Clinical Case 2

Clinical Case 2• 12-year-old boy was admitted to the hospital because of fever, chills, sweats, productive cough, nausea, and vomiting. • recurrent pneumonias since the age of 5 years. • physical exam: • febrile, tachycardic, and tachypneic; • diffuse rhonchi in both lungs. • finger clubbing, splenomegaly

• Blood cultures grew Staphylococcus aureus. • Dx: Chronic granulomatous disease

Clinical Manifestations

• Disease from S. aureus occurs in one of several ways– toxin formation– localized infection (pyogenic disease)– systemic infection (disseminated infection)


• Staph food poisoning– occurs through ingestion of a preformed enterotoxin (usually

staph enterotoxin A or B) in contaminated food– meats, potato salad, custards, ice cream - partially cooked or

come to room temperature and then refrigerated– usually the food appears normal– abrupt onset of salivation, N/V, abdominal pain, diarrhea

occurring 2 - 6 hours after ingestion– usually occurs in community outbreaks– self-limited: resolves in a few hours


• Toxic shock syndrome– associated with toxigenic staph strains producing

TSST-1• TSST-1: related to the enterotoxins and is a

superantigen– patients are colonized with the staph strain and

under certain conditions (low oxygen tension, low magnesium concentration, etc), toxin production begins


• Toxic shock syndrome - 2 scenarios clinical picture looks the same– Non-menstrual• usually occurs 48 hours after a surgical procedure • patient looks septic but wound looks good

– Menstrual• young women age 15-25 using tampons during menses


• TSS - clinical picture– abrupt onset of myalgias, fever, vomiting, diarrhea– confusion without focal neurologic deficits– severe hypotension, renal insufficiency, shock liver – rash with desquamation of palms and soles within

a week - often conjunctival injection


• TSS - Treatment– remove source of the staph (removes toxin

production) abscesses, fluid collections, tampons– supportive measures, immunoglobulins,

antibiotics• 3% mortality currently - long term neurologic

sequelae not uncommon

Clinical Manifestations• Pyogenic disease • Numerous types - clinical name used depends on

location and size of the S. aureus infection• Examples:– folliculitis– furuncles/carbuncles -

• deep seated inflammatory mass that evolves from folliculitis (zits) - a carbuncle is a coalescence of furuncles

– hidradenitis suppurativa • chronic infections of axilla, pubic area associated with

apocrine sweat glands

Furuncle

Carbuncle

hidradenitis

Clinical Manifestations• Pyogenic Diseases con’t– impetigo • Superficial infection of the skin• begins as a vesicular lesion, then changes to a crusty

erosion– cellulitis • Infection of the dermal, subcutaneous tissues

associated with dolor, rubor, calor, tumor– lymphangitis • Dissemination of infection through lymphatics - can

be a complication of pyogenic infection

impetigo

cellulitis

lymphangitis


• SSSS (Staph Scalded Skin Syndrome)– Ritter von Ritterschein disease (in newborns)– Toxins act on the dermis• Generalized

– Staph secretes a toxin systemically (usually can’t recover staph from the involved site)

– Nikolsky’s sign: detachment of the skin by rubbing• Localized

– Bullous impetigo– Blistering around an infected area

– Treatment is antistaph agents/local wound care

Scalded Skin Syndrome

SSSS vs TEN

• TEN (Toxic Epidermal Necrolysis)– Cleavage within the dermis or dermoepidermal

junction • epidermal involvement• High fatality rate• Can be difficult to distinguish from SSSS

– May need biopsy– Treatment with steroids (?)


• Disseminated infection– “Staph goes where the blood goes”– bacteremia/septicemia usually starts as a local

infection and overcomes host defenses– manifestations include endocarditis, vasculitis,

pericarditis, pneumonia, osteomyelitis, brain abscess

Treatment

• Remove foreign bodies if possible• Drain pus if possible• Duration of therapy depends on the

type of infection–bone, foreign body, heart require at least

4 weeks of antibiotics

Treatment• Antibiotic Therapy– guided by local susceptibility data– MSSA- methicillin sensitive S. aureus • good drug choices are B-lactams

– Hospital Acquired MRSA (HA-MRSA)• Most frequently due to altered penicillin binding

proteins (PBP2a)- mecA gene• resistant to more drugs than CA-MRSA• vancomycin best choice

– Community acquired-MRSA (CA-MRSA)• doxycycline, trim-sulfa, linezolid, vancomycin good

initial choices if CA-MRSA suspected• rifampin resistance occurs rapidly and combination

therapy is useful– VISA/VRSA• MRSA that is Vancomycin Resistant

– vancomycin intermediate-susceptible MRSA– vancomycin resistant MRSA

• consider linezolid or Synercid or daptomycin

Treatment

Antibiotic Susceptibility Testing

Vitek 2.0

Mueller-Hinton Agar Disk Diffusion

CA-MRSA

Coagulase Negative Staphylococci

• Coagulase Negative staph– 15 species are indigenous to man– 4 are clinically important• S. epidermidis (S. epidermidis)• S. hemolyticus• S. saphrophyticus• S. lugdunensis (infrequent, but severe)

