Staphylococcus

Question 1

Diseases of Staphylococcus Aureus

Answer 1

• pyogenic infections (e.g., endocarditis, septic arthritis,
  and osteomyelitis)
• food poisoning
• scalded skin syndrome
• toxic shock syndrome
• hospital-acquired pneumonia, septicemia, surgical-wound infections. - skin and soft tissue infections (folliculitis, cellulitis, impetigo)
• bacterial conjunctivitis

Question 2

Diseases of Methicillin-resistant Staphylococcus aureus (MRSA)

Answer 2

• pneumonia
• necrotizing fasciitis
• sepsis in immunocompetent patients.

Question 3

Diseases of Staphylococcus epidermidis

Answer 3

• prosthetic valve
  endocarditis
• prosthetic joint infections. - central nervous system shunt infections
• sepsis in newborns.

Question 4

Diseases of Staphylococcus
saprophyticus

Answer 4

urinary tract infections, especially
cystitis.

Question 5

Important Properties- Coagulase production

Answer 5

• Staphylococcus
  aureus coagulase positive.
• Staphylococcus
  epidermidis and S. saprophyticus are
  coagulase-negative.

Coagulase enzyme causes plasma to clot by activating prothrombin
to form thrombin which catalyzes activation
of fibrinogen to form the fibrin clot.

Question 6

Important Properties- staphyloxanthin

Answer 6

• Staphylococcus aureus produces carotenoid pigment staphyloxanthin.
• imparts a golden color to its colonies enhancing the pathogenicity of the
  organism by inactivating the microbicidal effect of superoxides and other reactive oxygen species within neutrophils.
• Staphylococcus epidermidis does not synthesize this
  pigment and produces white colonies.

Question 7

Important Properties- hemolysis of rbcs

Answer 7

• S. aureus do -> source of iron required for growth of the organism.
• S. epidermidis & S. saprophyticus do not.
• Iron in hemoglobin is recovered by the bacteria
  and utilized in the synthesis of cytochrome enzymes used
  to produce energy

Question 8

methicillin resistant
S. aureus (MRSA) or nafcillin-resistant S. aureus
(NRSA).

Answer 8

• strains contain plasmids
  that encode B-lactamase (enzyme degrades penicillins) but some strains of S. aureus are resistant to the β-lactamase–resistant penicillins, (methicillin
  & nafcillin) -> changes in
  penicillin-binding proteins (PBP) in cell membrane.
• mecA genes on the bacterial chromosome encode these altered PBPs.
• causes health care-acquired (HCAMRSA) [few produce P-V leukocidin]
  & community-acquired (CA-MRSA) [all produce P-V leukocidin] infections.

Question 9

S. aureus resistance to vancomycin

Answer 9

• Strains of S. aureus with intermediate (VISA) & full resistance to vancomycin (VRSA).
• Same cassette of genes
  encodes vancomycin resistance in S. aureus & enterococci.
• located in a transposon on a plasmid & encodes the enzymes that substitute d-lactate for
  d-alanine in the peptidoglycan.

Question 10

S. aureus 5 cell wall components
and antigens

Answer 10

(1) Protein A
(2) Teichoic acids & Lipoteichoic acids
(3) Polysaccharide capsule
(4) Surface receptors
(5) Peptidoglycan

Question 11

Protein A

Answer 11

• major protein in the cell wall.
• virulence factor -> binds to Fc portion of IgG at complement-binding site,
  preventing activation of complement -> no C3b is produced-> opsonization &
  phagocytosis of organisms reduced.
• used in clinical tests as binds to IgG and forms a “coagglutinate” with antigen– antibody complexes.
• coagulase-negative staphylococci do not produce protein A.

Question 12

(2) Teichoic acids & Lipoteichoic acids

Answer 12

• polymers of ribitol phosphate.
• mediate adherence of the staphylococci to mucosal
  cells.
• induction of
  septic shock inducing cytokines such as interleukin-1
  (IL-1) and tumor necrosis factor (TNF) from macrophages

Question 13

(3) Polysaccharide capsule

Answer 13

• virulence factor.
• 11 serotypes based on the antigenicity of the capsular polysaccharide, but types 5 and 8 cause
  85% of infections.
• Some strains of S. aureus are coated with microcapsule (small amount of polysaccharide capsule)
• poorly immunogenic makes producing effective vaccine difficult.

Question 14

(4) Surface receptors

Answer 14

• for specific staphylococcal bacteriophages
  permit the “phage typing” of strains for epidemiologic
  purposes.
• Teichoic acids are receptors.

