Gram-positive Cocci Flashcards

1
Q

the reservoirs of Staph aureus

A

• Normal flora of nares, skin, various mucosal surfaces

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2
Q

the reservoirs of Staph epidermidis

A

• Normal inhabitant of skin and mucous membranes

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3
Q

the transmission of Staph aureus

A
  • From endogenous flora to normally sterile site
  • Person-to-person via fomites, direct contact, respiratory droplets
  • Ingestion of food containing toxin
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4
Q

the transmission of Staph epidermidis

A
  • From normal flora to normally sterile site

* Spread person-to-person

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5
Q

Major diseases caused by Staph aureus

A

Cutaneous infections
Impetigo
o Primarily affects young children
o Flattened red spot → pus filled vesicle that crusts
Cellulitis
o Infection of skin and soft tissues (dermis and subcutaneous fat layers)
o Treat with systemic antibiotics
Folliculitis
o Infection of hair follicles
o Often resolves on own; may need systemic therapy
Furuncle (boil)
o Small, painful infection of skin and soft tissues
o Infection resolves with drainage or incision
Carbuncle
o When furuncles coalesce and extend to deeper tissue
o Usually on back of neck
o May result in bacteremia
Wound infections
o Staph colonizing skin is introduced during surgery or trauma
o Manage infection by draining pus and removing foreign object
o May require antibiotic therapy
Mastitis
o Colonized infant transfers Staph to mother during breastfeeding
o Pain, swelling, redness of breast tissue
Food poisoning
• Toxin-mediated = toxin grows in food
• Heat-stable, not affect appearance or taste of food
• Causes abdominal pain, severe vomiting, diarrhea
• Occurs 2-4 hrs after ingestion, lasts about 24 hrs
Toxic shock syndrome (TSS)
• Mediated by sugerantigen (TSST-1)
• Associated with tampon use or surgical packing
• Abrupt onset: fever, hypotension, diffuse erythematous rash, shock, desquamation of skin
• Multiple organs may be involved
• Fluid resuscitation is critical!
Scalded skin syndrome
• Mediated by toxin
• Abrupt onset of erythema and blisters over entire body, desquamation of top layer of epidermis
• Most common in neonates and young children
• Mortality rate is low
Bacteremia and endocarditis
• 50% of cases = following a surgical procedure or use of intravascular catheter
• With prolonged cases = dissemination to other body sites
• If go to heart → endocarditis
• Mortality rate approaches 50% (80% in MRSA endocarditis)
Pneumonia
• Associated with ventilator use
• Also from aspiration of oral secretions
• Seen in very young, elderly, CF patients COPD, post-influenza
Osteomyelitis
• From contiguous (adjoining) soft tissue infection or hematogenous dissemination to bone
• Staph aureus is main cause
Septic arthritis
• Staph aureus is primary cause

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6
Q

Major diseases caused by Staph epidermidis

A

leading nosocomial pathogen
Hospital acquired bacteremia
• #1 cause

Endocarditis
• Primarily involves prosthetic valves
• Indolent course of disease
• Need to replace heart valves

Catheter and shunt infection
• Access to blood stream → develop persistent bacteremia → endocarditis may result

Implanted medical device infection
• Prosthetic joints, breast implants, artificial lens
• Biofilms form
• Need to remove device

Surgical site infection

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7
Q

Virulence factors from Staph aureus

A
  • Techoic acid = binds fibronectin and aids in attaching to mucosal surface
  • Protein A = binds to Fc portion of IgG → inhibits Ab-mediated clearance by phagocytes
  • Capsule = anti-phagocytic

Toxins:
• Cytotoxins: α, β, Δ, γ, and Panton-Valentine (PV) leukocidin
o Damage cell membranes
o Mediate destruction of many cell types
o PV leukocidin seen in most community-acquired MRSA = forms pores = allows Staph aureus to penetrate tissues
• Exfoliative toxins
o Split intracellular bridges in stratum granulosum epidermis → desquamation = scalded skin syndrome
• Enterotoxins
o Heat stable
o Stimulate GI symptoms (vomiting)
o Produced by up to 50% of all Staph aureus
• Toxic shock syndrome toxin-1 (TSST-1)
o Nonspecific activation of 30-40% of T cells and cytokine release
o Superantigen = lots of cytokine release
o Produces leakage or destruction of endothelial cells

