B Virus (Macacine Herpesvirus 1, Herpes B) 

Updated: Jun 20, 2019
Author: Sandra G Gompf, MD, FACP, FIDSA; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD 

Overview

Practice Essentials

B virus, whose scientific name is macacine herpesvirus 1 (McHV-1), is commonly referred to as herpes B. Other terms include simian herpes, monkey B virus, herpesvirus simiae, and herpesvirus B. B virus produces infection in several species of Old World macaque and cynomolgus primates. Human contact with macaque and cynomolgus species may occur during laboratory work with captive monkeys. In addition, the risk of nonoccupational human encounters with Old World monkeys may be increasing with the popularity of travel to developing and exotic locales.

Primates with B virus infection are often asymptomatic, but B virus, in rare cases, can produce life-threatening disease in humans with mucosal or percutaneous contact (bite, scratch, splash, or needlestick) to primate saliva or other body fluids. Approximately 70% of untreated infections result in fatal encephalitis in humans.

Human-to-human transmission is unlikely, but antibody seroconversion has been documented in one case, in the wife of an infected animal handler after using an ointment on her skin with which she treated his wounds; she herself did not develop clinical illness.[1]

Contact with primate body fluids, however healthy-appearing the animal, must not be ignored. Exposed wounds or mucosa should be immediately washed with soap and water, followed by evaluation for prophylactic antiviral therapy. While laboratory protocols for handling of primates and occupational exposures exist, the general public and many clinicians remain unaware of B virus.

Prompt consultation with public health officials or an infectious disease specialist may facilitate assessment for antiviral prophylaxis of primate exposures.

Background

Macacine herpesvirus 1 (McHV-1) is an alphaherpesvirus that is enzootic to the rhesus (Macaca mulatta) and cynomolgus (Macaca fascicularis) members of the macaque genus, Macaca (as seen in the image below). Among the nonhuman-primate herpesviruses, only B virus is known to cause disease in humans. Its medical importance is its propensity to cause devastating central nervous system (CNS) infection after contact of infected saliva with mucosal fluids, wounds, or tissues. This fact is known in the research community, and there are published protocols for preventing exposures, as well as postexposure prophylaxis. While many clinicians and the lay public are unaware of the risk, opportunities for nonoccupational human encounters with Old World monkeys are increasing.

This is a photo of long-tailed macaques socializin This is a photo of long-tailed macaques socializing in the wild. The long-tailed macaque, Macaca fascicularis, is a major reservoir for the herpes B virus. (Photo courtesy of Carel van Schaik)

These primates may be found in close proximity to human habitation in the Caribbean and other parts of the world. Humans may be exposed to B virus during international travel and during travel to US territories. Originally imported for clinical research, some animals escaped, and free-ranging populations of rhesus and patas monkeys now inhabit rural and urban areas of Puerto Rico, as well as surrounding islands. A rhesus monkey colony has been established since the 1930s in Silver Springs State Park, Florida, where they were imported in the 1930s to boost tourism. Both populations have been observed to have antibodies to B virus and to shed reactivated virus in saliva.[2]

Similar to human herpes simplex virus (HSV), B virus belongs to the family Herpesviridae, subfamily Alphaherpesvirinae, genus Simplexvirus. It is properly referred to by its current taxonomic name, macacine herpesvirus 1 (McHV-1).[3] Adding confusion, it may also be identified in literature as macacine alphaherpesvirus 1 or under an older taxonomy, cercopithecine herpesvirus 1. The term herpes B was coined in 1934 from the initials of the first human case, which was described in detail by Sabin and Wright; "Dr. W.B." was a 29-year-old researcher who developed fatal meningoencephalitis and transverse myelitis following a bite on the hand from a seemingly healthy rhesus monkey.[4]

B virus contains double-stranded linear DNA and has a molecular weight of approximately 110 megadaltons (approximately 162 kilobase pairs). It shares about 50% of its genes with human herpes simplexviruses and expresses the same glycoprotein D (HSV-1 gD) binding proteins. However, infection of human cells may take different routes and is under study. Unlike human herpes simplexviruses, B virus gD does not bind herpesvirus entry mediator (HVEM) proteins, but fuses with human nectin-1, nectin-2, and, possibly, other surface proteins.[5, 6, 7]

Most macaques infected with B virus are asymptomatic. When symptoms do occur, they are very similar to those caused by HSV infection in humans. The most obvious manifestation of B virus infection is the presence of fluid-filled vesicles on the back of the tongue, lips, and elsewhere in the mouth; occasionally, the vesicles appear on the lips. When the vesicles rupture, they often give rise to ulcers and necrotic scabs, which may lead to secondary bacterial and fungal infections. Scabs typically heal within 7-14 days. Conjunctivitis of varying severity is another common symptom.

