MEASLES (Rubeola)

Measles
An acute communicable disease characterized by a temperature of 38.3C or more, cough, coryza, conjunctivitis, an erythematous maculopapular rash, and a pathognomonic exanthem called Koplik spots.

Measles
Three Stages:
1. 2.

3.

An incubation stage of 8-12 days with few signs and symptoms (ave, 10 days) Prodromal stage with an exangthem (Koplik spots ) on the buccal and pharyngeal mucosa, fever, conjunctivities and increasingly severe cough (catarrhal stage). Lasts for 2-4 days ( ave. 3 days) Exanthem period: Final stage with maculopapular rash over neck and face, body, arms and legs associated with high

Measles
Etiology: RNA virus of the family Paramyxoviridae genus Morbillivirus, with 1 serotype. During the prodomal period and shortly after rash appears, the virus is found in nasopharyngeal secretion, blood and urine. It can remain active for 34 hours at room temperature

Measles
Period of Infectivity Most contagious during prodomal period, about 7th 10th day after exposure up until 5 days after the rash has appeared.

Measles
Epidemiology: Transmitted by direct contact with infectious droplets, or by airborne spread The only natural hosts of measles virus are humans and primates. Maternal antibodies against measles protect child usually until 6 months of age, but this is variable.

Measles
Pathology: Measles in heavily populated but underdeveloped countries has its greatest incidence in children < 2 y/o.

Measles
Pathology: Characterized by widespread multinucleated giant cells. Two main types 1. Warthin Finkeldey cells found in the reticuloendothelium adenoids, tonsils, Peyer patches, appendix, lymph nodes, spleen and thymus. May contain more than 100

Measles
2. Epithelial giant cells which occur in the respiratory epithelium and other epithelial surfaces. Kopliks spots are similar to that of the skin rash.

Measles
Clinical manifestations: Typical illness: 1. Incubation period: 8-12 days (ave. 10 days) No outward sign of illness although some may have mild transient respiratory symptoms and fever 2. Prodromal period: 2-4 days (ave. 3 days)

Measles
Characterized by: General malaise symptoms fever worsen over coryza 4 day conjunctivitis and period photophobia cough (brassy)

2-

Measles
On 10th day, Koplik spots first appear on buccal mucosa opposite the lower molars. They are 1.0mm in size and described as whitish lesions on a bright red mucosal surface. From a few lesions, they become innumerable within 12 hours. During prodromal period posterior pharyngeal wall is erythematous and patient may

Measles
Exanthem Period: Measles exanthem appears on 14th day (maximum no. of Koplik spots have appeared and they will disappear over next 3 days). Measles rash first appears behind the ears and on the forehead at hair line, spread is CENTRIFUGAL from head to feet.

Measles
Over next 3-4 days, erythematous and maculopapular rash will spread from head to feet. Fever will peak on the 2nd or 3rd day of the rash and then falls after the 3rd or 4th day of the rash. Fever persisting beyond the 3rd or 4th day of the exanthem suggest

Measles
Rashes clear on 3rd to 4th day. From red color, rashes become coppery, then brownish in appearance. Finally, fine desquamation occurs with brownish discoloration.

Measles
Diagnostic tests: Usually made from typical clinical picture so lab confirmation rarely needed.

Measles
Lab tests:
1. 2. 3.

Measles virus isolation tissue culture Measles immunoglobulin (ig) M antibody Rise in IgG measles antibody titers in paired acute and convalescent serum specimen

Measles
Modified measles: Defined as an infection that occurs in the partially immune person. It follows the regular sequence of events but the illness in milder. There is no confluence of lesions occur in: 1. Those given immune serum globulin when exposed to a

Measles
2. Those younger than 9 months who still have maternal measles antibodies. 3. Live vaccine failure

Measles
Atypical measles: A clearly defined clinical syndrome occurring in previously immunized individual after exposure to natural measles. Described as bizarre Incubation period 7-14 days

Measles
Prodromal period: Sudden onset of fever (39.5 to 40.6C) - Koplik spots are Headache Abdominal pain Pleuritic chest pain

Measles
2-3 days after onset of illness, rash appears in distal extremities and goes cephalad. Rash is yellowish, involves palms and soles and ends its cephalad progression at the level of the nipples. Respiratory distress is common. Lesions on chest x-ray

Measles
Other findings: marked hepatosplenomegaly, hyperesthesia, weakness. Measles antibodies are very high by the 10th day of life.

