口腔微生物免疫學
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口腔微生物免疫學. Bacterial infection 細菌感染. 陳玉昆副教授 : 高雄醫學大學 口腔病理科 07-3121101~2755 [email protected] 學 習 目 標. Understand: Virulence factor of bacteria Koch postulates Two main oral bacterial lesions - Caries/periapical lesions - Periodontitis 4. Tuberculosis

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口腔微生物免疫學

Bacterial infection

細菌感染

陳玉昆副教授: 高雄醫學大學 口腔病理科

07-3121101~2755

[email protected]


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學 習 目 標

  • Understand:

  • Virulence factor of bacteria

  • Koch postulates

  • Two main oral bacterial lesions

  • - Caries/periapical lesions

  • - Periodontitis

  • 4. Tuberculosis

  • 5. Syphilis


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參考書目

References

  • Siqueira JF. Endodontic infections: Concepts, paradigms, and perspectives. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2002;94:281-93

  • Hoang MD et al, Secondary syphilis: a histologic and immunohistochemical evaluation. J Cutan Pathol 2004: 31: 595-9

  • Zeltser R & Kurban AK. Syphilis. Clin Dermatology 2004;22:461-8

  • Yepes JF et al, Tuberculosis: Medical management update. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2004;98:267-73

  • 結核病教學參考教材-衛生署疾病管制局

  • 黃吉志 結核病的歷史回顧與展望 高醫醫訊 94年7月

  • 張肇益 淺論牙周病病原菌、內毒素及宿主免疫反應 牙橋 2003;16:30-7

  • Slots J & Taubman MA. Contemporary oral microbiology & Immunology. First edition, 1992 Chapter 11, p. 165-190

  • Kaohsiung Medical University, Oral Pathology Department

  • Ficarra G, Carlos R. Syphilis: The renaissance of an old disease with oral implications. Head and Neck Pathol DOI 10.1007/s12105-009-0127-0


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Bacterial Infection

No damage

(latent/dormant)

Commensal

Host

Parasite

Pathogen

Damage

Virulence factors

Adherence, extracellular enzymes,

fibrinolysin, toxin


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Koch’s postulates

The microorganism occurs in every case of the

disease can account for the pathologic changes

and clinical course of the disease

The microorganism occurs in no other disease

as a fortuitous and nonpathogenic parasite


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After it is isolated from the diseased host & grown in pure

culture, the microorganism can induce the diseaseanew

Koch’s postulates

Organism isolated from lesions

Grown in pure culture in vitro

Pure culture

Animal

A similar disease

Organism reisolated

Help! I have been infected

哈 哈


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Shortcomings

Koch’s postulates

Isolated from patients both with and without cholera,

Vibrio choleraefailed to experimentally induce the

disease in animals

  • Place considerable emphasis on pathogenicity, which

  • resides particularly in the microorganism

  • Dependence on host susceptibility is an unquestionable issue

  • Emphasize the ability to cultivate the causative micro-

  • organism in pure culture

  • Some diseases, such as syphilis and leprosy, for which

  • the causative bacterium has not yet been cultured

Limitations


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Koch’s postulates

  • Imply that all strains of a given microbial species are

  • equally virulent

  • It is known that different strains within a species vary

  • in virulence

  • Suggest that only a single species causes each disease

  • There are some diseases, such as periradicular diseases, that are induced by a mixture of different microbial species

Limitations

  • Require that the suspected microorganism, after reino- culation into an animal, produce the S/S of the disease

  • Several human pathogens either do not cause the disease in animals or cause a disease with different characteristics from the human form of the disease


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牙 周 病

細 菌

口腔兩大疾病

病原菌:

Streptococus mutans

Gram (-)

Two Main Bacterial Infections

齲 齒

  • > 200 different microbial species can be found in infected

    root canals, usually in combinations of 4 to 7 species/canal

  • Theoretically, any one of these species would have the

  • potential to be an endodontic pathogen


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The microorganism must be present in sufficient number

to initiate and maintain the periradicular disease

The microorganism must possess an array of virulence

factors, which should be expressed during root canal

infection

The microorganism must be spatially located in the root canal system in such a way that it or its virulence factors can gain access to the periradicular tissues

The root canal environment must permit the survival and growth of the microorganism and provide signals or cues that stimulate the expression of virulence genes

Requirements for endodontic pathogen (1)


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Inhibiting microorganisms must be absent or present in low numbers in the root canal environment

The host must mount a defense strategy at the periradicular tissues, inhibiting the spread of the infection. This process will result in tissue damage