Enzymes
•	Coagulase
o	Converts fibrinogen to fibrin
o	Fibrin protects organism from phagocytosis
o	Best marker of acute virulence
•	Catalase
o	Catalyzes breakdown of toxic hydrogen peroxide (accumulates during bacterial metabolism)
•	Antibiotic resistance genes
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8
Q

Virulence factors from Staph epidermidis

A
  • Hydrophobic synthetic polymers = initial adherence to medical devices
  • Some strains produce viscous polysaccharide slime/biofilm
  • Provides additional adhesion
  • Acts as barrier to antimicrobials and host defense
  • Often resistant to beta-lactam antibiotics
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9
Q

Groups at risk for Staph aureus

A

o Menstruating women = toxic shock syndrome
o Neonates = scalded skin syndrome
o Patients with intravenous catheters or implanted medical devices = bacteremia and endocarditis
o Patients with immunocompromised pulmonary function or preceeding viral infection = pneumonia
o IV drug users = bacteremia and endocarditis
o Patients with neutrophil dysfunction or granulocytopenia = primarily skin and soft tissue infections
o Burn patients or patients with compromised skin integrity (including surgical wounds) = primarily soft tissue infections and bacteremia
o Healthy adults = cryptogenic bacteremia

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10
Q

Groups at risk for Staph epidermidis

A

o Patients with intravenous catheters

o Patients with prosthetic materials

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11
Q

Gram Stain reactions and lab tests for Staph aureus

A

Gram-positive cocci
o Clusters
o Catalase-positive
o Facultative

Culture
o	Coagulase-positive 
o	Facultative anaerobe but prefers O2
Sheep blood agar: 
•	Grows as 3-5 mm smooth white colonies
•	Non-mucoid (no capsule)
•	Commonly has golden color
•	Most colonies are hemolytic
Mannitol salt agar 
•	7.5% salt selects for staphylococci
•	Staph aureus ferments mannitol → turns media yellow
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12
Q

Gram Stain reactions and lab tests for Staph epidermis

A

Gram-positive cocci
o Clusters
o Catalase-positive
o Facultative

Culture:
o	Coagulase-negative 
Sheep blood agar: 
•	Small, grey to white colonies
•	Non-hemolytic 
Mannitol salt agar
•	Grows but does not ferment mannitol
•	Facultative anaerobe but prefers O2
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13
Q

Staph aureus prevention techniques

A
  • Hand hygiene
  • Chemoprophylaxis to prevent post-op surgical site infections (especially with cardiac and hip replacements)
  • Antiseptics applied to skin prior to surgical procedures
  • Proper cleaning of wounds
  • Women who have had TSS should not use tampons unless have detectable antibodies to TSST-1
  • Properly refrigerate foods
  • Food handlers with furuncles should not work
  • No anti-staphylococcal vaccine available
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14
Q

Staph epidermidis prevention techniques

A
  • Limit long-term catheter use
  • Prompt wound treatment
  • Chemoprophylaxis to prevent post-op surgical site infections (especially with cardiac and hip replacements)
  • Antiseptics applied to skin prior to surgical procedures
  • No vaccine yet
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15
Q

Treatment of Staph infections

A

o Penicillin-sensitive strains (rare) = penicillin
o Oral treatment of penicillin-resistant infections:
1) Methicillin (Nafcillin or Oxycillin) IV or Dicloxacillin
2) Other choices: cephalosporins, carbapenems, combination beta-lactam/beta-lactamase inhibitor durgs
3) Clindamycin if penicillin allergy
o For MRSA strains (Methicillin-resistant) = Vancomycin
• Other choices:
1) For MRSA pneumonia and soft tissue infections (but not bacteremias) = Linezolid
2) For severe infections (but not pneumonia) = Daptomycin
3) For soft tissue infections = clindamycin, trimethoprim-sulfamethoxazole, minocycline
o Vancomycin-resistant strains (VRS) = Linezolid or Daptomycin

