Transcript S. pyogenes

A菌
細菌名稱
B菌
診斷？
型態
生長特性
生化反應
血清學反應
疾病？症狀？
如何造成疾病？（致病機制）
細菌本身：侵襲性（毒力因素？ ）；產毒力（毒素？ ）
宿主因素：抵抗力？ 易感因素？
如何感染：途徑？ 媒介？
治療？
抗生素？ （抗藥性？ ） ；抗毒素？ ；症狀治療？
預防？
環境及個人衛生？ 疫苗？
Pyogenic Cocci
Staphylococcus
gram-positive
Streptococcus
gram-positive
Neisseria
gram-negative
Stapylococcus and related organisms
S. aureus: major pathogen for humans, may cause suppuration,
abscess formation, scalded skin syndrome, toxic shock
syndrome and food poisoning.
S. epidermidis: may cause infection from prosthetic devices.
S. saprophyticus: may cause urinary tract infections (UTI) in
young women.
S. capitis: endocarditis, UTI, and opportunistic infections.
S. haemolyticus: endocarditis, UTI, and opportunistic infections.
Micrococcus spp.: opportunistic infections.
Stomatococcus mucilaginosa: endocarditis, opportunistic
infections.
Alloiococcus otitidis: chronic middle ear infection.
Morphology and Identification
Staphylococci
Nonmotile, spores (-).
Grow readily on most
bacteriological media;
facultative anaerobic.
Grow most rapidly at 37 oC,
but form pigment best at room
temperature under aerobic
condition on solid medium.
Produce catalase.
Relatively resistant to drying,
heat and 10% NaCl.
Gram-positive cocci
(a bunch of grapes)
Structure of staphylococcal cell wall
Capsule
Not readily seen in vitro
At least 11 types in S. aureus
Inhibiting phagocytosis by polymorphonucleocytes
Slime layer
Loose-bound, water-soluble film
Facilitates bacterial adherence to tissues and
foreign bodies (important for the pathogenesis of
coagulase-negative staphylococci)
Peptidoglycan
Has endotoxin-like activity
induces production of cytokines
activates complement
induces aggregation of polymorphonucleocytes
Teichoic acids and lipoteichoic acids
Bind covalently to peptidoglycan; species-specific;
bind to fibronectin of host cells; antibodies may be
found in systemic staphylococcal disease,
particularly endocarditis.
Protein A: present on the surface of S. aureus
strains, but not other species. Binds to the Fc portion of
IgG except IgG3, preventing clearance of bacteria.
Coagulase (clumping factor)
Produced by most S. aureus on the cell wall surface; binds
to fibrinogen and aggregates the bacteria.
Coagulase-positive vs. coagulase-negative staphylococci
Other adhesins bind with collagen, elastin and fibronectin
Pathogenesis and Immunity
Staphylococci can produce diseases both through
invasiveness and production of toxins.
Toxins
Cytotoxins
Exfoliative (epidermolytic)
toxins: proteases that split
intercellular bridges in epidermis;
causes the generalized
desquamation of the
staphylococcal scalded skin
syndrome.
Toxic shock syndrome toxin-1
(TSST-1): superantigen,
associates with fever, shock,
desquamative skin rash of toxic
shock syndrome in humans.
Enterotoxins: superantigens
produced by about 50% of S.
aureus.
Heat-stable (100 oC, 30 min.)
and resistant to the gut
enzymes.
An important cause of food
poisoning. Enterotoxins are
produced in carbohydrate and
protein foods.
Causing emesis, a
characteristic of staphylococcal
food poisoning.
Enzymes
Coagulase: bound and free forms. May deposit fibrin on
the surface of staphylococci and alter their ingestion by
phagocytic cells or their destruction within such cells
(associated with invasiveness).
Fibrinolysin (staphylokinase): to dissolve fibrin clot.
Catalase: to remove H2O2.
Hyaluronidase: to facilitate spread of S. aureus in tissue.
Lipase: associated with superficial skin infection.
