MIKROBIOLOGI

PARASITOLOGI
RESPIRATION

AN
IMO 2019
1. INFLUENZA

Electron micrograph of influenza virus

A/Hong Kong/1/68(H3N2)
Epidemiology incidence
annual epidemics, often occurring in the winter

demographics
affects both adults and children, though with higher
frequency in children

risk factors
advanced or young age
pregnancy
immunosuppression
morbid obesity
pulmonary disease
Pathogenesis
Surface protein
hemagglutinin (H)
and neuraminidase
(N)

• Hemagglutinin
binds to sialic
acid and allows
for viral entry
into cells

• Neuraminidase
allows for
progeny virion
release from
cells
Clinical features
Treatment
 Prevention
Prevention
annual flu vaccine for
those 6 months or older

contains multiple killed

viral strains that are
thought to be likely to
appear during flu season
intramuscular
live-attenuated vaccine
Intranasal

Prognosis
may lead to severe
bacterial superinfections
most commonly S.
aureus, S. pneumoniae,
and H. influenzae
may be fatal
2. Haemophilus
Small, gram-negative rods / coccobaccilli, pleomorphic, facultative anaerobic, non
motile

Most important genera in the family Pasteurellaceae are along with Actinobacillus,
Aggregatibacter, and Pasteurella.

Present on the mucous membranes of humans

The growth of most species requires supplementation of media with one or both of
the following growth-stimulating factors:
Hemin (also called X factor for “unknown factor”) and

Nicotinamide adenine dinucleotide (NAD; also called V factor for “vitamin”).

Although both factors are present in blood-enriched media, sheep blood agar must be
gently heated to destroy the inhibitors of V factor. For this reason, heated blood
(“chocolate”) agar is used for the isolation of Haemophilus in culture.
H. Influenzae
Strains of H. influenzae is covered with a polysaccharide capsule, and six antigenic
serotypes (a through f)

In addition, species is subdivided into eight biotypes (I through VIII) as determined by

three biochemical reactions: indole production, urease activity, and ornithine
decarboxylase activity.

Pathogenesis transmission
respiratory droplets
Predisposing factors for infection
asplenia
H. influenza is one of the "SHiN" that poses particular risk to asplenic patients
Reservoir : nasopharynx
spreads nasopharynx -> lymphatics -> meninges in case of meningitis

Pili and nonpilus adhesins mediate colonization of the oropharynx with H.

influenzae.

Cell wall components of the bacteria (e.g., lipopolysaccharide and a low-molecular-

weight glycopeptide) impair ciliary function, leading to damage of the respiratory
epithelium.

Sometimes, bacteria can then be translocated across both epithelial and endothelial
cells enter the blood.
Molecular biology : encapsulated
capsular type B (antiphagocytic polysaccharide capsule) causes most severe
disease
type B contains ribose in place of hexose
type B capsule is polyribosyl-ribitol-phosphate
Non-encapsulated strains exist ("nontypable")
cause otitis media, sinusitis, and bronchitis
vaccine does not confer immunity to nontypable strains

IgA1 proteases are produced by H. influenzae (both encapsulated and

nonencapsulated strains) and may facilitate colonization of the organisms on
mucosal surfaces by interfering with humoral immunity.

The lipopolysaccharide lipid A may be responsible for initiating this response

in humans.

No antibodies against capsul high-grade bacteremia with dissemination to

the meninges or other distal foci, or epligottitis. (alongside with patient with
depletion complement and splenectomy)
3. Bordetella
Extremely small (0.2 to 0.5 × 1
μm), strictly aerobic, gram-
negative coccobacillus.

Eight species are currently

recognized, with four species
responsible for human disease
:

Bordetella pertussis, the

agent responsible for pertussis
or whooping cough;
• Infection and development of whooping cough (100-day cough) require
exposure to the organism, bacterial attachment to the ciliated epithelial
cells of the respiratory tract, proliferation of the bacteria, and production
of localized tissue damage and systemic toxicity.
• Attachment of the organisms to ciliated epithelial cells is mediated by
protein adhesins: pertactin, filamentous hemagglutinin, and fimbria.
(Similar proteins are also found in B. parapertussis and B. Bronchiseptica).
• Localized tissue damage is mediated by dermonecrotic toxin (produces
localized ischemia in mouse model) and tracheal cytotoxin (inhibits cilia
movement, disrupting normal clearance mechanisms in the respiratory
tree leading to the characteristic pertussis cough).

