Mikroorganisme Inf Sal Nafas

8/13/2019 Mikroorganisme Inf Sal Nafas

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Mikroorganisme Penyebab Infeksi

Saluran Pernafasan

dr.ACHSAN HARAHAP,MPH


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Sites of upper respiratory infections


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Lokasi:

Infeksi Saluran Nafas Bagian Atas

Infeksi Saluran Nafas Bagian Bawah

Mikroorganisme:

Bakteri

Virus

Jamur

Wabah yang mengancam nyawa :

SARS

Flu Burung


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Perbedaan diantara

MikroorganismeMikroorganisme

Pembiakanpd media

mati

Pembiakandgn

pembelahan

AsamNukleat

Ribosom Kepekaaninterferon

TerhadapAntiboitik

Bakteri

Mikoplasma

Riketsia

Klamidia

Virus

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DNA & RNA

DNA & RNA

DNA & RNA

DNA & RNADNA atau RNA

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Penyakit2 Virus System

Pernapasan 1.Acute Febrile Pharyngitis

2.Acute Respiratory Disease.

3.Bronchitis,Broncholitis,& CROUP 4.Common cold

5.Epidemic Myalgia

6.Hand,Foot,& Mouth Disease

7.Herpangina 8.Influenza,Flu Babi,Flu Burung

9.Pharyngoconjungtival Fever.

10.SARS

11.Viral Pneumonia


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I.Bacterial Upper Respiratory

Infections


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Group A beta hemolytic Streptococcu s pyogenes

Common in children 5-15 yrs old

Inhaling droplet nuclei from active cases or healthy

carriersOnset 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


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Haemophilus influenzaetype b,S. pneumoniae, S. aureus, H. influenzaetype non-b, H. parainfluenzae

Pathogenesis : Inflammation and edema of the epiglottis,

arytenoids, arytenoepiglottic folds, subglotticarea

Epiglottis pulled down into larynx andoccludes 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


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Microbial Causes of

Acute Maxillary SinusitisPREVALENCE MEAN (RANGE)

Adults Children

MICROBIAL AGENT (Bacteria) (%) (%)

Streptococcus p neumoniae 31 (20-35) 36

Haemophi lu s inf luenzae 21 (6-26) 23

(nonencapsulated)

S. pneumon iae and H. influ enzae 5 (1-9) --

Anaerobes (Bacteroides, Fuso bacter ium, 6 (0-10) --

Pepto streptoco ccu s, Vei l lonel la)

Staphy loco ccus aureus 4 (0-8) --

Streptococcus p yogenes 2 (1-3) 2

Branhamella (Moraxella) catarrhalis 2 19

Gram-negative bacteria 9 (0-24) 2


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II.Viral Upper Respiratory

Infections


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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 InfectionsSyndrome Commonly Associated

VirusesLess Commonly AssociatedViruses

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 parainfluenzaviruses, adenoviruses

Bronchopneumonia

Influenza virus, RSV,Adenoviruses

Parainfluenza viruses, measles,VZV, CMV


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Parainfluenza Virus

ssRNA virus

enveloped,

pleomorphicmorphology

5 serotypes: 1, 2, 3,4a and 4b

No common groupantigen

Closely related toMumps 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 byparainfluenza viruses Bronchiolitis,

Pneumonia, Flu-like tracheobronchitis, and

Coryza-like illnesses.


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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, genomeconsists of 8 segments

enveloped virus, with

haemagglutinin andneuraminidase 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.)


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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


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Influenza Virus

Figure 24.16


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Influenza Virus

Epidemiology Pandemics - influenza A pandemics arise

when a virus with a new haemagglutininsubtype emerges as a result of antigenic shift.

As a result, the population has no immunityagainst the new strain. Antigenic shifts hadoccurred 3 times in the 20thcentury.

Epidemics - epidemics of influenza A and Barise through more minor antigenic drifts as aresult of mutation.


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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/Acute idiopathicpolyneuritisrelated to an autoimmune

mechanism ,(flaccid paralysis)

Asthma attacks

P t A ti i Shift


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Past Antigenic Shifts

1918 H1N1Spanish Influenza 20-40 million

deaths1957 H2N2Asian Flu 1-2 million deaths

1968 H3N2Hong Kong Flu 700,000 deaths

1977 H1N1Re-emergence No pandemic

At least 15 HA subtypes and 9 NA subtypesoccur in nature.