In rare instances, B virus may cause systemic illness in macaques, including the occurrence of ulcerative lesions in the mouth, esophagus, and stomach and necrosis of the liver, spleen, and adrenal glands. While the virus is shed in saliva and in conjunctival, nasal, and genital fluids, viremia is uncommon.[8, 9, 2] Similar to human HSV infection, after acute infection, B virus remains latent in the ganglia of trigeminal and lumbosacral nerve roots and may reactivate intermittently owing to stress or illness. The animals commonly transmit infection to each other via shared ocular, nasopharyngeal, and venereal fluids.

Members of the genus Macaca (>16 species) are natural hosts of B virus, and almost all of these hosts naturally exist in Asia. Both wild and captive macaque populations generally exhibit high rates of herpes B virus infection, but most individuals exhibit few or no symptoms of infection. The strongest evidence for this pattern of high prevalence and mild infection comes from the rhesus, Japanese, and long-tailed (or cynomolgus) macaques, all of which are very closely related phylogenetically. In wild and semi–free-ranging populations of long-tailed and rhesus macaques, seroprevalence rates (or prevalence of serum-detected herpes B virus–induced antibodies) typically exceed 70%.

Captivity likely affects the risk of shedding, which is expected to be higher in stressed, breeding, or immunocompromised animals. In surveys of captive populations, 80%-100% of adults are seropositive for B virus.

Pathophysiology

In humans, B virus produces local infection at the inoculation site, with concomitant local and regional inflammatory changes. Vesicular eruption, local pruritus, numbness, or tingling may occur. Regional lymphadenitis and lymphangitis may also occur, and lymph nodes draining the entry site may demonstrate hemorrhage and focal necrosis on histopathology.

Within 4 weeks of inoculation, the virus progresses via peripheral nerves to the CNS, causing local and systemic inflammation and neurologic dysfunction along the way. Beginning with peripheral paresthesia at the site of infection, symptoms progress centrally to produce global CNS pathology, including meningitis and encephalitis, cranial nerve palsies, and brain stem impairment.[10, 11, 1] Systemic symptoms with fevers, rigors, conjunctivitis, sinusitis, and myalgias occur and may be the only manifestation in some cases. At least one case in which disease occurred years after exposure has been reported, suggesting that herpes B virus might be able to become latent and reactivate in humans.[12] Self-limited aseptic meningitis has been reported, but almost all cases produce substantial morbidity and mortality.

Epidemiology

Frequency

United States

Of roughly 45 well-documented cases of B virus infection in humans, two thirds occurred in the United States and the others were reported in Canada and Great Britain. Most of the well-documented human cases occurred in the 1950s and 1960s, when large numbers of rhesus macaques were used in the production and testing of poliomyelitis vaccines. In the late 1980s, several cases in Pensacola, Florida and Kalamazoo, Michigan, refocused attention on B virus, and several other cases have since been documented. The increase coincides with an increased use of macaques in human immunodeficiency virus (HIV) research.

International

Reports of human B virus infection from countries where macaques are prevalent and commonly interact with humans are uncommon. Whether the absence of these reports is due to the limited availability of B virus diagnostic facilities (ie, actual cases not identified) or if some other factors are responsible (eg, different animal-handling procedures) is unclear. B virus has been identified in wild macaque species in Asia and Southeast Asia. Increasing opportunities for human B virus infections is a concern because of increasing human encroachment upon natural habitats and increasingly adventurous travel.

Age

The average age of persons who develop B virus infection reflects the demographics of individuals involved with the care of primate hosts in research laboratories.

Transmission

Information regarding the epidemiology and transmission of B virus in primates is vital in order to understand how to prevent this high-mortality infection.