• Systemic toxicity is produced primarily by pertussis toxin. This toxin

inactivates the protein that controls adenylate cyclase activity, leading to
an increase in cyclic adenosine monophosphate (cAMP) levels and a
subsequent increase in respiratory secretions and mucus production,
characteristic of the paroxysmal stage of pertussis.
Clinical features
Treatment for pertussis is primarily supportive, with nursing supervision
during the paroxysmal and convalescent stages of the illness.

Antibiotics can ameliorate the clinical course and reduce infectivity,

particularly during the early stages of disease, but convalescence depends
primarily on the rapidity and degree to which the layer of ciliated epithelial
cells regenerates Macrolides (i.e., erythromycin, azithromycin,
clarithromycin)
Bordetella parapertussis

Bordetella pertussis

Bordetella parapertussis
Bordetella bronchisepta
• Small, gram-negative bacillus that
inhabits the respiratory tracts of canines,
in which it may cause “kennel cough” and
pneumonitis.

• It causes snuffles in rabbits and atrophic

rhinitis in swine. It is infrequently
responsible for chronic respiratory tract
infections in humans, primarily in
individuals with underlying diseases.

• It grows on blood agar medium. B

bronchiseptica has a silent copy of the
pertussis toxin gene.

• This organism possesses a β-lactamase

that renders it resistant to penicillins and
cephalosporins.
Bordetella holmesii
We describe the detection of Bordetella
holmesii as a cause of whooping cough in Spain.
Prevalence was 3.9% in 2015, doubling to 8.8%
in 2016. This emergence raises concern
regarding the contribution of B. holmesii to the
reemergence of whooping cough and the
effectiveness of the pertussis vaccine. -> CDC
4. Mycobacterium
Bacteria are classified in the genus
Mycobacterium on the basis of ;
(1) their acid-fastness
(2) the presence of cell wall
Mycolic acids
(3) a high (61% to 71% mol)
guanine plus cytosine (G+C)
content in deoxyribonucleic acid
(DNA).
Mycobacteria possess a complex,
lipid-rich cell wall that is
responsible for many of the
characteristic properties of the
bacteria
 Mycobacterium tuberculosis
Culture Growth
The media for primary culture
of mycobacteria should
Characteristics
Obligate aerobes and derive
include a nonselective energy from the oxidation
medium and a selective of many simple carbon
medium. compounds
There are three general Slower
formulations that can be used The doubling time of
for both the nonselective and tubercle bacilli is about 18
selective media. hours
1. Semisynthetic agar media Saprophytic forms tend to
grow more rapidly, to
(eg, Middlebrook 7H10 and
proliferate well at 22–33°C
7H11)
2. Inspissated egg media (eg,
LöwensteinJensen)
3. Broth media (eg,
Middlebrook 7H9 and 7H12)
Reaction to Physical and Chemical Variation
Agents pigmentation, virulence,
Resistant to chemical agents than other bacteria optimal growth
Acids and alkalies permit the survival of some temperature, and many
exposed tubercle bacilli and are used to help other cellular or growth
eliminate contaminating organisms and for characteristics.
“concentration” of clinical specimens.
Tubercle bacilli are resistant to drying and
survive for long periods in dried sputum. Pathogenicity of
Mycobacteria
Epidemiology There are marked
The disease is spread by close person-to-person differences in the ability
contact through the inhalation of infectious of different
aerosols. mycobacteria to cause
Regions with the highest incidence of disease are lesions in various host
China, India,Eastern Europe, Pakistan, sub-Saharan species
Africa, and South Africa.
Other populations at increased risk for M.
tuberculosis disease are homeless persons, drug
and alcohol abusers, prisoners, and people
infected with the human immunodeficiency virus
(HIV).
Constituents of Tubercle
Bacilli Pathology
Lipids The production and
Poteins development of lesions
Pollysaccharides and their healing or
progression are
determined chiefly by
Pathogenesis (1) the number of
Mycobacteria are emitted in mycobacteria in the
droplets smaller than 25 μm in inoculum and their
diameter
subsequent multiplication
when inhaled, to be deposited (2) the type of host and
in alveoli
immune response.
The host’s immune system
responds by release of
cytokines and lymphokines
that stimulate monocytes and Intracelullar Site of Growth
macrophages.( when in
Alveoli) When mycobacteria establish themselves in
Pathogenic lesions associated tissue, they reside principally intracellularly in:
with infection appear in the monocytes
lung 1–2 months after reticuloendothelial cells
exposure. giant cells
 2. Productive (proliferative) type
Two Principal A chronic granuloma, consists of three
Lesions zones:
1. Exudative Type (1) a central area of large, multinucleated
This consists of an acute giant cells containing tubercle bacilli
inflammatory reaction (2) a mid zone of pale epithelioid cells,
with edema fluid; often arranged radially
polymorphonuclear (3) a peripheral zone of fibroblasts,
leukocytes; and, later, lymphocytes, and monocytes.
monocytes around the peripheral fibrous tissue develops, and
tubercle bacilli the central area undergoes caseation
It may lead to massive necrosis. Such a lesion is called a tubercle
necrosis of tissue or may
develop into the second Spread of Organisms in the Host
(productive) type of
lession Tubercle bacilli spread in the host by
The tuberculin test result direct extension, through the lymphatic
becomes positive channels and bloodstream, and via the bronchi
and gastrointestinal tract.
In the first infection, tubercle bacilli
always spread from the initial site via the
lymphatics to the regional lymph nodes.
Primary Infection and Reactivation
Types of Tuberculosis Reactivation tuberculosis
is characterized by
When a host has first Reactivation -chronic tissue lesions
contact with tubercle bacilli, tuberculosis is the formation of
the following features are characterized by tubercles
usually observed:
-chronic tissue lesions -caseation
(1) An acute exudative the formation of -fibrosis
lesion develops and rapidly
spreads to the lymphatics tubercles Always begins at the
and regional lymph nodes. -caseation apex of the lung, where
The exudative lesion in -fibrosis the oxygen tension
tissue often heals rapidly. Always begins at the (PO2) is highest
(2) The lymph node apex of the lung, where
undergoes massive the oxygen tension
caseation, which usually (PO2) is highest
calcifies (Ghon lesion).
(3) The tuberculin test result
becomes positive.
 Clinical features, Lab Diagnosis

