MMI Part 3.1

Card Set Information

MMI Part 3.1
2013-03-08 16:38:20

Between quiz 2 and 3
Show Answers:

  1. Structure of Human skin
    • Epidermis: hair shaft
    •                   sweat pore
    • Dermis: Oil gland
    •               blood vessels
    •               hair follicle
    •               sweat gland
    •               nerve
    • Subcutaneous layer adipose tissue (fat)
  2. Skin
    • Poor environment for microbial growth: dry, high salt concentration, sebum; lysozyme, antimicrobial peptides
    • Microbial inhabitants often gram+
    • Washing reduces numbers but does not eliminate: quickly re-established from hair follicles, sweat glands
    • High moisture areas have larger microbial populations: groin, armpits, feet, etc
  3. Normal flora of the skin
    • Staphyloccocus epidermidis (G+): dormant
    • Propionibacterium acnes: anaerobic, gram + rod; help maintain low pH of skin
    • Staphyloccocus aureus (G+)
    • Pityrosporum sp. (fungus): grows on oily secretions (sebum); dandruff
    • Candida sp (fungus)
  4. Skins Diseases
    • Modes of infection: breach of intact skin, skin manifestation of systemic disease, toxin-mediated skin damage
    • Different infections can cause different types of lesions: can be used in classification and diagnosis
    • Focus of infection may be elsewhere, but rash is characteristic
  5. Vesicle
    • Type of skin lesion, small, fluid-filed lesion
    • Eg. Chickenpox
  6. Bulla
    • Type of skin lesion, fluid-filled lesion > 1cm
    • Eg. cellulitis
  7. Macule
    • Type of skin lesion, flat, reddened lesion
    • Eg. measles
  8. Pustule (papule)
    • Type of skin lesion, raised lesion
    • Eg. smallpox
  9. 4 types of skin lesions
    • vesicle
    • bulla
    • macule
    • pustule
  10. Infectious Diseases of the Skin - BACTERIAL
    • Staphylococcus aureus: folliculitis, sty, furuncle, carbuncle, toxemia (SSSS, TSS)
    • Streptococcus pyogenes: erysipelas, necrotizing fascilitis
    • BOTH Staphylylococcus sp. and Streptococcus sp: Impetigo, ecthyma, cellultitis
    • Pseudomonas aeruginosa: dermatitis, otitis externa
  11. Bacterial Diseases of Skin
    • Staphylococcal and Streptococcal infections are frequent causes of skin disease
    • Both organisms: Are well adapted to physiological conditions of skin; produce invasive enzymes and damaging toxins
  12. Staphylococcal Skin Infections
    • S. aureus often enters via hair follicle to cause disease:
    • -folliculitis: infected hair follicle (pimple)
    • -sty: infected eyelash follicle
    • -furuncle: abscess, "walled-off" folliculitis: difficult to treat - antibiotic penetration
    • -carbuncle: failure to wall off furuncle: result: progressive tissue invasion; generalized illness, fever
  13. Staphylococcal Toxemia
    • Staphylococcal scalded skin syndrome (SSSS): exfoliative toxin (superantigen), often babies <2 yrs old, Bacteria attack junctions of epidermal cells, necrotic epidermis peels off, painful and raw
    • Toxic shock syndrome (TSS): TSST-1; high absorbancy tampons, nasal packing, skin lesions, burns, surgical wounds; sunburn-like rash, fever, vomiting, low blood pressure, exfoliation, varied organ involvement
  14. Steps to Toxic Shock Syndrome is caused by a superantigen
    • Bacteria colonize
    • Bacteria releases toxin into host system
    • Polyclonal T cell activation that is NOT antigen-specific
    • Excess release of inflammatory cytokines (IL-1, TNF-alpha)
