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
Initial imaging in clostridium perfringins infxn?
X-ray–> reveals gas in soft tissues
Treatment for clostridium perfringins?
Immediate aggressive surgical debridement (most important) + clindamycin and third-gen CSN +/− hyperbaric oxygen
What infections are caused by corynebacterium?
Erythrasma, pittered keratolysis, Trichomycosis axilla, pubic, and capitis and cutaneous diphtheria
What bacteria causes erythrasma?
C. Minutissiumum, gram + filamentous rod.
Most common areas for erythrasma?
Moist, intertriginous zones like the groin and toe web spaces, axillae, inframammary, umbilicus and intergluteal
What color does erythrasma fluoresce with woods lamp and why?
Coral red, due to bacterial coproporphyrin III
What is the treatment for erythrasma?
20% aluminum chloride topically, topical clindamycin/erythromycin. If it is widespread or recalcitrant can try tetracyclines.
What organism most commonly causes pitted keratolysis?
Kytococcus Sedentarius
Mechanism of action for pitted keratolysis?
K. Sedentarius has two serine proteases (K1/K2) which degrade keratin in the stratum corneum
Other causes of pitted keratolysis?
Dermatophilus congolensis, Corynebacterium, and actinomyces
Presentation of pitted keratolysis?
Noninflammatory infection of weight-bearing areas of plantar> palmar skin. It has small crateriform pits and foul odor.
Does pitted keratolysis fluoresce?
NO!
What is the histology of pitted keratolysis?
Sharply demarcated, deep pits in startum corneum w/ gram + bacteria at the bases
Tx for pitted keratolysis?
Topical erythromycin (or clinida, mupirocin, or azole antifungals). You can also add aluminum chloride to help with sweating
What bacteria causes trichomycosis axillaris/pubis/capitis?
Corynebacterium tenuis
Presentation of trichomycosis?
Asymptomatic, adherent yellow-red concretions on axillary hair shafts -characteristic odor; sweat occasionally takes on a red color and stains clothing
Does trichomycosis fluoresce?
Yes, fluoresces pale yellow w/ Wood’s lamp.
Treatment for trichomycosis?
Shaving of axillary hair; may use topical erythromycin/clindamycin
What bacteria cause cutaneous diphtheria?
Both toxigenic (able to produce systemic dz) and non-toxigenic strains of Corynebacterium diphtheriae and Cornyebacterium ulcerans
Endemic areas for cutaneous diphtheria?
Vancouver, Latvia, Russia and Ukraine
How is cutaneous diphtheria spread?
Highly contagious through person to person spread
Clinica of cutaneous diphtheria?
Presents with an ulcer (favoring acral sites) with a punched-out appearance and variable gray “pseudomembranous” eschar +/- lymphadenopathy and rarely, toxin-mediated complications, such as myocarditis and polyneuritis
Risk factors for cutaneous diphtheria?
Poor hygiene, injection drug use, and skin trauma
Does the vaccine protect against skin diseases?
Not all the time.
What is the treatment for cutaneous diphtheria
First-line treatments include erythromycin and penicillin. For toxigenic strains, intravenous diphtheria antitoxin should be administered.
Contacts should be screened, and asymptomatic carriers should receive appropriate treatment.
What type of bacteria causes cutaneous anthrax?
Bacillus antracis (Gram + rod)
What are the forms of anthrax?
- cutaneous
- pulmonary
- GI
Cutaneous anthrax affects the skin, pulmonary anthrax affects the lungs, and gastrointestinal anthrax occurs through ingestion.
What form of anthrax is most common and what form carries the best prognosis?
Cutaneous on both accounts
What is the main risk factor for cutaneous anthrax?
Occupation-related exposure, especially through direct contact with infected animals (such as sheep, cows, horses, and goats).
What is the presentation of cutaneous anthrax?
- Onset: Typically presents 1 week post-exposure.
- Initial Lesion: Painless, purpuric papulovesicle (often called a “malignant pustule”) that drains serosanguinous fluid.
- Progression: The vesicle ulcerates, forming a painless, black, necrotic eschar with surrounding satellite vesicles and edema.
- Additional Symptoms: Lymphangitis and painful lymphadenopathy may occur, though systemic symptoms like fever, malaise, and headache are rare.
Pathology of cutaneous anthrax?