Measles
Complications of typical measles
1.

Pneumonia a. measles virus itself causing interstitial type of pneumonia b. Bronchopneumonia due to secondary bacteria, ex: Streptococcus pyogenes Strepcoccus pneumonia

Measles
2. Conjunctivitis- most common cause of blindness in the Philippines 3. Otitis media 4. Laryngitis and laryngotracheobronchitis 5. Myocarditis and pericarditis 6. Measles encephalitis occur during the period of the exanthem and within 8 days of

Measles
7. SSPE rare degenerative CNS disease of children and adolescents due to persistent measles virus infection. Mean incubation period between measles infection and onset of SSPE is 7 years.

Measles
Signs and symptoms Progressive behavioral and intellectual deterioration Motor incoordination Seizure, myoclonic jerks, blindness, speech difficulty Stupor, dimensia, decorticate rigidity

Measles
EEG: Burst suppression pattern synchronized with myoclonic jerks h. Appendicitis: caused by generalized mesenteric adenitis. Surgical removal in treatment of choice.

Measles
Treatment:
1. 2. 3. 4.

Supportive: antipyretics, bed rest, adequate fluid intake Vit. A administration For 6 months to 1 year: 100,000 IU single dose For 1 year of age and older: 200,000 in single dose

Measles
Differential diagnoses
1. 2. 3.

4. 5. 6. 7. 8.

Exanthem subitum Rubella Infection with other viruses: echovirus, coxsackie and adenovirus Infectious mononucleosis Rickettsial diseases Serum sickness Kawasaki disease Drug rashes

German Measles or Rubella

Rubella: 2 clinical types
1. 2.

Postnally Acquired congenital Common communicable diseases of childhood, consisting of mild constitutional symptom, rash similar to measles and tenderness of postoccipital, retroauricular and posterior lymph nodes.

Rubella
Etiology RNA containing virus in the family Togaviridae, genus Rubivirus. Present I nasopharyngeal secretions, blood, feces, and urine.

Rubella
Epidemiology Humans only natural host, spread by oral droplet, or transplacentally through congenital infection.

Rubella
Pathology Non specific Reticulum cell hyperplasia Inflammatory cell infiltration Follicular hyperplasia in spleen and lymph nodes No giant cells found

Rubella
Clinical Manifestations: Intubation period: 18 + 3 days Prodromal period: 1-5 days

Rubella
Exanthem period: Centrifugal pattern from head toward hand and feed; In 24 hours whole body is involved. Rash: erythematous maculopapular, and discrete, and no desquamation occurs.

Rubella
Lymphadenopathy is major linical sign in the suboccipital and posterior auricular nodes. Lasts for 5-8 days. Fever variable from being minimal to 40C Other signs and symptoms: pharyngitis, conjunctivitis, cough, headache and pruritus

Rubella
Diagnostic tests:
1. 2. 3.

Viral isolation from nose or throat specimen Rubella IgM antibody test IgG antibody in paired serum titers collected 1-2 weeks apart.

Rubella
Complications of Rubella: 1. Arthritis and arthralgia more common in adults than in prepubertal children; multiple joints involved and more women were experiencing joint pains compared to men.

Rubella
2. Neurological manifestation a. Encephalitis a rare complication and is similar to measles encephalitis but is less severe. Usually occurs 2-4 days after occurrence of rash. b. neuritis numbness and tingling

Rubella
3. Thrombocytopenic purpura Rash and purpura occur together. 4. Myocarditis and pericarditis Treatment Supportive

Rubella
Differential diagnosis Difficult to diagnose clinically except when a patient is seen during an epidermic 1. Mild type of measles 2. Roseola infantum 3. Drug rashes 4. Infectious mononucleosis 5. Enteroviral infections with rash

Rubella
Congenital Rubella Syndrome: Another clinical form of rubella In 1941, in Australia ophthalmologist named Gregg observed congenital defect in babies of mothers who had rubella during early pregnancies. Originally thought to just involve eyes, ears, brain and heart, in 1964 a big rubella pandemic in the US revealed much more anatomic defects

Rubella
The syndrome in the result of in utero fetal infection during first 12 weeks of pregnancies.

