You are on page 1of 11

Exanthems II

Dr Wael Hayajneh

NOTE: EVERYTHING WRITTEN IN ITALIC


FORM IS EXTRA INFO.

Done By Ahmad Shyoukh

Varicella Zoster Virus (VCV) and chickenpox:


It is an enveloped DNA virus that infects mucoepithelial cells, causing chickenpox
in children as a primary infection, and shingles in adults and elderly as a latent
reactivation infection. It remains latent in dorsal root ganglia.

Here we have different generations of lesions. (Necrotic, vesicles, papules, crusted


lesions). These are called pleomorphic/heterogenous lesions and are characteristic
of chicken pox caused by VZV. <<<< Pleomorphic rash means papules, vesicles,
pustules that are concurrently present.

The virus is transmitted through:


1) Airborne respiratory droplets from an infected host
2) Direct close contact with the characteristic rash (High viral titers are found
in the characteristic vesicles of chickenpox)
3) Vertical transmission >>> maternal varicella with viremia can
transplacentally be spread to the fetus causing neonatal varicella.
Pathophysiology:
VZV infects susceptible individuals via the conjunctivae or respiratory tract and replicates in the
nasopharynx and upper respiratory tract. Viral proliferation occurs in regional lymph nodes of
the upper respiratory tract 2-4 days after initial infection; this is followed by primary viremia on
postinfection days 4-6, and it infects the liver, the spleen, and other organs where the virus
replicates again and then a secondary viremia follows 14-16 days post infection, resulting in a
cutaneous infection with the typical vesicular rash. This viremia also spreads the virus to
respiratory sites and is responsible for the contagion of varicella before the appearance of the rash.
After primary infection, VZV is hypothesized to spread from mucosal and epidermal lesions to
local sensory nerves. VZV then remains latent in the dorsal ganglion cells of the sensory nerves.
Reactivation of VZV occurs by spread f the virus from the dorsal root ganglia through the sensory
nerve back to the skin, which results in the clinically distinct syndrome of herpes zoster
(shingles)characterized by a rash that is typically confined to the dermatome innervated by the
sensory ganglion, usually unilateral with local lymphadenopathy.
Exposure to VZV in a healthy child initiates the production of host immunoglobulin G (IgG),
immunoglobulin M (IgM), and immunoglobulin A (IgA) antibodies; IgG antibodies persist for life
and confer immunity. Cell-mediated immune responses are also important in limiting the scope
and the duration of primary varicella infection.
Epidemiology:
Chickenpox is largely a childhood disease, with more than 90% of cases occurring in children
younger than 10 years. The disease is benign and self-limited in the healthy child, and increased
morbidity occurs in adults and immunocompromised patients.

Since the introduction of widespread pediatric immunization in the United States in 1995, the
incidence of varicella has declined significantly.
Clinical Manifestations:
Chickenpox is usually diagnosed clinically on the basis of the characteristic rash and
successive crops of lesions.
The usual incubation period is 10-21 days. A history of exposure to an infected contact
within this period is also an important clue in the diagnosis.
Chickenpox is highly communicable in susceptible individuals. The patient is contagious
from 1-2 days before the appearance of rash until the lesions crust over, usually 5-6 days
after the rash first appears.
Q. How many days should we keep a patient with chicken pox at home?
Ans. They stay at home, until all the previous lesions are dry and crusted,
and no more new papular or vesicular lesions are present, to make sure they
are not infectious anymore. This approximately takes one week, but it can
differ between different patients.
Prodromal symptoms of low-grade fever, malaise, and anorexia may precede the rash by 1
day. The characteristic rash appears initially as small red papules that rapidly progress to
oval, "teardrop" vesicles on an erythematous base. The fluid progresses from clear to
cloudy, and the vesicles ulcerate, crust, and heal.
New crops appear for 3 to 4 days, usually beginning on the trunk followed by the head, the
face, and, less commonly, the extremities. There may be a total of 100 to 500 lesions, with
all forms of lesions being present at the same time.
If fever is prolonged, this may raise the suspicion of complications like varicella
pneumonia and bacterial skin infection, or immunodeficiency.
Pruritus is universal and marked.
Lesions may be present on mucous membranes.
Lymphadenopathy may be generalized.
An ill appearance should raise concern for pulmonary or neurologic complications or
serious bacterial superinfection.
The severity of the rash varies, as do systemic signs and fever, which generally abate after 3
to 4 days.
3

