Download scarlet fever - UMF IASI 2015

SCARLET FEVER
Epidemiology

The mortality has declined from 72% in
the preantibiotic era to 7 to 27%.
Pathogenesis

There are three mechanisms involved in the production
of scarlet fever: toxic, septic and immunologic.

The streptococcal erythrogenic toxin.

As a result of soft tissue infections may occurs otitis,
sinusitis, adenitis and bacteremia.

Immune mechanism: antibodies against different
streptococcal antigens
Clinical manifestations

Incubation period is usually 3-6 days.

The onset is abrupt with fever, headache, dysphagia, vomiting, with
approximately 3 days duration.

Exanthem – Characteristic:
Filatov’s mask
Pastia’s lines

The erythema abates in 7-9 days.

Enanthem consists of:
Characteristic appearance of tongue
Exudative or erythematous pharyngitis and
tonsillitis, and very rarely, ulcerative aspect of
tonsillitis.
Descuamation period starts after 7-14 days of illness
Laboratory features

Throat culture - positive for group A streptococci.

Rapid antigen detection tests in throat swab.

White blood cell count reveals leukocytosis,
hypereosinophilia, neutrophilia.

Increased ESR.

Intracutaneous administration of erythrogenic toxin
elicits local erythema (positive Dick test – not used at
the present time).
Differential diagnosis



Other infectious causes of tonsillitis
Different eruptive disease
Kawasaki
Complications of scarlet fever
 Suppurative
complications
 Nonsuppurative
complications: acute
rheumatic fever, acute glomerulonephritis
Treatment

To prevent primary attacks of rheumatic fever,
treatment should ensure penicillin levels for at
least 10 days.
This can be achieved by 7 days of penicillin G (24 million IU/day) followed by 3 administration of
benzathine penicillin (every 7 days).

If penicillin allergy is suspected, the drug of
choice is erythromycin (30-40 mg/kg/day).
MEASLES
 Measles
is a contagious disease
characterized by a prodrome of fever,
cough, coryza, and conjunctivitis,
followed by an erythematous,
maculopapular, confluent rash and a
pathognomonic enanthem (Koplik spots).
Etiology

measles virus, member of the genus Morbillivirus
(family Paramyxoviridae).
Measles virus is a spherical, enveloped RNA virus

Infected cells may also develop intranuclear and
intracytoplasmic inclusion bodies (a frequent
pathologic feature of persistent CNS infections).
Pathogenesis

Infection is spread between individuals by the respiratory
route.

In the second day, primary viremia occurs

On the 5th to 7th day after inoculation, secondary
viremia occurs

Between the 11th and 14th days after inoculation the
greatest viral content is noted; this is the moment when
prodrome starts followed by the occurrence of
exanthema.
Clinical manifestations


Incubation period is 10-14 days.
The prodromal stage (lasts for 3-4 days) - is
characterized by:
 fever, malaise,
 cough, coryza
 conjunctivitis photophobia
 diarrhea.
 Koplik spots are the pathognomonic lesions of the
measles:
 Sore throat and gingivitis are another two manifestations
of enanthem.
Clinical manifestations
The rash (persists for 6-7 days)

appears 3-4 days after the onset

the lesions are light, pink at the beginning (lesions blanched with
pressure), then, they become confluent;

maculopapular eruption begins behind the ears, involves the upper
part of the neck;

spreads centrifugally,

the exanthem begins to fade after 3 days of evolution

the end of the exanthem is marked by a fine
in the same period physical examination can reveals pharyngitis,
enlargement of cervical lymph nodes and fever

Clinical syndromes of measles

Atypical measles
It’s a form of measles that occurs in children with a
previous administration of measles vaccine.
Measles virus can not be isolated, but antibody levels
are very high.

Modified measles
Modified measles is a mild form that occurs in partially
immune persons:
 The
distinguishing features are: a longer
incubation period and a minimal
prodromal period.



Measles in pregnant women
In a pregnant woman, measles can lead
to spontaneous abortion and stillbirth.
Measles in immunocompromised
patients
In immunocompromised patients
measles infection evolves as a severe,
frequently fatal disease..
Complications

Complications may be consequences of viral infection or
secondary to bacterial infections:
Otitis media, mastoiditis, laryngitis, laryngotracheitis;





Pulmonary involvement
Neurologic complications
Post infectious encephalomyelitis
Measles inclusion-body encephalitis
Subacute sclerosing panencephalitis.
Laboratory diagnosis
 Serological
exams: ELISA and
hemagglutination-inhibition assay.
 Virus
isolation from nasopharyngeal
secretions is not a routine technique.
Differential diagnosis






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

rubella,
scarlet fever
erythema infectiosum
roseola infantum
enteroviral infection
Epstein-Barr virus exanthema
viral hepatitis
drug-induced exanthema
trichinosis.
Treatment

Bed rest must continue at least 8-10 days after
the appearance of rash.
Infection is contagious 5 days before and
another 5 days after the appearance of rash.

Treatment consists, primary, of symptomatic
relief.

If bacterial superinfection occurs antibiotics are
indicated.
Prevention
 Passive
immunization with human immune
globulin, intramuscularly, within 6 days
after exposure, is recommended in
children under 1 year of age, in chronically
ill patients, pregnant women,
immunosuppressed patients.
Active immunization
Two doses of vaccine are recommended for
all the children.
RUBELLA

Rubella (German measles or 3-days measles) is
an acute febrile illness characterized by a rash
and posterior auricular and suboccipital
lymphadenopathy that affects children and
young adults.

