Infectious diseases in children

2. Will focus on >>
• 1-Measles
• 2-Rubella
• 3-Mumps
• 4-Chicken pox
• 5-Roseola infantum
• 6-Pertussis
• 7-Hepatitis
• 8-CNS infections

3. For each infection will try to cover??
• Epidemiology:
• Causative agent:
• Clinical features:
• Diagnosis
• Complications:
• Treatment:
• Prevention:

4. Measles

5. Measles
• Measles is a highly contagious disease spread by
airborne means or by contact with respiratory
droplets.
• Cause: Measles—Paramyxovirus (ssRNA).
• Epidemiology: Outbreaks are rare because of
herd immunity resulting from near universal
immunization. Isolated cases occur within
communities with low immunization rates.
• Patients are generally contagious about 5 days
before to 4 days after the appearance of the
pathognomonic rash.

6. • Clinical manifestations: Prodrome of fever,
cough, coryza, conjunctivitis, and
• cough followed by the development of the
pathognomonic morbilliform rash which
appears approximately day 5 of illness in a
cephalocaudad progression fading in the order
that it appeared; skin may desquamate.
• Koplik's spots are pathognomonic gray/white
spots on buccal mucosa.
Measles

7. • Complications of the disease include otitis media,
pneumonia, croup, and subacute sclerosing
panencephalitis .
• subacute sclerosing panencephalitis which is a rare
degenerative encephalitis characterized by dementia
and intellectual deterioration and seizures occurring
many years after initial infection.
• Diagnosis: Clinical diagnosis can be verified with
serology.
• Treatment: Generally supportive. Vitamin A
supplementation can decrease mortality especially in
malnourished patient.
Measles

8. Rubella

9. Rubella
• Cause: Rubella–Togavirus (ssRNA).
• Epidemiology: Virus is transmitted by droplets
or direct contact.
• Infected individuals are contagious from a few
days before to 7 days after the onset of rash.
• Because of comprehensive vaccination and
routine antibody screening by obstetricians,
congenital rubella syndrome has nearly been
eliminated in some country like United States.

10. • Clinical manifestations: Asymptomatic infections are
common.
• Rubella infection can produce mild erythematous
maculopapular rash, fever, and lymphadenopathy.
• Transient polyarthralgias and polyarthritis are common
in adolescent females.
• The disease is of major medical importance because of
congenital rubella syndrome .
• Teratogenic-associated with congenital infection
causing cataracts, deafness, cardiac (PDA)
• Diagnosis: IgM serology.
• Treatment: Supportive.
Rubella

11. Roseola infantum (exanthem subitum)

12. Roseola infantum (exanthem subitum)
• Human Herpes Virus 6 & 7
• Epidemiology: Primary infection peaks
between 6 and 24 months of age.
• Transmission likely to occur from contact with
infected respiratory secretions from
asymptomatic adult caregivers.
• Once individuals have been infected, the virus
persists in latent form throughout life.

13. • Clinical manifestations:
• The illness typically presents with 3 to 5 days of
high fever followed by a macular papular rash
which appears on the trunk and spreads to the
extremities, neck, and face as the fever resolves.
• It may be associated with febrile seizures.
• Complications: Encephalitis and
encephalopathy have been seen.
• Diagnosis: Generally clinical, PCR when
available.
• Treatment: Supportive.
Roseola infantum

14. Measles VS Rubella VS Roseola
infantum

15. Mumps

16. Mumps
• Epidemiology: Transmitted by respiratory
droplets.
• Clinical manifestations: General symptoms of
fever, headache, malaise, and muscle aches with
swelling of one or more salivary gland (usually
parotid gland).
• Complications include meningoencephalitis,
orchitis in pubescent males, arthritis, myocarditis,
and pancreatitis. Note that orchitis causes
infertility infrequently.
• Diagnosis: Clinical diagnosis supported with
serology.
• Treatment: Supportive.

