About all

Salicylic acid for boils: The Difference Between a Pimple and a Boil

The Difference Between a Pimple and a Boil

You’ve probably experienced that dreadful feeling the moment you find a boil or a pimple on your skin. The ugly, red bumps can be painful. Plus, they can take weeks to fully heal, possibly leaving a scar in its wake. But before you consider treatment options, it’s important to first understand the difference between a pimple and a boil. Treating one like the other could jeopardize your skin’s health. (In the meantime, keep your skin in tip-top shape with these 17 skincare tips dermatologists follow themselves.)

Pimples 101

Just like blackheads, whiteheads, and cysts, pimples are a form of acne. (Fun fact: pimples are also called pustules). They pop up when pores become clogged by excess oils, dead skin cells, or bacteria like Propionibacterium acnes. Pimples usually don’t grow too much in size. They also come to a whitehead within a few days. Boils, on the other hand, will swell up and redden as the bump continues to fill with pus from the infection (most zits aren’t full of pus).

Boils 101

The key difference between a pimple and a boil is how they’re formed. Boils develop when the Staphylococcus aureus bacteria (commonly referred to as “Staph”) enters your skin through a cut, bug bite, or ingrown hair follicle and causes an infection. Boils and zits can be found anywhere on your skin, but boils are likely to show up in moist areas where the bacteria can thrive like your armpits, buttocks, and upper thighs.

Treating pimples

Whatever you do, it’s never wise to pop or squeeze a zit, no matter how strong the urge. Picking may make the unwanted bumps last longer by burrowing bacteria deeper into your body. Picking could also scar your skin. Here’s the one type of acne you should never pop.

A warm compress can help a zit come to a head, but a good daily skincare routine is important. Therefore, be sure to wash your skin with a mild cleanser containing benzoyl peroxide or salicylic acid twice a day to help prevent future breakouts. An exfoliating facial scrub once or twice a week can also help. It will keep dead skin cells from accumulating in your pores. Additionally, the Mayo Clinic suggests helpful topical treatments such as retinoids or salicylic acid, both of which can keep hair follicles from plugging.

Treating boils

The same words of caution apply here as they do with zits: resist the urge to pick and squeeze. However, the reasons are more serious than with a pimple. The difference between a pimple and a boil in this case is that unlike zits, boils carry a ton of bacteria that cause infections. If you touch an opened boil, you could spread the infection to other parts of your body. Always wash your hands with soap and water before and after you touch a boil. For an additional layer of protection, be aware of these reasons why your relaxing hot tub is actually pretty gross. Plus, never share your towels, razors, makeup brushes or anything that could come into contact with the bacteria inside the boil.

To treat boils, the University of Texas at Austin’s University Health Services recommends you apply a warm compress to the boil for 10 to 15 minutes up to three times daily. Doing this can help bring the pus to a head. Next, use water and antibacterial soap to gently clean the skin around your boil. Then place a sterile gauze bandage over the area, changing whenever the gauze becomes wet or dirty.

When it’s time to see a dermatologist

Usually, pimples and boils should heal within about three weeks. But sometimes, that’s not the case. If you have a boil with pain or swelling that worsens over the course of a few days, or if you experience fever or vision issues, the American Academy of Dermatology suggests paying a visit to a board-certified dermatologist. A dermatologist may need to drain the boil or give you a prescription to fight a possible infection.

Popular Videos

Salicylic acid: an old dog, new tricks, and staphylococcal disease

1. Ogston A. Micrococcus poisoning. J. Anat. 1882;17:24–58. [PMC free article] [PubMed] [Google Scholar]

2. Cabell CH, et al. Changing patient characteristics and the effect on mortality in endocarditis. Arch. Intern. Med. 2002;162:90–94. [PubMed] [Google Scholar]

3. Bayer, A.S., and Scheld, W.M. 2000. Endocarditis and intravascular infections. In Principles and practice of infectious diseases. G.L. Mandell, J.E. Bennett, and R. Dolin, editors. Churchill Livingstone. Philadelphia, Pennsylvania, USA. 857–902.

