Zoster is a common, predominantly dermal, and neurologic disorder caused by the varicella-zoster virus (VZV), a virus morphologically and

antigenically identical to the virus causing varicella (chickenpox). Difference in clinical manifestations between varicella and zoster apparently depends on the immune status of individual patients; those with no prior immunologic exposure to varicella virus, most commonly children, develop the clinical syndrome of varicella, while those with circulating varicella antibodies develop a localized recrudescence, zoster. Zoster probably results most often from a failure of the immune system to contain latent varicella-zoster virus replication. Whether other factors such as radiation, physical trauma, certain medications, other infections, or stress also can trigger zoster has not been determined with certainty. Nor is it entirely clear why circulating varicella antibodies and cell-mediated immune mechanisms do not prevent recurrent overt disease, as is common with most other viral illnesses. An inverse correlation appears to exist between the capacity of a host to mount a cellular immune response and the incidence of zoster. However, many patients with zoster apparently have normal immune systems. In these patients, zoster is postulated to occur when varicella-zoster virus antibody titers and cellular immunity drop to levels at which they no longer are completely effective in preventing viral invasion. Evidence for this hypothesis includes the observation that pediatricians, who presumably are reexposed to the varicella virus routinely and thus maintain high levels of immunity to varicella-zoster virus, seldom develop zoster. Zoster most commonly manifests in 1 or more posterior spinal ganglia or cranial sensory ganglia, presumably because viral particles have been preserved within these ganglia in a dormant state since the original episode of varicella. This results in pain and characteristic cutaneous findings (see History) along the corresponding sensory dermatomes of the involved ganglia. Less often, involvement of anterior and posterior horn cells, leptomeninges, and peripheral nerves is observed, with consequent muscle weakness or palsy, pleocytosis of spinal fluid, and/or sensory loss. Rarely, myelitis, meningitis, encephalitis, or visceral involvement may occur.

Shingles facts

Shingles is caused by the same virus that causes chickenpox and can be spread to people who have not had chickenpox. Shingles, also known as herpes zoster, is not related to thesexually transmitted herpes virus disease called herpes genitalis, or the oral herpes virus, herpes simplex. Shingles may cause pain that can continue after the rashdisappears. Steroids and antiviral drugs can help prevent long-term pain after shingles if they are started within the first two days of the appearance of the rash. The Zostavax vaccine is available for people over 60 years of age to reduce the incidence and severity of shingles.

What is shingles? What causes shingles?

Shingles is a skin rash caused by a nerve and skin inflammation from the same virus that previously caused chickenpox. This virus is called thevaricella zoster virus (VZV) and belongs to the herpes family of viruses. After an individual has chickenpox, this virus lives dormant in the nervous system and is never fully cleared from the body. Under certain circumstances, such as emotional stress, immune deficiency (from AIDS orchemotherapy), or with cancer, the virus reactivates and causes

shingles. In most cases of shingles, however, a cause for the reactivation of the virus is never found. Anyone who has ever had chickenpox is at risk for the development of shingles, although it occurs most commonly in people over the age of 60. It has been estimated that up to 1,000,000 cases of shingles occur each year in the U.S. The herpes virus that causes shingles and chickenpox is not the same as the herpes viruses that causes genital herpes (which can be sexually transmitted) or herpes mouth sores. Shingles is medically termed herpes zoster.

What are shingles symptoms and signs? How long does shingles last?
Even when there is no rash, the pain of shingles may be apparent. Before a rash is visible, the patient may notice several days to a week of burning pain and sensitive skin. When the characteristic rash is not yet apparent, it may be difficult to determine the cause of the often severe pain. Shingles rash starts as small blisters on a red base, with new blisters continuing to form for three to five days. The blisters follow the path of individual nerves that come out of the spinal cord in a specific "ray-like" distribution (called a dermatomal pattern) and appear in a band-like pattern on an area of skin. The entire path of the affected nerve may be involved, or there may be areas in the distribution of the nerve with blisters and areas without blisters. Generally, only one nerve level is involved. In a rare case, more than one nerve will be involved. Eventually, the blisters pop, and the area starts to ooze. The affected areas will then crust over and heal. The duration of the outbreak may take three to four weeks from start to finish. On occasion, the pain will be present but the blisters may never appear. This can be a very confusing cause of local pain.