Spores grow readily on all routine culture media at 37°C, with a “jointed bamboo-rod” cellular appearance and a unique “curled-hair” colonial morphology
Treatment for cutaneous anthrax?
First line (cutaneous anthrax): quinolone or doxycycline ×2 weeks (treat for 60 days if suspect bioterrorism or possible inhalation exposure) Antibiotic therapy does not alter the progression from vesicle to ulcer to eschar, as the process is toxin-mediated Vaccine for pre-and post-exposure prophylaxis Raxibacumab is a recombinant human immunoglobulin monoclonal antibody targeting the B. anthracis protective antigen
Importance of treatment timing in cutaneous anthrax?
Early treatment is key, untreated mortality is 20%, essentially 0 if treated
What is the lethal toxin involved with anthrax infection?
Protective toxin + Lethal factor. -This increases TNF-a and IL-1B –> septic shock
What is the edema toxin involved in anthrax infection?
Protective antigen + edema factor -Increases cAMP –> edema. Also, impairs neutrophil function and affects water homeostasis
What are the 3 virulence factors for anthrax?
Poly-D-glutamic acid capsule (resists phagocytosis) Lethal Toxin Edema Toxin
What bacteria causes erysipeloid?
Erysipelothrix rhusiopathiae (gram + non-motile rod)
Risk factors for erysipeloid?
Occupational –> fisherman, poultry/fish handlers. Occurs as a result of traumatic inoculation
Presentation of erysipeloid?
Acute, self-limited infection -Red-violaceous nonsuppurative cellulitis +/- hemorrhagic vesicles; classically affects the finger web spaces and spares the terminal phalanges
Treatment of erysipeloid?
Penicillin, ciprofloxacin if penicillin allergic. Should prevent by using gloves
Who does cutaneous listeria usually affect?
Most commonly neonatal septicemia from vertical transmission
What bacteria causes cutaneous listeria infection?
Listeria monocytogenes (motile Gram + rode)
Presenting a picture of cutaneous listeria infection?
Disseminated papules/pustules/vesicles which turn to petechiae and purpura –> granulomatous papules and nodules
Treatment for cutaneous listeria infection?
Ampicillin, TMP/SMX (second line)
What bacteria causes meningococcemia?
Neisseria Meningitidis (gram - diplococcus)
Risk factors for meningococcemia?
Children/young adults in close quarters like military recruits and college students. *important* asplenic pt’s are at risk due to deficiency in complement C3, terminal complement components (C5-C9), properdin, factor D or H, and immunoglobulins -This also can occur in patients on the terminal complement inhibitor eculizumab
Can you be an asymptomatic carrier of Neisseria meningitidis?
Yes, 15% of the population are asymptomatic carriers
How is N. Meningitidis spread?
Respiratory secretions
Presentation of meningococcemia?
1-10 days after exposure pts get fever, chills, headache and petechial rash in 30-50% of pts, retiform purpura can happen that has a “gunmetal gray” color or hemorrhagic bullae on legs and trunk. This can progress to septic shock and DIC (purpura fulminans related to this).
Histology of meningococcemia?
LCV w/ vascular thrombosis and Gram(-) rods in 70% biopsies
Best way to dx meningococcemia?
PCR assay most sensitive/specific (>blood/tissue/CSF cultures or latex agglutination studies)
What is chronic meningococcemia?
Less common; p/w recurrent fevers, arthralgias, and macular/papular eruption; condition self-resolves, only to recur days to weeks later
Treatment for meningococcemia?
Early treatment is critical! First line: high-dose IV penicillin (treatment of choice) Second line: quinolones or chloramphenicol (if PCN-allergic); third-generation CSN (resistant disease) Prophylactically treat all close contacts w/ ciprofloxacin, rifampin, or ceftriaxone
What is the main virulence factors for N. Meningitidis?
Polysaccharide capsule endotoxin –> septic shock and purpura fulminans
What type of bacteria is pseudomonas aeruginosa?
gram -, strictly aerobic, motile bacillus
What is green nail syndrome?
Green/blue-black nail discoloration a/w water exposure and nail trauma. It is caused by P Aeuruginosa and the pyocyanin pigment it produces
Tx for green nail syndrome?
Topical quinolone, vinegar soaks, or aminoglycoside solution ×4 months, topical application of 2% sodium hypochlorite (household bleach diluted 1:4)
Presentation of pseudomonal pyoderma?
