the major criteria?

A

Jones criteria

Major criteria:

  • Polyarthritis
  • Carditis
  • Subcutaneous nodules
  • Erythema marginatum
  • Sydenham’s chorea
93
Q

When is the heart involved in ARF?

A

In about half of cases - permanent damage usually requires several bouts of ARF, but can occur after just one episode

94
Q

What is the pathogenesis of ARF?

A

Due to molecular mimicry of anti-strep antibodies resulting in autoimmune assault on own tissues (autoantibodies against myosin, collagen and other native tissue components)

95
Q

Age range of ARF?

A

4-19 years

96
Q

Management of ARF?

A

Treat GAS infection with:

  • Penicillin V PO 2-3xdaily for 10/7 (<20kg = 250mg, >20kg = 500mg)
  • OR amoxicillin PO 50mg/kg/day od for 10/7 (max 1000mg)
  • OR single dose IM benzathine penicillin

Prevent subsequent infection with secondary prophylaxis:

  • Benzathine penicillin IM monthly
97
Q

What is PSGN?

A

Post-streptococcal glomerulonephritis.

An uncommon type III hypersensitivity reaction that occurs 10-21 days post-GAS infection.

98
Q

Symptoms and signs of PSGN?

A

Symptoms:

  • Pale skin
  • Lethargy
  • Loss of appetite
  • Headache
  • Dull back pain

Clinical findings:

  • Dark coloured urine
  • Oedema
  • High blood pressure
99
Q

Management of PSGN?

A

Supportive care

100
Q

How do you decide severity of CAP?

A

CURB65 score

C - confusion

U - urea >7mmol/L

R - respiratory rate >30/min

B - blood pressure SBP <90, DBP <60

Age >65

Low severity = 0-1

Moderate severity = 2

Severe = 3-5

101
Q

What investigations are required for low severity CAP?

A

None (other than CXR)

102
Q

What investigations are required for moderate severity CAP?

A

Blood cultures

Sputum

Pneumococcal +/- legionella urinary antigen

PCR for selected pathogen

103
Q

What investigations are required for severe CAP?

A

Blood cultures

Sputum culture

Pneumococcal + legionella urinary antigen

PCR for pathogens including viral and atypical pathogens

104
Q

Treatment of non-severe CAP?

A

Amoxicillin 500mg-1g PO tds for 7 days

105
Q

Treatment for suspected atypical CAP (or patients that do not get better after 24-48 hours of treatment)?

A

Erythromycin/roxithromycin

106
Q
A

Pathology and Laboratory Science (4 decks)

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