Nuclease: produced only by S. aureus.
Penicillinase
Epidemiology
Staphylococci can permanently or transiently colonize
various areas of the human body, with the anterior
nasopharynx as the most common colonization site
for S. aureus in older children and adults.
Nasopharyngeal or skin carriers of S. aureus are
responsible for many hospital infections.
S. aureus can be transmitted through direct personal
contact or contact with contaminated fomites.
Areas at highest risk for severe infections: new born
nursery, ICU, operating rooms and cancer
chemotherapy wards.
Clinical Diseases
S. aureus
Cutaneous infections (folliculitis,
e.g., stye and acne; furuncles;
carbuncles; impetigo): usually an
intense, localized painful
inflammatory reaction that
undergoes central suppuration
and heals quickly when the pus is
drained. Carbuncle patients
frequently have systemic signs.
Wound infections: can occur after surgery or trauma,
may involve skin, bone (osteomyelitis from an open
fracture) or meninges (meningitis from skull fracture.)
Clinical Diseases
S. aureus (continued)
Bacteremia
Results from surgery or continued
use of intravascular catheters.
Bacteria may spread to other body
sites and cause endocarditis,
hematogenous osteomyelitis and
septic arthritis, meningitis, and
pulmonary infection (hematogenous
pneumonia, and emphysema.)
Aspiration pneumonia caused by S.
aureus is seen in very young, very old,
cystic fibrosis patients, influenza, etc.
Septic embolism
Clinical Diseases
S. aureus (continued)
Staphylococcal scalded skin syndrome (SSSS disease)
Forms large
bullae or
cutaneous
blisters with
clear fluid that
contains no
bacteria or
leukocytes.
Occurs more
often to young
children.
Clinical Diseases
Food poisoning: caused
by ingestion of preformed
enterotoxin in food (meat
and carbohydrates). Short
incubation (1-8 hr). Violent
nausea, vomiting and
watery diarrhea; no fever;
rapid convalescence.
Staphylococcal
enterocolitis occurs in
patients who have received
broad spectrum antibiotics
(antibiotic-associated
diarrhea).
Toxic shock syndrome: abrupt
onset of high fever, vomiting,
diarrhea, myalgia, scarlatini form
rash, desquamation of palms and
soles, and hypotension with
cardiac and renal failure. This
disease has occurred in children
injected with contaminated
vaccine, and young women who
used tampons. This may also
occur in children or in men with
staphylococcal wound infections
(half cases are caused by
enterotoxin B and, rarely,
enterotoxin C.)
Clinical Diseases
S. epidermidis
and other coagulase-negative staphylococci
Endocarditis: caused by infection of native (rarely) or
prosthetic heart valves.
Catheter and shunt infections: a major medical problem,
because this usually occurs to critically ill patients. Slime
production that causes biofilm formation prevents the
bacteria from antibiotics and inflammatory cells. Persistent
bacteremia is generally observed.
Prosthetic joint infections: localized pain and failure of
the artificial joint. Systemic signs are not prominent.
Reinfection is increased in such patients.
Laboratory Diagnosis
Specimen: pus, sputum, blood, anterior nasal and
perineal swabs, left-over food etc.
Smear: except for abscess material, gram stain of the
smear is usually not informative.
Serology: antibodies against teichoic acid can be
detected in patients with staphylococcal endocarditis.
Culture and identification: catalase test; coagulase test.
Treatment
Tetracycline are used for long term treatment of
acne or furunculosis. Abscess and other closed
suppuration lesions are treated by drainage and
antibiotics.
Bacteremia, endocarditis, pneumonia and other
severe staphylococcal infections: prolonged i.v.
therapy with b-lactamase-resistant penicillins
(e.g. methicillin, oxacillin, etc.)
Vancomycin is the most effective drug against
staphylococci, but its use is restricted in most
hospitals.
Drug resistance of S. aureus
1) Resistance to penicillin G, ampicillin, and similar drugs is
common.
