Infections of the skin, muscle and soft tissue - DONE Flashcards

1
Q

What protects the epidermis from infections?

A

Protection of the epidermis depends on the mechanical barrier afforded by the stratum corneum

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2
Q

What can cutaneous inoculation cause?

A

intracellular infection of the squamous epithelium with vesicle formation may arise from cutaneous inoculation, as in HIV1 infection

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3
Q

What are the risk factors of staph infections of the skin and deep soft tissues?

A
  • chronic skin conditions (e.g. eczema)
  • skin damage (e.g. skin bites, minor trauma)
  • injections (e.g in diabetes)
  • poor personal hygiene
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4
Q

Where do we usually form pus-containing blisters?

A

hair follicles

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5
Q

S. aureus produce 3 types of toxins:

A
  • cytotoxins
  • pyrogenic toxin antigen
  • exfoliative toxin
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6
Q

When does illness usually occur when having S.aureus?

A

illness develops after toxin synthesis and absorption and the subsequent toxin-initiated host response

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7
Q

What is folliculitis?

staphylococcal infections

A

superficial infection that involves the hair follicle, with a central area of purulence (pus) surrounded by induration and erythema

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8
Q

Furuncle =

A

boil

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9
Q

Furuncles:

staphylococcal infections

A

= boil

  • more extensive than folliculitis
  • painful lesion that tend to occur in hairy, most regions of the body
  • extend from hair follicle to become a true abscess with an area of central purulence
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10
Q

Carbuncles:

staphylococcal infections

A
  • cluster of boils caused by infection (s. pyogenes also possible, but less common)
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11
Q

Where are carbuncles usually located?

staphylococcal infections

A

most often located in the lower neck and more severe and painful than furuncle

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12
Q

Staphylococcal skin infections - treatment:

- What is the most important therapeutic intervention?

A

The most important therapeutic intervention - surgical incision and drainage of all suppurative collections

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13
Q

Staphylococcal skin infections - treatment:

- If there is a risk of dissemination and bacteria?

A

Antibiotic therapy may be recommended:

-

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14
Q

MSSA treatment:

A

dicloxacillinPO 500 mg qidorcephalexinPO 500 mg qid, clindamycinPO 300 mg tid

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15
Q

MRSA treatment:

A

clindamycinPO 300 mg tid, TMP-SMX PO 480-960 bid, doxycyclinePO bid, linezolidPO 600 mg bid

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16
Q

Mastitis def:

A

infection of the breast which usually develops in 1-3% of nursing mothers

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17
Q

What are the etiologies of mastitis?

A
  • s. aureus (the most common)
  • s. epidermidis
  • streptococci
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18
Q

When does mastitis occur?

A

generally presents within 2-3 weeks after delivery

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19
Q

What are the clinical manifestations of mastitis?

A

range from cellulitis to abscess formation

- systemic signs, fever and chills, are often present in more severe cases

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20
Q

What is the treatment of mastitis?

A

cephalexin PO 500 mg qid, cephadroxil PO 1g once a day

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21
Q

SSSS =

A

Staphylococcal scaled-skin syndrome

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22
Q

Who is mainly affected by SSSS?

A

SSSS primarily affects newborns and children, much less common in adults

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23
Q

What are the symptoms of SSSS?

A
  • SSSS may vary from a localized blister to exfoliation of much of the skin surface
  • skin is usually fragile and often tender, with thin-walled, fluid-filled bullae
  • gentle pressure results in rupture of the lesion, leaving denuded underlying skin
  • generalized symptoms: fever, lethargy, poor feeding, dehydration
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24
Q

What causes SSSS?

A

exfoliative toxin-producing strains

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25
Q

What does SSSS usually follow?

A

SSSS usually follows localized skin infection

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26
Q

What is the treatment of SSSS?

A

anti-staphylococcal + supportivetherapy

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27
Q

What does the streptococcal superficial infections usually involve?

A
  • impetigo
  • erysipelas
  • cellulitis
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28
Q

What does the streptococcal deep seated infections involve?

A
  • necrotizing fascitis
  • myositis
  • myonecrosis
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29
Q

Impetigo =

A

pyoderma

- honeycomb-like crust

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30
Q

Impetigo (pyoderma) def:

A
  • superficial infection of the skin caused by primarily by the GAS, occasionally by other streptococci of s.aureus
  • not painful lesions
  • FEVER IS NOT A FEATURE OF IMPETIGO
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31
Q

Who usually gets Impetigo (pyoderma)?

A

most often in young children

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32
Q

What are the usual sites of involvement of Impetigo (pyoderma)?

A
  • face (around the nose and mouth)

- legs

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33
Q

What is the treatment of Impetigo (pyoderma)?

