Coagulase negative

Coagulase negative DEFAULT



  • Coagulase-negative staphylococci (CoNS) are aerobic, Gram-positive coccus, occurring in clusters.
    • Predominantly found on the skin and mucous membranes.
    • Heterogeneous group
    • Catalase positive but coagulase negative (S. aureus is coagulase positive).
  • Major pathogens:
    • S. epidermidis: colonies typically small, white-beige (about 1-2 mm in diameter).
    • S. haemolyticus: colonies typically small, golden yellow (about 1-2 mm in diameter).
    • S. lugdunensis: colonies are usually sticky, smooth, glossy, yellow-orange (2-4 mm).
      • Perhaps the most virulent of CoNS; it behaves similarly to S. aureus.
    • Over 40 recognized species of CoNS capable of causing human disease.
      • Others seen on occasion: Staphylococcus auricularis, Staphylococcus capitis, Staphylococcus hominis, Staphylococcus saprophyticus, and Staphylococcus simulans.
  • Many strains with a propensity to produce biofilm, allowing for adherence to medical devices.
  • Susceptibility profile for CoNS. Breakpoints vary by species.
    • Vancomycin (CLSI): MIC cutoffs
      • Sensitive: ≤ 4 mg/L
      • Intermediate: 8-16 mg/L
      • Resistant: ≥ 32 mg/L
      • Note: EUCAST states resistance is MIC > 4 mg/L
    • Oxacillin (CLSI)
      • S. epidermidis sensitive if ≤ 0.25 mg/L and Resistant if ≥ 0.5 mg/L.
      • S. lugdunensis sensitive if ≤ 2 mg/L and resistant if ≥ 4 mg/L.
    • Usually resistant to penicillin and typically (> 80%) to methicillin (oxacillin, nafcillin).
      • mecA gene encodes for low-affinity penicillin-binding protein.
      • Resistance can be heterotypic, so usually like to see multiple isolates determined as susceptible to beta-lactams, as only a minority of isolates typically express resistance phenotypes.
    • Linezolid resistance described but remains rare.

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Last updated: July 4, 2021


Auwaerter, Paul G. "Staphylococci, Coagulase Negative." Johns Hopkins ABX Guide, The Johns Hopkins University, 2021. Johns Hopkins Guide,

Auwaerter PG. Staphylococci, coagulase negative. Johns Hopkins ABX Guide. The Johns Hopkins University; 2021. Accessed October 13, 2021.

Auwaerter, P. G. (2021). Staphylococci, coagulase negative. In Johns Hopkins ABX Guide. The Johns Hopkins University.

Auwaerter PG. Staphylococci, Coagulase Negative [Internet]. In: Johns Hopkins ABX Guide. The Johns Hopkins University; 2021. [cited 2021 October 13]. Available from:

TY - ELEC T1 - Staphylococci, coagulase negative ID - 540517 A1 - Auwaerter,Paul,M.D. Y1 - 2021/07/04/ BT - Johns Hopkins ABX Guide UR - PB - The Johns Hopkins University DB - Johns Hopkins Guide DP - Unbound Medicine ER -


Coagulase-Negative Staphylococci

S. arlettaeYellow or beige+−Textile and tannery industrial effluentsCattle, goats, pigs, poultry, sheep−−BSI (+)S. auricularisWhite−−−−External auditory canal (principle habitat), seldom on other skin regions−BSI in preterm infant (?)S. capitis subsp. capitisChalk white−−−Cats, dogs, horsesPredominantly on the scalp and arms, less frequently on other skin regionsCRBI (+), PVIE (+), CAPD (+), DRBJI (++)BSI in neonates (+)S. capitis subsp. urealyticusdWhite, delayed yellow pigmentation in ∼70% of isolates−−−−Predominantly on skin (mostly from heads, primarily ears and foreheads)CRBI (+), PVIE (+)BSI in neonates (++)S. capraeNonpigmented−−−GoatsSkin, anterior naresCRBI (+), CAPD (+), CFDAI (+), DRBJI (+)UTI (+)S. carnosus subsp. carnosusGray-white−−Fermented food (starter cultures, soy sauce mash)Cattle−−−S. carnosus subsp. utilisCream colored after 48 h−−Fermented food (soy sauce mash, fermented fish)−−−S. chromogenesButyrous, orange, or creamy−−−Cattle, pigs, horses, goats, sheep−−−S. cohnii subsp. cohniiUnpigmented or, occasionally, tinted slightly yellowish+−−Dogs, goats, poultrySkinCRBI (++), DRBJI (++)BSI in burn patient (+)S. cohnii subsp. urealyticuseTranslucent with concentric ring patternsc+−−Apes, clams, monkeys, horsesSkin−BSI (+), infected pressure ulcer (?)S. condimentiCream colored after 48 h−−Fermented food and starter cultures−−−−S. devrieseiGray-yellow, yellow. or yellow-orange−−−Cattle−−−S. epidermidisGray or grayish white−−Fermented sausagesCats, cattle, dogs, goats, gorillas, horses, pigs, sheepSkin (preferentially axillae and the head; also arms and legs) and mucous membranes of the nasopharynxCAPD (!), CFDAI (!), DRBJI (!), PVIE (!), and virtually all other kinds of FBRIsBSI in neonates (!)S. equorum subsp. equorumWhite+−Fermented food (starter cultures)Cattle, goats, horses, sheep−DRBJI (+)−S. equorum subsp. linensWhite+−Smear-ripened cheese (starter culture)−−−−S. felisUnpigmented−−−Cats, horses−−−S. fleurettiiUnpigmented or cream colored++Milk cheeseGoats, pigs, small mammals−−−S. gallinarumYellow, yellowish tint, or unpigmented+−Chickens, pheasants−CRBI (+)−S. haemolyticusGray-white, white, or slight yellow tint−−Milk, fermented foodCats, cattle, dogs, horses, goats, pigs, sheepSkin (preferentially legs and arms)CAPD (+++), CFDAI (+++), DRBJI (++)BSI in neonates (+++)S. hominis subsp. hominisDull, gray-white to yellowish or yellow-orange−−Goat milk, fermented foodCats, dogs, goats, pigs, sheepSkin (preferentially axillae, arms, legs, and pubic and inguinal regions)CRBI (++), DRBJI (++)BSI in neonates (+)S. hominis subsp. novobiosepticusButyrous, gray-white−−−−−CRBI (++)BSI in neonates (+)S. jettensisYellow (after prolonged incubation)−−−−−CRBI (+)−S. kloosiiOpaque+−−Goats−CRBI (+)BSI (+)S. lentusGray-white to white or creamy++Soy bean oil meal, meat, milkClams, goats, horses, mink, pigs, poultry, sheep−CRBI (+)BSI (+), splenic abscess (+)S. lugdunensisCream-white to slightly yellow−−−Cats, chinchillas, dogs, goats, guinea pigsSkin (preferentially lower abdomen and extremities)PVIE (++), CFDAI (+), DRBJI (+)Native valve endocarditis (++), wound infection (++), SSI (++)S. massiliensisWhite−−−−Skin (?)−Brain abscess (+)S. microtiOpalescent whitish−−−Mice−−−S. muscaeButyrous, grayish white−−−Flies (trapped in cattle sheds)−−−S. nepalensisWhite+−Environment (not specified)Goats, pigs, squirrel monkeys, bats (guano), dry-cured ham−−Cystitis (?; recovered from human urine)S. pasteuriMostly yellow, also white−−Fermented sausagesPigs−CAPD (+), DRBJI (+), CRBI (?)BSI (+)S. petrasii subsp. croceilyticusPale creamy yellow−−−−Skin (?; so far only from acoustic meatus)−−S. petrasii subsp. petrasiiUnpigmented−−−−Skin (?)−BSI (?)S. pettenkoferiMostly white, also yellow−−−−Skin (?)CRBI (++)Wound infection (?), osteomyelitis (+)S. piscifermentansUnpigmented, white, yellowish orange−−−Dogs (feces), fermented food and starter cultures−−−S. rostriWhite−−−Pigs, poultry, water buffalo−−−S. saccharolyticusfGrayish white−−−GorillasSkin, particularly on the forehead and armPVIE (?)Spondylo-discitis (+), joint infection (?), pneumonia (?)S. saprophyticus subsp. bovisCreamy to pale orange, also unpigmented+−−Cattle−−−S. saprophyticus subsp. saprophyticusUnpigmented or slight yellow tint+−Horses, goats, sheep, cats, fermented foodSkinCRBI (+)UTI (!), BSI (+), NVIE (+)S. schleiferi subsp. schleiferi−−−Dogs, catsSkin (particularly preaxillary)CFDAI (+), CRBI (+), DRBJI (+), PVIE (+)BSI (+), wound infection (+), UTI (?)S. sciuri subsp. carnaticus++−Cattle, dolphinsSkin−BSI (?)S. sciuri subsp. rodentium++−Rodents, whalesSkin−BSI (?)S. sciuri subsp. sciuriGray-white with yellowish or cream-colored tint toward the center, yellowish (rare)++−Cats, cattle, clams, dogs and other carnivores, dolphins, goats, horses, insectivores, marsupials, monkeys, pigs, rodents, whalesSkinCAPD (+), CRBI (+), DRBJI (+)BSI (?), diabetic food infection (?), wound infection (?)S. simiaeWhite−−−Squirrel monkeys−−−S. simulansGray-white−−−Cattle, horses, sheepSkin (legs, arms, and heads of children; occasionally in adults)DRBJI (+)−S. stepanoviciiUnpigmented++−Insectivores, rodents−−−S. succinus subsp. caseiWhite+−Fermented foodInsectivores, rodents−−−S. succinus subsp. succinusWhite+−Amber, fermented food (starter cultures)Cattle, insectivores, rodents, songbirdsEye (single report)−BSI (?)S. vitulinusCream to yellow, rarely unpigmented++Fermented foodHorses, poultry−−Hip infection (?)S. warneriGray-white (20%), slightly yellowish colonial center to bright yellow-orange−−Fermented foodDogs, cats, goats, horses, insectivores, monkeys, pigs, prosimians, rodents, sheepSkin (preferentially nares, head, legs, and arms)CAPD (+), DRBJI (++)Septic arthritis (+)S. xylosusOrange-yellow, yellowish, or gray to gray-white+−Fermented food (starter cultures)Cats, clams, goats, horses, insectivores, lower primates, rodents, sheepSkin (rare)DRBJI (+)−
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Coagulase-negative staphylococci

