1. SCARLET FEVER

2. Epidemiology
The mortality has declined from 72% in the preantibiotic era to 7 to 27%.

3. 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

4. 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

5. 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).

6. Differential diagnosis
Other infectious causes of tonsillitis
Different eruptive disease
Kawasaki

7. Complications of scarlet fever
Suppurative complications
Nonsuppurative complications: acute
rheumatic fever, acute glomerulonephritis

8. 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 (2- 4 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).

9. MEASLES

10. 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).

11. 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).

12. 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.

13. Clinical manifestations
Incubation period is 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.

14. 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

15. 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:

16. The distinguishing features are: a longer incubation period and a minimal prodromal period.

17. 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..

18. 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.

19. Laboratory diagnosis
Serological exams: ELISA and hemagglutination-inhibition assay.
Virus isolation from nasopharyngeal secretions is not a routine technique.

20. Differential diagnosis
rubella,
scarlet fever
erythema infectiosum
roseola infantum
enteroviral infection
Epstein-Barr virus exanthema
viral hepatitis
drug-induced exanthema
trichinosis.

21. 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.

22. 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.

23. Active immunization
Two doses of vaccine are recommended for all the children.

24. RUBELLA

25. 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.

26. Acquired rubella

27. Pathogenesis
Infection occurs through the mucosa of the upper respiratory tract.

28. 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.

29. 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.

30. 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.

31. 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.

32. Congenital Rubella Syndrome

33. 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.

34. 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.

35. Laboratory diagnosis
Demonstration of rubella antibodies of the IgM class

36. Differential diagnosis
Includes other congenital infections: syphilis, toxoplasmosis, CMV and herpes simplex virus infection.

37. 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.

38. 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.

39. VARICELLA

40. Varicella (chickenpox) is a contagious, benign, acute illness characterized by a generalized vesicular rash, which results from primary infection with varicella-zoster virus (VZV).

41. Etiology
VZV belongs to the family Herpesviridae. The VZV genome consists of a double- stranded DNA molecule.

42. Pathogenesis
VZV is spread by air droplets from nasopharyngeal secretions.

43. Pathology
In the skin, VZV produces ballooning degeneration of epithelial cells in the malpighian layer of the epidermis.

44. 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.

45. 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.

46. 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.

47. 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)

48. 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.

49. Differential diagnosis
Differential diagnosis includes vesicular exanthems caused by: coxackievirus, disseminated HSV infection, diffuse impetigo, or rickettsialpox.