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ACEM Primary Written > Infectious diseases: Pathology - Bacterial infections > Flashcards

Infectious diseases: Pathology - Bacterial infections Flashcards

1
Q

What type of bacteria is Mycobacteria tuberculosis? Describe its structure

A

Acid-fast, weakly Gram positive, aerobic rods
Unique waxy cell wall composed of mycolic acid
Non-spore-forming, non-motile

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2
Q

List eight conditions which increase risk of contracting tuberculosis

A
  1. HIV
  2. DM
  3. Hodgkin lymphoma
  4. Chronic lung disease
  5. Chronic renal failure
  6. Malnutrition
  7. Alcoholism
  8. Immunosuppression
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3
Q

How does primary tuberculosis typically present?

A

Usually asymptomatic
May cause fever and pleural effusion

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4
Q

Where does tuberculosis typically initially implant when inhaled?

A

Upper part of lower lobe

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5
Q

Describe the pathogenesis of primary tuberculosis

A

First 3 weeks:
- M. tuberculosis inhaled and endocytosed by alveolar macrophages (several receptors involved)
- Replicates within phagosome by blocking fusion to lysosome, resulting in bacteraemia and seeding of multiple sites

After 3 weeks:
- TH1 response initiated by mycobacterial Ag entering lymph nodes, results in NO production and macrophage activation
- Formation of epithelioid granulomas (often with central caseating necrosis; type IV hypersensitivity response)

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6
Q

In what % of cases of primary tuberculosis does the cell-mediated immune response control the initial infection? How can this be confirmed clinically? What happens if the infection is not initially controlled?

A

95%
As demonstrated by positive tuberculin test
In remaining 5%, proceeds to progressive primary tuberculosis (in the form of tuberculous pneumonia or disseminated tuberculosis)

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7
Q

How does progressive primary tuberculosis present compared with secondary tuberculosis?

A

Progressive primary tuberculosis:
- Usually resembles an acute bacterial pneumonia with lower and middle lobe consolidation, hilar lymphadenopathy, and pleural effusion
- Cavitation is rare

Secondary tuberculosis:
- Classically involves apex of one or more lungs, with less involvement of regional lymph nodes but more cavitation compared with primary form

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8
Q

What is secondary tuberculosis?

A

Pattern of tuberculous disease that arises in a previously sensitised host
Most commonly occurs years after initial infection at a time of immunocompromise, and is usually due to reactivation of latent infection (but may also be due to exogenous re-infection, especially in high-prevalence areas/populations)

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9
Q

Describe the typical presentation of secondary tuberculosis

A

Symptoms often insidious and are initially related to cytokine release with low-grade relapsing-remitting fevers, night sweats, malaise, anorexia and weight loss
With progressive pulmonary involvement: mucopurulent sputum, haemoptysis (in 50%), pleurisy
Haematogenous spread produces extrapulmonary manifestations (e.g. kidneys, meninges, bone marrow)

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10
Q

What is disseminated tuberculosis?

A

Widespread tuberculous infection due to haematogenous spread of mycobacteria

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11
Q

What organs are most often affected in single organ tuberculosis?

A
  1. Adrenals (important cause of Addison’s disease)
  2. Kidneys
  3. Bone (tuberculous osteomyelitis)
  4. Female genital tract (salpingitis, endometritis)
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12
Q

What is miliary tuberculosis? Which organs are typically affected?

A

Tuberculous infection caused by massive haematogenous dissemination with widespread minute granulomatous foci
Affected organs include liver, bone marrow, spleen, adrenals, meninges, kidneys, fallopian tubes, epididymis

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13
Q

What is a Ghon focus? What is a Ghon complex?

A

Area of grey-white inflammation with consolidation which develops with immune sensitisation in primary tuberculosis
May develop central caseous necrosis and undergo scarring

Ghon complex is Ghon focus (parenchymal involvement) and draining regional lymph nodes (which may also caseate)

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14
Q

How does tuberculosis in HIV typically present, depending on the CD4+ count?

A

CD4+ count >300: typical secondary tuberculosis presentation
CD4+ count <200: progressive primary tuberculosis

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15
Q

How does the presentation of tuberculosis differ in HIV?