The definition of the heterogeneous group of coagulase-negative staphylococci (CoNS) is still based on diagnostic procedures that fulfill the clinical need to differentiate between Staphylococcus aureus and those staphylococci classified historically as being less or nonpathogenic. Due to patient- and procedure-related changes, CoNS now represent one of the major nosocomial pathogens, with S. epidermidis and S. haemolyticus being the most significant species. They account substantially for foreign body-related infections and infections in preterm newborns. While S. saprophyticus has been associated with acute urethritis, S. lugdunensis has a unique status, in some aspects resembling S. aureus in causing infectious endocarditis. In addition to CoNS found as food-associated saprophytes, many other CoNS species colonize the skin and mucous membranes of humans and animals and are less frequently involved in clinically manifested infections. This blurred gradation in terms of pathogenicity is reflected by species- and strain-specific virulence factors and the development of different host-defending strategies. Clearly, CoNS possess fewer virulence properties than S. aureus, with a respectively different disease spectrum. In this regard, host susceptibility is much more important. Therapeutically, CoNS are challenging due to the large proportion of methicillin-resistant strains and increasing numbers of isolates with less susceptibility to glycopeptides.


Coagulase-negative staphylococci (CoNS) as a significant etiological factor of laryngological infections: a review

Annals of Clinical Microbiology and Antimicrobialsvolume 19, Article number: 26 (2020) Cite this article

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This review article shows that coagulase-negative staphylococci (CoNS) are widely responsible for laryngological diseases. General characteristics of CoNS infections are shown in the introduction, and the pathogenicity in terms of virulence determinants, biofilm formation and genetic regulation mechanisms of these bacteria is presented in the first part of the paper to better display the virulence potential of staphylococci. The PubMed search keywords were as follows: CoNS and: nares infections, nasal polyps, rhinosinusitis, necrosing sinusitis, periprosthetic joint infection, pharyngitis, osteomyelitis of skull and neck bones, tonsillitis and recurrent tonsillitis. A list of laryngological infections and those related to skull and neck bones was presented with descriptions of the following diseases: rhinosinusitis, necrotizing sinusitis, nasal polyps, nares and nasal skin infections, periprosthetic joint infections, osteomyelitis, pharyngitis, and tonsillitis. Species identification and diagnostic problems challenging for diagnosticians are presented. Concluding remarks regarding the presence of CoNS in humans and their distribution, particularly under the effect of facilitating factors, are mentioned.

General characteristics of coagulase-negative staphylococci (CoNS) infections

The significance of CoNS in infectious medicine became apparent in the late 1970s following a series of articles on the isolation of these bacteria from diagnostically documented infections in humans, as shown by several authors [1,2,3,4,5,6]. The definition of CoNS as a heterogeneous group of staphylococci is based on diagnostic procedures that fulfil the clinical need to differentiate between Staphylococcus aureus, commonly known as strongly pathogenic, and other staphylococci classified as non- or less pathogenic [7]. CoNS are characterized by fewer virulence factors than S. aureus, especially factors responsible for aggression, so they are considered less pathogenic. However, the virulence of both CoNS and coagulase-positive staphylococci (CoPS), represented by S. aureus, were compared using various animal models of experimental infections [8,9,10,11,12,13]. The authors showed that some CoNS species demonstrated skin lesions similar to the lesions generated by S. aureus [11]. Generally, the pathogenic potential of CoNS could be accepted when both biochemical and genetic molecular methods were introduced to analyze the pathogenesis and mechanisms of infections [7, 14]. In the last two decades, the medical importance of this group of bacteria has increased, as reported by clinicians and microbiologists [15, 16]. There is evidence that CoNS are responsible for a variety of infections that differ in localization, manifestation or course of infection. However, staphylococcal bacteria are opportunistic pathogens that are present in the skin and mucous membranes of healthy individuals and become true pathogens mostly for predisposed patients, i.e., immunocompromised individuals, patients with catheters, prosthetic implants, dialysis, and oncological diseases, and neonates [17,18,19,20].

As pathogens, CoNS are involved in a broad range of diseases in deep organs, including bones, the central nervous system, the heart or joints [21]. However, CoNS are typical opportunistic bacteria that not only colonize healthy individuals but also represent one of the major hospital pathogens with a substantial increasing impact on human life and health [7]. The presence of CoNS in the skin and mucous membranes of the host is a main source of endogenous infections [7, 22]. In addition, bacteria are transmitted among diverse hosts by crossing species barriers and during medical procedures, especially invasive ones [23, 24]. Regarding otorhinolaryngology, CoNS are always present in the skin and mucous membranes of the nose, respiratory tract, oral cavity and alimentary canal [25, 26]. In the field of laryngology, the main papers on CoNS pathogenicity focus on diseases such as bacteremia, septicemia, pneumoniae, endocarditis or urinary tract infections, but there are few reports on laryngological diseases such as rhinosinusitis and sinusitis, both acute and chronic, and infections of the frontal sinus, throat, larynx, nares, polyps, tonsils, and trachea. A dozen of the over 50 described CoNS species have been commonly reported in these diseases, including Staphylococcus epidermidis, Staphylococcus haemolyticus, Staphylococcus lugdunensis, Staphylococcus warneri, Staphylococcus xylosus, Staphylococcus hominis, Staphylococcus capitis, Staphylococcus simulans, Staphylococcus sciuri, Staphylococcus cohnii, Staphylococcus lentus, and Staphylococcus chromogenes, although other rare species, such as Staphylococcus pettenkoferi, have been documented [7, 27, 28].

Pathogenicity: virulence determinants, biofilm formation and genetic regulation of CoNS species

CoNS possess numerous diverse strategies to both cause infection and survive in the host. In comparison to S. aureus, this group of bacteria exhibits lower pathogenic potential, but less is known about CoNS virulence mechanisms. Recent studies have focused on the ability of CoNS to produce a variety of extracellular enzymes, such as proteases, elastases, esterases, lipases, and phospholipases [29,30,31,32], as well as the production of toxins, such as families of hemolysins, enterotoxins, exfoliative toxins, and even TSST-1 (Toxic shock syndrome toxin-1) [7, 33,34,35,36]. The enzymes and toxins presented play crucial roles in some of the effects of staphylococci on host organisms, including virulence factors in tissue destruction and additionally as spreading factors facilitating invasion into nearby tissues. In general, CoNS species lack the virulence determinants responsible for aggression, but they possess the ability to adhere, invade and persist [14, 31]. Furthermore, a critical CoNS property is the ability to colonize the surfaces of medical devices by the formation of a three-dimensional structured matrix composed of bacteria and extracellular biopolymers-biofilm. Increasing evidence suggests that biofilms may form on abiotic surfaces of medical devices or on biotic surfaces, such as host factor-coated foreign material or host tissue [37, 38]. Biofilm-associated infections are extremely difficult to eradicate because within the biofilm, bacteria are protected against the immune system of the patient and antibiotic therapy [39, 40]. Identification of the factors that increase CoNS pathogenicity is a great need, especially for clinicians and microbiologists. Studies described to date have demonstrated that S. epidermidis isolates differ regarding antibiotic resistance gene acquisition (e.g., SCCmec), biofilm forming capacities (e.g., ica locus), metabolism (e.g., arginine catabolic mobile element ACME) and the presence of insertion sequence (IS) elements (e.g., IS256) [41,42,43,44]. It is very important to extend such studies to a larger number of isolates and species, but there is strong evidence that horizontal gene transfer is responsible for virulence factor transmission between species [45,46,47,48]. Staphylococcal pathogenesis is a process involving an array of extracellular proteins and biofilm and cell wall components that are coordinately expressed in different phases of infection. The expression or suppression of two divergent loci, accessory gene regulator (agr) and staphylococcal accessory regulator (sar), are recognized as key regulators of virulence in staphylococcal infections [49, 50]. The agr system is known to modulate virulence factors such as nucleases, proteases, lipases and the expression of surface binding proteins, and sar can modulate both the agr system and independently form an agr locus of cell wall-associated proteins such as fibronectin-binding protein, adhesins, protein-A and exo-proteins. When the bacterial population is low, the expression of adherence proteins is triggered for attachment to host tissue and toxins are produced once the infection is established [51].

General descriptions of laryngological infections

Laryngology, otolaryngology, is generally a broad medical discipline that covers the diagnosis, therapy, and prophylaxis of diseases of the upper respiratory tract and additional organs present in the neck and head, including throat, larynx, nose, ears, and other organs in these parts of body [52]. Recently, important medical questions in laryngology have been raised regarding oncological and infectious diseases [53, 54]. Statistically viral and bacterial infections of the respiratory tract that spread into other anatomical niches are the most identified in epidemiological analysis. Staphylococci, particularly CoNS, can cause local infections, but they are also responsible for pathological complications after expanding from laryngological areas to other areas, including skin, and heart, and even sepsis in newborns as well as nosocomial infections [55,56,57,58,59,60,61]. Moreover, an increasing number of fungal infections has recently been reported in laryngology studies, and these infections are related to the overconsumption of antibiotics and patients with immune disorders.