Infection during early pregnancy may result in
serious abnormalities of the fetus, referred to as
the congenital rubella syndrome.

Rubella virus, a member of the Togaviridae
family, is the sole member of the Rubivirus
genus.
Acquired rubella
Pathogenesis
Infection occurs through the mucosa of
the upper respiratory tract.
Clinical Findings
Incubation takes 2-3 weeks.

The rash starts on the face, extends over the trunk and extremities
and lasts 1-5 days.

Ocasionally, an enanthem consisting of small, red macules on the
soft palate precedes/accompanies the rash.

Posterior auricular and suboccipital adenopathy

Rare complications include thrombocytopenic purpura,
myocarditis, Guillain-Barre syndrome, bone marrow aplasia and
encephalitis.
Laboratory diagnosis
 isolation
of virus
 evidence of seroconversion.
 Differential
diagnosis: scarlet fever,
enterovirus infection, measles, adenovirus
infection, human parvovirus B19 disease,
sunburn, allergic rash, infectious
mononucleosis.
Treatment

Rubella is a mild, self-limited illness and no
specific treatment is given.
Laboratory-proved rubella in the first 3-4 months
of pregnancy is almost uniformly associated with
foetal infection.
Therapeutic abortion is the only means of avoiding
the risk of malformed infants in such cases.
Prevention

Attenuated live rubella vaccines have been
available since 1969 as a single antigen or
combined with measles and mumps vaccine.

Vaccinated children pose no threat to mothers
who are susceptible and pregnant.

The vaccine induces immunity in at least 95%
of recipients and will endure at least 10 years.
Congenital Rubella Syndrome
Pathogenesis

Maternal viremia associated with rubella
infection during pregnancy may result in
infection of the placenta and fetus. Mother
may be either symptomatic or
asymptomatic.
Clinical Findings




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Transient effects in infants
Permanent manifestations
congenital heart diseases
total or partial blindness
growth retardation; failure to thrive,
hepatosplenomegaly,
thrombocytopenic purpura, anemia,
osteitis and meningoencephalitis.
Developmental abnormalities that appear and progress
during childhood and adolescence:


Differential diagnosis includes other congenital
infections: syphilis, toxoplasmosis, CMV and herpes
simplex virus infection.
Laboratory diagnosis

Demonstration of rubella antibodies of
the IgM class
Differential diagnosis
 Includes
other congenital infections:
syphilis, toxoplasmosis, CMV and herpes
simplex virus infection.
Treatment:

There is no specific treatment for congenital
rubella.

Many abnormalities can be corrected by surgery
or may respond to medical therapy.

Specific lesions are managed clinically without
regard to their etiology.
Prevention
 To
eliminate rubella and the congenital
rubella syndrome, it is necessary to
immunize women of childbearing age, as
well as all school-age children.
VARICELLA
 Varicella
(chickenpox) is a contagious,
benign, acute illness characterized by a
generalized vesicular rash, which results
from primary infection with varicella-zoster
virus (VZV).
Etiology
VZV belongs to the family Herpesviridae.
The VZV genome consists of a doublestranded DNA molecule.
Pathogenesis
 VZV
is spread by air droplets from
nasopharyngeal secretions.
Pathology
 In
the skin, VZV produces ballooning
degeneration of epithelial cells in the
malpighian layer of the epidermis.
Clinical manifestations

Incubation period: 15 days (10-20 days)

Prodrome symptoms (last for 1-2 days):
Exanthem : pink macular (at the beginning) that
quickly become papular and develop into vesicle 1 to 4
mm in diameter surrounded by a zone of erythema.
The lesions become pustules as inflammatory cells
migrate into the vesicular fluid.
Enanthem: vesicles also involve mucosal surfaces, and
rapidly evolve into shallow ulcerations.
 Varicella
occurring during the first
trimester of pregnancy has been
associated with congenital abnormalities
 Neonatal
varicella may occur when the
mother develops the disease within a
period of 5 days before to 2 days after
delivery.
 Varicella
in immunocompromised persons
is a serious and potentially fatal infection.
Clinical manifestations
1.Bacterial superinfection
2. Varicella pneumonia
3.Neurologic complications:




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Reye’s syndrome
Cerebellar ataxia
Encephalitis
Transverse myelitis
Aseptic meningitis
4.Other rare complications: hepatitis, arthritis, Lyell
syndrome, pancreatitis.
Laboratory tests

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Culture of VZV
By electron microscopy and histopathology
Detection of VZV antigens in a scrapping
obtained from the base of a vesicle;
Direct fluorescent antigen detection;
PCR
Serologic techniques (a fourfold rise in antibody
titers is considered diagnostic)
Diagnosis

The history of exposure/no prior history of
chickenpox and the clinical appearance of the
exanthem (diffuse vesicular rash).

The presence of virus, viral antigens, or virus
associated cytopathic effect within the lesions.

Documentation of VZV - antibody production.
Differential diagnosis
 Differential
diagnosis includes vesicular
exanthems caused by: coxackievirus,
disseminated HSV infection, diffuse
impetigo, or rickettsialpox.