4. Outbreaks of community-associated methicillin-resistant Staphylococcus aureus skin infections: Los Angeles County, California, 2002–2003. MMWR Morb. Mortal. Wkly. Rep. 2003;52:88. [PubMed] [Google Scholar]

5. Daum RS, et al. A novel methicillin-resistance cassette in community-acquired methicillin-resistant Staphylococcus aureus isolates of diverse genetic backgrounds. J. Infect. Dis. 2002;186:1344–1347. [PubMed] [Google Scholar]

6. Vancomycin-resistant Staphylococcus aureus: Pennsylvania, 2002 [erratum 2002, 51:931] MMWR Morb. Mortal. Wkly. Rep. 2002;51:902. [PubMed] [Google Scholar]

7. Lowy FD. Medical progress: Staphylococcus aureus infections. N. Engl. J. Med. 1998;339:520–532. [PubMed] [Google Scholar]

8. Foster TJ, Höök M. Surface protein adhesins of Staphylococcus aureus. Trends Microbiol. 1998;6:484–488. [PubMed] [Google Scholar]

9. Palma M, Haggar A, Flock JI. Adherence of Staphylococcus aureus is enhanced by an endogenous secreted protein with broad binding activity. J. Bacteriol. 1999;181:2840–2845. [PMC free article] [PubMed] [Google Scholar]

10. Hussain M, et al. Identification and characterization of a novel 38.5-kilodalton secretory protein of Staphylococcus aureus with extended-spectrum binding activitiy for extracellular matrix and plasma. J. Bacteriol. 2001;183:6778–6786. [PMC free article] [PubMed] [Google Scholar]

11. Sinha B, et al. Heterologously expressed Staphylococcus aureus fibronectin-binding proteins are sufficient for invasion of host cells. Infect. Immun. 2000;68:6871–6878. [PMC free article] [PubMed] [Google Scholar]

12. Que YA, et al. Reassessing the role of Staphylococcus aureus clumping factor and fibronectin-binding protein by expression in Lactococcus lactis. Infect. Immun. 2001;69:6296–6302. [PMC free article] [PubMed] [Google Scholar]

13. Cheung AL, Nast CC, Bayer AS. Selective activation of sar promoters with the use of green fluorescent protein transcriptional fusions as the detection system in the rabbit endocarditis model. Infect. Immun. 1998;66:5988–5993. [PMC free article] [PubMed] [Google Scholar]

14. Xiong Y-Q, et al. Activation and transcriptional interaction between agr RNAII and RNAIII in Staphylococcus aureus in vitro and in an experimental endocarditis model. J. Infect. Dis. 2002;186:668–677. [PubMed] [Google Scholar]

15. Durack DT. Experimental bacterial endocarditis. IV. Structure and function of the very early lesions. Br. J. Exp. Pathol. 1975;115:81–80. [PubMed] [Google Scholar]

16. Clawson CC, White JG, Herzberg MC. Platelet interaction with bacteria. VI. Contrasting the role of fibrinogen and fibronectin. Am. J. Hematol. 1980;9:43–53. [PubMed] [Google Scholar]

17. Herrmann M, Lai QJ, Albrecht RM, Mosher DF, Proctor RA. Adhesion of Staphylococcus aureus to surface-bound platelets: role of fibrinogen/fibrin and platelet integrins. J. Infect. Dis. 1993;167:312–322. [PubMed] [Google Scholar]

18. Siboo IR, Cheung AL, Bayer AS, Sullam PM. Clumping factor A mediates binding of Staphylococcus aureus to human platelets. Infect. Immun. 2001;69:3120–3127. [PMC free article] [PubMed] [Google Scholar]

19. Sullam PM, Bayer AS, Foss WM, Cheung AL. Diminished platelet binding in vitro by Staphylococcus aureus is associated with reduced virulence in a rabbit model of infective endocarditis. Infect. Immun. 1996;64:4915–4921. [PMC free article] [PubMed] [Google Scholar]

20. Heilmann C, Herrmann M, Kehrel BE, Peters G. Platelet-binding domains in 2 fibrinogen-binding proteins of Staphylococcus aureus identified by phage display. J. Infect. Dis. 2002;186:32–39. [PubMed] [Google Scholar]