Requirements for endodontic pathogen (2)

Ref: 1


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病 原 菌

Specific

Non- specific

Specific

Gram (-)

A. Actinomycetemcomitans

P. gingivalis

P. Intermedia

C. Rectus

B. Forsythus

Spirochete

Amoeba

Bacteroides

Spirochete

1890

1930

1990

1970

牙 周 病

細 菌

牙科兩大 疾病

Two Main Bacterial Infections

齲 齒


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牙 周 病 特 定 病 原 菌 的 條 件

該種細菌必須能夠大量於發病時存在,

而於健康時則僅有少數或甚至沒有

該種細菌所引發之抗體價在血清,唾液

或牙齦溝液中必須要高

清除或抑制該種細菌將迅速去除或舒緩病症

病巢部的組織,若使用該種細菌之抗體來操作

螢光抗體染色法,病巢部之組織能被染色標記

該種細菌必須能夠產生致病毒素或致病原因子

該種細菌之接種必須能夠讓實驗室的無菌動物

也引發相同的病程及症狀


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Principal bacteria associated with

periodontal diseases

Adult periodontitis

Refractory

periodontitis

Localized juvenile

periodontitis

Periodontitis in

juvenile diabetics

Pregnancy

gingivitis

ANUG

Porphyromonas gingivalis,

Prevotella intermedia,

B. forsythus,

Campylobacter rectus

Bacteroides forsythus,

P. gingivalis,

Campylobacter rectus,

P. intermedia

P. intermedia,

Intermediate-sized-

spirochetes

Actinobacillus actinomycetemcomitans,

Capnocytophaga

Capnocytophaga

Actinobacillus actinomycetemcomitans,

P. intermedia


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牙 周 組 織

牙 周 病 病 原 菌

直 接 效 應

間 接 效 應

Inhibition of PMN

Leukotoxin, chemotaxis inhibitors,

phagocytosis & intracellular killing,

resistance to C-mediated killing

Lymphocyte alterations

Endotoxicity

IgA, IgG proteases

Fibrinolysin

Superoxide dismutase

Catalase

Enzymes

Collagense, hyaluronidase,

phospholipase, phosphatases

Exotoxin

Endotoxin

Cell inhibitors

Ammonia

Fimbria

牙 周 病 病 原 菌 之 致 病 力


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Endotoxin - lipopolysaccharide (LPS)

化學結構

O antigen

Side chain

Core Polysaccharide

Lipid A

O antigen

polysaccharide

Core polysaccharide

Lipid A

Outer membrane

Smooth- 8-10 O antigen

Phospholipid

Lipoprotein

Semi-rough- 1-2 O antigen

Peptidoglycan

Rough- no O antigen

Inner membrane

Refs: 7,8


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Endotoxin - lipopolysaccharide (LPS)

毒性強, 可直接對組織產生傷害,

亦會產生不良的免疫反應

可 :

造成 Leukopenia

活化XII blood clotting factor, 影響凝血機制

活化變異的補體反應

毒害fibroblast

引發骨吸收

活化巨噬細胞以製造IL-1,TNF-種種組織分解酶

亦產生過氧化物或離子基


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Tuberulosis

Granulomatous inflammation &

tubercle

Lung

Caseation necrosis

(liquefy, cavitation,

fibrosis & calcification)

Ghon complexe

(radiodensities)

Mycobacterium tuberculosis

Miliary tuberculosis

Koch phenomenon (partial immunity to reinfection)

High lipid content

Difficult to destain with acid once stained

(acid-fast stain)

Virulence factor: Cord factor ( a glycolipid of trehalose & mycolic acid)

inhibition of PMN, attack mitochondrial memb causing

damage to respiratory &/or oxidative system, elicit

granulomatous formation

: PPD (purified protein derivative)

(no toxin)

Aerosols

Hematogenate route

Ref: 9


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Ref: 5


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結核桿菌 Mycobacterium tuberculosis

Ref: 5


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M tuberculosis

Bacilli

Fc receptors

High molecular

weight lipids

Glycolipids

Mycolic acids

Surfactant protein

receptor

Complement

receptors

CD 14

Cell wall

Cell wall

  • Aerobic

  • Non-motile

  • Non-spore forming

  • Slow growing

Refs: 4, 9


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Latent

Primary Infection

Coughing

Bacilli

Pulmonary

manifestation

80-84%

Active

Extrapulmonary

manifestation

16-20%

  • Immunosuppression

  • Malnutrition

  • Vitamin D deficiency

Refs: 4, 9


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結 核 病 的 傳 染 途 徑

Ref: 5


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Ref: 5


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只要number of cells = 10 可被感染

Ref: 5


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Ref: 5


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Ref: 5


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Ref: 5


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Ref: 5


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2002年 各國結核病發生率比較

台灣肺結核

Ref: 6


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Bacilli

New cases – 14,486 (2001)