The rhinosinus is the space in the front part of the facial skeleton that is filled with air and mucous membranes with ciliated epithelium, including mucous glands. In addition, inflammation proceeds synchronously because of the anatomical and physiological relations of the mucous membranes of the nose and rhinosinus, which is the reason for the Latin name used for inflammation of mucous membranes of nose and rhinosinus–rhinosinusitis. Acute rhinosinusitis (ARS) appears the most frequently in the course of viral cold disease, whereas chronic rhinosinusitis (CRS) is a common source of CoNS isolation [62]. CRS represents a heterogeneous group of diseases resulting from the multifaceted interactions between the individual patient and environment. Chronic rhinosinusitis is one of the most common chronic disorders, present in up to 28% of European or American populations [63]. The mechanisms of this disease are still under careful molecular analysis. The main underlying causes of rhinosinusitis are various bacteria, but the most commonly isolated are gram-positive cocci. The predominant organisms identified are streptococci and staphylococci. Bacterial infection plays an important role in CRS as either a causative or exacerbating factor [64, 65]. However, the role of CoNS in CRS remains “controversial” [66]. For a significant subpopulation of patients, only CoNS were isolated, while another population had other positive cultures, and a small group had no bacterial growth [66].

Microbiological analysis of samples from CRS patients revealed that mainly CoNS were identified, followed by S. aureus and gram-negative rods, including Pseudomonas aeruginosa, Stenotrophomonas maltophilia, Escherichia coli, and Serratia marcescens [65]. The most frequently found CoNS species in CRS patients was S. epidermidis, and other CoNS, such as S. lugdunensis, S. capitis, Staphylococcus saprophyticus, S. haemolyticus, and Staphylococcus saccharolyticus and to a lesser degree other minor CoNS, were present in 87% of cases [63, 67].

Molecular genetic studies have shown that the pathologic ability of CoNS such as S. epidermidis depends on genes associated with biofilm formation that have only been found in certain strains [68]. However, knowledge of the importance of bacteria and microbial biofilms in the etiology of CRS is still incomplete. Some authors have determined the association between positive CoNS culture at the time of functional endoscopic sinus surgery (FESS) and CRS severity. Simultaneously, bacteria other than CoNS have been isolated: Streptococcus pneumoniae (30–70%), Streptococcus pyogenes (3–7%), Streptococcus spp., Moraxella catarrhalis (12–28%), Enterobacter spp., Cutibacterium acnes [66], S. aureus (27%), Haemophilus influenzae (27%), P. aeruginosa (22%), Peptostreptococcus spp. (20%), Bacteroides spp. (19%), Klebsiella pneumoniae (11%), and E.coli (11%) [69]. Other authors analyzed the exacerbation of CRS in 125 patients and identified CoNS as the most common organism, followed by S. aureus [70]. Studies on cultures from 394 CRS patients revealed that aerobes were predominant, and CoNS were common (24%), followed by S. aureus (19%) and Streptococcus viridans (10%) [71]. Despite the high prevalence of CoNS and their controversial effect on CRS, some reports have shown that the bacteria as the sole positive culture result did not result in increased CRS disease burden [66]. The presence of CoNS alone was independently associated with no history of prior FESS. However, some authors showed no significant difference in CRS disease severity between patients with CoNS as the sole positive culture result and no bacterial growth, but phenomena such as horizontal virulence gene transfer, quorum sensing, and mechanisms of gene expression/suppression necessitate further studies on a larger number of patients and isolates to evaluate whether the effect of CoNS differs in various subgroups [66, 69]. The role of CoNS in CRS pathogenesis is not completely understood because the bacteria that colonize the nasal cavity under physiological conditions have been interpreted as contamination in microbiological analysis by few authors. Most authors have reported an important role for CoNS in CRS pathogenesis and the mechanism of the disease because of the extracellular production of virulence factors such enzymes and toxins, biofilm formation, and virulence or resistance gene transfer among the bacteria colonizing these anatomical areas. However, there are few factors that may affect the detection of CoNS as etiological factors in such infections. The frequency of CoNS isolation at the infection site and the molecular typing of CoNS to determine the clonality of the isolates is crucial in determining the real etiological factor. Moreover, the presence of invasive medical devices and the immune status of patients should be considered, as immunocompromised patients are more susceptible to CoNS infection.

Necrotizing sinusitis

Necrosing sinonasal infection often involves infectious agents such as viruses, bacteria, fungi, and parasites [72,73,74]. However, the only reported CoNS species responsible for acute necrotizing sinusitis is S. lugdunensis, which was reported in hospitalized patients with metastatic prostate adenocarcinoma [75]. Additionally, severe acute necrotizing sinusitis was complicated by periorbital cellulitis and ulceration from the maxillary sinus to the hard palate. The only pathogen to be identified in three independent biopsy samples was S. lugdunensis [75]. The species identification of organisms was verified by the Health Protection Agency Respiratory and Systematic Infection Reference Laboratory using advanced methodology. Interestingly, S. lugdunensis, in addition to being a skin commensal of the limbs, groin and nose vestibule of healthy adults, has also been isolated from acute oral infections [76], prosthetic joints, endovascular, skin and soft tissue infections; in individual cases, S. lugdunenesis has been isolated as an agent of osteomyelitis, which can lead to laryngological implications in terms of significant effects on the head or face bones. Moreover, S. lugdunensis is a major pathogen for heart valves, both native and prosthetic, as it causes very aggressive endocarditis [75, 77].

Nasal polyps

Many staphylococci colonize the human nose vestibule; however, the main question relates to S. aureus, as it is unknown whether and how this bacterium adapts to this particular ecological niche during colonization. Staphylococci are among the bacterial species associated with increasing invasive diseases and drug resistance distribution in humans [78]. The analysis of the composition of the human nasal culturome revealed that S. epidermidis colonizes almost all individuals (97%), followed by S. haemolyticus (44%), S. hominis and S. capitis (each 41%), S. warneri (32%) and S. lugdunensis (26%) [79]. The basis of colonization with strains carrying virulence determinants and/or resistance results from fibronectin-, fibrinogen-, and collagen-binding surface proteins responsible for adhesion and further infection [80]. Polyps are abnormal growth tissue complexes that originate from mucous membranes and are generally present in any organ. In laryngology, polyps are interpreted as disorders or lesions of an inflammatory nature or caused by injury; most cases involve a history of trauma [81]. Therefore, polyps occur elsewhere in the body where there is a mucous membrane. The presence of polyps and accompanying mucosal edema is one of the main observations at examination [82]. The polyps may be involved in chronic sinusitis. CRS with polyps can be present not as a single disease entity but as nasal symptoms of many different diseases [83]. Environmental microorganisms affect the host and cause symptoms in CRS. Bacteria involved in the disease play an important role, and bacterial biofilms present in CRS patients are responsible for noneffective therapy even after surgical and antibiotic interventions [63]. A group of patients with nasal polyps may have different disease etiologies, and it is well documented that culture results are difficult in post-ESS patients. CRS patients with CoNS as the sole positive culture result were significantly more likely to have nasal polyps [66]. Analysis of the bacteriological profile of the patients showed that CoNS, S. aureus, Streptococcus sp., Haemophilus sp., Enterobacter sp., and Corynebacterium sp. appear to be more frequently associated with patients with chronic rhinosinusitis (CRS) with nasal polyps than with patients with CRS without nasal polyps or control individuals, where the most common aerobic bacteria were CoNS, Corynebacterium spp., S. aureus, and H. influenzae. Additionally, few anaerobic bacteria and fungi have been isolated from various study groups [84]. Authors of another project reported no significant differences in isolation rates among three groups of CRS patients, i.e., with polyps, without polyps, and the control group, although the two most common bacterial species were CoNS and Corynebacterium spp. in CRS with polyps group; CoNS, Corynebacterium spp., and S. aureus in CRS without polyps group; and CoNS, and S. aureus in the control group. Finally, CoNS were the most common species among the three groups [85].

Nares and nasal skin infections

The human nares and skin flora are normally largely composed of different species of CoNS and coryneforms, as reported by many authors [1, 2, 86,87,88]. Among all aerobic bacteria, CoNS are the group of organisms with the best characteristics for growth and multiplication in cutaneous recesses enriched with sebum and sweat because of the many extracellular enzymes they produce, enabling the use of skin substrates, particularly neutral fatty acids of sebum [89,90,91]. Infections with Staphylococcus bacteria can result in a variety of skin conditions, including cellulitis, furuncles, impetigo or staphylococcal scalded skin syndrome (SSSS). Some CoNS strains, such as S. epidermidis and S. haemolyticus, share the same habitats as S. aureus and permanently or transiently colonize the anterior nares, nose vestibule, and other regions of skin and mucous membranes, acting as a source of infection [92]. Therefore, both S. aureus and CoNS are often recovered from the same diagnostic specimen in parallel [93].

CoNS infections of nares or nasal skin have been reported in a minority of cases in comparison to S. aureus infections, and they are always combined with immunocompromised or directly post-surgery hospitalized patients [94, 95]. Common types of nasal staphylococcal infections include folliculitis, which is an infection of one or many hair follicles; furuncle, also known as boils, which are deep infections around the hair follicle or oil glands that contain pus; or nasal vestibulitis, an infection of the front area of the nasal cavity that may cause crusting and bleeding. There are various symptoms of nasal staphylococcal infections, such as crusting, swelling, lesions with pus secretion, light bleeding, pain, redness or fever [96]. Therefore, nasal carriage of CoNS, especially methicillin-resistant CoNS, appears to play a key role in the epidemiology and pathogenesis of infections in nares or upper respiratory tracts [94]. Increasing evidence suggests that nasal CoNS are also reservoirs for mupirocin resistance, which may therefore be transmitted to S. aureus. Mupirocin is the first-line drug treatment to eradicate S. aureus nasal colonization, which may fail, although rarely, due to the transfer of underlying genetic elements from CoNS to S. aureus [97, 98]. Over the last few years, CoNS have become important as causative agents of hospital-acquired bacteremia and surgical site infections. Thus, CoNS colonizing anterior nares and skin are severe pathogens responsible for infections and are additionally often associated with multiple antimicrobial-resistance mechanisms, including antibiotic resistance of various other pathogens [51, 52].