21. Yeaman MR. The role of platelets in antimicrobial host defense. Clin. Infect. Dis. 1997;25:951–968. [PubMed] [Google Scholar]

22. Bayer AS, et al. Hyperproduction of alpha-toxin by Staphylococcus aureus results in paradoxically reduced virulence in experimental endocarditis: a host defense role for platelet microbicidal proteins. Infect. Immun. 1997;65:4652–4660. [PMC free article] [PubMed] [Google Scholar]

23. Nicolau DP, et al. Reduction of bacterial titers by low-dose aspirin in experimental aortic valve endocarditis. Infect. Immun. 1993;61:1593–1595. [PMC free article] [PubMed] [Google Scholar]

24. Taha TH, Durrant SS, Mazeika PK, Nihoyannopoulos P, Oakley CM. Aspirin to prevent growth of vegetations and cerebral emboli in infective endocarditis. J. Intern. Med. 1992;231:543–546. [PubMed] [Google Scholar]

25. Nicolau DP, Tessier PR, Nightingale CH. Beneficial effect of combination antiplatelet therapy on the development of experimental Staphylococcus aureus endocarditis. Int. J. Antimicrob. Agents. 1999;11:159–161. [PubMed] [Google Scholar]

26. Kupferwasser LI, et al. Acetylsalicylic acid reduces vegetation bacterial density, hematogenous bacterial dissemination, and frequency of embolic events in experimental Staphylococcus aureus endocarditis through antiplatelet and antibacterial effects. Circulation. 1999;99:2791–2797. [PubMed] [Google Scholar]

27. Kupferwasser LI, et al. Salicylic acid attenuates virulence in endovascular infections by targeting global regulatory pathways in Staphylococcus aureus. J. Clin. Invest. 2003;112:222–233. doi:10.1172/JCI200316876. [PMC free article] [PubMed] [Google Scholar]

28. Cheung AL, et al. Diminished virulence of a sar-/agr- mutant of Staphylococcus aureus in the rabbit model of endocarditis. J. Clin. Invest. 1994;94:1815–1822. [PMC free article] [PubMed] [Google Scholar]

29. Novick RP. Autoinduction and signal transduction in the regulation of staphylococcal virulence. Mol. Microbiol. 2003;48:1429–1449. [PubMed] [Google Scholar]

30. Proctor RA, et al. Two diarylurea electron transport inhibitors reduce Staphylococcus aureus hemolytic activity and protect cultured endothelial cells from lysis. Antimicrob. Agents Chemother. 2002;46:2333–2336. [PMC free article] [PubMed] [Google Scholar]

31. Kahl B, et al. Persistent infection with small colony variant strains of Staphylococcus aureus in patients with cystic fibrosis. J. Infect. Dis. 1998;177:1023–1029. [PubMed] [Google Scholar]

32. Yarwood JM, McCormick JK, Paustian ML, Kapur V, Schlievert PM. Repression of the Staphylococcus aureus accessory gene regulator in serum and in vivo. J. Bacteriol. 2002;184:1095–1101. [PMC free article] [PubMed] [Google Scholar]

33. Wolz C, Goerke C, Landmann R, Zimmerli W, Fluckiger U. Transcription of clumping factor A in attached and unattached Staphylococcus aureus in vitro and during device-related infection. Infect. Immun.> 2002;70>:2758–2762. [PMC free article] [PubMed] [Google Scholar]

34. Teichberg S, Farber BF, Wolff AG, Roberts B. Salicylic acid decreases extracellular biofilm production by Staphylococcus epidermidis: electron microscopic analysis. J. Infect. Dis. 1993;167:1501–1503. [PubMed] [Google Scholar]

35. Muller E, Al Attar J, Wolff AG, Farber BF. Mechanism of salicylate-mediated inhibition of biofilm in Staphylococcus epidermidis. J. Infect. Dis. 1998;177:501–503. [PubMed] [Google Scholar]

36. McKenney D, et al. Broadly protective vaccine for Staphylococcus aureus based on an in vivo-expressed antigen. Science. 1999;284:1523–1527. [PubMed] [Google Scholar]