Macaques transmit B virus to each other through oral, ocular, or genital contact of mucous membranes or lesioned skin. B virus can be shed asymptomatically, including through bodily fluids (eg, semen, mother's milk, saliva, perhaps even in aerosol form). The animal stools could also conceivably transmit the virus. In captive macaques, transmission may often occur during routine colony management protocols involving tube sharing, common instrumentation, or contaminated gloves. Animals usually become infected as juveniles, at the onset of sexual activity; however, younger animals can become infected through contact with another virus-shedding animal. For example, a nursing mother has repeated opportunities to transmit the virus in buccal or conjunctival fluids to a nursing infant during grooming.

Conclusively determining transmission pathways may not be possible because most human cases of B virus infection involve individuals who regularly work with monkeys, thus providing many potential means of exposure. Suspected transmission modes include monkey bites, monkey scratches, or cage scratches; direct contamination of a preexisting wound with macaque saliva; respiratory exposure to aerosol macaque saliva; mucosal splash exposure; cuts sustained from culture bottles containing macaque kidney cells; needle-stick injuries following needle use in macaques; and cleaning a rhesus macaque skull without gloves. In addition, one apparent case of human-to-human herpes B virus transmission involved a woman with dermatitis on her finger; she touched her husband's herpetiform lesion (resulting from a monkey bite).[10]

Given the myriad potential transmission pathways and abundance of macaques in contact with people, the fact that relatively few documented cases of B virus infection occur in humans may seem surprising. Nevertheless, although most macaques test positive for B virus antibodies, only a small percentage (ie, 0-2%) shed the virus at any given time. In most animals, the virus is latent in the trigeminal ganglia and becomes reactivated only when the macaque experiences psychological stress, pharmacological stress, or diminished immunocompetence.[12]

The widely observed pattern of increasing frequency with age suggests that horizontal transmission is far more common than vertical transmission (ie, mother to offspring). Whether this horizontal transmission occurs most commonly via oral or genital contact, including sexual behavior, is unresolved.

Prognosis

Historically, human B virus encephalitis carries a case-fatality rate of up to 80%, a rate similar to that of untreated HSV encephalitis. Most individuals with encephalitis succumb to the infection despite antiviral therapy.

As with HSV encephalitis, many survivors of B virus infection have substantial residual neurologic deficits.

Patient Education

There is currently no commercially available vaccine against B virus.

All workers who handle macaque and cynomolgus monkeys should be aware of the risk, preventive procedures, and postexposure prophylaxis protocols for B virus infection. Some percentage of captive populations may be expected to be shedding the virus at any point in time.

Known habitats for macaque and cynomolgus monkeys include Asia, Southeast Asia, Silver Springs State Park in Florida, and Puerto Rico.

Travelers to rural and developing areas that these primates may inhabit should be aware of the risk posed by contact with primates and other animals and should be counseled to avoid feeding or touching them. In addition to pre-exposure prophylaxis against rabies, travelers should consider access to healthcare and local availability of postexposure antivirals for a monkey bite. The prospect of B virus infection may diminish the allure of photographs with these animals, regardless of the social media impact. Avoidance of contact is entirely effective for preventing B virus infection.[2, 1, 13]

 

Presentation

History

The incubation period of B virus infection ranges from 2-30 days, with progression of symptoms over 7-10 days. Following potential exposure to B virus in humans, the individual exposed and the primate (if available) should be monitored (see Laboratory Studies).

Early symptoms (variably present) may include the following:[1]

  • Pain or pruritus at exposure site
  • Vesicles or ulcers at or near exposure site
  • Local lymphadenopathy or lymphadenitis

Intermediate symptoms (variably present) may include the following:[1]

  • Fever
  • Malaise
  • Diffuse myalgias
  • Headache
  • Numbness or paraesthesias at or near exposure site
  • Nausea and/or abdominal pain
  • Persistent hiccups

Late manifestations may include the following:[1]

  • Persistent headache
  • Alteration of mentation
  • Focal neurological symptoms

Physical Examination

Findings of B virus infection include progressive neurologic deterioration that suggests a multifocal hemorrhagic encephalitis or encephalomyelitis. This finding contrasts with the temporal lobe localization of herpes simplex encephalitis. The progression of signs and symptoms may be modified by early antiviral therapy. Asymptomatic human B virus infection is unknown, if not nonexistent. Typical physical signs include the following:[1]

  • Meningismus
  • Confusion progressing to coma
  • Brain stem findings, which may include diplopia, dysarthria, dysphagia, cerebellar signs (including ataxia), and/or cranial nerve palsies
  • Signs of meningoencephalomyelitis, which may include seizures, hemiparesis or hemiplegia, progressive ascending paralysis, and/or transverse myelitis
  • Non-CNS signs, which may include conjunctivitis, chorioretinitis, and/or sinusitis

Complications

Aseptic meningitis results in a moderate lymphocyte pleocytosis and erythrocytes, moderately elevated cerebrospinal fluid (CSF) protein level, and normal CSF glucose. In humans, B virus can be grown from CSF, skin lesions, and urine.

