Staphylococcus hominis merupakan bagian dari bakteri genus staphylococcus

baktergi gram positif dengan bentuk sel lonjong dalam kluster. Biasanya bakteri ini secara
umum tidak berbahaya dan terletak pada kulit manusia dan hewan, dan dikenal sebagai
bakteri yang bertanggung jawab untuk mensekresi komposisi thioalkohol pada tubuh yang
berkontribusi dalam bau badan. Koloni dari S. homini berbentuk kecil, 1-2mm dengan
diameter setelah inkubasi 24 jam dalam suhu 35o, memiliki warna putih atau putih keruh
kecoklatan. Biasanya bakteri ini resisten terhadap novobiocin, dan dapat membingungkan
untuk resisten spesie lain (cth : S. saprophyticus)

Bakteri ini merupakan satu dari dua bakteri Staphylococcus yang sensitif terhadap
desferrioxamin, selain S. epidermis. Tidak seperti S. epidermis, S. hominis memproduksi
asam dari trehalose, sehingga dapat dilakukan tes untuk mengidentifikasi kedua spesies.
Banyak bakteri koagulasi negatif staphylococcus pada kulit manusia. Diantara spesies
tersebut, S. epidermis dan S. hominis merupakan yang paling banyak. S. epidermis lebih
banyak terdapat pada bagian atas tubuh, sementara S. hominis berkolonisasi di daerah yang
mempunyai glandula apokrin, seperti aksila dan regio pubis. Dalam studi kasus, S. hominis

Numerous coagulase-negative staphylococci appear commonly on the skin of human. Of

these species, S. epidermidis and S. hominis are the most abundant. While S. epidermidis
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, S. hominis
was calculated to account for 22% of the total staphylococcal species recovered from
individuals, second to S. epidermidis at 46%. S. hominis is the predominant species on the
head, axillae, arms, and legs. S. hominis, as well as most other staphylococcal species
common on the human skin, is able to produce acid aerobically from glucose, fructose,
sucrose, trehalose, and glycerol. Some strains were also able to produce acid from turanose,
lactose, galactose, melezitose, mannitol, and mannose. Most strains colonize on the skin for
relatively short periods of time compared to other Staphylococcus species. They, on average,
stay on the skin for only 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 cells are Gram-positive cocci, usually 1.2 to 1.4 μm in diameter.
They appear normally in tetrads and sometimes in pairs

Based on a total of 240 strains, all were resistant to lysozyme, some were slightly resistant to
lysostaphin, 77% were susceptible to penicillin G, 97% to streptomycin, 93% to
erythromycin, 64% to tetracycline, and 99% to novobiocin.[4]

Multi drug resistant strains of s. hominis have been isolated from blood and wound cultures
in humans.

When grown in agar cultures, colonies are usually circular, 4.0 to 4.5 mm 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 seem to
be around 7.5%, and a salt concentration of 15% yielded poor growth to no growth at all. The
optimal growth temperature range was around 28 to 40 °C, but good growth is still observed
at 45 °C, while no growth is observed at 15 °C. S. hominis can be differentiated from
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
suggest a close relationship between S. hominis and S. epidermidis, S. haemolyticus, and S.
warneri

S. hominis is normally found on human skin and is usually harmless, but can sometimes
cause infections in people with abnormally weak immune systems. Most, if not all, strains are
susceptible to penicillin, erythromycin, and novobiocin, but a divergent strain, S. hominis
subsp. novobiosepticus (SHN), was isolated between 1989 and 1996.[6] This strain was
named so because of its unique resistance to novobiocin and 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 hominis is
commonly found isolated from human skin, but as of 1998, no SHN isolate from human skin
had been reported.[7]

The SHN is so similar to the original S. hominis, now called S. hominis subsp. hominis, that
in 2010, a MicroScan system that clinical microbiology laboratories used, identified 7 of 31
S. hominis novobiosepticus cultures as S. hominis hominis. The relationship between the two
was unknown, but antibiotic-resistant isolates of S. hominis belonged only to SHN. [8]

SHN strains seems to have thickened cell walls, which can be the result of a genetic
background that also allows for vancomycin resistance. The thickened cell walls exist in
subspecies with and without vancomycin resistance which suggests this subspecies did not
originate from the acquiring of resistance genes

The combined resistance to novobiocin and oxacillin is hypothesized to have originated from
a simultaneous introduction of genes controlling the resistance to the two. These genes were
believed to have been 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 groups. The larger genome size of the SHN compared to that of S. hominis
hominis may be the result of the acquiring of heterologous DNA. This new, divergent strain
was first described in 1998, and was first implicated in causing bacteremia in 2002. Another
hypothesis is the insertion of the mec A gene and its flanking sequence into the chromosome
of SHN might have affected the expression of a closely linked gene, which converted the host
to become novobiocin-resistant