Periprosthetic joint infections

In laryngology, temporomandibular joint (TMJ) infections are still a challenge, because there is no single leading disease [99]. The TMJ joins the mandible with the skull, and pain can mimic infections of the inner ear. The TMJ is part of a larger system known as the stomatological system or locomotor system of the masticatory apparatus. This is a very complex system under permanent and dynamic changes throughout life. Infections of the TMJ in both intracapsular and pericapsular courses are rare diseases [100]. The predisposing factors for contributing to TMJ infections are divided into local factors, such as blunt trauma, history of joint diseases and burn, and systemic factors including autoimmune disease and overconsumption of medicines with special reference to steroids [57, 101, 102]. Therefore, there are various reasons for TMJ infections; however, it is difficult to indicate the most important. Some authors have shown fatigue of TMJ muscles, orthodontic disorders, trauma of the head or spine, and stress as reasons for TMJ infections [103]. Analysis of ankylosis and arthritis showed that the most common causes of the disease are trauma and infection [104], and psychological aspects have also been reported as factors in nonorganic TMJ dysfunction [105]. The invasion of bacteria into the joint space can occur through several routes, but hematogenous spread indicates that blood circulation is the most common route. The other methods are adjacent, contiguous infected tissues and direct centesis into the joint cavity by direct inoculation [100]. Among these, the most prevalent route is hematogenous spread originating from primary infection sites [106]. The typical bacteria causing TMJ infections are Streptococcus spp., S. aureus, S. epidermidis, Neisseria gonorrhoeae, H. influenzae, and P. aeruginosa [107, 108]. The tests used to confirm species identifications showed that CoNS, such as S. lugdunensis, S. epidermidis, S. haemolyticus, S. xylosus, S. warneri, and S. hominis, were isolated from fluid secreted by the temporomandibular joint of patients with muscle pain [109]. Additionally, S. capitis, a multidrug-resistant strain with documented potential for both human disease and nosocomial spread, was isolated from a group of patients [110]. An accompanying chronic orofacial muscle pain is associated with membrane-damaging toxins from CoNS (MDT-CoNS) or S. aureus. Previous reports suggest that membrane-damaging toxins produced by CoNS are associated with the development of chronic disease [111, 112]. Additionally, an evaluation in the distribution of Staphylococcus spp. in different phases of prosthetic joint infection (PJI) was observed, and the predominant pathogens were CoNS followed by S. aureus. Almost equal proportions of CoNS and S. aureus were observed in the delayed phase. CoNS were the predominantly identified organisms in the early phase, whereas S. aureus was observed primarily in the late phase [113]. In many medical disciplines, such as infectious laryngology, orthopedic infections due to CoNS presenting antibiotic-resistant profiles are increasing. Soft tissues and bone implant-associated infections are caused by CoNS, with the most prevalent species being S. epidermidis. These infections are considered difficult to treat because of the ability of the bacteria to grow in biofilms and form small-colony variants, including persistent organisms [114, 115].


The discipline of laryngology also concerns diseases of the skull and neck bones. Osteomyelitis generally refers to laryngology-related inflammatory diseases of bones caused by microorganisms and leads to bone destruction. The most frequent microorganisms isolated from osteomyelitis are S. aureus and CoNS, with a predominance of S. epidermidis [116]. However, a new CoNS species, S. pettenkoferi, has been described as causing human osteomyelitis [117]. The disease otitis or otitis externa can also cause complications such as skull base osteomyelitis (SBO) [118]. In particular, orthopedic devices are used for bone fixation or joint replacement and are receptive/susceptible to commensal bacteria, mainly CoNS. The therapy of such infections is expensive, and the infections result in high patient morbidity [119]. Bone infections caused by CoNS are associated with a high prevalence of methicillin resistance, and broad spectrum oral antibiosis was demonstrated in a predominantly diabetic population [116]. In advanced laryngology concerning surgical reconstructions of bones and/or accompanying soft tissues, infections due to CoNS and methicillin-resistant strains are increasing [114]. CoNS are often responsible for cases of chronic osteomyelitis and otitis, especially in patients with orthopedic prostheses or implants. Chronic courses of osteomyelitis or ostitis were caused by the following CoNS species: S. epidermidis, S. haemolyticus, S. simulans, S. warneri, S. sciuri, S. cohnii, S. hominis, S. lentus, S. chromogenes, and S. pettenkoferi [120]. Additionally, other chronic forms of osteomyelitis such as suppurative osteomyelitis of the jaws are caused by various bacteria, with a significant portion being CoNS [121].

Pharyngitis, throat infection

Pharyngitis is a disease of the throat, infection and inflammation caused by viruses, eubacteria, or Mycoplasma pneumoniae. The bacteria, that cause these infections include group A/C/G/B streptococci, Fusobacterium, and N. gonorrhoeae, but Str. pyogenes and other streptococci are the predominant species [52]. CoNS are generally considered nonpathogenic, and their presence in clinical material has been interpreted as contamination by normal microbiota present in the mucous membranes of the oral cavity and upper respiratory tracts. However, there are few reports on CoNS in cultures from throat infections, but these studies were mostly in children, and the role of CoNS as causative agents should be further investigated [122,123,124].

Tonsillitis (T) and recurrent tonsillitis (RT) are caused by viruses, bacteria, Chlamydia and fungi. The symptoms of tonsillitis and pharyngitis are similar. The most frequently isolated organisms from T or RT are S. aureus strains, from 70% of patients, followed by Streptococcus sp. from groups A, B, and C (and G), and the following species dominant as well: beta-hemolytic Str. pyogenes, H. influenzae, Haemophilus parainfluenzae, Klebsiella pneumoniae, Klebsiella oxytoca, Moraxella catarrhalis, Citrobacter koseri, Enterobacter cloacae, Enterobacter aerogenes, E. coli, and P. aeruginosa [125,126,127]. Aside from streptococci, all other species are considered able to colonize the throat and could be found in recurrent tonsillitis due to gastroesophageal reflux. CoNS have also been isolated in cultures from T and RT infections, but they are reported as accompanying bacteria and culture contaminants [128, 129]. Such results and the involvement of S. aureus in the etiology of T and RT have not yet been fully understood because CoNS and occasionally S. aureus constantly colonize mucous membranes of the oral cavity and upper respiratory tracts. Furthermore, staphylococcal internalizations in deeper layers or even inside of tonsils, as well as in single cells of patients, have been observed [125, 130].

Species identification and diagnostics problems

Challenging identification processes may lead to a lack of noted infections caused by staphylococci other than S. aureus and their spread in the environment. Commonly used routine diagnostic methods, such as culture-dependent phenotypic tests, including automated systems such as Vitek 2 (bioMérieux, La Balme Les Grottes, France), BD Phoenix (BD Diagnostic Systems, Sparks, MD, USA), and matrix-assisted laser desorption ionization–time of flight mass spectrometry (MALDI-TOF MS), both with 16S rRNA gene sequencing, are usually not precise enough to carefully assign Staphylococcus species [28, 131,132,133,134]. Many members of the Staphylococcus genus are closely phylogenetically related, and the real impact of CoNS species as infectious etiological factors may remain underreported. The implementation of reliable genetic methods in clinical practice will improve the identification process and result in faster and more precise diagnosis of staphylococcal infections. As shown in our review article, in laryngological infections, staphylococci often coexist with other opportunistic and pathogenic bacteria, complicating the identification process. The new genetic diagnostics approach, based on next generation sequencing, may be used for the identification of whole species content in polymicrobial clinical samples. The well-curated and publicly available reference sequence dataset for Staphylococcus species will allow the introduction of this approach in all microbiological laboratories with access to NGS (next-generation sequencing) platforms and may be used in diagnosing laryngological infections [28, 135, 136].

Concluding remarks

CoNS are a heterogeneous group of gram-positive bacteria that colonize human or animal skin and mucous membranes and are distributed from these niches into the environment. Although CoNS are present everywhere, they multiply in humans or animals only. Under physiological conditions, CoNS are typical saprophytes, but under exposure to additional conditions, known as infection-facilitating factors, their character changes from saprophytic to pathogenic. Therefore, CoNS are responsible for various infections of different localizations, manifestations or courses. This review article showed that CoNS are widely present in laryngological diseases. Their presence in clinical materials originating from laryngological patients presents a new challenge for both clinicians and microbiologists; showing these bacteria in new light. Known in the past as “skin staphylococci”, CoNS were interpreted as accompanying bacteria or contamination in diagnostic samples. Today, based on recent reports from advanced microbiological laboratories using molecular diagnostic methods, it is known that CoNS are severe pathogens and require increased infection prevention programs with hygiene discipline in hospitals. Moreover, improved didactic programs are needed to better understand the role of CoNS in laryngological diseases with the primary aim of reducing the number of staphylococcal infections in patients.

Availability of data and materials


Arginine catabolic mobile element

Accessory gene regulator

Acute rhinosinusitis

Coagulase-negative staphylococci

Coagulase-positive staphylococci

Chronic rhinosinusitis

Functional endoscopic sinus surgery

Insertion sequence

Membrane-damaging toxins from coagulase-negative staphylococci

Next-Generation Sequencing

Prosthetic joint infection

Recurrent tonsillitis

Staphylococcal accessory regulator

Skull base osteomyelitis

Staphylococcal scalded skin syndrome


Temporomandibular joint

Toxic shock syndrome toxin-1


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Negative coagulase

Coagulase negative staphylococci

HomeTopics A–ZCoagulase negative staphylococci

Author: Dr Linda Chan, Senior Resident Medical Officer, Department of Dermatology, Concord General Repatriation Hospital, Sydney, Australia. DermNet New Zealand Editor in Chief: Hon A/Prof Amanda Oakley, Dermatologist, Hamilton, New Zealand. Copy Editor: Gus Mitchell. October 2017.

Coagulase negative staphylococci — codes and concepts

What are coagulase-negative staphylococci?