Up until 1997, only viruses of H1, H2, and H3are known to infect and cause disease inhumans.

Avian Influenza


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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 chickensand 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 theirnatural avian hosts.

H9N2

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

The disease was mild all patients made a complete

recovery & there was no evidence of reassortment


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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 genes

between human and avian influenza virusesthrough a third host.

There is good evidence that this occurred inthe 1957 H2N2 and the 1968 H3N2

pandemics.2. Recycling of pre-existing strainsthis

probably occurred in 1977 when H1N1 re-surfaced.

3. Gradual adaptation of avian influenzaviruses to human transmission. There issome evidence that this occurred in the1918 H1N1 pandemic.


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Avian Influenza (Flu Burung)

Laboratory Diagnosis Detection of Antigen - a rapid diagnosis can

be made by the detection of influenza antigenfrom nasopharyngeal aspirates and throat

washings by IFT and ELISA Virus Isolation - virus may be readily isolated

from nasopharyngeal aspirates and throatswabs.

Serology - a retrospective diagnosis may bemade by serology. CFT most widely used.HAI and EIA may be used to give a type-specific diagnosis


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Common cold

Rhinoviruses the most common cause of colds

Coronaviruses the 2ndmost common cause

Cold viruses more often spread by fomitesthan by close contact with infected persons

Treatment with remedies that alleviate some

symptoms

Different combinations of interferons and other

factors being explored to control rhinovirus

infections


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Common ColdOver 200 viruses

Virus typeSerotypes

Adenoviruses 41Coronaviruses 2

Influenza viruses 3

Parainfluenza viruses 4

Respiratory syncytial virus 1

Rhinoviruses100+

Enteroviruses60+


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Lower respiratory tract disorders


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I.BACTERIAL LOWER

RESPIRATORY INFECTION1.Pertussis

2.Pneumonia

3.Mycoplasma Pneumonia

4.Legionaeires disease

5.Tuberculosis

6.Psittacosis

7.Q.fever

8.Nocardiosis


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Bordetella pertussis, small, aerobic,

encapsulated, Gram-neg coccobacillus

Transmitted by respiratory droplets

Treated with antitoxin and erythromycin

Vaccine prevents the disease

Complications and deaths

Whooping cough or pertussis(violent cough, cough of 100 days)


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Classified by site of infection as lobar or bronchial

Transmitted by respiratory droplets and carriers

Klebsiella pneumoniais more severe than

Pneumococcal pneumoniaKlebsiella usually treated with cephalosporins

PNC is drug of choice for Pneumococal pn.

Mycoplasma pneumoniae causes primary atypical

pneumonia.

The disease called walking pneumonia

Pneumonia


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Mycoplasma Pneumonia

Figure 24.14

Mycoplasma

pneumoniae:

pleomorphic, wall-

less bacteria

Also called primary

atypical pneumonia

and walking

pneumonia

Common in childrenand young adults

Diagnosis by PCR or

by IgM antibodies

Legionnaires disease


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1976 war veterans attending a convention in

Philadelphia, 29 deaths

Legionella pneumophila, a weakly Gram-neg,

strictly aerobic bacillus with fastidious nutritional

requirements.Most Legionella are free living in soil or water and

do not ordinarily cause disease.

Some strains live as intracellular parasites ofamoebas,Acanthamoeba, Naegleria, Hartmanella,

and Echinamoeba.



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Some of these amoebas colonize wet areas.

Legionellosis is transmitted when organisms

growing in soil or water become airborne and enter

patients lungs as an aerosolAir conditioners, ornamental fountains, cooling

tower, shower heads, humidifiers, vaporizers in

patient rooms should be regularly desinfected

2-10 days incubation; fever, chills, headache,

diarrhea, vomiting, fluid in the lungs, pain in the chest

and abdomen



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Tuberculosis

Mycobacterium tuberculosis, Robert Koch in 1882

White plague of Europe

Atypical mycobacteria, M. avium-intracellulare

complex (MAC) in AIDS patients.