A
  • the same as in streptococcal pharyngitis
  • if s.aureus etiology is possible, empirical treatment should cover both streptococci and s.aureus
  • CloxacillinPO 500 mg qidorcephalexinPO 250 mg qid–10 days
  • Topical mupirocin ointment is also effective
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34
Q

What do we do if the empirical treatment of Impetigo (pyoderma) is ineffective?

A

If epimirical treatment is ineffective – MRSA infection is possible (culture should be taken)

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35
Q

Erysipelas def:

A
  • infection involving the skin and subcutaneous tissues, develops over a few hours
  • protal of entry - any break in the skin
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36
Q

What are the distinctive features of erysipelas?

A

well-defined indurated margins and intense pain

- flaccid bullae may develop during the second or third day of illness, but extension of deeper soft tissue is rare

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37
Q

What are the clinical features of erysipelas?

A
  • pain
  • intense red colour
  • lesion is warm to the touch
  • appears shiny and swollen
  • fever and chills are common
38
Q

Which areas of the body gets erysipelas?

A
  • face

- lower extremities

39
Q

What happens to erysipelas after 5-10 days?

A

After 5-10 days desquamation of the involved skin occurs

40
Q

Erysipelas treatment:

A
  • PenicillinG IV 3 mln U qid orV-penicillin PO 1.5 mln U tid–10 days
  • Clindamycin IV or PO 600 mg tid–10 days
41
Q

Cellulitis def:

A

Streptococcal cellulitis tends to develop at anatomy sites in which normal lymphatic drainage has been disrupted (e.g. sites of prior cellulitis, the arm ipsilateral to a mastectomy and axillary lymph nodes dissection, lower limb with previous deep vein thrombosis)

42
Q

What causes cellulitis?

A
  • fissures of the skin- a portal of entry for streptococci
  • cellulitis may also involve recent surgical wounds
  • infection may also be associated with lymphangitis manifested by red streaks extending proximally along superficial lymphatics from the infection site
43
Q

What is the treatment of cellulitis?

A

penicillinG, clindamycin–as in erysipelas; cephazolinIV 1-2g tid, ampicillin/sulbactam1.5-3 g IV qid

44
Q

Necrotizing fascitis

A
  • may be associated with GAS or mixed aerobic-anaerobic bacteria or may occur as a component of gas gangrene caused by clostridium perfringens
45
Q

What are the early manifestations of necrotizing fascitis

A
  • early diagnosis is difficult - pain and unexplained fever is the only presenting manifestation
46
Q

What does necrotizing fascitis look like after the early manifestations?

A
  • swelling develops and is followed by browny edema and tenderness -> dark-red induration of the epidermis -> bullae filled with blue or purple fluid -> skin becomes friable and takes on a bluish, maroon, black colour
47
Q

How does the spread of necrotizing fscsitis occur?

A

rapid spread occur along fascial planes through venous channel and lymohatics

48
Q

What happens in the late stages of necrotizing fascitis?

A

toxic shock and multiorgan failure

49
Q

What are the predisposing factors of necrotizing fascitis?

A
  • peripheral vascular disease
  • diabetes mellitus
  • surgery
  • penetrating injury to the abdomen
50
Q

Fournier’s gangrene:

A

Leakage into the perineal are result in a syndrome called Fournier’s gangrene - massive swelling of the scrotum and penis with extension into the perineum or the abdominal wall and legs

51
Q

What is the frequency of myositis occurring concomintantly?

A

in 20-40% of cases, myositis occurs concomitantly

52
Q

In how many cases does the myonecrosis occur concomitantly with fascitis?

A

in 50% - both are a part of the toxic shock syndrome

53
Q

What may induce primary myositis (streptococcal necrotizing myositis)

A

S. pyogenes may induce primary myositis (streptococcal necrotizing myositis) in association with severe systemic toxic shock syndrome.

54
Q

What is the treatment of necrotizing fascitis?

A
  • early surgical exploration
  • GAS: clindamycinIV 600-900 mg q6h plusPenicillinG IV 4 mln U q4h orCephalosporin(first or second generation)
  • Mixed aerobesand anaerobes:
    • AmpicilinIV + ClindamycinIV + CiprofloxacinIV
    • VancomycinIV + MetronidazoleIV + CiprofloxacinIV
55
Q

Gas gangrene:

A

usually follows severe penetrating injuries that result in interruption of the blood supply and introduction of soil to wounds

56
Q

What causes gas gangrene?

A

caused by the clostridial species:

  • c. perfringens
  • c. septicum
  • c. histolytium
57
Q

Spontaneous non-traumatic gangrene-

A

among patients with neutropenia, gastrointestinal malignancy, recent radiation therapy, etc. (Cl. septicum)

58
Q

When does the gas gangrene of the uterus occur?

A
  • after abortion
  • vaginal delivery
  • cesarean section
59
Q

What causes gas gangrene of the uterus?

A

C. sordelli

60
Q

What is the clinical picture of gas gangrene of the uterus?