Nonfatal cases of human B virus infection may result in complete recovery, but residua are common and include the following:

  • Extremity paresis or plegia
  • Aphasia
  • Dysarthria
  • Residual chorioretinitis

Because of prolonged or long-term use of antiviral therapy in surviving patients, the frequency of asymptomatic or symptomatic reactivation and/or viral shedding occur is unclear.[1]

 

DDx

 

Workup

Laboratory Studies

Evaluation of the potential primate vector

Obtain virus cultures from buccal mucosa (for saliva exposure), conjunctivae, and the urogenital area (for urine exposure) of the involved primate. If a cage was involved, acquire swab cultures from the monkey that was most recently housed there.

Because B virus is a Biosafety Level class 4 pathogen, cultures should be performed only at a designated reference laboratory.

Serologic evaluation of the exposed patient

If frozen serum from the last 6 months is not available, acquire, freeze, and store a serum sample.

Obtain a follow-up serum sample approximately 3 weeks after exposure or after the onset of illness (as close to 3 wk as possible) to test with the initial specimen for herpes B virus seroconversion.

Perform serologies in a reference laboratory to minimize cross-reacting HSV antibodies. Although further research is required, newer recombinant DNA techniques may allow for differentiation of herpes B virus infection from HSV infection.[14]

Some human cases of herpes B virus infection have resulted in a slow or minimal rise in virus-specific antibody, confounding serological confirmation.

Polymerase chain reaction

Polymerase chain reaction (PCR) technology may permit faster and more accurate assessment of both human and primate cases. Newer studies are aimed at developing a PCR test that is not only sensitive but also specific, allowing for differentiation from HSV.[15]

Other Tests

Veterinary evaluation of monkeys

The importance of evaluating the primate should be weighed against the potential of further injuries if the monkey must be recaptured without anesthesia.

After anesthesia, the monkey should be examined for oral lesions, genital lesions, or conjunctivitis.

High-risk exposure includes any injury associated with an ill, immunocompromised, or lesioned animal.

Remember that asymptomatic shedding of herpes B virus may occur and is more likely during breeding season or times of stress.

Serial serologies can be obtained from the primate because a rise suggests primary infection and a higher risk of viral shedding. Stable serologies do not predict shedding, which occurs in only 2-3% of cases.

 

Treatment

Approach Considerations

Treatment for B virus infection is not recommended in the case of exposure to non-macaque primates or exposure of intact skin to a source that is not high-risk (see below).

All macaque species must be presumed to be infected with B virus at the time of a human exposure, as previous serologic testing may not reflect a recently acquired infection.

High-risk exposures

Treatment for B virus infection is recommended for high-risk exposures, as follows:

  • Skin or mucosal exposure to a high-risk source (eg, primate is clinically ill, immunosuppressed, actively shedding B virus, or has lesions suggestive of B virus infection)
  • Inadequately cleansed exposure to nonintact skin (with or without injury)
  • Inadequately cleansed mucosal splash
  • Laceration of the head, neck, or upper body
  • Deep puncture bite
  • Puncture or laceration with needle, device, or other object either (1) contaminated with fluid from monkey oral or genital lesions or with nervous system tissues or fluid or suspicious skin lesions or (2) known to contain B virus
  • Culture positive for B virus performed after the wound was cleansed

Medium-risk exposures

Treatment should be considered for medium risk exposures, as follows:

  • Needlestick injury with a needle containing blood from a clinically ill or immunosuppressed macaque
  • Laceration or broken skin or mucosa contaminated with other body fluids or possibly infected cell culture
  • Mucosal splash with adequate cleansing

Medical Care

Refer to the most recently published guidelines for a detailed discussion.[10] The substance of these guidelines is delineated below. Prompt attention to a potential exposure is vital to minimize the risk of this disease, which carries high morbidity and mortality rates.

