Herpes Zoster

Camila K Janniger, MD

16 juni 2016

Herpes zoster is caused by VZV infection. VZV is an enveloped, double-stranded DNA virus belonging to
the Herpesviridae family; its genome encodes approximately 70 proteins. In humans, primary infection
with VZV occurs when the virus comes into contact with the mucosa of the respiratory tract or
conjunctiva. From these sites, it is distributed throughout the body. After primary infection, the virus
migrates along sensory nerve fibers to the satellite cells of dorsal root ganglia where it becomes
dormant.

Reactivation of VZV that has remained dormant within dorsal root ganglia, often for decades after the
patient’s initial exposure to the virus in the form of varicella (chickenpox), results in herpes zoster.
Exactly what triggers this reactivation has not yet been determined precisely, but likely candidates
(alone, or in combination) include the following:

• External reexposure to the virus

• Acute or chronic disease processes (particularly malignancies and infections)

• Medications of various types

• Emotional stress

Known risk factors for developing herpes zoster relate to the status of cell-mediated immunity to VZV.
Risk factors in children and adults include the following:

• VZV-specific immunity and cell-mediated immunity, which generally declines with age

• Immunosuppression (eg, by HIV infection or AIDS)

• Immunosuppressive therapy

• Primary VZV infection in utero or in early infancy, when the normal immune response is
decreased

• Anti-tumor necrosis factor (TNF)-a agents (may pose an increased risk)

• Immune reconstitution inflammatory syndrome

• Acute lymphocytic leukemia and other malignancies

Epidemiologi
Fewer than 10% of zoster patients are younger than 20 years, and only 5% are younger than 15 years.
Even though zoster is primarily a disease of adults, it has been noted as early as the first week of life,
occurring in infants born to mothers who had primary VZV infection (chickenpox) during pregnancy.

The incidence of herpes zoster increases with age. In the general population, the lifetime incidence rate
of herpes zoster is 10-20%, which rises to 50% in those individuals surviving to age 85 years. More than
66% of patients are older than 50 years.

Sign symptom

• Patchy erythema, accompanied by induration, in the dermatomal area

• Regional lymphadenopathy

• Grouped herpetiform vesicles developing on the erythematous base

• Pain in the dermatomal area of involvement

• Vesicular involution – Vesicles initially are clear but eventually cloud, rupture, crust, and
involute, a process that may be greatly accelerated by treatment

• After vesicular involution, slow resolution of the remaining erythematous plaques, typically
without visible sequelae

Diagnosis of herpes zoster is based primarily on the history and physical findings—specifically, the
characteristic location and appearance of the skin eruption in association with localized pain.

Therapeutic choices generally depend on the host’s immune state and on the presentation of zoster.
Conservative therapy includes nonsteroidal anti-inflammatory drugs (NSAIDs); wet dressings with 5%
aluminum acetate (Burow solution), applied for 30-60 minutes 4-6 times daily; and lotions. Medications
used include steroids, analgesics, anticonvulsants, and antiviral agents. Varicella-zoster virus (VZV)
vaccine is used for preventive purposes. Varicella-zoster immune globulin (VZIG) is used to prevent or
modify clinical illness in susceptible persons who are exposed to varicella or zoster.

Measles

Selina SP Chen, MD, MPH

30 Maret 2015

The cause of measles is the measles virus, a single-stranded, negative-sense enveloped RNA virus of the
genus Morbillivirus within the family Paramyxoviridae. Humans are the natural hosts of the virus; no
animal reservoirs are known to exist. This highly contagious virus is spread by coughing and sneezing via
close personal contact or direct contact with secretions.

Risk factors for measles virus infection include the following:

• Children with immunodeficiency due to HIV or AIDS, leukemia, alkylating agents, or

corticosteroid therapy, regardless of immunization status
 • Travel to areas where measles is endemic or contact with travelers to endemic areas

• Infants who lose passive antibody before the age of routine immunization

Risk factors for severe measles and its complications include the following:

• Malnutrition

• Underlying immunodeficiency

• Pregnancy

• Vitamin A deficiency

Although measles is historically a disease of childhood, infection can occur in unvaccinated or partially
vaccinated individuals of any age or in those with compromised immunity.