Superficial erosive infection w/ blue-green purulent exudate, “moth-eaten” appearance to the skin surface, with “mousy” or “grape-like” odor; may arise at burn sites, in mixed toe web infections and other chronic wounds
Presentation of blastomycosis-like pyoderma?
Large verrucous plaques with multiple pustules and elevated borders. Histologic examination reveals pseudoepitheliomatous hyperplasia with intraepidermal abscesses; fungi are NOT seen, and fungal cultures are negative
Treatment of pseudomonal pyoderma and blastomycosis-like pyoderma?
Systemic antipseudomonal antibiotics, topical antiseptics, debridement, and drying agents -Additional treatment options for blastomycosis-like pyoderma include acitretin, surgical excision, electrodesiccation and curettage, and ablative laser therapy
Presentation of otitis externa?
Can be caused from P. aeuruginosa, p/w edema, skin maceration, and purulent green exudate; tympanic membrane intact; classically severe pain upon pinna manipulation
Who is at risk for malignant otitis externa?
Usually only in diabetics or immunosuppressed
Presentation of malignant otitis externa?
Persistent drainage w/ excessive granulation tissue extending to bony portion of ear → may result in osteomyelitis of skull base; +/- LAD, parotid swelling
Tx for otitis externa?
Topical antipseudomonal agents (ear drops)
Presentation of hot tub folliculitis?
Self-resolving P. aeurginosa infection arising from poorly chlorinated hot tubs/whirlpools; p/w red, perifollicular papulopustules 1 to 2 days postexposure; commonly affects areas covered by bathing suit
Treatment for hot tub folliculitis?
Spontaneously resolves within 2 weeks for most, can use warm compresses with 2% acetic acid + topical polymyxin B or gentamycin Widespread, immunosuppressed: oral quinolone
How do you get pseudomonas hot-foot syndrome?
Arises from wading in pools w/ high concentrations of pseudomonas
Presentation of hot-foot syndrome?
Painful red-violaceous plaques/nodules on weight-bearing areas of plantar surface
Treatment of hot-foot syndrome?
None, self-resolving
What is ecthyma gangrenosum a sign of?
Pseudomonal septicemia, these lesions are essentially septic emboli of pseudomonas
Risk factors for ecthyma gangrenosum?
Immunosuppressed patients w/ severe neutropenia (often BMT patients)
Presentation of ecthyma gangrenosum?
+ fever, hypotension, alterations in consciousness, p/w a small number of purpuric macules –> progresses to hemorrhagic bullae –> bullae rupture –> ulcer w/ necrotic black eschar and tender, red skin surrounding eschar
What are the most common sites of cutaneous involvement for ecthyma gangrenosum?
Anogenital region and extremities
Histology of ecthyma gangrenosum?
Necrotizing hemorrhagic vasculitis, Gram-negative rods can be seen in the medial and adventitial walls of deeper vessels (intima is spared)
Treatment for ecthyma gangrenosum?
IV aminoglycoside + antipseudomonal PCN
What factors portend to worse prognosis in ecthyma gangrenosum?
of lesions, delay in dx, and prolonged neutropenia
What are the 3 main bartonella species which cause dz in humans?
B. henselae (cat scratch dz, bacillary angiomatosis) B. quintana (trench fever, bacillary angiomatosis) B. bacilliformis (Carrion dz, bartonellosis)
What is bartonellosis?
Caused from B. bacilliformis, has two phases: oroya fever and verruga peruana (peruvian wart). Potentially life-threatening
What is the vector for b. bacilliformis?
Phlebotomine sand flies (Lutzomyia verrucarum)
Describe the two phases of bartonellosis?
1) Oroya fever: an acute febrile disease with associated hemolytic anemia, die 2/2 bacterial infection often with Salmonella enterica (2) Verruga peruana: (Peruvian wart), a chronic disease characterized by cutaneous vascular lesions (resembles pyogenic granuloma or Kaposi sarcoma)
How do you make the diagnosis of bartonellosis?
The presence of organisms within red blood cells or within the cytoplasm of endothelial cells is diagnostic; blood and/or tissue cultures, immunologic testing (ELISA, immunoblot), PCR assays
What is the vector for cat scratch disease among cats?
Flea, Ctenocephalides felis
Vector for cat scratch disease for humans?
90% report cat scratch/bite
Presentation of cat-scratch disease?