How long is shingles contagious?

Shingles is contagious and can be spread from an affected person to babies, children, or adults who have not had chickenpox. But instead of developing shingles, these people develop chickenpox. Once they have had chickenpox, people cannot catch shingles (or contract the virus) from someone else. Once infected, however, people have the potential to develop shingles later in life.

What does shingles look like?

Shingles is contagious to people who have not previously had chickenpox, as long as there are new blisters forming and old blisters healing. Similar to chickenpox, the time prior to healing or crusting of the blisters is the contagious stage of shingles. Once all of the blisters are crusted over, the virus can no longer be spread and the contagious period is over.

How is shingles diagnosed?

The clinical appearance of shingles, with characteristic painful blisters localized to the region of a specific nerve, is usually sufficient to establish the diagnosis. No diagnostic tests are usually required. However, particularly in people with impaired immune function, shingles may sometimes not display the characteristic clinical pattern. In these cases, samples from the affected area may be tested in a laboratory, either by culturing the tissue for growth of the virus or by identifying the genetic material of the virus.

What is the treatment for shingles? Should I visit my health care professional?
There are several effective treatments for shingles. Drugs that fight viruses (antivirals), such as acyclovir (Zovirax),valacyclovir (Valtrex), or famciclovir(Famvir), can reduce the severity and duration of the rash if started early (within 72 hours of the appearance of the rash). In addition to antiviral medications, pain medications may be needed for symptom control. Both nonsteroidal antiinflammatory medications and narcotic pain-control medications may be used for pain management in shingles. The affected area should be kept clean. Bathing is permitted, and the area can be cleansed with soap and water. Cool compresses and anti-itching lotions, such ascalamine lotion, may also provide

relief. An aluminum acetate solution (Burow's orDomeboro solution, available at your pharmacy) can be used to help dry up the blisters and oozing.

What are the complications of shingles?

Generally, shingles heals well and problems are few. However, on occasion, the blisters can become infected with bacteria, causingcellulitis, a bacterial infection of the skin. If this occurs, the area will become reddened, warm, firm, and tender. You might notice red streaks forming around the wound. If you notice any of these symptoms, contact your health care professional. Antibiotics can be used to treat these complications. A more worrisome complication occurs when shingles affects the face, specifically the forehead and nose. In this situation, it is possible, although not likely, that shingles can affect the eye (known as herpes zoster ophthalmicus), leading to loss of vision. If you have shingles on your forehead or nose, your eyes should be evaluated by a health care professional. A rare complication of shingles is known asRamsay Hunt syndrome. In this case, the cranial nerves (cranial nerves V, IX, and X) are involved. Symptoms may include peripheral facial nerve weakness anddeafness. The typical rash is often observed around the ear and ear canal.

Picture: How the varicella zoster virus causes shingles and postherpetic neuralgia

What is postherpetic neuralgia?

The most common complication of shingles is postherpetic neuralgia. This occurs when the nerve pain associated with shingles persists beyond one month, even after the rash is gone. It is a result of irritation of the nerves of sensation by the virus. The pain can be severe and debilitating. Postherpetic neuralgia occurs primarily in people over the age of 50 and affects 10%-15% of people with shingles. There is evidence that treating shingles with antiviral agents can reduce the duration and occurrence of postherpetic neuralgia. The pain of postherpetic neuralgia can be reduced by a number of medications. Tricyclic antidepressant medications (amitriptyline [Elavil] and others), as well as antiseizure medications (gabapentin[Neurontin], carbamazepine [Tegretol],pregabalin [Lyrica]), have been used to relieve the pain associated with postherpetic neuralgia. In 2012, the FDA approved the use of gabapentin enacarbil (Horizant), previously used for the management of restless legs syndrome, for the treatment of postherpetic neuralgia. Capsaicin cream(Zostrix), a derivative of hot chili peppers, can be used topically on the area after all the blisters have healed, to reduce the pain.Lidocaine pain patches (Lidoderm) applied directly to the skin can also be helpful in relieving nerve pains by

numbing the nerves with local lidocaine anesthetic. These options should be discussed with your health care professional.