Wound decontamination and culture

Cleansing of the exposed area within minutes of the episode is the only means of preventing a contaminated wound from progressing to actual infection. B virus is likely to enter host cells within 5 minutes.

At least 15 minutes of scrubbing and/or irrigating the exposed area is recommended. Sterile saline or rapidly flowing water is used for the eye, and decontaminants (eg, soap solution, povidone-iodine, chlorhexidine) can be used at other sites.

Dakin solution (0.25% hypochlorite) has been suggested for high-risk deep lacerations or needle sticks, as it may inactivate herpesviruses. The solution must be fresh, and standard decontaminants should be used after a 5-minute treatment. Dakin solution should never be used to wash the eyes or mucous membranes.

After cleansing of a high-risk wound, cultures for B virus should be performed.

Antiviral therapy

Antiviral therapy is clearly indicated for suspected clinical cases of human B virus infection; use of prophylactic antiviral therapy is problematic.

The decision regarding postexposure prophylaxis should be individualized and made by a health care provider experienced with the evaluation, treatment, and prevention of B virus infection. Early prophylaxis may prevent either overall or symptomatic infection; on the other hand, infection is quite rare compared with the number of exposures.

The ability of therapy to prevent B virus infection is not documented, and therapy can suppress shedding and seroconversion, further complicating diagnosis. In addition, the length of therapy is undefined.[10]

B Virus Postexposure Prophylaxis

Postexposure prophylaxis is recommended up to 5 days after exposure or longer if a postcleansing wound culture is positive for B virus, given that results may be delayed. The exposed person should be evaluated frequently and monitored with serologic testing for B virus, for example, at 1, 2, and 4 weeks postexposure. Because postexposure prophylaxis may delay seroconversion, patients receiving antivirals should be retested for antibodies 12 weeks postexposure. Positive postcleansing wound culture findings should prompt cultures of conjunctivae, oropharynx, and any unhealed suspicious skin lesions 1-2 weeks after completion of antiviral therapy. A culture positive for B virus at any point warrants intravenous therapy (see Treatment of B Virus Infection, below).

Postexposure prophylaxis regimens include the following:

  • Valacyclovir 1000 mg PO every 8 hours for 14 days
  • Acyclovir 800 mg PO 5 times per day for 14 days

Treatment of B Virus Infection

Advanced encephalitis is often fatal despite antiviral therapy. Duration and discontinuation of treatment is based on expert guidance. B virus is believed to behave similarly to other human herpesviruses and is reported to have reactivated from latent infection in at least one human case.

Treatment regimens for early symptoms without CNS symptoms include the following:

  • Acyclovir 12.5-15 mg/kg IV every 8 hours OR
  • Ganciclovir 5 mg/kg IV every 12 hours

Treatment for CNS symptoms consists of ganciclovir 5 mg/kg IV every 12 hours.

Acyclovir is preferred in pregnant patients. Currently, treatment with intravenous (IV) antivirals is recommended until symptoms resolve and two sets of cultures yield negative results for 14 days. Thereafter, treatment can be deescalated to oral therapy, as for postexposure prophylaxis, for 6-12 months. Thereafter, a lower oral dose may be considered and continued indefinitely for long-term suppression.[10]

Surgical Care

Incision of wounds directed at diagnosis or treatment is usually of little benefit and can increase the risk of secondary bacterial infection. Therefore, it is not generally recommended.[10]

Consultations

For prevention protocol and specimen testing, obtain appropriate consultation from occupational health personnel of primate centers. In addition, the National Institute of Health’s National Center for Research Resources funds the National B Virus Resource Center, which is an excellent resource for numerous topics related to herpes B virus, including both diagnostic testing and education. Other resources include the Centers for Disease Control and Prevention Emergency Operations Center (available 24/7 at 770-488-7100) and the National Institute for Occupational Safety and Health.

Prevention

Developing herpes B virus–free colonies

The endeavor to develop virus-free colonies has found some success, especially in the United States, where the National Center for Research Resources took a leading role in the 1990s by promoting experimental strategies in husbandry and management.

Achieving completely herpes B virus–free colonies has proven difficult because some macaques may show no antibodies but may retain latent herpes B virus particles. Furthermore, the B virus may become reactivated and shed without any visible symptoms.

