Professional Documents
Culture Documents
Microbiology Department
Medical Faculty,
University of Sumatera Utara
Parainfluenza virus
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 undert 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
Mumps
Mumps
Mumps
Pathogenesis
Transmitted by droplet spread or direct contact
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
Parotid glands show interstitial oedema and
serofibrinous exudate with mononuclear cell
infiltration
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
Rubeola (Measles)
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
Influenza virus
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.
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 (1020days 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
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
Candida species
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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