Bacterial disease Flashcards
What organism causes bacillary angiomatosis?
Bartonella henselae
What percent of people with bacillary angiomatosis recall some bite or scratch?
Only 20%
How are rickettsial organisms transmitted?
Arthropod is host/vector (ticks, fleas, lice, and mites)
What two rickettsial diseases don’t have eschar?
Rocky Mountain spotted fever and typhus group
The differential diagnosis for lesions with eshcar?
Ecthyma gangrenosum, pyoderma gangrenosum, ecthyma/ulcerating impetigo, rickettsiosis, non-rickettsiosis (anthrax, barnella, tularensis, trachomatis, etc), non-infectious
What is the pneumonic and diseases with sporitrichoid spread?
Cat scratch disease Atypical mycobacteria Tuberculosis Nocardia Sporotrichosis Phaeophyphmycoses Leishmaniasis Anthrax Tularemia
Is impetigo contagious?
Yes, direct person to person contact or through fomites is how it is spread
Types of impetigo?
Non-bullous (70%) and bullous (30%)
Most common organism for non-bullous impetigo?
S. aureus > strep pyogenes
Most common location for impetigo?
It is often seen in children and it is often seen on the face, perioral/perinasal areas
Most common organisms for bullous impetigo?
Phage group II (types 55 and 71) staph aureus
What is the pathophysiology of bullous impetigo?
The phage group II staph produce exfoliatoxins A and B which cleaves desmoglein 1 and leads to subcorneal/intragranular acantholysis
What is the distribution of bullous impetigo compared with non-bullous impetigo?
The bullous form is more generalized. Like the non-bullous from it is more common in children
The appearance of bullous impetigo lesions?
early on: small vesicles enlarge into 1-2 cm superficial bullae late: flaccid, transparent bullae measuring up to 5cm in diameter; after rupture, there is a collarette of scale, but no thick crust, little surrounding erythema
Is the risk of acute post-streptococcal glomerulonephritis affected by treatment of impetigo w/ antibx?
No, risk same if caused from strep even w/ tx
What is the most common causative organism of bacterial folliculitis?
S. Aureus folliculitis
Most common location of s. aureus folliculitis?
face or beard area
What is sycosis barbae?
Large red papulopustules with or without plaques and small pustules
What is the major risk factor for pseudomonal folliculitis?
Poorly chlorinated hot tubs/whirlpools
Treatment for staph folliculitis?
Chlorhexidine washes or sodium hypochlorite (.5cups of bleach in a full 40-gallon bathtub or .5-1 tsp per gallon in a spray bottle
if it is widespread can do a beta lactam antibx
Tx for gram-negative folliculitis?
isotretinoin
Tx for pseudomonal folliculitis?
self-resolves, but can give cipro if severe
What is the difference between abscess vs furuncle vs carbuncle?
Abscess are inflamed and fluctuant nodule that can arise anywhere. Furuncle: only occurs with hair follicles on hair-bearing sites, often the head and neck > intertriginous zones, thighs or other sites of friction. Carbuncle: a collection of furuncles, often deeper with multiple draining sinuses. Most often on the posterior neck, back and thighs and systemic sx’s can occur in these.
Which of the 3, furuncle, abscess or carbuncle is MRSA most commonly associated with?
Most commonly associated with furunculosis, often mistaken for a spider bite. Can be associated with cellulitis and necrotic plaques?
What is the mechanism of MRSA’s resistance to methacillin?
mecA gene encodes the penicillin-binding protein, PBP2a which decreases the affinity for beta-lactams.
How is the mecA gene stored/shared?
The mecA gene is on a mobile genetic element called the staphylococcal cassette chromosome mec (SSCmec)
The acquisition of these elements by S. Aureus has led to different strains of MRSA like healthcare-associated versus community-associated
Major virulence factor with community-acquired MRSA?
Panton-Valentine leukocidin (PVL) which is a pore-forming cytotoxin that causes destruction of leukocytes and tissues and is associated with increased virulence
What is blistering dactylitis?
Initially presents with darkening of the skin of the distal finger (more than toe) and volar fat pad, progresses to purulent vesicles and bulla on erythematous background in a week.
Who gets blistering dactylitis?
Children, most commonly from picking their noses or local skin trauma
Most common organism of blistering dactylitis?
S. Pyogenes > S. Aureus
What is the treatment for blistering dactylitis?
I&D + 10 day course of oral beta-lactam
What is ecthyma?