Straight or slightly curved rods that stain acid-fast.

Waxes and long-chain mycolic acids in

mycobacterial cell walls, difficult to Gram stain


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Tuberculosis

Obligate aerobes sensitive to slightdecreases in O2 conc., in apical or upperportions of the lungs which highly

oxygenated. Pathogenic mycobacteria long generation

time (12-18 hours), up to 8 weeks to producea visible colony on laboratory

Highly resistant to drying and remain viablefor 6-8 months in dried sputum, sensitive todirect sunlight


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Mycobacterial cell wall


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TB Transmission

Infectious disease cause by the bacterium,

Mycobacterium tuberculosis

Spread by airborne droplets, droplet nuclei, 1to 5 microns in size

Droplet nuclei generated when a person with

TB disease coughs, sneezes, speaks, or sing

TB infection occurs when a susceptible person

inhales droplet nuclei containing the bacteria

becomes established in the body


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Probability TB Will Be Transmitted

Infectiousness of person with TB

Environment in which exposure

occurred

Duration of exposure

Virulence of the organism


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Psittacosis or parrot fever

Associated with psittacine birds, parrots(burungnuri), and parakeets(burung betet).

At least 130 different species of birds, including

ducks, chickens, and turkeys(kalkun), disease

referred to ornithosis(peny.pada burung,ditularkanpada man.oleh Clamydia psittaci.Pada man disebut

Psittacosis.)

Chlamydia p si t tac i, by direct contact from birds.

Most cases are mild and self-limiting, but some

developed a serious pneumonia

Incubation 1-2 weeks, sore throat, coughing,

difficulty in breathing, headache, fever and chills.


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Q Fever

1stdescribed in Queensland, Australia.

Q : query, which organism caused it remained a

question for a long time

Caused by Coxiel la bu rnett i, among the rickettsias

Exist all over the world, especially in cattle-and

sheep-raising areas.

Transmitted via tick bites, feces, and genitalsecretions of infected animals

Treatment with antibiotics

A vaccine for workers with occupational exposure


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Q fever

Figure 24.15

N di i


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NocardiosisCharacterized by tissue lesions and abscesses

Nocardia asteroides, aerobic, acid-fast staining,filamentous bacterium

Found in soil and water

By inhalationPrimary site is the lungs, can originate in the skin

and other organs

Usually occurs in immunosuppressed patients

Diagnosis based finding the organism in sputum

or other specimens

Sulfonamide and trimethoprim


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II.Viral Lower Respiratory

Infections

1.RSV

2.SARS

R i t S ti l Vi


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Respiratory Syncytial Virus

(RSV)

ssRNA enveloped virus.

belong to the genus Pneumovirus of theParamyxovirus family.

Considerable strain variation exists, may beclassified into subgroups A and B bymonoclonal sera.

Both subgroups circulate in the community atany one time.

Causes a sizable epidemic each year.


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Respiratory Syncytial VirusClinical Manifestations

Most common cause of severe lowerrespiratory tract disease in infants,

responsible for 50-90% of Bronchiolitis and 5-40% of Bronchopneumonia

Other manifestations include croup (10% ofall cases).

In older children and adults, the symptomsare much milder: it may cause a coryza-likeillness or bronchitis.


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Respiratory Syncytial VirusInfants at Risk of Severe Infection

1. Infants with congenital heart disease

2. infants who were hospitalized within the first few

days of life with congenital disease3. Infants with underlying pulmonary disease -

especially bronchopulmonary dysplasia, are at risk

of developing prolonged infection with RSV.

4. Immunocompromized infants - children who areimmunosuppressed or have a congenital

immunodeficiency disease may develop lower

respiratory tract disease at any age.


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Acute Respiratory Disease

Mild to severeSore throat, cough, cold symptoms, fever,

headache, and malaise

Adenoviruses cause about 5% of ARD cases in

children under 5 yrs old.