Specimens

chronic cough and spitting of blood (next) fresh sputum

Meningitis or urinary tract involvement can gastric washings
occur in the absence of other signs of urine
tuberculosis pleural fluid
Miliary tuberculosis with lesions in many cerebrospinal fluid
organs and a high mortality rate. joint fluid
biopsy material
blood or other suspected
material
Treatment
The two major drugs used to treat tuberculosis are
INH, RMP ((PZA) (EMB)
Regimens begin with 2 months of isoniazid (isonicotinylhydrazine [INH]),
ethambutol, pyrazinamide, and rifampin,
Followed by 4 to 6 months of INH and rifampin or alternative combination
drugs. Second-line drugs include kanamycin, capreomycin, ethionamide,
cycloserine, ofloxacin, and ciprofloxacin

Chemoprophylaxis

The regimens that have been recommended include daily or twice weekly INH
for 6 to 9 months, or daily rifampin for 4 months.
Patients who have been exposed to drug-resistant M. tuberculosis should
receive prophylaxis with pyrazinamide and either ethambutol or levofloxacin for
6 to 12 months.
Mycobacterium leprae
Leprosy (also called Hansen disease) is caused by Mycobacterium leprae.

Characteristic :
-Typical acid-fast bacilli
-singly, in parallel bundles, or in globular masse (are regularly found in scrapings from
skin or mucous membranes (particularly the nasal septum) in patients with
lepromatous leprosy
Diagnosis
Scrapings with a scalpel blade from skin or nasal mucosa or from a biopsy of
earlobe skin are smeared on a slide and stained by the Ziehl-Neelsen technique.
Biopsy of skin or of a thickened nerve gives a typical histologic picture.

