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Niemann, S.; , . Staphylococcus schweitzeri. Encyclopedia. Available online: (accessed on 21 June 2024).
Niemann S,  . Staphylococcus schweitzeri. Encyclopedia. Available at: Accessed June 21, 2024.
Niemann, Silke, . "Staphylococcus schweitzeri" Encyclopedia, (accessed June 21, 2024).
Niemann, S., & , . (2022, May 19). Staphylococcus schweitzeri. In Encyclopedia.
Niemann, Silke and . "Staphylococcus schweitzeri." Encyclopedia. Web. 19 May, 2022.
Staphylococcus schweitzeri

The Staphylococcus aureus-related complex is formed by the Staphylococcus aureusStaphylococcus schweitzeriStaphylococcus argenteusStaphylococcus roterodami and Staphylococcus singaporensis. Within this complex, S. schweitzeri is the only species mainly found in African wildlife, but it is rarely detected as a colonizer in humans or as a contaminant of fomites. The few detections in humans are most likely spillover events after contact with wildlife. However, since S. schweitzeri can be misidentified as S. aureus using culture-based routine techniques, it is likely that S. schweitzeri is under-reported in humans. The low number of isolates in humans, though, is consistent with the fact that the pathogen has typical animal adaptation characteristics (e.g., growth kinetics, lack of immune evasion cluster and antimicrobial resistance); however, evidence from selected in vitro assays (e.g., host cell invasion, cell activation, cytotoxicity) indicate that S. schweitzeri might be as virulent as S. aureus. In this case, contact with animals colonized with S. schweitzeri could constitute a risk for zoonotic infections. 

Staphylococcus schweitzeri Zoonosis One Health Africa

1. The S. aureus Complex

S. aureus, S. schweitzeri, S. argenteus, S. roterodami and S. singarporensis form the S. aureus complex [1][2][3][4]. The members of the S. aureus complex other than S. schweitzeri will be briefly introduced here.
S. aureus is a globally occurring human commensal, as well as a pathogen in humans and animals [5][6][7]. Infections caused by S. aureus are of particular concern due the virulence of the pathogen, as well as to the frequent occurrence of antimicrobial (multi) resistance [8]. Given the wealth of literature on S. aureus, any more detailed discussion here is precluded for the sake of the review format of this article.
S. argenteus was originally described as a community-acquired (CA) methicillin-resistant S. aureus (MRSA) lineage belonging to the clonal complex (CC) CC75. The first isolates were recovered from patients with CA-MRSA infections in Australian Aboriginal communities [9]. Subsequently, the complex was delineated as S. argenteus [2]. In the meantime, S. argenteus has been found worldwide, e.g., in Thailand, Japan, France, Belgium, Trinidad, Tobago and Africa, both in humans and animals; however this species seems to be predominantly associated with humans [1][10][11][12][13][14][15][16][17][18]S. argenteus and S. aureus differ in the amino acid sequence contained in peptidoglycan, while S. argenteus and S. schweitzeri possess the same peptidoglycan type [2]. At the molecular level, the nucleotide sequences of S. argenteus display 87.4% identity with S. aureus [19]. The pathogenicity of S. argenteus appears to be comparable to that of S. aureus, and 76.6% of the virulence genes of S. aureus have also been found in S. argenteus [19]. Some isolates also produce Panton–Valentine leukocidin (PVL) [9][20], a toxin associated with S. aureus isolates causing skin and soft tissue infections [21][22]. The absence of the pigment staphyloxanthin in S. argenteus results in the whitish color of the colonies [2][23]. Many S. argenteus isolates are penicillin-resistant [12], while other antibiotic resistances are less frequent; for instance, methicillin-resistance was found in isolates from Australia or Denmark [9][24].
S. roterodami was first described in 2021 by Schutte et al. [4]. This species was isolated from a human foot wound infection in the Netherlands. However, the patient probably became infected with S. roterodami in Bali after suffering an injury to his foot. There is only this one isolate described so far. The strain was originally identified as S. argenteus. Antimicrobial susceptibility was determined using the Vitek 2 susceptibility testing card for Gram-positive bacteria, and S. roterodami was found to be susceptible to all antibiotics tested. An analysis of cellular fatty acids showed several differences in fatty acid proportions compared to S. aureusS. argenteus and S. schweitzeri [4].
In 2021, S. singaporensis was described by Chew et al. following a retrospective clinical laboratory cohort study of non-S. aureus complex members in Singapore [3]. Six out of forty-three isolates stood out as genetically distinct from S. argenteusS. singaporensis was found in infectious diseases in humans, and the clinical features of these infections were similar to S. aureus infections. The isolates did not contain some of the virulence genes typically associated with S. aureus, i.e., staphylococcal enterotoxins, tst (toxic shock syndrome Toxin-1), or pvl (Panton–Valentine leukocidin). The S. singaporensis isolates did not reveal antibiotic resistance [3].