17. Pertussis

18. • Diagnosis: PCR, or culture. Peripheral blood
leukocytosis with lymphocytosis.
• Treatment: Infants younger than 6 months
commonly require hospitalization for supportive care.
• After paroxysmal phase begins, treatment does not
lessen severity of disease but may limit spread. Treat
with erythromycin for 14 days or azithromycin for 5
days.
• Prevention: Infants are routinely immunized with
the DTaP vaccine at several intervals within the first 2
years of life (2, 4, 6, and 15 months) as well as at 4
years of age.
• Those exposed to pertussis, regardless of immunization
status, should be treated prophylactically with a
macrolide to prevent spread.
Pertussis

19. Pertussis
• Epidemiology: Respiratory infection caused by Bordetella
pertussis, a gram-negative aerobic coccobacillus.
• Adolescents and adults often serve as a source of infection
for infants and young children as their symptoms are not
recognized as pertussis.
• Clinical manifestations: Begins with a mild upper
respiratory prodrome for a week (catarrhal stage), followed
by severe cough for 1 to 3 months (paroxysmal stage) that
may be associated with a classic inspiratory whoop; during
convalescent stage, symptoms resolve gradually.
• Patients are usually afebrile throughout the illness.
• Older children and adults usually have milder URI
symptoms.

20. Chicken pox

21. Epidemiology
• In the prevaccine era, the peak age of
occurrence was 5 to 10 years, with peak
seasonal infection in late winter and spring.
• Transmission is by direct contact, droplet, and
air.

22. Etiology
• Chickenpox and zoster are caused by varicella-zoster virus (VZV),
double-stranded DNA virus that is a member of the herpesvirus
family.
• Humans are the only natural host.
• Chickenpox (varicella) is the manifestation of primary infection.
• After resolution of chickenpox, the virus persists in latent infection
in the dorsal root ganglia cells. Zoster (shingles) is the
manifestation of reactivated latent infection of endogenous VZV.
• VZV (chickenpox) is highly communicable among susceptible
individuals, with a secondary attack rate of more than 90%.
• The period of communicability ranges from 2 days before to 7 days
after the onset of the rash, when all lesions are crusted.

23. Clinical Manifestations
• The incubation period of varicella is generally 14 to 16
days, with a range of 11 to 20 days after contact.
• Primary infection with VZV results in chickenpox.
• Prodromal symptoms of fever, malaise, and anorexia
may precede the rash by 1 day.
• The characteristic rash appears initially as small red
papules that rapidly progress to nonumbilicated, oval,
"teardrop" vesicles on an erythematous base.
• The fluid progresses from clear to cloudy, and the
vesicles ulcerate, crust, and heal.

24. • 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.
• Pruritus is universal and marked.
• Lesions also may be present on mucous
membranes.
• Lymphadenopathy may be generalized.
• The severity of the rash varies, as do systemic
signs and fever, which generally abate after 3 to 4
days.
Clinical Manifestations

25. Laboratory Studies
• Laboratory testing confirmation for diagnosis
is usually unnecessary.
• Infection can be confirmed by detection of
varicella-specific antigen in vesicular fluid by
immunofluorescence using monoclonal
antibodies, or by demonstration of a fourfold
antibody increase of acute and convalescent
sera.

26. Treatment
• Symptomatic therapy of varicella includes
nonaspirin antipyretics, cool baths, and
careful hygiene.
• The routine oral administration of acyclovir is
not recommended in otherwise healthy
children because of the marginal therapeutic
benefit, the lack of difference in
complications, and the cost of acyclovir
treatment.

27. Complications
• Although VZV infection is generally a mild disease, complications
are common.
• Secondary infection of skin lesions by streptococci or staphylococci
is the most common complication.
• Thrombocytopenia and hemorrhagic lesions or bleeding also may
occur, known as varicella gangrenosa.
• Pneumonia is uncommon in healthy children.
• Myocarditis, pericarditis, orchitis, hepatitis, ulcerative gastritis,
glomerulonephritis, and arthritis may complicate varicella.
• Reye syndrome may follow varicella; aspirin use is contraindicated
during varicella infection.
• Neurologic complications frequently include post-infectious
encephalitis, cerebellar ataxia, nystagmus, and tremor. Less
common neurologic complications include Guillain-Barré syndrome,
transverse myelitis, cranial nerve palsies, optic neuritis, and
hypothalamic syndrome.