Specific treatments:
o Abscesses = incision and drainage; may use antibiotics
o Bacteremia and endocarditis = prolonged IV therapy
o TSS = reapid resuscitation with massive amounts of IV fluids, source control, antibiotic therapy

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16
Q

Staph saprophyticus

A

o Coagulase negative staph
o Colonizes skin and urethral area
o May result in UTI

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17
Q

Group A Strep reservoirs

A

skin, upper respiratory tract, may be carried in nasal and pharyngeal mucosa

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18
Q

Streptococci transmission

A

o Person-to-person via direct contact with secretions or respiratory droplets via coughing or sneezing

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19
Q

Major diseases caused by Group A Strep (Strep pyogenies)

A

Pharyngitis
• Acute inflammation of pharynx and tonsils
• Result: fever, painful swallowing
• Incubation period of 2-4 days
• Group A strep = most common bacterial cause of pharyngitis in school age children
• Most sore throats NOT due to Strep but from viral infection or mycoplasma
• Clinical features alone only 50-75% accurate in Strep pharyngitis diagnosis
• Must culture throat or do rapid antigen test
• Complication: Scarlet Fever
• Occurs when infecting strain is lysogenized by bacteriophage → production of exotoxin
• Develop diffuse erythematous rash 1-2 days after pharyngitis symptoms
• Strawberry tongue common
Impetigo
• Skin colonization plus trauma (insect bites)
• Pus-filled vesicles rupture and crust over
• Also from Staph aureus alone or in combination with Strep pyogenes
Erysipelas
• Skin infection with spreading of erythema and edema with well-demarcated edges
• Usually in children and older adults
• Commonly seen in legs rather than face
Cellulitis
• Acute inflammation of skin and deeper subcutaneous CT
• Not clearly defined edges of infection
• Caused: Group A Strep, Staph aureus, others
Necrotizing fasciitis
• Infection deep in subcutaneous tissues
• Extensive tissue destruction
• Requires debridement of non-viable tissue
Streptococcal Toxic shock syndrome
• Begins with soft tissue inflammation at site of infection
• Pain fever, chills, non-specific symptoms
• Progresses to shock and multi-organ failure
• Patients are bacteremic; most have necrotizing fasciitis
• Need debridement or amputation
• Associated with streptococcal pyrogenic exotoxin (acts as superantigen)
• High mortality: 30-40%
• Other form = S. aureus
• Most are tampon-related
• Mortality low (<1%)

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20
Q

Diseases caused by Group B Strep

A

o Peuperal (during childbirth) and neonatal sepsis
o Neonatal bacteremia, pneumonia, or meningitis
o Adult infections (bacteremia, pneumonia, skin and soft tissue infections)

21
Q

Diseases caused by Group D Strep

A

o Urinary tract infection
o Surgical wound infection
o Endocarditis

22
Q

Diseases caused by Viridans α-hemolytic Strep

A

(normal flora of oral cavity, GI, and GU tract)
o Dental caries
o Bacteremia and endocarditis

23
Q

Diseases caused by Strep Pneumoniae

A

o Pneumonia
o Otitis media in children
o Sinusitis
o Meningitis

24
Q

Diseases caused by Anaerobic strep (Peptostreptococcus)

A

normal flora of mouth, vagina, intestines
o Peritonitis
o Intra-abdominal abscess
o Aspiration pneumonias

25
Q

Virulence factors in Strep

A

M (protein)
• Antiphagocytic
• Promotes binding to surface fibronectin
• Cross-reaction with cardiac or renal antigens
• Role in post-streptococcal rheumatic fever and glomerulonephritis

Lipoteichoic acid and protein F
• Mediate attachment to epithelial cells by binding fibronectin

