CocciCocci
Gram positive and negative cocciGram positive and negative cocci
Classification
G+
: Staphylococcus
Streptococcus
Pneumococcus
G-
:
Meningococcus
Gonococcus
§1 Staphylococcus
I. Morphology
II. Culture
III. Antigenic structure
IV. Resistance
Biological characters
MorphologyMorphology
※※ Gram positiveGram positive
※※ Grape like-clustersGrape like-clusters
Culture characteristics
S.SaprophyticusS.EpidermidisS.Aureas
※※ Facultative anaerobesFacultative anaerobes
※ Low nutritional required and grow rapidly
※ Colonies : circular, 2-3 mm in diameter with a
smooth, shiny opaque surface;
※ Pigments : golden 、 grayish white or lemon
※ Hemolysis on sheep blood agar plate
Important properties
※ Mannitol fermentation
※ Produce catalase
H2O2 →O2 + H2O ( hydrogen
peroxide )
※ Coagulase : S aureus, can clot citrated plasma
(-) (+)
Antigenic StructureAntigenic Structure
★★ Staphylococcus protein AStaphylococcus protein A ,, SPASPA
Binds to the Fc portion of IgG at the complementBinds to the Fc portion of IgG at the complement
binding sitebinding site
SignificanceSignificance
※※ Preventing the activation of complementPreventing the activation of complement
※※ anti-phagocytosisanti-phagocytosis
※※ coagglutinationcoagglutination
PHAGOCYTEPHAGOCYTE
Fc receptorFc receptor
Protein AProtein A
immunoglobulinimmunoglobulin
Bacterium, etc.
immunoglobulinimmunoglobulin
Bacterium, etc.
Staphylococcus protein AStaphylococcus protein A ,, SPASPA
Binds to the Fc portion of IgG at the complementBinds to the Fc portion of IgG at the complement
binding sitebinding site
SignificanceSignificance
※※ Preventing the activation of complementPreventing the activation of complement
※※ anti-phagocytosisanti-phagocytosis
※※ coagglutinationcoagglutination
Antigen+antibody+SPA→compound with High molecular weight
Resistance
Thermotolerance : 60 1h or 80 30min℃ ℃
Salt tolerance : can grow in 10-15% sodium chloride solution.
resistant to common disinfectants
Antibiotics resistance : multidrug resistant
MRSA (methicillin resistant staphylococcus aureus)
▲ Catalase
▲ Coagulase and clumping factor
▲ Hyaluronidase and Lipaseipase
▲ Hemolysin or sphingomyelinase Csphingomyelinase C
▲ Leukocidin
▲ Exfoliative Toxin (superantigen)
▲ Toxic Shock Syndrome Toxin
(superantigen)
▲ Enterotoxins (superantigen)
PathogenesisPathogenesis
PathogenesisPathogenesis
H2O2 →O2 + H2O
▲ Destruction of the bactericidal activity of hydrogen peroxide
▲ Differentiate the staphylococci from the streptococci
※ catalase
▲ Coagulase: an enzyme-like protein that clots citrated
Coagulase
prothrombin
+
Enzymatically active(thrombin-like)→fibrin
polymerization
Free coagulase
※ Coagulase and clumping factor Coagulase=
↓
☆ Coagulase can deposit fibrin on the surface of the
agent, altering their ingestion by phagocytic cells and
their destruction within such cells, so coagulase
production is considered synonymous with invasive
pathogenic potential.
▲ Clumping factor: a surface compound of S.aureus
and adherence of the agents to fibrinogen and fibrin
S.aureus(clumping factor)
+
plasma
Clumps forms
BoundBound coagulase
※ Coagulase and clumping factor Coagulase=
※ Hemolysin
Hemolysin is a exotoxin that cause lysis of red blood cells, white blood
cells, platelet and macrophages in vitro and in vivo.
Alpha-hemolysin,
a transmembrane heptamer
αhemolysin: a broad spectrum of eukaryotic cells
βhemolysin: a broad spectrum of eukaryotic cells
γhemolysin: white blood cells
δhemolysin: play a role in S.aureus diarrheal diseases.
Can increase cation permeability
※ Leukocidin
Leukocidin: a pore forming toxin, so it can form
pores in white blood cell membrane especially the
neutrophil and increase cation permeability.
This toxin may be an inportant virulence factor
in community associated methicillin resistant S.
aureus infection.
※ Exfoliative toxins Epidermolytic toxins=
Dsg-1:desmoglein 1; Dsg-3:desmoglein 3
Responsible for staphylococcal scalded skin syndrome (SSSS), a
disease predominantly affecting infants and characterized by the loss of
superficial skin layers, dehydration, and secondary infections
Superantigen
※ Toxin shock syndrome toxin-1
Toxic shock syndrome toxin (TSST) is a superantigen
with a size of 22 KDa produced by 5 to 25% of Staphylococcus
aureus isolates. It causes toxic shock syndrome (TSS) by
stimulating the release of large amounts of interleukin-1,
interleukin-2 and tumor necrosis factor. In general, the toxin
is not produced by bacteria growing in the blood; rather, it is
produced at the local site of an infection, and then enters the
blood stream.
Superantigen
TSST-1 binds to MHC- molecules, yielding T cellⅡ
stimulation, which promotes the protean manifestations of the
toxic shock syndrome.
※ Enterotoxins Superantigen
Staphylococcal enterotoxin is an enterotoxin
produced by Staphylococcus aureus. It is a common
cause of food poisoning, with severe diarrhea, nausea
and intestinal cramping often starting within a few
hours of ingestion. Being quite stable, the toxin may
remain active even after the contaminating bacteria are
killed. It can withstand boiling at 100 for a about 30℃
minutes. Gastroenteritis occurs because the toxin is a
superantigen, causing the immune system to release a
large amount of cytokines that lead to significant
inflammation.
※ Enterotoxins
Superantigen
The emetic effect of enterotoxin is
probably the result of central nervous system
stimulation (vomiting center) after the toxin
acts on neural receptors in the gut.
Formation conditions of staphylococcal enterotoxin
Storage Temperature: below 37 , the higher of the℃
temperature, the shorter of the time of toxin
production;
Storage location: easy form enterotoxin in
environment of poorly ventilated, low partial
pressure of oxygen.
Types of food: rich in carbohydrate and protein
Physicochemical properties : Low molecular weight
proteins, heat-resistant, protease-resistant.
Formation conditions of staphylococcal
enterotoxin
Mechanism of action :
▲ Acting on the gastrointestinal mucosa, result in
inflammatory changes such as congestion, edema,
erosion and metabolic disturbance of electrolyte
and eventually diarrhea.