Can shingles be prevented with a vaccine?

In May 2006, the U.S. Food and Drug Administration (FDA) approved the first vaccine for adult shingles. The vaccine known as Zostavax, is approved for use in adults ages 50 and over who have had chickenpox. The U.S. Centers for Disease Control and Prevention recommends the vaccine for people 60 years of age and over who have had chickenpox. It is a onetime injection (shot) that does not need to be repeated. The shingles vaccine contains a booster dose of the chickenpox vaccine usually given to children. Tests over an initial four-year period showed that the vaccine significantly reduced the incidence of shingles in these older adults. The single-dose vaccine was shown to be more than 60% effective in reducing shingles symptoms, and it reduced the incidence ofpostherpetic neuralgia (PHN, see above) by at least two-thirds. Studies are ongoing to evaluate the effectiveness of the vaccine over a longer term. Even if you have had shingles, you can still have the vaccine to help prevent future outbreaks. There are certain contraindications to receiving the shingles vaccine. People with weakened immune systems due to immune-suppressing medications, cancer treatment,HIV disease, or organ transplants should not receive the shingles vaccine because it contains live, weakened viral particles. There is not enough information available from researchers to decide at this point whether Zostavax may be beneficial in people younger than 60 years of age.Pregnant women should not receive the shingles vaccine. The shingles vaccine has not been shown to cause any serious side effects or health consequences. Minor side effects include redness, soreness, swelling, or itching at the shot site, and headache. It is safe for those who have received the shingles vaccine to be around babies or those with weakened immune systems. It has not been demonstrated that a person can develop chickenpox from getting the shingles vaccine, although some people who receive the vaccine may develop a mild chickenpox-like rash near the injection site. This rash should be kept covered and will disappear on its own. Since the chickenpox vaccine is now recommended for children, the incidence of chickenpox has been reduced. This is also expected to reduce the incidence of shingles in adults in the future as these vaccinated children age.

Is shingles dangerous in pregnant women?

Pregnant women are susceptible to shingles, but fortunately, shingles inpregnancy is very rare. The antiviral medications described above are considered safe to use in pregnant women, as are most pain-relieving drugs. In the later stages of pregnancy, women should not take nonsteroidal antiinflammatory medications such as ibuprofen (Advil) ornaproxen (Aleve). However, acetaminophen(Tylenol) is considered safe even in the late stages of pregnancy.