Don’t get confused with ecthyma gangrenosum. This is a deep variant of non-bullous impetigo
Who gets ecthyma?
Most common in children
What is the most common causative organism of ecthyma?
Streptococcus pyogenes
Presentation of ecthyma?
Few vesicopustules, most commonly on legs –> develop into “punched out” ulcers with purulent base and hemorrhagic crust (rather than yellow!)
Tx for ecthyma?
dicloxacillin or cephalexin
Who most commonly gets staph scalded skin and why?
Infants/young children who lack neutralizing anitbodies and have decreased renal clearence. It can also be seen in adults with chronic renal failure (high mortality >50% in this population as compared to 5% in the kids).
Presentation of staph scalded skin syndrome?
febrile prodrome, purulent rhinorrhea or conjunctivitis, widespread skin tenderness; skin eruption begins on face (periorificial radial fissuring [an important sing]) and intertriginous zones –> generalizes within 48 hrs as wrinkled appearing skin w/ flaccid bullae and + nikolsky sign.
Prognosis of staph scalded skin syndrome?
Very good prognosis in young children (low mortality <5%) Bad prognosis in chronic renal failure (>50%) The desquamation from infxn will last about a 1 week and then heal without scarring
What type of staph is involved in staph scalded skin?
Phage group II (types 55 and 71) s. aureus and then these produce exfoliatoxins A and B and then these go into the bloodstream and you get widespread cleavage of desmoglein 1.
What is a difference in the histology between staph scalded skin and bullous impetigo?
staph scalded skin is not directly from the bacteria in lesions but from the toxin so the subcorneal/intragranular acantholysis is not accompanied by bacteria or inflammatory cells
Treatment for staph scalded skin syndrome?
Clindamycin is given to reduce bacterial toxin production but up to 50% of strains are resistant so this should not be used as monotherapy. Use dicloxacillin or similar penicillin or cephalexin or other first generation cephalosporin
One key pathophysiology difference between staph scalded skin and bullous impetigo?
SSS has hematogenously disseminated exfoliators rather than local ones like in bullous impetigo
What is the most common primary site of infection in children for staph scalded skin?
Nasopharynx or conjunctivae
What is the most common primary site of infection in adults for staph scalded skin?
Pneumonia and bacteremia
What are the two types of staphylococcal toxic shock syndrome?
Menstrual toxic shock syndrome (<50%) and non-menstrual (>50%) [Nasal packing is a big cause, surgery skin or other internal infection]
Sx’s of staphylococcal toxic shock syndrome?
Both forms p/w high fever (>102°F) + rash + systemic symptoms (myalgias, vomiting, diarrhea, headache, pharyngitis) + hypotension (100%)
Which type of staphylococcal toxic shock syndrome has better prognosis?
Menstrual associated (<5% as compared to <20 for the other forms)
Presentation of staphylococcal toxic shock syndrome?
Mucocutaneous eruption classically starts w/ scarlantiniform eruption (initially on trunk → becomes generalized), redness and edema of palms/soles, “red strawberry tongue,” conjunctival hyperemia → palmoplantar desquamation (1 to 3 weeks later), Beau’s lines, onychomadesis; usually negative blood cultures (<15% positive); low mortality (<5% for menstrual TSS and <20% for nonmenstrual TSS)
Pathogenesis of toxic shock syndrome?
Production of toxic shock syndrome toxin-1 (TSST-1) by certain strains of S. aureus → TSST-1 acts as superantigen, binding to Vβ region of TCR and class II MHC on APCs → nonspecific activation of T-cells + cytokine storm (↑TNF-α, IL-1, IL-6, TLR2, and TLR4)
Tx for toxic shock syndrome?
B-lactamase resitant ABX + clinda +/- IVIG for neutralizing toxin
What is the major difference between staph and strep toxic shock syndrome?
The strep is much worse prognosis (30-60% vs 3-20%), less florid primary site infection, more frequent rash, far more frequent blood cx positivity (>50%)
What areas are accentuated in staph scalded skin compared to TEN?
Areas of sparing seen in TEN but you get flexural accentuation of SSSS
What is the difference of the facial lesions seen in TEN as compared to SSSS?
Perioral and periocular crusting and radial fissuring with mild facial swelling is seen with SSSS In TEN you get vermilion lip erosions and crusting.
What are the age groups affected by streptococcal toxic shock syndrome?
Affects young/healthy adults as compared to infants and those with chronic renal dz.
What types of lesions is streptococcal toxic shock syndrome associated with?
Florid skin/soft-tissue infections like necrotizing fasciitis vs the occult infections of SSSS.