History should include if there is any exposure to varicella at school, daycare, or among
family members, whether the child has previously received varicella vaccine, and if the
child is immunocompromised (including recent systemic steroid use).
Laboratory and Imaging Studies:
It is usually unnecessary because diagnosis is mainly clinical, but it may be
required for conformation.
Vesicles exhibit polymorphonuclear leukocytes.
Cytology and electron microscopy of vesicular fluid or scrapings may reveal intranuclear
inclusions, multinucleated giant cells (which indicates herpes infection but not specific for
VZV), and virus particles.
Serology: Detection of varicella-specific antigen in vesicular fluid by immunofluorescence
using monoclonal antibodies or demonstration of a fourfold antibody increase of acute
and convalescent sera are diagnostic.
White blood cell count: Most children with varicella have leukopenia in the first 3 days,
followed by leukocytosis. Marked leukocytosis may indicate a secondary bacterial
infection but is not a dependable sign. Most children with significant secondary bacterial
infections do not have leukocytosis; neutrophilic leukocytosis and neutrophilia occur in
only a few cases involving serious bacterial infections. Investigations cannot be relied on to
diagnose or exclude bacterial infection.
Complications:
1) Pneumonia:
Perhaps the most serious complication of varicella is viral pneumonia, which primarily occurs in
older children and adults causing morbidity and mortality, but it is Uncommon in young children.
Respiratory symptoms usually appear 3-4 days after the rash. The pneumonia may be
unresponsive to antiviral therapy and may lead to death.
2) Secondary bacterial infections (most common complication)
Varicella may predispose patients to secondary bacterial infections. Signs and symptoms of such
infections can be indistinguishable from uncomplicated varicella during the first 3-4 days. These
lesions provide a portal of entry for virulent organisms; rapidly spreading cellulitis, septicemia,
4

necrotizing fasciitis and other serious infections may occur. Superficial infection with impetigo is
suggestive of potential bacterial superinfection. The most common infectious organisms are group
A streptococci and Staphylococcus aureus. SO either mild infections as impetigo or severe as toxic
shock syndrome and nerotizing fasciitis.
3) Neurological complications
Acute postinfectious cerebellar ataxia is the most common neurological complication,
with an incidence of 1 case per 4000 patients with varicella. Ataxia has sudden onset that
usually occurs 2-3 weeks after the onset of varicella. Manifestations may range from mild
unsteadiness to complete inability to stand and walk, with accompanying incoordination
and dysarthria.
Encephalitis : manifests few days after rash onset. Lethargy, drowsiness, and confusion are
the usual presenting symptoms.
Other reported neurological complications are Reye syndrome, Guillain-Barre syndrome
and aseptic meningitis.
4) Hemorrhagic complications:
Thrombocytopenia and purpura secondary to VZV infection. Hemorrhagic complications are
more common in the immunocompromised or immunosuppressed populations, although healthy
children and adults have been affected.
Treatment of chickenpox:
It is usually self-limited. Some cases are treated with systemic Acyclovir (oral
antiviral medication). IV (intravascular) Acyclovir medication is given in severe
cases.
Symptomatic therapy of varicella includes nonaspirin antipyretics, cool baths, and careful
hygiene. With antihistamine such as diphenhydramine for pruritus.
Early administration of acyclovir, famciclovir, or valacyclovir for chickenpox may decrease the
incidence of varicella pneumonia. Early therapy with antivirals in immunocompromised persons
is effective in preventing severe complications, including pneumonia, encephalitis, and death from
varicella.
================================================================================
5

HERPES ZOSTER: (SHINGLES)