The shingles vaccine should not be administered to pregnant women. It is recommended that a woman wait three months before trying to become pregnant after she has received the shingles vaccine. Having chickenpox during pregnancy has the potential to cause birth defects, depending upon when in the pregnancy the infection occurs. The risk of birth defects is believed to be lower with shingles than with primary chickenpox infection. If you do not know if you have had chickenpox, a blood test can determine whether you have antibodies (immune protection) against the virus. Those who received the chickenpox vaccine as well as those who have previously had chickenpox will have antibodies in their blood that are directed against the VZV virus.
Herpes simplex viruses are ubiquitous, host-adapted pathogens that cause a wide variety of disease states. Two types exist: herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2). Both are closely related but differ in epidemiology. HSV-1 is traditionally associated with orofacial disease, while HSV-2 is traditionally associated with genital disease; however, lesion location is not necessarily indicative of viral type. Up to 80% of herpes simplex infections are asymptomatic. Symptomatic infections can be characterized by significant morbidity and recurrence. In immunocompromised hosts, infections can cause lifethreatening complications. The prevalence of HSV infection worldwide has increased over the last several decades, making it a major public health concern. Prompt recognition of herpes simplex infection and early initiation of therapy are of utmost importance in the management of the disease. HSV (both types 1 and 2) belongs to the family Herpesviridae and to the subfamily Alphaherpesvirinae. It is a double-stranded DNA virus characterized by the following unique biological properties: [1] Neurovirulence (the capacity to invade and replicate in the nervous system) Latency (the establishment and maintenance of latent infection in nerve cell ganglia proximal to the site of infection): In orofacial HSV infections, the trigeminal ganglia are most commonly involved, while, in genital HSV infection, the sacral nerve root ganglia (S2-S5) are involved. Reactivation: The reactivation and replication of latent HSV, always in the area supplied by the ganglia in which latency was established, can be induced by various stimuli (eg, fever, trauma, emotional stress, sunlight, menstruation), resulting in overt or covert recurrent infection and shedding of HSV. In immunocompetent persons who are at an equal risk of acquiring HSV-1 and HSV-2 both orally and genitally, HSV-1 reactivates more frequently in the oral rather than the genital region. Similarly, HSV-2 reactivates 8-10 times more commonly in the genital region than in the orolabial regions. Reactivation is more common and severe in immunocompromised individuals.[2] Dissemination of herpes simplex infection can occur in people with impaired T-cell immunity, such as in organ transplant recipients and in individuals with AIDS. HSV is distributed worldwide. Humans are the only natural reservoirs, and no vectors are involved in transmission. Endemicity is easily maintained in most human communities owing to latent infection, periodic reactivation, and asymptomatic virus shedding.[3] HSV is transmitted by close personal contact, and infection occurs via inoculation of virus into susceptible mucosal surfaces (eg, oropharynx, cervix, conjunctiva) or through small cracks in the skin. The virus is readily inactivated at room temperature and by drying; hence, aerosol and fomitic spread are rare.

