Coagulase-negative staphylococci (co.n.s) are a diverse group of Gram-positive bacteria known for their role as opportunistic pathogens associated with nosocomial and community-acquired infections, particularly in immunocompromised patients and those with implanted medical devices. They exhibit resistance to various antimicrobial agents, with a significant percentage being methicillin-resistant (MR-co.n.s), and their pathogenicity is enhanced by the ability to form biofilms. Co.n.s are implicated in a variety of infections, including skin infections, endocarditis, and bloodstream infections, making their prevention and control critical in healthcare settings.

1. Coagulase negative staphylococci
Presentation
By
Marwa A. Al-Asady

2. General overview of Co.N.S
• Staphylococcus genus consists of 47 species and 23 subspecies, of these, 38
described as coagulase-negative species.
• Coagulase-negative staphylococci (Co.N.S) is characterized by a gram-
positive, spherical cell of (0.5-1.5µm) in diameter, occurring as single cocci,
in pairs, as a tetrad, short chains, or irregular cluster. Furthermore no-motile,
no-spore forming, encapsulated, catalase positive, cytochrome negative in
modified oxidase teste, also susceptible to lysostaphin and resistance to
bacitracin and they are grown in presence of 10% NaCl between 18℃ and
40℃.
Marwa A. Al-Asady

3. General overview of Co.N.S
• These groups of bacteria are facultative anaerobes so they can grow in the presence
or absence of oxygen.
• Besides, they are reduced nitrate to nitrite, fermenting carbohydrate and producing
pigments when growing on media that vary from white to deep yellow. Colonies
appearance round, smooth, raised and glistening on solid media.
• Called coagulase-negative staphylococci because they lack coagulase is a surface
protein, which can convert fibrinogen to fibrin and resulting in clot formation in
plasma.
Marwa A. Al-Asady

4. General overview of Co.N.S
• The cell walls of Co.N.S contain important cell-adherence factor:
peptidoglycan, teichoic acids, and protein.
• Their peptidoglycan chain cross-linked pentaglycine residue (affected by
lysostaphin); micrococci do not have glycine-residue in their peptide bond
(resistant to lysostaphin) and neither do they have teichoic acids.
• Recently Co.N.S got an important opportunistic pathogen associated with
nosocomial infection and community-acquired infection.
Marwa A. Al-Asady

5. General overview of Co.N.S
• They can adhere to medicinal instruments and surfaces through slime layer which
has a mucopolysaccharide arrangement, therefore they can simply colonize and
spread with-in the hospital environment. The slime feature also assistances in
pathogenicity by protective them from phagocytosis, chemotaxis, and anti-microbial
agents.
• Co.N.S are the most commonly isolated organism related with clinical infection and
communal bacteria residents of the skin, and mucous membranes humans.
• They are causes a variety of infections in immune-compromised individuals and
people with implanted medicinal devices.
Marwa A. Al-Asady

6. General overview of Co.N.S
• The incidence of sepsis infections in neonates caused by Co.N.S is still very
high and preventing and treating disease remain difficult in nosocomial
patient and cause a significant number of death.
• Co.N.S isolated from hospital environments are sometimes resistant to
various anti-microbial agents.
• About 80%–90% of Co.N.S isolates related with hospital infections are
methicillin-resistant (MR-Co.N.S).
Marwa A. Al-Asady

7. Co.N.S Species
• Co.N.S include many species:-
• S. epidermidis, S. caprae, S. sacchrolyticus, S. capitis(ssp.capitis ,ssp.urealyticus)
• S. haemolyticus, S. devriesie, S. jeffensis,
• S. hominis (ssp.hominis, ssp.novobisepticus),
• S. petrasii (ssp.croceilyticus, ssp.petrasii)S.lugdunensis
• S. warneri , S. pasteuri
• S. Saprophyticus (ssp. saprophyticus, ssp. bovis) S. equorum (ssp. equorum,
ssp.linens), S.xylosus
• S. Succinus (ssp.succinus, ssp.casei), S .gallinarum S. pettenkoferi, S. massiliensis