A

Increased extrapulmonary involvement (especially with increasing levels of immunosuppression)
Increased false negative sputum smears and tuberculin tests
Higher bacterial load in spite of false negative tests (likely due to decreased cavitation into airways)
Absence of characteristic granulomas in tissues due to lack of competent immune response

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16
Q

Six infectious syndromes caused by Staphylococcus aureus

A
  1. Skin infections (abscess, carbuncle, furuncle, impetigo, wounds)
  2. Endocarditis
  3. Pneumonia
  4. Osteomyelitis
  5. Food poisoning
  6. Toxic shock syndrome
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17
Q

Three virulence factors of Staphylococcus aureus

A
  1. Surface proteins involved in adherence (e.g. surface receptors for fibrinogen and fibronectin)
  2. Secreted enzymes (e.g. lipase degrades fatty acids on the skin)
  3. Toxins (including exotoxins A and B which produce staphylococcal scalded-skin syndrome; endotoxin which causes food poisoning; superantigens which cause toxic shock syndrome)
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18
Q

How do staphylococci vs streptococci grow?

A

Both Gram positive cocci
Staphylococci in bunches
Streptococci in pairs (diplococci) or chains

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19
Q

Five specific streptococcal species and their infective syndromes

A
  1. S. pyogenes (group A beta-haemolytic): pharyngitis, scarlet fever, erysipelas, impetigo, rheumatic fever, TSS, glomerulonephritis
  2. S. agalactiae (group B beta-haemolytic): neonatal sepsis and meningitis, chorioamnionitis in pregnancy (colonises female genital tract)
  3. S. pneumoniae (alpha-haemolytic): CAP, meningitis in adults
  4. Viridans-group streptococci (includes several alpha-haemolytic and non-haemolytic species): endocarditis
  5. S. mutans: dental caries
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20
Q

What is enterococcus?

A

Gram positive cocci that grows in chains
Previously considered “group D streptococci”

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21
Q

What infections are caused by enterococcus?

A

UTI
Endocarditis

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22
Q

Outline six virulence factors of streptococcal species, giving examples where relevant

A
  1. Antiphagocytic capsules: S. pneumoniae, S. agalactiae, S. pyogenes
  2. M protein (also antiphagocytic): S. pyogenes
  3. C5a peptidase (degrades C5a): S. pyogenes
  4. Secreted exotoxins: S. pyogenes
  5. Pneumolysin (lyses host cell membranes): S. pneumoniae
  6. Lactic acid production from sucrose (demineralises tooth enamel): S. mutans
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23
Q

What kind of bacteria is anthrax?

A

Large spore-forming Gram positive rod

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24
Q

What are the three syndromes produced by Bacillus anthracis? Give a brief description of each

A
  1. Cutaneous anthrax:
    - 95% of naturally occurring infections
    - Pruritic papule -> vesicle -> ruptured vesicle with formation of black eschar -> eschar falls off
  2. Inhalational anthrax:
    - Spores germinate in lymph nodes -> haemorrhagic mediastinitis -> bacteraemia -> meningitis -> shock, death (within 1-2 days)
  3. GI anthrax:
    - From contaminated meat
    - Causes nausea and vomiting, abdominal pain, dysentery
    - Mortality >50%
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25
Q

What are the two main virulence factors of Bacillus anthracis?

A
  1. Antiphagocytic capsule
  2. Exotoxins:
    - Oedema factor (EF): increased cAMP causes water efflux from cell
    - Lethal factor (LF): protease which produces cell death (mechanism unclear)
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26
Q

What type of organism is Haemophilus influenzae?

A

Polymorphic Gram negative

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27
Q

What three infective syndromes are caused by Haemophilus influenzae?

A
  1. Epiglottis
  2. Laryngotracheobronchitis (croup)
  3. Meningitis in young children
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28
Q

What morphological changes are characteristic of atypical pneumonia?

A

Patchy inflammatory changes in lungs, largely confined to alveolar septa and interstitium

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29
Q

What is the usual clinical presentation of atypical pneumonia?

A

Moderate sputum
No physical findings of consolidation
Lack of alveolar exudate
Moderate WCC elevation

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30
Q

Four causes of atypical pneumonia. Which is most common?

