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THE

STAPHYLOCOCCI
FEBRUARY 6, 2008
CASE 1
 M.M., 17 YEAR OLD FEMALE
 CHIEF COMPLAINT: FEVER
 HPI: 2 DAYS PTA, SHE STARTED
EXPERIENCING HIGH-GRADE FEVER, WITH
CHILLS AND BODY MALAISE.
FOOD INTAKE WAS LIMITED, DUE TO
NAUSEA NAD VOMITING. SHE NOTICED
RASHES ON HER ABDOMEN, AND HER
PERINEAL AREA WAS PAINFUL.
 MENSTRUAL HISTORY: SHE IS ON DAY
4 OF HER CYCLE.
 PERTINENT PE FINDINGS
BP: 80/50 mmHg
PR:120 /MIN
T: 103 F
 BUCCAL MUCOSA AND TONGUE WERE
CONGESTED
 ERYTHEMATOUS MACULOPAPULAR
RASH SEEN ON HER ABDOMEN ,
LOWER EXTREMITIES AND HANDS
 GYNE EXAM SHOWED HYPEREMIC
VAGINAL WALLS, (+) TENDERNESS
 REST OF THE PE WAS NORMAL
 IMPRESSION?
 Gram-positive
 cluster-forming coccus

 Nonmotile
 nonsporeforming
 facultative anaerobe

 fermentation of glucose produces mainly lactic acid


 catalase positive
 coagulase positive
 golden yellow colony on agar (S.aureus)
 White colonies (S. epidermidis/ albicans)
 normal flora of humans found on nasal passages, skin
and mucous membranes
S. aureus
STAPHYLOCOCCUS
MSA
STAPH INFECTIONS
 suppurative infections
 superficial skin lesions such as boils, styes and
furunculosis
 Pneumonia
 Mastitis
 Phlebitis
 Meningitis
 urinary tract infections
 deep-seated infections, such as osteomyelitis and
endocarditis.
VIRULENCE FACTORS
 1) surface proteins that promote colonization
of host tissues;
 (2) invasins that promote bacterial spread in
tissues (leukocidin, kinases, hyaluronidase);
 (3) surface factors that inhibit phagocytic
engulfment (capsule, Protein A);
 (4) biochemical properties that enhance their
survival in phagocytes (carotenoids, catalase
production);
VIRULENCE FACTORS
 (5) immunological disguises (Protein A, coagulase,
clotting factor); and
 (6) membrane-damaging toxins that lyse eukaryotic
cell membranes (hemolysins, leukotoxin, leukocidin;
 (7) exotoxins that damage host tissues or otherwise
provoke symptoms of disease (, TSST)
 (8) inherent and acquired resistance to antimicrobial
agents.
ALPHA-TOXIN
 most potent membrane-damaging toxin of S.
aureus I
 binds to the membrane of susceptible cells
 Toxin subunits create a central pore through
which cellular contents leak
 platelets and monocytes
 Septic shock
BETA-TOXIN
 sphingomyelinase
 damages membranes rich in this lipid
 classical test for ß-toxin is lysis of sheep
erythrocytes
 majority of human isolates of S. aureus do not
express ß-toxin
LEUKOCIDIN
 protein toxin which creates pores in the
membranes
 hemolytic, but less so than alpha hemolysin.
 Only in 2% of all of S. aureus
 90% of the strains isolated from severe
dermonecrotic lesions
 important factor in necrotizing skin infections.
COAGULASE
 extracellular protein
 binds to prothrombin in the host to form a
complex called staphylothrombin
 The protease activity characteristic of
thrombin
 result in the conversion of fibrinogen to fibrin
 No evidence that it is a virulence factor.
STAPHYLOKINASE
 lyses fibrin
 associated with lysogenic bacteriophages
 staphylokinase + plasminogen = dissolution
of fibrin clots.
AVOIDANCE OF HOST
RESPONSE
 surface polysaccharide serotype 5 or 8
 Microcapsule: visualized only by electron
microscopy
 rapidly lose the ability when cultured in the
lab
 impede phagocytosis in the absence of
complement
PROTEIN A
 surface protein of S. aureus
 binds IgG molecules by their Fc region
 In serum, binding occurs in a wrong
orientation on the IgG
 disrupts opsonization and phagocytosis.
SUPERANTIGENS
 enterotoxins
 six antigenic types