2. Pathogenicity

Although no clinical infections with S. schweitzeri have been detected yet, it has been shown in vitro that S. schweitzeri has many of the pathogenicity factors already known from S. aureus. Of 111 virulence genes of S. aureus examined, 86 (77.5%) were also found in S. schweitzeri. It has been discussed that the pan-genome of these bacteria contains all virulence genes necessary for the pathogenicity of S. aureus [19].
S. schweitzeri belongs to the coagulase-positive staphylococci and most isolates are able to coagulate human, rabbit, canine and equine plasma, but not porcine or avian plasma [25][26]. Capsular polysaccharides (CP) are virulence factors that can protect the pathogen to evade opsonophagocytic killing [27]. Many S. schweitzeri isolates contain the cap5 gene encoding for CP type 5, and only few contain genes encoding for CP type 8 [19][25]. In contrast, African S. aureus isolates from humans as well as from non-human primates were shown to contain the genes for CP5 and CP8, either equally distributed (non-human primates) or biased towards CP8 (humans) [28][29][30]. Many S. schweitzeri isolates are positive for the edinB (epidermal cell differentiation inhibitor) gene in combination with the exfoliative toxin D (etd) [25]. EDIN catalyze the inactivation of RhoA, a regulator of the host cell actin cytoskeleton, while ETD is a serine protease [31][32]. Other protease genes found in the genome of S. schweitzeri are sspA and sspP, but not aur or sspB [25].
The pathogen is capable of forming a biofilm in vitro [25]. Numerous virulence factors regulate biofilm formation such as the thermostable nuclease Nuc. The primary structures of Nuc from S. schweitzeri (NucM) and S. aureus (Nuc1) were found to be different (identity 78.1–80.4%, similarity 92.4–94.1%); however, the nuclease activities were identical, as well as the biofilm formation [25][33]. In experiments, the ability of S. schweitzeri to form biofilms was significantly lower than that of S. epidermidis, which may be related to the fact that the genome of S. schweitzeri harbors the genes icaC and icaD, which are important for biofilm formation, but neither bap nor icaA [25].
The S. schweitzeri genome can contain enterotoxin genes such as sebsegseh, sei, sel, sen and the toxic shock toxin (tst) gene. For alpha-toxin (Hla), a membrane-damaging toxin that can lead to cell permeability and induce cell necrosis, higher released Hla protein levels were detected in S. schweitzeri than in S. aureus [34]. Researchers demonstrated a cell-destructive efficacy of S. schweitzeri supernatant on A549 cells, a human alveolar epithelial cell line, and on Vero cells, a kidney epithelial cell line derived from an African green monkey, comparable to that of S. aureus [25]. This cytotoxic effect might also be attributable to alpha-toxin.
Traditionally, S. aureus has been considered a pyogenic extracellular pathogen, but S. aureus can also be taken up into host cells, such as epithelial and endothelial cells [35]. In this process, S. aureus binds to the α5β1-integrin of the host cell via a fibronectin bridge with the help of the fibronectin-binding proteins (FnBPs). This leads to integrin clustering, the initiation of intracellular signaling cascades, and finally reorganization of the actin cytoskeleton and S. aureus uptake into the host cell [36]. The adhesins FnBPA and FnBPB, which are important for the binding of S. aureus to fibronectin and thus also for uptake into host cells, are also present in S. schweitzeri. In line with this, S. schweitzeri can be taken up by epithelial cells in the same way as S. aureus [25]. The invasion of non-professional phagocytes is followed by the activation of the host cells, leading e.g., to an increase in cytokine production. In addition, many S. aureus isolates are able to translocate from the phagolysosomes into the cytoplasm, similarly to S. schweitzeri [25][37]. This phagolysosomal escape is a prerequisite for the bacteria to kill the host cells from the inside [38][39]. Escaping into the cytoplasm as well as intracellular cytotoxicity has also been shown for S. schweitzeri isolates [25]. In addition to the adhesins FnBPA and FnBPB, S. schweitzeri harbors genes for the adhesin clumping factors A and B (ClfA, ClfB), collagen-binding adhesin CNA, extracellular matrix binding protein Ebh, elastin binding protein Ebp, and the extracellular fibrinogen-binding protein Efb [19][25]. The absence of map (eap) in the genome of S. schweitzeri is striking. Interestingly, only fragments and not the complete map gene were detected in African S. aureus isolates [25][40].
During infection bacteria need iron which can be obtained from the blood. S. aureus uses a hemoglobin receptor, IsdB, to bind to hemoglobin and to steal iron-containing heme. IsdB from S. schweitzeri has only 77% similarity to S. aureus; however, it binds hemoglobin from primates with a similar pattern of species preference as S. aureus [41].
In summary, these results show that S. schweitzeri shares many virulence features with S. aureus.

