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Bacterial_infection

VIEWS: 42 PAGES: 90

									Bacterial infections


     Dr. Majdy Naim
Bacterial Infections
    Impetigo
    Folliculitis
    Furunculosis
    Erysipelas/ Cellulitis
    Tuberculosis of the skin
    Leprosy




                Majdy Naim Bacterial infections 10.01.2010   2
Impetigo




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Impetigo
 A highly contagious gram-positive bacterial
  infection of the superficial layers of the
  epidermis.
 Occurs in all ages
 Children younger than 6 years have a higher
  incidence of impetigo than adults




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Impetigo
Encouraging factors

 Hot humid weather
 Crowded living conditions
 Poor personal hygiene
 Unhygienic work environment




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Forms of Impetigo
 2 forms
     nonbullous impetigo
     bullous impetigo




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Nonbullous impetigo
         Impetigo Contagiosa
         Crusted Impetigo




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Nonbullous Impetigo
 Etiology:
      β-haemolytic strains of Streptococci, S
       aureus, or a mixture of both organisms.


 Clinical picture:
      Thin-walled blisters, which rupture very easilly
       and leave exudation and yellowish crusting
      Often multiple and particulary arround the face
      most often in children aged 2-4 years

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Nonbullous Impetigo
 Diffirential diagnosis:
      Varicella
      Herpes simplex
      Tinea corporis
      Recurrent impitigo of the head and neck,
       should prompt a search for scalp lice
      eczema



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  Nonbullous Impetigo

 Complications
     2–5% of cases of impetigo are associated with the
      development of acute glomerulonephritis




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Nonbullous Impetigo
Treatment:
 For severe cases systemic antibiotics (such as
  flucloxacillin, erythromycin, penicillin or cefalexin) are
  needed

 For minor cases the removal of crusts by
  compressing them and application of a topical
  antibiotic such as neomycin, fusidic acid , mupirocin
  or bacitracin will suffice




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Bullous Impetigo
 Bullous impetigo begins as a rapid onset of
  blisters that enlarge and rupture.




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Bullous impetigo
 Etiology:
     Staphylococccus aureus

 Epidemiology:
     most common in neonates and infants




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Staphylococcal scalded skin
syndrome




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 Bullous Impetigo

 Treatment:
     Topical antibiotics
     Systemic antibiotics (e.g. dicloxacillin, cephalexin
      or erythromycin)
     Not pennicillin




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                   Erysipelas

 Acute, superficial cellulitis with infection and
  inflammation in the dermis and upper
  subcutaneous tissue involving the superficial
  dermal lymphatics




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Cellulitis

This inflammation of the skin occurs at a deeper
level than erysipelas




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Erysipelas                      Cellulitis
 Causes
     Streptococcus 80% of cases
     Staphylococcus aureus has been implicated in
      cases of recurrent erysipelas secondary to
      lymphedema




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Erysipelas                        Cellulitis
 Portals of entry
       local factors, such as venous insufficiency,
       stasis ulcerations, inflammatory dermatoses,
       Fungal infections, insect bites, and surgical
       incisions




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Erysipelas                     Cellulitis
 In all age groups, but the peak incidence in
  patients aged 60-80 years

 More severe infections may exhibit numerous
  vesicles and bullae along with petechiae and
  even frank necrosis




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Erysipelas                     Cellulitis
 The first warning of an attack is often malaise,
  shivering and a fever




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Cellulitis




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Facial cellulitis – caused by Haemophilus
influenzae




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 Complications


 Complications occur in 13-17% of patients with
  erysipelas.
 The most common complications include
  abscess, gangrene, and thrombophlebitis.
 Less common complications (<1%) are acute
  glomerulonephritis, endocarditis, septicemia,



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Therapy I
 Elevation and rest of the affected limb are
  recommended to reduce local swelling and
  inflammation
 Complete rest
 Saline wet dressings




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Therapy II
 Systemic antibiotics:
     Penicillin
     Cephalosporin
     Dicloxacillin.
     At least 10 days


 Treatment the portal of entry



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Prophylaxis
(at least 6 months)
      if three relapses within a few years
      benzathine penicillin 1.2 – 1.5 mega units im.
       every 4 weeks or more frequently or
       erythromycin 250mg 3xdaily




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Folliculitis
 An inflammation of the hair follicles caused by
  infection (coagulase-positive staphylococci)




