| Staphylococcus hominis | |
|---|---|
| Scientific classification | |
| Kingdom: | Bacteria |
| Phylum: | Firmicutes |
| Class: | Bacilli |
| Order: | Bacillales |
| Family: | Staphylococcaceae |
| Genus: | Staphylococcus |
| Species: | S. hominis |
| Binomial name | |
| Staphylococcus hominis Kloos & Schleifer 1975 |
|
Staphylococcus hominis is a coagulase-negative member of the bacterial genus Staphylococcus, consisting of Gram positive, spherical cells in clusters. It occurs very commonly as a harmless commensal on human and animal skin. However, like many other coagulase-negative staphylococci, S. hominis may occasionally cause infection in patients whose immune system is compromised, for example by chemotherapy or predisposing illness.
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Colonies of S. hominis are small, usually 1–2 mm in diameter after 24 hours' incubation at 35 degrees Celsius, and white or tan in colour. Occasional strains are resistant to Novobiocin and may be confused with other resistant species (e.g. S. saprophyticus.)
It is one of only two species of Staphylococcus that display sensitivity to desferrioxamine, the other being S. epidermidis. Unlike S. epidermidis, S. hominis produces acid from trehalose, so the two tests together serve to identify the species.
Numerous coagulase-negative staphylococci appear commonly on the skin of human. Of these species, Staphylococcus epidermis and Staphylococcus hominis are the most abundant. While S. epidermis tends to colonize the upper part of the body, S. hominis tends to colonize in areas with numerous apocrine glands, such as axillae and the pubic region. In a certain study, it was calculated that the S. hominis species attributed for a mean 22% of the total staphylococci species recovered from individuals. This was second to only S. epidermidis, which attributed for a mean of 46%. S. hominis is the predominant species on the head, axillae, arms, and legs. S. hominis, as well as most other staphylococci species that are common on the human skin, are able to produce acid aerobically from glucose, fructose, sucrose, trehalose, glycerol. Some strains were also able to produce acid from turanose, lactose, and galactose, melezitose, mannitol, and mannose. Most strains colonize on the skin for relatively short periods of time compared to other Stapholococcus species. They, on average, stay on the skin for only about several weeks or months. The cell wall contains low amounts of teichoic acid and glutamic acid. The cell wall teichoic acid contains glycerol and glucosamine. S. hominis cell are gram-positive cocci and are usually 1.2 to 1.4 micrometers in diameter. They appear normally in tetrads and sometimes in pairs.[1]
Based on a total of 240 strains, all were resistant to lysozyme, some were slightly resistant to lysostaphin, seventy- seven percent were susceptible to penicillin G, 97% to streptomycin, 93% to erythromycin, 64% to tetracycline, and 99% to novobiocin.[2]
When grown in agar cultures, colonies are usually circular, 4.0 to 4.5 micrometers in diameter. Agar colonies usually have wide edges and an elevated center. They are commonly smooth with dull surfaces, and are yellow-orange pigmented in the center of the opaque colonies. They grow both in aerobic and anaerobic conditions, but tend to grow significantly less in the latter. Optimal NaCl concentrations of the agar culture for the growth of S. hominis seems to be around 7.5%, and NaCl concentration of 15% yielded poor growth to no growth at all. The optimal growth temperature range was around 28 to 40 degrees Celsius, but good growth is still observed at 45 degrees Celsius while no growth is observed at 15 degree Celsius. S. hominis can be differentiated between other staphylococci by its colony morphology and pigmentation patterns, predominant tetrad cell arrangement, poor growth in thioglycolate, low tolerance of NaCl, and carbohydrate reaction pattern. Each species is also significantly different in cell wall composition, lactic acid configuration, temperature extremes of growth, coagulase activity, hemolysis acetylmethylcarbinol production, nitrate reduction, and phosphatase, DNase, and bacteriolytic activities. Similarities in these properties between S. hominis and several other species suggests that there is a close relationship between S. hominis and S. epidermidis, S. haemolyticus, and S. warneri.[3]