▲ stimulate the visceral ['v sərəl] branch of the vagusɪ
nerve, and result in reflex vomiting
Pathogenesis of staphylococcal infectionsPathogenesis of staphylococcal infections
Skin (local) infectionSkin (local) infection
※※ Furuncle:Furuncle:Protein A, Leukocidin, HemolysinProtein A, Leukocidin, Hemolysin
※※ Stye:Stye: lipaselipase
※※ Impetigo:Impetigo:contagiouscontagious
※※ Epidermal necrolysisEpidermal necrolysis
※※ Exfoliative Dermatitis:Exfoliative Dermatitis: Exfoliative toxinExfoliative toxin
※※ MastitisMastitis
※※ Abscess (deep tissue); granulation:Abscess (deep tissue); granulation: coagulase, hyaluronidasecoagulase, hyaluronidase
(burn, wound)(burn, wound)
Systemic infectionSystemic infection
Bactermia (from abscess, wound, burn)Bactermia (from abscess, wound, burn) ,, Osteomyelitis (tibiaOsteomyelitis (tibia
['t biə])ɪ['t biə])ɪ ,, PneumoniaPneumonia
Clinical findings
Invasive infections
Food poisoningFood poisoning
Toxic shock syndromeToxic shock syndrome
scalded skin syndrome Babiesscalded skin syndrome Babies
ExfoliatinExfoliatin
feverfever
scarlatiniformscarlatiniform rashrash
desquamationdesquamation
vomitingvomiting
diarrheadiarrhea
myalgiasmyalgias
not a human infectionnot a human infection
food contaminated from humansfood contaminated from humans
- growth- growth
- enterotoxin- enterotoxin
onset and recovery both occur within few hoursonset and recovery both occur within few hours
VomitingVomiting// nauseanausea// diarrheadiarrhea// abdominalabdominal //painpain
Toxic diseases
※※ Cause vomiting and watery, nonbloody diarrheaCause vomiting and watery, nonbloody diarrhea
※※ SuperantigenSuperantigen
※※ Heat-resistant (100 30min)℃Heat-resistant (100 30min)℃
EnterotoxinEnterotoxin
Food poisoningFood poisoning
Toxic shock syndromeToxic shock syndrome
scalded skin syndrome Babiesscalded skin syndrome Babies
ExfoliatinExfoliatin
feverfever
scarlatiniformscarlatiniform rashrash
desquamationdesquamation
vomitingvomiting
diarrheadiarrhea
myalgiasmyalgias
not a human infectionnot a human infection
food contaminated from humansfood contaminated from humans
- growth- growth
- enterotoxin- enterotoxin
onset and recovery both occur within few hoursonset and recovery both occur within few hours
VomitingVomiting// nauseanausea// diarrheadiarrhea// abdominalabdominal //painpain
No feverNo fever
Toxic shock syndrome toxin 1Toxic shock syndrome toxin 1
※※ Cause toxic shockCause toxic shock
◆◆ Tampon['tæmp n]ɑːTampon['tæmp n]ɑː 止血棉塞止血棉塞–– usingusing
menstruating womenmenstruating women
◆◆ Individuals with wound infectionIndividuals with wound infection
◆◆ Patients with nasal packing used to stop bleedingPatients with nasal packing used to stop bleeding
from the nosefrom the nose
※※ SuperantigenSuperantigen
Food poisoningFood poisoning
Toxic shock syndromeToxic shock syndrome
scalded skin syndromescalded skin syndrome BabiesBabies
ExfoliatinExfoliatin
feverfever
scarlatiniformscarlatiniform rashrash
desquamationdesquamation
vomitingvomiting
diarrheadiarrhea
myalgiasmyalgias
not a human infectionnot a human infection
food contaminated from humansfood contaminated from humans
- growth- growth
- enterotoxin- enterotoxin
onset and recovery both occur within few hoursonset and recovery both occur within few hours
VomitingVomiting// nauseanausea// diarrheadiarrhea// abdominalabdominal //painpain
ExfoliatinExfoliatin
※※ Cause scalded skin syndrome in young childrenCause scalded skin syndrome in young children
※※ Acts as protease that cleavesActs as protease that cleaves
desmosomedesmosome ,, leadingleading
to the separation of the epidermis at the granularto the separation of the epidermis at the granular
cell layercell layer
§2 Streptococcus§2 Streptococcus
MorphologyMorphology
Gram-positive, spherical or ovoid, arrange inGram-positive, spherical or ovoid, arrange in
chainschains, no spore and flagella; in very young cultures,
the capsules are noticeable.
※※ Facultative anaerobeFacultative anaerobe
※※ Much higher nutritional requirement, growMuch higher nutritional requirement, grow
well on enriched media.well on enriched media.
※※ colonies: 1-2 mm in diametercolonies: 1-2 mm in diameter with a smooth,
shiny opaque surface, different hemolytic zone, different hemolytic zone
around the colonies.around the colonies.
Culture and typical biochemical reaction
CatalaseCatalase negativenegative
(staphylococci are catalase positive)(staphylococci are catalase positive)
 α-hemolytic streptococcus
Incomplete hemolysis, green zone around colonies
* Opportunistic pathogens
ClasssificationClasssification
(1) According to the Hemolytic activity:(1) According to the Hemolytic activity:
 β-hemolytic/pyogenic streptococcus
Complete hemolysis, clear zone around colonies
*major human pathogens
 γ-streptococcus
No hemolyzation, no pathogenicity.
( 2 ) According to the antigenic structure
Group-specific cell wall antigen: on the basis of this antigen,
streptococci can be classified in to A-H and K-U groups.
Chemical property: carbohydrate, the serologic specificity of
this antigen is determined by an amino sugar.
M protein:
▲ The foundation of subtype within groups.
▲ Major virulence factor of group A S.pyogenes.
Group A : more than 100 serotypes
Group B: 4 serotypes
Group C : 13 serotypes
Pathogenesis
Virulence factors
exotoxin
Invasive enzyme
Hyaluronidase
Streptokinase
DNAases
Streptolysin (O, S)
Pyrogenic exotoxin
LTA
M protein
Attachment
(1) Attachment: Surface structure
* LTA (lipoteichoic acid) : Adhere to sensitive cell
* M-protein :
◆ Anti-phagocytotic
◆ Common antigen -- heart muscle cell, glomerular basement membrane
cells, etc.
◆ M Ag-Ab complex: type Ⅲ hypersensitivity
Such as: poststreptococcal acute glomerulonephritis, rheumatic fever,
rheumatic heart disease.
There is common antigenicity between M protein and Myocardial
cells, glomerular [ 'l mrj lə] basement membrane cells, so theɡ ɒ ʊ
antibody just against M protein can also combine with these cells,
activate complements and result type Ⅱ hypersensitivity
▲ Hyaluronidase :
Destroy the polysaccharide (hyaluronic acid) that holds animal cells
together, making it easier for the pathogen to spread through the tissues of
the host organism.