A
  1. Mycoplasma pneumoniae (most common)
  2. Viruses (influenza, RSV, human metapneumovirus, adenovirus, rhinovirus, rubeola, varicella)
  3. Chlamydia pneumoniae
  4. Coxiella burnetti (Q fever)
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31
Q

What kind of bacteria are clostridia?

A

Anaerobic spore-producing Gram positive bacilli

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32
Q

What four infective syndromes are caused by Clostridium perfringens and septicum?

A
  1. Cellulitis and myonecrosis (gas gangrene)
  2. Uterine myonecrosis (associated with illegal abortions)
  3. Mild food poisoning
  4. Necrotising colitis
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33
Q

Virulence factor of Clostridium perfringens

A

Produces 14 exotoxins including alpha-toxin (phopholipase C)

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34
Q

Virulence factor of Clostridium tetani

A

Secretes neurotoxin tetanospasmin which inhibits neurotransmitter release (especially GABA) to induce convulsive skeletal muscle reactions

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35
Q

Virulence factor of Clostridium botulinum

A

Secretes neurotoxin botulinum toxin which inhibits neurotransmitter release (especially ACh) to induce severe paralysis of respiratory and other skeletal muscles

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36
Q

Where does botulinum toxin grow?

A

In adequately sterilised canned foods

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37
Q

Virulence factor of Clostridium difficile

A

Produces toxin A (stimulates chemokine production) and toxin B (directly cytopathic)

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38
Q

What is the difference between clinical presentation of clostridial cellulitis vs gas gangrene

A

Cellulitis: foul odour, thin discoloured exudate, rapid and wide destruction with granulation tissue at borders
Gas gangrene: life-threatening, marked oedema and enzymatic necrosis of muscle cells 1-3 days post injury, with large bullous vesicles and subcutaneous emphysema (inflamed muscles eventually become soft, blue-black, friable and semi-fluid)

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39
Q

What type of bacteria is chlamydia trachomatis?

A

Gram negative coccobacillus
Obligate intracellular pathogen of columnar epithelial cells

40
Q

Four infective syndromes caused by Chlamydia trachomatis

A
  1. Urogenital infections
  2. Lymphogranuloma venereum
  3. Trachoma (ocular infection of children)
  4. Inclusion conjunctivitis or pneumonitis in infants born to mothers with C. trachomatis cervicitis
41
Q

What is Reiter syndrome? Who does it typically affect?

A

Triad of polyarthritis, conjunctivitis and urethritis
Typically occurs in men aged 20-40 with HLA association

42
Q

What is lymphogranuloma venereum and how does it present? Describe the histopathology

A

Chronic ulcerative disease:
- Initially produces papules on mucosa
- Subsequent swelling and rupture of draining lymph nodes
- May cause fibrosis and anogenital strictures

Histopathology:
- Mixed granulomatous and neutrophilic reaction

43
Q

In which two forms does chlamydia trachomatis exist?

A
  1. Elementary body (EB; infectious form):
    - Metabolically inactive, does not divide
    - Taken up by endocytosis and prevents endosome and lysosome fusion
    - Differentiates into reticulate body
  2. Reticulate body (non-infectious form):
    - Metabolically active, produces new elementary bodies which infect additional cells
44
Q

What is the most common sexually transmitted infection?

A

Chlamydia trachomatis

45
Q

What type of bacteria is Neisseriae?

A

Encapsulated Gram negative diplococcus, aerobic

46
Q

What does Neisseria meningitidis cause?

A

Meningitis in children less than 2yrs old

47
Q

What infective syndromes are caused by Neisseria gonorrhoea?

A
  1. Urethritis in men
  2. Often asymptomatic in women but causes pelvic inflammatory disease and salpingitis
  3. Pharyngitis
  4. Proctitis
  5. Perinatal ophthalmic infection and blindness
  6. Disseminated infection in setting of immunodeficiency -> presents as septic arthritis
48
Q

What are two complications of Neisseria gonorrhoea seen in men, and four complications seen in women?

A

Men:
1. Urethral strictures
2. Chronic infections of epididymis, prostate, seminal vesicles

Women:
1. Tubo-ovarian abscess
2. Scarring
3. Infertility
4. Increased risk of ectopic pregnancy

49
Q

Three virulence factors of Neisseria gonorrhoea

A
  1. Capsule prevents phagocytosis
  2. Antigenic variation
  3. Adherence via pili proteins (also subject to antigenic variation)
50
Q

How is perinatal ophthalmic infection by Neisseria gonorrhoea prevented?