2) Resistance to nafcillin, methicillin and oxacillin
MRSA (ORSA): methicillin (oxacillin)-multiresistant S.
aureus, resulting from acquisition of mecA, which
encodes a novel PBP (PBP2’)
3) MRSA strains are usually also resistant to tetracyclines,
erythromycins and aminoglycosides.
4) Remain susceptible to vancomycin.
Prevention and control
Chief sources of infection: shedding human lesions,
contaminated fomites, human respiratory tract and skin.
Prevention of infection: cleansing of the wound and the
application of an effective disinfectant.
Prevention of wide dissemination from staphylococci
carriers is very important (aerosols and UV of air have
little effect). Rifampin plus a second antibiotics, or some
topical agents, may suppress or cure of nasal carriage.
Areas at highest risk for severe infections: new born
nursery, ICU, operating rooms and cancer
chemotherapy wards.
Impetigo
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Carbuncle
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Streptococci
Morphology and Identification
Gram-positive cocci arranged in chains.
Most group A, B, and C strains produce capsules.
Most strains grow as discoid colonies, 1-2 mm in diameter.
Catalase-negative.
Grow better in media enriched with blood or tissue fluid.
For most species
growth and hemolysis
are aided by
incubation in 10%
CO2.
Classification
Hemolysis
a-hemolysis: incomplete lysis with the formation of
green pigment.
b-hemolysis: complete hemolysis
No hemolysis
Lancefield classification
a serologic classification (A to V)
Biochemical reactions
used for species that can not be classified into the
Lancefield classification, e.g. viridans streptococci
Antigenic Structure
Capsule: the capsule of group A streptococci is
composed of hyaluronic acid; antiphagocytosis
Group-specific cell wall antigen
Lancefield groups A-V
Carbohydrate
Specificity is determined by an amino sugar.
M protein
F protein: a major adhesin of S. pyogenes, binding
with fibronectin.
Pathogenesis
Pathogenesis of group A streptococci
Adherence to the epithelial cells;
>10 adhesion molecules
invasion into the epithelial cells;
mediated by M protein and F protein
important for persistent infections and invasion into
deep tissues
avoiding opsonization and phagocytosis;
M protein, M-like proteins, and C5a peptidase
producing enzymes and toxins
Pathogenesis
Enzymes and toxins
Streptokinases (fibrinolysins)
Can lyse blood clots and may be responsible for the rapid
spread of the organism.
DNases A to D (streptodornases)
Decrease viscosity of DNA in the abscess and facilitate
spread of the organism.
Hyaluronidase (spreading factor):
Destroys connective tissue and aids in spreading infecting
bacteria.
C5a peptidase
Prevents streptococci from C5a-mediated recruitment and
activation of phagocytes, and is important for survival of S.
pyogenes in tissue and blood.
Pathogenesis
Streptococcal pyrogenic exotoxins (Spe)
Produced by both the scarlet fever strains and new
invasive S. pyogenes strains.
Four serologically distinct toxins (SpeA, B, C and F).
Biological activities (except SpeB, which is a cysteine
protease):
Pyrogenicity
Cytotoxicity
Immunosuppression
Superantigen
Spe is associated with toxic shock-like syndrome or
other invasive S. pyogenes diseases.
Pathogenesis
Hemolysins
Streptolysin O: active in the reduced state; causes
hemolysis deep in blood agar plates. ASO (antistreptolysin
O) titer >160-200 units suggests recent infection or
exaggerated immune response to an earlier infection
(except for skin infection).
Streptolysin S: cell-bound, not antigenic. O2-stable.
Causes b-hemolysis on the surface of blood agar plates.
Kills phagocytes by releasing the lysosomal contents after
engulfment.
Epidemiology
S. pyogenes can transiently colonize the oropharynx.
Diseases are caused by recently acquired strains that can
establish an infection of the pharynx or skin.
S. pyogenes causes pharyngitis mainly in children of 5 to
15 years old.
The pathogen is spread mainly by respiratory droplets.
Crowding increases the opportunity for the pathogen to
spread, particularly during the winter months.