Capsule
• Made of hyaluronic acid
• Anti-phagocytic activity

Streptococcal pyrogenic exotoxins (SPEs)
• Act as superantigens = interact with both macrophages and helper T cells
• Mediate production of rash in scarlet fever
• Responsible for multisystem effects in toxic shock syndrome

Hemolysins (Streptolysin O and S)
• Lyse leukocytes, platelets, and erythrocytes
• Responsible for beta-hemolysis on blood agar plates
• Streptolysin O = immunogenic
• Presence of antibodies to Streptolysin O is basis for Anti-Streptolysin O test (ASO)
• Documents Group A strep infections

Other enzymes
Contribute to tissue invasion and destruction 
Contribute to inflammation
Ex.
•	Streptokinase
•	DNAase
•	Hyaluronidase 
Erythrogenic toxin of Group A strains
•	Causes Scarlet fever
•	Produced by lysogenic phage
26
Q

Discuss which groups of individuals are at increased risk for developing infections caused by Strep organisms

A
School-age children
o	Pharyngitis
o	Acute rheumatic fever
Young children
o	Impetigo 
Surgical patients, burn patients
o	Other conditions with damage skin: measles, chickenpox
Postpartum women
o	Puerperal sepsis (no longer common)
College students, military recruits
27
Q

Explain the suppurative complications of streptococcal pharyngitis and that it is caused by direct extension of Group A strep.

A

Suppurative
o Peritonsillar abcess (1%)
o Pneumonia with empyema
o Bacteremia, distant metastatic infection (very rare)

28
Q

List the two major nonsuppurative complications (sequelae) of streptococcal infections

A

Acute rheumatic fever

Post-streptococcal glomerulonephritis (PSGN)

29
Q

Acute rheumatic fever

A

o Inflammatory changes involving heart and CT of joints and skin
o Mediated by B and T cells that cross-react with heart and other tissues
o Can be caused by Group A strep
• Certain M types are more rheumatogenic
o Associated with strep pharyngitis but not cutaneous strep infections
• Prevented if strep pharyngitis treated quickly
o Can recur with subsequent strep throat infections from different M types
• Result: damage to heart valves and Rheumatic heart disease

o Diagnose: Jones criteria
• 2 major or 1 major + 1 minor criteria
• Plus lab evidence of Group A strep infection
–Major criteria: carditis, polyarthritis, chorea, subcutaneous nodules, erythema
–Minor criteria: fever, arthralgia, increased PR interval on ECG, increased ESR, WBC or CRP, preceding beta-hemolytic strep infection, previous rheumatic fever or inactive RHD
o Can affect any age group
Treat with aspirin

30
Q

Post-streptococcal glomerulonephritis (PSGN)

A

o Acute inflammation of renal glomeruli → kidney failure
o Mediated by antigen-antibody complexes that deposit in glomerular BM
o Caused by specific nephritogenic M strains of Group A strep
• Can follow skin infections (impetigo) and pharyngitis
o More common in children than adults
o Can’t prevent with treatment
Treat: supportive only

31
Q

Streptococci antigens

A
Capsular
•	Polyhyaluronic acid for ALL strep 
•	Not immunogenic 
•	Antiphagocytic 
C (polysaccharide) = Lancefield grouping
•	A-H, K-T (18 groups)
•	Precipitin test
M (protein) = Lancefield typing
•	Type specific surface protein associated with S. pyogenes
•	Only for Group A
•	Approximately 70 types
•	Precipitin test
•	Antiphagocytic, promote adherence 
•	Immunity to Group A strains 
•	A major virulence factor!
Variety of extracellular enzymes
•	Many are antigenic and also virulence factors
•	Ex. Streptolysins 

Latex agglutination antigen deletion
o Rapid diagnosis of Group A Strep Pharyngitis

32
Q

Streptococci treatment

A

o S. Pyogenes = susceptible to penicillin (Drug of choice)
o Drainage and surgical debridement for soft tissue infection
o Antibiotic therapy for pharyngitis
• Increase symptom relief by 1-2 days
• Decrease transmission to others
• Prevents rheumatic fever and peritonsillar abscess if started within 10 days

