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Mikroorganisme Penyebab Infeksi Saluran Pernafasan

Dr. Tetty Aman Nasution, M.Med.Sc

Departemen Mikrobiologi FK USU

The Respiratory Tract

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LokasiLokasi ::

• Infeksi Saluran Nafas Bagian Atas

• Infeksi Saluran Nafas Bagian Bawah

MikroorganismeMikroorganisme ::

� Bakteri

� Virus

� Jamur

Wabah yang mengancam nyawa :Wabah yang mengancam nyawa :

� SARS

� Flu Burung

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Sites of upper respiratory infections

Bacterial Upper Respiratory Infections

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• Group A beta hemolytic Streptococcus pyogenes

• Common in children 5-15 yrs old

• Inhaling droplet nuclei from active cases or healthy carriers

• Onset is usually abrupt, with chills, headache, acute throat soreness (upon swelling), nausea and vomiting

• Diagnosis by positive throat culture

• Immediate treatment needed

• 3% cases untreated cases interact with immune system and give rise to rheumatic fever

Streptococcal Pharyngitis

• Haemophilus influenzae type b, S. pneumoniae, S. aureus, H. influenzae type non-b, H. parainfluenzae

Pathogenesis :

• Inflammation and edema of the epiglottis, arytenoids, arytenoepiglottic folds, subglottic area

• Epiglottis pulled down into larynx and occludes the airway

Epiglottitis

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• Corynebacterium diphteriae

• Pseudomembrane block the airway

• Spread by respiratory droplets

• Treated with antitoxin and antibiotics

• Prevented by DPT vaccine

Diphteria

Viral Upper Respiratory Infections

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Microbial Causes of Acute Maxillary Sinusitis

PREVALENCE MEAN (RANGE)

Adults Children MICROBIAL AGENT (Bacteria) (%) (%) Streptococcus pneumoniae 31 (20-35) 36 Haemophilus influenzae 21 (6-26) 23

(nonencapsulated) S. pneumoniae and H. influenzae 5 (1-9) --

Anaerobes (Bacteroides, Fusobacterium, 6 (0-10) -- Peptostreptococcus, Veillonella)

Staphylococcus aureus 4 (0-8) --

Streptococcus pyogenes 2 (1-3) 2 Branhamella (Moraxella) catarrhalis 2 19

Gram-negative bacteria 9 (0-24) 2

Microbial Causes of Acute Maxillary Sinusitis

PREVALENCE MEAN (RANGE)

Adult Children MICROBIAL AGENT(Virus) (%) (%)

Rhinovirus 15 --

Influenza virus 5 -- Parainfluenza virus 3 2 Adenovirus -- 2

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Viruses Associated with

Respiratory Infections

Syndrome Commonly Associated Viruses

Less Commonly Associated Viruses

Corza Rhinoviruses, Coronaviruses

Influenza and parainfluenza viruses, enteroviruses, adenoviruses

Influenza Influenza viruses Parainfluenza viruses, adenoviruses

Croup Parainfluenza viruses Influenza virus, RSV, adenoviruses

Bronchiolitis RSV Influenza and parainfluenza viruses, adenoviruses

Bronchopneum onia

Influenza virus, RSV, Adenoviruses

Parainfluenza viruses, measles, VZV, CMV

Parainfluenza Virus

• ssRNA virus

• enveloped, pleomorphic morphology

• 5 serotypes: 1, 2, 3, 4a and 4b

• No common group antigen

• Closely related to Mumps virus

(Linda Stannard, University of Cape Town, S.A.)

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Parainfluenza Virus Clinical Manifestations

• Croup (laryngotraheobroncitis) - most common manifestation of parainfluenza virus infection.

• However other viruses may induce croup e.g. influenza and RSV.

• Other conditions that may be caused by parainfluenza viruses Bronchiolitis, Pneumonia, Flu-like tracheobronchitis, and Coryza-like illnesses.

• Rhinitis, pharyngitis, bronchitis, sometimes pneumonia

• Paramyxoviruses attack the mucous membranes of the nose and throat

• Symptoms can progress to a barking cough and high-pitched, noisy respiration (stridor)

• 2 parainfluenza viruses can cause croup ( acute obstruction of the larynx)

• Inactivated by drying, increased temperature, most desinfectants.