    • Acute fever, shock, multi-organ failure
  15. Staphylococcus sp.
    • Gram positive cocci in clusters
    • Non-motile, non spore forming, + capsules
    • 3 important species to know:
    • S. aureus (primary pathogen)
    • S. epidermidis (opportunistic)
    • S. saphrophyticus (primary pathogen in the urinary tract, young women)
  16. S. aureus "coagulase positive staphylococci"
    • Produce coagulase (differentiating characteristic from other staph species): coagulase catalyzed fibrinogen (soluble) to fibrin (insoluble)
    • Produce catalase (breaks down H2O2)
    • Salt tolerant: tolerant to drying
    • Often yellowish colonies
  17. Catalase Test
    • 1. One drop of hydrogen peroxide H2O2 on a slide, add bacteria and mix
    • 2. Formation of bubbles = gas (enzyme is present and breaking down the peroxide, releasing oxygen gas)
  18. Treatment (for S. aureus)
    • Semi-synthetic penicillins: many strains of S. aurues produce beta-lactamase; nafcillin, oxacillin
    • Vancomycin (alternative)
    • Supportive therapy: i.v. rehydration
  19. Streptococcal Skin Infections
    • Various skin/soft tissue infections: Impetigo, erysiplelas, cellulitis, ecthyma, necrotizing fasciitis
    • Streptococci can cause many other disease states as well: meningitis, pneumonia, sore throat, otitis media, endocarditis, puerperal fever, dental caries (all in later lectures)
    • Streptococcus gram (+) cocci grow in chains
  20. Virulence factors (Streptococci)
    • Streptococci produce many substances that aid in the spread of infection:
    • streptokinase: dissolves blood clots
    • hyaluronidase: breaks down connective tissue
    • dexoyribonuclease: degrades DNA
    • proteases: break down proteins (eg. IgA protease breaks down IgA antibody)
    • spe toxins: Superantigen: responsible for tissue and muscle breakdown; eg. eryotherogenic toxin; strains that express theses toxins are very aggressive and can cause necrotizing fasciitis
    • Not all of the enzymes/toxins listed above will be expressed by every strain
  21. Streptokinase
    streptococci virulence factors; dissolves blood clots
  22. Hyaluronidase
    streptococci virulence factors; breaks down connective tissue
  23. Deoxyribonuclease
    streptococci virulence factors; degrades DNA
  24. Proteases
    streptococci virulence factors; break down proteins (eg. IgA protease breaks down IgA antibody)
  25. Spe toxins
    • streptococci virulence factors: superantigen
    • Responsible for tissue and muscle breakdown
    • Eg. Erythrogenic toxin
    • Strains that express these toxins are very aggressive and can cause necrotizing fasciitis
  26. Streptococcal hemolysins
    • Hemolysin: bacterial enzyme that can lyse red blood cells and break down hemoglobin (Hb); can lyse other cell types as well- contributes to pathogenicity
    • Streptococci are divided into 3 groups based on their hemolytic reactions on Blood Agar Plates (BAP)
    • -Alpha-hempolytic: partial breakdown
    • -Beta-hemolytic: complete breakdown
    • -Gamma-hemolytic: no breakdown
  27. Beta-hemolytic Streptococci
    • Often associated with human disease
    • Lancefield groups A-T:
    • -serological classification: based on antigenic carbohydrates in cell walls
    • -Group A = Streptococcus pyogenes: Most Streptococal infections are caused by variants of Group A strep
    • -Group B = Streptococcus agalactiae: part of normal flora in 10-35% of healthy adults (lower intestine, vagina); may be passed to babies during birth- meningitis, sepsis, pneumonia, etc.; may result in permanent damage or death (10-20%)
  28. M protein (Streptococcus)
    • Virulence factor
    • Greatly contributes to a particular strain's pathogenicity
    • Different strains = differences in antigenicity of M protein