28. • Prognosis: Primary varicella usually resolves
spontaneously
• Prevention: Children with chickenpox should
not return to school until all vesicles have
crusted. A hospitalized child with chickenpox
should be isolated in a negative-pressure
room to prevent transmission.
• A live attenuated varicella vaccine is recommended
as a single dose for all children at age 12 to 18
months and for children age 19 months to the 13th
birthday without a history of chickenpox

29. Hepatitis

30. Hepatitis
• Definition: Acute hepatitis is defined as less than 6 months
of liver inflammation, and chronic hepatitis indicates an
inflammatory process which has been present for 6 or
more months.

31. • EPIDEMIOLOGY:
• 70% to 80% of all new cases of viral hepatitis are
related to HAV,
• 5% to 30% are related to HBV,
• and 5% to 15% are related to HCV.
• The major risk factors for HBV and HCV are
injection drug use, frequent exposure to blood
products (hemophilia, organ transplants, chronic
renal failure), and maternal infection.
• HBV and HCV cause chronic infection, which may
lead to cirrhosis and is a significant risk factor for
hepatocellular carcinoma and represents a
persistent risk of transmission.

32. Hepatitis
• ETIOLOGY:
• There are five primary hepatotropic viruses, which differ in
their virologic characteristics, transmission, severity,
likelihood of persistence, and subsequent risk of
hepatocellular carcinoma .
• HAV and hepatitis E virus (HEV) are transmitted by the
fecal-oral route.
• HBV, HCV, and hepatitis D virus (HDV) are transmitted
parenterally by IV drug use and sexual and perinatal modes.
• HDV, also known as the delta agent, is a defective virus that
requires HBV for spread and causes either coinfection with
HBV or superinfection in chronic HBsAg carriers.
• HBV, HCV, and HDV infections can result in chronic
hepatitis, or a chronic carrier state, which facilitates spread.

33. • CLINICAL MANIFESTATIONS :
• There is considerable overlap in the characteristic clinical courses
for HAV, HBV, and HCV .
• The preicteric phase, which lasts approximately 1 week, is
characterized by headache, anorexia, malaise, abdominal
discomfort, nausea, and vomiting and usually precedes the onset of
clinically detectable disease.
• Jaundice and tender hepatomegaly are the most common physical
findings and are characteristic of the icteric phase. Prodromal
symptoms, particularly in children, may abate during the icteric
phase.
• Asymptomatic or mild, nonspecific illness without icterus is
common with HAV, HBV, and HCV, especially in young children.
• Hepatitic enzymes may increase 15-fold to 20-fold.
• Resolution of the hyperbilirubinemia and normalization of the
transaminases may take 6 to 8 weeks.

34. LABORATORY AND IMAGING STUDIES
• Alanine aminotransferase and aspartate
aminotrans-ferase levels are elevated and
generally reflect the degree of parenchymal
inflammation.
• Alkaline phosphatase, 5'-nucleotidase, and total
and direct (conjugated) bilirubin levels indicate
the degree of cholestasis, which results from
hepatocellular and bile duct damage.
• The prothrombin time is a good predictor of
severe hepatocellular injury and progression to
fulminant hepatic failure

35. • Hepatitis A : The diagnosis of viral hepatitis is confirmed by
characteristic serologic testing .
• The presence of IgM-specific antibody to HAV with low or
absent IgG antibody to HAV is presumptive evidence of
HAV.
• There is no chronic carrier state of HAV.
• Hepatitis C :
• Serocon-version after HCV infection may occur 6 months
after infection.
• A positive result of HCV ELISA should be confirmed with the
more specific recombinant immunoblot assay, which
detects antibodies to multiple HCV antigens.
• Detection of HCV RNA by PCR is a sensitive marker for
active infection, and results of this test may be positive 3
days after inoculation.