In 2002 and 2003, 32 isolates of SHN were found in 21 patients. Twenty-three of these were
from blood cultures, six from catheters, one from cerebrospinal fluid, one from a wound, and
one from external ear fluid. Eighteen of the 21 patients from whom these isolates were
recovered were neonates, one was a 13-year-old boy, and two were adults. Thirteen of these
cases were confirmed as sepsis in neonates resulting from SHN infection. These were the first
clinical reports of SHN causing bacterimia in hospitalized patients. SHN infections were high
in morbidity, but had a low rate of mortality. More undocumented instances of SHN
infections may not have been reported because not all coagulase-negative staphlococcal
infections (CONs) 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 neonatal ICUs. Formal investigation regarding the mode of transmission this
microbe uses were not conducted, but infants are believed to serve as reservoirs for the
microorganism, and transmission takes place with contact between health workers and the
infants. In addition, staphylococcal isolates from the nasopharynges and hands of health care
workers were shown to be 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. If SHN indeed takes residence on human skin, it probably exists in
small numbers and would require enrichment for detection. [11]

SHN has also been responsible for nosocomial outbreaks elsewhere. SHN strains have been
causing bloodstream infections, but have still been classified as vancomycin-susceptible.[12]

In May 2015, two babies from Simojovel rural communities of Chiapas, Mexico, were killed
and about 30 required medical attention after receiving vaccines for Hepatitis B, the Mexican
Social Security Institute (IMSS) launched an investigation to identify the cause of suchs
events, the preliminary results showed that the cause was external contamination with
Staphylococcus hominis

Vancomycin merupakan antimikroba golongan glikopeptida atau campuran glikopeptida

yang diproduksi oleh strain Amycolaptosis orientalis.

Struktur kimia Vancomycin

Indikasi Vancomycin:
Pengobatan infeksi yang disebakan oleh spesies staphylococcus dan streptococcus digunakan
oral untuk enterocolitis, staphylococcus atau untuk antibiotik yang berhubungan dengan
kolitis pseudomembran yang disebabkan oleh C.difficile.

Kontra Indikasi:
Hipersensitif terhadap vankomisin atau komponen lain dalam sediaaan; Hindari
penggunaannya pada pasien yang pernah mengalami hilang pendengaran.

Dosis dan Cara Pemakaian:

Dosis lazim:

 Bayi > 1 bulan dan anak-anak: 10-15 mg/kg setiap 6 jam.

 Dewasa: IV: 2-3 g/hari (20-45 mg/kg/hari) dalam dosis terbagi setiap 6-12 jam,
maksimum 3 g/hari.

Dosis: untuk indikasi khusus:

 Bayi > 1 bulan dan anak-anak:

 Meningitis: IV: 15 mg/kg setiap 6 jam, intratekal 5-20 mg/hari.

 Profilaksis infeksi endokarditis: IV: bedah dental, oral atau saluran pernapasan atas:
20 mg/kg 1jam sebelum pembedahan.

 Infeksi gram positif: IV: 10 mg/kg setiap 6 jam.

 Dewasa: Meningitis (pneumococcus atau staphylococcus): IV: 30-45 mg/kg/hari

dalam dosis terbagi setiap 8 sampai 12 jam atau 500-750 mg setiap 6 jam.

 Intratekal: sampai 20 mg/hari.

 Profilaksis infeksi endokarditis: IV: bedah dental, oral atau saluran penapasan atas: 1
g, 1 jam sebelum pembedahan.

 Infeksi gram positif: IV: 15-20 mg/kg/dosis (sekitar 750-1500 mg) setiap 12 jam.

Efek Samping Vancomycin:

Mulut pahit, mual, muntah, stomatitis, eosinopilia, nefritis interstisial, ototoksisitas, gagal
ginjal, ruam kulit, trombositopenia, vaskulitis, hipotensi eritematus pada wajah dan bagian
tubuh atas.

Peringatan dan atau Perhatian:

1. Dapat menyebabkan nefrotoksisitas, faktor risiko yang umum adalah gangguan ginjal,
penggunaan bersama obat nefrotoksik, peningkatan usia dan dehidrasi.

2. Hentikan penggunaan jika ada tanda nefrotoksisitas

3. kerusakan ginjal biasanya dapat pulih.

4. Mungkin dapat menyebabkan neurotoksisitas.

5. Ototoksisitas sebanding dengan jumlah obat yang diterima dan durasi pengobatan.

6. Penggunaan IV cepat dapat menyebakan hipotensi, eritema, urtikaria dan/atau pruritus

7. kecepatan infus seharusnya lebih dari 60 menit.

Bentuk dan Kekuatan Sediaan: Injeksi: 500 mg/vial.

Penyimpanan dan Stabilitas: Vial 500 mg dan 1 gram yang sudah direkonstitusi stabil dalam
suhu ruangan atau di lemari es selama 14 hari.

Pustaka:
-MIMS Indonesia Edisi 15 Tahun 2014.
-ISO Indonesia Volume 46 Tahun 2011-2012

SEMAKIN RENDAH NILAI MIC SEMAKIN TINGGI SENSITIVITAS DARI

ANTIBIOTIK TERHADAP MIKROBA