Treatment
Sulfones such as dapsone are first-line therapy for both tuberculoid and
lepromatous leprosy. RMP and/ or clofazimine generally are included in the
initial treatment regimens.
Pseumdomonas aeruginosa
• motile
• straight or slightly curved
• arranged in pair
• Obligate aerobic
• Cytochrome oxidase (+)
• Glucose oxidizer
• Nonfermentative
• Capsule
Virulence factor : Epidemiology
Pseudomonas has minimal
• Adhesin : flagella, pili, LPS, alginate nutritional requirements
Resistant to many
• Exotoxin A : disrupt protein synthesisby blocking antibiotics
peptide chain elongation. (EF-2) Contributes to Intrinsic resistance : low
the dermatonecrosis that occurs in burn movement of antibiotics
wounds, acting like Diphtheria toxin through the outer
membrane pores + rapid
• Pyocyanin -> catalyzes superoxide and hydrogen efflux of antibiotics
peroxide and stimulates interleukin (IL)-8 release Acquired resistance :
mutation of gene
• Pyoverdin bind to iron (fullfill metabolic Adaptive resistance :
demand) and regulates secretion of ETA (act as stimuli or specific antibiotic
siderophore/iron chelation)
Patients at high risk ->
• LasA (serine protease) and LasB (zinc neutropenic or
metalloprotease)-> degrade elastin lung immunocompromised
parenchymal damage and hemorrhagic lesions patients, CF patients, burn
(ecthyma gangrenosum)
patients, and individuals
• Alkaline protease & Phospolipase C : tissue
receiving broad-spectrum
destruction-> spreading
antibiotics
• Exoenzymes S and T
B-Hemolysys
Grape-like odor
Flat colonies
Spreading border

Tx : combination of active antibiotics

 Pearls of pathogenic fungi classification:
True Pathogenic fungus Opportunistic Pathogenic
fungus
Thermal Dimorphism Does not express Thermal What is a thermal
Dimorphism dimorphism?
Mostly intracellular Mostly extracellular in yeast Thermal dimorphism is a
form feature unique on true
Can cause clinical Clinical manifestation heavily pathogenic fungus in that
manifestations not depended depends on immune they:
on immune competency competency • At bodily
temperature(37C)
Systemic manifestation is most Manifestation site is random they turn from their
common (lung) saphrobic form into
Usually invoke Th1 pathway Usually invoke Th17 pathway their yeast form
domination involvement domination involvement
although usually it failed in the
end
Examples including : Examples including :
Histoplasma capsulatum Aspergillus spp.
Blastomyces dermatitidis Candida spp.
Coccidioides immitis Penicillium spp.
Paracoccidioides brasiliensis Cryptococcus spp.
 FUNGUS NAME SAPROBIC PHASE PARASITIC PHASE
observables observables

Histoplasma Large flower Intracellular yeast

capsulatum macroconidia/ inside macrophages
tuberculate
macroconidia
Blastomyces Chlamydospore Budding yeast/
dermatitidis blastoconidia/
daughter cell
Paracoccidioides Chlamydospore ‘Pilot-wheel’
brasiliensis appearance

Coccidioides immitis Barrel-shaped Endospore

Arthroconidia

Penicillium/Talaromy Sporulating Capsule-like yeast

ces marneffei structures
Blastomyces Laboratory investigation :
Skin lesion scrapping or pus and sputum
Cultured on Saboraud dextrose agar
dermatitidis without cycloheximide
 Ecology : Decaying organic material Positive result : Mycelial structure on 25-
(route of transmission : spore 30 and Daughter cell yeast appearance
inhalation) after 37
 Incubation period : 4-6 weeks Other test : Immunodiffusion test using
 Clinical manifestation : Antigen A of the blastomyces
1. Lung blastomycosis acute and Treatment :
chronic
2. Cutaneous chronic blastomycoses Mild to moderate : itraconazoles is the
(manifested from chronic lung drug of choice
dissemination) usually Severe to life-threatening : Amphotericin
granulomatous to ulcerative B intravenous+itraconazole follow-on
lesions with well-demarcated therapy (12-24 MONTHS :APPLY TO ALL
edge)
3. Osteomyelitis WHO USE AMPHOTERICIN B)
4. Arthritis
5. Meningitis (immunocompromised)
Usually healthy patient will recover by
itself after 2-12 weeks after initial
symptoms of acute lung blastomycoses
Coccidioides Laboratory investigation :
Sputum,pus and biopsy
immitis Detection of endospores on lung biopsy gives
positive result
Culture of arthroconidia is highly not
 Alternative agent : Coccidioides recommended,since it is very infectious
posadasii (biosafety level 3)
 ecology : desert soil and other Immunodiffusion test : antibodies detected
barren area (dust transmission) after 1-3 weeks after infection but become
 Is also called ‘great immitator’ negative after 2-6 months
 Incubation period : 1-3 weeks Treatment :
 Clinical manifestation : Mild to moderate : Itraconazoles is the drug of
1. Primary coccidioidomycoses : choice too for severe and disseminated
asymptomatic to flu-like illness coccidioidomycoses
2. San Joaquin valley fever : Severe : intravenous amphotericin B only IF
pneumonia-like illness present AZOLES NOT EFFECTIVE
with granulomatous lesion
(mimicking tuberculosis)
3. Dissemination on
immunocompromised
individuals usually after 3-12
months post-initial symptoms
Paracoccidioides brasiliensis
 Ecology : southern America soil
transmitted fungus
 Clinical manifestations :
1. Acute lung paracoccidioidomycoses
to disseminated manifestations in
children and immunocompromised
2. Ulcerative granulomatous lesion in
oral and nasal mucosa (head
granulomatous lesion, DD :
Actinomycetoma,Mycetoma)
 Laboratory diagnosis : findings of
pilot-wheel yeast on biopsy
materials
 Treatment :
1. Mild to moderate : Itraconazole oral
2. Severe or refractory : Amphotericin
B intravenous
Histoplasma capsulatum
 Ecology : pigeon or bat droppings found on soil
(high on nitrogen)
 Variant : Histoplasma capsulatum var.
capsulatum : all around the world
Histoplasma capsulatum var.
duboisii: only in Africa
 the difference between the two is that var.
duboisii is larger :
Var capsulatum : 2-4 mikrometer, Var duboisii :
10-15 mikrometer
 Incubation period : 1-3 weeks
 The case is characteristic to prior history of
cave explorations,presumably exposed to bat
guano
 CLINICAL MANIFESTATIONS OF
HISTOPLAMOSIS
Histoplasma capsulatus var Histoplasma capsulatum var
capsulatum duboisii
1. PULMONARY INFECTIONS 1. NON-PULMONARY
• Acute transient INFECTIONS
• Chronic • SKIN
• Symptoms usually not • BONES
specific and primarily flu- • ABDOMINAL ORGANS NON
like symptoms INTESTINAL
2. DISSEMINATED ON
IMMUNOCOMPROMISED

