Breastfeeding Mother with Chickenpox (Varicella) By Shella Riana, MD Introduction Varicella-zoster, also known as Chickenpox, is quite familiar and a worldwide disease. This infectious disease can affect anyone, especially those who have not received immunization. In Indonesia, data records for cases of varicella or chickenpox nationally remains inadequate and limited only in some certain areas. Data from the Banyumas (Central Java Province) District of Health Office states, during the period from January to November 2007, there were 691 persons affected by varicella. Varicella caused by Varicella-Zoster Virus (VZV), which is a worldwide epidemic. Although Varicella-zoster infection is classified as a mild infection, due to its high probability to become a severe sickness and high possibility of death in immunocompromised patients, this infection should be treated and prevented carefully. VZV is a family of human herpes viruses. The virus consists of a double stranded DNA genome, covered in a nucleus containing protein and wrapped by glycoprotein. The VZV can cause primary, latent, and recurrent infections. Primary infection manifests as varicella (chickenpox); reactivation of latent infection causes herpes zoster (also known as ‘shingles’). This disease is very contagious with characteristic reddish vesicle lesions. The latent reactivation of the VZV generally occurs in the sixth decade with the appearance of shingles characterized as vesicular lesions limited to a specific dermatomes and accompanied by severe pain.BANNER 728 x 90 Definition Chickenpox is a viral infectious disease caused by the Varicella-Zoster virus which can manifest into varicella (chickenpox) and its latent reactivation causes herpes zoster (shingles).1 Varicella is usually a limited disease that lasts for four to five days and some symptoms often characterized by fever, malaise, and generalized vesicular rashes usually consisting of 250-500 lesions. Infants, adolescents, adults, and immunocompromised people are at higher risk for complications. Etiology Chickenpox and shingles are caused by VZV, a family of the herpes virus, very similar to the Herpes Simplex Virus. This virus has an envelope, icosahedral shape, and a double chain DNA that encodes more than 70 kinds of proteins. VZV is a Human Herpes Neurotropic virus that causes less than four million cases of smallpox each year. After smallpox, VZV becomes latent in the cranial nerves, dorsal roots and autonomic nervous system ganglia along the neuraxis. VZV or herpes virus, consists of a double-chain DNA genome surrounded by protein and contained in an envelope of icosahedral and lipids on the outer membrane. The VZV genome has 69 different genes that encode proteins to form viruses and enter the host cell. Viral DNA replication and new virion synthesis spreads to adjacent uninfected cells VZV, like other human herpes viruses, is a threat to hematopoietic cell transplant recipients (HCT). During primary infection, which causes varicella, VZV remains in dorsal sensory root ganglia cells. Among adult HCT patients, most VZV infections indicate reactivation of latent viruses. Classic herpes zoster, with a dermatomal vesicular rash is the most common clinical symptom caused by VZV reactivation, but some HCT recipients have a general vesicular exanthema that resembles varicella, neuropathic pain syndrome, or organ involvement not associated with any rash.5 Epidemiology There are no differences according to sex or race. This contagious disease has rate of ± 90% among vulnerable people. The incidence ranges from 65-86% with a period of transmission between 24-48 hours before skin lesions appear and between 3-7 days after the lesion appears. About 50% of cases occur in children aged 5-9 years, many are found in ages 1-4 years and 10-14 years. There were 11,000 cases of varicella hospitalization with 100 people die each year.1 A lethal perinatal varicella may occur if pregnant women infected by varicella within five days before delivery or 48 hours after giving birth. Death is related to the low immune system among the neonates. Congenital varicella is often characterized by limb hypoplasia, skin lesions, and microcephaly. Overall, the incidence of herpes zoster is 215 per 100,000 people per year. About 75% of the cases occur over the age of 45 years and the incidence will increase in patients with a low immune system The epidemiology of chickenpox seems to change. There had been a shift in the age distribution of cases over the past 20 years. This condition is shown in the increased consultation for chickenpox in general practice and more deaths due to varicella in England and Wales. Based on hospital admissions data for chickenpox in young adults, there is similar evidence in the United States. Epidemiological changes have important consequences for the future such as death and risk of infection in health workers and pregnant women.6 Chickenpox is generally considered a mild disease in countries where