    • -antiphagocytic
    • -aids in adherence to mucous membranes
  29. Laboratory and Treatment (Streptococcus)
    • Culture: G+ aerobic, cooci; Beta-hemolytic (on BAP - Blood Agar Plate)
    • Serology: anti-streptolysin O antibodies present (ASO+)
    • Treatment**:
    • -penicillin G (i.v if severe) or amoxicillin
    • -alternative: macrolides (erythromycin)
    • -surgical debridement (removal of affected tissue) for necrotizing fasciitis
    • **It is important to treat all strep infections with antibiotics to reduce all the potential for post-infection complications such as glomerulonephritis and toxic shock syndrome
  30. Streptococcal Skin Infections
    • Impetigo (topical, stratum corneum): vesicles/honey colored erosions
    • Ecthya (epidermis): crusts/erosions
    • Erysipelas (upper dermis): tender, red plaque with sharp borders
    • Lymphangitis (lower dermis): red streaks (usually on an extremity)
    • Cellutlitis (fat): tender, red plaque
    • Characteristics of infection are different depending upon how deep the infection is
    • Usually localized
    • Highly destructive if infection reaches deeper tissue
    • Staphylococci may also cause these types of infections, but most commonly Streptococci
  31. Impetigo
    • Typically Streptococci skin infection, though can be Staphylococci
    • In the stratum corneum (top)
    • Vesicles/honey colored erosions
  32. Ecthyma
    • Typically Streptococci skin infection, though can be Staphylococci
    • In the epidermis
    • Crusts/erosions
  33. Erysipelas
    • Typically Streptococci skin infection, though can be Staphylococci
    • In the upper dermis
    • Tender, red plaque with sharp borders
  34. Lymphangitis
    • Typically Streptococci skin infection, though can be Staphylococci
    • In the lower dermis
    • Red streaks (usually on an extremity)
  35. Cellulitis
    • Typically Streptococci skin infection, though can be Staphylococci
    • In the Fat layer
    • Tender, red plaque
  36. Streptococcal Skin Infections - Pathogenesis
    • Trauma inoculates bacteria in skin
    • Bacteria colonize
    • Inflammation
    • Pustular lesions and honeycomb-like crusts form at site of inoculation (impetigo)
    • Deeper infection results in erysipelas, ecthyma or cellultitis
    • Local tissue destruction and/or sepsis may occur
    • Treatment with penicillin or spontaneous recovery
  37. Impetiga
    • Often in newborns and young children, caused by Staphylococcus aureus and Streptococcus pyogens
    • Infection of epidermal layer
    • Treatment: removal of crusts, washing of lesions and application of topical antibiotics - oral antibiotics only if infection spreads
  38. Erysipelas
    • Infection of the dermal layer of skin
    • Can progress to septicemia and fatal outcome
    • Can begin as pharyngitis
    • Treatment: antibiotic (most often IV penicillin)
  39. Complications - Glomerulonephritis (of Strep)
    • Glomeruli: site of blood filtration in the kidney
    • "Clumps" of antibodies bound with antigen accumulate in the blood and get stuck in the glomeruli
    • Symptoms of glomerulonephritis: Early - may have no symptoms; blood in urine; edema (swelling); kidney failure
    • Treatment: rest; antibiotics to treat infection; may restrict sodium and protein to allow the kidneys to recover; treatment usually continues for 1-2 weeks after tests show normal kidney function
  40. Glomeruli
    Site of blood filtration in the kidney
  41. Streptococcal Skin Infections - Necrotizing Fasciitis
    • Symptoms:
    • severe pain
    • swelling
    • discoloration
    • bleeding into the skin
    • visibly dead (necrotic) tissue
    • skin breaks (open wound)
    • skin around the wound feels hot (inflamed)
