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OPath Block 2 > 3. Bacterial Infections > Flashcards

3. Bacterial Infections Flashcards

1
Q

What is impetigo?

A

Superficial infection of skin caused by Staphylococus aureus and/or Streptococus pyogenes

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2
Q

What allows bacteria to cause impetigo?

A

Breaks of skin:

cut

scratch

abrasion

dermatitis

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3
Q

What populations tend to get impetigo?

A

Children

adults with systemic conditions

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4
Q

What determines if a patient will develop impetigo when bacteria enters?

A

Immune status

bacterial load

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5
Q

How does impetigo clinically progress?

A

Vesicles with clear fluid at site of injury → large bullae or ulcerated/crusted

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6
Q

Dx of impetigo?

A

clinilcal presentation & history

pattern corresponds to scratches/breaks of skin

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7
Q

Tx of impetigo

A

prevention and topical antibiotics

will heal by itself in most cases

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8
Q

Which pathogen that causes impetigo is most worrysome? why?

A

MRSA

Resistant to typical antibiotics and if left untreated will spread systemically

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9
Q

Steptococcus pyogenes is aka what?

A

Group A ß-hemolytic streptococcus (GAS)

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10
Q

What is pharyngitis/tonsilitis?

A

Infection in the throat. the two conditoins usually occur together

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11
Q

How is pharyngitis spread?

A

Respiratory droplet

Oral secretion

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12
Q

What kind of pathogen causes the majority of pharyngitis? Tx?

A

Virus

No Tx needed or suppurative

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13
Q

What bacteria causes the majority of bacterial pharyngitis?

A

GAS

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14
Q

What population is most commonly affected by bacterial pharyngitis?

A

School aged children who then spread it to their family

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15
Q

S/S of bacterial phayrngitis

A

Sore throat

redness of oropharynx and tonsil

cervical lymphadenopathy

NO VESICLES unlike viral pharyngitis

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16
Q

Dx of bacterial pharyngitis?

A

Rapid direct antigen test (5-10 mins)

culture (gold standard, 1-2 days)

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17
Q

Bacterial pharyngitis Tx

A

Antibiotics

Necessary to prevent complications

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18
Q

How does scarlet fever begin?

A

Untreated strep throat that has spread throughout body but has not developed antitoxin Ab

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19
Q

What causes the red skin in scarlet fever?

A

GAS produces erythrogenic toxin.

The toxin attacks small blood vessels cusing the skin rash all over hte body and mucosa

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20
Q

What is exanthem?

A

skin rash

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21
Q

What is enanthem?

A

Mucosa rash

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22
Q

What population is most often affected by scarlet fever?

A

Children

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23
Q

How does the skin rash in scarlet fever resolve?

A

Fades in a week followed by desquamation

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24
Q

Where is oral cavity petechiae most obvious in scarlet fever?

A

Soft palate

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25
Q

How is the tongue affected in scarlet fever?

A

Hyperplastic

erythematous fungiform papillae against white background

Initially white strawberry; later red strawberry (5-7 days). White coat (keratin) sheds off like the skin rash leaving the red coloration

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26
Q

What complications from pharyngitis are most concerning?

A

Rheumatoid fever

Glomerulonephritis

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27
Q

Why do bacterial pharyngitis systemic complications occur?

A

GAS produces M protein which the body forms ABs against

Due to M proteins similarity to host tissue, the M protein ABs will cross react with antigens from host tissue causing tissue damage

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28
Q

Why are recurrent infections of bacterial pharyngitis concerning?

A

Recurrent infections will increase M protein Ab production which will cause significant organ destruction from constant cross reaction

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29
Q

If a patient with GAS infection has a family history of RF, how does this affect treatment?

A

Pt with family history of Rf requires a post therapeutic lab test to ensure that all of the bacteria has been cleared

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30
Q

What pathogen causes tuberculosis?

A

Mycobacterium tubercolosis

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31
Q

What characteristic of M. tuberculosis confers it so much strength? What adidtional strengths are gained?

A
  • High lipid content of its cell wall
    • Resistance to killing by phagocytosis
    • Inhibits penetration of antimicrobial agents
    • Resistance to drying and remain viable in dried sputum
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32
Q

Tx for M tuberculosis?

A

Combination of antibiotics

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33
Q

What is tuberculosis?

A

Communicable chronic granulomatous dz

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34
Q

What populations are most affected by TB?

A

Elderly

Poor

AIDS

Immunocompromised

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35
Q

What is the #1 risk factor for TB?

A

AIDS

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36
Q

What is the leading cause of death in HIV infected pts?

A

TB

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37
Q

What causes damage in TB?

A

NOT toxin mediated

Host immune response causes damage (type IV hypersensitivity)

Bacterial antigens are presented to t cells. T cells become sensitized and release cytokines that attract macrophages and T cells to get rid of Mycobacterium.

Macrophages are ineffective in killing mycobacterium. Inability to kill mycobacterium causes T cells to continue releasing cytokines which recruits more T cels and macrophages.

Macrophages then fuse to form giant cells. This walls off bacteria for containment

this forms granules called tubercles with central necrosis called caseous

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38
Q

What are the two classifications of TB?