(2) Invasive enzyme
▲ Streptokinase (SK) = fibrinolysin [ fa brə'n l s n]ˌ ɪ ɒ ɪ ɪ
▲ Streptodornase (SD):
an enzyme produced by hemolytic streptococci that catalyzes the
depolymerization of deoxyribonucleic [di ksi ra bə nu 'kli k] acidːˌɒ ː ɪ ʊ ː ːɪ
(DNA).
a protein secreted by several species of streptococci which can bind
and activate human plasminogen [plæz'm nəd ən]ɪ ʒ 血浆酶原
plasminogen Streptokinase plasmin digest
Fibrin and other proteins
Spreading factorSpreading factor
(3) exotoxin:
(i) Pyrogenic exotoxins (erythrogenic toxin)
▲ Coded by lysogenic phage.
▲ superantigen
▲ Low molecular weight proteins, heat-resistant.
Biological activity
▲ Pyrogenic
▲ increased the permeability of blood-brain barrier
▲ cytotoxicity: have cytotoxic activity to spleen cells and macrophages
cultured in vitro
▲ Increase the sensitivity of Animal to endotoxin
(ii)hemolysins
Streptolysin S – alters membrane permeability; lyses RBCs, leukocytes, and
other cells containing sterols in membrane
Streptolysin O – forms membrane penetrating channels (porin) leading to
membrane defects and cell lysis
Streptococcus can produce two hemolysins:
△ Cytotoxic to RBCs and many tissue cells, particularly cardiotoxic
△ Antigenic - anti-streptolysin O (ASO) antibody used to diagnose recent
infection
property
Streptolysin S has no antigenicity
Pathogenesis of S. pyogenes infections.
[ er 's p l s]ˌ ə ɪ ə ə
Invasive disease
Clinical findings
pharyngitis
Pyoderma
Dermatocellulitis
necrotizing fascitis
erysipelas
puerperal fever
……
▲ systemic infection
septicemia
▲ local purulent infections:
Scarlet fever
Toxin-Mediated diseases
Caused by Hemolytic streptococcus B group A,
Acute respiratory infectious disease. Clinical features: fever, pharyngitis,
genernal diffused fresh red eruption and obvious desquamation
Complication: heart, kidney and joints diseases
Scarlet fever is characterized by:
▲ Sore throat
▲ Fever
▲ Bright red tongue with a "strawberry" appearance
▲ Forchheimer spots (fleeting small, red spots on the soft palate) may occur
▲ spares the face (although some circumoral [ s kəm'o rəl] pallorˌ ɜː ʊ 口周苍
白 is characteristic)
▲ Characteristic rash:
△ fine, red and rough-textured
△ blanches upon pressure
△ Pastia lines (where the rash runs together in the armpits and groin)
appear and can persist after the rash is gone.
Strawberry tongue
Pastia lines 帕斯蒂亚
(1) acute glomerulonephritis ( group A)
[glə merj lə nef'ra t s]ʊ ʊ ʊ ɪ ɪ
(2) Rheumatic fever
(3) rheumatic heart disease
poststerptococcal diseases (hypersensitive disease)
Prevention & treatmentPrevention & treatment
※※ Treat the pharyngitis and tonsillitis in time,Treat the pharyngitis and tonsillitis in time,
avoid the post streptococcal diseases.avoid the post streptococcal diseases.
※※ Antibiotics and chemical agents: penicillin G forAntibiotics and chemical agents: penicillin G for
the first choicethe first choice
Gram stain of pure culture Urethral exudate
§3 Neisseria§3 Neisseria
※※ Gram negative cocci, usuallyGram negative cocci, usually
arranged in pairs and the flat orarranged in pairs and the flat or
concave sides are adjacent.concave sides are adjacent.
※※ Some are normal inhabitants inSome are normal inhabitants in
respiratory tract. Others arerespiratory tract. Others are
human pathogenshuman pathogens
※※ Gram negative cocci, kidney-shaped, in pairs haveGram negative cocci, kidney-shaped, in pairs have
capsules and pilicapsules and pili
※※ Need enriched mediaNeed enriched media :: grow best on mediagrow best on media
containing complex organic substances such ascontaining complex organic substances such as
heated blood, hemin and in an atmosphereheated blood, hemin and in an atmosphere
containing 5% COcontaining 5% CO2.2.
Common biological characteristicsCommon biological characteristics
Gonococci and meningococci are the main pathogens in
neisseriae, and they are closely related, with 70% DNA
homology.
The main differences between these two agents
△ Meningococci have polysaccharide capsules, but gonococci do
not.
△ Meningococci rarely have plasmids whereas most gonococci
do.
△ Meningococci cause meningitis, whereas gonococci cause
genital infections.
※※ Resistance: relativelyResistance: relatively fragilefragile organism, susceptibleorganism, susceptible
toto temperature changes, drying, uv light,temperature changes, drying, uv light, andand
other environmental conditions.other environmental conditions.
※ They are rapidly killed by drying, sunlight, moist heat and
many disinfectants.
※ produce autolytic enzymes that result in rapid swelling and
lysis in vitro at 25℃
gonococci and their coloniesgonococci and their colonies
Neisseria gonococciNeisseria gonococci
GonoGonococcal colonies on chocolate agar plate: grayish
white, round, convex, smooth, opaque.
1. Pili
2. Por proteins
3. Opa
4. Rmp
5. Lipooligosaccharide (LOS):
Antigenic structure
N. gonorrhoeae is capable of changing its surface antigens
(particularly pilin) rapidly to avoid host defenses.
N. gonorrhoeae (Gonococcus)
Pathogenicity and immunityPathogenicity and immunity
1. Pathogenicity:
(1) Human is the only natural host.
(2) Virulence factor:
※ Pili — key factor in anchorage of organisms to mucosal epithelium.
Nonpiliated gonococci are avirulent
※ Capsule-antiphagocytosis
※ Endotoxin (lipooligosaccharide: LOS)-main pathogenic substance
※ IgA1 protease: can split and inactivate secretory IgA1, a major
mucosal immunoglobulin of human.
Has no long O-antigen side chains
▲ Porin proteins (Por) : form porins and mediate
resistance to neutrophil and serum killing, allow
intracellular survival of the bacteria[ also called
protein I].
▲ Opacity proteins (Opa) : associated with opaque
colonies; an outer membrane protein functioning
in attachment to host cells[ also called protein Ⅱ].
▲ Reduction-modifiable proteins (Rmp) : stimulates
antibodies that block serum bactericidal
activity [also called protein Ⅲ].
※※ Outer membrane proteins (OMPs):Outer membrane proteins (OMPs):
Pathogenesis
Attachment to mucosal cells (requires pili) →Invade into the
cells and multiply (Opa mediates tighter association with and
invasion of host cells; Por inhibits phagolysosome fusion)
→Pass through the cells into the subepithelial space
→Establish infection (LOS stimulates inflammatory
response; Rmp blocks bactericidal activity)
Establishment of infection
Pathogenesis and Pathology
Gonococci attack mucous
membrane of the
genitourinary tract, eye,
rectum, and throat,
producing acute suppuration
that lead to tissue invasion;
this is followed by chronic
inflammation and fibrosis.