8. Co.N.S Species
• S. conhii (ssp.conhii , ssp.urealyticus),
• S. nepalensis S. klossi , S .arletta
• S. sciuri(ssp.sciuri, ssp.carnaticus, ssp.rodentium)
• S. fleurettii, S. lentus, S. stepanovicii, S. vitulinus, S .simulans, S. carnosus (ssp.utilis,
ssp.carnosus),
• S. codimenti, S. piscifermentans, S. muscae, S. microti, S.rosteri
• S. auricularis
Marwa A. Al-Asady

9. Pathogenesis of Co.N.S
• The pathogenesis of Co.N.S infection typically depends on their ability to
produce biofilms on polymer.
• Formation of biofilms around microorganisms protected them from the
host’s immune defense mechanisms lead to cause chronic infection, extra
resistant to various disinfectants, anti-microbial treatment than their
planktonic cell and from environment variables factors make them difficult
to eradicate.
Marwa A. Al-Asady

10. Virulence factors of Co.N.S
• To start an infection, bacteria need possess a group of molecules named
virulence factors that are critical for its invasion of the host, its persistence
within the host, and the initiation of the clinical symptoms.
• Co.N.S contain various virulence factors that promote colonization host
tissue, immune-evasion, immune-stimulation, develops antibiotic resistance,
also methicillin-resistant.
Marwa A. Al-Asady

11. Virulence factors of Co.N.S
• The virulence factor that produce and dangerous to host tissue, include
toxins, and degradative exoenzymes: metallo-protease with elastase activity,
cysteine protease, serine, protease, lipase, fatty-acid modifying enzymes
(FAME) and δ-toxin also can form biofilm is an important one.
Furthermore, produces lantibiotics are bacteriocins such as epidermin, which
are active to inhibit other gram-positive bacteria.
Marwa A. Al-Asady

12. Infection caused by Co.N.S
• Skin infection
• Endocarditis
• Endophthalmitis
• Bloodstream infections
• Foreign body-related infections
• Urinary tract infection
• Other infections (cerebrospinal shunt infections, meningitis, ventriculitis).
Marwa A. Al-Asady

13. Mechanism of antimicrobial resistance
• Antimicrobial resistance may be acquired through mutation and selection of
resistant bacterial strains or horizontal transfer of resistance genes from
other bacteria of the same or different species.
• The common famous resistance mechanisms in Co.N.S are the production
of enzymes that inactivate or destroy the antibiotics (e.g., stated by the genes
ermA, ermB, ermC, Blaz, and aac-apD), active deletion of antibiotics from the
cell (e.g., efflux-mechanisms pumps), and decrease of the antibiotic binding
affinity to the drug.
Marwa A. Al-Asady

14. Mechanism of antimicrobial resistance
• A large and theatrical increase in the number of resistant strains has
detected, in particular to penicillin, oxacillin, methicillin, clindamycin,
erythromycin, ciprofloxacin, and gentamicin.
• Resistance to β-lactams, that is, MR-Co.N.S (methicillin-resistant Co.N.S) is
determined by the presence of mecA gene, which encodes other penicillin
binding protein (PBP-2a) and is inserted into a mobile-gene element (MGE),
called the staphylococcal cassette chromosomal mec (SCCmec).
Marwa A. Al-Asady

15. Mechanism of antimicrobial resistance
• The mecA gene, which encodes a PBP-2a, with reduced affinity for
methicillin compared with the attractions of other PBP. In addition to
methicillin resistance, Co.N.S strains have acquired resistance to several other
antibiotics, including rapamycin, fluoroquinolones, gentamycin, tetracycline,
erythromycin, chloramphenicol, clindamycin and sulphonamides
Marwa A. Al-Asady

16. Thank you for lessening
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