    • oozing puslike fluid - yellowish clear or yellowish bloody
    • fever
    • general ill feeling
    • Treatment:
    • Penicillin G (iv)
    • Surgical debridement of damaged tissue
  42. Pseudomonas infections in healthy people
    • Pseudomonas dermatitis: self-limiting rash; (~2 weeks); often associated with pools, hot tubs, saunas
    • Otitis externa: painful external ear canal infection; competition swimmers
  43. Infections by Psuedomonads
    • Psuedomonas aeruginosa: most prominent species: aerobic gram (-) bacilli; produces exotoxin and endotoxin; produces a blue-green iridescent pigment call pyocyanin; results in blue-green pus; fruity odor; opportunistic pathogen; very hardy; ubiquitous in soil and water; relatively resistant to antibiotics
    • Infection is rare in healthy people
    • Often nosocomial: grows on medical tubes/devices; can grow in flower vases, mop buckets, dilute disinfectants
    • Respiratory infections in immunocompromised individuals: colonizes lungs in CF patients; often causes infections in burn patients
    • Infection in immunocompromised can cause septicemia, septic shock and death
  44. Treatment (Pseudomonads)
    • Usually use 2 antibiotics together because resistance can arise quickly
    • Beta-lactam + aminoglycoside or quinolone
    • Silver sulfadiazine is used to treat burn infections
  45. Infectious Diseases of the Skin - VIRAL
    • Papilloma virus: warts
    • Herpesviridae: HSV-1- Herpes simplex virus-1 (cold sore)
    • Paramyxoviridae: Rubeola - measles virus
    • Togaviridae: Rubella - German measles, congential rubella syndrome
    • Parvoviridae: Human Parvovirus B19 - fifth disease (Erythema infectiosum)
  46. Viral Diseases of Skin
    • Often systemic
    • Transmitted by respiratory routes etc.
    • Skin rash is a manifestation of systemic infection
  47. Warts
    • Caused by papilloma virus (DNA, nonenveloped)
    • Virus causes proliferation of skin cells "tumour growth" - most are benign
    • Transmitted by direct contact - genital warts: STC, certain types cause cancer (16,18)
    • -plantar warts: usually acquired at swimming pools, public showers
    • -most warts disappear spontaneously with time
  48. Herpesviruses
    • "Herpes" means to crawl or creep
    • 8 viruses in group that are human pathogens
    • HSV-1            (cold sores)(Herpes simplex)
    • HSV-2             (genital Herpes lesions)
    • HHV-3 (VZV)   (chickenpox and shingles)
    • HHV-4 (EBV)   (infectious mononucleosis)
    • HHV-5 (CMV)  (congenital disease + disease in immunocompromised)
    • HHV-6            (roseola)
    • HHV-7          (sometimes roseola, otherwise?)
    • HHV-8          (Kaposi's Sarcoma-associated)
  49. HSV-1
    • Herpes simplex virus
    • Infection often in infancy
    • Transmission: oral, respiratory
    • Often subclinical: serology: 90% infected (US)
    • Treatment: acyclovir: also works for prevention
    • recurrence triggered by:
    • -excessive UV exposure
    • -emotional stress
    • -hormonal changes (menstruation), etc
    • Complications:
    • -herpetic keratitis (cornea)
    • -herpes encephalitis (brain): up to 70% mortality if untreated
  50. Measles
    • Rubeola virus: paramyxoviridae; enveloped ssRNA virus
    • Extremely contagious: infectious prior to appearance of symptoms; quarantine not effective
    • Transmission and development: respiratory aerosol droplets; incubation 10-12 days; contagious 2 days before to 4 days after rash
    • Symptoms: Fever, cough, conjunctivitis; maculopapular rash (beginning face->trunk->extremities); Koplik's spots: read patches with central white specks on oral mucosa next to molars (diagnostic indicator)
    • Complications: Middle ear infections; pneumonia (vial or 2o bacterial); encephalitis (1 in 1000)