33
Q

Streptococci prevention

A

o Long term antibiotic prophylaxis to prevent ARF recurrences in children and young adults with history of rheumatic fever
o Detection and early treatment of respiratory and skin infections
o No specific antibiotic treatment or prophylaxis for glomerulonephritis
o No vaccines yet

34
Q

Describe the reservoir of Strep pneumoniae

A

o Colonized nasopharynx or throat
o Depends on age and season
• 35% carriage rates in pharynx during winter
o Highest carrier rates = children in winter

35
Q

Transmission of Strep. pneumoniae

A

o Endogenous, airborne spread from nasopharynx to distal sites (lung, sinuses, blood, etc.)

Requires a susceptible host:
• Preceding viral infection or condition interfering with bacterial clearance
• Ex. COPD, alcoholism, splenectomy

36
Q

Major diseases of Strep pneumoniae

A

Otitis media
• Bulging, red non-motile tympanic membrane
• Most frequent childhood illness
• Responsible for 3-40% of cases

Mastoiditis
• Infection of mastoid bone usually after a middle ear infection
• Virtually eliminated now with antibiotics

Sinusitis
• Infection of paranasal sinuses when outflow from one of sinuses is decreased/blocked
• Accounts for 30% cases sinusitis (#1 cause)

Community-acquired pneumonia
• With or without bacteremia, empyema
• Classically in lobar lung consolidation pattern, but now rarely
• Number 1 cause of death due to infection
• Abrupt start with chills and high fever; cough with production of pink to rusty colored sputum (RBCs present) is common

Bacteremia
• Travels to bloodstream
• Can invade other tissues, including CNS

Acute meningitis
•	10-30% mortality 
•	Treatment:
•	With widespread high-level penicillin resistance: vancomycin 15 mg/kg Q 12 hrs + ceftriaxone 2 gm Q 12 hrs
•	Dexamethasone 10 mg Q 6 hr IV x 4 days
•	Vaccine for susceptible
37
Q

Virulence factors of Strep pneumoniae

A

Capsular polysaccharide
Causes inflammatory response in lung
• With bacteremia and meningitis = in blood and meninges = SIRS (systemic inflammatory response syndrome)
• Neutrophilic infliltration and edeam in lung → consolidation → respiratory failure
• In meningitis → brain edema
If extreme → septic shock
90 serotypes are known
• Detect by Quellung test or precipitation
• Serotype 3 causes most of the serious invasive disease
Capsule interferes with complement deposition (C3b) → evades phagocytosis
Unencapsulated strains are not virulent
Basis for vaccine
• Protective opsonizing antibodies form to specific capsular antigen

o Other factors
• Aid in adhesion, colonization, tissue destruction
• Help elicit host immune response

38
Q

Discuss which groups of individuals are at risk for developing pneumococcal infections and significant risk factors.

A

o Elderly (>60 years)
o Infants (<2 years)
o Sickle Cell disease, other hemoglobinopathy
• High risck pneumococcal meningitis
o Post-splenectomy (greatest risk in first 2 years)
o Post-influenza and other viral respiratory infections (due to loss of respiratory cilia)
o Hypogammaglobulinemia
• Myeloma, lymphoma, leukemia, nephrotic syndrome
• Antibody is needed for opsonization
o Alcoholism (due to frequent aspiration)
o Diabetes mellitus
o COPD or heart disease
o CSF leaks following trauma
• Risk of secondary meningitis
o Persons with cochlear implants
o Crowded living conditions (dorms, prisons, childcare centers)

39
Q

Explain the Gram stain reaction and laboratory tests used to identify S. pneumoniae

A

Morphology:
o Gram-positive, lancet-shaped diplococci commonly surrounded by unstained capsule