A

Primary - non-sensitized individuals contacting TB for first time

Secondary - reactivation or re-infection of the bacilli in a previously sensitized host

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39
Q

When does sensitivity occur in primary TB?

A

Second week of infection patient will develop immune response. No initial imune response because pt is not sensitized

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40
Q

How does primary TB manifest in pts?

A

Arrested/self-limited

Tubercle is walled off by calcified connective tissue

Walling off of organism prevents active disease and spread of TB from patient

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41
Q

How is TB reactived to cause secondary TB?

A

Imunosuppression

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42
Q

how does damage occur in secondary TB?

A

An immune response will occur within 2-3 dys after reactivation or reexposure causing greater inflammation which leads to significant destruction of lung tissue

43
Q

How can TB become systemic?

A

Granulomatous lesions can break into blood causing systemic infection. Only occurs in small percentage of secondary patients

44
Q

What is primary progressive TB?

A

Pts that are immunosuppressed and quickly develop systemic TB from primary TB because they cannot effectively wall off bacteria.

45
Q

What patients tend to develop primary progressive TB?

A

HIV patients with high degree of immunosuppression

46
Q

how does oral TB occur?

A

cut in the oral mucosa contaminated by sputum with M. tuberculosis.

Very rarely, occurs in patients with systemic TB (PPT or secondary)

47
Q

S/S of oral TB?

A

Chronic non-healing ulcer or swellings (granulation tissue like)

Osteomyelitis in pts with systemic TB (very rare)

48
Q

Dx of oral TB

A

Biopsy is a must.

Cannot tell from clinical presentation

49
Q

Dx of TB?

A
  • Mantoux test (PPD skin test)
    • inject purified protein isolated from bacteria
    • if body has antigen against bacteria (sensitized), will illicit a reaction within 2-3 days against protein
    • great for screening but not very accurate
  • Culture
    • Takes a long time (3-6 weeks)
    • Gold standard
    • Good for determining use of treating antibiotic
  • Stain
    • acid fast bacilli
    • non-specific
  • PCR
    • quick and specific
    • $$$
50
Q

What is leprosy?

A

Chornic granulomatous dz from Mycobacterium leprae

51
Q

Transmission of leprosy

A

Unclear but possibly ihalation of contaminated respiratory droplets

52
Q

Site of leprosy involvement?

A

Skin and nerves (main)

mucous membrane and resp tract (minor)

53
Q

What are the two classifications of leprosy?

A

Tuberculoid (Paucibacillary)

Lepromatous (Multibacillary)

54
Q

What population of pts develop paucibacillary leprosy?

A

Pts with high immune response

55
Q

Test for paucibacillary leprosy?

A

Positive lepromin test (a skin test to heat killed bacteria)

56
Q

Is paucibacillary leprosy localized or diffuse?

A

Localized

57
Q

S/S of paucibacillary leprosy

A

Manifests as small number of well circumscribed, hypopigmented skin lesions

Nerve involvement leads to loss of sensation in affected skin

58
Q

Paucibacillary leprosy histology

A

granulomatous inflammation with well formed granulomas (multinucleated giant cells surrounded by lymphocytes)

Acid fast stain will show some but few bacteria demonstrating proper immune system function

59
Q

what kind of patients develop multibacillary leprosy?

A

Pts with reduced immune response

60
Q

Test for multibacillary leprosy?

A

Negative lepromin test due to poor immune fxn

61
Q

Is multibacillary leprosy diffuse or localized?

A

Diffuse

62
Q

S/S of multibacillary leprosy

A

numerous ill defined hypopigmented lesions

With time, lesions become thickened

loss of skin appendages (replaced with granulomatous inflammation)

skin enlargement leads to facial distortion

All areas of involvement have no sensation

Nerve involement spread to most of body

63
Q

Histology of multibacillary leprosy?

A

Granulation tissue with ill formed granuloma (multinucleated giant cells mixed with T lymphocytes)

Numerous bacteria in acid-fast stain demonstrating poor immune response

64
Q

What oral lesions manifest in multibacillary leprosy?

A

Soft tissue – ulceration, necrosis and loss of tissue

Bone - resorption and perforation of palate

Facies leprosa - resorption of anterior nasal spine and anterior maxillary alveolar edge (pts end up with collapsed nose and lose front teeth)

65
Q

Dx of leprosy?

A

Characteristic skin lesions with diminished sensation

Prove presence of M. leprae

66
Q

Tx for leprosy

A

Eradicate infection with MDR

Treat complication of nerve drug

Reconstruction of damage

67
Q

What bacteria causes Syphilis?

A

Treponema pallidum

68
Q

Transmission of syphilis?

A

Sexual contact

Mother to fetus

bacteria is vulnerable to drying

69
Q

What accounts for the recent hike in syphilis cases?

A

Unprotected oral sex and AIDs

70
Q

What condition complicates syphilis?

A

AIDS

71
Q

What stages of syphilis are treatable by antibiotics?

A

All (primary, secondary, tertiary)

72
Q

Wha is the trend of a patients infectiousness after contracting syphilis?