  51. Measles vaccine
    • 1963: vaccine licensed
    • -live attenuated vaccine
    • -no animal reservoir; eradication is possible
    • -some people still not vaccinated
  52. Measles Diagnosis
    • Isolate virus from nasopharyngeal secretions, blood or urine
    • Identify Warthin-Finkelday cells (multinucleated gaint cells with inclusion bodies) in respiratory secretion
    • Serology
  53. Rubella (German Measles)
    • Togaviridae: enveloped ssRNA virus
    • Milder disease than rubeola (in adults)
    • Congenital rubella syndrome in fetus if infection occurs during first trimester
    • Aerosol transmission
    • Fever followed by rash
    • Infection results in lifelong immunity
    • Vaccine: live attenuated; part of MMR (measles, mumps, rubella)
    • Treatment: none self-limiting
  54. Rubell (German Measles)
    • Congenital rubella syndrome
    • Severe birth defects in pregnant woman contracts rubella during 1st trimester
    • 35% chance of fetal damage: spontaneous abortion, deafness, cataracts, heart defects, mental retardation, death (15% die within 1st year)
    • Infant with CRS may transmit the virus up to age 2 - complicates control of infection
    • Pregnant women are screened for immunity: vaccine is not given to pregnant women for fear of fetal infection
    • Last severe epidemic (UG): 1964-1965: ~20,000 severely impaired children born
  55. Fifth Disease (Erythema infectiosum)
    • Parvoviridae: non-enveloped ss linear DNA virus; human parvovirus B19
    • "Fifth" disease because it is one of the 5 most common pediatric diseases with rash
    • Characteristic "slapped cheek" facial rash
    • Symptoms: mild influenza-like symptoms; fever, cough, myalgia, sore throat; asymptomatic in 20%
    • Can lead to chronic severe anemia in immunocompromised patients
    • Infection leads to immunity
  56. Infectious Diseases of the Skin - FUNGAL
    • Trichophyton, Microsporum, Epidermophtyon
    • -cutaneous mycosis
    • Candida albicans
    • -oral thrush (candidiasis)
    • Mycosis = fungal infection of the body
    • Characterization based on level of tissue involvement
    • Fungi are particularly suited to skin environment: high osmotic pressure (high [salt]), low moisture
    • ALSO recall that fungi are eukaryotes -> treatment is difficult
  57. Cutaneous Mycoses
    • Dermatophytes:
    • -colonize hair, nails and outer layer of epidermis (stratum corneum)
    • -commonly known as tinea or ringworm
    • -infection spreads circularly
    • -can't grow subcutaneously even if they gain access
    • Grow on keratin
    • Transmitted by fomites or from dogs/cats
    • Generally infect moist areas: groin, feet, scalp
  58. Laboratory and Treatment for cutaneous mycoses
    • Diagnosis: microscopy, culture on selective media
    • Treatment: Drugs specific to whether or not it involves hair or nails.
  59. Candidiasis
    • Yeast infection
    • Usually suppressed by normal flora
    • Antibiotic treatment or immunosuppression can allow dissemination of Candida: systemic disease can be fatal
    • Treatment; topical or oral drugs, depending on severity: monistat = miconazole
  60. Microbial Disease of the Eye
    • Outer surface of eye is exposed to the external environment and infectious organisms
    • Eyelid serves as a mechanical barrier to organisms
    • Tears with lysozyme and IgA: chemical barrier
    • Conjunctiva: especially susceptible to infection: vulnerable epithelial surface; covered by eyelid, creates warm, moist conditions
  61. Difference between an eye infection caused by a bacterium and a virus?
    Bacterial infections more often present with pus than viral infections, sometimes large amounts that glue the eye shut.