△ Gonorrhea occurs only in humans.
△ Gonorrhea is transmitted by sexual contact
△ 95% infected men and 50% infected women have
acute symptoms. So, asymptomatic carriage is more
common in women than in men.
△ Rectal and pharyngeal infections are more
commonly asymptomatic than genital infections.
Epidemiology
※ Gonorrhea (sexually transmitted disease STD)
in male: acute urethritis
in female: pelvic inflammatory
※ Ophthalmia [ f'θælm ə]ɒ ɪ
neonatorum [ni næ't r m]ːɒ ɔː ʌ →blindness
Symptoms
1. Male: urethritis with yellow, creamy pus and
painful urination. The process may extend to
the epididymis [ epə'd dəm s]ˌ ɪ ɪ .
As suppuration subsides in untreated
infection, fibrosis occurs, sometimes leading to
urethral strictures (sterility).
2. Female: infection starts from the endocervix, and
results in vagina discharge, dysuria, and abdominal
pain. Uterine ['ju təra n]ː ɪ tubes may be involved,
causing salpingitis , fibrosis, and obliteration of the
tubes (20% may become infertile). When
gonococcal cervicitis is either asymptomatic or
unrecognized, the patient may progress to pelvic
inflammatory disease (PID).
3. Gonococcal ophthalmia neonatorum : bilateral
conjunctivitis often follows vaginal delivery from an
infected mother. The symptoms are eye pain,
redness, and a purulent discharge. The organism
can cause permanent injury to the eye in a very
short time; prompt recognition and treatment are
essential to avoid blindness. prevention:
tetracycline, erythromycin or silver nitrate.
4. Gonococcal bacteremia (1-3% of infected women
and much lower percent of infected men) can lead
to fever, pustular rash over the extremities,
tenosynovitis [ teno s nə'va t s]ˌ ʊˌ ɪ ɪ ɪ 腱鞘炎 and
suppurative arthritis.
※ Specimen:
purulent secretion of genitourinary tract
*note: “fragile” →bed-side inoculation
※ Isolation and identification:
direct smear, isolation and culture,
biochemical tests, antigen detection, etc.
Laboratory diagnosisLaboratory diagnosis
Prevention and treatment
Penicillin, Spectinomycin 奇霉素 ,
Ceftriaxone[seftra' æksn]ɪ 头孢三嗪 , and so on
※ Treatment
△ neonatorum ophthalmia - silver nitrate
△ Strengthen health education and prohibit dirty sex
△ No vaccine
※ Prevention
Infection rate can be reduced by:
1. avoiding multiple sexual partners;
2. early diagnosis and treatment;
3. finding cases and contacts through education
and screening of population at high risk.
4. combined with doxycycline 强力霉素 or azithromycin
[e z θrə'ma s n]ɪ ɪ ɪ ɪ 阿奇霉素 for dual infections with
Chlamydia
※ Prevention
meningococci and their coloniesmeningococci and their colonies
Neisseria meningococciNeisseria meningococci
Meningococcal colonies on chocolate agar plate:
Colorless, round, convex, smooth, transparent and just like
Dew drops.
1. Capsular polysaccharide: more than 13 serogroups
have been identified (serogroups A, B, C, X, Y, and
W135 are most commonly isolated).
2. Pili (allow bacterial colonization of nasopharynx).
3. Outer membrane proteins: these are analogues to the
Por and Opa proteins of gonococci.
4. Lipooligosaccharide (LOS): responsible for diffuse
vascular damage in meningococcal infections.
Antigenic structure
1. Pathogenicity:
(1) Meningococci are pathogenic only for humans under natural conditions.
Child: susceptible
(2) virulence factor:
*Pili– attach to nasopharyngeal mucosa
*capsule – antiphagocytosis
*endotoxin – main pathogenic substance →capillary, small blood vessel
*IgA1 protease: can split and inactivate IgA1, a major mucosal
immunoglobulin of human.
Pathogenicity and immunity
Symptoms: begins suddenly, with intense headache,
vomiting, and stiff neck, and progress to coma
within a few hours.
Mortality: nearly 100% if untreated; <10% in patients treated
promptly with appropriate antibiotics.
Neurologic sequelae: uncommon; hearing deficit, Intellectual
impairment
Pathogenesis
Like gonococci, meningococci are able to invade the
epithelial cells. The capsule of meningococci protects the
bacteria from phagocytic destruction.
2. Pathogenesis:2. Pathogenesis:
Epidemic cerebrospinal meningitisEpidemic cerebrospinal meningitis
Clinical typing: common, outbreak, septicemic typeClinical typing: common, outbreak, septicemic type
(1) Organisms(1) Organisms →→ attach to epithelial cells of nasoparynxnasoparynx with the aid of
pili ( nasopharyngeal infection : asymptomatic , most are carriers,( nasopharyngeal infection : asymptomatic , most are carriers,
only 2~3% go to next stage )only 2~3% go to next stage )
(2) Blood stream <fever, skin ecchymosis[ ekə'mo s s] >ˌ ʊ ɪ(2) Blood stream <fever, skin ecchymosis[ ekə'mo s s] >ˌ ʊ ɪ →→cross the braincross the brain
barrier <severe headache ,vomitting, stiff neck > (meningococcemia.barrier <severe headache ,vomitting, stiff neck > (meningococcemia.
bacteremia or septicemia. blood contain cocci )bacteremia or septicemia. blood contain cocci )
(3) Meninges [mə'n nd i z] (meningitis. meninges pyogenic inflammation.ɪ ʒ ː(3) Meninges [mə'n nd i z] (meningitis. meninges pyogenic inflammation.ɪ ʒ ː
spinal fluid contain cocci )spinal fluid contain cocci )
Clinical cause: 3 stagesClinical cause: 3 stages
※※ Immunity:Immunity:
Group-specific antibody(subclinicalGroup-specific antibody(subclinical and
symptomaticsymptomatic infection).infection).
※※ Prevention and treatmentPrevention and treatment
1. Polysaccharide vaccine (group A, C)1. Polysaccharide vaccine (group A, C)
2. Penicillin; cefotaxime [sefə 'tæksa m]ʊ ɪ2. Penicillin; cefotaxime [sefə 'tæksa m]ʊ ɪ
头孢噻肟头孢噻肟 ; chloramphenicol; chloramphenicol
Exercises:Exercises:
Staphylococcus protein A , SPA Coagulase
Toxin shock syndrome toxin-1 Streptolysin O
Lipooligosaccharide (LOS) Streptokinase (SK)
Streptodornase (SD)
1.The pathogenic substances and pathogenicity of cocci?
2.The main pathogenic substances and pathogenicity of
strptococci?