 Laboratory diagnosis : findings of yeast cells on biopsy materials

 Treatment :
1. Mild to moderate : Itraconazoles
2. Moderate to severe chronic lung : Amphotericin B IV+follow-on
Itraconazole 12-24 months
3. Severe CNS involvements : Amphotericin B IV + follow-on fluconazole 9-
12 months
Penicillium/Talaromyces marneffei
 Unique cases often rise on immunocompromised
individuals in Southeast Asia
 However,it is important to note that this fungus is
not an opportunistic, since it can also induce non-
specific flu-like symptoms
 Clinical manifestations :
 present with fever, cough, pulmonary infiltrates,
lymphadenopathy, organomegaly, anemia,
leukopenia, and thrombocytopenia.
 Skin lesions reflect hematogenous dissemination
and appear as molluscum contagiosum–like
lesions on the face and trunk.
 Laboratory diagnosis : ‘capsule’ yeast cell on
sputum,pus or other biopsy material
 Treatment :
1. Amphotericin B for 2 weeks+followed by
itraconazole for another 10 weeks.
2. Prophylaxis : life-long Itraconazole is the drug of
choice
PARAMYXOVIRIDAE
• The paramyxoviruses is most important agents of respiratory infections
of infants and young children as well as causative agents of two of the
most common contagious diseases of childhood.
• All members of the Paramyxoviridae family initiate infection via the
respiratory tract.
 Structure and Replication
• (-) sense RNA
genome,
envelope
• helical
nucleocapsid
• Viral attachment
protein: HN of
parainfluenza
virus and mumps,
H of measles
virus, and G of
RSV.
• Virus replicates in
the cytoplasm.
 Measles Virus
• Measles virus binds to the CD46 present
on most cell types, nectin 4 on epithelial
cells, and also CD150 which is expressed on
activated T and B cells.
• Measles is highly contagious and is
transmitted from person to person by
respiratory droplets.
• Cell-mediated immunity is essential to Epidemiology
control infection. Transmission Inhalation
• Has large enveloped virion  easily of large-droplet aerosols
inactivated by dryness and acid. High risk unvaccinated
• The characteristic maculopapular measles people Malnourished
rash is caused by immune T cells targeted people and who have
to measles-infected endothelial cells lining more serious outcomes
small blood vessels. Immunocompromised
• T-cell–deficient children who are infected people
with measles have an atypical presentation Virus found worldwide :
consisting of giant cell pneumonia without endemic from autumn to
a rash.
spring, possibly because
of crowding indoors.
Laboratory Diagnosis
• Measles antigen 
immunofluorescence in
pharyngeal cells or
urinary sediment
• Measles genome 
(RT-PCR) in respiratory
tract secretions, urine,
blood, and brain tissue
 characteristic
cytopathologic effects,
multinucleated giant
cells with cytoplasmic
inclusion bodies.
• IgM  when rash is
present.
Treatment, Prevention, and Control