Soft tissue infections are preceded by skin colonization and
the organisms are introduced into the superficial or deep
tissue through a break in the skin.
Clinical Diseases
1. Local infection with S. pyogenes
Streptococcal sore throat (pharyngitis), and scarlet fever.
Streptococcal pyoderma (impetigo, local infection of superficial
layers of skin).
2. Invasion by S. pyogenes
Invasion from respiratory tract: otitis media, sinusitis,
pneumonia, meningitis, osteomyelitis, and arthritis.
Invasion from skin: erysipelas, cellulitis, and necrotizing facitis.
Diffuse and rapidly spreading infection that extends along
lymphatic pathways with only minimal local suppuration.
Sepsis (toxic shock-like syndrome, TSLS): the organism is
introduced into the subcutaneous tissue through a break in the
skin -> cellulitis -> necrotizing faciitis -> systemic toxicity,
multiple organ failure, and death (mortality > 40%).
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Clinical Diseases
3. Poststreptococcal diseases (occurs 1-4 weeks after
acute S. pyogenes infection, hypersensitivity responses)
Rheumatic fever: most commonly preceded by infection of
the respiratory tract. Inflammation of heart (pancarditis),
joints, blood vessels, and subcutaneous tissue. Results from
cross reactivity of anti-M protein Ab and the human heart
tissue. This disease can be reactivated by recurrent
streptococcal infections, whereas nephritis does not.
Acute glomerulonephritis: preceded by infection of the skin
(more commonly) or the respiratory tract. Symptoms: edema,
hypertension, hematuria, and proteinuria. Initiated by Ag-Ab
complexes on the glomerular basement membrane.
Clinical Diseases
S. agalactiae (group B, b-hemolytic, contains typespecific capsular polysaccharide)
Neonatal sepsis or meningitis
Early-onset (during the first week of life): infection acquired
in utero or at birth.
Late-onset (older infants): infection acquired from an
exogenous source.
Infection of pregnant women
Urinary tract infections, amnionitis, endometritis, and wound
infections
Infection in men and nonpregnant women
Patients are generally older and have underlying conditions.
Bacteremia, pneumonia, bone and joint infections, skin and
soft tissue infections. Mortality: 15%-32%.
Clinical Diseases
Viridans streptococci (a-hemolytic or nonhemolytic, most
are nongroupable)
These streptococci colonize the oropharynx, GI tract, and GU
tract; rarely on the skin surface.
Diseases:
Subacute endocarditis
Intra-abdominal infections
Dental caries (mostly associated with S. mutans)
Cariogenicity of S. mutans is related to its ability to
synthesize glucan from fermentable carbohydrates as well
as to modify glucan in promoting increased adhesiveness.
S. pneumoniae
Laboratory Diagnosis
Smears: useful for soft tissue infections or pyoderma, but not for
respiratory infections.
Antigen detection tests: commercial kits for rapid detection of
group A streptococcal antigen from throat swabs.
Direct detection by DNA probes.
Culture: Specimens are cultured on blood agar plates in air. 10%
CO2 although speeds hemolysis, the growth of inhibitory bacteria
is also enhanced.
Identification
Serological test
ASO; anti-DNase B and antihyaluronidase;
antistreptokinase; anti-M type-specific antibodies.
Identification of Gram-positive cocci
None
Treatment
All S. pyogenes are sensitive to penicillin G.
Effective doses of penicillin or erythromycin for 10
days can prevent poststreptococcal diseases.
Drainage and aggressive surgical debridement must
be promptly initiated in patients with serious soft
tissue infections.
Antibiotic sensitivity test is helpful for treatment of
bacterial endocarditis.
Prevention and Control
Most streptococci are normal flora of the human body.
Source of S. pyogenes is a person harboring these organisms
(carrier).
Control:
1. Prompt eradication of streptococci from early infections.
2. Prophylactic antibiotic treatment for rheumatic fever patients.
3. Eradication of S. pyogenes from carriers.
4. Dust control, ventilation, air filtration, UV irradiation and
aerosol mists are of doubtful efficacy.