  62. Conjuncitivitis
    • Inflammation of conjunctiva
    • Numerous causes: bacteria, virus, protozoa; bacteria usually originate from skin and upper respiratory tract
    • Increased incidence due to contact lenses
  63. Karatitis
    Inflammation of the cornea
  64. Nematodes in the eye
    • Most eye infections result from upper respiratory and skin, but can come from the blood and nervous system
    • Inner regions of the eye can be infected by worms and protozoans eg. children and toxocara
  65. Bacterial Diseases of the Eye
    • Neonatal Gonorrheal Ophthalmia
    • C. trachomatis
    • Tracoma
  66. Neonatal Gonorrheal Ophthalmia
    • Caused by Neisseria gonorrhea
    • Acquired during passage through birth canal (infected mother)
    • Large amounts of pus -> cornea ulceration (in untreated)
    • High risk of blindness
    • Treatment of newborns with silver nitrate eye drops (preventative)
    • Now use antibiotics: Chlamydia is frequent co-infection
  67. C. trachomatic
    • Ocular: types A-C
    • Not ever sexually transmitted
    • Gential: types D-K, LGV
    • *Note that you can infect your eye with a gential Chlamydia, this is then called inclusion conjunctivitis
  68. Inclusion Conjunctivitis
    An eye infection that has been transferred from genital Chlamydia, Types D-K
  69. Trachoma
    • Chlamydia trachomatis
    • greatest infectious cause of blindness in the world today -PREVENTABLE!!
    • Worldwide:
    • ~500 million active cases
    • ~7 million blinded victims
    • Conjunctivitis
    • Blindness is caused by mechanical abrasion: scarring, turned-in eyelashes, secondary bacterial infections
    • Education, sanitary practices, antibiotics and simple surgery could prevent blindness!!!! tetracycline, erythromycin OR single dose azithromycin
  70. Wounds
    Potential concerns:
    • Pathogens can gain entrance
    • Poor or no circulation: lack of blood flow to deliver nutrients, drugs, oxygen, immune cells, antibodies, etc.
    • Poor infiltration by antimicrobials
    • Presence of dirt or debris from trauma: keeps inflammation going, source of pathogens
  71. Anaerobic wounds
    • Anaerobic conditions common in crushed wounds, puncture wounds
    • Anaerobes important!!
  72. Wounds
    Wounds expose tissue components that are normally protected by skin or mucous membranes: collagen, fibronectin, fibrin/fibrinogenSome pathogens (Staphylococcus sp., Streptococcus sp.) have receptors for these
  73. 3 steps to Wound repair
    • 1. Inflammation (24-48 hours)
    • 2. New tissue formation (5-10 days)
    • 3. Remodelling (1-12 months)
  74. Step 1 of wound repair
    • Inflammatory response:
    • Damaged cells and resident macrophages in damages area send signals (cytokines) to the blood vessels
    • Surrounding blood vessels dilate: neutrophils migrate to wound site, fibrinogen (from Plasma) is converted to fibrin to form clot
  75. Step 2 of wound repair
    • Formation of new tissue and blood vessels
    • Formation of new epithelial layer (under scab)
    • Main immune cell in the wound switches from neutrophils to macrophages: they clean up the mess
  76. Step 3 of Wound repair
    • Remodeling
    • Scar formation
    • Collagen fills in the wound site
    • New epithelium and dermis do not contain the normal skin appendages
  77. Consequences of Infection of Wounds
    • 1. Delayed healing
    • 2. Formation of abscesses
    • 3. Dissemination or spread of the infection into nearby tissues, bones or the blood/lymph
  78. Abscess
    • Localized lesion with accumulation of pus anywhere in the body
    • Result of external infection or internal (eg. after peritonitis)
    • Often polymicrobial (eg. appendicitis) "intra-abdominal abscess"
  79. Wound abscesses
    • Localized accumulation of pus
    • Area of inflammation surrounds the pus and walls it off from surrounding tissue, trying to prevent spread of infection
    • Difficult to treat with antibiotics only as they diffuse poorly in inflamed tissue
    • Surgical draining it often necessary
  80. Wound abscesses
    Anaetobic wounds
    • Anaerobic conditions common in crushed wounds, puncture wounds
    • Anaerobes important!!!