Pengertian Poxvirus merupakan virus lengkap yaitu virion dan dari inti asam nukleat yang dikelilingi lapisan protein yang bersifat antigenik yang disebut dengan kapsid dan terdapat selubung luar (envelope) yang terdiri dari protein dan lipid. Poxvirus ini berasal dari family poxviridae, merupakan penyakit penyebab cacar. Biasanya terjadi infeksi pada kulit. virus ini menyebar dari orang ke orang dengan menyentuh kulit yang terkena. Penanggulangan Cacar dapat dilakukan dengan vaksinasi dalam waktu tiga hari setelah terinfeksi akan mencegah atau secara signifikan mengurangi keparahan gejala cacar di sebagian besar orang. Vaksinasi empat sampai tujuh hari setelah terinfeksi dapat menawarkan beberapa perlindungan dari penyakit atau dapat memodifikasi keparahan penyakit. Selain vaksinasi, pengobatan cacar, seperti perawatan luka dan pengendalian infeksi, terapi cairan, dan bantuan ventilator. Pengertian Poxvirus merupakan virus lengkap yaitu virion dan dari inti asam nukleat yang dikelilingi lapisan protein yang bersifat antigenik yang disebut dengan kapsid dan terdapat selubung luar (envelope) yang terdiri dari protein dan lipid. Ciri mencolok dari DNA poxvirus adalah bahwa kedua untai komplementer bergabung. Intermediet replikatif, hadir dalam sitoplasma, yang concatemers khusus berisi pasang genom tersambung baik kepala atau ekor. Poxvirus ini berasal dari family poxviridae, merupakan penyakit penyebab cacar. Biasanya terjadi infeksi pada kulit. virus ini menyebar dari orang ke orang dengan menyentuh kulit yang terkena. Virus ini juga dapat menyebar dengan menyentuh permukaan dengan virus di atasnya, seperti handuk, pakaian, atau mainan. Setelah seseorang memiliki virus, benjolan dapat menyebar ke bagian lain dari tubuh mereka dengan menyentuh atau menggaruk benjolan dan kemudian menyentuh bagian lain dari tubuh. Siklus hidup poxvirus rumit dengan memiliki bentuk infeksi ganda, dengan mekanisme yang berbeda dan masuk ke sel. Poxvirus adalah unik di antara virus DNA dalam bahwa mereka bereplikasi dalam sitoplasma sel bukan di inti. Untuk mereplikasi, poxvirus menghasilkan berbagai protein khusus yang tidak diproduksi oleh virus DNA lainnya, yang paling penting yang merupakan virus terkait DNAdependent RNA polimerase. Kedua virion menyelimuti dan unenveloped yang menular. Virus ini terbuat dari membran Golgi dimodifikasi mengandung virus-spesifik polipeptida, termasuk hemaglutinin. Infeksi dengan baik variola besar atau variola minor menciptakan kekebalan terhadap yang lain. Proses Replikasi Virus DNA yaitu pada Poxvirus transkripsi terjadi pada inti dan terjemahan dalam sitoplasma. Umumnya, transkrip primer, yang dihasilkan oleh RNA polimerase II, lebih besar daripada mRNA ditemukan pada ribosom, dan dalam beberapa kasus, sebanyak 30% dari RNA ditranskripsi tetap diterjemahkan dalam nukleus. Para utusan virus, bagaimanapun, seperti sel-sel hewan, yang monocistronic. Transkripsi memiliki organisasi temporal, dengan virus DNA yang paling hanya sebagian kecil dari genom ditranskripsi menjadi utusan awal. Sintesis protein awal adalah langkah awal penting dalam replikasi DNA virus. Setelah sintesis DNA, sisa genom ditranskripsi menjadi utusan terlambat. Virus kompleks memiliki gen awal langsung, yang dinyatakan di hadapan inhibitor sintesis protein, dan tertunda gen awal, yang membutuhkan sintesis protein untuk berekspresi. Regulasi dilakukan oleh protein hadir dalam virion, atau ditentukan oleh gen virus atau selular, berinteraksi dengan urutan peraturan di ujung 5 gen.

