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MICROBIOLOGY PPT LECTURE NOTES | Karya Tulis Ilmiah

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17/9/7 microbiology 8-year course 1

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Biological Features

Structure and chemical composition

Developmental cycle

Staining properties

Antigens

Growth and metabolism

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Structure and chemical composition

a nonreplicating, infect

ious particle called the

elementary body (EB)

an intracytoplasmic for

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Structure and chemical composition

The elementary body, which is covered by a rigid cell wall, contains a DNA geno

me with a molecular weight of 66 X 107 (about 600 genes, one-quarter of the g enetic information present in the DNA of Escherichia coli).

A cryptic DNA plasmid (7,498 base pairs) is also found. It contains an open read

ing frame for a gene involved in DNA replication.

 the elementary body contains an RNA polymerase responsible for the transcripti

on of the DNA genome after entry into the host cell cytoplasm and the initiation of the growth cycle.

Ribosomes and ribosomal subunits are present in the elementary bodies. Throu

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Developmental cycle

EBs attach to the microvilli of susceptive cells.

Penetration into the host cell via endocytosis or pinocytosis and for

ming phagosomes

Fusion of lysomes with the EB-containing phagosome are inhibitedEBs reorganize into the metabolically active RBs.

RBs synthesize their own DNA, RNA and protein but lack the necess

ary metabolic pathways to produce high-energy phosphate compou nds.

Energy parasites.

RBs replicate by binary fission and inclusion forms.RBs begin reorganizing into EBs.

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Staining properties

 EBs stain purple with Giemsa stain—in contrast to the blue

of host cell cytoplasm.

 RBs stain blue with Giemsa stain.

 The Gram reaction of chlamydiae is negative or variable and

is not useful in identification.

 Inclusions stain brightly by immunofluorescence ,with

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Antigens

 Group(fenus)-specific antigens:

– heat-stable LPS as an immunodominant component. – Antibody to these antigens can be detected by CF an

d immunofluorescence

 Species-specific or serovar-specific antigens

– Antigens are mainly outer membrane proteins(MOM P).

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Growth and metabolism

Unable to synthesize ATP and depend on the host cell for energy requirement

s.

Grow in cultures of a variety of eukaryotic cell lines

McCoy cells are used to isolate chlamydiae

C pneumoniae grows better in HL or Hep-2 cells.

All types of chlamydiae proliferate in embryonated eggs,particularly in th e yolk sac.

The replication of chlamydiae can be inhibited by many antibacterial drugs.

Cell wall inhibitors (penicillins) result in the production of morphologicall y defective forms but are not effective in clinical diseases.

Inhibitors of protein synthesis (tetracyclines,erythromycins)are effective in most clinical infections.

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Classification

C trachomatis

Biovar trachoma

Biovar lymphogranuloma venereum

Biovar mouse

C pneumoniaeC psittaci

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Pathogenicity

transmission

Who is at risk

Virulence factor

Clinical syndromes

Epidemiology

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Transmission

C. trachomatis

– Sexually transmitted;most frequent bacterial pathogen in united states.

– Infected patients , who may be asymptomatic. – Inoculation through break in skin or membranes.

– Passage to new born at birth.

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Transmission

C. pneumoniae

– Person-to-person spread by inhalation of infecti ous aerosols.

– No animal reservoir

C. psittaci

– Infection acquired by contact with infected bir d or animal(may appear healthy).

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Who is at risk?

C. trachomatis

– People with multiple sexual partners.

– Homosexuals,who are more at risk for LGV. – Newborns born of infected mothers.

– Reiter’s syndrome: young white men.

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Who is at risk?

C. pneumoniae

– High prevalence of infections throughout life;m ost infections asymptomatic.

– Diease most common in adults.

C. psittaci

– Disease most common in adults.

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Virulence factors

C. trachomatis

– Intracellular replication,

– prevention of phagolysosomal 吞噬溶酶体 fusi

on,

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Virulence factors

C. pneumoniae

– Intracellular replication;

– prevention of phagolysosome 吞噬溶酶体 fusi

on;

– ability to infect and destroy ciliated epithelial c ells of respiratory tract,smooth muscle cells,end othelial cells,and macrophages;

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Virulence factors

C. psittaci

– Intracellular parasite,

– prevention of phagolysosomal fusion,

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Clinical syndromes

C. trachomatis

– Trachoma

– Adult inclusion conjunctivitis

– Neonatal conjunctivitis

– Infant pneumonia

– Ocular lymphogranuloma venereum

– Urogenital infections – Reiter’s syndrome

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Clinical syndromes

C. pneumoniae

– Bronchitis

– Pneumonia

– Sinusitis 鼻窦炎

– Pharyngitis

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Clinical syndromes

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Epidemiology

Trachoma

– Trachoma is still prevalent in Africa and Asia, and sporadic cases o ccur all over the world.

– The disease flourishes in hot, dry areas where there is a shortage of water and where standards of hygiene are low.

– The agent is spread to the eyes by flies, dirty towels, fingers, or co smetic eye pencils.

– The initial infection usually occurs in childhood, and the active dis ease eventually appears (mostly by 10 to 15 years of age). Tracho ma may leave a residuum of permanent lesions that can lead to bli ndness.