Which one (staph or strep) toxic shock syndrome is more likely to have + blood cx’s?
Much more likely to occur with strep
What is the presentation of streptococcal toxic shock syndrome
Classically presents with severe localized pain in extremity w/ redness, swelling or necrotizing fasciitis –> within 24 hrs you get systemic sx’s and hypotension
What types of strep and what toxins are involved in strep associated toxic shock syndrome?
Beta-hemolytic strep, M types 1 and 3, which produce SPE A, B, C, streptococcal mitogenic toxin Z (SMEZ), streptolysin O
Pathophysiology of strep mediated toxic shock syndrome?
Toxins act as superantigens, binding to the Vbeta region of the TCR and class II MHC on APC’s –> non-specific activation of T-cells and cytokine storm (increased TNF-a, IL-1, IL-6, TLR2, and TLR4)
What is the epidemiology of scarlet fever?
Young children (1-10yrs old); caused by group A beta-hemolytic streptococcus
Pathophysiology of scarlet fever?
Streptococci generate streptococcal pyrogenic toxins A,B,C and then these generate the sx’s
Presentation of scarlet fever?
Most commonly in setting of streptococcal pharyngitis/tonsillitis; p/w sore throat, high fevers, and systemic symptoms → 1 to 2 days later, macular erythema on upper trunk/neck → soon develop classic “sandpaper-like” papular eruption, Pastia’s lines (linear petechiae; favors flexural sites), flushed cheeks with circumoral pallor, and “white strawberry tongue” (white background + red papillae) → later “red strawberry tongue,” purulent exudate from throat → 1 to 2 weeks later, palmoplantar desquamation The throat is red and edematous, developing an exudate after 3–4 days; palatal petechiae and tender cervical adenopathy are often present
What are the linear petechiae seen in (often) flexural sites in scarlet fever called?
Pastia’s lines
What laps will be + in scarlet fever?
Positive throat/nasal culture is confirmatory, also have elevated DNase B and ASO titers
What is the tx of choice for scarlet fever?
Penicillin, amoxicillin or erythromycin if PCN allergic
What are the two major complications of scarlet fever?
Acute glomerulonephritis and rheumatic fever
Can scarlet fever happen without purulent pharyngitis?
Usually, not, this is almost always present
What percentage of patients with strep throat develope scarlet fever?
10%
What is erysipelas?
More superficial variant of cellulitis (upper-mid dermis vs deep dermis and subcutaneous tissues of cellulitis).
What cutaneous structure is prominently involved in erysipelas?
The lymphatics
What are the most common areas for erysipelas?
The lower extremity > face
Major risk factor for erysipelas?
Lymphedema
What is the primary organism that causes erysipelas?
Group A beta-hemolytic strep
What do the labs in erysipelas show?
Cx’s usually negative, best confrimator tests are increased DNase B and ASO titers
Tx in erysipelas?
Penicillin for 10-14 days, erythromycin if PCN-allergic
Presentation of perianal/vulvovaginal streptococcal skin infection?
Usually boys >4 years old, presents with sharply defined red plaques spreading up to 3 cm from the anus; a/w pain upon defecation and blood in the stool. -Can be associated with a guttate psoriasis outbreak
Is perianal/vulvovaginal strep always preceded by pharyngitis?
Not always, plus-minus in terms of association. However, it is almost always associated with + pharyngeal cx for strep pyogenes even in asymptomatic patients
What is the treatment for perianal/vulvovaginal strep
Oral cefuroxime or pencillin (less effective)
Most common cause of cellulitis in adults vs kids?
Beta-hemolytic strep in adults and S. Aureus in children
What is the presentation of cellulitis?
Infection of deep dermis/SQ most commonly affecting adults w/ skin barrier disruption; p/w tender/red/warm, ill-defined plaques w/ fever/chills/lymphangitis In severe cases, may see necrosis, bullae, vesicles
Most common causative bacteria in cellulitis?
Group A beta-hemolytic strep>staph aureus (most common in kids though)
What are the most common sites for cellulitis?
Head/neck in children and lower extremities in adults. and IV injection sites on arms.
What gives clues that MRSA may be involved?
Abscess or necrotizing cellulitis are clues to MRSA
Risk factors for cellulitis?
- Lymphedema, alcoholism, diabetes mellitus, injection drug use, and peripheral vascular disease
- Lymphatic damage from prior cellulitis and lymph node dissection –> increased risk of recurrent cellulitis
What will the blood cx show in cellulitis?