THANKS

9 cocci

  • 1.
  • 2.
    Gram positive andnegative cocciGram positive and negative cocci
  • 3.
  • 4.
    §1 Staphylococcus I. Morphology II.Culture III. Antigenic structure IV. Resistance Biological characters
  • 5.
    MorphologyMorphology ※※ Gram positiveGrampositive ※※ Grape like-clustersGrape like-clusters
  • 6.
    Culture characteristics S.SaprophyticusS.EpidermidisS.Aureas ※※ FacultativeanaerobesFacultative anaerobes ※ Low nutritional required and grow rapidly ※ Colonies : circular, 2-3 mm in diameter with a smooth, shiny opaque surface; ※ Pigments : golden 、 grayish white or lemon ※ Hemolysis on sheep blood agar plate
  • 7.
    Important properties ※ Mannitolfermentation ※ Produce catalase H2O2 →O2 + H2O ( hydrogen peroxide ) ※ Coagulase : S aureus, can clot citrated plasma (-) (+)
  • 8.
  • 9.
    ★★ Staphylococcus proteinAStaphylococcus protein A ,, SPASPA Binds to the Fc portion of IgG at the complementBinds to the Fc portion of IgG at the complement binding sitebinding site SignificanceSignificance ※※ Preventing the activation of complementPreventing the activation of complement ※※ anti-phagocytosisanti-phagocytosis ※※ coagglutinationcoagglutination
  • 10.
    PHAGOCYTEPHAGOCYTE Fc receptorFc receptor ProteinAProtein A immunoglobulinimmunoglobulin Bacterium, etc. immunoglobulinimmunoglobulin Bacterium, etc.
  • 11.
    Staphylococcus protein AStaphylococcusprotein A ,, SPASPA Binds to the Fc portion of IgG at the complementBinds to the Fc portion of IgG at the complement binding sitebinding site SignificanceSignificance ※※ Preventing the activation of complementPreventing the activation of complement ※※ anti-phagocytosisanti-phagocytosis ※※ coagglutinationcoagglutination
  • 13.
  • 14.
    Resistance Thermotolerance : 601h or 80 30min℃ ℃ Salt tolerance : can grow in 10-15% sodium chloride solution. resistant to common disinfectants Antibiotics resistance : multidrug resistant MRSA (methicillin resistant staphylococcus aureus)
  • 15.
    ▲ Catalase ▲ Coagulaseand clumping factor ▲ Hyaluronidase and Lipaseipase ▲ Hemolysin or sphingomyelinase Csphingomyelinase C ▲ Leukocidin ▲ Exfoliative Toxin (superantigen) ▲ Toxic Shock Syndrome Toxin (superantigen) ▲ Enterotoxins (superantigen) PathogenesisPathogenesis
  • 16.
  • 17.
    H2O2 →O2 +H2O ▲ Destruction of the bactericidal activity of hydrogen peroxide ▲ Differentiate the staphylococci from the streptococci ※ catalase
  • 18.
    ▲ Coagulase: anenzyme-like protein that clots citrated Coagulase prothrombin + Enzymatically active(thrombin-like)→fibrin polymerization Free coagulase ※ Coagulase and clumping factor Coagulase= ↓
  • 19.
    ☆ Coagulase candeposit fibrin on the surface of the agent, altering their ingestion by phagocytic cells and their destruction within such cells, so coagulase production is considered synonymous with invasive pathogenic potential. ▲ Clumping factor: a surface compound of S.aureus and adherence of the agents to fibrinogen and fibrin S.aureus(clumping factor) + plasma Clumps forms BoundBound coagulase ※ Coagulase and clumping factor Coagulase=
  • 20.
    ※ Hemolysin Hemolysin isa exotoxin that cause lysis of red blood cells, white blood cells, platelet and macrophages in vitro and in vivo. Alpha-hemolysin, a transmembrane heptamer αhemolysin: a broad spectrum of eukaryotic cells βhemolysin: a broad spectrum of eukaryotic cells γhemolysin: white blood cells δhemolysin: play a role in S.aureus diarrheal diseases. Can increase cation permeability
  • 21.
    ※ Leukocidin Leukocidin: apore forming toxin, so it can form pores in white blood cell membrane especially the neutrophil and increase cation permeability. This toxin may be an inportant virulence factor in community associated methicillin resistant S. aureus infection.
  • 22.
    ※ Exfoliative toxinsEpidermolytic toxins= Dsg-1:desmoglein 1; Dsg-3:desmoglein 3 Responsible for staphylococcal scalded skin syndrome (SSSS), a disease predominantly affecting infants and characterized by the loss of superficial skin layers, dehydration, and secondary infections Superantigen
  • 23.
    ※ Toxin shocksyndrome toxin-1 Toxic shock syndrome toxin (TSST) is a superantigen with a size of 22 KDa produced by 5 to 25% of Staphylococcus aureus isolates. It causes toxic shock syndrome (TSS) by stimulating the release of large amounts of interleukin-1, interleukin-2 and tumor necrosis factor. In general, the toxin is not produced by bacteria growing in the blood; rather, it is produced at the local site of an infection, and then enters the blood stream. Superantigen TSST-1 binds to MHC- molecules, yielding T cellⅡ stimulation, which promotes the protean manifestations of the toxic shock syndrome.
  • 24.
    ※ Enterotoxins Superantigen Staphylococcalenterotoxin is an enterotoxin produced by Staphylococcus aureus. It is a common cause of food poisoning, with severe diarrhea, nausea and intestinal cramping often starting within a few hours of ingestion. Being quite stable, the toxin may remain active even after the contaminating bacteria are killed. It can withstand boiling at 100 for a about 30℃ minutes. Gastroenteritis occurs because the toxin is a superantigen, causing the immune system to release a large amount of cytokines that lead to significant inflammation.
  • 25.
    ※ Enterotoxins Superantigen The emeticeffect of enterotoxin is probably the result of central nervous system stimulation (vomiting center) after the toxin acts on neural receptors in the gut.
  • 26.
    Formation conditions ofstaphylococcal enterotoxin Storage Temperature: below 37 , the higher of the℃ temperature, the shorter of the time of toxin production; Storage location: easy form enterotoxin in environment of poorly ventilated, low partial pressure of oxygen. Types of food: rich in carbohydrate and protein Physicochemical properties : Low molecular weight proteins, heat-resistant, protease-resistant.
  • 27.
    Formation conditions ofstaphylococcal enterotoxin Mechanism of action : ▲ Acting on the gastrointestinal mucosa, result in inflammatory changes such as congestion, edema, erosion and metabolic disturbance of electrolyte and eventually diarrhea. ▲ stimulate the visceral ['v sərəl] branch of the vagusɪ nerve, and result in reflex vomiting
  • 28.
    Pathogenesis of staphylococcalinfectionsPathogenesis of staphylococcal infections
  • 29.
