THE STAPHYLOCOCCI

FEBRUARY 6, 2008

CASE 1
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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?

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Gram-positive cluster-forming coccus Nonmotile nonsporeforming facultative anaerobe fermentation of glucose produces mainly lactic acid

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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

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S. aureus

STAPHYLOCOCCUS

MSA

STAPH INFECTIONS
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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
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(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

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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
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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

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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
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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
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lyses fibrin associated with lysogenic bacteriophages staphylokinase + plasminogen = dissolution of fibrin clots.

AVOIDANCE OF HOST RESPONSE
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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
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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
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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
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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
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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
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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
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CAUSES TOXIC SHOCK SYNDROME TSST-1 is responsible for 75% of TSS, including all menstrual cases enterotoxins B and C cause 50% of nonmenstrual cases of TSS.

TOXIC SHOCK SYNDROME
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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
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Prodromal period of 2-3 days Pain at site of infection Fever and/or chills Nausea and/or vomiting

SIGNS AND SYMPTOMS:TSS
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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
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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
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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
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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
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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

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Culture all potentially infected sites (including blood) CXR: pulmonary edema. XRAYS: soft-tissue swelling. 2D ECHO: wall-motion abnormality, toxic cardiomyopathy.

TREATMENT :TSS
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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

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Hyperbaric oxygen therapy: necrotizing softtissue 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)
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Ritter Disease affects infants and children under the age of 5.

SIGNS AND SYMPTOMS: SSS
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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
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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
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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
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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
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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

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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
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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.

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VISA, VRSA

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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, trimethoprimsulfamethoxazole, and tetracycline

IMPRESSION FOR CASE 1

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