The human skin is the first line of defence between the body and the outside world. As a result, the skin is physiologically colonised by a host of microorganisms, including at least 47 species of coagulase-negative staphylococci [1]. Coagulase-negative staphylococci are gram-positive, aerobicorganisms distinguished from the closely related Staphylococcus aureus by the group's inability to form coagulase, an enzyme that promotes thrombus formation via the conversion of fibrinogen into fibrin [2]. They were first identified by the microbiologists Louis Pasteur and Alexander Ogston in the 1880s [1]. 

Coagulase-negative staphylococci are an important part of normal skin microbiota, and they also colonise mucous membranes in adults and children from a few weeks of age [1]. Staphylococci prefer humid areas and are therefore commonly found in the axillae, gluteal, and inguinal regions as well as anteriornares and the conjunctiva [3]. 

Below is a list of common coagulase-negative staphylococcal species and their preferred sites of colonisation. 

  • S. epidermidis tends to occur in the axillae, groin, perineum, toe webs, anterior nares, and conjunctiva.
  • S. haemolyticus and S. hominis both occur in the axillae and pubic areas high in apocrineglands.
  • S. capitis tends to surround the sebaceous glands on the forehead and scalp following puberty.
  • S. lugdunensis occurs in the axillae, pelvis and perineum regions, groin & lower extremities.

Until two decades ago, coagulase-negative staphylococci were commonly perceived as contaminants in clinical specimens. Now, with the increasing use of implanted medical equipment, they have become leading pathogens for nosocomialinfections owing to their ability to form biofilms on foreign material [1,2]. The S. epidermidis group of coagulase-negative staphylococci are of particular importance.

    • There are between 10 and 24 strains of S. epidermidis on healthy adult skin.
    • This group comprises predominantly of S. epidermidis, S. haemolyticus, S. capitis, S. hominis, S. simulans and S. warneri [1].  
    • S. epidermidis accounts for > 50% of staphylococci isolated from human skin and > 75% of coagulase-negative staphylococci in all clinical specimens [2].
    • Collectively, S. epidermidis and S. haemolyticus account for the majority of foreign body and premature neonatal infections due to coagulase-negative staphylococci [1]. 
Skin conditions associated with staphylococci

Coagulase-negative staphylococcal skin conditions 


S. epidermidis can induce miliaria, a disorder characterised by the retention of sweat within the eccrine glands. Skin biopsies have shown that periodic acid–Schiff (PAS)–positive material tends to block the upper eccrine sweat ducts. Miliaria is associated with:

  • Overgrowth of commensalbacteria, especially coagulase-negative staphylococci
  • An occlusive environment (occlusive dressings and thermal stimulation) 
  • S. epidermidis strains that produce PAS-positive extracellular polysaccharide substances (EPS) [4].

Miliaria is not associated with non-EPS producing strains of S. epidermidis or another coagulase-negative staphylococcus, such as S. haemolyticus and S. hominis. Of note, up to 62% of S. epidermidis strains on the forehead and back produce EPS [4,5].

Occluded sweat ducts may also lead to hyperhidrosis and anhidrosis, which may occur in chronicdermatoses such as psoriasis, atopicdermatitis and systemic sclerosis [5].

Atopic dermatitis

Coagulase-negative staphylococci are implicated in the 'double-hit' phenomenon, a theory used to explain the cause of atopic dermatitis. The abnormal stratum corneum (skin surface) is attributed to the combined effects of an abnormal FLGgene and an unknown environmental trigger. The specific environmental trigger may be subclinical miliaria, as PAS-positive material has been discovered in the eccrine ducts of patients with atopic dermatitis. The PAS-positive material may arise from S aureus and EPS–producing strains of S. epidermidis. Rather than causing the usual miliaria lesions, in patients with a FLG defect, occlusion of the eccrine ducts may trigger a flare of atopic dermatitis by activating the innate immune system [3].  

In the study described above, all skin samples from patients with atopic dermatitis contained drug-resistant staphylococci. S. aureus accounted for 42% and S. epidermidis in 20%, and all were positive for EPS and biofilms [3].

Competing against pathogens

Coagulase-negative staphylococci are competitors against S. aureus, a common pathogen, on the surface of normal skin. All organisms use quorum–sensing systems in which virulence factors are only expressed in a dense population of bacteria that is adapting to a changing environment. The quorum-sensing system for staphylococci is known as the accessory gene regulator (agr) system. Each staphylococcal subspecies has pheromones that can block the agr system of foreign species.

  • S. epidermidis produces a pheromone that inhibits the agr response in three subgroups of S. aureus; therefore, inhibiting the expression of many virulence factors [6].
  • It is also thought that the serine protease produced by S. epidermidis destroys any biofilm formed by S. aureus [7].  

Skin samples from patients with atopic dermatitis patients are colonised with greater proportion of S. aureus than healthy controls, which are colonised with S. epidermidis [3]. Skin colonisation by S. epidermidis may confer protection against atopic dermatitis, particularly in patients with the FLG gene defect. 

Who gets coagulase-negative staphylococcal infections?

Despite their abundance on the skin, coagulase-negative staphylococci rarely cause disease in intact skin. The main risk factor for coagulase-negative staphylococcal infection is a medical implant on which the organism can colonise, proliferate, and gain access to the systemic circulation [1,2,8].

Specific risk factors for coagulase-negative staphylococcal infection are:

  • Prosthetic heart valves (metallic and porcelain), pacemakers, defibrillators, cardiac stents and prosthetic joints [2]
  • Neutropenic, systemic immunosuppressive therapy [1,2]
  • Intravascular devices, such as central venouscatheters, peripherally inserted central venous catheters and arterial lines, which are associated with up to 40% of nosocomial bloodstream infections [1,9].  
  • Orthopaedic implants — risks include previous joint surgery, prolonged surgery, concurrent infection at the time of implant, and rheumatoid arthritis [8]
  • Prematurity, very low birth weight (< 1500 g at birth), and the use of umbilical or central catheters in neonates (accounting for 31% of all neonatal intensive care infections in the United States) [1].

What are the symptoms and signs of coagulase-negative staphylococcal infections?

Clinical signs such as fever, hypotension and leukocytosis are helpful in differentiating between true infections from coagulase-negative staphylococcal contamination [2].

Certain microbiological findings can support a diagnosis of infection, as opposed to contamination.

  • Incubation time to a positive culture occurs in ≤ 25 hours [8].
  • Growth occurs in both aerobic and anaerobic culture bottles [2,10].
  • There are ≥ two positive cultures with identical species. If there are two isolates with different genetic makeup, contamination is likely [2,10].
  • Positive results appear more quickly from blood drawn from a suspected catheter than from a peripheral blood sample. A ≥ 2–hour difference in positivity is considered a sensitive and specific marker of catheter-associated bacteraemia [8].

How are coagulase-negative staphylococci identified and infection diagnosed?

Coagulase-negative staphylococci are identified in the laboratory.

  • Clinical specimens are first cultured on non–selective blood agar plates and an enrichment broth.
  • The organism group is then identified via examining morphology, physiological testing results and antibiotic susceptibility [1].
  • Clonal diversity among coagulase-negative staphylococci is discerned through multilocus sequence typing (MLST) of housekeeping genes and whole-genome sequencing with 70–90% accuracy in identifying specific staphylococcal species [1,2].

Surgical site infections

Coagulase-negative staphylococci are more often cultured from superficial incisionalwounds than from deeper wounds. A diagnosis is obtained by finding they are the predominant microorganisms or by repeated isolation of the same organism in serial cultures [9].


Two sets of blood cultures should be obtained in a patient with fever and signs of bacteraemia [8].  If the patient has an indwelling central catheter, one of the blood cultures should be collected through the catheter [10].

Intravascular device infection

Diagnosis is achieved by a positive culture of the catheter tip, which is considered the gold standard [10].

Prosthetic vascular graft infections

Prosthetic vascular graft infection is most commonly associated with grafts distal to the inguinal region (1–6%). Infection can occur within 30 days of grafting, but more commonly occurs months to years later. It is diagnosed by physical examination and imaging, which shows sinus tracts or pseudo-aneurysms (pockets of blood in the bloodstream) at the site of vascular anastomosis (a connection between blood vessels) [8].

Prosthetic valve endocarditis

Endocarditis is due to S. epidermidis in 15–40% cases. Diagnosis is achieved via repeated positive blood cultures with suggestive transthoracic echo findings (80% will have valve dysfunction and intracardiac abscess), usually > 12 months after valve placement.

Native valve endocarditis

This form of endocarditis is rarely caused by coagulase-negative staphylococci, occurring in only 8% of cases of endocarditis. It is due to haematogenous seeding of previously damaged or malformed heart valves and endocardium [8].

Cardiac pacemaker infection

Coagulase-negative staphylococcus, predominantly S. epidermidis, is the culprit pathogen in 25% of pacemaker infections. About 25% of infections occur within 1–2 months of insertion of the device, due to inoculation at the time of placement of the device. Symptoms include inflammation at the pacer pocket site, systemic bacteraemia, and right-sided endocarditis.

Diagnosis is achieved via culture of the generator pocket and of the device itself, or by multiple positive sequential blood cultures with the same strain of bacteria [8]. 

Orthopaedic prosthetic device infections

Coagulase-negative staphylococci are usually are inoculated at the time of surgery, but remain indolent and is only present between 3 months and two years later. S. epidermidis is the main pathogen in these infections with a few cases being caused by S. lugdunensis.

Diagnosis is determined through reports of unexplained joint pain together with a high erythrocyte sedimentation rate, positive bone scan findings and culture of the prosthesis. There can be culture-negative prosthetic joint infections, which manifest as aseptic joint loosening [8].

Central nervous system shunt infections

Coagulase-negative staphylococci are responsible for more than 50% of central nervous system shunt infections. Risk factors are:

  • Age < 6 months
  • Reinsertion of shunt
  • Lack of experience of the surgeon 
  • A lengthy operation. 

