Staphylococci Lecture 11 Flashcards
Enterococcus
Normal flora of the large bowel and feces;
antibiotic resistance is common;
fourth leading cause of nosocomial infections
E. Faecium, and E faecalis
Physiology and structure of Enterococcus
Gram positive cocci in pairs or short chain
grow both aerobic and anerobic in a broad in a broad range of temps (10-45 C)
catalase negative
bacitricin resistant
variable hemolysis
can grow in presence of 6.5 NaCl
can tolerate 40% bile salt
can hydrolyze esculin
source and transmission of enterococcus
enteric bacteria
found in large intestine and genitourinary tract
human infection orginate from patients bowel flora
virulence factors: entercoccus
aggregation substance
carbohydrate adhesins
cytolysin: inhibits gram positive bacter and induce local tissue damage
gelatinase
antibiotic resistant: resistant to aminoglycoside, beta lactams, and vancomycin
lab diagnosis of entercocus
biochemical test: resistant to optochin
do not dissolve when exposed to bile
TX of entercoccus
ampicillin can be used for senstive strains
combination of an aminoglycoside and vancomycin for resistant strains: Vanc resistant enterococci (VRE) have a substititue for the D ala D ala in peptidoglycan that is the target for vancomycin
Viridans streptococci
a major part of tnormal flora of the mouth and teeth
identification: Alpha hemolytic, resistance to optochin and no lancefield antigens
Groups C and G streptococci: non rheumatogenic but otherwise specture of infections like group A
viridans streptococci: sub actue endocarditis (#1 causative agents), central role in dental carries
TX of streptococcal endocarditis: penicillin and antibiotic prophylaxis
Summary of strep infections
GAS: Gram +, catalase -, doesn’t like oxygen, capsule, M proteins, C5a peptidase; GBS: capsule
suppartive: pharyngitis, scarlet fever, impetigo, cellulitis, erysipelas
non supparative: PSGN, acute rheumatic fever
GBS: neonatal meningitis and sepsis, CAMP testing
strep pneumo: polysaccharide, bile, IgA protease, vaccine, pneumonia, meningitis, sinusitis, otitis media
entercoccous, resistance to antibiotics, normal flora, VRA, hospital acquired UTI
Staphylcocci
gram positive cocci in bunches
Abscesses, systemic diseases, food poisoning, and toxic shock syndrome
General characteristics of Staphylcocci
gram +: most resistant of the non spore formers to adverse conditions
non motile
facultatively anaerobic
catalase +; coagulase +/-
can grow: medium containing 10% NaCl
genus: 40 species; 16 are found on humans
S. aureus (coagulase +)
CNS: S. Epidermidis, and S. Saprophyticus
Properties of S. Aureus
frequency of disease: common
Coagulase +
color of colonies: Bronze
Mannitol fermentation: +
Novobiocin resistance: -
Properties of S. Epidermidis
frequency of disease: common
Coagulase -
Color of colony: White
Mannitol fermentation: -
Novobiocin resistance -
Properties of S Saprophyticus
Frequency: Occasional
Coagulase -
color of colonies: White
Mannitol fermentation -
novobiocin resistance +
Physiology and structure of Staphylococci
capsule: more common in vivo. Helps in adherence, inhibiting chemotaxis, phagocytosis. More important in coagulase negative strains
protein A: S aureus only
Techoic acid: glycerol TA (SE), Ribitol TA (SA)
Coagulase (clumping factor): S. Aureus
Enzyme: lipase, hyaluronidase
staphylococcus aureus
gram positive cluster forming coccus
non motile, non spore forming facultative anaerobe
fermentation of glucose produces mainly lactic acid
ferments mannitol (distinguishes from S. Epidermidis)
catalse positive; coagulase positive
golden yellow colny on agar
normal flora of humans found on nasal passages, skin and mucous membranes
pathogen of humans, causes a wide range of suppurative infection as well as food poisoning and toxic shock syndrome
MRSA- Methicillin resistant SA
the gene encodes the protein PBP2A (penicillin binding protein 2A). PBP2A has a low affinity for beta lactam antibiotics such as methicillin and penicillin. This enables transpeptidase activity in the presence of beta lactams, preventing them from inhibiting cell wall synthesis
the mecA gene responsible for methicillin resistance is located on a mobile genetic element called staphylococcal cassette chromosome
MRSA is almost ubiquitous, which is a serious clinical and economical problem
multiple drug resistant SA, resistant to tet, macroides, lincosamides, fluoroquinolones, and aminoglycosides
SA resistant to vancomycin
genetic transfer of a high level vancomycin resistant isolate of S A has been identified
mecA gene analysis
Agarose gel electrophoresis
mecA gene is detected my polymerase chain reaction
Source and transmission of MRSA or SA
source: part of normal flora. There are three major reservoris of hospital associated MRSA: patients, healthcare workers, and the inanimate environment.