Unvaccinated young children are at the highest risk. Age-specific attack rates may be highest in
susceptible infants younger than 12 months, school-aged children, or young adults, depending on local
immunization practices and incidence of the disease.

The first sign of measles is usually a high fever (often >104o F [40o C]) that typically lasts 4-7 days. This
prodromal phase is marked by malaise, fever, anorexia, and the classic triad of conjunctivitis, cough, and
coryza (the “3 Cs”). Other possible associated symptoms include photophobia, periorbital edema, and
myalgias.

The characteristic enanthem generally appears 2-4 days after the onset of the prodrome and lasts 3-5
days. Small spots (Koplik spots) can be seen inside the cheeks during this early stage

The exanthem usually appears 1-2 days after the appearance of Koplik spots; mild pruritus may be
associated. On average, the rash develops about 14 days after exposure, starting on the face and upper
neck (see the image below) and spreading to the extremities. Immunocompromised patients may not
develop a rash.

Laboratory confirmation is achieved by means of serologic testing for immunoglobulin G (IgG) and M
(IgM) antibodies, isolation of the virus, and reverse-transcriptase polymerase chain reaction (RT-PCR)
evaluation.

A complete blood cell count (CBC) may reveal leukopenia with a relative lymphocytosis and
thrombocytopenia. Liver function test (LFT) results may reveal elevated transaminase levels in patients
with measles hepatitis.

Consult public health or infectious disease specialists for recommendations and guidelines for diagnostic
confirmation of cases and prophylaxis of susceptible contacts.
Treatment of measles is essentially supportive care with maintenance of good hydration and
replacement of fluids lost through diarrhea or emesis. Intravenous (IV) rehydration may be necessary if
dehydration is severe.

Vitamin A supplementation, especially in children and patients with clinical signs of vitamin A deficiency,
should be considered. Postexposure prophylaxis should be considered in unvaccinated contacts; timely
tracing of contacts should be a priority.

Patients should receive regular follow-up care with a primary care physician for surveillance of
complications arising from the infection. Antiviral, vaksin, ig

Mumps

Germaine L Defendi, MD, MS, FAAP

26 april 2016

After the initial entry into the respiratory system, the virus replicates locally. Viremic dissemination then
occurs to target tissues, such as the salivary glands (parotid glands) and extrasalivary locations (CNS).
These findings are based on experimentally induced mumps infection by Henly et al in 1948.

A secondary phase of viremia that occurs before the immune response is due to the replication of the
virus at the target organs. Viruria is also common, via blood transmission of the virus into the kidneys,
where active replication occurs. Therefore, impaired renal function (glomerulonephritis) may occur.

Risk factors

Lack of immunization, international travel, and immune deficiencies are all factors that increase risk of
infection by the Paramyxovirus mumps virus.

Symptoms in the patient’s history consist mostly of fever, headache, and malaise. Within 24 hours,
patients may report ear pain localized near the ear lobe that is aggravated by a chewing movement of
the jaw. Older children may describe a swelling sensation at the mandibular angle and an associated
sour taste in the mouth. Fever usually subsides within 7 days, notably before parotid gland edema
disappears. Sudden hearing loss may occur due to a vestibular reaction.

Diffuse, tender swelling of the thyroid gland (thyroiditis) may occur about 1 week after parotitis.
Antithyroid antibodies are detected in the serum.

Pancreatitis is a severe but, fortunately, rare complication. A sudden onset of mid-epigastric pain and
tenderness occurs, accompanied by fever, chills, nausea, and vomiting. Patients generally recover within
1 week with appropriate supportive treatment.

Orchitis can occur in up to 50% of postpubertal males, and as many as 30% have bilateral involvement.
Orchitis presents acutely with fever, chills, nausea, vomiting, and lower abdominal pain. After the fever,
the testes begin to swell rapidly. Increase in testicular size can be minimal or as much as 4 times normal
size. As the fever decreases, the accompanying testicular pain and edema subside. Loss of turgor is
noticed, with up to 50% of cases demonstrating atrophy.

Oophoritis in postpubertal females is associated with abdominal and/or pelvic pain and tenderness.