Symptom are mild and nonspecific-stuffy nose,

cough, and nasal discharge

Adenovirus pneumonia accounts for about 10% ofall childhood pneumonia and is occasionally fatal


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Adenovirus

ds DNA virus

non-enveloped

At least 47serotypes are

known

classified into 6subgenera: A to F

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


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SARS

(Severe Acute RespiratorySyndrome)

Coronaviridae

The coronaviruses (order Nidovirales, familyCoronaviridae, genus Coronavirus) are

members of a family of large, enveloped,

positive-sense single-stranded RNA viruses that

replicate in the cytoplasm of animal host cells


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SARS

Multiple specimens, extracts of lung and

kidney tissue by virus isolation or PCR;

bronchoalveolar lavage specimens byvirus isolation,electron microscopy and

PCR; sputum or upper respiratory tract

swab, aspirate, or wash specimens byPCR


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Coronavirus

ssRNA Virus

Enveloped,

pleomorphicmorphology

2 serogroups: OC43

and 229E


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Fever with a body temperature of > 38.0C (100.4F), amain criteria in the current WHO case definition for

suspected or probable SARS.

Sputum production, sore throat, coryza/ingus, nausea,

and vomiting are less common

Ribavirin, a "broad spectrum" agent, which is active

against various RNA viruses which has been used

extensively in SARS patients

There are currently no commercial veterinary vaccines

to prevent respiratory coronavirus infections, except for

infectious bronchitis virus infections in chickens.

SARS


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FUNGAL RESPIRATORY

INFECTION1.Coccidiodomycosis

2.Histoplasmosis

3.Cryptococcosis4.Pneumocystis Pneumonia

5.Aspergillosis


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Coccidioidomycosis


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Coccidioidomycosis

Figure 24.19

Coccidioides immitis


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Histoplasmosis

Histoplasma capsulatum, soil fungus

Thrives in soil mixed with feces and especially

in chicken houses and in caves containing bat

feces

Enters the body by the inhalation of conidia

Diagnosis by microscopic identification

Supportive therapy and amphotericin B


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Histoplasmosis

Figure 24.17

Histoplasma capsulatum, dimorphic fungus

(a) 37 (a) >35


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Cryptococcosis

Filobasidiella (Cryptococcus) neoformans,budding, encapsulated yeast

Through the skin, nose or mouth

Thrives in pigeon droppings

Birds do not suffer from cryptococcosis, but

disseminate the opportunistic yeast

Mild symptoms can became systemic in largequantities of the spores inhaled by debilitated

patients

Flucytosine and amphotericin B

P ti i


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Pneumocystis pneumonia

Pneumocyst is car in i i, an opportunistic fungus

Occurs in infants, elderly and the

immunocompromised

Invade cell of the lungs and causes alveolar

septa to thicken and the epithelium to rupture

Can spread to other organs and cause

extrapulmonary infections

Diagnosis by finding organisms in biopsied lung

tissue or bronchial lavage

Combination of trimethoprim and

sulfametoxazole

Pneumocystis


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Pneumocystis

Figure 24.21

The mature cyst contains8 intracystic bodies.

The cystruptures,releasing thebodies.

The bodiesdevelop intotrophozoites.

1

2

3Thetrophozoitesdivide.

4

Each trophozoitedevelops into amature cyst.

5

Cyst

Intracystic

bodies

Trophozoite

A ill i


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Aspergillosis

Farmers lung disease

Aspergillus fumigatusorA. flavusoccurs in the

lungs

Fungal spores inhaled from piles of rotting

vegetation or compost may cause clinical allergy

such as asthma, or invasive infection in the lower

respiratory tract.Fungus ball or aspergilloma may be seen on X

rays


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Aspergillosis

Obstruct gas exchange, cause death by

asphyxiation

Aspergillus growing in the lungs may serveas antigens that trigger chronic asthma

Immunosuppresed, immunodeficient (AIDS),

diabetic patients are at higher than normal

risk Amphotericin B

O t i ti f i i l d i i t di


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Aspergillus Rhizopus

Mucor

Opportunistic fungi involved in respiratory disease:

Mucor rouxi i

Figure 12.2b, 12.4


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REFF.

1. REVIEW OF MEDICAL

MICROBIOLOGY,JAWETZ

2. Virologi Klinik ,ProfSoedarto,DTMH,PhD,2010

3. Mikrobiologi Dasar,Edisi ketiga,Satish

Gupte


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