Because of the relative ease of monkey-to-monkey transmission, even a single animal infected with herpes B virus may compromise the virus-free status of an entire facility.

Current research focuses on the development of techniques (eg, PCR) to reduce false-negative results and the implementation of regular screening protocols that quickly identify infected monkeys.

Accepting moderate to high infection rates in macaques but minimizing human exposure to herpes B virus

Minimizing social, nutritional, pharmacological, and psychological stress (especially overcrowding and shipping) can reduce viral shedding by monkeys. Promoting good veterinary care and immunocompetence also can reduce shedding.

Eliminating transmission pathways can prevent human exposure. Some means of prevention include the use of protective suits, gloves, eye shields, and similar devices. Given the difficulties and costs of achieving herpes B virus–free colonies, these methods may remain the reality at most facilities, at least for the near future.

Nonmacaque species are highly susceptible to herpes B virus infection. The risk of infection in these animals can be easily minimized by housing macaques in separate nonadjacent cages. A failure to follow this precaution has sometimes led to cross-species infection and fatalities.

Immunoprevention

Immunoprevention has been attempted in animal studies using several different vaccines. Most recently, a recombinant vaccinia virus that expresses herpes B glycoprotein D appears promising in preventing infection and/or latency.

 

Medication

Medication Summary

Specific antiviral agents are recommended as soon as possible to attempt prevention of herpes B virus disease progression in humans or when prophylaxis is indicated. No treatment is currently approved for herpes B virus infection by the US Food and Drug Administration. Early treatment has been successful in modifying infection in some animal models, but human data, albeit anecdotal, have been mixed. The progression of complications seems to be limited in some human reports. The dosing, especially for prophylaxis, is not clearly delineated. Because of its bioavailability profile, valacyclovir seems preferable to acyclovir for oral use in either treatment or prophylaxis.

Topical antiseptic compounds or preparations are used topically on potentially contaminated or infected body surfaces or on inanimate objects. In these cases, the topical antiseptics are used to inactivate any herpes B virus remaining in the wound after irrigation.

Antivirals

Class Summary

Nucleoside analogs are initially phosphorylated by viral thymidine kinase to eventually form a nucleoside triphosphate. These molecules inhibit HSV polymerase with 30-50 times the potency of human alpha-DNA polymerase. Herpes B virus thymidine kinase has only recently been characterized. Initial in vitro study has suggested that, under experimental conditions, B virus thymidine kinase is less susceptible to several commonly used antiherpes drugs, including acyclovir and ganciclovir. This may lead to further research aimed at developing more effective alternatives than the currently accepted drugs for this infection.[16]

Acyclovir (Zovirax)

Synthetic purine nucleoside analogue with activity against a number of herpesviruses, including herpes B. Primarily available in preparations for PO and IV use. Highly selective for virus-infected cells because of high affinity for viral thymidine-kinase enzyme. This effect serves to concentrate acyclovir monophosphate into virus-infected cells. The monophosphate is then metabolized into triphosphate active form by cellular kinases.

Valacyclovir (Valtrex)

Hydrochloride salt of the L-valyl ester of acyclovir. Rapidly converted into acyclovir after prompt absorption from the gut via first-pass intestinal or hepatic metabolism. An alternative to acyclovir for prophylaxis (or possibly treatment).

Topical antiseptics

Class Summary

These agents are to be used for decontamination of affected areas. Scrubbing should persist for at least 15 min.

Povidone-iodine (Betadine)

Broad-spectrum germicidal agent used topically on skin or mucous membranes. Used as a surgical scrub or topical cleanser. Elemental iodine is the active form.

Chlorhexidine oral (Hibiclens, Peridex, PerioChip)

Effective, safe, and reliable topical wash or PO mouthwash antiseptic. A polybiguanide with bactericidal activity; usually is supplied as a gluconate salt. At physiologic pH, the salt dissociates to a cation that binds to bacterial cell walls. Commercially available central venous catheters impregnated with chlorhexidine and silver sulfadiazine are available.

Dakin solution

Originally described by Dakin in 1915. Made from sodium carbonate, salt, bleaching powder, and boric acid. Today, commonly referred to 0.5% sodium hypochlorite (a 1:10 dilution of household bleach). Solution deteriorates with time and should be made fresh. Further dilutions also can be made. Some physicians use it as part of pressure ulcer management. Because of potential injury, other topical antiseptics usually are used.