3. Animal Adaption

While many S. schweitzeri characteristics suggest a possible transfer of the pathogen from animals to humans, the pathogen also shows characteristics that suggest an adaptation to its animal hosts. For instance, S. schweitzeri seems to grow better than S. aureus at 34 °C and 40 °C, which correspond to the respective body temperatures of bats and monkeys [25].
Adaptation to a new host such as humans would require S. schweitzeri to overcome the host’s immune defenses, such as T-cell-mediated immunity, the complement system, neutrophils, and phagocytes. In S. aureus, the acquisition and loss of mobile genetic elements (MGEs) often leads to host-specific adaptation. Sa3int phages, which are integrated into the hlb locus-encoding beta-hemolysin (Hlb), have a special role in this process. These phages carry the scnchp, and sak genes, encoding the human-specific immune evasion factors staphylococcal complement inhibitor, and chemotaxis inhibitory protein and plasminogen activator staphylokinase, respectively [42][43]. Up to 96% of human S. aureus nasal isolates carry the Sa3int phages; these isolates typically have a truncated hlb and are thus unable to produce Hlb as visible by the absence of double hemolytic zones [42]. The transfer of human-adapted isolates to livestock is accompanied by the loss of Sa3int phages. Monkey-adapted S. aureus also lack the immune evasion factors [44]. The same was shown for S. schweitzeri, and the hlb gene was found to be intact [25]. However, S. schweitzeri possesses in its genome the integrase groups φ1–3, indicating the presence of the prophages [19]. Whether S. schweitzeri can also integrate Sa3int phages has not yet been investigated.
The bi-component leukotoxin PVL is also phage-encoded. In sub-Saharan Africa, about half of the S. aureus isolates from humans are PVL-positive, whereas in Germany PVL is almost absent [40]. PVL has a high species specificity, targets the human C5a receptor, and therefore attacks only human neutrophils. It has no cytolytic effect, e.g., on Java monkey neutrophils [45]. It is therefore not surprising that PVL has not been found in S. schweitzeri yet [25]. In contrast, a leukocidin LukAB similar to that of S. aureus was also detected in S. schweitzeri. This has a similar high cytotoxic activity with respect to human dendritic cells compared to S. aureus, but the effect on human neutrophils, monocytes and macrophages is reduced [46].
Many bacteria have a defense system against foreign genes, since these can also harm the bacteria. The CRISPR-Cas (clustered regularly interspaced short palindromic repeats and the CRISPR-associated genes (Cas)) system can protect bacterial cells from the integration of foreign genes in their genome. So far, little is known about the role of CRISPR-Cas in S. aureus, and only a few S. aureus seem to bear this system [47]. For S. schweitzeri, this has not yet been investigated.
It has not yet been shown that S. schweitzeri can overcome the human immune system. This could also be the reason why the pathogen has, to date, almost only been detected in animals. So far, it is still questionable whether S. schweitzeri can acquire genes from S. aureus via horizontal gene transfer that allow it to adapt to humans


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