HIV+ IV drug user, carrying SA in nose. Colonization lasting for a year
transmission: person to person direct contact or through contact with fomites
food poisoning: ingestion of food or diary product (eg procesed meat, custard, potato salad, ice cream)
pneumonia: aspiration of oral secretions
bacterimia: hematogenous spread from localized infection
Protein A SA
present on the surface of most S A
it is covalently linked with the peptidoglycan layer
unique affinity to bind Fc portion of IgG
Protects: opsonization and phagocytosis
CLumping factor (coagulase) SA
the outer surface of S aureus contains bound coagulase
it converts fibrinogen to fibrin
protect bacteria under fibrin mash
staphylococcal toxins
cytolytic toxins: alpha, beta, gamma, delta, panto-valentine leukocidin
exofolative toxin: two exofoliative toxins (A+B)
enterotoxins: eight enterotoxins toxins (A to E, G to I)
toxic shock syndrome toxin - 1 (TSST-1)
exofoliative toxin A, the enterotoxins, and TSST-a are superantigens
panton valentine leukocidin SA
active against PMNs and macrophages causing cell lysis
makes SA more resistant to phagocytosis
necrotizing pneumonia, mortality rate reaching 60%
airway bleeding, erythroderma and leucopenia, often caused by MRSA
SA infections
skins: impetigo, folliculitis, furuncles (boils), carbuncles
wound infections (traumatic, surgical)
scaled skin syndorome in young children (ritter’s disease)
bullous impetigo: localized form of SSSS
food poisoning
toxic shock syndrome: mostly in women during use of tampons
Cutaneous infections: SA
impetigo: superficial skin infections
folliculitis: pyogenic infection in the hair follicles
furuncles (boils): extension of folliculitis (E.G. Stye)
carbuncles: infection extends to the deeper subcutaneous tissue (chills and fever due to systemic spread)
Staphylococcal scalded skin syndrome (ritter’s disease)
perioral erythema covers entire body within 2 days
+ nikolsky sign large blisters with clear fluid
exofoliative toxin destroys the intracellular connections in the skin
Bullous impetigo
localized staphylococcal scalded skin syndrome
culture positive
no nikolsky’s sign
highly communicable
pustular impetigo
pus filled vesiscles
crusted lesions
S A or SA and GAS together
Entertoxins; food poisoning
food will not appear or taste tinted
mean incubation = 4 hours and lasts for 24 hours.
Severe vomiting and diarrhea (non bloody)
abdominal cramp or nausea with no fever
only 30-50% of SA strains producing them
Bacteremia and endocarditis
SA is common cause. however, the initial infection loci are unclear in about 1/3 cases. many are associated with hospitaliztion
prolonged episodes are associated with dissemination to other body parts such as the heart
Pneumonia and empyema SA
aspiration pneumonia in very young, the aged, CF, influenza, COPD, bronchiectasis: pathy infiltrates with consolidation or abscess
hematogenous pneumonia from bacteremia or endocarditis
empyema, SA is a major cause (30%)
SA infections
OSteomyelitis (#1 causative agent in acute and chronic infection of the bone marrow), trauma or hematogenous spread
infective arthritis (#1 causatie agent in adut #1 cause of septic arthritis in young children)
acute endocarditis (#1 causitive agent) infects normal, abnormal and prosthetic valve
bacteremia and sepsis: #1 causative agent
host defense against SA
phagocytosis is the major mechanism for combating SA infection
antibodies are produced which neutralize toxins and promote opsonization. However, the bacterial capsule and protein A may interfere with phagocytosis
biofilm growth on implants is also impervious to phagocytosis
staphylococci may be difficult to kill after phagocytic engulfment because they produce carotenoids and catalse which neutralize singlet oxygen and speroxide which are primary phagocytic killing mechanisms within the phagolysososme
TX SA
penicillinase (beta lactamase) resistant penicillin
cephalosporins: skin infection
clindamycin: skin infection
IF MRSA, treat it with intravenous vancomycin
topical bacitracin prophylaxis
Staphylococcus Epiidermidis (SE)
G+ cocci in clusters
coagulase -
virulence factors: glycocalyx: the exopolysaccharide “slime” helps in adhesion, antiphagocytic and makes it resistance to antibiotics
betalactamase
mutant penicillin binding protein
Source and transmission of SE
found common on the skin
patients at risk include those with prosthetic devices, intravascular catheters or other foreign bodies in place and immunocompromised hosts
transmitted: introduced through a contaminated catheter (bacteremia)
infection of previously damaged or artificial heart valve (endocarditis)
Staphylococcus saparophyticus (SS)
coagulase -
virulence related to binding to epithelium
almost entirely associated with UTI
SX: infected women usually have dysuria (pain on urination), pyuria (pus in urine) and numerous organisms in urine
Summary of staph infections
abscess in the breast, cellulitis, endocarditis, food poisoning, furuncle, carbuncle, impetigo, osteomyelitis, pneumonia, scalded skin syndrome, septic arthritis, toxic shock syndrome, and wound infection
preformed toxin, food poisoning occurs quickly. Same with TSS
Formation of abscess in the breast or lung, empyema
IV catheter sites, prothetic implants (heart valves, vascular grafts) get infected
UTI
penicillin works. MRSA
Nosocomial infections, screening for HCWs