37. Heilmann C, et al. Molecular basis of intercellular adhesion in the biofilm-forming Staphylococcus epidermidis. Mol. Microbiol. 1996;20:1083–1091. [PubMed] [Google Scholar]

38. Kullik I, Giachino P. The alternative sigma factor ςB in Staphylococcus aureus: regulation of the sigB operon in response to growth phase and heat shock. Arch. Microbiol. 1997;167:151–159. [PubMed] [Google Scholar]

39. Chavakis T, et al. Staphylococcus aureus extracellular adherence protein serves as anti-inflammatory factor by inhibiting the recruitment of host leukocytes. Nat. Med. 2002;8:687–693. [PubMed] [Google Scholar]

40. Lee LY, et al. The Staphylococcus aureus Map protein is an immunomodulator that interferes with T cell–mediated responses. J. Clin. Invest. 2002;110:1461–1471. doi:10.1172/JCI200216318. [PMC free article] [PubMed] [Google Scholar]

Furuncle, furuncle treatment in Moscow

Sign up online

  • Published: 14 October 2018

  • Article updated: April 4, 2023

The disease is characterized by the development of inflammation in the area of ​​the hair follicle. In this case, the pathological process extends not only to the sac of the hair bulb, but also to the surrounding connective tissue.

Causes

The reason for the appearance of boils is the penetration of pathogenic pathogens into the hair follicle. The most common inflammation is caused by Staphylococcus aureus. Infection is promoted by the following factors:

  • pronounced decrease in the body’s immune defenses;
  • metabolic disorders such as diabetes mellitus;
  • increased sebum secretion;
  • excessive sweating;
  • eating habits (abuse of salty, sweet, fatty foods with low fiber content).

Also, the cause of a boil can be microtraumatization of the skin on the face, for example, during shaving.

Symptoms

The development of a boil is characterized by the following signs:

  • the appearance of a painful vesicle on the skin;
  • a rod is formed in the center of the bubble, in place of which necrosis develops;
  • redness of the skin;
  • after opening the formation, the wound heals by scarring.

Most often, inflammatory elements are localized in the area of ​​the skin:

  • hips;
  • neck;
  • back;
  • persons;
  • armpits;
  • neck.

Diagnosis of a boil

The following examinations are used to make the correct diagnosis:

  • examination and palpation at a specialist’s appointment;
  • blood test to determine the level of ESR and leukocytes;
  • determination of blood sugar level;
  • determination of causative agents of tuberculosis, syphilis.

Treatment

Topical remedies such as:

  • ethyl alcohol;
  • salicylic acid;
  • alcohol solution of methylene blue, brilliant green;
  • antibiotics;
  • keratolytic preparations;
  • electrophoresis, UHF.

It is obligatory to remove the boil if it is localized on the face. At the same time, it is opened, drained, followed by anti-inflammatory, detoxification, specific immune therapy. Armpit furuncle is also treated.

Diet

Patients with boils should adhere to the following dietary principles:

  • avoid sweet, salty, fatty foods;
  • restriction of spices, smoked meats;
  • introduction to the diet of foods rich in fiber;
  • increasing the share of dairy and vegetable products in the diet.

Danger

The most dangerous complications of the disease, which may include the following:

  • sepsis;
  • purulent meningitis;
  • phlebitis of ophthalmic, facial veins;
  • thrombosis of the longitudinal and cavernous sinuses of the dura mater;
  • boil abscess;
  • phlegmon with localization on the upper lip or side slopes of the nose.

How to prevent a boil

The risk group for the development of this disease includes people who:

  • neglect personal hygiene rules, do not treat the skin after shaving;
  • have excessive sweating;
  • have an increased oiliness of the skin.

Prevention of the development of this disease includes the following principles:

  • personal hygiene;
  • treatment with alcohol solutions of injured skin areas;
  • prevention of skin microtrauma.

Furuncle treatment in the network of NEARMEDIC clinics

How to treat a boil – a specialist decides. Qualified assistance can be obtained in the surgical department of NEARMEDIC clinics. The surgeon will open and treat the abscess, give recommendations for the prevention of the disease. It is possible to take tests, cure any surgical diseases in an outpatient clinic and a hospital. All manipulations are carried out in sterile conditions, painlessly, using the latest equipment and medicines.