S. hominis is normally found on human skin and is usually harmless, but it can sometimes cause infections in people with abnormally weak immune system. Most, if not all, strains of S. hominis are susceptible to penicillin, erythromycin, and novobiocin, but a divergent strain of S. hominis subsp. novobiosepticus was found not too long ago. This strain was named so because of its unique characteristics of having the ability to resist novobiocin and also its failure to produce acid aerobically from trehalose and glucosamine. In addition, the 26 isolated strains of this new subspecies are resistant to nalidixic acid, penicillin G, oxacillin, kanamycin and streptomycin. They were also somewhat resistant to methicillin and gentamicin, and most strains were resistant to erythromycin, clindamycin, chloramphenicol, trimethoprim/ sulfamethoxazole and ciprofloxacin as well. In addition, S. hominis subsp. hominis is commonly found isolated from human skin, but there are no reports of the isolation of S. hominis subsp. novobiosepticus from the human skin.[4]
The S. hominis subsp. novobiosepticus is so similar to the original S. hominis, now called S. hominis subsp. hominis, that a MicroScan system that clinical microbiology laboratories use identified 7 of 31 S. hominis subsp. novobiosepticus as S. hominis subsp. hominis. The relationship between the two is currently unknown, but antibiotic-resistant isolates of S. hominis belong only to S. hominis subsp. novobiosepticus. [5]
It has been observed that SHN strains seems to have a thickened cell wall, and this tendency may be the result of a genetic background that also allows for vancomycin resistance. The fact that the thickened cell wall exists in subspecies with and without vancomycin suggests that this subspecie strain did not originate from the acquiring of resistance genes. [6]
It is hypothesized that the combined resistant to novobiocin and oxacillin may have originated from a simultaneous introduction of genes controlling the resistance to the two. It is believed that these genes were acquired originally through heterologous DNA from a methicillin resistant strain of one of the novobiocin-resistant species belonging to the S. sciuri or the S. saprophyticus group. The larger genome size of the S. hominis novobiosepticus compared to that of S. hominis subsp. hominis may be the result of the acquiring of heterologous DNA. This new divergent strain was first described in 1998, and it was first implicated in 2002 that this microbe could cause bactermia. Another hypothesis says that the insertion of the mec A gene and its flanking sequence into the chromosome of S. hominis subsp. novobiosepticus might have affected the expression of a closely linked gene, which convereted the host to become novobiocin-resistant.[7]
Within the years 2002 and 2003, 32 isolates of S. hominis subsp. novobiosepticus were found in 21 patients. 23 of these were from blood cultures, six from catheters, one from cerebrospinal fluid, one from a wound, and one from external ear fluid. 18 of the 21 patients from which these isolates were recovered were neonates, one was a 13-year-old boy, and two were adults. 13 of these cases were confirmed as sepsis in neonates resulting from SHM (S. hominis subsp. novobiosepticus) infection. These were the first clinical reports of SHM causing bactermia in hospitalized patients. SHN infections were high in morbidity but had a low rate of mortality. There may be more undocumented instances of SHN infections that were not reported because not all CONS (Coagulase-Negative Staphlococcal Infections) are identified to the species level. Molecular epidemiology was successful in tracing 13 cases of sepsis in neonates to a single clone of SHN during a two year study period in NICU. Formal investigation regarding the mode of transmission that this microbe uses were not conducted, but it is believed that infants serve as reservoirs for the microorganism and transmission takes place with contact between health workers and the infants. In addition, it has been shown that Staphylococcal isolates from the nasopharynges and hands of health care workers are genetically similar to those that colonize or cause disease in neonates. This supports the idea that health workers serve as a form of nosocomical transmission of CONS. It is suggested that if SHN indeed takes residence on human skin, it probably exists in small numbers and would require enrichment for detection. [8]
SHN has also been responsible for nosocomical outbreaks elsewhere. Nosocomical outbreaks are outbreaks of infection that result from one being treated in a hospital or healthcare service unit. SHN strains have been causing bloodstream infections, but have still been classified as vancomycin-susceptible.[9]