– Others: S. capitis, S. caprae, S. warneri, S. auricularis, S. intermedius, S. simulans, S. cohnii, S. chormogenes

S. epidermidis

• normal resident bacteria on skin, mucous membranes (S.epi - 65% - 90%)

• type, location, and amount of S.epi on skin can be altered by many factors

• eg. - antibiotic use, S. aureus colonization

• Contains numerous plasmids coding for antibiotic resistance and can easily transfer them within or between species, genus

S. epidermidis

• usually highly antibiotic resistant–>80% methicillin resistant–>50% are resistant to: erythromycin,

clindamycin, Chloramphenicol, and tetracyclines– Sensitive to: vancomycin, rifampin, and

ciprofloxacin• Nearly all infections are nosocomial (hospital

acquired)

S. epidermidis

• Coagulase negative• Catalase positive• Growth on blood agar:– Non-hemolytic (gamma

hemolysis)– Whitish creamy color– Grows readily (16 hours)

S. aureus

S. epidermidis

S. epidermidis

• no known pathogenic exoproteins or toxins• mainly causes infection on “hardware” and is

introduced onto foreign body during procedure from hospital environment, hands of personnel– eg - IVs, dacron grafts, CSF shunts, pacemaker

wires, artificial valves and joints, implants (breast, eye)

S. epidermidis

• Exopolysaccharide layer produced by the organism (biofilm) is the major reason it causes infection on hardware–Biofilm protects S. epidermidis from

host defenses such as opsonization and decreases penetration of antibiotics– some surface antigens produced by S.

epidermidis may promote its adherence

CoNS Pathogenesis

Von Eiff, et al. Lancet Infect Dis 2002;2:677-85

silicone ventricular catheter (Cordis®)

before inoculation 30 minutes

12 hours 24 hours

• DO NOT take blood cultures from Lines!• Intravenous Catheter Infections– S. epidermidis- most common associated

organism– Can lead to bacteremia and can also be

associated with significant morbidity/mortality (“line sepsis”)

– Infection can occur at the insertion site or the tip

– Remove catheter + Vancomycin



• Bacteremia– S. epidermidis often recovered from blood cultures– most common blood contaminate and rarely causes native

valve endocarditis• most common cause of “line sepsis” • major cause of sternal osteomyelitis after

cardiothoracic surgery• common cause of prosthetic joint infection


• Infective Endocarditis (IE)– Native valve IE

• 5% of all cases are due to S. epidermidis• occurs with seeding of damaged valves, endocardium

when S. epidermidis crosses skin barrier– Prosthetic valve IE

• 40% of all cases are due to S. epidermidis• if it develops in the first months after valve

replacement, seeding probably occurred during surgery


• IE (continued)– Diagnosis• Multiple sets of positive blood cultures • echocardiography• high level of clinical suspicion

– Treatment• Vancomycin + gent + rifampin• Removal & replacement of valve


• S. epidermidis endophthalmitis: – Most common cause after

cataract surgery/lens implantation

– Also occurs in intravenous drug abusers (IVDA)

– Dx - clinical exam– Tx - vitrectomy or enucleation

with IV vancomycin +intravitreal antibiotics


• Urinary Tract Infections– S. epidermidis usually causes UTIs in elderly,

hospitalized patients with catheters in place–Very different than clinical setting of UTIs

with S. saprophyticus

S. hemolyticus

• (2nd most common cause of CoNS infections) • normal resident bacteria on skin, mucous

membranes• Infections: similar to S. epidermidis-– Line infections, endocarditis, septicemia– Others: UTI, Wound, bone, and joint

• Lab: similar to S. epidermidis: catalase positive coagulase negative, non-hemolytic on blood agar

S. saprophyticus

• Catalase positive• Coagulase negative• Non-hemolytic on blood agar• Novobiocin resistant• True urinary pathogen (rarely a

contaminant)• UTI clinical presentation similar to that of infection with GNRs such as E. coli: frequency, urgency,

dysuria: pyuria on UA

S. saprophyticus

• Infection occurs in healthy young women in an outpatient setting– 70% report sex within 24 hours preceding symptoms– 2nd most common pathogen (after E. coli) in young

women– can cause symptoms, pyuria, with <105 cfu/ml– may be cause of acute urethral syndrome– Tx - quinolones, Bactrim• may recur in 10% of patients

S. lugdunensis• Infrequent, but important cause of infections• Very aggressive endocarditis with frequent valve replacement, congestive heart

failure, and high mortality rate• Bacteremia, arthritis, UTI, central line infections, wound infections• Key lab features:

– Beta hemolytic on blood agar– Coagulase negative– pyrrolidonyl-α-naphthylamide hydrolysis (PYR) positive

• Detects L-pyrrolidonyl arylamidase• Paper disk impregnated with reagent• (most staph are negative): good rapid screening test

– Rapid ornithine decarboxylase positive (all other staphylococci are negative)

PYR positivePYR negative

Definitive ID to SpeciesBiochemical Reactions

AutomatedVitek 2.0

Remel Staph RapID BioMerieux API Staph

Manual Methods

Definitive ID to Species16S rRNA gene sequencing

Search Sequence Database of Organisms

Documents

Clinical Case 2