Symptoms include unexplained fevers within two months of shunt placement or shunt dysfunction. Definitive diagnosis is determined through positive culture from cerebrospinal fluid drawn from the shunt or ventricles, or positive culture of the shunt [8].

How do coagulase-negative staphylococci cause systemic infection?

Coagulase-negative staphylococci gain entry through breached skin surfaces, commonly during medical or nursing procedures. The key mechanism is the ability of the bacteria to form biofilms on the surfaces of implanted medical equipment, where the bacteria replicate and disseminate within the systemic circulation [9].

The key steps are:

  1. Coagulase-negative staphylococci bind to the biotic surface (the host tissue) or abiotic surface (the medical device), coating it with adhesins (bacterialappendages that attach to the skin surface).
  2. The bacteria multiply and adhere to each other in multi-layered cell aggregates via the production of cell-wall-anchored proteins and surface-associated proteins, forming a biofilm.  
  3. The biofilm's polysaccharide intercellularadhesion (PIA) helps it to gradually mature into a complex, multi-layered structure with fluid-filled channels ensuring all layers have sufficient nutrients for growth. It is tolerant to antibiotics and can evade host defences, such as phagocytosis [1,8].
  4. Single cells or groups of cells dissociate from the biofilm and disseminate to other sites via the bloodstream to start colonisation and new biofilm formation [1,8,9].

What is the treatment for the coagulase-negative staphylococcal infection?

When treating coagulase-negative staphylococcal infections, the clinician should consider the:

  • Site of infection
  • Host's immune status
  • Presence of indwelling medical equipment [1].

The mainstay of treatment is appropriate systemic antibiotic therapy and removal of the culprit implant [8].

Approximately 90% of infections are resistant to penicillin. Vancomycin is the drug of choice. If the organism is confirmed to be susceptible to methicillin, vancomycin can be replaced by lactamase–resistant penicillin or a first– or second-generation cephalosporin. Newer antibiotics with activity against coagulase-negative staphylococci are daptomycin, linezolid, clindamycin, telavancin, tedizolid and dalbavancin [1,9]. Gentamicin or rifampicin can be added for deep-seated infections.

The duration of treatment depends on the site of infection. (Detailed information on the duration of treatment can be found in guidelines published by the Infectious Diseases Society of America).

  • Isolated bacteraemia with no visceral involvement:  > 7–14 days [9]
  • Intravascular catheter infection if the offending intravascular catheter is removed, seven days [8]
  • Cardiac pacemaker infection: remove the device and give 4–6 weeks of intravenous antibiotics [8]
  • Central nervous system infection: remove the shunt, drain the ventricles, and give intravenous and intraventricular vancomycin and gentamicin plus oral rifampicin; the new shunt should be inserted after the cerebrospinal fluid has been sterilised
  • Prosthetic joint infections — this involves a two-stage replacement procedure with 99% success rate:
    • Stage 1: resection of the involved prosthesis and affected tissues with six weeks of antibiotic therapy
    • Stage 2: New joint re-implantation after antibiotic treatment [8].

Other treatments

Due to the correlation between mucosa colonisation and subsequent bacteraemia, treatment can be given to decrease mucosal colonisation with coagulase-negative staphylococci. One suggested the approach is topicalmupirocin for nasal decolonisation and an oral glycopeptide, such as ramoplanin, for intestinal decolonisation [11].

What is the outcome of coagulase-negative staphylococcal infection?

Coagulase-negative staphylococcal bacteraemia is a serious medical condition associated with significant morbidity and mortality.

  • Septic shock has been reported in 22% of patients, with a mortality rate of 37%.
  • Approximately 50% of deaths in patients with septic shock are secondary to coagulase-negative staphylococcal bacteraemia [10].
  • Coagulase-negative staphylococcal cardiac pacemaker infection also has a high mortality rate of up to 66% [8].
  • Coagulase-negative staphylococcal prosthetic valve endocarditis has a mortality of 24–36% [8,10].
  • Although neonatal coagulase-negative infections carry relatively low mortality at 0.3–1.6%, these infections are associated with morbidity and prolonged hospital stays [8].
  • Prosthetic graft infections carry a 17% mortality and 40% morbidity, usually from amputation. The mortality rate for aortic grafts is around 50% [8].

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Related information



  1. Becker K, Heilmann C, Peters G. Coagulase–negative staphylococci. Clin. Microbiol. Rev. 2014; 27: 870–926. Journal 
  2. Tufariello JM, Lowy F. Infection due to coagulase-negative staphylococci: Epidemiology, microbiology, and pathogenesis. UpToDate. Updated 30 September 2015. Available at: (accessed July 2017).
  3. Allen HB, Vaze ND, Choi C, Leyden JJ. The presence and impact of biofilm-producing staphylococci in atopic dermatitis. J Am Acad Dermatol 2014: 150: 260–5. DOI: 10.1001/jamadermatol.2013.8627. Journal
  4. Mowad CM, McGiley KJ, Foglia A et al. The role of extracellular polysaccharide substance produced by Staphylococcus epidermidis in miliaria. J Am Acad Dermatol 1995; 33: 729–33. PubMed
  5. Wenzel F, Horn T. Non–neoplastic disorders of the eccrine glands. JAAD 1998; 38: 1–17. PubMed
  6. Otto M, Echner H, Voelter W, Götz F. Pheromone cross–inhibition between Staphylococcus aureus and Staphylococcus epidermidis. Infect Immun. 2001 March 69: 1957–60. DOI: 10.1128/IAI.69.3.1957-1960.2001. Journal
  7. Iwase T 1, Uehara Y, Shinji H et al. Staphylococcus epidermidis Esp inhibits Staphylococcus aureus biofilm formation and nasal colonization. Nature 2010: 465(7296): 346–9. DOI: 10.1038/nature09074. PubMed
  8. Rogers K, Fey P & Rupp M. Coagulase–Negative Staphylococcal Infections. Infectious Disease Clinics of North America, 2009; 23(1): 73–98. DOI: 10.1016/j.idc.2008.10.001. PubMed
  9. Tufariello JM, Lowy F. Clinical manifestations of infection due to coagulase–negative staphylococci. UptoDate. Updated 11 April 2017. 
  10. Rupp M & Archer G. Coagulase–Negative Staphylococci: Pathogens Associated with Medical Progress. Clinical Infectious Diseases 1994; 19(2): 231–243. PubMed
  11. Costa SF, Miceli MH & Anaissie, EJ. Mucosa or skin as source of coagulase–negative staphylococcal bacteraemia? The Lancet Infectious Diseases, 2004; 4(5): 278–86. DOI: 10.1016/S1473-3099(04)01003-5. PubMed

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Microbiology: Coagulase Test

OVERVIEW: What every clinician needs to know

Pathogen name and classification

There are more than 45 recognized species of coagulase-negative staphylococci (CoNS). CoNS are gram-positive cocci that divide in irregular “grape-like” clusters and are differentiated from S. aureus by their inability to produce coagulase and coagulate rabbit plasma. Species of CoNS that have important traits and are more frequently associated with clinical disease are S. epidermidis (biomaterial-based and prosthetic device infections), S. lugdunensis (skin and soft-tissue infections, bacteremia, endocarditis), S. saprophyticus (uncomplicated urinary tract infections in sexually active women), and S. haemolyticus (often less-susceptible to vancomycin).

What is the best treatment?

  • Vancomycin is generally the cornerstone for treatment of infections due to S. epidermidis and other CoNS, because 80-90% of strains responsible for nosocomial infections are resistant to semi-synthetic, penicillinase-stable penicillins, such as oxacillin and nafcillin. Dosing of vancomycin is based on actual weight and renal function. The benefit of higher-dose vancomycin (trough levels of 15-20 ug/mL) is not well-defined for CoNS infections and may lead to increased risk of nephrotoxicity. Many clinicians add rifampin (600 mg/day) to regimens containing vancomycin when treating a biomaterial-based infection (prosthetic joint infection, prosthetic valve endocarditis, etc.).

  • A characteristic of CoNS infections involving medical devices (intravascular catheters, vascular grafts, prosthetic joints, CSF shunts, etc.) is the presence of biofilm and “persister” cells. Biofilm-associated CoNS are generally much less susceptible to antibiotics than planktonic cells, and, oftentimes, effective therapy of biomaterial-based infections requires removal of the device.

    Continue Reading

  • CoNS responsible for nosocomial infections are almost always resistant to multiple classes of antimicrobial agents.

    Approximately 95% of strains of S. epidermidis isolated from well-defined healthcare-associated infections are resistant to penicillins due to production of beta-lactamase. Most strains are also resistant to methicillin due to mecA-mediated production of PBP2A. Further complicating the picture is the fact that phenotypic expression of methicillin resistance is much more heterotypic than observed in S. aureus. In addition, resistance to other classes of antibiotics is common, including resistance to fluoroquinolones, macrolides, lincosamides, and trimethroprim-sulfamethoxazole.

    To detect heterotypic oxacillin-resistance in CoNS, the MIC breakpoint is lower for CoNS (except S. lugdunensis) than S. aureus (0.5 ug/mL versus 4 ug/mL, respectively). Commercial assays are available for detection of mecA or PBP2A. The commercially available automated identification and susceptibility testing systems (e.g., MicroScan, Vitek, etc.) perform adequately in defining susceptibility to other classes of antibiotics.

    Fortunately, several newer antibiotics have been introduced that have activity against multiple-resistant CoNS. These newer antibiotics include linezolid, daptomycin, tigecycline quinupristin-dalfopristin, televancin, and ceftaroline.

How do patients contract this infection, and how do I prevent spread to other patients?

  • Epidemiology

    CoNS are commensal flora of the human skin and mucous membranes and rarely cause primary disease. Their pathogenic potential resides in their ability to colonize biomaterials and cause medical device infections. CoNS, largely S. epidermidis, are the leading cause of nosocomial bloodstream infections and are responsible for approximately 30% of these infections, which are chiefly due to intravascular catheters. Similarly, CoNS are a leading cause of various other device-associated infections, including vascular grafts, cerebro-spinal fluid (CSF) shunts, prosthetic joints, and artificial heart valves. As the use of such devices has increased in developed countries, the incidence of infection due to CoNS has increased in tandem.