Laboratory Tests
Inoculated onto sheep blood agar = α-hemolytic 1-3 mm opaque colonies
• Often umbilicated
• Mucoid (due to capsule)
• Grow better with 10% CO2
• Optochin test:
• To identify α-hemolytic isolate as pneumococcus = must exclude Strep viridans (also α-hemolytic streptococcus with same morphology)
• Place disk with optochin on streaked area
• If inhibited growth after 24 hours = susceptible organism → identified as S. pneumoniae
• Pneumococcus also: soluble in bile, has mouse virulence and quelling
Antigen detection in serum or CSF

40
Q

Prevention of Strep pneumoniae

A

Don’t smoke
Moderate alcohol consumption
Pneumococcal vaccine
• 23-valent polysaccharide vaccine
• For elderly and immunocompromised
• One of the standard vaccines of childhood (all infants in 1st year)
• 50% efficacy against bacteremia or meningitis caused by homologous vaccine strains
Educate asplenics of risk
• Medi-alert bracelets, letters to carry, antimicrobial prophylaxis (children 4 bouts/year)

41
Q

Treatment of Strep pneumoniae

A

o Problem with penicillin-resistant strains over past 5 years
• Penicillin ineffective for meningitis, otitis media, sinusitis
• Risk factors for infection with penicllin-resistant pneumococci
• Age 70 years
• Children and staff in day care centers
• Recurrent or chronic otitis media
• Prolonged or recent hospitalizations
• Prior β-lactam therapy, especially with amoxicillin or oral cephalosporins
• Crowding (ex. Jails)
• Major underlying disease, especially C.F., cirrhosis, cancer, AIDS

o Otitis media: amoxicillin 80 mg/kg/d or erythromycin
o Sinusitis: amoxicillin –clavulinate or FQ (fluoroquinolones)
o Community-Acquired Pneumonia: ceftriaxone + macrolide or FQ
o Meningitis: ceftriazone + vancomycin

42
Q

Describe the reservoirs of the enterococci

A

o Found in soil, food, water

o Normal flora of animals, birds, humans

43
Q

Enterococci transmission

A

o By endogenous strains gaining access to sterile sites
o Hardy organism (can survive on surfaces)
o Person to person transmission
• Directly on hands
• By contaminated medial equipment
o Nosocomial spread with multi-drug resistant strains = major problem

44
Q

Major enterococci diseases

A

Community- acquired infection:
• Endocarditis
• Urinary tract infection

Hospital-acquired infections
• UTI
• Bacteremia
• Surgical wound/intra-abdominal abscesses (usually polymicrobial)

45
Q

Enterococci virulence factors

A

o No significant factors
o But = combination of adhesions, bacteriocins that inhibit competing flora, resistance to common antibiotics (ampicillin, vancomycin)

46
Q

Discuss the risk factors associated with enterococcal infections

A
  • Exposure to invasive devices (especially urinary or intravascular catheters)
  • Prolonged or prior hospitalization
  • Use of broad spectrum antibiotics
  • Surgery (especially GI or cardiothoracic)
  • Age >60 years
  • Major underlying disease
47
Q

Explain the Gram stain reaction and lab tests used to identify the enterococci.

A

Gram Stain:
o Catalase-negative, aerobic Gram-positive cocci
o Most common species: E. faecalis and E. faecium

Culture:
o Grow on blood agar as small cream-white colonies
o Can grow in bile (bile-esculin test), 6% NaCl
o Can be α, β (rare), or non-hemolytic
• Most are non-hemolytic

48
Q

Enterococci treatment

A

o Based on site of infection and susceptibility data
o Ampicillin or amoxicillin if susceptible
o Endocarditis = combo of penicillin plus gentamicin
• Adding an aminoglycoside to a beta-lactam produces cidal activity (needed to treat endocarditis)
o Vancomycin if susceptible
• If vancomycin resistant → use linezolid, daptomycin, or quinapristin-dalfopristin

49
Q

Enterococci prevention

A
  • Reduce antibiotic pressure
  • Restrict broad spectrum antimicrobials
  • Limit long-term use of intravascular devices
  • Implement appropriate infection control practices to prevent nosocomial spread