Question 15

(5) Peptidoglycan

Answer 15

• endotoxin-like
  properties (stimulate macrophages to produce
  cytokines & activate complement & coagulation
  cascades).
• ability of S. aureus to cause septic shock not possess endotoxin.

Question 16

Transmission of S.aureus

Answer 16

• nose -> main site of colonization
• chronic carriers have increased risk of skin infections caused by S. aureus in hospital personnel and patients (Diabetes & intravenous drug use).
• Hand contact -> mode of transmission
• handwashing decreases transmission.
• found in the vagina->
  toxic shock syndrome.
• shedding from human lesions and fomites
  such as towels and clothing contaminated by these lesions
• heavily contaminated
  environment (e.g., family members with boils)
  and a compromised immune system.
• Reduced humoral
  immunity, low levels of antibody, complement, or
  neutrophils, predisposes to staphylococcal infections.
• Patients with chronic granulomatous
  disease (CGD) [defect in ability of neutrophils to kill bacteria] prone infections.

Question 17

Transmission of S.epidermidis

Answer 17

• on human skin
• enter bloodstream at site of intravenous catheters that penetrate through the skin

Question 18

Transmission of S.saprophyticus

Answer 18

• on mucosa of the genital tract in young women site
• ascend into the urinary bladder cause urinary
  tract infections

Question 19

S.aureus pathogenesis

Answer 19

• causes disease by producing toxins & inducing pyogenic inflammation.
• typical lesion -> abscess
• undergo central necrosis & drain to outside
  (e.g., furuncles and boils), but organisms may disseminate via bloodstream.

Question 20

Exotoxin-Enterotoxin

Answer 20

• food poisoning with vomiting (cytokines
  from lymphoid cells stimulate enteric nervous
  system activates vomiting center in brain) & diarrhea.
• Superantigen within gastrointestinal tract
  stimulating release of large amounts of IL-1 and IL-2 from macrophages and helper T cells, respectively.
• heat-resistant ->not inactivated by brief cooking.
• resistant to stomach
  acid & enzymes in stomach and jejunum.
• six immunologic types of enterotoxin, types A–F.

Question 21

Exotoxin- Toxic shock syndrome toxin (TSST)

Answer 21

• causes toxic
  shock (tampon-using menstruating women or
  in individuals with wound infections)
• patients with nasal packing used to stop bleeding from the nose.
• produced locally in
  vagina, nose, or infected site.
• enters bloodstream, causing toxemia.
• Blood cultures do
  not grow S. aureus.
• superantigen causes toxic shock stimulating release of large amounts of IL-1, IL 2, and TNF.
• Toxic Shock occurs in people who do not have antibody against
  TSST.

Question 22

Exotoxin- Exfoliatin

Answer 22

• causes “scalded skin” syndrome in young
  children.
• epidermolytic protease
  cleaves desmoglein in desmosomes -> separation
  of epidermis at granular cell layer.

Question 23

Exotoxin- Alpha toxin
[can kill leukocytes (leukocidins)
and cause necrosis of tissues in vivo.]

Answer 23

• marked necrosis of the skin & hemolysis.
• cytotoxic effect of alpha toxin -> formation
  of holes in cell membrane & consequent loss of
  low-molecular-weight substances from the damaged cell

Question 24

Exotoxin- P-V leukocidin
[can kill leukocytes (leukocidins)
and cause necrosis of tissues in vivo.]

Answer 24

• pore-forming toxin that kills wbcs by damaging cell membranes.
• 2 subunits of toxin assemble in cell membrane form pore through which cell contents leak out.
• encoding gene located on a lysogenic phage.
• virulence factor for
  CA-MRSA & plays a role in severe skin and soft tissue
  infection caused by organism.
• severe necrotizing
  pneumonia caused by strains of S. aureus that produce P-V leukocidin.

Question 25

Enzymes produced by S.aureus

Answer 25

coagulase, fibrinolysin, hyaluronidase,
proteases, nucleases, and lipases.