    Pulse field gel electrophoresis (PFGE) is generally regarded as the best test to address questions of short-term molecular epidemiology. There is great diversity in pulse-field patterns. Finding indistinguishable PFGE patterns in the context of an outbreak or in complex clinical situations is a reliable indicator of clonality. Longer-term population analysis is better addressed by multi-locus sequence typing (MLST).

  • Infection control issues

    CoNS are ubiquitously present on human skin and lack the intrinsic virulence of S. aureus. Standard infection control measures (hand hygiene, routine environmental cleaning and disinfection) are adequate.

    Prevention of infection due to CoNS becomes more relevant in the setting of surgical implantation of prosthetic medical devices and insertion and care of intravascular catheters. Central venous catheters should be inserted using full sterile barrier precautions following disinfection of the skin with chlorhexidine. Catheter insertion and maintenance can be successfully introduced using a “bundle” approach. In the operating room, when a prosthetic device is to be placed, great care should be exercised in preparing the skin at the operative site with emphasis placed on adequate disinfection of the skin and removal of hair, if necessary, through use of surgical clippers. Many surgeons elect to use vancomycin as a prophylactic antibiotic when placing a prosthetic device in which contamination and infection due to CoNS is relevant (heart valve, prosthetic joint, vascular graft, etc).

    Although efforts to develop a vaccine against S epidermidis are in progress, there is currently no commercially available vaccine for CoNS.

What host factors protect against this infection?

  • The key immune system factor that protects against invasion by CoNS is intact skin and mucosal barriers and functional neutrophils.

  • Patients at higher risk of infection because of CoNS are those with intravascular catheters and prosthetic medical devices. In addition, neonates and neutropenic patients are at higher risk of infection. S. saprophyticus causes urinary tract infection in pre-menopausal, sexually active women. S. lugdunensis behaves more similarly to S. aureus than other CoNS and can cause invasive infection in normal hosts.

  • Histopathology of CoNS biomaterial-associated infections often reveals evidence of acute and chronic inflammation, as well as foreign body reaction (multi-nucleated giant cells). In animal models of antibiotic treated CoNS biomaterial-associated infection, organisms are often cleared from the immediate interface between the device and tissue but persist in the peri-implant tissues. In addition, viable organisms are often recovered from the biofilm that is a hallmark of CoNS biomaterial-based infections.

What are the clinical manifestations of infection with this organism?

S. epidermidis is most commonly associated with medical device infections. Infections are often indolent and may be clinically difficult to define. Differentiating culture contamination from true infection may be challenging.

Intravascular Catheter Infections: CoNS, usually S. epidermidis, are the most common cause of intravascular catheter infections. Although patients with infected intravascular catheters may present with signs of sepsis (bacteremia, hypotension, etc.), the catheter site itself usually appears innocuous. Occasionally, there are local signs of inflammation or purulent drainage at the catheter site. In general, short-term, non-tunneled, central venous catheters (CVCs) infected with CoNS should be removed. In patients with infected long-term CVCs who do not have signs of severe sepsis, it is reasonable to attempt treatment with the catheter in-situ.

Prosthetic Valve Endocarditis (PVE): CoNS cause 15-40% of cases of PVE. Patients may present acutely or in an amore indolent fashion. Clinical manifestations include fever and evidence of valve dysfunction. The diagnosis is confirmed by documenting persistently positive blood cultures and finding evidence of endocarditis via transesophageal echocardiogram. Surgery is almost always required, and antibiotic treatment usually consists of a combination of vancomycin and rifampin, often with gentamicin for the first 2 weeks.

Pacemaker Infection: CoNS account for 50-60% of pacemaker endocarditis. Patients generally present with evidence of inflammation at the generator pocket site along with positive blood cultures. Transesophageal echocardiography is recommended for all patients with suspected pacemaker infection, and successful treatment usually requires complete removal of the device.

Vascular Graft Infection: 20-30% of vascular graft infections are caused by CoNS. Infections usually present in an indolent fashion over weeks to months with a false aneurysm, fistula, or sinus track at the graft site. Blood cultures may be negative, because the infection may not extend into the graft lumen. Surgery is needed for cure and prolonged antibiotic therapy is often employed.

Orthopedic Infections: CoNS cause 30-45% of prosthetic joint infections. Although it is believed that most of these infections stem from contamination of the device at the time of implantation, the presentation of infection may be delayed for months or years. Joint pain is usually the only symptom, and fever or other systemic signs or symptoms are rare. The diagnosis is supported by finding elevated inflammatory markers (erythrocyte sedimentation rate, C-reactive protein). Cure is best assured with a two-step exchange procedure and 6-8 weeks of antibiotic therapy.

Cerebrospinal Fluid Shunt Infections: CoNS cause approximately one-half of infections of CSF shunts. Signs and symptoms of CSF shunt infection usually develop within 2-3 months of shunt implantation and consist of local signs of inflammation, as well as fever, nausea, vomiting, shunt malfunction, and increased intracranial pressure. The diagnosis is confirmed by recovery of CoNS from CSF obtained from the shunt. As is true of most prosthetic device infections, surgical removal is generally required and antibiotic treatment with agents active against methicillin-resistant strains is employed. In the case of CSF shunt infections, vancomycin and gentamicin are often given intraventricularly and rifampin is administered orally.

Peritoneal Dialysis Catheter-Associated Peritonitis: CoNS account for 25-50% of peritoneal dialysis-associated peritonitis. Manifestations of infection include abdominal pain and tenderness, fever, nausea, and vomiting. Unlike other prosthetic device infections, peritoneal catheter-associated peritonitis can often be successfully treated with antibiotics in the dialysate fluid without removal of the catheter. Recalcitrant peritonitis is, however, an indication for catheter removal.

Other common CoNS prosthetic device infections:

  • Endophthalmitis following intraocular lens implantation

  • Breast implant infection

  • Penile prosthesis infection

  • Left-ventricular assist device and other cardiac device infections

  • Orthopedic hardware and fracture fixation device infection

  • Surgical mesh infection

Infections due to S. lugdunensis present in an acute fashion similar to infections due to S. aureus. Common infections include skin and soft tissue infection (e.g., cellulitis, furunculosis) and native valve endocarditis.

S. saprophyticus is a common cause of urinary tract infection in pre-menopausal women and presents with typical signs and symptoms, such as urgency, frequency, dysuria, and pelvic discomfort. Pyuria and hematuria are common. For unknown reasons, S. saprophyticus urinary tract infection has a late summer and fall seasonal predilection and often follows sexual intercourse or menstruation.

What common complications are associated with infection with this pathogen?

  • Complications of infection due to CoNS are usually due to direct extension of infection in peri-medical device tissues and/or device malfunction. For example, as CoNS prosthetic valve endocarditis progresses, valvular dysfunction, heart failure, and cardiac conduction abnormalities develop. Because CoNS do not produce exotoxins or other pro-inflammatory compounds (as does S. aureus), rarely do patients develop overt signs of severe sepsis or septic shock, even with endovascular infections associated with high-grade bacteremia. Rarely, patients exhibit immunologic phenomena associated with chronic bacteremia; immune complex deposition in the kidneys causes shunt nephritis. More specific information regarding complications can be found in sections addressing specific organ system infection topics.

How should I identify the organism?

CoNS are gram-positive cocci that divide in “grape-like” clusters and are catalase-positive. CoNS are readily recovered from biologic specimens with use of commercially-available automated blood culture systems or standard solid or broth media (sheep blood agar, Mueller-Hinton, brain-heart-infusion, trypticase soy, etc).

Because of the number of biochemical tests needed, it is difficult to routinely identify all of the CoNS to species level. However, the majority of systems used in modern clinical microbiology laboratories can accurately identify those species most commonly associated with clinical disease, S. epidermidis, S haemolyticus, and S sapophyticus. A method to rapidly identify S. lugdunensis from other CoNS involves documenting a positive L-pyrrolidonyl-beta-naphyhylamide (PYR) test and ornithine decarboxylase test. Molecular methods that identify CoNS to the species level have been developed based on phylogenetic analysis of several conserved DNA sequences.

The recovery of CoNS from biofilms and biomaterial-based infections has been enhanced by sonication of devices and PCR protocols. However, because CoNS are normal commensal organisms of the skin and mucous membranes, detecting low numbers of CoNS by polymerase chain reaction (PCR) from surgically removed devices and peri-device aspirates often raises the question of whether the finding is consistent with contamination or true infection.

In the situation of recovery of CoNS from blood cultures, the clinician is often faced with determining whether the culture result represents true infection or contamination. Factors that can assist in this determination include host situation (is the patient at higher risk of infection due to CoNS [neonate, neutropenic, presence of an intravascular prosthetic device, such as a cardiac valve, vascular graft, or ventral venous catheter?]); multiple positive blood cultures with the same strain of CoNS (same species, same phenotype – antibiogram or biotype – same genotype – indistinguishable PFGE pattern); culture positivity within 24 hours (indicative of larger numbers of organisms); and positive differential time to positivity test (DTP).

The DTP test is helpful in patients with a CVC and is predicated on the principle that a blood sample from an infected CVC will have a higher number of microbes present than an equal amount of blood obtained from the periphery. If the blood culture obtained from the periphery “turns positive” greater than 2 hours longer than blood obtained from the CVC, it is a reasonably sensitive and specific indicator of a CoNS CVC-associated infection.

How does this organism cause disease?

CoNS are able to cause disease because of two features: their natural niche on human skin, resulting in ready access to medical devices implanted or inserted across the skin, and their ability to adhere to biomaterials and to elaborate biofilm. S. epidermidis possesses genetic elements, such as Arginine Catabolic Mobile Element (ACME) that are important in its ability to thrive in the relatively dry and acidic conditions found on human skin. It produces antibiotics (e.g., epidemin, epilancin, epicidin) that may play a role in bacterial interference and successful persistence on the skin.