most cases occur in children. In immunocompetent children, complications rarely occur with fewer than 2 deaths per 100,000 cases in children aged 1-14 years. Though, in adults, chickenpox is more often associated with complications and death. Varicella can lead to pneumonia in 1 out of 400 cases and is very severe in smokers. Encephalitis is a more serious complication, with 10% mortality and long-term up to 15% of victims Varicella is mainly occurs in children under 20 years, especially 3 to 6 years and only about 2% occurs in adults. In America, varicella often occurs in children under the age of 10 years and 5% of cases occur at the age of more than 15 years and in Japan, generally occurs in children under the age of 6 as much as 81.4%. Pathogenesis VZV is a contagious in 1-2 days before skin lesions appear. It can be transmitted through the respiratory tract and cause lesions in the oropharynx. These lesions facilitate the spread of the virus through the respiratory tract pathway. In this phase, transmission occurs through droplets to the mucous membranes of healthy people, such as the conjunctiva. The incubation period lasts around 14 days, where the virus will spread to the lymph glands, then expand to the liver and mononuclear cells. VZV in mononuclear cells begins to disappear 24 hours before the onset of the skin rash; in immunocrompomised patients, the virus disappears later that is 24-72 hours after the onset of the skin rash. These viruses migrate and replicate from capillaries to skin tissue and cause maculopapular, vesicular and crustal lesions. This infection causes fusion of epithelial cells to form multinucleus cells characterized by intranuclear eosinophilic inclusions. The development of vesicles is related to the event of “ballooning”, which can be observed by degeneration of epithelial cells, which will cause a room filled with fluid. The spread of lesions on the skin is known to be caused by the presence of ORF47 kinase protein, which is useful in the process of viral replication. VZV can cause disseminated infections that are usually associated with a low immune system. In most infected patients, replication of the virus can defeat the body’s immature defense mechanisms, continued by the second viral replication cycle that occurs in the liver and spleen, which results in secondary viremia. In this phase, the virus particles will spread throughout the body and reach the epidermis between 14 to 16 days, which results in the appearance of lesions on the typical skin. A child who has varicella will transmit it to others ranging from two-days before and up to five-days after the onset of the lesion on the skin.2 In herpes zoster, the pathogenesis is not yet fully known. During varicella, VZV moves from skin lesions and mucosal surfaces to sensory nerve endings and centripetally transported through sensory nerve fibers to the sensory ganglion. In the ganglion latent infection occurs, where the virus is no longer contagious and does not multiply, but still has the ability to turn into an infectious virus reactivation.2 Clinical Manifestation It starts with prodromal symptoms such as fever, malaise, headache, and abdominal pain, which last between 24 to 48 hours before skin lesions appear. Systemic symptoms such as fever, fatigue, and anorexia can occur along with skin lesions. Symptoms of the respiratory tract and vomiting rarely occur. Initial skin lesions of the scalp, face, body, are usually very itchy, in the form of a reddish macula, then turn into small vesicle lesions and contain fluid in them, similar to the appearance of teardrops. Healing is characterized by the formation of new skin epithelial cells that appear from the base of the lesion. Hypopigmentation can occur due to healing of the lesion. Scarring due to varicella infection is rare. 1 Lesions in varicella, beginning in the face and scalp area, then extending to the chest (centripetal spread) and then can extend to the extremities. Lesions can also be found in the oral and genital mucosa. Lesions in varicella are usually very itchy and often shown all stages of the lesion simultaneously. At first, a small erythematous macule arises in the face and chest area, and then changes rapidly within 12-14 hours to become a papule and then develops into clear vesicles containing erythematous fluid.2 The vesicles formed with an erythematous base have a classic form, which is superficial and has thin walls so that it looks like a tear drop, 2-3 mm in diameter, elliptical in shape, with an axis that is parallel to the skin fold or visible vesicles like dew points on the leaves of a rose (dew drop on a rose petal). Vesicle fluid quickly becomes cloudy due to the entry of inflammatory cells so that on day 2 it will turn into pustules. The lesions will dry out beginning at the center so that they form umbilization (delle) and eventually become crust within 1-3 weeks. In the healing phase, varicella rarely forms scar, if not accompanied by bacterial