Rubella
Most common manifestation
1.

clinical

General: growth retardation and high infant mortality rate a. growth retardation: 50-85% weigh less than 2.5 kg. b. high infant mortality rate: due to congenital pneumonia, heart defects, hepatitis, encephalitis thrombocytopenia, immune

Rubella
2. Eye findings 1/3 of all babies have cataracts and other eye defects, e.g. retinopathy, microphthalmia, congenital glaucoma 3. Auditory defects Sensorineural deafness. All patients born to mothers who had rubella during first half of pregnancy should have periodic hearing tests for 1st 5 years of

Rubella
4. Cardiovascular finding: a. PDA most common defect b. Pulmonary artery stenosis 2nd most common c. Pulmonary valvular stenosis 3rd most common d. Myocarditis

Rubella
Others (Expanded Congenital Rubella Syndrome): Interstitial pneumonitis Hepatitis Nephritis Bone radiolucencies Myositis Chronic rash Hemolytic and hypoplastic anemia Meningoencephalitis Myocarditis

Rubella
Diagnosis: Not difficult in known maternal exposure. But diagnosis of the syndrome in an uneventful pregnancy is more difficult.

Rubella
Diagnosis
1. 2.

Serum IgM Viral isolation best method; specimens from nose, throat, urine, CSF, buffy coat and blood

Rubella
Treatment: Isolation: most babies are contagious and so should be isolated. Rubella viral shedding occurs for more than a year. 2. Multiple congenital problems: team approach , refer to various subspecialties.
1.

Rubella
Prevention of mothers exposed to rubella: Susceptible mothers in 1st 20 weeks of pregnancy exposed to a rubella infected person may be given 20 ml of immune globulin within 72 hours post exposure.

Roseola Infantum/Exanthem Subitum (Human Herpesvirus or Sixth Disease) In 1981, a new virus isolated from blood of AIDS patients named human herpesvirus 6 (HHV-6). This virus was subsequently related to roseola infantum or exanthem subitum.

Etiology:

Roseola Infantum (6 disase)

th

HHV-6 is one of 7 human herpesvirus. It is a large, enveloped, double stranded DNA virus. A-variant: commonly isolated from AIDS adult patients B-variant: associated with infants. HHV-6 closely related to human cytomegalovirus.

Roseola Infantum (6 disease)

Epidemiology:

th

Maternal antibodies present in newborns, but drop by 4-6 months of age. Peak incidence: 6-12 months old; 90% occurrence within 1st 2 years of life; about 1/5 of all children experience roseola

Roseola Infantum (6 disease)

Pathogenesis:

th

Mode of acquisition: frequent detection of virus in saliva suggest horizontal spread by oral viral shedding.

Roseola Infantum (6 disease)

th

Virus has long-lived state of latency in humans as proven by high levels of antibody in adults, frequent viral shedding in saliva and presence of viral nucleic acids in salivary glands and in blood cells of seropositive children and adults.

Roseola Infantum (6 disease)

Clinical Manifestations:

th

HHV-6 is the etiologic agents of roseola is at least 8092% of cases. Others probably due to HHV 7 or enteroviral or less common pathogens

Roseola Infantum (6 disease)

Typical case:

th

Onset sudden with fever as high as 39.4 41.2C; associated with bulging anterior fontanelle or convulsions (5-35% of cases)

Roseola Infantum (6 disease)

th

Fever falls by 3-4th day. When the temp. is normal, macular or maculopapular rashes start on trunk, then to arms and neck, and involve face and legs. Rash fades within 3 days with no desquamation or pigmentation.

Roseola Infantum (6 disease)

th

Associated signs and symptoms

1. 2. 3. 4.

Occipital or cervical adenopathy: 30-35% Respiratory signs or symptoms: 50-55% Mild diarrhea: 55-70% Seizures: 5-35%

Roseola Infantum (6 disease)

th

5. Edema of eyelids: 0-3% 6. Bulging anterior fontanelle: 2630% 7. Papular pharyngitis: 65%

Roseola Infantum (6 disease)

Complications: RARE
1. 2. 3. 4.

th

Extreme hyperpyrexia Persistent seizures Severe encephalitis Fetal hepatitis

Roseola Infantum (6 disease)

LAB findings:

th

WBC ct. during 1st few days: about 8,000/mm2 By 3rd to 4th day of fever: WBC ct. drops to 6,000/mm2, and lymphocytosis as high as 90% CSF usually normal

Roseola Infantum (6 disease)

Diagnosis:
1. 2.

th

Viral isolation Antibody assay after 1st week of primary infection: a. immunofluorescence b. neutralization c. immunoblot d. enzyme immunoassays

Roseola Infantum (6 disease)

th

3. PCR techniques detect HHV-6 antigen in immunocompromised patients. Prophylaxis and treatment: - None - Management purely supportive For HIV patients, may try antiviral agents like ganciclovir and foscarnet.

