scarlet fever - UMF IASI 2015
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Transcript 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
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
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:
Reye’s syndrome
Cerebellar ataxia
Encephalitis
Transverse myelitis
Aseptic meningitis
4.Other rare complications: hepatitis, arthritis, Lyell
syndrome, pancreatitis.
Laboratory tests
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.