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Folliculitis
 Supeficial folliculitis
      folliculitis
 Deep Folliculitis
      Furunculosis (boils)




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Folliculitis




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Furuncle




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Furunculosis




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Folliculitis / Furunculosis

 Predisposing risk factors :
      Friction
      Hyperhidrosis
      Occlusion
      Shaving, Epilation




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Folliculitis / Furunculosis

Other predisposing risk factors
     Preexisting dermatitis
     Reduced host resistance, such as patients
      with diabetes mellitus or immunologic
      disorders
     Staphylococcal nasal carriers
     Skin injuries, abrasions, surgical wounds, and
      draining abscesses
     Skin occluded for topical corticosteroid
      therapy
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Folliculitis

 The primary lesion in folliculitis is a papule or
  pustule with a central hair.

 Typical body sites affected are the face,
  scalp, thighs, axilla, and inguinal area
 Deep folliculitis inflames the entire follicular
  structure and tends to be more symptomatic.



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Therapy
    Wash with antibacterial soaps to prevent or
     control mild cases of folliculitis.
    Topical antibiotics may be used.
    Systemic antibiotics with coverage of S aureus
     often are needed, since S aureus is the most
     common pathogen. This organism often is
     penicillin resistant; therefore, dicloxacillin or a
     cephalosporin is the first choice



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Ecthyma
 Deep, punched out, ulcerative, painful,
  cutaneous infection
 Typically develops on legs and buttocks at
  sites of minor trauma, insect bites or
  excoriations
 Often occurs in the setting of malnutrition or
  poor hygiene



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Pathogenesis
 Caused by Streptococcus pyogenes most
 commonly, or Staphylococcus aureus




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Treatment


 Local wound care with gentle cleansing and
 debridement
 Topical and systemic antibiotics




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Tuberculosis




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Cutaneous tuberculosis
Cutaneous tubeculosis
 A chronic granulomatous disease caused by
  Mycobacterium tuberculosis, Mycobacterium
  bovis or BCG (bacillus Calmette-Guerin)




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Route of infection
 Exogenous by inoculation
 Endogenous




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Mode of infection
 Inhalation of droplets expelled from patients
 Direct inoculation of the organism into the
  skin




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Primary tuberculosis complex
 Previously uninfected
 Typically occurs in a wound
 Lesion develops 2–4 weeks after inoculation
 Presents as a red-brown papule with ‘apple
  jelly’ translucence on diascopy that may
  ulcerate or crust
 Associated with regional lymphadenopathy



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Tuberculosis verrucosa cutis
 Previously infected
 Presents with large verrucous papule or
  plaque at the site of re-inoculation
 Due to strong immunity and hypersensitivity
  against M. tuberculosis




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Scrofuloderma

 Caused by direct extension of the organism
  to the skin overlying an infected lymph node
  or bone
 Lesions are most common over the cervical
  lymph nodes
 May ulcerate or form draining sinuses
 Heals with scar

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Tuberculosis cutis orificialis

 Autoinoculation of the mucous membranes
  Occurs at the mouth, nose, anus, urinary
  meatus or genitalia from infected secretions
  or visceral involvement
 Presents as painful punched-out ulcers with
   undermined edges
 Indicates failing resistance to disease

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Lupus vulgaris
 The most common form
 Chronic, very slowly progressive cutaneous
  form
 Associated with strong immunity to M.
  tuberculosis
 Presents with atrophic red-brown plaques
   on the head and neck in ~90% of cases
 Lesions can ulcerate and cause ectropion or
   eclabium
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Lupus vulgaris




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Metastatic tuberculosis
(Tuberculosis gumma)
 Occurs in patients with internal tuberculosis
  and decreased immunity
 Presents with ulcerated nodules and sinuses
 Most commonly on extremities




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Miliary tuberculosis of the skin
 Presents with generalized macules, papules,
  pustules, nodules or purpura associated with
  fulminant pulmonary or meningeal involvement
 Systemically ill with poor prognosis




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Diagnosis
 Positive tuberculin test
 Histopathology
 Culture of tissue
 Polymerase chain reaction for M. tuberculosis
  DNA in tissue




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Treatment

 Isoniazid (10–15 mg/kg per day) and rifampin
  (10–20 mg/kg per day) for 9 months
  Pyrazinamide, ethambutol or streptomycin is
  added for the initial 2 months of therapy if drug
  resistance is a consideration (Hispanic or Asian
  population), or if the duration of therapy is
  limited to 6 months