Differential diagnosis:

Roseola Infantum (6 disease)

th

Timing of fever with the appearance of rash key factor in diagnosis 1. Rubella 2. Rubeola or measles 3. Dengue H fever 4. Enteroviral infection difficult to 5. Adrenoviral infections

Chicken Pox or Varicella

Varicella-Zoster Virus (VZV) 2 forms: 1. Primary infection: varicella or chicken pox 2. Latent infection in dorsal root ganglia: Herpes zoster or shingles

Varicella
Etiology: A human herpes virus. It is an enveloped, double streaked DNA virus

Varicella
Pathology: Transferred via respiratory secretions or direct contact with skin lesion of chickenpox or herpes zoster. 1. Incubation period: 10-23 days (ave. 14 days) VZV spread to regional lymph nodes, undergo multiplication and cause a primary low grade viremia

Varicella
2. Viremic phase: Virus is delivered to the skin causing the skin rash. Rash begin as macular, and develop rapidly to papules, vesicles, pustules and scabs. Lesions in zoster and chicken pox are the same. Hallmark: multinucleated giant cell and intranuclear inclusions

Varicella
Clinical Manifestation: Typical Varicella: Prodromal phase in children unusual, but in adults 1-2 days of malaise and fever before rash appears are common Rash more intense on trunk and head than on extremities and evolves as a series of crops oer 1-2

Varicella
Clinical Manifestation: Typical varicella: adult suffer more severe infections: attributed to lower cell-mediated responses (CMI) to VZV in adults compared to children. Newborns, however, develop sever varicella if infected by mothers due to immature CMI response.

Varicella
Clinical Manifestation: Typical varicella: In varicella: cells localized in the epidermis, where ballooning degeneration of cells in deeper layers is accompanied by intercellular edema. An edema progresses, the cornified layers separate to form a thinly roofed vesicles. An exudate of

Varicella
In zoster in addition to skin lesions resembling chicken pox, there is also mononuclear inflammatory infiltrate in the dorsal root ganglion of the affected dermatone. May also have necrosis of ganglion cells and demyelination of axon.

Varicella
Treatment:
1.

2.

Supportive, non specific measures: frequent bathing, antihistaminem, calamine lotion, paracetamol Specific antiviral therapy Acyclovir (ACV, an inhibitor of DNA polymerase and a DNA chain terminator.

Varicella
A.

Patient with severe or potentially severe VZV infections: Treat with IV ACV Adults: 30mg/kg/day Children: 1,500 mg/m2/day

Varicella
B. In healthy adults and children treatment is controversial because infection are self limited. Should be given within 24 hours of onset of rash. Children: 80mg/kg/day in 4 divided Adults: 4g/day doses for 5 days Effect: no. of lesions was

Varicella
Other drugs: 1. Penciclovir 2. Valacyclovir in adults only Prognosis: Excellent, zoster has better prognosis than varicella because it is only a secondary infection.

Varicella
Immunization: 1. Passive use of Varicella-Zoster immunoglobulin (VZIG) for exposed immunocompromised children, newborn infants with mothers who have active varicella, and hospitalized preterm infants.

Varicella
Infants with mothers who have chickenpox whose onset of rashes is 5 days or less before delivery, or within 48 hours after delivery should be given 1 vial of VZIG.

Varicella
Complication of varicella:
1.

2.

Most frequent: bacterial superinfection skin, lungs, bones, caused by Staph. Aureus or group A Beta hemolytic streptococci. CNS complication a. transient cerebellar ataxia b. cerebral encephalitis c. aseptic meningitis d. transverse myelitis e. less common arthritis, glomerulonephritis, myocarditis and purpura fulminans

Varicella
3. Primary varicella pneumonia in immunocompromised patients, in adults, and in neonates. 4. In immunocompromised patients with HIV, malignancy, CMI defects, on high steroid treatment varicella may be severe or even fatal due to pneumonia, and DIC manifestation

Varicella
Clinical Manifestation of Zoster: A localized unilateral vesicular skin eruption involving 1-3 dermatomal segments. Skin lesion are like varicella but tend to be more confluent and are very painful especially in adults.