    Skin (local) infectionSkin(local) infection ※※ Furuncle:Furuncle:Protein A, Leukocidin, HemolysinProtein A, Leukocidin, Hemolysin ※※ Stye:Stye: lipaselipase ※※ Impetigo:Impetigo:contagiouscontagious ※※ Epidermal necrolysisEpidermal necrolysis ※※ Exfoliative Dermatitis:Exfoliative Dermatitis: Exfoliative toxinExfoliative toxin ※※ MastitisMastitis ※※ Abscess (deep tissue); granulation:Abscess (deep tissue); granulation: coagulase, hyaluronidasecoagulase, hyaluronidase (burn, wound)(burn, wound) Systemic infectionSystemic infection Bactermia (from abscess, wound, burn)Bactermia (from abscess, wound, burn) ,, Osteomyelitis (tibiaOsteomyelitis (tibia ['t biə])ɪ['t biə])ɪ ,, PneumoniaPneumonia Clinical findings Invasive infections
  • 30.
    Food poisoningFood poisoning Toxicshock syndromeToxic shock syndrome scalded skin syndrome Babiesscalded skin syndrome Babies ExfoliatinExfoliatin feverfever scarlatiniformscarlatiniform rashrash desquamationdesquamation vomitingvomiting diarrheadiarrhea myalgiasmyalgias not a human infectionnot a human infection food contaminated from humansfood contaminated from humans - growth- growth - enterotoxin- enterotoxin onset and recovery both occur within few hoursonset and recovery both occur within few hours VomitingVomiting// nauseanausea// diarrheadiarrhea// abdominalabdominal //painpain Toxic diseases
  • 31.
    ※※ Cause vomitingand watery, nonbloody diarrheaCause vomiting and watery, nonbloody diarrhea ※※ SuperantigenSuperantigen ※※ Heat-resistant (100 30min)℃Heat-resistant (100 30min)℃ EnterotoxinEnterotoxin
  • 32.
    Food poisoningFood poisoning Toxicshock syndromeToxic shock syndrome scalded skin syndrome Babiesscalded skin syndrome Babies ExfoliatinExfoliatin feverfever scarlatiniformscarlatiniform rashrash desquamationdesquamation vomitingvomiting diarrheadiarrhea myalgiasmyalgias not a human infectionnot a human infection food contaminated from humansfood contaminated from humans - growth- growth - enterotoxin- enterotoxin onset and recovery both occur within few hoursonset and recovery both occur within few hours VomitingVomiting// nauseanausea// diarrheadiarrhea// abdominalabdominal //painpain No feverNo fever
  • 33.
    Toxic shock syndrometoxin 1Toxic shock syndrome toxin 1 ※※ Cause toxic shockCause toxic shock ◆◆ Tampon['tæmp n]ɑːTampon['tæmp n]ɑː 止血棉塞止血棉塞–– usingusing menstruating womenmenstruating women ◆◆ Individuals with wound infectionIndividuals with wound infection ◆◆ Patients with nasal packing used to stop bleedingPatients with nasal packing used to stop bleeding from the nosefrom the nose ※※ SuperantigenSuperantigen
  • 34.
    Food poisoningFood poisoning Toxicshock syndromeToxic shock syndrome scalded skin syndromescalded skin syndrome BabiesBabies ExfoliatinExfoliatin feverfever scarlatiniformscarlatiniform rashrash desquamationdesquamation vomitingvomiting diarrheadiarrhea myalgiasmyalgias not a human infectionnot a human infection food contaminated from humansfood contaminated from humans - growth- growth - enterotoxin- enterotoxin onset and recovery both occur within few hoursonset and recovery both occur within few hours VomitingVomiting// nauseanausea// diarrheadiarrhea// abdominalabdominal //painpain
  • 35.
    ExfoliatinExfoliatin ※※ Cause scaldedskin syndrome in young childrenCause scalded skin syndrome in young children ※※ Acts as protease that cleavesActs as protease that cleaves desmosomedesmosome ,, leadingleading to the separation of the epidermis at the granularto the separation of the epidermis at the granular cell layercell layer
  • 36.
  • 37.
    MorphologyMorphology Gram-positive, spherical orovoid, arrange inGram-positive, spherical or ovoid, arrange in chainschains, no spore and flagella; in very young cultures, the capsules are noticeable.
  • 38.
    ※※ Facultative anaerobeFacultativeanaerobe ※※ Much higher nutritional requirement, growMuch higher nutritional requirement, grow well on enriched media.well on enriched media. ※※ colonies: 1-2 mm in diametercolonies: 1-2 mm in diameter with a smooth, shiny opaque surface, different hemolytic zone, different hemolytic zone around the colonies.around the colonies. Culture and typical biochemical reaction CatalaseCatalase negativenegative (staphylococci are catalase positive)(staphylococci are catalase positive)
  • 39.
     α-hemolytic streptococcus Incompletehemolysis, green zone around colonies * Opportunistic pathogens ClasssificationClasssification (1) According to the Hemolytic activity:(1) According to the Hemolytic activity:
  • 40.
     β-hemolytic/pyogenic streptococcus Completehemolysis, clear zone around colonies *major human pathogens
  • 41.
  • 42.
    ( 2 )According to the antigenic structure Group-specific cell wall antigen: on the basis of this antigen, streptococci can be classified in to A-H and K-U groups. Chemical property: carbohydrate, the serologic specificity of this antigen is determined by an amino sugar. M protein: ▲ The foundation of subtype within groups. ▲ Major virulence factor of group A S.pyogenes. Group A : more than 100 serotypes Group B: 4 serotypes Group C : 13 serotypes
  • 43.
  • 44.
    (1) Attachment: Surfacestructure * LTA (lipoteichoic acid) : Adhere to sensitive cell * M-protein : ◆ Anti-phagocytotic ◆ Common antigen -- heart muscle cell, glomerular basement membrane cells, etc. ◆ M Ag-Ab complex: type Ⅲ hypersensitivity Such as: poststreptococcal acute glomerulonephritis, rheumatic fever, rheumatic heart disease. There is common antigenicity between M protein and Myocardial cells, glomerular [ 'l mrj lə] basement membrane cells, so theɡ ɒ ʊ antibody just against M protein can also combine with these cells, activate complements and result type Ⅱ hypersensitivity
  • 45.
    ▲ Hyaluronidase : Destroythe polysaccharide (hyaluronic acid) that holds animal cells together, making it easier for the pathogen to spread through the tissues of the host organism. (2) Invasive enzyme ▲ Streptokinase (SK) = fibrinolysin [ fa brə'n l s n]ˌ ɪ ɒ ɪ ɪ ▲ Streptodornase (SD): an enzyme produced by hemolytic streptococci that catalyzes the depolymerization of deoxyribonucleic [di ksi ra bə nu 'kli k] acidːˌɒ ː ɪ ʊ ː ːɪ (DNA). a protein secreted by several species of streptococci which can bind and activate human plasminogen [plæz'm nəd ən]ɪ ʒ 血浆酶原 plasminogen Streptokinase plasmin digest Fibrin and other proteins Spreading factorSpreading factor
  • 46.