Blood cx are always negative in immunocompetent patients
What type of bacteria is associated with more frequent blood cx positivity and leukocytosis?
H. Influenzae
Treatment for cellulitis?
Uncomplicated: dicloxacillin, cephalexin, or clindamycin -MRSA: TMP/SMX, minocycline/doxycycline, and clindamycin
What is pyomyositis?
Infection of skeletal muscle. Presents with 1-2 weeks febrile prodrome then muscle pain and soft tissue mass w/ surrounding woody induration –> muscle abscess +/- septicemia
Treatment for pyomyositis?
I&D and IV antibiotics
What is the best dx tool for pyomyositis?
MRI (early), US-guided aspiration (later)
What is botryomycosis and what organisms usually cause it?
Deep granulomatous and suppurative infection most frequently caused by S. aureus (others: Pseudomonas, Proteus, Moraxella, Serratia, and Corynebacteria spp)
Other complications of botryomycosis?
May extend to skeletal muscle and bone; affects all ages; a/w ↓T-cell counts and other defects in cellular immunity
How does botryomycosis present?
70% have skin-limited disease (rarely visceral in severely immunosuppressed patients; lung most common); p/w deep, ulcerative plaques/nodules with multiple draining sinuses that drain yellow granules
What is the histology of botryomycosis?
Large granules w/ basophilic center (nonfilamentous bacteria) and eosinophilic/hyaline periphery d/t host immunoglobulin response (Splendore-Hoeppli phenomenon; comprised of IgG and C3 deposits), granules are surrounded by abscess and granulomatous inflammation; granules are PAS+, Giemsa+, and Gram(+)
What is the name of the host response that surrounds the botryomycosis infection with hyalin like material and IgG and C3 deposits?
Splendore-Hoeppli
Work-up for botryomycosis?
Bacterial + fungal cultures, biopsy for H&E, KOH prep
Treatment for botryomycosis?
Surgical debridement + anti-staphylococcal antibiotics
What is necrotizing fasciitis?
Rapidly progressive, life-threatening (up to 50% mortality) necrotizing infection of skin, SQ, and fascia
What is the most common site for necrotizing fasciitis?
Extremities > trunk
What is the most common species to cause necrotizing fasciitis?
Type 1 Polymicrobial (#1 in adults), a mix of streptococci, S. Aureus, E. Coli, clostridium and Bacteroides) at least one anaerobe in addition to facultative anaerobes Type 2: Monomicrobial; usually group A beta-hemolytic strep M types 1 and 3 (#1 cause in children) Type 3: Gram-negative marine organisms (Vibrio and Aeromonas) Type 4: Fungi; Post-trauma or immunocompromised state
Presentation of necrotizing fasciitis?
Initially p/w severely painful indurated/”woody” plaque (“pain out of proportion to visible skin changes”) → over 1 to 2 days and rapidly progresses → color changes from erythematous → dusky purple/gray +/− hemorrhagic bullae/ulceration, crepitus, foul-smelling discharge; patients always severely toxic-appearing (fever, tachycardia, and septic shock) → late in course and skin becomes anesthetic (nerves destroyed)
What is necrotizing fasciitis of the genitalia/perioneum/ lower abdominal wall called?
Fournier’s gangrene
What is it called with polymicrobial necrotizing fasciitis occurs arising as a postoperative complication?
Meleney’s gangrene
What is the treatment for necrotizing fasciitis?
Fasciotomy + IV abx (piperacillin/tazobactam + clindamycin + ciprofloxacin
Risk factors for necrotizing fasciitis?
Risk factors: diabetes, immunosuppression, PVD, CRF, trauma, IVDA, bevacizumab therapy, and recent surgery
Risk factors for worsened mortality in necrotizing fasciitis?
older age, increased time to the first debridement, increased extent of the infection, females, increased lactic acid, and increased creatinine
If you see a necrotizing soft tissue infection and imaging shows gas, what type of organisms might you be worried about?
Clostridium perfringens
What type of bacteria is clostridium perfringins?
Gram +, spore-forming rod. Ubiquitous in soil and is an obligate anaerobe
How do infections with clostridium perfringins usually occur?
Due to traumatic inoculation mostly like surgery or crush/penetrating injuries.
How does clostridium perfringins exert their pathologic effects?
bacteria proliferate freely in anaerobic environment, producing CO2 and cleaving lipids → clinically p/w crepitus, foul-smelling brown exudate (“dirty dishwater” color), w/ variable skin changes