Varicella
Complication of zoster:
1.

2.

Postherpetic neuralgia where pain at site of lesions may persist for months to years. Described as aching, jabbing or boring. May be severe and common (35% incidence) in bone marrow transplant patients.

Varicella
Lab Diagnosis
1. 2.

Determination of viral antigens from skin scrapings Isolation of VZV from skin vesicles by immunofluorescence. a. Patients with creatinine clearance less than 50 ml/min 1.73m2 should receive to 1/3 of this dosage. ACV in general is

Varicella
3. PCR using skin scrapings, vesicular fluid, respiratory secretion and CSF. 4. Antibody determination a. latex agglutination b. enzyme linked immunosorbent assay c. fluorescent antibody to membrane antigen method.

Varicella
2. Active immunization against varicella vaccine developed n Japan 25 years ago. Few side effects but vaccine may develop a mild rash several weeks after immunization in 5% of healthy children. Not all are protectted completely, 15-30 percent may have a modified (<50 lesions) breakthrough illness, but severe varicella is prevented. Vaccine failure:

Varicella
Another clinical variation: Congenital varicella syndrome In 1947, Laforet and Lynch discovered an infant with multiple congenital anomalies after maternal chicken pox during 1st or 2nd trimester of pregnancy. Features: Cicatricial scars of skin (70%)

Varicella
Hypoplasia of right lower extremities Clubfoot Cerebral cortical atrophy: early cataract; and death Chorioretinitis Torticollis

Erythema Infectiosum or Fifth Disease (PARVOVIRUS B19) In 1983, Small DNA containing virus called parvovirus B19 was identified as the cause of erythema infectiosum. (EI). A mild systemic illness characterized by fever in 1530% of cases, followed by a distinctive rash 7-10 days later.

Erythema Infectiosum (5th Disease)

The facial rash is intensely red with a slapped cheek appearance accompanied by circumoral pallor. Aside from the facial rash, there is a symmetric, maculopapular lace like, pruritic rash on the trunk, arms, buttocks and thighs. The rash can wax and wane with changes in temperature and exposure to sunlight for weeks or months.

Erythema Infectiosum (5th Disease)

Etiology: Parovirus B19 member of the genus Parvovirus in the formle Parvoviridae. It is a single stranded DNA.

Erythema Infectiosum (5th Disease)

Epidemiology and Transmission
-

Common; worldwide in distribution 70% of cases occur in children 515 years old 40-60% of adults have evidence of prior infection with serologic survey. Transmission is via respiratory route, via large droplet spread. Incubation

Pathogenesis and Immunity

Erythema Infectiosum (5th Disease)

The target of Parvovirus B19 is the erythroid cell line, specifically erythroid precursors near the pronormoblast stage. The virus lyzes these cells, leading to depletion and arrest of erythropoiesis. The viremia ends with the appearance of specific IgM antibody. Humoral

Erythema Infectiosum (5th Disease)

Clinical Manifestations: Parvovirus B19 causes a spectrum of clinical manifestation Most common; Erythema Infectiosum (fifth disease because it was fifth in the classification of childhood exanthems) Has 3 stages.

Erythema Infectiosum (5th Disease)

First stage: occurs 18 days after acquiring the infection and is characterized by the slapped check appearance Second stage: occurs 1-4 days after onset of facial involvement with appearance of maculopapular rash on trunk and limbs, sparing palms and soles. Extensor surfaces are more prominently affected.

Erythema Infectiosum (5th Disease)

Third stage: last with waxing rashes related factors. from 1-3 weeks and waning of to environmental

Other clinical manifestation: 1. Transient aplastic crisis infection with B19 may lead to fall in hemoglobin in patients with preexisting hemolytic conditions such as thalasemia, hereditary spherocytosis and sickle cell disease 2. Arthritis and arthralgia - more common in adults 3. Persistent anemia is

Erythema Infectiosum (5th Disease)

Erythema Infectiosum (5th Disease)

4. Fetal infections primary maternal infection leading to fetal hydrops and fetal death: mechanism of fetal disease due to lysis of erythroid precursors leading to profound anemia, high output cardiac failure and hydrops seen at every stage of gestation. 5. Neurologic illness: Aseptic meningitis and

Erythema Infectiosum (5th Disease)

Diagnosis:
1. 2.