SE-A, B, C, D, E and G
 SUPERANTIGEN:activate 20% of the T cells

(normal is 0.001%)
response is not specific to the antigen
“useless” immune response
 Superantigens evade the immune system
STAPHYLOCOCCAL FOOD
POISONING
 foods contaminated with toxins
 most common way: contact with food workers
who carry the bacteria or through
contaminated milk and cheeses.
 salt tolerant
 As the bacteria multiplies in food-produces
toxins
 resistant to heat, resistant to cooking.
Staph food poisoning
 highest risk of contamination:
sliced meat,
puddings
pastries
sandwiches
SIGNS AND SYMPTOMS
 fast acting toxins
 cause illness in as little as 30 minutes
 Average: one to six hours after eating
contaminated food.
 nausea, vomiting
 Crampy abdominal pain
 diarrhea.
Staph food poisoning
 Lab diagnosis:
 Identification of the bacteria in stool and
vomitus
 toxin can be detected in food items
 generally based only on the signs and
symptoms
 High index of suspicion
 Testing is usually reserved for outbreaks
involving several persons
Staph food poisoning
 The illness is mild
 recover after one to three days
 Supportive treatment
 Antibiotics are not useful
 Patients with this illness are not contagious
SUPERANTIGEN :TSST-1
 CAUSES TOXIC SHOCK SYNDROME
 TSST-1 is responsible for 75% of TSS,
including all menstrual cases
 enterotoxins B and C cause 50% of non-
menstrual cases of TSS.
TOXIC SHOCK SYNDROME
 Mostly in females
 Cases reported also in males (e.g.surgical site
infection)
 Menstrual-related TSS
 Non-mentrual related TSS
TSS
SIGNS AND SYMPOTOMS :TSS
 Prodromal period of 2-3 days
 Pain at site of infection
 Fever and/or chills
 Nausea and/or vomiting
SIGNS AND SYMPTOMS:TSS
 Profuse watery diarrhea with abdominal pain
 Lightheadedness and/or syncope
 Myalgias and/or arthralgias
 Pharyngitis and/or headache
 Confusion (more common with staphylococcal
TSS than with streptococcal TSS)
The Centers for Disease Control and
Prevention (CDC) criteria for the diagnosis of
staphylococcal TSS
 Fever, hypotension, and rash
 Involvement of 3 or more organ systems
 Absence of serologic evidence of Rocky
Mountain spotted fever, leptospirosis, measles,
hepatitis B, antinuclear antibody, positive
Venereal Disease Research Laboratory
(VDRL) test results, and antibodies at
Monospot testing
SKIN RASH
 Diffuse rash, occasionally patchy and
erythematous, with desquamation occurring
approximately 1-2 weeks later
 Rash initially appearing on trunk, spreading

to arms and legs, and involving palms and


soles
SKIN RASH: TSS
SKIN RASH: TSS
MULTI-ORGAN INVOLVEMENT:
TSS
 ventricular arrhythmias, renal failure, or hepatic
failure
 Disseminated intravascular coagulation (DIC)
 Acute respiratory distress syndrome
 Necrotizing fasciitis and/or myositis
 Altered consciousness (CNS involvement)
 Mucosal inflammation (eg, vaginitis,
conjunctivitis, pharyngitis
STRAWBERRY TONGUE:TSS
TSS
 Fever higher than 102°F
 Systolic BP less than 90 mm Hg

 orthostatic decrease in systolic BP of 15

mm Hg
LAB EXAMS:TSS
 The CBC: leukocytosis , mild anemia, and/or
thrombocytopenia.
 ElectrolyteS:hyponatremia, hypokalemia,
hypocalcemia out of proportion to hypoalbuminemia,
hypophosphatemia, and hypomagnesemia.
 Liver function test: hyperbilirubinemia , elevated
aspartate aminotransferase (SGOT) level , and an
elevated alanine aminotransferase (SGPT)
 Coagulation studies:elevated activated partial
thromboplastin time (aPTT) and fibrin split products.
LAB EXAMS:TSS
 Azotemia and/or acute tubular necrosis
 Urinalysis:sterile pyuria, myoglobinuria, and
red cell casts.
 Increased Creatine kinase
levels:rhabdomyolysis
 ABG: metabolic acidosis secondary to
hypotension and/or hypoxia.
Lab exams :TSS
 Culture all potentially infected sites (including
blood)
 CXR: pulmonary edema.
 XRAYS: soft-tissue swelling.
 2D ECHO: wall-motion abnormality, toxic
cardiomyopathy.
TREATMENT :TSS
 Fluid resuscitation
 Crystalloids may be administered. As much as
10-20 L/d often is necessary.
 Administer supplemental oxygen therapy to
maximize tissue oxygenation and to correct
hypoxia and/or acidosis.
 Assisted ventilation may be required if acute
respiratory distress syndrome develops.
TREATMENT:TSS
 Hyperbaric oxygen therapy: necrotizing soft-
tissue infections
 Cardiac monitoring
 Foley catheter
 Tampons and packing materials, if present,
should be removed.
 menstruation-related TSS:irrigation of vagina
with isotonic sodium chloride solution or
povidone-iodine solution
EXFOLIATIN TOXIN
 separation within the epidermis, through the
stratum granulosum of the epidermis.
 Staphylococcal exfoliative toxin B has been
shown to specifically cleave desmoglein 1, a
cadherin that is found in desmosomes in the
epidermis.
SCALDED SKIN
SYNDROME(SSS)
 Ritter Disease
 affects infants and children under the age of 5.
SIGNS AND SYMPTOMS: SSS