In contrast to S aureus that produces a large number adhesins, toxins, and factors to avoid host defense, CoNS possess relatively few defined virulence factors. The ability of S epidermidis to adhere to biomaterials and to form biofilm appears to be the most important virulence trait. Also, the ability to secrete poly-gamma-DL-glutamic acid (PGA) and phenol soluble modulins (PSM) appear to aid in the capacity to cause disease.

Adherence: Biomaterials placed within the human host are quickly coated with a “conditioning film” consisting of various host serum matrix proteins, such as fibrinogen, fibronectin, and elastin. S. epidermidis is able to bind directly to plastics because of action of autolysins and to interact with the conditioning film due to various adhesins.

Biofilm: CoNS growing in a biofilm are much less susceptible to antibiotics and are more resistant to host defense than unattached planktonic cells. In addition, it is thought that metabolically quiescent cells found in biofilms allow for tolerance to antibiotics and persistence of infection that is hallmark of a CoNS biomaterial-based infection. Extracellular DNA (eDNA) and polysaccharide intercellular adhesin (PIA) appear to be major functional components of S. epidermidis biofilm. In addition, alternative proteinaceous biofilm components, such as Accumulation-Associated Protein (AAP) and Biofilm-associated protein (Bap), have been described. S epidermidis produces PSMs under quorum-sensing global regulation and are important in the ability of the organisms to detach from the biofilm and disperse to other sites. Multiple species of CoNS produce PGA that appears to inhibit host defense and facilitate colonization of human skin.

WHAT’S THE EVIDENCE for specific management and treatment recommendations?

Daroucihe, RO. “Treatment of infections associated with surgical implants”. N Engl J Med. vol. 350. 2004. pp. 1422-9. (CoNS are a major cause of infection of surgical implants. This review article outlines principles of treatment and the need for surgical intervention.)

Fey, PD, Olson, ME. “Current concepts in biofilm formation of “. Future Microbiol. vol. 5. 2010. pp. 917-33. (This review article discusses current knowledge of S. epidermidis adherence, biofilm formation, and virulence.)

Hall, KK, Lyman, JA. “Updated review of blood culture contamination”. Clin Microbiol Rev. vol. 19. 2006. pp. 788-802. (Approximately 1-5% of blood cultures yield contaminants, and 70-80% of blood culture contaminants are CoNS. Hall and Lyman discuss the clinical significance of blood culture contamination, how to differentiate contamination from true infection, and how to prevent contamination.)

Lewis, K, Spoering, AL, Kaldalu, N, Keren, I, Shah, D, Pace, JL, Rupp, ME, Finch, RG. “Persisters: specialized cells responsible for biofilm tolerance”. Biofilms, infection, and antimicrobial therapy. 2006. pp. 241-56. (This source is a review of biofilm infections, antibiotic tolerance, and persister cells.)

Mermel, LA, Allon, M, Bouza, E. “Clinical practice guidelines for the diagnosis and management of intravascular catheter-related infection: 2009 update by the Infectious Diseases Society of America”. Clin Infect Dis. vol. 49. 2009. pp. 1-45. (CoNS are the most common cause of nosocomial bacteremia and intravascular catheter infections. In this evidence-based guideline from the Infectious Diseases Society of America [IDSA], the diagnosis and treatment of intravascular-catheter related infections due to CoNS are discussed.)

Raad, I, Hanna, HA, Alakech, B, Chatzinikolaou, I, Johnson, MM, Tarrand, J. “Differential time to positivity: a useful method for diagnosing catheter-related bloodstream infections”. Ann Intern Med. vol. 140. 2004. pp. 18-25. (The use of the differential-time-to-positivity test is put to the test in this study.)

Rogers, KL, Fey, PD, Rupp, ME. “Coagulase-negative Staphylococcal infections”. Infect Dis Clin N Am. vol. 23. 2009. pp. 73-98. (This is an overview of pathogenesis, clinical features, and treatment of infections due to CoNS.)

Sader, HS, Jones, RN. “Antimicrobial susceptibility of Gram-positive bacteria isolated from US medical centers”. Diagnos Microbiol Infect Dis. vol. 65. 2009. pp. 158-62. (This is a large surveillance study from 27 US medical centers testing 1153 strains of CoNS recovered from patients in 2007 and 2008. This study documents the multi-resistant phenotype common in isolates recovered from patients with healthcare-associated infections.)

Copyright © 2017, 2013 Decision Support in Medicine, LLC. All rights reserved.

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Coagulase-Negative Staph Infection


Coagulase-negative staphylococci (CoNS) are a type of staph bacteria that commonly live on a person’s skin. Doctors typically consider CoNS bacteria harmless when it remains outside the body. However, the bacteria can cause infections when present in large amounts, or when present in the bloodstream.

Doctors often divide staph bacteria into coagulase-positive and coagulase-negative types. Coagulase is an enzyme needed to make blood clot. This enzyme is present in Staphylococcus aureus (S. aureus) bacteria. Doctors typically associate this type with causing more serious infections.

Infection types

Several different types of CoNS bacteria fall within this category. Often, each bacteria type may cause a different infection. Examples of these types include the following:

S. epidermidis

This CoNS bacteria type commonly live on the skin and don’t usually cause infections. A person who has a condition that compromises the immune system, such as lupus, is more likely to experience this infection type. Higher risk is also seen in people who have a foreign body implant, such as:

This bacterium causes skin infections and fever. The skin may be red, swollen, and inflamed. Sometimes the skin may leak pus.

S. saprophyticus

This CoNS bacteria type can collect in the urinary tract and cause urinary tract infections (UTIs). Symptoms associated with UTIs include:

  • pain when urinating
  • fever
  • flank pain, or pain in the lower back that radiates to the stomach
  • blood-tinged urine

S. lugdunensis

This bacteria species can cause infectious endocarditis. This is a serious infection on the heart valves, which can affect heart function and vessels away from the heart. The infection itself closely resembles endocarditis caused by S. aureus.

Symptoms of endocarditis may include:

  • fever
  • chills
  • aching joints
  • shortness of breath
  • chest pain when breathing
  • a new-onset heart murmur

These aren’t the only CoNS bacteria types. Others include:

  • S. simulans
  • S. hominis
  • S. haemolyticus
  • S. warnerii

The CoNS bacteria tend to thrive in warm, moist environments. These include the:

  • armpits
  • feet
  • groin
  • behind the knees
  • in the crook of the elbow
  • in the folds of the stomach

What are the causes and risk factors of coagulase-negative staph?

According to a 2007 review, most CoNS infections are nosocomial. This means a person is exposed to the bacteria in a hospital. A person may have had surgery or an illness that required a stay in the hospital where CoNS bacteria outside the body got into the body.

For this reason, it’s important that healthcare providers practice excellent hand hygiene. It’s also vital they practice sterile techniques when inserting catheters, starting IVs, and performing surgery.

Those who are at greatest risk for CoNS infections include:

  • People with a compromised immune system. This includes people with cancer, older adults, the very young, or those who have an autoimmune disorder.
  • People with an indwelling urinary catheter.
  • People with a central IV line. An example is a peripherally inserted central catheter (PICC) line.
  • People who’ve undergone certain procedures. This includes people who’ve had joint replacement surgery, a cerebrospinal fluid shunt, or a pacemaker, ocular, or cosmetic implant.

The presence of these risk factors is why many orthopedic surgeons won’t perform a joint replacement surgery on someone who has a skin infection. They will wait until the infection has healed.

What are the treatment options?

Treating CoNS infections are traditionally difficult because many bacterial strains have become resistant to antibiotics. The medications doctors normally prescribe to kill the bacteria aren’t effective.

If a person has a CoNS infection, a doctor may perform what’s called a culture. They’ll take a sample of blood, tissue, body fluid, or all of these and send it to a laboratory.

Laboratory staff will then identify the infecting organism. They can do this in two different ways, using either the Kirby-Bauer antibiotic testing method or an automated system.

For the Kirby-Bauer method, a laboratory technician puts the bacteria into a special dish that has different types of antibiotics. For the automated method, a sample of bacteria is placed in a device that automatically exposes the bacteria to changing concentrations of antibiotic. For both methods, if the bacteria stops growing, a doctor can tell which antibiotic will kill the infection.

Smaller hospitals prefer the first method. Most academic centers prefer an automated system.

Doctors have been doing this for years. It’s given them a strong idea of the types of mediations that will kill different types of staph bacteria. This means doctors can start treating people as quickly as possible.

Doctors often initially prescribe a very strong antibiotic called vancomycin to treat CoNS infections. They usually give this medication through an IV. Then, based on the antibiotic data, they can choose a better antibiotic.

What are the possible complications and emergency symptoms?

If a person has a severe CoNS infection, they may experience a condition known as sepsis. This occurs when the immune system triggers an inflammatory response due to the side effects of fighting the infection.

Sepsis can result in low blood pressure, which affects the body’s ability to send blood to vital organs. A person can experience organ failure due to sepsis. This makes it a life-threatening illness.

Symptoms associated with severe infection and sepsis include:

  • fast heart rate
  • fever, which may occur with shivering
  • mental confusion
  • pain or discomfort at a surgical site or IV access site
  • problems breathing and shortness of breath
  • sweaty or clammy skin

Seek immediate emergency medical attention if you suspect you or a loved one has sepsis.

What’s the outlook for coagulase-negative staph?

When looking at all staph bacteria, CoNS bacteria tend to be less virulent. This means they cause fewer and less severe infections than other bacteria types. However, some people may experience severe infections related to these bacteria. This is especially the case for people with a compromised immune system.

Because CoNS infections are traditionally hard to treat, it’s important that a person see a doctor as early as possible. Early treatment will prevent the bacteria from continuing to multiply.


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