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Important Pathogenic Virus

During Child Growth (2)

Microbiology Department
Medical Faculty,
University of Sumatera Utara
Parainfluenza virus
Causing a spectrum of respiratory illness from
upper respiratory tract symptoms in healthy
children to severe pneumonia in the
immunosupressed
Member paramyxoviridae, genus
Paramyxovirus, species parainfluenza virus
RNA virus single stranded
Parainfluenza virus
Pathogenesis
Transmission is by droplet spread.
Replication occurs in cells of the respiratory
epithelium.
Clinically , illness most frequently involves
larger airways of the lower respiratory tract,
causing croup (laryngotracheobronchitis).
Parainfluenza virus
Pathogenesis (cont)
Re-infection may occur and tends to cause
milder upper airway disease, probably
representing waning of immunity.
Antigenic variation is not progressive (unlike
influenza virus)
Mucosal immunity is most important for
resisting infection. CD8 T cells are important in
viral clearance.
Parainfluenza virus
Clinical Feature
Upper respiratory tract illness (Children under
5 years )
Otitis media
Croup
Bronchiolitis (infants under 6 months)
Severe pneumonia in the immunosupressed
Parainfluenza virus
Diagnosis
Viral isolation by tissue culture and
immunofluorescence is the standard
PCR based tests are faster and can distinguish
viral type
Respiratory Syncytial Virus
RSV is a major cause of lower respiratory tract
infection in young children (bronchiolitis)
An important nosocomial infection
Member of the Paramyxoviridae family, genus
pneumovirus, species Respiratory Syncytial Virus
ssRNA virus
May survives up to 24 hour in patient secretions
depositing on non-porous surface and around an
hour on porous surfaces (tissue, fabric, skin)
Respiratory Syncytial Virus
Pathogenesis
Incubation between 2 and 8 days. Inoculation
is by nose and eye, with infection confined to
the respiratory tract.
Lymphocytic infiltration of the areas around
the bronchioles with wall and tissue oedema
is followed by proliferation and necrosis of
the bronchiolar epithelium : bronchiolitis
Respiratory Syncytial Virus
Pathogenesis (cont)
Sloughed epithelium and mucus blocks small airway
lumens leading to air trapping and hyperinflation.
Air absorbed distal to obstructed airways leads to
multiple areas of atelectasis
Disease is due to the vulnerability of the small
airways of the very young to inflammation and
obstruction (resistance to air flow being inversely
related to the cube of the radius) ,
Respiratory Syncytial Virus
as well as immunopathology , perhaps
immune complex formation.
The severest forms are experienced by infants
when maternally derived specific antibody is
at a high level and severe disease was seen in
children vaccinated with a trial inactivated
vaccine in the 1960s
Respiratory Syncytial Virus
Clinical Feature
Young children : pneumonia and bronchiolitis
Older children : a severe common cold
Respiratory Syncytial Virus
Diagnosis
Clinical diagnosis can be made with some
confidence in children during an outbreak
Serology is only useful epidemiologically
Cell culture : nasopharingeal aspirate provides the
best sample with a high rate of virus isolation. It
should be inoculated into cell lines as soon as
possible.
Respiratory Syncytial Virus
Diagnosis (cont)
Infection is characterized by the typical
syncytial appearance , and the cytopathic
effect is visible at around day 3-7
Rapid test : immunofluorescence antibody
test (IFAT), PCR and enzyme immunoassays
are all available.
Respiratory Syncytial Virus
Prevention
Active immunization is not available.
RSV monoclonal antibody reduces morbidity
in infants at risk of severe RSV.
Infection control in hospital.
Mumps
Acute generalized viral infection of children
and adolescents causing swelling and
tenderness of the salivary glands and rarely
epididymo-orchitis.
A member of the Paramyxoviridae family,
genus rubulavirus, species mumps virus
RNA virus, single stranded
Mumps
Mumps
Pathogenesis
Transmitted by droplet spread or direct
contact
Most infectious just before parotitis
Incubation is 2-4 weeks
During incubation the virus proliferates in the
upper respiratory tract with consequent
viraemia and localization to glandular and
neural tissue
Mumps
Pathogenesis (cont)
Parotid glands show interstitial oedema and
serofibrinous exudate with mononuclear cell
infiltration
Cases of orchitis are similiar with the addition
of interstitial haemorrhage,
polymorphonuclear infiltration and areas of
local infarction due to vascular compromise
Mumps
Clinical feature
Prodrome of fever, headache and anorexia
Earache and ipsilateral parotid tenderness.
The gland swells over 2-3 days. Swelling can
lift the ear lobe up and outward
The other side follows within a couple of days
in most cases
Mumps
Diagnosis
Lab confirmation is required for
epidemiological purposes or when disease is
atypical
Leucocytosis may be seen particularly with
meningitis, orchitis, or pancreatitis
Serum amylase is elevated in parotitis or
pancreatitis
Mumps
Diagnosis (cont)
Serology : most reliably determined using ELISA for
IgM
Virus isolation : present in saliva from 2 days before
symptom onset to 5 days after onset