36. • Hepatitis B:
• The presence of HBsAg signifies acute or chronic infection with HBV.
• Antigenemia appears early in the illness and is usually transient, but
also is diagnostic of the carrier state.
• Hepatitis B e antigen (HBeAg) appears in the serum with acute HBV.
• The continued presence of HBsAg and HBeAg in the absence of
antibody to e antigen (anti-HBe) indicates high risk of
transmissibility that is associated with ongoing viral replication.
• Clearance of HBsAg from the serum precedes a variable window
period followed by the emergence of the antibody to surface
antigen (anti-HBs), which indicates development of lifelong
immunity.
• Antibody to core antigen (anti-HBc) a useful marker for recognizing
HBV infection during the window phase (when HBsAg has
disappeared, but before the appearance of anti-HBs).
• Anti-HBe is useful in predicting a low degree of infectivity during the
carrier state.

37. Typical course of hepatitis B infection. After exposure to hepatitis B virus (HBV; arrow), the
earliest detectable serum marker is a rise in HBsAg, which may appear at any time (weeks 1 to
10) postexposure; HBV DNA and HBAg follow closely. HBeAg is detectable 2 to 8 weeks before the
onset of the symptomatic phase, which is heralded by an increase in alanine aminotransferase
(ALT) levels, serum bilirubin concentrations, and constitutional signs. Clearance of HBsAg by
immune aggregation with anti–hepatitis B core antigen (HBc) occurs by 6 to 8 months
postinfection; those who fail to clear are termed HBsAg carriers. Anti-HBc, which appears just
before the symptomatic phase, is the first detectable, host-induced immunologic marker of
hepatitis B infection. Anti-HBc of the IgM class may be the only marker of HBV infection in serum
after clearance of HBsAg and before a rise in anti-HBs. Anti-HBc is not a neutralizing antibody and
therefore, in contrast to anti-HB, is not protective.

38. TREATMENT
• The treatment of acute hepatitis is largely supportive
and involves rest, hydration, and adequate dietary
intake.
• Hospitalization is indicated for persons with severe
vomiting and dehydration, a prolonged prothrombin
time, or signs of hepatic encephalopathy.
• When the diagnosis of viral hepatitis is established,
attention should be directed toward preventing its
spread to close contacts.
• For HAV, hygienic measures include hand washing and
careful disposal of excreta, contaminated diapers or
clothing, needles, and other blood-contaminated
items.

39. • Chronic HBV infection may be treated with
interferon alfa-2b or lamivudine,
• and HCV may be treated with interferon alfa
alone or more often in combination with oral
ribavirin.
TREATMENT

40. COMPLICATIONS
• A protracted or relapsing course may develop
in 10% to 15% of cases of HAV in adults,
lasting for 6 months with an undulating course
before eventual clinical resolution.
• Fulminant hepatitis with hepatic
encephalopathy, gastrointestinal bleeding
from esophageal varices or coagulopathy, and
profound jaundice is uncommon, but is
associated with a high mortality rate.

41. PROGNOSIS
• Most cases of acute viral hepatitis resolve without specific therapy,
with less than 0.1% of cases progressing to fulminant hepatic
necrosis.
• HBV, HCV, and HDV may persist as chronic infection with chronic
inflammation, fibrosis, and cirrhosis and the associated risk of
hepatocellular carcinoma.
• Five percent to 10% of adults with HBV develop persistent infection,
defined by persistence of HBsAg in the blood for more than 6
months compared with 90% of children who acquire HBV by
perinatal transmission.
• Approximately 85% of persons infected with HCV remain chronically
infected, which is characterized by fluctuating transaminase levels.
• Approximately 20% of persons with chronic infection develop
cirrhosis, and approximately 25% of those develop hepatocellular
carcinoma.