Urutan ini dapat menanggapi di trans untuk produk yang dihasilkan oleh gen lain dan bertindak dalam cis pada gen yang terkait. Kelas yang berbeda mungkin gen ditranskripsi dari untai DNA yang berbeda dan oleh karena itu dalam arah yang berlawanan misalnya polyomaviruses. Transkrip dapat menjalani proses pasca-transkripsi sehingga urutan intervensi yang tidak penting akan dihapus. Modus replikasi adalah semikonservatif tetapi sifat intermediet replikatif tergantung pada cara replikasi. Penyakit cacar dalam bahasa medis disebut variola, sedangkan dalam bahasa Inggris disebut small pox. Penyakit yang disebabkan oleh virus poks (pox virus) ini sudah ada sejak berabad-abad yang lalu dan sangat mudah menular. Gejala yang terjadi bagi yang terinfeksi adalah demam, dan muncul gelembung-gelembung berisi nanah secara serentak di kulit daerah wajah, tangan, kaki, dan akhirnya seluruh tubuh. Penyakit ini kerap berakibat fatal, terutama bila mengenai bayi atau lanjut usia. Bagi yang bisa sembuh pun, akan memberikan bekas di kulit berupa bopeng-bopeng. Penyakit cacar yang disebabkan oleh poxvirus ini ada beberapa macam diantaranya yaitu cacar air, cacar ular dan cacar monyet. Cacar air, walaupun namanya mirip dengan cacar, merupakan penyakit yang berbeda. Cacar air, dalam bahasa medisnya disebut varisela, dan dalam bahasa Inggris dinamai chicken pox. Penyakit ini disebabkan oleh virus yang bernama virus varisela-zoster. Gejala berupa gelembung yang muncul kecil-kecil dan tidak serentak, yang dimulai dari bagian tubuh penderita lalu menjalah ke anggota tubuh lainnya. Secara umum, penyakit cacar air ini jauh lebih ringan dan tidak berbahaya seperti penyakit cacar. Cacar ular adalah nama awam untuk penyakit Herpes Zoster. Penyakit ini merupakan bentuk reaktivasi penyakit cacar air (varisela) yang pernah diderita seseorang sebelumnya. Perlu diketahui, bila seseorang terkena infeksi virus varisela-zoster untuk pertama kali, maka akan timbul penyakit cacar air. Setelah sembuh, virus tersebut tidaklah musnah seluruhnya dari tubuh penderita, melainkan berdiam di dalam tubuh penderita, tepatnya di ganglion saraf tepi penderitanya. Virus yang berdiam dalam tubuh penderita ini dapat sewaktu-waktu muncul kembali dan menyebabkan penyakit yang dinamai Herpes Zoster. Walaupun di dalam tubuhnya terdapat virus ini, namun kebanyakan orang memang tidak mengalami penyakit Herpes Zoster. Hal ini disebabkan daya tahan tubuh yang baik yang dapat menekan virus ini berkembang. Sebaliknya, pada orang yang daya tahannya sedang menurun, tak jarang penyakit ini tiba-tiba muncul menyerang. Istilah cacar monyet memang relatif tidak sepopuler istilah cacar lainnya yang telah disebutkan di atas. Penyakit ini nama ilmiahnya adalah impetigo bulosa, atau ada pula yang menamakan impetigo vesikulo-bulosa. Berbeda dengan jenis cacar lainnya yang disebabkan karena infeksi virus, cacar monyet ini disebabkan oleh bakteri Staphylococcus aureus. Secara klinis, penderita tidak mengalami demam ataupun gejala umum seperti pada cacar air ataupun herpes zoster. Gejala yang didapatkan adalah adanya gelembung yang munculnya terutama di ketiak, dada, dan punggung. Gelembung yang muncul ini cepat pecah dan jumlahnya tidak begitu banyak, namun kerap kali disertai pula oleh miliaria (biang keringat). Penanggulangan Cacar dapat dilakukan dengan vaksinasi dalam waktu tiga hari setelah terinfeksi akan mencegah atau secara signifikan mengurangi keparahan gejala cacar di sebagian besar orang. Vaksinasi empat sampai tujuh hari setelah terinfeksi dapat menawarkan beberapa perlindungan dari penyakit atau dapat memodifikasi keparahan penyakit. Selain vaksinasi, pengobatan cacar, seperti perawatan luka dan pengendalian infeksi, terapi cairan, dan bantuan ventilator.

Warts are benign proliferations of skin and mucosa caused by the human papillomavirus (HPV). Currently, more than 100 types of HPV have been identified. Certain HPV types tend to infect skin at particular anatomic sites; however, warts of any HPV type may occur at any site. The primary clinical manifestations of HPV infection include common warts, genital warts, flat warts, and deep palmoplantar warts (myrmecia). Less common manifestations of HPV infection include focal epithelial hyperplasia (Heck disease),[1] epidermodysplasia verruciformis, and plantar cysts. Warts are transmitted by direct or indirect contact, and predisposing factors include disruption to the normal epithelial barrier. Treatment is difficult, with frequent failures and recurrences. Many warts, however, resolve spontaneously within a few years even without treatment. A small number of high-risk HPV subtypes are associated with the development of malignancies, including types 6, 11, 16, 18, 31, and 35. Malignant transformation most commonly is seen in patients with genital warts and in immunocompromised patients. HPV types 5, 8, 20, and 47 have oncogenic potential in patients with epidermodysplasia verruciformis. Warts can affect any area on the skin and mucous membranes. The HPV virus infects the epithelium, and systemic dissemination of the virus does not occur. Viral replication occurs in differentiated epithelial cells in the upper level of the epidermis; however, viral particles can be found in the basal layer.