Immunocompetent hosts: benign, self-limited illness characterized by tender, regional lymphadenitis that lasts for weeks to months -2-4 weeks after scratch/bite develop LAD that can last for 2-6 months, usually single axillary lymph node + swelling/erythema of overlying skin; +/- fevers, malaise, fatigue, weakness, and headaches
- Additional manifestations such as encephalopathy, hepatic granulomas, osteomyelitis, and pulmonary involvement develop in up to 15% of patients
Histology of nodes affected w/ Bartonella henselae?
Affected lymph nodes display central necrosis surrounded by histiocytic and epithelioid cells with an inner palisading layer
What stain is needed on histology to see the Bartonella henselae?
Warthin–Starry silver stain demonstrates bacilli within areas of necrosis
What bacteria cause bacillary angiomatosis?
Bartonella henselae or Bartonella quintana
Risk factors for bacillary angiomatosis?
Mostly in HIV + pt’s with CD4 count <200; unlike cat-scratch disease only 20% recall cat bite/scratch
Presentation of bacillary angiomatosis?
- Lesions are dome-shaped, vascular papulonodules
- More developed lesions can have a friable eroded appearance, resembling pyogenic granulomas
- vascular proliferation(s) caused by bacterial angiogenic factor
- Can involve lymph nodes, bone, and viscera
Histology of bacillary angiomatosis?
In H&E-stained sections, interstitial clumps of bacilli appear as purplish granular material -Warthin-Starry stain needed to see the organisms
What causes brucellosis?
Gram- coccobacillus Brucella spp.
Where do you get brucella bacteria from?
Endemic in Middle East from consuming unpasteurized goat milk/cheese. In the US it is more of an occupational dz, farmers, butchers, and veterinarians from direct contact/inhalation
Presentation of brucellosis?
Undulating fevers, arthralgias, LAD, hepatosplenomegaly, and rarely (<10% skin findings)
Skin findings in brucellosis?
Disseminated violaceous papules, erythema nodosum, extensive purpura, morbilliform eruptions
Tx for brucellosis?
Multi-drug regimens of doxycycline + other antibiotics (streptomycin, rifampin, TMP/SMX, quinolones, and aminoglycosides)
What causes Glanders?
Non-motile, strictly aerobic, non-pigment-producing, gram-negative bacillus Burkholderia mallei
Risk factors for Glanders?
Contact w/ infected horses, donkeys, or mules
4 forms of Glanders?
-Localized—hemorrhagic, ulcerative papulopustule at the inoculation site, the superficial portion of the lesion sloughs, producing an ulcer with a gray–brown base -Chronic—multiple soft tissue nodules (“farcy buds”) on skin overlying lymphatics -Septicemic form—mortality rate >95% without treatment and 50% w/ treatment -Pulmonary form—mortality like septicemic form
Tx of Glanders?
Localized disease: 60- to 150-day course of amoxicillin/clavulanate, doxycycline, or TMP/SMX Septicemic: IV carbapenems + ciprofloxacin or doxycycline
What bacteria causes melioidosis?
Caused by mobile, obligately aerobic, intracellular, non-spore-forming Gram (-) bacillus found in soil and water, Burkholderia pseudomallei
Presentation of melioidosis?
A/w direct contact w/ contaminated water or soil, risk factors are DM, alcoholism, immunosuppression adn IVDU. Otherwise presents like Glanders
Treatment for melioidosis?
Current guidelines recommend an initial intensive phase with intravenous administration of ceftazidime or a carbapenem for at least 10–14 days, followed by an eradication phase with oral TMP-SMX or amoxicillin/clavulanate for ≥3 months
What is malakoplakia?
Chronic granulomatous infection as a result of the inability of macrophages to kill phagocytosed E. coli (also Pseudomonas, Proteus, Klebsiella, Staphylococcus, Shigella, Enterococcus, Rhodococcus, and Mycobacterium spp.)
Who gets malakoplakia usually?
Most commonly affects immunosuppressed (BMT + other transplant patients > HIV/AIDS)
Most commonly affected areas in malakoplakia?
Most commonly affects GU tract; may affect skin of perianal/genital region (ulcerations, abscesses with multiple draining sinuses, yellow-to-pink soft papules, and erythematous indurated nodules)
Presentation of malakoplakia?