• Live attenuated vaccine  combination with

mumps and rubella (measles-mumps-
rubella [MMR] vaccine) and the varicella
vaccines.
• Vaccination schedule: after 12 months of age
and at age 4 to 6 years or before junior high
school (12 years of age).
• High-dose vitamin A treatment reduces the
risk of measles mortality.
 Parainfluenza Viruses
• Cause mild coldlike symptoms Pathogenesis and Epidemiology
but can also cause serious
respiratory tract disease. Parainfluenza viruses infect
• Four serologic types within the epithelial cells of the upper
parainfluenza genus are human respiratory tract causes
pathogens. giant cell formation and
• Types 1, 2, and 3  severe cell lysis.
lower respiratory tract infection Virus stay in the upper
in infants and young children  respiratory tract, causing
laryngotracheobronchitis only coldlike symptoms.
(croup). Can spreads to the lower
• Type 4 causes  mild upper respiratory tract
respiratory tract infection in laryngotracheobronchitis.
children and adults. Transmission by inhalation
• Parainfluenza viruses do not of large-droplet aerosols.
cause viremia or become Risk : Children mild
systemic.
disease or croup and adults
reinfection with milder
symptoms .
Clinical features, Laboratory Diagnosis
• Parainfluenza viruses 1, 2, isolated from nasal washings
and 3 : mild coldlike upper and respiratory secretions and
respiratory tract infection grows well in primary monkey
to bronchiolitis and kidney cells .
pneumonia. Finding of syncytia and is
• Croup results in subglottal identified with
swelling. Hoarseness, a immunofluorescence.
“seal bark” cough, Rapid RT-PCR techniques are
tachypnea, tachycardia, and the method of choice to detect
suprasternal retraction and identify parainfluenza
develop in infected patients viruses from respiratory
after a 2- to 6-day secretions.
incubation period.
Treatment, Prevention, and Control
Croup : nebulized cold or hot steam and
careful monitoring of the upper airway.
Vaccination with killed vaccines is ineffective.
Mumps Virus
• Mumps virus is the cause of
acute, benign viral parotitis
(painful swelling of the
salivary glands).
• Virus infects epithelial cells of
respiratory tract.
• Infection of parotid gland,
testes, and central nervous
system occurs.
• Principal symptom is swelling
of parotid and other glands
caused by inflammation.
• Cell-mediated immunity is
essential for control of
infection and responsible for
causing some of the symptoms
 Epidemiology, Clinical features
• Transmission  inhalation
of large-droplet aerosols.
• Risk : unvaccinated people Usually present as parotitis almost bilateral with
and immunocompromised fever.
people.
Oral examination reveals redness and swelling of
• Virus is found worldwide.
the ostium of the Stensen (parotid) duct.
• Virus is endemic in late
winter and early spring. The swelling of other glands.

Treatment, Prevention,
Laboratory Diagnosis
and Control
Present in saliva for approximately 5 days after
Vaccines provide the only the onset of symptoms and in urine for as long
effective means for as 2 weeks.
preventing the spread of Mumps virus grows well in monkey kidney cells
mumps infection. multinucleated giant cells.
Live attenuated vaccine RT-PCR detection of viral genomes .
(Jeryl Lynn strain) is part of ELISA, immunofluorescence, and
measles-mumps-rubella hemagglutination inhibition tests to detect
vaccine. mumps virus, antigen, or antibody.
Respiratory Syncytial Virus
• It is the most common cause of
fatal acute respiratory tract
infection in infants and young
children. Epidemiology
• Virus causes localized infection Transmission : Inhalation of
of respiratory tract. large-droplet aerosols.
• Virus does not cause viremia High risk :
or systemic spread. Infants: lower respiratory tract
• Pneumonia results from infection (bronchiolitis and
cytopathologic spread of virus. pneumonia)
• Maternal antibody is Premature neonates: serious
insufficient to protect infant disease
from infection. Children: spectrum of disease
• Necrosis of the bronchi and from mild to pneumonia
bronchioles leads to the Adults: reinfection with milder
formation of “plugs” of mucus, symptoms
fibrin, and necrotic material Immunocompromised, chronic
within smaller airways. heart and lung problems:
serious disease
Clinical features
• Bronchiolitis, pneumonia,
or both : Fever, cough,
dyspnea, and cyanosis in
children < 1 year.
• Febrile rhinitis and
pharyngitis : Children.
• Common cold : Older
children and adults.