• Coagulase, by
  clotting plasma, serves to wall off the infected site, retarding migration of neutrophils into site.
• Staphylokinase
  is a fibrinolysin that can lyse thrombi

Question 26

Pathogenesis of Staphylococcus epidermidis & Staphylococcus
saprophyticus

Answer 26

• coagulase-negative staphylococci -> does not produce exotoxins -> does not cause food poisoning or toxic shock syndrome.
  cause pyogenic infections.
• pyogenic infections on
  prosthetic implants such as heart valves and hip joints
• urinary tract infections, especially cystitis

Question 27

Staphylococcus aureus: Pyogenic Diseases

Skin and soft tissue infections

Answer 27

• abscess, impetigo, furuncles, carbuncles, paronychia, cellulitis, folliculitis, hidradenitis suppurativa,
  conjunctivitis, eyelid infections (blepharitis and
  hordeolum), and postpartum breast infections (mastitis), Lymphangitis (forearm)
• Severe necrotizing infections -> MRSA strains produce P-V leukocidin.
• community-acquired-> homeless and intravenous drug users.
• Athletes (wrestlers and football players)

Question 28

Staphylococcus aureus: Pyogenic Diseases

Septicemia (sepsis)

Answer 28

• originate from any localized lesion, wound infection, or intravenous
  drug abuse.
• similar to sepsis caused by gram-negative bacteria (Neisseria meningitidis).

Question 29

Staphylococcus aureus: Pyogenic Diseases

Endocarditis

Answer 29

• occur on normal or prosthetic heart valves
  [right-sided endocarditis (tricuspid valve)] in intravenous drug users.

(Prosthetic valve endocarditis is often caused by S. epidermidis.)

Question 30

Staphylococcus aureus: Pyogenic Diseases

Osteomyelitis and septic arthritis

Answer 30

• arise by hematogenous spread from distant infected focus
• introduced locally at a wound site
• children

Question 31

Staphylococcus aureus: Pyogenic Diseases

postsurgical wound infections

Answer 31

• cause of morbidity and mortality in hospitals.
• S. aureus and S. epidermidis infections at cardiac pacemakers sites

Question 32

Staphylococcus aureus: Pyogenic Diseases

Pneumonia

Answer 32

• postoperative patients or
  following viral respiratory infection (influenza).
• Staphylococcal pneumonia leads to empyema or lung
  abscess -> cause of
  nosocomial pneumonia in general & ventilator associated pneumonia in ICU.
• CA-MRSA causes severe necrotizing pneumonia.

Question 33

Staphylococcus aureus: Pyogenic Diseases

Conjunctivitis

Answer 33

• unilateral burning eye pain, hyperemia of the conjunctiva, and a
  purulent discharge.
• transmitted by contaminated fingers.
• Staphylococcus aureus, S. pneumoniae & Haemophilus influenzae common in children.
• Gonococcal and nongonococcal (Chlamydia trachomatis) conjunctivitis acquired by infants during passage through birth canal.

Question 34

Staphylococcus aureus: Pyogenic Diseases

Abscesses

Answer 34

• occur in any organ when S. aureus circulates in bloodstream
• “metastatic abscesses” -> occur by spread of bacteria from original infection site (skin)

Question 35

Staphylococcus aureus: Toxin-Mediated Diseases

Food poisoning

Answer 35

• ingestion of enterotoxin preformed in foods
• short incubation period (1–8 hours).
• vomiting prominent than diarrhea.

Question 36

Staphylococcus aureus: Toxin-Mediated Diseases

Toxic shock syndrome

Answer 36

• fever; hypotension; a diffuse, macular, sunburn-like rash that goes on to desquamate; liver, kidney, gastrointestinal tract,
  central nervous system, muscle, or blood.

Question 37

Staphylococcus aureus: Toxin-Mediated Diseases

Scalded-skin syndrome

Answer 37

• fever, large bullae, & erythematous macular rash.
• Large areas of skin slough, serous fluid exudes, & electrolyte
  imbalance can occur.
• Hair and nails can be lost. - Recovery 7–10 days.
• Young children

Question 38

Staphylococcus aureus: Kawasaki Disease

Answer 38

• resemble TSS caused by superantigens of
  S. aureus (and S. pyogenes).
• vasculitis involving
  small and medium-size coronary arteries.
• high fever of at least
  5 days’ duration; bilateral nonpurulent conjunctivitis;
  lesions of the lips and oral mucosa (e.g., strawberry tongue, edema of the lips, and erythema of the oropharynx); cervical
  lymphadenopathy; a diffuse erythematous, maculopapular rash; and erythema and edema of the hands and feet that often ends with desquamation.
• myocarditis, arrhythmias, and regurgitation involving mitral or aortic valves.
• cause of morbidity and mortality -> aneurysm of coronary arteries.
• children of Asian ancestry, leading to speculation that certain major histocompatibility
  complex (MHC) alleles may predispose to the
  disease.
• no definitive diagnostic laboratory test
• Effective therapy consists of high-dose immune globulins (IVIG) plus high-dose aspirin, which promptly reduce fever & aneurysms.