Ulcerations, abscesses with multiple draining sinuses, yellow-to-pink soft papules, and erythematous indurated nodules, most commonly in the perianal/genital area
Histology of malakoplakia?
*high yield* Michaelis-Gutmann bodies: comprised of incompletely killed bacteria within calcified phagolysosomes; intracytoplasmic laminated concretions that represent accumulations of calcified, iron-containing phagolysosomes; they stain with PAS, von Kossa, Perls’, and Giemsa stains -Von Hansemann cells: large macrophages that contain Michaelis–Gutmann bodies; stain positively for CD68, lysozyme, and alpha-1 antitrypsin
Treatment of malakoplakia?
Localized: surgical excision Nonsurgical candidates: difficult to treat; may try long courses of ciprofloxacin, TMP/SMX, or clofazimine
What causes tularemia?
Gram - coccobacillus, non-motile, Francisella tularensis
note: reportable in the US d/t concern for biological weapon status
What is the mode of transmission for tularemia?
Contact w/ rabbit carcasses (most classic exposure), deer flies, and ticks; increased risk in hunters and animal handlers
What is the most common presentation of tularemia?
Most common presentation is ulceroglandular = 80% (>pneumonic>glandular, typhoidal>oropharyngeal >oculoglandular), which p/w necrotic, punched-out ulcer at inoculation site w/ suppurative lymphadenopathy
What is the treatment for tularemia?
streptomycin (treatment of choice) -Jarisch–Herxheimer-like reaction may occur following the initiation of therapy
Presentation of Haemophilus influenzae cellulitis?
Classically affects infants, p/w deep red-violaceous/blue facial cellulitis (most commonly periorbital or buccal) following a URI-like illness Usually positive blood cultures
Tx for Haemophilus influenzae cellulitis?
Third gen cephalosporin
What bacteria causes rhinoscleroma?
Inhalation of Klebsiella rhinoscleromatis (gram-negative coccobacillus that is a subspecies of K. pneumoniae)
Where do you see rhinoscleroma?
Mostly in tropical locations
Risk factors for rhinoscleroma?
Immune defects –> it is caused by the inability of macrophages to kill phagocytosed bacteria
What are the 3 clinical phases of rhinoscleroma?
- Catarrhal phase (rhinitis, obstruction from soft tissue edema)
- Granulomatous/infiltrative phase (granulomatous nodules in nose/URT, epistaxis, dysphonia, anesthesia of soft palate, and Hebra nose)
- Sclerotic phase (extensive scarring requires tracheotomy and nasal reconstruction)
Histology of rhinoscleroma?
dense pan-dermal infiltrate of (*High Yield* Mikulicz cells containing bacteria (seen w/ Warthin-Starry, Giemsa)) and Russell bodies (plasma cells with aggregates of condensed plasma cells)
Skin findings associated with salmonellosis?
Rose spots: 2-8mm pink, blanching, grouped papules on the trunk. Bacteria can be cultured from rose spots *This will be seen in the background of N/V, diarrhea, headache
Treatment for salmonellosis?
Quinolones, third-generation cephalosporin in children
What bacteria causes rat-bite fever?
Streptobacillus moniliformis (gram negative)
Vector for rat-bite fever?
Rats, increased incidence in urban areas w/ high rat concentration
Presentation of rat-bite fever?
Classic triad (paroxysmal fever, migratory polyarthritis, and acral rash) -p/w redness, edema, and ulceration at bite site –> paroxysmal fever w/ systemic symptoms –> 2 to 4 days later, migratory polyarthritis + acral eruption (palms and soles most common) of petechial red macules/papules, vesicles, or pustules Up to 15% mortality
Treatment of rat-bite fever?
Penicillin for 1 week (6 weeks if septicemic)
What bacteria causes plague?
Yersinia pestis - gram - bipolar bacillus that looks like a safety pin
What is the reservoir of plaque and how does it usually get transmitted to humans?
Rodents are a reservoir and usually gets transmitted to humans by flea bites (>rodent contact, inhalation)
3 forms and presentations of plague?
- Bubonic (most common): pustule or ulcer at inoculation site (10%) + painful, suppurative regional lymphadenopathy = “buboes” (groin, axillae most common); 25% to 50% mortality rate if untreated May simulate tularemia, rat-bite fever, sporotrichosis, tuberculosis, streptococcal ecthyma, syphilis, or lymphogranuloma venereum.