secondary infection. Shingles in children is rarely preceded by prodromal symptoms. Symptoms that can be found are radicular pain, paresthesia, malaise, headache and fever, usually occurring 1-3 weeks before the rash appears on the skin. Skin lesions that are typical of herpes zoster are usually unilateral localization and rarely cross the midline of the body. Locations that are often found are in T3 to L2 dermatomes and cranial nerve V and VII. Initial lesions in the form of erythematous macules and papules, then within 12-24 hours will develop into vesicles and will continue to become pustules on days 3-4 and finally on the 7th day crusts will form and can heal without scarring, unless there is a secondary bacterial infection.2 Additional Examination Laboratory tests are very important for diagnosing patients suspected of having varicella or herpes zoster and for determining appropriate antiviral therapy. Leukopenia occurs in the first 72 hours, followed by lymphocytosis. Examination of liver function (75%) also increased. Patients with neurological disorders due to varicella usually experience lymphocytic pleocytosis and increased protein in cerebrospinal fluid and glucose, which are generally remains in normal limits. Tzank test Some specimens are taken from the scraping base of the new vesicles, then stained with hematoxylin-eosin, Giemsa’s, Wright’s, toluidine blue or Papanicolaou’s. Through a light microscope, multinucleated giant cells will be found. This test sensitivity is around 84% This test cannot distinguish between varicella zoster virus and herpes simplex virus. PCR technique Virological methods by detecting viral DNA or viral proteins are used as one of the methods of diagnosing VZV infection. Specimens should be stored in ice or refrigerator at a temperature of -70ºC if storage is carried out for a longer period of time. Serology techniques One of the serological methods used to diagnose VZV infection is based on the examination of acute serum and convalescence, namely IgM and IgG. VZV IgM examination has low sensitivity and specificity. VZV reactivation triggers IgM, which is sometimes difficult to distinguish from the presence of IgM in primary infection. One of the reasons for checking IgG antibodies is to determine a person’s immune status, where the history of varicose veins is unclear. IgG examination has clinical importance, in order to know passive antibodies or have received an active vaccine against varicella. The presence of IgG is basically a sign of latent infection unless the patient has received passive antibodies from immunoglobulins. Another technique is to use membrane antigen assay fluorescents. This examination can detect antibodies that are bound to cells infected by VZV. This test is very sensitive and specific, almost similar to the examination of enzyme immunoassay or immunoblotting. Another supportive serological examination is latex agglutination, to determine the status of immunity against VZV. Treatment Varicella and herpes zoster in immunocompetent children usually do not require specific treatment unless it is symptomatic:2 If the lesion is still in the form of vesicles, powder can be given so that it is not easily broken. If the vesicle has ruptured or causing crust formation, antibiotic ointment can be given to prevent secondary infection. Antipyretics and analgesics (except the group of salicylates (aspirin) to avoid the occurrence of Reye’s syndrome). The fingernails must be cut to prevent secondary infection from scratching. Provision of antiviral drugs can reduce the duration of illness, severity and healing time will be shorter. Antiviral drugs should be within a period of less than 48-72 hours after the eruption in the skin appears. Antiviral drug classes that can be given are acyclovir, valacyclovir and famasiklovir. Oral antiviral doses for the treatment of varicella and herpes zoster that can be given are: Neonate: Acyclovir 500 mg / m2 IV every 8 hours for 10 days Children (2-12 years): Acyclovir 4 × 20 mg / kg BB / day / oral for 5 days Teenager and adults: Acyclovir 5 × 800 mg / day / oral for 7 days Valacyclovir 3 × 1 gr / day / oral for 7 days Famasiklovir 3 × 500 mg / day / oral for 7 days. (2) Acetaminophen can reduce discomfort due to fever; antipruritus such as diphenhydramine 1.25 mg / kg every 6 hours or hydroxine 0.5 mg / kg every 6 hours. Topical and systemic antibiotics can be given to treat bacterial superinfection. Antiviral therapy reduces mortality because it can prevent progressive pneumonia, and alters the prognosis of varicella infection in high-risk children. Acyclovir therapy in immunodeficient children should begin 24 to 72 hours after a skin rash appears. Due to the low oral absorption, the drug is given intravenously with each dose of 500 mg / m2 in 8 hours. Therapy is continued for 7 days or until no new lesions appear within 48 hours. Complications Varicella The most common complication caused by varicella infection is an infection of