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Leprosy


   Dr. Majdy Naim


                    62
                  Leprosy
 Chronic granulomatous infection of the skin,
  nasal mucosa, nerves and eyes




                       63
     Mode of transmission
 Droplet infection
 Contact through the skin
 From lepromatous mother to her fetus
 From the placenta and even milk of
  lepromatous leprosy mothers




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Pathogenesis
 Infection caused by Mycobacterium leprae
 Low infectivity (Incubation period ~5 years)
 Transmission is not fully known although
  droplet infection via an upper respiratory
  route is suspected
 Genetic predisposition may play a role in
  disease development
 Animal reservoirs: armadillos and monkeys


                        65
Pathogenesis
 By defect of macrophage-monocyte series
 and T-helper lymphocytes survive M.leprae
 and replicate inside the macrophage and
 Schwann cell of non-myelinated nerves




                     66
Disease classification
 Tuberculoid leprosy
 Borderline tuberculoid leprosy
 Borderline borderline leprosy
 Borderline lepromatous leprosy
 Lepromatous leprosy




                        67
Tuberculoid leprosy
 <3 skin lesions which are anesthetic and
  anhidrotic
 Highest immune resistance and reactivity
 Organisms are not identified in tissues
  (paucibacillary)
 Nerve involvement
 Strong positive reaction to the lepromin
   skin test

                       68
Borderline tuberculoid leprosy
 Few (3–10) skin lesions
 May have enlarged nerves with mild motor
  impairment




                       69
Borderline borderline leprosy
 Indeterminate type
 Multiple asymmetric annular plaques
 Host resistance is unstable
 Organisms may be identified




                       70
Borderline lepromatous leprosy

 Skin lesions are symmetrical and numerous
 Nerve involvement is not prominent




                      71
Lepromatous leprosy


 Diffuse skin infiltration with characteristic
  leonine facies and loss of the eyebrows
 No host resistance or reactivity
 Organisms are numerous (multibacillary)
 No reaction to lepromin skin test




                        72
Diagnosis

 Slit skin smears stained with Ziehl–Neelsen
  reveals organisms
 Organisms cannot be cultured in vitro
 Histopathology




                       73
Treatment

   Dapsone
   Rifampin
   Clofazimine
   systemic corticosteroids




                           74
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Syphilis


 Caused by the spirochete Treponema
  pallidum
 Incubation period: 9–90 days after initial
  exposure




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Primary stage

 Initial lesion at the site of inoculation
  (chancre)
 Presents as a painless ulcer that heals over
  1–6 weeks
 Typically found on the genitalia, but can also
 be seen on the lips, tongue, areola or hands




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Secondary stage

 Begins 2–10 weeks after healing of the
  primary chancre
 Results from hematogenous spread
 Constitutional signs: generalized
 lymphadenopathy, hepatosplenomegaly
 Classic findings: diffuse papulosquamous
   eruption, specifically involving the palms and
   soles

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 Other skin findings: condyloma lata, split
  papules, moth-eaten alopecia and, mucous
  patches




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Subclinical, latent phase

 No signs or symptoms except for reactive
  serology
 May last 1–40 years




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Tertiary or late stage

 Develops in one-third of untreated cases
 Typically presents 3–5 years after the initial
   infection
 Presents with nodular lesion or gummas
 Can involve the bones, CNS and
  cardiovascular systems




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Diagnosis

 Venereal Disease Research Laboratory
  (VDRL) test; typically positive within 5–6
  weeks of infection. Negative with therapy and
  in late syphilis

 Fluorescent treponemal antibody absorption
  (FTA-ABS) test; typically positive at 2–3
  weeks after infection and remains positive for
  life

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Treatment

 Parenteral penicillin G is the treatment of
  choice in all stages of syphilis, and is the only
  antibiotic with documented efficacy in
  pregnancy and in neurosyphilis
 Primary and secondary: benzathine penicillin
 G 50 000 units/kg intramuscularly up to 2.4
  million units, in a single dose
 Latent: benzathine penicillin G 50 000
  units/kg IM up to 2.4 million units with three
  doses at1-week intervals
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 Neurosyphilis: aqueous crystalline penicillin G
   200 000–300 000 units/kg per day
  intravenously for 10 days
 Penicillin-allergic patients can be treated with
   Doxycycline, Tetracycline or Erythromycin




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