  81. Osteomyelitis
    • Infection of the bone: by nearby site of infection, after trauma (like a fracture, or from circulating microbes)
    • Most common cause from blood is S. aureus
    • Most common cause from nearby site is polymicrobial (mix of G- and G+)
  82. Surgical Infections
    • Contamination of surgical site during operation or infection of the sutures after surgery
    • Associated with: hygienic conditions in the operating room; immune status of the patient; competence of the surgeon
    • Not uncommon to have normal flora infection a surgical site: upper body: primarily Staphylococcus sp, Lower body and abdominal infections: (primarily fecal flora: Gram negatives and enterococci)
  83. Cellultits
    • Acute spreading infection of the skin
    • Involves subcutaneous tissues
    • Originates from superficial skin lesion or trauma: eg. boils or ulcers
    • Majority of cases caused by S. aurerus and S. pyogenes
  84. Anaerobic cellulitis
    • Areas of traumatized tissue or poor blood circulation
    • Diabetics very prone to cellulitis of the feet
    • Causative organism depend on type of trauma:
    • foul-smelling exudate, marked swlling and gas
    • Treatment usually antibiotics and surgical debridement of the wound
  85. Gas Gangrene (clostridial myonecrosis)
    • Classical gas gangrene usually caused by Clostridium perfringens (G+ anaerobic spore forming bacilli)
    • C. perfingens spores in soil and feces
    • Usually a result of traumatized tissue with poor blood supply, with anaerobic conditions in the wound
    • Buttocks and perineum common sites
    • Organisms multiply in subcutaneous tissues and invade deeper tissues, thrive on dead tissue
    • Produce gas as a by-product of metabolism crackling sound on palpitation
    • Cause an anaerobic cellulitis followed by necrosis
    • Alpha-toxin destroys tissue cells and WBS, collagenase, hyaluronidase further break down tissue
  86. Symptoms of Bite Infection
    • Most common symptoms:
    • Localized cellulitis
    • Pain at site of injury
    • Purulent discharge, often gray and foul-smelling
    • Symptoms in <10% of victims:
    • Temperature >37.2 C
    • Regional adenopathy (swollen lymph nodes)
    • Lymphangitis
    • Puncture wounds most often infected: snake bites, human bites and "clenched fist" injuries
  87. Snake bites
    • 8000 American's bitten/yr
    • Venom causes tissue necrosis where infection can develop
    • Pseudomonas aeruginosa common cause of infections, but also other organisms, eg. Salmonella arizonae, CNS...
  88. Human Bites and "Clench Fist" injuries
    • Most often infected than animal bites
    • Both aerobic and anaerobic bacteria implicated (oral flora)
    • Eikonella corrodens important pathogen
  89. What to do when bitten by an animal?
    • Wash the wound with soap and water if possible, 20 min
    • Dress wound with sterile compresses, stop the bleeding and seed medical advice
    • Cat or sometimes dog bites can result in an infection with Pasteurella multocida, which causes lymphangitis and if untreated septic shock
    • Tetanus shot and rabies prophylaxis can be necessary
  90. Intraveous catheter: 4 sources of infection
    • 1. Microbial contamination at insertion site
    • 2. Hub
    • 3. Contaminated infusate
    • 4. Hematogenous seeding from a distant site
    • Blatant signs of infection in only ~ 50% of cases
  91. IVDU
    • Intravenous drug users
    • Immunosuppresed, many infections
    • Often get cellulitis, or lymphangitis with Staphylococcus aureus
  92. Burns
    • Infections result from a disruption in the normal homeostasis
    • Mortality rate with burns > 40% of body surface area high
    • Important to maintain blood flow to affected area
    • Necrotic (dead) tissue - good medium for growth of bacteria
    • Decreased immune defenses in large burns (cells 'burn out')
  93. Burns (what to do)
    • Close burn wound asap and use topical antibiotics prophylactically as well as surgical excision of necrotic tissue
    • Hemorrhage, eschar formation or greenish discolourization indicate infection
    • Often both gram - and gram + mixed infections
    • Pseudomonas aeruginosa commonly infects burn wounds