42. Meningitis
• Infection and inflammation of the meninges
surrounding the brain by direct inoculation or
hematogenous spread.

43. • Epidemiology:
• can be caused by bacteria, viruses, or, rarely, fungi.
• Viral meningitis is caused principally by entero-viruses, including
coxsackieviruses, echoviruses, and, in unvaccinated individuals,
polioviruses.
• The organisms commonly causing bacterial meningitis : S.
pneumoniae , N. meningitidis and H. influenzae type b .
• Incidence of H. influenzae type b meningitis has decreased
dramatically as a result of immunization.
• the most frequent pathogens varied according to age as follows:
• ≥1 month and <3 months—GBS (39%), gram-negative bacilli (32%),
S. pneumoniae (14%), N. meningitidis (12%).
• ≥3 months and <3 years—S. pneumoniae (45%), N. meningitidis
(34%), GBS (11%), gram-negative bacilli (9%).
• ≥3 years and <10 years—S. pneumoniae (47%), N. meningitidis
(32%).
• ≥10 years and <19 years—N. meningitidis (55%).
Meningitis

44. • Clinical manifestations: Preceding upper respiratory tract
symptoms are common.
• Rapid onset is typical of S. pneumoniae and N. meningitidis.
• Indications of meningeal inflammation include headache, irritability,
nausea, nuchal rigidity, lethargy, photophobia, and vomiting. Fever
usually is present.
• Kernig and Brudzinski signs of meningeal irritation usually are
positive in children older than 12 months of age.
• In young infants, signs of meningeal inflammation may be minimal
with only irritability, restlessness, depressed mental status, and
poor feeding.
• Focal neurologic signs, seizures, arthralgia, myalgia, petechial or
purpuric lesions, sepsis, shock, and coma may occur.
• Increased intracranial pressure is reflected in complaints of
headache, diplopia, and vomiting.
• A bulging fontanel may be present in infants.
• Ptosis, sixth nerve palsy, anisocoria, bradycardia with hypertension,
and apnea are signs of increased intracranial pressure with brain
herniation.
• Papilledema is uncommon, unless there is occlusion of the venous
sinuses, subdural empyema, or brain abscess.
Meningitis

45. • Neurologic sequelae include focal deficits,
seizures, hearing loss, and vision impairment.
The most common permanent neurologic
sequel is hearing loss.
• Complications: include subdural effusion,
intracranial infection (subdural empyema,
brain abscess), cerebral infarction,
hydrocephalus, diabetes insipidus, and
disseminated infection (arthritis, pneumonia).
Meningitis

46. Diagnosis
Cerebrospinal Fluid Evaluation (CSF)
Normal Bacterial Viral Tuberculosis
WBC per mL 0–5 (allow up
to 30 in
neonates)
100–100,000 50–1,000 100 s
Glucose
(mg/dL)
45–65 Low Normal Low
Protein
(mg/dL)
20–45 High Slightly
increased
High
Gram stain Negative Positive Negative Negative
Meningitis

47. Treatment
• In neonates, initiate ampicillin plus cefotaxime.
• Cefotaxime will treat GBS and gram-negative enterics and penetrates the
CSF. Ampicillin is mainly used for its effectiveness against Listeria
monocytogenes.
• In infants and children outside of the neonatal age group, third-
generation cephalosporin & Vancomycin
• third-generation cephalosporin is generally used empirically, as it treats
pathogens most likely recovered at this age, including S. pneumoniae, N.
meningitidis & H. influenzae type b . Vancomycin is added for resistant S.
pneumoniae.
• Duration of treatment is 10 to 14 days for S. pneumoniae, 5 to 7 days for
N. meningitidis, and 7 to 10 days for H. influenzae.
• Dexamethasone shown to decrease hearing loss in those with meningitis
due to H. influenzae type b (given before or concurrently with first dose of
antibiotics).
• Antibiotic prophylaxis of close contacts to those with meningococcal
meningitis and H. influenzae type b meningitis is indicated.
Meningitis