A
  • little or no fever
  • lack of purulent discharge
  • refractory hypotension
  • extensive peripheral edema and effusions
  • markedly elevated WBC
61
Q

What is the treatment of gas gangrene?

A
  • aggressive surgical exploration
  • visualization of the deep structures
  • removal necrotic tissue
  • reducing compartment pressure
  • obtaining material for gram staining and for cultures
62
Q

What is the primary antibiotic for gas gangrene?

A
  • Clindamycin + Penicillin G
63
Q

What is the alternative treatment of gas gangrene?

A
  • Clindamycin + Cefoxitin
64
Q

What are the most common infections complicated serious burns are:

A
  • pneumonia
  • septicemia
  • cellulitis
  • wound infection
65
Q

what is the most predominant causes of burn-wound infection in pre-antibiotic era, but still remains important?

A
  • strep

- staph

66
Q

What is a major problem in burn-wound management?

A
  • pseudomonas aeruginosa
67
Q

What is an increasingly important pathogens when it comes infectious complications of burns?

A

fungi (c. albicans, aspergillus)

68
Q

Burn-wound impetigo:

A

Characterized by loss of epithelium from a previously re-epithelialized surface

69
Q

Invasive infection in unexcised burn wounds

A
  • Secondary to a partial or full-thickness burn wound and is manifested by separation of the eschar or by violaceous, dark brown, or black discoloration of the eschar
70
Q

Green discolouration of the wound or subcutaneous factor erythema gangrenosum

A

susp. Invasive P. aeruginosa infection

71
Q

Infection of burn wounds - diagnosis:

and sepsis

A
  • changes in temperature
  • hypotension
  • tachycardia
  • neutropenia
  • thrombocytopenia
  • renal failure
72
Q

Burn-surgical wounds are found in up to……

A

39% of patients

73
Q

What is the treatment of infections of burn wounds?

A
  • closure and healing of wounds
  • topical antimicrobial agents
  • systemic treatment
  • alternative treatment: vancomycin and ciprofloxacin
  • linezolid
74
Q

Linezolid:

infections of burn wounds

A

efficacy in reducing bacterial growth and toxic shock syndrome

75
Q

What are the topical agents used in treating infections of burn wounds?

A
  • silver sulfadiazine cream
  • mafenide acetate cream
  • sillver nitrate cream
  • mupirocin (MRSA)

dramatically decrease incidence of infection

76
Q

What are the systemic treatment of infections of burn wounds?

A
  • antibiotic active against gram-positive bacteria plus drugs active against P. aeruginosa and other gram-negativees
77
Q

What are the alternative treatment of infections of burn wounds?

A
  • vancomycin

- ciprofloxacin

78
Q

infectious complications of bites:

A

the microbiology of bite- wound infections in general reflects the oropharyngeal flora of the biting animal, although organims from the soil, the skin of the animal and victim, and the animal´s feces may also be involved

79
Q

Of all animal bites how many are from dogs?

A

80% of all animal bite wounds -> 15-20% become infected

80
Q

When is the infection manifested after the bite?

A

infection manifests 8-24h after the bite - cellulitis with purulent discharge, fever, lymphadenopathy, lymphangitis

81
Q

The microbiology of dog-bite wound infections usually mixed:

A
  • ß-hemolytic streptococci, Pasteurella sp, Staphylococcus sp, Eiknella corodens,
  • anaerobic bacteria such as Actinomyces, Fusobacterium, Prevotella, Porphyromonas
82
Q

Infection with C. canimorsus (Gram-NEGATIVE) may result……

A

in fulminant sepsis, especially in host with impaired hepatic function, after splenectomy or immunocompromised

83
Q

What is the treatment of dog bites and cat bites?

A
  • amoxicillin/clavulanate

- clindamycin + ciprofloxacin

84
Q

C. canimorsus (Gram-NEGATIVE) treatment?

A

penicillin G IV every 4h

85
Q

Cat bites treatment?

A

same as in dog bites

86
Q

Cat bites:

A

cat bites are more likely to cause septic arthritis and osteomyelitis (mainly localized in hand) compared to dogs

87
Q

Pasteurella multocida:

cat bites

A
  • gram-negative coccbacillus
  • implicated in the majority of cat-bite wound infection, but the microflora is usually mixed
  • tend to advance rapidly (within hours)
  • causing severe inflammation with purulent drainage
88
Q

% of the human bites that gets infected:

A

wounds infected in 10-15% of cases of human bites

89
Q

Aerobic species in human bite infections:

A
  • strep
  • s.aureus
  • E.corrodens
  • H. influenzae
90
Q

Anaerobic species human bite infections:

A
  • Fusobacterium
  • Prevotella
  • Porphyromonas
  • Peptostreptococcus
91
Q

Flora of hospitalized patients:

human bite infections

A

Flora of hospitalized patients may include Enterobacteriacea

92
Q

What is the treatment of human bite infections:

A

amoxicillin/clavulanate or fluoroquinolone