Prevention
Vaccination is more than 95% effective and takes
place at 12-15 months and preschool as part of
MMR
Rubeola (Measles)
An acute highly infectious disease of children
characterized by cough, coryza, fever and rash
A member of the family Paramyxoviridae,
genus Morbillivirus, species Measles virus
ss RNA
This virus sensitive to light and drying but can
remain infective in droplet form for some
hours
Immunity after infection is lifelong
Rubeola (Measles)
Rubeola (Measles)
Pathogenesis
Airborne, spread by contact with aerosolized
respiratory secretions and one of the most
communicable of the infectious diseases
Patients are most infectious during the late
prodromal phase when coughing is at its peak.
Virus invades the respiratory epithelium and
local multiplication leads to viraemia and
leucocyte infection.
Rubeola (Measles)

Pathogenesis (cont)
Reticulo-endothelial cells become infected and their
necrosis leads to a secondary viraemia
The major infected blood cell is the monocyte
Tissue that become infected include the thymus,
spleen, lymph node, liver, skin and lung
Rubeola (Measles)
Pathogenesis (cont)
Secondary viraemia leads to infection of the
entire respiratory mucosa with consequent
cough and coryza
Kopliks spots and rash appear a few days after
respiratory symptoms (may represent host
hypersensitivity to the virus)
Rubeola (Measles)