A

High -> Low

Primary > secondary > tertiary

73
Q

S/S of primary syphilis?

A

Chancre (Most often at genitalia but oral cavity, lip is most common extragenital site)

Ulcer

Regional lymphadenopathy

highly infectious

74
Q

Dx of primary syphlis

A
  • Serology
    • Microscopy (IHC or dark-field)
    • only good for chancre on genitals not oral cavity bc oral cavity naturally has spirochete bacteria
75
Q

how does secondary syphilis develop?

A

If primary syphilis is untreated, will develop secondary syphilis 4-10 weeks after initial infectoin.

May overlap with primary syphilis

76
Q

how does secondary syphilis resolve?

A

spontaneously heal in 3-12 weeks

May relapse

77
Q

Dx of secondary syphilis

A

Serology

Microscopy

PCR

78
Q

S/S of secondary syphilis?

A

Maculopapular rash

  • often on face, trunk and **palmar and plantar areas **
  • rarely in oral cavity

Mucous patch

  • elevated white patch in oral cavity
  • split papules when on commissure of mouth

Lues maligna

  • appear on skin and mucosa
  • most severe form of secondary syphlis (aka malignany syphilis)
  • multiple nodules that become encrusted very quickly then heal with scars that may lead ot disfigurement
  • mostly seen in HIV pts

Condyloma lata

  • skin and mucosa
  • wart-like lesions
79
Q

What is the typical patient that develops tertiary syphilis now?

A

HIV+ patients

80
Q

What kind of systemic damages arise from tertiary syphilis?

A

CV and CNS damage

81
Q

S/S of tertiary syphilis?

A

Gummas

82
Q

What is congenital syphilis?

A

Transplacental infection of T. pallidum during fetal development

83
Q

What is the most common clinical manifestation of congenital syphilis?

A

Hutchison’s triad

84
Q

What is hutchnson’s triad?

A
  1. Dental anomalies (hutchinson’s incisors and mulberry molars)
  2. Deafness (8th nerve damage)
  3. Blindness (interstitial keratosis)
85
Q

What is the pathology of Bartonella in healthy patients?

A

Pt mounts an immune response and forms granulomatous inflammation

This reaction is normally sufficient in eradicating bacteria without Tx

example = cat scratch dz

86
Q

What is the pathology of bartonella in immunocompromised patients?

A

Pt cannot mount immune response and bacteria promotes vessel formation (angiogenesis)

Leads to bacillary angiomatosis which is a bartonella infection that looks like a tumor

Requires antibiotic

87
Q

What is cat scratch dz?

A

Benign self limiting infection of bartonella hensellae transmitted from cat to human via scratch

88
Q

S/S of cat scratch dz?

A

1-2 weeks: primary skin lesion along scratch line

3-7 weeks: regional lymphadenopathy, may have fever. Primary lesion may be resolved

Scratch on face usually develop submandibular lymphadenopathy

89
Q

Dx of cat scratch dz

A

Base on clinical history and demonstrate the bacteria in the specimen or a positive titer of Ab to B. henselae

Culture not effective

90
Q

Tx of cat scratch dz

A

None needed

follow up with patient to ensure resolution (usually clear by 4 weeks)

91
Q

What is Actinomyces?

A

Gram + filamentous anaerobic bacteria mostly present in head and neck region

92
Q

What is the most common Actinomyces in oral flora?

A

A. isrealii

93
Q

S/S of actinomycosis

A

Acute deep suppurative abscess with an associated draining sinus tract

Colonies of actinomycotic organisms surrounded by neutrophils

Sulfur granules (yellowish flecks seen clinically representing colonies of actinomyces)

94
Q

Dx of actinomycosis

A

Histology + culture

95
Q

Tx of actinomycosis

A

Surgical drainage/debridement and antibiotics

96
Q

What is tonsillar concretions?

A

When a large mass forms into the invaginations of the crypts of the palatine tonsils

97
Q

What is tonsillolithiasis?

A

When the tonsillar concretions become calcified

98
Q

S/S of tonsillar conretions and tonsillolithiasis

A

Usually asymptomatic

Radiograph will show tonsilloliths in ramus area of mandible

If pts feel mass, gargle salt water to prevent further accumulation and growth

99
Q

Tx of tonsillar concretions and tonsillolithiasis?

A

Usually unneeded

surgery if symptomatic

100
Q

What is a noma?

A

opportunistic infection caused by components of the normal flora in patients that are severely immunocompromised (HIV & malnourished children)

101
Q

S/S of noma

A

Begins as necrotizing ulcerative gingivitis, extends to involve adjacent soft tissue and beyond

normal flora becomes flesh eating

most patients will die without treatment

Extensive necrosis and marked tissue destruction

facial disfigurement

102
Q

Noma Tx

A

correct underlying dz

antibiotics

debridement

103
Q

What are gummas?

A

granulomatous inflammation causing ulceration and necrosis

extensive tissue destruction
can involve many tissues including perforating the palate

104
Q

How long does it take for primary syphilis to develop and resolve?

A

Develops in 3-90 days and heals spontaneously in 3-8 weeks

OPath Block 2 (10 decks)

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