A

By prophylaxis with silver nitrate

51
Q

What type of bacteria is Treponema pallidum? Describe its structure

A

Gram negative spiral-shaped (spirochetes), microaerophilic
Periplasmic flagella wound around helical protoplasm, covered in membrane called outer sheath

52
Q

What are the three stages of syphilis and their timeframes?

A
  1. Primary syphilis (3 weeks post contact)
  2. Secondary syphilis (2-10 weeks post primary chancre)
  3. Tertiary syphilis (at least 5 years of latent infection)
53
Q

How does primary syphilis present?

A

Single firm non-tender raised red lesion (chancre) at the site of invasion on penis, cervix, vaginal walls, or anus
Haematogenous and lymphatic spread of treponemes occurs even before chancre appears

54
Q

Are chancre infectious?

A

Yes, spirochetes are plentiful within chancre

55
Q

How long does chancre take to heal?

A

3-6 weeks

56
Q

In what % of untreated people does secondary syphilis occur?

A

75%

57
Q

What causes secondary syphilis?

A

Due to haematogenous and lymphatic spread and proliferation of treponemes within skin and mucocutaneous tissues

58
Q

How does secondary syphilis present?

A

Painless spirochete-containing skin lesions (variable morphology: maculopapular, scaly), frequently on palms and soles
Condylomata lata (plaques) on moist areas of skin
May be accompanied by white oral lesions, fever, lymphadenopathy, headache, arthritis, and (rarely) immune complex nephritis

59
Q

How long does secondary syphilis last?

A

Several weeks

60
Q

What are the three main manifestations of tertiary syphilis? Which is most common?

A
  1. Cardiovascular syphilis (most common, occurs in 80%): aortitis leading to aneurysm formation and aortic regurgitation
  2. Neurosyphilis: meningovascular disease, tabes dorsalis, generalised paresis
  3. Benign: gummas (nodular lesions due to delayed-type hypersensitivity) arising mainly in bone, skin and upper airways
61
Q

When is perinatal transmission of syphilis most likely to occur?

A

During primary and secondary syphilis

62
Q

Describe the three presentations of congenital syphilis

A
  1. Intrauterine or perinatal death (25%)
  2. Infantile (early): nasal congestion, desquamating rash, hepatomegaly, skeletal abnormalities
  3. Tardive (late): triad of interstitial keratitis, Hutchinson teeth, and CN VIII deafness
63
Q

Describe three morphological features of syphilis

A
  1. Obliterative endarteritis
  2. Treponemas on silver stain
  3. Plasma cell infiltrates
64
Q

What are the two types of serological tests for syphilis?

A
  1. Non-treponemal: anti-cardiolipin
  2. Treponemal: antibodies to T. pallidum
65
Q

When do non-treponemal syphilis tests become positive?

A

Positive after 4-6 weeks
However negative in tertiary syphilis

66
Q

When do treponemal syphilis tests become positive?

A

Positive after 4-6 weeks
Remains positive

67
Q

Four conditions which can produce a false positive on a non-treponemal syphilis test

A
  1. SLE
  2. Pregnancy
  3. Hypergammaglobulinaemia
  4. Other acute infections
68
Q

What type of bacteria is Bordatella pertussis?

A

Gram negative coccobacillus

69
Q

Three virulence factors of Bordatella pertussis

A
  1. Haemagglutinin adhesin
  2. Exotoxin pertussis toxin (inactivates Gs receptors and paralyses cilia)
  3. Haemolysin
70
Q

What infective syndrome is caused by Bordatella pertussis? What three features are seen in severe cases?

A

Laryngotracheobronchitis
Severe cases feature mucosal erosion, hyperaemia, and copious mucopurulent sputum

71
Q

What type of bacteria is Corynebacterium diphtheriae?

A

Gram positive bacillus

72
Q

How is Corynebacterium diphtheriae transmitted?

A

By aerosols or skin exudate

73
Q

Does immunisation prevent colonisation with Corynebacterium diphtheriae?

A

No, does not prevent colonisation but protects from lethal effects

74
Q

How does diphtheria toxin function?