What is molluscum contagiosum?

A single molluscum bump on the neck of an adult man. Typical bumps are approximately 3-5 mm in diameter. Image courtesy Scott Norton, MD, MPH, Dept. of Dermatology, Walter Reed Army Medical Center View large image >Molluscum contagiosum is caused by a virus and usually causes a mild skin disease. The virus

affects only the outer (epithelial) layer of skin and does not circulate throughout the body in healthy people. The virus causes small white, pink, or flesh-colored raised bumps or growths with a dimple or pit in the center. The bumps are usually smooth and firm. In most people, the growths range from about the size of a pinhead to as large as a pencil eraser (2 to 5 millimeters in diameter). The bumps may appear anywhere on the body, alone or in groups. They are usually painless, although they may be itchy, red, swollen and/or sore. Molluscum usually disappears within 6 to 12 months without treatment and without leaving scars. Some growths may remain for up to 4 years. Top

Who gets molluscum contagiosum?

Molluscum infections occur worldwide but are more common in warm, humid climates and where living conditions are crowded. There is evidence that molluscum infections have been on the rise in the United States since 1966, but these infections are not routinely monitored because they are seldom serious and routinely disappear without treatment. Molluscum is common enough that you should not be surprised if you see someone with it or if someone in your family becomes infected. Although not limited to children, it is most common in children 1 to 10 years of age. People with weakened immune systems (i.e., HIV-infected persons or persons being treated for cancer) are at higher risk for getting molluscum, and their growths may look different, be larger, and be more difficult to treat. Top

How do people become infected with the molluscum virus?

The virus that causes molluscum is spread from person to person by touching the affected skin. The virus may also be spread by touching a surface with the virus on it, such as a towel, clothing, or toys. Once someone has the virus, the bumps can spread to other parts of their body by touching or scratching a bump and then touching another part of the body. Molluscum can be spread from one person to another by sexual contact. Although the virus might be spread by sharing swimming pools, baths, saunas, or other wet and warm environments, this has not been proven. Researchers who have investigated this idea think it is more likely the virus is spread by sharing towels and other items around a pool or sauna than through water. Top

How would I know if I had molluscum contagiosum?

Close-up view of typical molluscum bumps. Typical bumps are approximately 3-5 mm in diameter. Image courtesy Dave Bray, MD, WRAMC View large image >
Only a health care provider can diagnose molluscum infection. If you have any unusual skin irritation, rash, bump(s), or blister(s) that do not disappear in a few days, you should see a health care provider. If you have molluscum, you will see small white, pink, or flesh-colored raised bumps or growths with a pit or dimple in the center. The bumps are usually smooth and firm. They can be as small as the head of a pin and as large as a pencil eraser (2 to 5 millimeters in diameter). The growths are usually painless but may become itchy, sore and red and/or swollen. They may occur anywhere on the body including the face, neck, arms, legs, abdomen, and genital area, alone or in groups. The bumps are rarely found on the palms of the hands or the soles of the feet. Top

What should I do if I think I have molluscum contagiosum?

If you have any unusual skin irritation, rash, bumps, or blisters that do not disappear in a few days, contact a health care provider. Only a health care professional can diagnose molluscum. He or she will discuss treatment options and how to care for the affected skin. Top

How can I avoid becoming infected with molluscum?

The best way to avoid getting molluscum is by following good hygiene habits.

Do not touch, pick, or scratch any skin with bumps or blisters (yours or someone elses). Good hand hygiene is the best way to avoid getting many infections including molluscum. For handwashing tips, see the Clean Hands Saves Lives sitelet at http://www.cdc.gov/cleanhands. By washing your hands frequently you wash away germs picked up from other people or from contaminated surfaces. Top

What is the correct way to wash my hands?

First wet your hands and apply soap. Next rub your hands vigorously together and scrub all surfaces. Continue for 1015 seconds. Soap combined with scrubbing action helps dislodge and remove germs. Rinse well and dry your hands.