The nose is made up of various components including, but not limited to, skin, nasal mucosa, bone and cartilage. What gives the nose its structure and integrity are the nasal bones superiorly, the upper and lower lateral cartilages inferiorly, and the cartilaginous nasal septum. The nasal vestibule is made up of hair-bearing skin anteriorly and transitions to nasal mucosa posteriorly. The epithelial wall of the nostril interiorly is fully keratinized and includes sebaceous gland, apocrine sweat glands, and hair follicles [1]. The angular and nasolabial veins draining the nasal vestibule are valveless. Therefore, infections in this area have the potential to spread to structures such as the cavernous sinus via these facial veins if treatment is inadequate. This area has been called the “danger triangle” for this reason [2].

The most common bacterial flora found in the nose includes coagulase-negative staphylococci (12–81 %) which includes Staphylococcus epidermidis, Staphylococcus hominis and Staphylococcus haemolyticus, aerobic diphtheroids (6–68 %), and S. aureus (6–34 %). Other aerobic species like Streptococcus viridians, pneumococci, meningococci, enteric bacteria and Moraxella species are also commonly found [3, 4].

S. aureus, one of the most common bacteria that cause nasal vestibulitis, produces penicillinase, a beta-lactamase that inactivates penicillin and extended-spectrum penicillins. Beta-lactamase inhibitors, such as potassium clavulanate help to overcome this resistance, unless methicillin-resistant S. aureus (MRSA) is present. MRSA accounts for 25–60 % of all strains of S. aureus in hospitals in the United States [4].

Immunosuppressed patients may be prone to infection with different pathogens such as Pseudomonas aeruginosa, mycobacteria, or invasive fungi like mucormycosis or aspergillus [5]. Herpes simplex virus, herpes zoster and other viruses can affect the nasal vestibule as well as the oral cavity and lips.

There have been a few case reports of rare organisms causing nasal vestibulitis in adult patients, but none in pediatric patients. Nocardiopsis dassonvillei was found in a 55-year-old diabetic patient in Mandya, Karnataka, India that recurred after a 10 day course of cefuroxime [6]. He fully recovered 4 weeks after receiving a week of clarithromycin and levofloxacin. Burkholderia pseudomallei was found to cause sinonasal Melioidosis and sepsis in 51-year-old diabetic man with hepatitis B who suffered from alcohol abuse in Melbourne, Australia who needed incision and drainage, debridement and endoscopic sinus surgery for infection of the nasal vestibule with a septal abscess [7]. He travelled from Vietnam, an endemic area for these particular bacteria. He was treated with IV meropenem, then IV ceftazidime for 8 weeks, followed by 3 months of Bactrim DS and doxycycline. Because of inadequately sterilized surgical equipment at a hospital in Mexico City, 22 (27.5 %) of 81 patients who underwent rhinoplasty from December 1987 to April 1988 developed nasal cellulitis due to Mycobacterium chelonae [8].

Symptoms of typical nasal vestibulitis include localized pain and swelling of the nasal vestibule, usually of sudden onset [5]. Nose picking or excessive blowing can precipitate the disease process and can result in crusting or bleeding near the nasal hair follicles. Nasal steroid use does not usually precipitate nasal vestibulitis, but intranasal drug use can lead to chronic nasal sores with ulceration. Nasal obstruction is not usually present. On physical examination, the nose can be swollen, tender to palpation, crusting, erythematous and warm. Sometimes a pimple-like lesion is present. A chronic nasal sore that does not heal after appropriate time and treatment may need to be biopsied to rule out other, more unusual causes such as systemic disease like Wegener’s granulomatosis with polyangitis (GPA) or sarcoidosis, or more rarely, lethal midline granuloma or sinonasal lymphoma. A neoplastic process such as basal cell or squamous cell carcinoma should also be ruled out. Eczema can also be on the differential diagnosis as well [2]. Dahle and Sontheimer have mentioned in the past a term they coined the “Rudolf sign,” as in Rudolf the Red Nosed Reindeer, in their case report of typical nasal vestibulitis that resolved with mupirocin ointment. The authors describe the “Rudolf sign” as unilateral, or sometimes bilateral, tender erythema of the nasal tip [9]. Involvement of both sides of the nose is rare, as is frank abscess. Systemic symptoms such as fever and chills are very uncommon. Spontaneous resolution, though, is very common. Symptoms can be more common in winter months.

There are many bacteria that can colonize the nose. Even if there is not a clear cut correlation between colonization and active nasal vestibulitis, nasal colonization has significant importance, especially with regard to invasive disease in other parts of the body. Staphylococcus aureus is by far the most studied, with the anterior nasal cavity being the most frequent carriage site [1]. Carrier status can be classified as persistent (20 %), intermittent (30 %) or non-carriage (50 %), with persistent carriers having a higher bacterial load and a higher risk of acquiring an infection than intermittent carriers [1]. Adults have lower persistent carriage rates than children with a transition from persistent to intermittent to non-carrier states during the adolescent years [1]. Carrier rates tend to be higher in white people, in men, in patients with diabetes mellitus, those undergoing hemodialysis, patients with end stage liver disease, patients with HIV, obese patients, patients with a history of stroke and patients skin diseases (psoriasis or eczema) that can pre-dispose them to skin infections [1]. Transmission of bacteria is usually via direct contact, but rarely can be transmitted via airborne dispersal. Family members tend to have the same carrier state. Being hospitalized is also an important risk factor for nasal carrier state. The second most common cause of hospital-acquired bloodstream infections is S. aureus with approximately 20 % of surgical patients acquiring at least one nosocomial infection [1]. This rate varies by institution. For community-acquired methicillin-resistant Staphylococcus aureus (MRSA), carrier rates are still low, but seem to be rapidly escalating in certain parts of the world.

A prospective observational study conducted at Brooke Army Medical Center in Ft. Sam Houston, Texas [10], determined the prevalence of nasal colonization with MRSA in patients hospitalized at five different units at the hospital. Colonization status was determined at admission and longitudinally over a 3 month period. Of the 26 patients who were initially colonized with MRSA, 5 (19 %) developed an infection involving MRSA. This was about 10 times the incidence in patients colonized with methicillin-susceptible S. aureus (MSSA), with a significant difference in relative risk (RR, 13; 95 % CI, 2.7–64; p < .01) for patients colonized with MRSA initially. Twelve (2.0 %) of the 595 patients who were initially not colonized with S. aureus developed MRSA infection, thus determining a higher relative risk (RR, 9.5; 95 % CI, 3.6–25; p < .01). Statistical analysis in this study showed MRSA infection to be more prevalent in older patients (mean age, 69 year) and in patients who were more prolonged admissions (mean length of stay, 16 days). Davis , et al., also mentioned that 12 (3.0 %) patients acquired MRSA colonization during their hospital admission. Nine of the 12 had no S. aureus colonization at admission while 3 were colonized with MSSA. There was a higher relative risk of MRSA infection (RR, 12; 95 % CI, 4.0–38; P < .01) for patients who acquire MRSA colonization during their hospitalization. This study is consistent with previous reports in the literature about the natural history of MRSA colonization in the nose.