Question 39

Staphylococcus epidermidis clinical findings

Answer 39

• coagulase-negative staphylococcus
• hospital acquired
• normal human
  flora on the skin & mucous membranes enter bloodstream (bacteremia) & cause metastatic infections at site of implants.
• infects intravenous
  catheters & prosthetic implants
• sepsis in neonates
  & of peritonitis in patients with renal failure who
  are undergoing peritoneal dialysis through an indwelling catheter.
• cerebrospinal
  fluid shunt infections.
• Strains produce glycocalyx adhere to prosthetic implant materials infect these implants than
  strains that don’t produce glycocalyx.
• Hospital personnel
  -> major reservoir for antibiotic-resistant strains

Question 40

Staphylococcus saprophyticus clinical findings

Answer 40

• coagulase-negative staphylococcus
• community-acquired
• urinary tract infections,
  (sexually active young women within the previous 24 hours).
• second to Escherichia coli as a cause of community-acquired urinary tract infections in young women.

Question 41

Staphylococcus lugdenensis clinical findings

Answer 41

• uncommon coagulase-negative staphylococcus
• causes prosthetic valve endocarditis and skin infections.

Question 42

Laboratory Diagnosis

Answer 42

• Smears -> gram-positive
  cocci in grapelike clusters
• S. aureus -> golden-yellow colonies-> β-hemolytic.
• S. aureus ferments mannitol -> lowers pH ->
  agar turns yellow
• S. epidermidis does not ferment mannitol & agar remains pink.
• coagulase-negative staphylococci -> nonhemolytic white colonies.
• distinguished by reaction
  to antibiotic novobiocin: S. epidermidis is sensitive; S. saprophyticus is resistant.
• No serologic or skin tests used for diagnosis of acute staphylococcal infection.
• TSS -> isolation of S. aureus not
  required but include isolation of TSST producing
  strain of S. aureus & development of antibodies
  to toxin during convalescence
• S. aureus subdivided based on susceptibility of clinical isolate to lysis by variety of bacteriophages.
• person carrying S. aureus of the same phage group as that which caused the outbreak may be the source of the
  infections.

Question 43

Treatment for S. aureus

Answer 43

• S. aureus strains are
  resistant to penicillin G -> produce B-lactamase.
• treated with β-lactamase–resistant penicillins (nafcillin or cloxacillin), cephalosporins, or vancomycin.
• combination of a β-lactamase–sensitive penicillin (amoxicillin) & β-lactamase inhibitor (clavulanic acid).
• vancomycin + gentamicin - Daptomycin
  -Trimethoprimsulfametho
  xazole or clindamycin ->
  non–life-threatening infections
• MRSA resistant to all β-lactam drugs-> penicillins & cephalosporins.
• Ceftarolinefosamil -> treatment of MRSA infections.
• Daptomycin (Cubicin) or Quinupristin-dalfopristin (Synercid) treat VISA & VRSA strains
• TSS ->correction
  of shock using fluids, pressor drugs, & inotropic
  drugs
• administration of β-lactamase–resistant
  penicillin (nafcillin) & removal of tampon or
  debridement of infected site.
• Pooled serum globulins contain antibodies against TSST
• Mupirocin topical antibiotic for skin
  infections & reduce nasal carriage of organism in hospital personnel
  & patients with recurrent infections.
• topical skin antiseptic (chlorhexidine) added
  to mupirocin.
• Tolerance result from failure of drugs inactivating inhibitors of autolytic enzymes degrading organism.
• treated with drug combinations
• Drainage -> abscess treatment.
• Previous infection
  provides only partial immunity to reinfection.

Question 44

Treatment for S. epidermidis

Answer 44

• highly antibiotic resistant.
• produce β-lactamase but sensitive to β-lactamase–resistant drugs (nafcillin) -> methicillin-sensitive strains (MSSE).
• vancomycin + rifampin or an aminoglycoside can
  be added.
• Removal of catheter or other device necessary.

Question 45

Treatment for S. saprophyticus

Answer 45

• urinary tract infections treated with trimethoprim-sulfamethoxazole
  or a quinolone (ciprofloxacin)

Question 46

Prevention

Answer 46

• no vaccine
• Cleanliness, frequent
  handwashing, and aseptic management of lesions control spread of S.aureus.
• Persistent colonization
  of nose reduced by intranasal mupirocin
  or oral antibiotics (ciprofloxacin or
  trimethoprim- sulfamethoxazole); difficult to eliminate completely.
• Shedders removed from
  high-risk areas (operating rooms & newborn nurseries).
• Cefazolin -> prevent surgical-wound infections.