Staphylococcal carriage status: implications, mechanisms, and practical treatment guidelines

Atreyo Chakraborty

doi:10.4103/ijdd.ijdd_26_22

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Year : 2023 | Volume : 9 | Issue : 1 | Page : 1-4

Staphylococcal carriage status: implications, mechanisms, and practical treatment guidelines

Atreyo Chakraborty
Department of Dermatology Venereology and Leprosy, All India Institute of Medical Sciences, Rishikesh, India

Date of Submission	20-Oct-2022
Date of Acceptance	09-Dec-2022
Date of Web Publication	24-Aug-2023

Correspondence Address:
Atreyo Chakraborty
Department of Dermatology Venereology and Leprosy, All India Institute of Medical Sciences, 26 C Selimpore Lane, Rishikesh, Dhakuria, Kolkata 700031
India

Source of Support: None, Conflict of Interest: None

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DOI: 10.4103/ijdd.ijdd_26_22

Abstract

Staphylococcal carriage status is very common, and it is important for the dermatologist to be aware of its clinical manifestations, the mechanisms by which they produce colonization, and the therapeutic options available to eliminate them.

Keywords: Carriage elimination, mupirocin, skin and soft tissue infection, staphylococcus carriage

How to cite this article:
Chakraborty A. Staphylococcal carriage status: implications, mechanisms, and practical treatment guidelines. Indian J Drugs Dermatol 2023;9:1-4

How to cite this URL:
Chakraborty A. Staphylococcal carriage status: implications, mechanisms, and practical treatment guidelines. Indian J Drugs Dermatol [serial online] 2023 [cited 2023 Sep 23];9:1-4. Available from: https://www.ijdd.in/text.asp?2023/9/1/1/384289

Introduction

Staphylococcus aureus is an important commensal of the human skin and an important constituent of the cutaneous microbiome. While it has been implicated in a number of conditions such as recurrent furunculosis, abscesses, staphylococcal scalded skin syndrome, and so on, it remains dormant in a large number of populations viz hospital workers, sanitation workers, the immunocompromised and so on. When they greatly exceed their presence in the normal skin, they often cause symptoms.

Factors Allowing Staph Aureus to Adapt to the Skin Microbiota

By adapting itself to the local skin milieu, Staph aureus has become a successful member of the cutaneous microbiota.^[1],[2] However, for any bacterium (note: the singular of bacteria is bacterium) to successfully adapt to host conditions, the following conditions, must be fulfilled:

A. Staph aureus possesses a multitude of virulence factors for example ET A, B, and many more that allow it to quickly lyze the cell and cause havoc to the immune system. However, if such virulence was allowed to continue, Staph aureus would have been quickly detected by the host immune response and destroyed. Hence, to avoid detection, Staph aureus tightly downregulates its virulence during its stay as commensal.

B. It develops an adhesion mechanism. There is evidence that adhesion to cell membranes is tighter in Staph aureus colonizing the skin than in pathogenic virulent ones. The tighter adherence ensures it is not rubbed off the skin regularly during washing/itching.

C. In a similar way, gene products that enhance colonization such as defense against reactive oxygen species (remember nose is exposed to a lot of oxygen), evasion of the immune response, and so on are upregulated.

Colonization Risk Factors

There are many risk factors postulated for Staphylococcal carriage status and these include living in a hot and humid environment, healthcare occupation, having anemia or other hematological deficiencies, and metabolic diseases such as diabetes, gout, and blood dyscrasias.

Colonization Sites

Various sites have been reported to have been colonized by Staph aureus and they include:^[3],[4] the squamous epithelium on the nasal septum adjacent to the nasal ostium, axillae (8%), chest and abdomen (15%), the perineum (22%), the intestines (17–33%), vagina (5%) and the pharyngeal wall (4–64%).^[3],[4]

Types of Carriage

Based on the methods of sampling, three types of carriage have been detected: persistent, intermittent, and noncarriage.^[4]

Persistent is defined as two or more cultures performed at 1 week apart and both are positive. Intermittent is defined as only one out of two cultures performed at 1 week apart and is positive. When both cultures are negative it is termed as noncarriage. It is well known that persistent carriers have a higher bacterial load than nonpersistent carriers.

Duration of Carriage

The duration of carriage is 4–14 days postinoculation for intermittent and noncarriers whereas it is on average 154 days for persistent carriers.^[5]

Determinants of Bacterial Carriage

There are many factors both from the host site and from the bacteria side which determine whether successful bacterial colonization will occur or not. They are:

A. Bacterial determinants
- i) Expression of adhesion molecules sdr C. sdr D, sdr E. In general, the skin is exposed to a lot of rubbing and scrubbing which in a normal setting usually dislodges the bacteria. These adhesion molecules ensure tight adhesion to the cell membranes, particularly of the skin.
- ii) Clumping proteins clf A, clf B, fnb A, fnb B: They also help in the formation of clumping of RBCs around them to protect them from further attacks of leukocytes.
- iii) Biofilm formation by binding of clf B to CK 8 and 10 on keratinocytes: This phenomenon is one of the most important strategies to evade the host immune response. A biofilm is a collection of bacterial slime, bacteria, and host keratinocyte sloughs which results in a tough membrane, restricting the access of antibiotics and host immune cells. In fact, biofilm formation is now implicated for many cases of emerging bacterial resistance.
- iv) Other bacterial flora: Corynebacteria on the nose and strep pneumonia significantly reduce Staph carriage.
- v) Quorum sensing: Staphylococcus can self-regulate their number on many occasions—if the number is too great, the cells signal to other cells to stop multiplying and in this way, the population is kept in check. This mechanism might explain why staphylococcus has been so successful in colonization our skin because any excess bacteria would be detected by the immune cells and rapidly killed.
B. Host determinants^[6]
- i) Toll-like receptor polymorphisms: Toll-like receptors (TLR) are a part of the natural immune system that is innate. Their signaling is mediated through protein receptors on the surface that look like lamp posts, hence the name Toll. They detect molecular patterns that are common to all pathogens and thereby mount an immune system in a nonspecific manner. There are around 20 types of Toll like receptor (TLR) discovered so far and each has specific functions—for example, TLR 2 works with gram-negative organisms and has been implicated in acne. TLR 4 deals with gram-positive organisms and their polymorphism means they do not work the same way in everyone—hence such polymorphism can enhance susceptibility to Staphylococcal carriage
- ii) Defensin and Cathlicidin polymorphism: They are natural antipathogenic molecules, which are reduced in some conditions such as atopic dermatitis. Their deficiency can account for increased staphylococcal carriage in these conditions as well as host carriage.
- iii) Mutations in glucocorticoid receptor genes: A 80% reduced carriage is seen with those with a particular mutation in Glucocorticoid receptors (GCR).
- iv) Reduced Vit D levels.
- v) Chronic Inflammation—viz atopic eczema.

The Risks of Staphylococcal Carriage Status

The carriage has been identified as an important risk factor for serious infections in these patients: Those undergoing surgery; those on hemodialysis or Continuous ambulatory peritoneal dialysis (CAPD); Those with HIV infection and AIDS; those with intravascular devices and those colonized with Methicillin-resistant Staphylococcus aureus (MRSA).^[7]

Elimination of carriage has been found to reduce the infection rates in surgical patients and those on hemodialysis and CAPD. Elimination of carriage appears to be an attractive preventive strategy in patients at risk.

A. Staphylococcal niche sites: These are the sites where staphylococcus is most often found and include:
- i) Nose: The anterior nares, at the junction where the bony nasal septum meets the mucosa.
- ii) Axillae.
- iii) Chest and abdomen, particularly periumbilical.
- iv) Perineum.
- v) Posterior pharyngeal mucosa.

How to Eliminate Staphylococcal Carriage

Various drugs or antiseptics have been in use for the elimination of staphylococcal carriage. They are summarized in the following [Table 1].^[8],[9],[10]

Table 1: Drug treatment of staphylococcal carriage

Click here to view

Guidelines for Staphyloccal Elimination Carriage

Indications of Staphylococcal carriage elimination:

A. Recurrent SSTI around mouth and nose: These most often take the form of recurrent furunculosis and abscesses. Perinatal abscesses are also seen. Sometimes even cellulitis has been seen. The benefits of weekly pulses of mupirocin are well established—in a recent study, the relative incidence before and after mupirocin prophylaxis was 0.84 vs. 0.03, which was statistically significant. The regimen being very cheap and effective should be the first line for the management of recurrent skin and soft tissue infections around the nose.^[11] The regimen was equally effective for community-acquired methicillin-resistant Staphylococcus aureus vs. methicillin-sensitive Staphylococcus aureus.

B. Before undertaking surgery of skin and soft tissues: This is associated with a reduced rate of postoperative infections. This has also been validated in major surgeries involving infected sites.^[12] Many times dermatologists are called to advice and give clearance for surgery, often involving minor infections at the proposed sites—in such situations elimination of staphylococcus by either systemic or topical means is conducive to a better outcome.

C. Community-acquired pneumonia and bacteremia prevention in the elderly and other immunocompromised: Nasal elimination of staphylococcus can often be lifesaving for at-risk population, such as those on peritoneal hemodialysis—the incidences of pneumonia and other fatal infections are also reduced. The dermatologist can advise their colleagues regarding the same. Yearly or twice-yearly prophylaxis is probably enough to reduce carriage status; however, formal studies are needed.^[13]

D. Predictor of pneumonia in postburn patients: Staphylococcus carriage status is one of the best predictors of pneumonia and bacteremia in postburn patients. Elimination of carriage status might help improving survival among these patients.^[14]

E. Severe recalcitrant hand eczema: The evidence that in noninfected hand eczema, elimination of Staphylococcal carriage results in improvement is at best equivocal. It is mostly derived from the coincident elimination of hand Staphylococcal aureus when mupirocin is also applied in the nasal nares. In many cases, improvement is also seen, coincident with such elimination.^[15]

High-Level Mupirocin Resistance

High-level, plasmid-mediated mupirocin resistance has been documented in some nations, warranting the necessity of the other regimens listed above.^[16] Since mupirocin resistance is mediated via the mupA gene, which distorts the isoleucine t-RNA synthase, related groups of drugs are also incapable to clear such organisms. In such circumstances, other options listed above should be tried. However, the real clinical implications of such resistance are still unknown.^[17]

Conclusion

The dermatologist should familiarize themselves with the various modalities available to eradicate staphylococcus from the skin, which often translates to a reduction in systemic and skin and soft tissue infections. Being simple, cost-effective and of a relatively shorter duration, such prophylaxis should be given wherever indicated.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

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