S. aureus or Streptococcus pyogenes (group A beta haemolytic streptococcus). Antibiotics can actually be used to reduce the risk of death, unless there is sepsis. Secondary infections due to bacteria are usually characterized by the appearance of bullae or cellulitis, regional lymphadenitis and subcutaneous abscesses can appear. S. pyogenes generally causes invasive gangrenous varicella. Other manifestations are pneumonia, arthritis, and osteomyelitis. Reye’s syndrome, which is a non-inflammatory encephalopathy with fatty degeneration in the liver can be a difficult complication. Children who suffer from varicella should not be given aspirin, because it can increase the risk of Reye’s syndrome. Neurological complications such as meningoencephalitis and cerebral ataxia are common. Complications in the central nervous system usually occur in children under 5 years and over the age of 20 years. Varicella vein encephalitis usually resolves on its own within 24 to 72 hours. Cerebellar ataxia usually disappears in some time. Symptoms such as bleeding, petechiae, purpura, epistaxis, haematuria, gastrointestinal bleeding, and Disseminated Intravascular Coagulation are caused by complications in the form of thrombocytopenia, occurring 1 to 2 weeks after varicella infection. Viral arthritis can also occur due to the presence of varicella viruses in the joint. Joint infections usually heal within 3 to 5 days. Other complications that may also occur, but rarely found are myocarditis, pericarditis, pancreatitis, and orchitis. Herpes Zoster A common complication of herpes zoster is PHN (Post Herpetic Neuralgia). From some data it was found that 9% of cases of herpes zoster were related to PHN for 4 weeks to reach 10 years. Permanent pain is felt by 22% of patients who get this syndrome. The risk of NPH is actually associated with an increase in age and immunodeficiency conditions of the patient. Prolonged risk of PHN increases by 40 to 50% at the age of more than 60 years Shingles can attack the central nervous system and cause encephalitis, but this is very rare, only about 0.2-0.5% of all patients. Spread from the skin to cause encephalitis occurs within 9 days to 6 weeks. Symptoms: disruption of sensory function, headache, photophobia, meningismus, and abnormal electroencephalogram. Cranial and peripheral nerve paresis can occur due to complications of herpes zoster in the central nervous system. Usually encephalitis due to varicella only occurs around 16 days Encephalitis due to herpes zoster rarely causes death, most patients recover without a certain disability. Encephalitis is also usually associated with acute vasculitis. Another symptom that usually occurs is cerebral angitis, which is a syndrome consisting of vasculitis, thrombosis and microinfarction associated with herpes zoster ophthalmicus and reactivation of cranial nerves in elderly individuals. Prevention In immunocompetent children who have suffered varicella, no precautionary measures are needed. Prevention are aimed at groups at high risk for fatal varicella such as neonates, puberty or adults, with the aim of preventing or reducing symptoms of varicella.2 Passive Immunization In 1962, Ross summarized the literature limited to severe cases of varicella and then conducted a classic study of the use of gamma globulin to modify disease. A significant advance in providing an increased supply of high potential gamma globulin results from the selective use of blood banks as indicated by complement fixation, so that varicella antibodies increase significantly. (7) Passive immunization can also use VZIG (Varicella-Zoster Immumoglobin) (Lubis, 2008). Varicella zoster immunoglobulin (VZIG) is an IgG antibody to VZV with a dose of one vial for 10 kg of body weight intramuscularly (IM). VZIG prophylaxis is indicated for high-risk individuals, including immunodeficient children, pregnant women who have had direct contact with varicella patients, neonates exposed to varicella-infected mothers, at least no more than 96 hours. Antibodies given after the onset of symptoms cannot reduce the severity that occurs Giving in 3 days (less than 96 hours) after exposure to VZV, immunocompetent children have been shown to prevent varicella while in immunocompromised children VZIG administration can relieve varicella symptoms. VZIG can be given to children less than 15 years old who have had varicella or herpes zoster, at the age of puberty of more than 15 years who have never had varicella or herpes zoster and do not have antibodies to VZV, in newborns, whose mothers suffer from varicella within 5 days before or 48 hours after delivery, preterm infants and babies aged ≤14 days whose mothers have never had varicella or herpes zoster, and children suffering from leukemia or lymphoma who have never had varicella.2 Active immunization In 1974, Takahashi et al reported that live self-developed virus vaccines by them had prevented the spread of varicella in a hospital. The Oka virus strain has