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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


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



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



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


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


penicillin works. MRSA

Nosocomial infections, screening for HCWs