Professional Documents
Culture Documents
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
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
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