been obtained from varicella cases in 3-year-old boys. Attenuation of the strain followed by 11 parts of the building structure of the human embryonic lung at 34 ° C and 12 parts in the cell guinea pig embryo at 37 ° C. Oka strains remain an important element of vaccines at this time. Takahashi vaccines produced by the Biken Institute are widely used in Japan and other far east countries. In 1984, Varilrix, a Smith Kline Beecham product, was first licensed in Europe and is now licensed in around 40 countries. In the 1980s Pasteur Merieux serum and Vaccins SA began research from vaccines in France. Varivax, manufactured by Merck and Company, has been licensed in the United States in 1995 followed by 14 years of extensive collaborative research organized by Dr. Anne Gershon. Therefore, vaccines are now universally available. The VZV vaccine uses a varicella virus vaccine (Oka strain) and acquired immunity can last up to 10 years. This vaccine has been used in America since 1995 with protection against varicella ranging from 71-100%. The vaccine is effective if given at the age of 1 and is recommended given at the age of 12-18 months. Children aged ≤13 years who do not suffer from varicella are recommended to take a single dose and older children are given in 2 doses at a distance of 4 to 8 weeks and given subcutaneously. Side effects that can be caused by fever or local reactions such as maculopapular rash or vesicles, occur in 3-5% of children and occur 10-21 days after administration at the injection site. Another type of varicella vaccine is Varivax. It should not be given to pregnant women due to risk of congenital varicella. The incidence of varicella is at the highest among children aged 1-6 years. Therefore, applying vaccination requirements for child care and entering school has a major impact on reducing the incidence of disease. The Advisory Committee on Immunization Practices (ACIP) recommends that all countries require children who will enter child care facilities and primary schools to receive the varicella vaccine or have other evidence of immunity to varicella. Other evidence of getting immunity must consist of a doctor’s diagnosis or have had varicella, or serological evidence of immunity. To ensure that adolescents are not affected by varicella in adulthood, varicella immunization must be considered. Data from the United States and Japan obtained from households, hospitals, and communities shows that varicella vaccines are effective in preventing disease or reducing varicella severity if given within 3-5 days after exposure. ACIP now recommends vaccines for use in people who are vulnerable after exposure to varicella. If varicella exposure does not cause post-exposure infection, vaccination can protect the subsequent exposure. Regular vaccination is recommended for all vulnerable health workers and is the preferred method of preventing varicella in a health care environment. Varicella outbreaks in several places (for example, child care facilities, schools, institutions) can last for 3-6 months. Varicella vaccine has been used successfully by the health department and by the military to prevent and control epidemics. Breastfeeding mothers and varicella At anytime breastfeeding mothers can get infectious diseases, one of them is varicella, a mother has the potential to transmit the disease to her baby. However, by terminating breastfeeding does not contribute to prevent the exposure and may reduce the protection of babies through maternal antibodies. These protective factors are found in breast milk. Therefore, varicella infection that occurs in a breastfeeding mother is not a contraindication to breastfeed her baby. In a study among mothers with varicella infection and their babies, mothers were allowed to breastfeed their babies with full attention to hygiene, avoiding contact lesions and the use of face masks by mothers. The result was none of the 42 infants acquired infection from their mothers. In another scientific journal, it was mentioned that exclusive breastfeeding is the optimal method for feeding babies in the first six months of life for healthy babies. There are many benefits associated with breastfeeding, including nutrition, immunological, psychological, developmental, environmental, social, economical and health, as well as transmission of infectious diseases. To promote protection and supports for the breastfeeding process, every effort must be made to minimize “contraindications” to breastfeeding. Actually, there are only a few disease in Indonesia that make mothers unable to breastfeed their babies. The dyads must still be monitored for their immunization status. In a journal, it was mentioned that varicella-infected mothers were encouraged to continue breastfeeding their babies with regard to hand hygiene. If the lesion is in the breast, delay until the lesion becomes crusty or dries. The mothers have to take the medication, which is considered safe for breastfeeding mothers. Moreover, according