Ref: 5


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Ref: 5


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Risk Group

(RG) = 3

Ref: 5


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Primary

(10 days to 10 wks, average 3 wks after contact)

Chancre (genitalis,

oral, perineal)

Lymphadenopathy

(lymph node)

Tertiary

(months or years

after 2nd stage)

Skin (gumma),

CNS (tabes

dorsalis),

Circulatory

system (aortic

aneurysm)

Secondary

(2 to 12 wks, after chancre)

Generalized rash,

Flu symptoms,

Bone lesions

(anywhere or

everywhere)

Placenta

Congenital

Hutchinson triad

Wassermann Ab

Non-specificity

IgM

Index of severity

Treponemal Ab

Specificity

IgG

Index of severity

3 wks

Syphilis

Treponema pallidum


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Exposure

Primary incubation

Central nervous

system invasion

10-90 days from exposure

Primary syphilis

25-60%

Chancre formation

Secondary incubation

4-10 weeks after chancre formation

Early

neurosyphilis

Secondary syphilis

Transmittable

sexually

or mother to

child

Symptomatic in

only 5%

Early latent syphilis (asymptomatic)

1 year or less postinfection

Recurrence

Meningitis

Cranial neuritis

Ocular involvement

Meningiovascular disease

Transmittable

mother to

child

Late latent syphilis (asymptomatic)

More than 1 year postinfection

Tertiary syphilis

late neurosyphilis

Tertiary syphilis: cardiovascular syphilis

Non-

Transmittable

10% (20-30 years postinfection)

Tabes dorsalis (2-9%)

(Onset 3-50 years postinfection)

Tertiary syphilis: gummatous disease

General paresis (2-9%)

(Onset 2-30 years postinfection)

15% (1-46 years postinfection)

Natural history of untreated syphilis

Ref: 3


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Natural history of untreated syphilis

TERTIARY SYPHILIS

Ref: 10


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Constitutional and mucocutaneous manifestations of secondary syphilis

Symptoms: fever, malaise, weight loss

Skin rash (symmetrical and generalized), alopecia

Condyloma latum in intertriginous areas

Lymphadenopathy

Oral involvement: multiple mucous patches covered by grayish,

white pseudomembranes and surrounded by erythema

Ocular involvement: uveitis, iritis, optic neuritis

Arthritis, periostitis

Hepatitis

Glomerulonephritis

Neurologic involvement: headache, meningitis, cranial nerve

paralysis, cerebrovascular accident

Ref: 10


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Syphilis: The Renaissance of an Old Disease with Oral Implications

Painless oral ulcer

Oral chancer

An important diagnostic criteria

Ref: 3


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(頂端切平)

Secondary syphilis: truncal macular- papular eruption

Manifestations of untreated syphilis

Chancer

Ref: 3


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Manifestations of untreated syphilis

Secondary syphilis: oral mucous patch

Secondary syphilis: papular syphilis of the palms

Ref: 3


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Manifestations of untreated syphilis

Secondary syphilis: moth-

eaten alopecia of the scalp

Congenital syphilis: mulberry molar

Tertiary syphilis: ulcerated gumma of the leg

Secondary syphilis:

loss of lateral eyebrow

Ref: 3


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Manifestations of untreated syphilis

Secondary syphilis: maculopapular skin lesions of the neck

Secondary syphilis: maculopapular and scaly lesions of the plantar area

Secondary syphilis:

moth-eaten alopecia

Macerated plaques (condylomata lata) of the toe webs

(浸軟)

Ref: 10


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Manifestations of untreated syphilis

Ulceronodular skin lesion of lue maligna

Secondary oral syphilis: mucous patches covered by grayish, white pseudo-membranes of the lower vestibular mucosa

Ref: 10

Secondary oral syphilis:

with lesions on the soft palate

Oral chancre in a promiscuous woman who had unprotected oral sex


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Detection of spirochytes

Silver stain

Immunocyochemical stain

Immunocyochemical stain

Immunocyochemical stain

Ref: 2


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Summaries

  • Knowing:

  • Virulence factor of bacteria

  • Koch postulates

  • Two main oral bacterial lesions

  • - Caries/periapical lesions

  • - Periodontitis

  • 4. Tuberculosis

  • 5. Syphilis


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