These pictures represent dermatomal distribution of vesicles. The picture on the


left represents a patient with an infection of the maxillary, mandibular and
ophthalmic branches of the trigeminal nerve on the left side only.
It is a delayed complication of varicella, herpes zoster infection, occurs months to years after the
primary infection in about 15% of patients. The complication is caused by virus that persists in the
sensory ganglions.
Herpes zoster consists of a unilateral vesicular rash, limited to 1-3 dermatomes. The rash is often
painful in older children and adults. Among the health benefits of routine varicella immunization
in childhood may be a lifelong decreased risk for reactivation of the virus as shingles.
Clinical Manifestations of zoster
The pre-eruption phase of zoster includes intense localized and constant pain and
tenderness (acute neuritis) along a dermatome, accompanied by malaise and fever.
6

In several days, the eruption of papules, which quickly vesiculate, occurs in the dermatome
or in two adjacent dermatomes. Groups of lesions occur for 1 to 7 days and then progress to
crusting and healing.
Thoracic and lumbar regions are typically involved. Lesions generally are unilateral and
are accompanied by regional lymphadenopathy. In one third of patients, a few vesicles
occur outside the primary dermatome.
Any branch of cranial nerve V may be involved, which also may cause corneal and
intraoral lesions. Involvement of cranial nerve VII may result in facial paralysis and ear
canal vesicles (Ramsay Hunt syndrome)
===============================================================================
Erythema Infectiosum (fifth disease):

The picture above represents a 5 year old patient that came to the emergency room
this morning with a very high fever that lasted for the previous five days. Today he
developed an ugly rash on the face, trunk, and upper extremities. No drug or food
allergy. No previous similar attacks.
7

This disease is called Erythema Infectiosum, or Slapped Cheek or Fifth


Disease, caused by the Parvovirus B19 (AKA erythrovirus).
Parvovirus B19 is a small single-stranded DNA virus that is transmitted via respiratory
droplets. It infects RBCs and human bone marrow erythroid progenitor cells (erythroblasts) that
are mitotically active and inhibits their growth by inducing cell cycle arrest and apoptosis,
resulting in impairment in normal erythrocyte development. It can infect other hematopoietic
precursors.
The rash here is characteristically lacy (joined to one another). Unlike the
petechial rash that occurs with meningococcal disease.
Clinical presentation of this disease:
Fever, Headache, malaise, myalgia as a prodrome, followed after one week
by the Distinctive "slapped cheek" facial rash with circumoral pallor, and
then the rash spreads
Arthritis or arthralgia
Hemolysis
Bone marrow suppression and A-plastic crises in patients with hemolytic
anemia and sickle cell disease.
After an incubation period of 4 to 12 days, a mild illness appears, characterized by fever, malaise,
headache, myalgia, and itching in varying degrees. A confluent, indurated rash appears on the face,
giving a "slapped-cheek" appearance. The rash spreads in 1 or 2 days to other areas, particularly
exposed surfaces such as the arms and legs, where it is usually maculopapular and reticular (lacelike). During the acute phase, generalized lymphadenopathy or splenomegaly may be seen, along
with a mild leukopenia and anemia. Parvovirus infections often are associated with mild
neutropenia and thrombocytopenia, but instances of transient pancytopenia also have been
reported.
The mechanism producing the dermatologic and rheumatologic features is unknown but thought
to represent antigen-antibody (Ag-Ab) complexes in the skin and joints.
The illness of erythema infectiosum lasts 1 to 2 weeks, but rash may recur for periods of 2 to 4
weeks thereafter, exacerbated by heat, sunlight, exercise, and emotional stress..
8