Parainfluenza Virus Clinical Manifestations

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Influenza Virus

• RNA virus, genome consists of 8 segments

• enveloped virus, with haemagglutinin and neuraminidase spikes

• 3 types: A, B, and C

• Type A undergoes antigenic shift and drift.

• Type B undergoes antigenic drift only and type C is relatively stable(Courtesy of Linda Stannard, University of Cape Town, S.A.)

Influenza Virus

• Antigenic shift

– Changes in H and N spikes

– Probably due to genetic recombination between different strains infecting the same cell

• Antigenic drift

– Mutations in genes encoding H or N spikes

– May involve only 1 amino acid

– Allows virus to avoid mucosal IgA antibodies

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Influenza Virus • Orthomyxoviruses

• Enzyme neuraminidase, penetrate the mucus layer protecting the respiratory epithelium, budding of new virus particles from infected cells

• Tendency to undergo antigenic variations or mutations that affect viral antigens

• Inhalation of virus-containing droplets or indirect contact with infectious respiratory secretions

•Hemagglutinin (H) : attachment to host cells

•Neuraminidase (N) :release virus from cell

Influenza Virus

Figure 24.16

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Influenza Virus Epidemiology

• Pandemics - influenza A pandemics arise when a virus with a new haemagglutinin subtype emerges as a result of antigenic shift.

• As a result, the population has no immunity against the new strain. Antigenic shifts had occurred 3 times in the 20th century.

• Epidemics - epidemics of influenza A and B arise through more minor antigenic drifts as a result of mutation.

Influenza Virus Diagnosis

• Viral culture - tissue culture

• Fluorescent-labeled murine monoclonal Ab - shell viral cell culture - viral Ag

• PCR

• CF - at onset and 2 weeks

4-fold-rise in Ab titre

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Influenza Virus Complications

• Bacterial superinfection

– Otitis media

– Sinusitis

– S. pneumoniae, H. influenzae, B. catarrhalis

• Guillain-Barre Syndrome

• Asthma attacks

Past Antigenic Shifts

1918 H1N1“Spanish Influenza” 20-40 million deaths

1957 H2N2“Asian Flu” 1-2 million deaths

1968 H3N2“Hong Kong Flu” 700,000 deaths

1977 H1N1 Re-emergence No pandemic

At least 15 HA subtypes and 9 NA subtypes occur in nature. Up until 1997, only viruses of H1, H2, and H3 are known to infect and cause disease in humans.

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Avian Influenza (Flu Burung)

H5N1

• An outbreak of Avian Influenza H5N1 occurred in Hong Kong in 1997, 18 persons were infected of which 6 died.

• The source of the virus probably from infected chickens and the outbreak controlled by a mass slaughter of chickens in the territory.

• All strains of the infecting virus were totally avian in origin and there was no evidence of reassortment.

• However, the strains involved were highly virulent for their natural avian hosts.

H9N2

• Several cases of human infection with avian H9N2 virus occurred in Hong Kong and Southern China in 1999.

• The disease was mild all patients made a complete recovery & there was no evidence of reassortment

Avian Influenza (Flu Burung)

• A(H5N1) avian influenza

• No signs from person to person

• Epidemic among poultry allows more and more opportunities for person-to-person contact to occur

• Right recombination event between the H5N1 strain and a coexisting human influenza strain."

• People and equipment are responsible for spreading about from farm to farm

• Persons with symptoms cover their nose, mouth with a tissue when coughing or sneezing; making hand hygiene products, tissues available in waiting areas; containers for disposal of used tissues; masks to symptomatic patients.

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Theories Behind Antigenic Shift1. Reassortment of the H and N genesbetween human and avian influenza viruses

through a third host.

There is good evidence that this occurred in the 1957 H2N2 and the 1968 H3N2 pandemics.

2. Recycling of pre-existing strains – this probably occurred in 1977 when H1N1 re- surfaced.

3. Gradual adaptation of avian influenza viruses to human transmission. There is some evidence that this occurred in the 1918 H1N1 pandemic.

Avian Influenza (Flu Burung) Laboratory Diagnosis

• Detection of Antigen - a rapid diagnosis can be made by the detection of influenza antigen from nasopharyngeal aspirates and throat washings by IFT and ELISA

• Virus Isolation - virus may be readily isolated from nasopharyngeal aspirates and throat swabs.

• Serology - a retrospective diagnosis may be made by serology.