to book by Thomas Hale, varicella drugs are consisted of acyclovir, valaciclovir, and famciclovir, which are considered safe if taken by breastfeeding mothers. REFERENCES Kurniawan, M., N. Dessy & M. Tatang, 2009. Varisela zoster pada anak. Medicinus, 3(1), hal. 23-31. Lubis, RD., 2008. Varisela dan Herpes Zoster. Makalah. Departemen Ilmu Kesehatan Kulit dan Kelamin Fakultas Kedokteran Universitas Sumatera Utara, Medan. Centers for Disease Control and Prevention (CDC), 1999. Prevention of Varisela: updated recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR U.S. Department of Health & Human Services, 48(6), p. 1-5. Gilden, L. Williams & Cohrs, 2002. Clinical features of Varisela Zoster Virus infection of the nervous system. Review Article ANCR, 2(2), p. 7-10. Arvin, AM., 2000. Varisela-zoster virus: Pathogenesis, immunity, and clinical management in hematopoietic cell transplant recipients. Biology of Blood and Marrow Transplantation, 6(1), p. 219-230. Fairley, CK. & E. Miller, 1996. Varisela-Zoster Virus Epidemiology-A Changing Scene?. The Journal of Infectious Diseases, 174(3), p. 314-319. Fitzpatrick TB, Wolff K, Allen R. Color atlas & Synopsis of Clinical Dermatology , 6th edition. New York: McGraw-Hill Inc, 2009.p. 833-49 Dorothy M. Sendelbach and Pablo J. Sanchez. Varicella, Influenza: Not Necessary to Separate Mother and Infant. Pediatrics 2012;130;e464 Dr Noni E MacDonald. Maternal infectious diseases, antimicrobial therapy or immunizations: Very few contraindications to breastfeeding. Can J Infect Dis Med Microbiol Vol 17 No 5 September/October 2006 Thomas W. Hale, Ph.D, Hilaru E. Rowe, PharmD. Medications & Mother’s Milk 2014. A Manual of Lactation Pharmacology. CASE REPORT Name: Mrs. S Age: 28 years old Obstetric history: P2A0. Baby Name: An. A Female, 1 year 4 months, 2nd born of Mrs.S Birth history: Sectio Caesaria Birth weight: 3400 gr Current weight: 8400 gr Nutritional status: Good History of Immunization: varicella vaccine at the first day after the mother was diagnosed with varicella History of breastfeeding: 1st child: 3 years old, exclusive breastfeeding +, breastfeeding until the age of 1 year because the mother is pregnant with her second child. 2nd child: exclusive breast milk +, direct breastfeeding baby, good complementary feeding February 11, 2017 The patient is a mother who is breastfeeding her baby aged 1 year 4 months. Major complains were fever, and lesions arising 2 days after the onset of the fever. The lesions arise reddish and filled with fluid in the hands and chest area, then spread to the back. Lesions do not arise on the nipple or on the areola. After being diagnosed with varicella, the patient consulted to a pediatrician who also works as a lactation counselor and has an IBCLC certification (International Board Certified Lactation Consultant). The doctor recommended the patients to still give breastfeeding to the babies with extra caution that they pay attention to cleanliness. For example, covering all lesions with plaster, wearing long sleeves, washing hands before touching or nursing a baby, and also always wear a mask. The babies should get immunization. If the lesion is exposed to the areola or nipple, the baby may breastfeed on the healthy breast next to it. Mothers get oral antiviral therapy, antiviral ointment, itching medication, and antipiretic drug. February 12, 2017 The lesions are spreading, but not to the areola and nipples. The patient continues to breastfeed the baby. The baby showed no sign of infection. Immunization was done for both children. Doctors advised that if there was a sign of infection in the baby observed, then the baby should go to the hospital. February 24, 2017 The patient says the lesion starts to dry out and there are no active lesions. During this time the patient continued the direct breastfeeding. The baby also had no signs of infection. The drugs had been stopped. Discussion Through this case, one can conclude that breastfeeding mothers with varicella can still be able to keep breastfeeding their babies. One important aspect is that the breastfeeding process monitored by pediatrician who is also a lactation consultant. The mother also did all the advice given by the doctor: keep breastfeeding while maintaining the hygiene of the mother and baby so that the baby is not exposed to lesions from the mother. For mothers affected by varicella, they can continue to breastfeed their babies. Extra requirements needed to preventing transmission such as: by covering all lesions with tape, wearing long sleeves clothing, trousers, washing their hands every time they want to breastfeed a baby, and also wearing a mask. In addition, the mothers have to take medication and vaccinate their babies as to prevent the infection. In the end, babies who remain breastfed by mother will also get natural immunity that is present in breast milk without contracting varicella. When this case was written, the mother had weaned her baby at the age of 2 years.