Clinical Features
A prodromal phase of malaise, fever, anorexia,
conjunctivitis and cough is followed by Kopliks spot
then rash.
Rash begins on the face and proceed down
involving palms and soles last. It last around 5 days
and may desquamate as it heals
Rubeola (Measles)
Diagnosis
Usually clinically
Lab confirmation is useful in atypical cases
Virus isolation possible in renal cell lines,
useful in the immunodeficient where antibody
responses may be minimal
Serology, a fourfold increase in measles
antibody titres between acute and
convalescent specimens is diagnostic
Rubeola (Measles)
Diagnosis (cont)
ELISA is capable of detecting specific IgM on a
single sample
Immunofluoresent microscopy of cells in
secretions
PCR
Rubeola (Measles)
Prevention
Measles vaccine is given as part of measles,
mumps, rubella (MMR), at 12 months and
preschool.
Passive immunization with immunoglobulin is
recommended for those exposed susceptible
people at risk of severe or fatal measles. It
must be given within 6 days of exposure to be
effective.
Rubeola (Measles)
Prevention ( cont)
Such groups include :
- Children with malignant disease, particularly if
receiving chemo or radiotherapy
- Children with HIV should be given
immunoglobulin after exposure even if
already vaccinated
Influenza virus
One of the commonest infectious disease of man,
primarily causing epidemics of upper respiratory tract
infection
Influenza is a moderate to severe illness most often
caused by influenza A or B viruses.
Members of family Orthomyxoviridae
ss RNA viruses
Have haemagglutinin (HA) or neuraminidase(NA)
activities as key antigenic components and may alter by
mutation (antigenic drift)
Influenza virus
Three distinct influenza viruses :
- Influenza A (16 HA and 9 NA variants have been
identified). Example of subtype: H1N1, H5N1, etc
Typical influenza syndrome and can precipitate
pandemics.
- Influenza B
causes the typical influenza syndrome but does not
cause pandemic
Influenza C (does not possess neuraminidase
structures)
causes afebrile common cold like syndrome and does
not occur in epidemics.
Influenza virus
Pathogenesis
It is highly infectious
Its short incubation period (1-2 day) can
rapidly cause large epidemics and pandemics
Virus enters respiratory epithelial cells,
replicates and progeny are released, the cell
dies.
Viral shedding may start within 24 hour of
infection - Illness follows 24 hour later
Influenza virus
Pathogenesis (cont)
There is diffuse infammation of the trachea and
bronchi with an ulcerative, necrotizing
tracheobronchitis in severe cases.
Primary viral pneumonia is uncommon but is
severe when it occurs.
Bacterial superinfection is common, facilatated by
damage to the mucociliary escalator, and virus-
induced defects in lymphocyte and leucocyte
function.
Influenza virus
Pathogenesis (cont)
Viral levels fall rapidly after 48 hour of illness,
becoming undetectable by 5-10 days.
Influenza virus
Clinical features
1-2 day incubation is followed by an abrupt
onset of symtomps. Fever, chills, headache,
malaise, myalgia, eye pain, anorexia, dry
cough, sore throat, and nasal discharge.
Attack rates are highest in children, who may
present with croup .
Influenza virus
Diagnosis
In the context of a community outbreak, the
diagnosis of influenza can be made with some
confidence on clinical criteria alone
Viral culture, virus is readily isolated from
sputum, throat, or nasal swabs. It is cultured
in cell lines and detected within 3-5 days by its
cytophathic effect
Influenza virus
Diagnosis (cont)
Viral antigen detection : rapid detection within
1-2 days is possible with immunofluoresence
or ELISA. PCR are in increasing use.
Serology : acute and convalescent (10-20days
apart) samples showing a fourfold rise in
antibody titre.
Influenza virus
Prevention
Inactivated vaccines are the main control measure
They are prepared each year containing two type
A and one type B strain
Two doses are required in children under 9 years.
Protection is around 70% and last for 1 year.
Rubella virus
Acute mild exanthematous viral infection of
children and adults resembling mild measles
Potential to cause fetal infection and birth defects
A member of Togaviridae family, genus Rubivirus,
species rubella virus
Rubella is also called German Measles and third
disease, measles and scarlet fever being the first
and second exanthematous infections in children
Rubella virus
Rubella virus
Pathogenesis
Spread is by droplets
Moderately contagious
Incubation is 12-23 days
Patients are at their most contagious when the
rash is erupting
Virus may be shed from 10 days before to 2
weeks after its appearance
Rubella virus
Pathogenesis (cont)
Rash appears as immunity develops and viral
titres fall
Primary viraemia follows infection of the
respiratory epithelium, secondary viraemia
occurs a few days later once the first wave of
infected leucocytes release virions
After infection or vaccination most people
develop lifelong protection
Rubella virus
Clinical feature
Many cases are subclinical
The main symtomps are lymphadenopathy
and a maculopapular rash
Rubella virus
Diagnosis
Its mild nature makes clinical diagnosis difficult
Serology , positive Ig M on a single sample or a
fourfold rise in IgG in paired sera is diagnostic.
Serological diagnosis of congenital rubella in
neonates need analysis of several samples over
time to determine whether antibody titres are
falling (maternal antibody) or rising (recent
infection)
Rubella virus
Diagnosis ( Cont)
Detection of rubella Ig M in newborns serum
indicates infection
Intrauterine diagnosis has been made by
placental biopsy and by cordocentesis with
detection by PCR
Rubella virus
Prevention
Vaccination achives a seroconversion rate of
95%
All women of child bearing age should be
vaccinated before pregnancy
Women should not become pregnant in the 3
months following vaccination
Important Pathogenic Fungi
During Child Growth

Microbiology Department
Medical Faculty,
University of Sumatera Utara
Candida species

A yeast and the most common cause of fungal


infection
Candida albicans is responsible for 90% of infection
Small ovoid cells that reproduce by budding
C. albicans may be found in soil, food and hospital
environment. They are commensal of human (skin,
sputum, GI tract, female genital tract, etc)
Candida species
Candida species
Pathogenesis
The rise of Candida sp. infection relates to the
increase in medical intervention :
- The use of antibiotics (supressing normal
bacterial flora and permitting proliferation of
Candida organism
- Intravenous catheters (providing route of
entry)
Candida species
Pathogenesis (cont)
Immune supression mediated by disease
(e.g.HIV) or therapy such as steroids are also
associated with increase rates of infection
Immune response to Candida infection is
mediated by humoral and cellular mechanism
Candida sp. virulence factors include surface
molecules that permit organism adherence to
other structures ( human cells), acid protease
Candida species
Clinical features : Oral thrush
Oral candidiasis characterized by white,
creamy patches on the tongue and oral
mucosa.
Candida species

Diagnosis
Can be confirmed using a KOH smear or gram stain
to demonstrate hyphae and yeast form
Culture : smooth white colony
Presumtive identification of C. albicans is possible
by inoculating organism from a colony into a small
tube of serum, germ tube should form within 90
minutes.

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