A

Blocks host cell protein synthesis

75
Q

Describe the pathogenesis of diphtheria

A

Causes epithelial necrosis -> fibrinosuppurative exudate -> coagulates on ulcerated necrotic surface with marked vascular congestion, interstitial oedema, and fibrin exudate -> membrane sloughs off, may cause bleeding and asphyxiation
May also cause hyperplasia of spleen and liver
Exotoxin can cause myocardial fatty change and (less commonly) fatty change and necrosis in liver, kidneys and adrenals

76
Q

What kind of bacteria is Pseudomonas aeruginosa?

A

Gram negative bacillus
Aerobic

77
Q

In which three populations is Pseudomonas a deadly pathogen?

A
  1. Cystic fibrosis
  2. Severe burns
  3. Neutropenia
78
Q

Five infective syndromes caused by Pseudomonas aeruginosa and populations at risk of each

A
  1. Chronic respiratory infection in cystic fibrosis
  2. Skin infections (e.g. in burns), especially hospital-acquired
  3. Corneal keratitis in contact lens wearers
  4. Endocarditis and osteomyelitis in IVDUs
  5. Otitis externa (including malignant otitis externa in diabetes mellitus)
79
Q

Six virulence factors of Pseudomonas aeruginosa

A
  1. Pili and adherence proteins
  2. Alginate secretion (forms biofilm)
  3. Exotoxin A (diphtheria-like: inhibits Gs to prevent host protein synthesis)
  4. Exoenzyme S (inhibits Gs that regulates cell growth and metabolism)
  5. Phospholipase C (lyses RBCs, degrades surfactant) and elastase (degrades IgG, ECM)
  6. Produces iron-containing compounds that are toxic to endothelium
80
Q

Morphological feature of Pseudomonas aeruginosa

A

“Fleur-de-lis” pattern of necrotising pneumonia

81
Q

What type of bacteria is Legionella pneumophilla?

A

Gram negative coccobacillus (but stains poorly)

82
Q

Where is Legionella pneumophila typically found and how is it transmitted?

A

Typically found in aerosols from cooling systems of buildings, water cooler towers
Transmission due to inhalation of aerosols or aspiration of contaminated water

83
Q

Describe the pathogenesis of Legionalla pneumonia

A

Facultative intracellular parasite of macrophages
Fails to induce respiratory burst
Blocks phagosome from fusion with lysosome

84
Q

What infective syndrome is caused by Legionella pneumophila? What patient groups are particularly at risk?

A

Multifocal pneumonia, fibropurulent type
Increased susceptibility in those with predisposing disease including cardiac, renal, immunologic and haematological (organ transplant recipients especially vulnerable)

85
Q

Describe the typical morphology of infection with Legionella pneumophila

A

High ratio of mononuclear phagocytes to neutrophils

86
Q

What type of bacteria is Listeria monocytogenes?

A

Gram positive coccobacillus, facultative intracellular

87
Q

How is Listeria monocytogenes transmitted?

A

Via contaminated food (e.g. dairy products, chicken, hot dogs)

88
Q

What three infective syndromes are caused by Listeria monocytogenes?

A
  1. Severe food-borne infection
  2. In pregnancy and neonates: amnionitis, abortion, stillbirth, neonatal sepsis
  3. In neonates and immunosuppression: disseminated disease, exudative meningitis
89
Q

Three virulence factors of Listeria monocytogenes

A
  1. Internalins (leucine-rich proteins which bind E-cadherin on host cells)
  2. Listeriolysin O and two phospholipases (enable bacteria to escape phagolysosome -> multiples in cytosol)
  3. Surface protein ACTA (induces actin polymerisation -> enables bacteria to infect adjacent cells)
90
Q

Which cytokine mediates protection against Listeria monocytogenes?

A

IFN-y

91
Q

What organism causes leprosy?

A

Mycobacterium leprae

92
Q

What type of bacteria is Mycobacterium leprae?

A

Acid-fast bacilli
Obligate intracellular

93
Q

What infective syndrome is produced by Mycobacterium leprae?

A

Leprosy: produces skin and peripheral nerve nodules

94
Q

What causes plague?

A

Yersinia pestis

95
Q

What type of bacteria is Yersinia pestis?

A

Gram negative coccobacillus
Facultative intracellular

ACEM Primary Written (150 decks)

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