Mainly based on clinical observation of the typical rash. Determination of anti-B19 IgM and IgG

Erythema Infectiosum (5th Disease)

Differential Diagnosis
1. 2. 3. 4. 5.

Rubella Scarlet fever Drug reactions Measles Collagen vascular diseases such as SLE, juvenile rheumatoid arthritis

Erythema Infectiosum (5th Disease)

Treatment
1. 2. 3.

IV immunoglobulin No specific antiviral therapy Blood transfusion in patient with aplastic crisis

Herpes Simplex Virus

Herpes means to creep in Greek; used to describe cutaneous, spreading lesions including fever blisters described by Hippocrates. The herpes simplex virus has a variety of clinical manifestation affecting the skin, mucous membrane, eye, central nervous system and genital tract. It also causes generalized systemic

Herpes Simplex Virus

2 types of Herpes simplex virus
a.

b.

HSV-1 commonly infects, mucous membranes, above the waist, also causes cerebral disease: ORAL TYPE HSV-2 infects the genitalia and the neonatal and congenital infections. TRANSMITTED SEXUALLY called GENITAL TYPE

Herpes Simplex Virus

Two types of infection:
1.

2.

Primary infection: a susceptible hosts first experience with the virus. Usually this is a subclinical infection but there are also systemic reactions and superficial lesions. Occur early in childhood. Recurrent herpetic lesions represent reactivation of a

Herpes Simplex Virus

Etiology: A double stranded DNA containing enveloped virus. The envelope contains glycoproteins that are important target antigens of the humoral and cellular response.

Herpes Simplex Virus

Epidemiology: Tranferred by infected oral or genital secretions. Incubation period 2-12 days (ave. 6 days) Humans are the primary host. Most of cases are subclinical (about 85%). Once infected, majority continue to carry the virus in a latent state and maintain a constant level of

Herpes Simplex Virus

Pathogenesis/Pathology HSV tends to infect calls of ectodermal origin and therefore affects: skin, mucous membranes, and the CNS. After primary HSV infection, the virus remain latent, and reactivation of latent HSV is affected by a variety of factors such as: exposure to sunlight,

Herpes Simplex Virus

1.

Neonatal infections: Infection is acquired by ascending spread prior to delivery or at the actual vaginal delivery from a mother with genital infection (HSV-2) within few days to weeks. Skin vesicular appear and patients are acutely ill and present with jaundice, shock, bleeding or respiratory distress. In some

Herpes Simplex Virus

The affected infant should be isolated and treated with acyclovir for 1421 C/S is recommended for mothers with obvious cervical or vaginal lesions.

Herpes Simplex Virus

2. Gingovastomatisis Multiple oral ulcers on tongue, buccal and gingival mucous extending to pharynx. Cervical lymph nodes are swollen and tender. Duration 7-14 days Differential diagnosis herpangina, aphthous stomatitis, thrush, and Vincents

Herpes Simplex Virus

Treatment: Hydration, topical anesthetics

Herpes Simplex Virus

3. Vulvovaginitis or urethritis Vesicles or ulcers on the valva, vagina, or penis, accompanied by fever of flulike symptoms in the primary infection. Primary infections last 10-21 day.

Herpes Simplex Virus

Differential diagnosis. Trauma, syphillis chancroid, bullous impetigo and chemical irritation Treatment: Analgesics, psychologic support

Herpes Simplex Virus

4. Cutaneous infections Presence of vesicles or ulcers in skin. Differential diagnosis impetigo or varicella Treatment deep skin lesions dry: use of systemic analgesics: antibiotics in secondary

Herpes Simplex Virus

5. Recurrent cutaneous disease milder than primary infection treat with sun block lip balm 6. Keratoconjunctivitis: Caused to spread from infected saliva in primary infection. In cases caused by reactivation of virus latent in the ciliary ganglion, it produces photophobia, pain and eventially dendritic corneal ulcers. Steroids should never be used in this condition. Topical preparations: trifluridine solution, vidarabine

Herpes Simplex Virus

7. Encephalitis HSV is most common cause of sporadic severe encephalitis. Associated with fever, headache, seizures. Differential diagnosis: mumps encephalitis, rabies, brain abscess and bacterial meningoencephalitis