    (3) exotoxin: (i) Pyrogenicexotoxins (erythrogenic toxin) ▲ Coded by lysogenic phage. ▲ superantigen ▲ Low molecular weight proteins, heat-resistant. Biological activity ▲ Pyrogenic ▲ increased the permeability of blood-brain barrier ▲ cytotoxicity: have cytotoxic activity to spleen cells and macrophages cultured in vitro ▲ Increase the sensitivity of Animal to endotoxin
  • 47.
    (ii)hemolysins Streptolysin S –alters membrane permeability; lyses RBCs, leukocytes, and other cells containing sterols in membrane Streptolysin O – forms membrane penetrating channels (porin) leading to membrane defects and cell lysis Streptococcus can produce two hemolysins: △ Cytotoxic to RBCs and many tissue cells, particularly cardiotoxic △ Antigenic - anti-streptolysin O (ASO) antibody used to diagnose recent infection property Streptolysin S has no antigenicity
  • 48.
    Pathogenesis of S.pyogenes infections. [ er 's p l s]ˌ ə ɪ ə ə
  • 49.
    Invasive disease Clinical findings pharyngitis Pyoderma Dermatocellulitis necrotizingfascitis erysipelas puerperal fever …… ▲ systemic infection septicemia ▲ local purulent infections:
  • 50.
    Scarlet fever Toxin-Mediated diseases Causedby Hemolytic streptococcus B group A, Acute respiratory infectious disease. Clinical features: fever, pharyngitis, genernal diffused fresh red eruption and obvious desquamation Complication: heart, kidney and joints diseases
  • 51.
    Scarlet fever ischaracterized by: ▲ Sore throat ▲ Fever ▲ Bright red tongue with a "strawberry" appearance ▲ Forchheimer spots (fleeting small, red spots on the soft palate) may occur ▲ spares the face (although some circumoral [ s kəm'o rəl] pallorˌ ɜː ʊ 口周苍 白 is characteristic) ▲ Characteristic rash: △ fine, red and rough-textured △ blanches upon pressure △ Pastia lines (where the rash runs together in the armpits and groin) appear and can persist after the rash is gone. Strawberry tongue Pastia lines 帕斯蒂亚
  • 52.
    (1) acute glomerulonephritis( group A) [glə merj lə nef'ra t s]ʊ ʊ ʊ ɪ ɪ (2) Rheumatic fever (3) rheumatic heart disease poststerptococcal diseases (hypersensitive disease)
  • 53.
    Prevention & treatmentPrevention& treatment ※※ Treat the pharyngitis and tonsillitis in time,Treat the pharyngitis and tonsillitis in time, avoid the post streptococcal diseases.avoid the post streptococcal diseases. ※※ Antibiotics and chemical agents: penicillin G forAntibiotics and chemical agents: penicillin G for the first choicethe first choice
  • 54.
    Gram stain ofpure culture Urethral exudate §3 Neisseria§3 Neisseria
  • 55.
    ※※ Gram negativecocci, usuallyGram negative cocci, usually arranged in pairs and the flat orarranged in pairs and the flat or concave sides are adjacent.concave sides are adjacent. ※※ Some are normal inhabitants inSome are normal inhabitants in respiratory tract. Others arerespiratory tract. Others are human pathogenshuman pathogens
  • 56.
    ※※ Gram negativecocci, kidney-shaped, in pairs haveGram negative cocci, kidney-shaped, in pairs have capsules and pilicapsules and pili ※※ Need enriched mediaNeed enriched media :: grow best on mediagrow best on media containing complex organic substances such ascontaining complex organic substances such as heated blood, hemin and in an atmosphereheated blood, hemin and in an atmosphere containing 5% COcontaining 5% CO2.2. Common biological characteristicsCommon biological characteristics
  • 57.
    Gonococci and meningococciare the main pathogens in neisseriae, and they are closely related, with 70% DNA homology. The main differences between these two agents △ Meningococci have polysaccharide capsules, but gonococci do not. △ Meningococci rarely have plasmids whereas most gonococci do. △ Meningococci cause meningitis, whereas gonococci cause genital infections.
  • 58.
    ※※ Resistance: relativelyResistance:relatively fragilefragile organism, susceptibleorganism, susceptible toto temperature changes, drying, uv light,temperature changes, drying, uv light, andand other environmental conditions.other environmental conditions. ※ They are rapidly killed by drying, sunlight, moist heat and many disinfectants. ※ produce autolytic enzymes that result in rapid swelling and lysis in vitro at 25℃
  • 59.
    gonococci and theircoloniesgonococci and their colonies Neisseria gonococciNeisseria gonococci GonoGonococcal colonies on chocolate agar plate: grayish white, round, convex, smooth, opaque.
  • 60.
    1. Pili 2. Porproteins 3. Opa 4. Rmp 5. Lipooligosaccharide (LOS): Antigenic structure N. gonorrhoeae is capable of changing its surface antigens (particularly pilin) rapidly to avoid host defenses. N. gonorrhoeae (Gonococcus)
  • 61.
    Pathogenicity and immunityPathogenicityand immunity 1. Pathogenicity: (1) Human is the only natural host. (2) Virulence factor: ※ Pili — key factor in anchorage of organisms to mucosal epithelium. Nonpiliated gonococci are avirulent ※ Capsule-antiphagocytosis ※ Endotoxin (lipooligosaccharide: LOS)-main pathogenic substance ※ IgA1 protease: can split and inactivate secretory IgA1, a major mucosal immunoglobulin of human. Has no long O-antigen side chains
  • 62.
    ▲ Porin proteins(Por) : form porins and mediate resistance to neutrophil and serum killing, allow intracellular survival of the bacteria[ also called protein I]. ▲ Opacity proteins (Opa) : associated with opaque colonies; an outer membrane protein functioning in attachment to host cells[ also called protein Ⅱ]. ▲ Reduction-modifiable proteins (Rmp) : stimulates antibodies that block serum bactericidal activity [also called protein Ⅲ]. ※※ Outer membrane proteins (OMPs):Outer membrane proteins (OMPs):
  • 63.
    Pathogenesis Attachment to mucosalcells (requires pili) →Invade into the cells and multiply (Opa mediates tighter association with and invasion of host cells; Por inhibits phagolysosome fusion) →Pass through the cells into the subepithelial space →Establish infection (LOS stimulates inflammatory response; Rmp blocks bactericidal activity) Establishment of infection
  • 64.
    Pathogenesis and Pathology Gonococciattack mucous membrane of the genitourinary tract, eye, rectum, and throat, producing acute suppuration that lead to tissue invasion; this is followed by chronic inflammation and fibrosis.