The clinical consequences are generally trivial, unless patients are already compromised by a
chronic hemolytic process, such as sickle cell disease or thalassemia, in which maximal
erythropoiesis is continually needed to counterbalance increased destruction and decreased lifespan of circulating erythrocytes. The hematocrit of these patients may drop as much as 10-15% per
day during acute infection
Primary infection by parvovirus B19 in such individuals often produces an acute, severe, and
sometimes fatal anemia manifested as a rapid fall in red blood cell count and hemoglobin. These
patients may present initially with no clinical symptoms other than fever; this is commonly
referred to as aplastic crisis (reticulocytopenia).
In pregnant woman primary infections in the first 20 weeks of pregnancy, there
will be transplacental transmission of parvovirus B19 from the mother to the baby,
and this will cause hydrops fetalis, which leads to death of fetus. The fetus will
have no hemoglobin (due to bone marrow suppression and hemolysis), thus will
have intrauterine anemia. This results in heart failure. The fetus will be edematous,
and will eventually die.
The infectious stage of this disease is prior to the appearance of the rash. Once the
rash appears, the patient is no longer infectious, and thus will not transmit the
disease. Patients with aplastic crisis continue to be viremic and infectious until
RBC recovery occurs.
Detection of serum parvovirus B19-specific IgM antibody is the preferred diagnostic test. A
positive IgM test result indicates that infection probably occurred within the past 2 to 4 months.
There is no specific therapy. Routine supportive care includes maintaining adequate hydration
and antipyretics. Transfusions may be required for transient aplastic crisis. Intravenous
immunoglobulin may be used for immunocompromised persons with severe anemia.
===============================================================================

ROSEOLA INFANTUM: (AKA SIXTH DISEASE or EXANTHEM SUBITUM)

The case seen in the picture above is a two year old male patient, brought this
morning to the emergency room with mild diffused skin lesions on the back and
anterior chest. He also has mild suboccipital lymphadenopathy
He is Afebrile, conscious, alert and happy, with normal appetite. Physical
examination apart from these skin lesions is normal. He has no itching, took no
recent medications. The patient was febrile, three days prior to appearance of rash.
This disease is called Roseola Infantum or Sixth Disease or Exanthem
Subitum. It is caused by Human Herpes Virus 6 (HHV-6) in most cases, and may
be caused by HHV-7. It is characteristically presented as a diffused transient rash,
that occurs following a sudden, abrupt relief of a high fever, which lasted for about
three days duration.
This is a very common disease that affects almost 100% of children around 2 years
of age! Some are mild cases and others with obvious symptoms.
HHV-6 and HHV-7 are large, enveloped double-stranded DNA viruses that are members of the
herpesvirus family. They infect T lymphocytes and mature mononuclear cells and cause a
relatively prolonged (3 to 5 days) viremia during primary infection. They can be detected in the
saliva of healthy adults, which suggests, as with other herpesviruses, the development of lifelong
latent infection and intermittent shedding of virus.
10

They spread via respiratory route, saliva, and direct close contact with asymptomaic adults who
periodically shed these viruses.
Transplacental antibody protects most infants until 6 months of age. The incidence of infection
increases as maternally derived antibody levels decline. By 12 months of age, approximately 60%
to 90% of children have antibodies to HHV-6, and essentially all children are seropositive by 2 to
3 years of age. The virus is likely acquired from asymptomatic adults who periodically shed these
viruses. HHV-6 is a major cause of acute febrile illnesses in infants and may be responsible for
20% of visits to the emergency department for children 6 to 18 months of age.
Clinical Manifestations
Roseola is characterized by high fever (often >40 C) with an abrupt onset that lasts 3 to 5 days.
A maculopapular, rose-colored rash erupts coincident with defervescence (disappearance),
although it may be present earlier. The rash usually begins on the trunk and then spreads to the
face, neck and legs. The rash usually lasts 1 to 3 days but may fade rapidly and is not present in all
infants with HHV-6 infection. Upper respiratory symptoms, nasal congestion, erythematous
tympanic membranes, and cough may occur. Roseola is associated with approximately one third
of febrile seizures. Roseola caused by HHV-6 and HHV-7 is clinically indistinguishable, although
HHV-6-associated roseola typically occurs in younger infants. Reactivation of HHV-6 following
bone marrow transplantation may result in bone marrow suppression.
There is no specific therapy for roseola. Routine supportive care includes maintaining adequate
hydration and antipyretics.
==============================================================================

He who studies medicine without books sails an uncharted sea, but he


who studies medicine without patients does not go to sea at all.
William Osler
The End
Original Lecture By Yara Abdou
Edited and Modified By Ahmad Shyoukh
11

You might also like