Doctors

Who treat Furuncle disease

More doctors

To make an appointment with the clinic, you can contact the single contact center:
+7 (495) 6-171-171

Or use the online appointment:

Boil. He is Furuncle / News of the Society of Krasnoyarsk and the Krasnoyarsk Territory / Newslab.Ru

09/28/2010

Many have encountered this disease – a painful pimple suddenly appears on the skin, which increases in size day by day, then opens, leaving behind an ulcerated surface and a scar.

Sometimes the process is accompanied by an increase in temperature. In the people, this formation is called a boil, and doctors prefer the official name – boil.

Furuncle is an inflammation of the hair follicle – a “pouch” immersed in the skin, containing the hair root and blood vessels that supply it. The disease is caused by bacterial flora penetrating the thickness of the skin through microcracks on its surface.

Normally, the immune system provides protection against such invasion (there are special antibodies on the surface of the skin, and the damaged epithelium is able to quickly recover). However, when immunity is weakened, bacteria can multiply at the mouth of the hair follicle, which leads to its inflammation with the formation of a large amount of pus. As a result, redness appears on the skin, then a painful cone-shaped tubercle that increases in size over several days.

After some time, the tubercle opens and on the damaged area you can see a torn hair shaft surrounded by pus – fragments of the normal contents of the follicle. The boil is emptied and a small scar remains in place of the healed ulcer.

Do not confuse a boil with manifestations of acne: acne is an inflammation of the sebaceous glands, into the ducts of which dirt from the surface of the skin enters. This process is typical for adolescence, when due to increased production of sebum and insufficient skin cleansing, clogging of pores occurs. Acne, as you know, passes without a trace and does not cause significant pain. Furuncle can appear in people of any age, and its treatment often requires medical attention.

Boils are formed not only on the face, but also on the neck, back of the head, shoulders, back and buttocks. Theoretically, any area of ​​the skin where there is hair (and there are none only on the palms and soles of the feet) can be affected by them. A condition in which a person has several boils at the same time is called furunculosis. This is a sign of serious malfunctions in the immune system and a reason to consult a doctor without fail: both to treat the disease itself and to diagnose the cause that caused it. So in adulthood, people with sudden onset of furunculosis are most often diagnosed with latent diabetes mellitus.

What to do if a furuncle appears on the skin? You can try to cure it yourself, unless it is located on the skin above the upper lip. With such localization, it is worth fearing the spread of infection along the anterior facial vein and cavernous sinus into the cranial cavity, which can lead to the development of meningitis or thrombosis of the cavernous sinus. Such a development of the situation is not uncommon, there are even cases of death after an attempt to squeeze out a “pimple” in this area.

Remember – inflammatory formations on the skin of the face are not always harmless!

Even acne is recommended to be treated by rubbing the face with alcohol lotions, without resorting to squeezing out their contents (skin microtrauma resulting from “mechanical cleaning” is a sure way to spread infection and new inflammation).

As for boils localized in the area of ​​the nasolabial triangle, they should be treated only in a hospital under the constant supervision of a doctor: this will allow you to notice the deterioration in the patient’s well-being in time and take all necessary measures to prevent complications. And while waiting for hospitalization (I repeat once again, this is a necessity!) You should avoid unnecessary contractions of the facial muscles and muscles of the lower jaw (to reduce blood circulation in the affected area) – and, therefore, talk less and eat liquid food.

Treatment of an uncomplicated boil consists in treating the affected skin area with 70% ethyl alcohol solution, 2% salicylic acid alcohol solution or brilliant green solution. In the treatment of boils in a hospital, the affected area is chipped with antibiotic solutions with novocaine or antibiotic electrophoresis.

In severe cases, under local anesthesia, the boil is opened with subsequent removal of purulent-necrotic masses. Then the wound is treated with antiseptic solutions and a bandage is applied with an antibacterial ointment (tetracycline, erythromycin, gentamicin, synthomycin).

After cleansing the wound of pus, the patient is prescribed physiotherapeutic procedures: UV irradiation, UHF therapy, and others.