  • 65.
    △ Gonorrhea occursonly in humans. △ Gonorrhea is transmitted by sexual contact △ 95% infected men and 50% infected women have acute symptoms. So, asymptomatic carriage is more common in women than in men. △ Rectal and pharyngeal infections are more commonly asymptomatic than genital infections. Epidemiology
  • 66.
    ※ Gonorrhea (sexuallytransmitted disease STD) in male: acute urethritis in female: pelvic inflammatory ※ Ophthalmia [ f'θælm ə]ɒ ɪ neonatorum [ni næ't r m]ːɒ ɔː ʌ →blindness
  • 67.
    Symptoms 1. Male: urethritiswith yellow, creamy pus and painful urination. The process may extend to the epididymis [ epə'd dəm s]ˌ ɪ ɪ . As suppuration subsides in untreated infection, fibrosis occurs, sometimes leading to urethral strictures (sterility).
  • 68.
    2. Female: infectionstarts from the endocervix, and results in vagina discharge, dysuria, and abdominal pain. Uterine ['ju təra n]ː ɪ tubes may be involved, causing salpingitis , fibrosis, and obliteration of the tubes (20% may become infertile). When gonococcal cervicitis is either asymptomatic or unrecognized, the patient may progress to pelvic inflammatory disease (PID).
  • 69.
    3. Gonococcal ophthalmianeonatorum : bilateral conjunctivitis often follows vaginal delivery from an infected mother. The symptoms are eye pain, redness, and a purulent discharge. The organism can cause permanent injury to the eye in a very short time; prompt recognition and treatment are essential to avoid blindness. prevention: tetracycline, erythromycin or silver nitrate.
  • 70.
    4. Gonococcal bacteremia(1-3% of infected women and much lower percent of infected men) can lead to fever, pustular rash over the extremities, tenosynovitis [ teno s nə'va t s]ˌ ʊˌ ɪ ɪ ɪ 腱鞘炎 and suppurative arthritis.
  • 71.
    ※ Specimen: purulent secretionof genitourinary tract *note: “fragile” →bed-side inoculation ※ Isolation and identification: direct smear, isolation and culture, biochemical tests, antigen detection, etc. Laboratory diagnosisLaboratory diagnosis
  • 72.
    Prevention and treatment Penicillin,Spectinomycin 奇霉素 , Ceftriaxone[seftra' æksn]ɪ 头孢三嗪 , and so on ※ Treatment △ neonatorum ophthalmia - silver nitrate △ Strengthen health education and prohibit dirty sex △ No vaccine ※ Prevention
  • 73.
    Infection rate canbe reduced by: 1. avoiding multiple sexual partners; 2. early diagnosis and treatment; 3. finding cases and contacts through education and screening of population at high risk. 4. combined with doxycycline 强力霉素 or azithromycin [e z θrə'ma s n]ɪ ɪ ɪ ɪ 阿奇霉素 for dual infections with Chlamydia ※ Prevention
  • 74.
    meningococci and theircoloniesmeningococci and their colonies Neisseria meningococciNeisseria meningococci Meningococcal colonies on chocolate agar plate: Colorless, round, convex, smooth, transparent and just like Dew drops.
  • 75.
    1. Capsular polysaccharide:more than 13 serogroups have been identified (serogroups A, B, C, X, Y, and W135 are most commonly isolated). 2. Pili (allow bacterial colonization of nasopharynx). 3. Outer membrane proteins: these are analogues to the Por and Opa proteins of gonococci. 4. Lipooligosaccharide (LOS): responsible for diffuse vascular damage in meningococcal infections. Antigenic structure
  • 76.
    1. Pathogenicity: (1) Meningococciare pathogenic only for humans under natural conditions. Child: susceptible (2) virulence factor: *Pili– attach to nasopharyngeal mucosa *capsule – antiphagocytosis *endotoxin – main pathogenic substance →capillary, small blood vessel *IgA1 protease: can split and inactivate IgA1, a major mucosal immunoglobulin of human. Pathogenicity and immunity
  • 77.
    Symptoms: begins suddenly,with intense headache, vomiting, and stiff neck, and progress to coma within a few hours. Mortality: nearly 100% if untreated; <10% in patients treated promptly with appropriate antibiotics. Neurologic sequelae: uncommon; hearing deficit, Intellectual impairment
  • 78.
    Pathogenesis Like gonococci, meningococciare able to invade the epithelial cells. The capsule of meningococci protects the bacteria from phagocytic destruction.
  • 79.
    2. Pathogenesis:2. Pathogenesis: Epidemiccerebrospinal meningitisEpidemic cerebrospinal meningitis Clinical typing: common, outbreak, septicemic typeClinical typing: common, outbreak, septicemic type (1) Organisms(1) Organisms →→ attach to epithelial cells of nasoparynxnasoparynx with the aid of pili ( nasopharyngeal infection : asymptomatic , most are carriers,( nasopharyngeal infection : asymptomatic , most are carriers, only 2~3% go to next stage )only 2~3% go to next stage ) (2) Blood stream <fever, skin ecchymosis[ ekə'mo s s] >ˌ ʊ ɪ(2) Blood stream <fever, skin ecchymosis[ ekə'mo s s] >ˌ ʊ ɪ →→cross the braincross the brain barrier <severe headache ,vomitting, stiff neck > (meningococcemia.barrier <severe headache ,vomitting, stiff neck > (meningococcemia. bacteremia or septicemia. blood contain cocci )bacteremia or septicemia. blood contain cocci ) (3) Meninges [mə'n nd i z] (meningitis. meninges pyogenic inflammation.ɪ ʒ ː(3) Meninges [mə'n nd i z] (meningitis. meninges pyogenic inflammation.ɪ ʒ ː spinal fluid contain cocci )spinal fluid contain cocci ) Clinical cause: 3 stagesClinical cause: 3 stages
  • 80.
    ※※ Immunity:Immunity: Group-specific antibody(subclinicalGroup-specificantibody(subclinical and symptomaticsymptomatic infection).infection). ※※ Prevention and treatmentPrevention and treatment 1. Polysaccharide vaccine (group A, C)1. Polysaccharide vaccine (group A, C) 2. Penicillin; cefotaxime [sefə 'tæksa m]ʊ ɪ2. Penicillin; cefotaxime [sefə 'tæksa m]ʊ ɪ 头孢噻肟头孢噻肟 ; chloramphenicol; chloramphenicol
  • 81.
    Exercises:Exercises: Staphylococcus protein A, SPA Coagulase Toxin shock syndrome toxin-1 Streptolysin O Lipooligosaccharide (LOS) Streptokinase (SK) Streptodornase (SD) 1.The pathogenic substances and pathogenicity of cocci? 2.The main pathogenic substances and pathogenicity of strptococci?
  • 82.