Mumps can also cause aseptic meningitis, a CNS complication which usually is indistinguishable from
other viral etiologies, such as enteroviruses, herpesviruses, or poxviruses. CSF analysis reflects less than
WBC 500 cells/µL with a lymphocytic predominance.

Serum amylase is elevated in mumps parotitis (amylase-S) and in pancreatitis (amylase-P). Serum lipase
is elevated in pancreatitis.

Viruria is present, even in uncomplicated cases, with the mumps virus detected in urine within the first 2
weeks of illness

Mumps virus can be isolated from nasopharyngeal swabs, blood, and fluid from the buccal cavity
typically within the window of 7 days before, up until 9 days after, the onset of parotitis. The virus can
also be isolated in a cell culture inoculated with throat washings, urine, or spinal fluid. CNS involvement
usually shows a lymphocytic pleocytosis. Polymerase chain reaction (PCR) assay of the CSF can be used
to detect viral mumps RNA and fosters a rapid confirmation modality for the diagnosis.

Mumps infection can be confirmed by a positive mumps-specific immunoglobulin M (IgM) titer or by

demonstration of a significant rise in mumps-specific immunoglobulin G (IgG) antibody titers between
acute and convalescent sera specimens. IgG titers can be detected by complement fixation,
hemagglutination inhibition, or enzyme immunoassay. Interpretation of titer rise may have limitations
due to potential mumps cross-reaction with other parainfluenza viruses.

Encouraging oral fluid intake is essential, as maintenance of adequate hydration and alimentation of
patients is important. Refrain from acidic foods and liquids as they may cause swallowing difficulty, as
well as gastric irritation.

Prescribe analgesics (acetaminophen, ibuprofen) for headaches or discomfort due to parotitis. Topical
application of warm or cold packs to the swollen parotid area may soothe the region.

Stronger analgesics may be required for patients with orchitis. Bed rest, scrotal support, and ice packs
are recommended.

Chikunguya

Suganthini Krishnan Natesan, MD

19 agustus 2015

Chikungunya virus is an alpha virus that belongs to the Togaviridae family. It is a single-stranded RNA
virus and is approximately 11.8 kb long with a capsid and a phospholipid envelope. Phylogenetic analysis
has revealed 3 distinct groups based on partial sequences of NS4 and E1 genes: (1) the West African, (2)
the East-Central-South African (ECSA), and (3) the Asian.

Chikungunya virus is transmitted to humans through day-biting mosquitoes that belong to the Aedes
genus. Being an arbovirus, the virus is maintained in the environment between humans or other animals
and mosquitoes. Humans serve as major reservoirs during epidemics.

Chikungunya fever is an acute febrile illness with an incubation period of 3-7 days. It affects all age
groups and both sexes equally, with an attack rate (percentage of individuals who develop illness after
infection) of 40%-85%.

Patients present with abrupt onset of high-grade fever often reaching 102°-105°F, with shaking chills that
last 2-3 days. The fever may return for 1-2 days after an afebrile period of 4-10 days, hence called a
“saddle-back fever.”

Prodromal symptoms are uncommon. However, sore throat, headache, abdominal pain, constipation,
and retro-orbital pain have been reported during the acute phase of the illness.

Chikungunya virus–specific IgM antibodies usually appear upon cessation of viremia, usually by day 5-7
into the illness, and stay positive for 3-6 months. Immunoglobulin G (IgG)–neutralizing antibodies appear
after 7-10 days and may persist for several months. These antibodies are detected with an enzyme-linked
immunoassay (ELISA) test that is available through the CDC and several state health departments.

Chikungunya virus may be isolated in culture within the first 3 days of illness during the period of active
viremia by inoculation of blood into mice or mosquitoes. Culture-based detection is also available
through the CDC.

RT-PCR has been standardized using both structural and nonstructural domains of the Chikungunya virus
genome and is available through the CDC. A genotyping assay has also been developed that would help
in outbreak settings. The molecular assay detects viral RNA during the first 7-8 days of the illness.

Management includes hydration, monitoring of hemodynamic status, collection of blood specimens for
diagnosis, and antipyretic therapy. Severe arthralgia may be managed with nonsteroidal anti-
inflammatory drugs (NSAIDS) (once dengue is excluded) and physiotherapy.