Laboratory Diagnosis
Presence of the viral genome in
infected cells and nasal washings can
be detected by RT-PCR techniques.
immunofluorescence and enzyme
immunoassay tests are available for
detection of the viral antigen.
Treatment, Prevention, and Control

• Supportive, consisting of administration of oxygen,

intravenous fluids, and nebulized cold steam.
• Aerosolized ribavirin is approved for treatment of
infants with severe disease.
• Prophylactic and therapeutic passive immunization
with anti-RSV immunoglobulin or monoclonal
antibody (palivizumab) is available for young children
at high risk to serious disease.
• Infected children must be isolated.
• hand washing and wearing gowns, goggles, and
masks.
 Epidemiology
Human metapneumoviruses
Metapneumovirus are ubiquitous and
distributed worldwide.
Infections occur common in
• Human metapneumovirus is
able to cause a wide range pediatric patients.
of respiratory illnesses from The median age of
mild upper respiratory metapneumovirus-positive
symptoms to severe lower hospitalized children is 6–12
respiratory tract disease in
all age groups. months, older than seen
• Human metapneumovirus with RSV (2–3 months).
infects only humans.
• The incubation period for
metapneumovirus is Clinical Syndrome
estimated to be from 4 to 9
days. Children usually display rhinorrhea, cough, and
• Replication is limited to fever and may develop acute otitis media.
respiratory epithelial cells in Lower respiratory tract illnesses may occur,
infected hosts and cell including bronchiolitis, pneumonia, croup, and
surface receptor for human
metapneumovirus appears exacerbation of asthma.
to be αvβ1-integrin. Healthy adults tend to develop cold and flu-like
symptoms.
 Laboratory Diagnosis, Treatment and
Control
• The best specimens for
detection of human
metapneumovirus are
nasopharyngeal Supportive care is the only therapy
aspirates or swabs. available for these infections.
There is no specific therapy for
• Detection of viral human metapneumovirus infections,
antigens in respiratory and no vaccine is available.
specimens by direct
immunofluorescence
staining is sensitive for
children due to higher
viral loads but poorer
for adults.
 Rubella Virus
• Rubella is a respiratory virus and
does not cause readily
detectable cytopathologic
effects.
• Rubella, meaning “little red” in
Latin, was first distinguished
from measles and other
exanthems by German physicians
 Germany Measles
• Maternal rubella infection has
since been correlated with
several other severe congenital
defects.
• Rubella infects the upper
respiratory tract and then
spreads to local lymph nodes.
• The infected person can shed
virus in respiratory droplets
during the prodromal period
Epidemiology Clinical Syndrome
• Transmission : After a 14- to 21-day incubation period
Respiratory route. symptoms in children consist of a 3-day
• High risk : maculopapular or macular rash and swollen
- Children: mild glands.
exanthematous
disease Infection in adults can be more severe and
- Adults: more include problems such as bone and joint pain
severe disease with (arthralgia and arthritis) and (rarely)
arthritis or thrombocytopenia or postinfectious
arthralgia encephalopathy.
- Fetus < 20 weeks:
congenital defects
Treatment, Prevention, and Control
The best means of preventing
Laboratory Diagnosis rubella is vaccination with the
Presence of the virus can be detected by RT- live cold-adapted RA27/3
PCR detection of viral RNA. vaccine strain of virus.
The diagnosis is usually confirmed by the The live rubella vaccine is
presence of antirubella-specific IgM. usually administered with the
Antibodies to rubella are assayed early in measles and mumps vaccines
pregnancy to determine the immune status of (MMR vaccine) after 12
the woman. months of age.
Congenital Infection
• Rubella infection in
a pregnant woman Clinical Syndrom of Congenital Infection
can result in serious
congenital Cataracts and other
abnormalities in the ocular defects
child. Heart defects
• If the mother does Deafness
not have antibody, Intrauterine growth
the virus can retardation
replicate in the Failure to thrive
placenta and spread Mortality within the
to the fetal blood first year
supply . Microcephaly
Mental retardation