 fever
 Generalized erythema
 skin slips off with gentle pressure leaving wet
red areas (Nikolsky sign)
 exfoliation or desquamation
 painful skin
SSS
SSS
SSS
LAB EXAMS: SSS
 Complete blood count
 cultures of the skin and throat
 skin biopsy
 Serum electrolytes
TREATMENT: SSS
 Fluid rehydration is initiated with Lactated
Ringer solution at 20 cc/kg initial bolus.
Repeat the initial bolus as clinically indicated
 maintenance therapy with consideration for
fluid losses from exfoliation of skin being
similar to a burn patient.
TREATMENT:SSS
 Topical wound care: saline AND topical
antibiotic ointment.
 A chest radiograph should be considered to
rule out pneumonia as the original focus of
infection.
 Steroids are not indicated at this time.
PROGNOSIS:SSS
 Healing begins in about 10 days following treatment.
 A full recovery is expected.
 Possible Complications
septicemia
dehydration or electrolyte imbalance
poor temperature control (in young infants)
cellulitis
 The disorder may not be preventable; Prompt
treatment
COAGULASE-NEGATIVE STAPH
 S. epidermidis;75% of clinical isolates
 S, haemolyticus
 S. hominis
 S. capitis
 S. saprophyticus
 increased use of implants such as CSF shunts,
IV lines, cardiac valves, pacemakers, artificial
joints, urinary catheters
 increasing number of severely debilitated
patients in the hospitals.
 morphologically similar to S.aureus, however
they form white colonies, and are coagulase
negative.
S.epidermidis
DISEASE CAUSED BY
COAGULASE-NEGATIVE STAPH
 Prosthetic valve endocarditis
 Meningitis
 Peritonitis
 UTI in pregnant women(S. saprophyticus)
 Treatment is with Vancomycin, if not resistant.
S. saprophyticus responds to trimethoprim or
to quinolones.
ENDOCARDITIS
STAPH DRUG RESISTANCE
 (1) mutation in chromosomal genes followed
by selection of resistant strains
 (2) acquisition of resistance genes as
extrachromosomal plasmids, transducing
particles, transposons, or other types of DNA
inserts.
MRSA
 occur in otherwise healthy people who have
not been recently (within the past year)
hospitalized
 had a medical procedure (such as dialysis,
surgery, catheters)
 community-associated (CA)-MRSA infections
skin infections: abscesses, boils, and other
pus-filled lesions
MRSA RESERVOIRS
 In hospitals, the most important reservoirs of
MRSA are infected or colonized patients
 HOSPITAL PERSONNEL: commonly
identified as a link for transmission between
colonized or infected patients.
MODE OF
TRANSMISSION:MRSA
 via hands (especially health care workers'
hands) which may become contaminated by
contact with
 a) colonized or infected patients
 b) colonized or infected body sites of the
personnel themselves,
 c) devices, items, or environmental surfaces
contaminated with body fluids containing
MRSA.
 Hospital-associated MRSA isolate is resistant to :
erythromycin
clindamycin
tetracycline
 community-associated MRSA isolates resistant:
ß-lactam agents
erythromycin.
TREATMENT: MRSA
 vancomycin
 in Georgia, Texas, and California, the
prevalence of CA-MRSA is widespread.
VRSA
 1996, MRSA strains with decreased
susceptibility to vancomycin

 VISA: if the MIC for vancomycin is 4-8µg/ml,


 VRSA :MIC is >16µg/ml.
VISA, VRSA
 several underlying health conditions (such as
diabetes and kidney disease)
 previous infections with methicillin-resistant
Staphylococcus aureus (MRSA)
 intravenous [IV] catheters)
 recent hospitalizations
 recent exposure to vancomycin and other
antimicrobial agents.
TREATMENT FOR VRSA
 limited treatment options for VISA/VRSA
infections
 rifampin, gentamicin, imipenem,
chloramphenicol, trimethoprim-
sulfamethoxazole, and tetracycline
 IMPRESSION FOR CASE 1

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