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Epidemiology

Lymphogranuloma venereum

– Lymphogranuloma venereum persists in the genital tract of infecte d persons.

– LGV is a chronic sexually transmitted disease caused by serotype L1,L2,and L3.

– Because C trachomatis is able to infect both the eyes and the urog enital tract, antitrachoma campaigns involving only ocular treatme nts are futile.

– It occurs sporadically in North America ,Australia ,and Europe but is highly prevalent in Africa, Asia and South America.

– Male homosexuals are the major reservoir of disease.

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Epidemiology

Chlamydia pneumoniae

Chlamydia pneumoniae spreads in human populations by respiratory tract infections.

– It is the agent of atypical pneumonia in hospitalized pat ients as well as in young individuals with an acute respi ratory disease.

– It has caused epidemics in Scandinavia.

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Epidemiology

Chlamydia psittaci

– the cause of psittacosis in birds and occasionall y in humans,

– it is carried by wild and domestic birds, includi ng poultry.

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Immunity

C. trachomatis

– Untreated infections tend to be chronic with per sistence of the agent for many years.

– Little is known about active immunity.

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Immunity

C. pneumoniae

Little is known about active or potentially prote

ctive immunity.

Prolonged infections can occur with C. pneumo

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Immunity

C. psittacosis

– Immunity in animals and humans is incomplete. – A carrier state in humans can persist for 10

years after recovery.

– During this period, the agent may continue to be excreted in the sputum.

– Live or inactivated vaccines induce only partial resistance in animals.

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Diagnosis

Most diseases caused by the chlamydiae are

diagnosed on the basis of

their clinical ma

nifestations.

Eye damage caused by

C trachomatis

is typ

ical, as are the vesicles in the infected uroge

nital tract.

Diagnosis of pneumonitis requires laborator

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Diagnosis

Chlamydia trachomatis can be identified microscopically i

n scrapings from the eyes or the urogenital tract. Inclusion bodies in scraped tissue cells are identified by iodine staini ng of glycogen present in the cytoplasmic vacuoles in infe cted cells.

To isolate the agent, cell homogenates that contain the chla

mydial elementary bodies are centrifuged onto the cultured cells (e.g., irradiated McCoy cells).

After incubation, typical cytoplasmic inclusions are seen in

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Diagnosis

Staining with iodine can distinguish between inclusion bod

ies of C trachomatis and C psittaci, as only the former cont ain glycogen.

Each chlamydial agent can also be identified by using spe

cific immunofluorescent antibodies prepared against either

C trachomatis or C psittaci.

Homogenates or exudates of infected tissues also have bee

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Diagnosis

Sera and tears from infected humans are use

d to detect

anti-

Chlamydia

antibodies

by the

complement fixation or microimmunofluore

scence tests.

The latter is useful for identifying specific s

erotypes of

C trachomatis.

Fluorescent monoclonal antibodies are used

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Diagnosis

It is possible to diagnose C trachomatis in tissue biopsy sp

ecimens by in situ DNA hybridization with cloned C trach omatis DNA probes.

DNA from C trachomatis isolates can be examined by rest

riction endonuclease analysis.

The DNA cleavage pattern of C trachomatis isolates differ

s greatly from that of DNA from C psittaci isolates.

DNAs of the agents of trachoma and lymphogranuloma ve

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Diagnosis

Chlamydia pneumoniae DNA has 10 percent homology

with C trachomatis or C psittaci;

C pneumoniae isolates have 100 percent homology. Chl

amydia pneumoniae isolates can be diagnosed by hybrid ization with a specific DNA probe that does not hybridi ze to other chlamydiae.

Two additional serologic tests are in use:

the microimmunofluorescence test with C pneumoniae

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Prevention and control

C. trachomatis

– It is difficult to prevent C. trachomatis infection s because the population with endemic disease f requently has limited access to medical care.

– It is difficult to eradicate the disease within a po pulation and to prevent reinfections.

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Prevention and control

C. pneumoniae

– Treatment is with tetracycline or erythromycin. – Failures are common.

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Prevention and control

C. psittaci

– Tetracycline or erythromycin is used for treatm ent.

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Treatment

C. trachomatis

– Ocular,genital & respiratory infections

– In endemic areas,sulfonamides,erythromycins,and tetracyclines have b een used to suppress chlamydiae and bacteria that cause eye infections. – Genital infections & inclusion conjunctivitis

– It is essential that chlamydial infections be treated simultaneously in bo th sex partners and in offspring to prevent reinfection.

– tetracyclines are commonly used in non pregnant in fected females. – Erythromycin is given to pregnant women.

– LGV

– The sulfonamides and tetracyclines have been used with food results es pecially in the early stages.

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Treatment

C. pneumoniae

– It is susceptible to the macrolides and tetracyclines and to some fluoroquinolones.

– Treatment with doxycycline, azithromycin,or clarithro mycin appears to benefit patients with the infection. – The symptoms may continue after routine courses of th

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Treatment

C. psittacosis

– tetracyclines. Are the drugs of choice and shoul d be continued for 10 days.

– It may not free the patient from the agent.

– Intensive antiviotic treament may also delay the normal course of antibody development.

– Strains may become drug-resistant.

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