- Septicemic: vesiculopustular eruption w/ petechiae, purpura; hemorrhagic and necrotic lesions in nasopharyngeal and GI tracts; 100% mortality if untreated
- Pneumonic: acute pneumonitis; 100% mortality if untreated
Treatment of plague?
- First line: aminoglycosides (streptomycin and gentamicin) -Plague meningoencephalitis: chloramphenicol (high penetration of blood-brain barrier)
- Postexposure prophylaxis: doxycycline or ciprofloxacin ×7 days (highly effective)
Risk factors for vibrio vulnificus infection?
Liver diseases (hemochromatosis, cirrhosis, alcoholism), diabetes or other things causing peripheral neuropathy/vasculopathy predisposing them to wounds, GI dz, immunosuppression and ESRD
Reservoir of vibrio vulnificus?
Shellfish
What are the two modes of infection for vibrio vulnificus?
Cutaneous exposure from contaminated seawater/shellfish and consumption of raw/undercooked shellfish
Cutaneous manifestation of vibrio vulnificus infection?
- Cutaneous exposure: primary skin infection, or superinfection of preexisting wound –> may progress to necrotizing fasciitis, myositis, or septicemia
- Consumption exposure: most commonly from raw oysters; septicemia, abdominal cramps, and hypotension; 75% have skin findings – red-purple macules/vesicles –> progress to hemorrhagic bullae and necrotic plaques, reminiscent of purpura fulminans
Treatment of vibrio vulnificus infection?
Doxycycline + third-gen cephalosporin
What are the main spirochetes to cause lyme by location?
Borrelia burgdorferi (#1 in the US), Borrelia garinii and B. Afzelii (#1 in Europe)
How long does the tick usually have to stay attached to transmit dz?
Low transmission risk of Borrelia during the first 48 hrs of tick attachment
What is the Reservoir of B. Burgdorferi?
White-tailed deer and white-footed mouse
What is the Vector of B. Burgdorferi?
Ixodes species of ticks; specific type varies by region.
What is the most common vector of B. burgdorferi in the US?
Ixodes scapularis: prevalent in the eastern US and great lakes area
What is the most common vector for B. burgdorferi in the western US?
Ixodes pacificus
What is the most common vector for B. burgdorferi in europe?
Ioxdes ricinus
What is the most common vector for B. burgdorferi in Asia?
Ixodes persulcatus
What is a borrelial lymphocytoma and what from of Borrelia is most commonly associated with it?
- Lymphocytoma is a benign, reactive form of lymphoid hyperplasia that can be attributed to various stimuli, including Borrelia infection
- Occurs during the early disseminated stage of Lyme disease d/t spread of spirochetes; ~1% of patients with Lyme disease in Europe; strongly a/w B. afzelii and B. Garinii -p/w firm, plum-colored tender nodule/plaque on earlobes (children), or nipple/areola (adults); +/- regional LAD
Histopathology of borrelial lymphocytoma?
Grenz zone, dense dermal infiltrate of lymphocytes forms a pattern that closely resembles the architecture of a lymphoid follicle
What is acrodermatitis chronica atrophicans?
- Seen in up to 10% of patient’s with Lyme disease in Europe d/t strong a/w B. afzelii and B. garinii
- Occurs months to years after initial infection; two clinical phases: -Erythematous/violaceous plaques and nodules with “doughy”/swollen skin on distal extremities (early phase; easily treated/reversible)
- Progresses to atrophic “cigarette-paper” skin w/ telangiectasias (chronic phase; recalcitrant to treatment) and subcutaneous fibrous nodules overlying joint
How does the skin findings in lyme dz differ by how widespread the infection is?
The initial lesion, erythema migrans is an expanding large bullseye appearing lesion (classically) that can grow quite large. The more disseminated form can have multiple smaller lesions that may not be as a bullseye in appearance but rather look like red rings without scale.
What causes yaws, pinta, and endemic syphilis (Bejel)?
T. Pallidum subspecies that are morphologically and antigenically identical to the organism that causes venereal syphilis but they are not venereal
Which endemic treponematoses affect children?
Yaws and endemic syphilis (all but Pinta commonly affect children)
Most common presenting areas of rash for endemic treponematoses?
All except Bejel most commonly begin on legs
Treatment for endemic treponematoses?
