Staphylococcus Flashcards
Gram-positive cocci
1
Q
Diseases of Staphylococcus Aureus
A
- 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
2
Q
Diseases of Methicillin-resistant Staphylococcus aureus (MRSA)
A
- pneumonia
- necrotizing fasciitis
- sepsis in immunocompetent patients.
3
Q
Diseases of Staphylococcus epidermidis
A
- prosthetic valve
endocarditis - prosthetic joint infections. - central nervous system shunt infections
- sepsis in newborns.
4
Q
Diseases of Staphylococcus
saprophyticus
A
urinary tract infections, especially
cystitis.
5
Q
Important Properties- Coagulase production
A
- 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.
6
Q
Important Properties- staphyloxanthin
A
- 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.
7
Q
Important Properties- hemolysis of rbcs
A
- 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
8
Q
methicillin resistant
S. aureus (MRSA) or nafcillin-resistant S. aureus
(NRSA).
A
- 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.
9
Q
S. aureus resistance to vancomycin
A
- 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.
10
Q
S. aureus 5 cell wall components
and antigens
A
(1) Protein A
(2) Teichoic acids & Lipoteichoic acids
(3) Polysaccharide capsule
(4) Surface receptors
(5) Peptidoglycan
11
Q
Protein A
A
- 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.
12
Q
(2) Teichoic acids & Lipoteichoic acids
A
- 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
13
Q
(3) Polysaccharide capsule
A
- 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.
14
Q
(4) Surface receptors
A
- for specific staphylococcal bacteriophages
permit the “phage typing” of strains for epidemiologic
purposes. - Teichoic acids are receptors.
15
Q
(5) Peptidoglycan
A
- endotoxin-like
properties (stimulate macrophages to produce
cytokines & activate complement & coagulation
cascades). - ability of S. aureus to cause septic shock not possess endotoxin.
16
Q
Transmission of S.aureus
A
- 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.
17
Q
Transmission of S.epidermidis
A
- on human skin
- enter bloodstream at site of intravenous catheters that penetrate through the skin
18
Q
Transmission of S.saprophyticus
A
- on mucosa of the genital tract in young women site
- ascend into the urinary bladder cause urinary
tract infections
19
Q
S.aureus pathogenesis
A
- 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.
20
Q
Exotoxin-Enterotoxin
A
- 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.
21
Q
Exotoxin- Toxic shock syndrome toxin (TSST)
A
- 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.
22
Q
Exotoxin- Exfoliatin
A
- causes “scalded skin” syndrome in young
children. - epidermolytic protease
cleaves desmoglein in desmosomes -> separation
of epidermis at granular cell layer.
23
Q
Exotoxin- Alpha toxin
[can kill leukocytes (leukocidins)
and cause necrosis of tissues in vivo.]
A
- 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
24
Q
Exotoxin- P-V leukocidin
[can kill leukocytes (leukocidins)
and cause necrosis of tissues in vivo.]
A
- 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.
25
Enzymes produced by S.aureus
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
26
Pathogenesis of Staphylococcus epidermidis & Staphylococcus
saprophyticus
- 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
27
Staphylococcus aureus: Pyogenic Diseases
Skin and soft tissue infections
- 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)
28
Staphylococcus aureus: Pyogenic Diseases
Septicemia (sepsis)
- originate from any localized lesion, wound infection, or intravenous
drug abuse.
- similar to sepsis caused by gram-negative bacteria (Neisseria meningitidis).
29
Staphylococcus aureus: Pyogenic Diseases
Endocarditis
- 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.)
30
Staphylococcus aureus: Pyogenic Diseases
Osteomyelitis and septic arthritis
- arise by hematogenous spread from distant infected focus
- introduced locally at a wound site
- children
31
Staphylococcus aureus: Pyogenic Diseases
postsurgical wound infections
- cause of morbidity and mortality in hospitals.
- S. aureus and S. epidermidis infections at cardiac pacemakers sites
32
Staphylococcus aureus: Pyogenic Diseases
Pneumonia
- 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.
33
Staphylococcus aureus: Pyogenic Diseases
Conjunctivitis
- 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.
34
Staphylococcus aureus: Pyogenic Diseases
Abscesses
- occur in any organ when S. aureus circulates in bloodstream
- “metastatic abscesses” -> occur by spread of bacteria from original infection site (skin)
35
Staphylococcus aureus: Toxin-Mediated Diseases
Food poisoning
- ingestion of enterotoxin preformed in foods
- short incubation period (1–8 hours).
- vomiting prominent than diarrhea.
36
Staphylococcus aureus: Toxin-Mediated Diseases
Toxic shock syndrome
- fever; hypotension; a diffuse, macular, sunburn-like rash that goes on to desquamate; liver, kidney, gastrointestinal tract,
central nervous system, muscle, or blood.
37
Staphylococcus aureus: Toxin-Mediated Diseases
Scalded-skin syndrome
- 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
38
Staphylococcus aureus: Kawasaki Disease
- 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.
39
Staphylococcus epidermidis clinical findings
- 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
40
Staphylococcus saprophyticus clinical findings
- 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.
41
Staphylococcus lugdenensis clinical findings
- uncommon coagulase-negative staphylococcus
- causes prosthetic valve endocarditis and skin infections.
42
Laboratory Diagnosis
- 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.
43
Treatment for S. aureus
- 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.
44
Treatment for S. epidermidis
- 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.
45
Treatment for S. saprophyticus
- urinary tract infections treated with trimethoprim-sulfamethoxazole
or a quinolone (ciprofloxacin)
46
Prevention
- 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.