Benzathine Penicillin (although recently oral azithromycin was sown to be non-inferior to benzathine penicillin for yaws, so for yaws azithro is first-line)
Skin findings of yaws?
Legs most commonly affected, p/w indurated, red, painless papules that enlarge then ulcerate this is the “mother yaw”, 2nd stage: multiple smaller widespread “daughter yaws”, 3 stage: necrotic and ulcerative abscesses that heal w/ severe/deforming scars + bony damage
Skin findings in Pinta?
First stage: legs most commonly affected; p/w papules surrounded by red halo; enlarges over months up to 12 cm. Secondary stage: smaller scaly papules and psoriasiform plaques erupt “pintids” and change in color from red –> blue –> brown –> gray/black 3rd stage: vitiligo-like lesions over bony prominences w/ atrophic epidermis
Skin findings in endemic syphilis?
1st stage: rarely noticed, p/w inconspicuous papules or ulcer in the mouth or on nipples of breastfeeding women (not legs). 2nd stage: mucous membrane lesions and generalized LAD 3rd stage: gumma formation of mucous membranes, skin and bones *remember that endemic syphilis attacks “enside” surfaces
What are the cutaneous manifestations of leptospirosis?
Cutaneous manifestations include erythematous macules, papules, patches, and/or plaques in a widespread distribution or (especially with L. interrogans serovar Autumnalis) localized to the shins, as well as petechiae and purpura secondary to vascular involvement
How is leptospirosis transmitted?
Transmitted via contact of non-intact skin or mucous membranes with urine or other body fluids (with the exception of saliva) from infected mammals (e.g. rodents, dogs, livestock, wild animals), either directly or from drinking or swimming in contaminated water
How often is leptospirosis icteric?
10%, more severe
Treatment of leptospirosis?
Self-limited; oral doxycycline, amoxicillin, or azithromycin and (for more severe disease) intravenous penicillin or third-generation cephalosporins
What bacteria causes actinomycosis?
Actinomyces israelili, gram +, nonacid fast and anaerobic microaerophilic filamentous bacteria
Presentations of actinomycosis?
- Cervicofacial (most common, accounts for 70%): “lumpy jaw disease,” red-brown nodules with fistulous abscesses draining characteristic yellow sulfur granules (= clumps of bacteria); a/w poor dental hygiene and dental procedures
- Pulmonary/thoracic: as a result of aspiration, p/w pulmonary cavities at base of lungs -GI: as a result of trauma or inflammatory disease, p/w granulomatous lesions in bowel wall
Histology of actinomycosis?
Dense granulomatous and suppurative inflammation with “granules” with basophilic center (Gram(+) branching filaments of Actinomyces) and eosinophilic rim (Splendore-Hoeppli phenomenon)
Treatment of actinomycosis?
Penicillin G or ampicillin
What is the bacteria that causes nocardiosis?
Nocardia brasiliensis (#1 cause of actinomycotic mycetoma) and nocardia asteroides (#1 cause of pulmonary/systemic nocardiosis)
What type of bacteria is nocardia?
Gram + weakly acid-fast, filamentous bacteria
Most common site and presentation of actinomycotic mycetoma?
50% of cases of actinomycotic mycetoma are caused by Nocardia species, traumatic inoculation causes a painless nodule that enlarges, suppurates, and drains via the sinus tracts, purulent discharge contains sulfur granules. **foot is the usual site of involvement, may involve underlying muscle and bone
Treatment of nocardiosis?
Sulfonamides
What is the difference between an eschar and a scab?
Eschar is from necrotic tissue
DDx of eschar lesions?
- Rickettsiosis: tick-born (not RMSF); Mite-born: 10-30% of scrub typhus; Flea-born: R. Relis
- Non-rickettsiosis: B. Antracis (surrounded by non-pitting edema); Bartonella, F. Tularensis, c. Trachomatis, Y. pestis, P. Multicida
- Non-infection: full-thickness burn, warfarin and heparin-induced necrosis, vasculitis, brow-recluse spider bite
- Ecthyma gangrenosum: pseudomonas -Pyoderma gangrenosum -Ecthyma/ulcerating impetigo
DDx for sporotrichoid lymphocutaneous infection?
Cat scratch disease (bartonella henselae) Atypical mycobacteria especially marinum Tuberculosis Nocardia Sporotrichosis Phaeohyphomycosis (deep fungal infections) Leishmaniasis Anthrax Tularemia