5. Intrapartum penicillin to mother at risk of giving birth to an
infant with invasive group B disease.
S. pneumoniae
Morphology and Physiology
Gram-positive lancet-shaped diplococci for typical organisms.
Form small round colonies on the plate, at first dome-shaped
and later developing a central plateau with an elevated rim.
a-hemolytic (pneumolysin is similar to streptolysin O).
Autolysis is enhanced in bile salt.
Growth is enhanced by 5-10% CO2.
Capsular polysaccharide:
type-specific, 90 types.
Smooth (capsular polysaccharideproducing) vs. rough colonies
S. pneumoniae
Pathogenesis and Immunity
Pneumococci produce disease through their ability to multiply in the
tissues (invasiveness). Major virulence factor: capsule.
40-70% of humans are at sometimes carrier of virulent pneumococci.
Major host defense mechanisms: ciliated cells of respiratory tract and
spleen. The normal respiratory tract has natural resistance to the
pneumococcus. Loss of natural resistance may be due to:
1. Abnormalities of the respiratory tract (e.g. viral RT infections).
2. Alcohol or drug intoxication; abnormal circulatory dynamics.
3. Patients undergone renal transplant.
4. Malnutrition, general debility, sickle cell anemia, hyposplenism
or splenectomy, nephrosis or complement deficiency.
5. Young children and the elderly.
S. pneumoniae
Clinical diseases
Pneumococcal pneumonia develops when the bacteria
multiply rapidly in the alveolar space after aspiration. The
affected area is generally localized in the lower lobes of
the lungs (lobar pneumonia). Children and the elderly can
have a more generalized bronchopneumonia. Resolution
occurs when specific anticapsular antibodies develop.
Sudden onset with fever, chills and sharp chest pain. Bloody,
rusty sputum. Empyema is a rare but significant complication.
Complications caused by spreading of pneumococci to other
organs: sinusitis, meningitis, endocarditis, septic arthritis,
middle ear infection.
S. pneumoniae
Laboratory diagnosis
Examination of sputum
Stained smears: a rapid diagnosis.
Quellung test with multivalent anticapsular antibodies.
Culture
Specimen: sputum, aspirates from sinus or middle ear, CSF.
Cultured on blood agar in CO2.
Identification: bile solubility, optochin sensitivity, etc. for
differentiation from other a-hemolytic streptococci.
Antigen detection: detect capsular polysaccharide in body fluids.
S. pneumoniae
Treatment, Prevention, and Control
Penicillins are the drugs of choice. However, penicillinresistant strains are common nowadays.
Penicillin-resistant pneumococci cause problems in
treatment of meningitis.
Healthy carriers are the source of dissemination. In the
development of illness, predisposing factors are more
important than exposure to the bacteria.
Vaccination of high-risk population (too old, too young,
and people losing natural resistance) with vaccines
containing multiple capsular polysaccharide types.
M protein
Forms hair-like projections (fimbriae)
from the cell membrane.
Major virulence factor of S.
pyogenes.
Resists phagocytosis by PMNs.
Enhances degradation of C3b.
Promotes adherence to epithelial
cells.
Induces type-specific protective
immunity.
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Erysipelas
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Neisseria
N. gonorrhoeae (gonococcus): gonorrhea
N. meningitidis: meningitis
Morphology and Identification
Gram-negative cocci
(kidney-shaped),
usually in pairs.
Human pathogens (i.e.
N. gonorrhoeae and
N. meningitidis) are
typically found
associated with or
inside PMN cells.
Morphology and Identification
Menigococci have polysaccharide capsule;
gonococci have a loose capsule-like structure.
Grow best under aerobic conditions
Produce oxidase (oxidase-positive).
Meningococci and gonococci grow best in medium
containing complex organic substances (e.g. blood,
hemin, and animal proteins), and in an atmosphere
containing 5% CO2.
Meningococci and gonococci are rapidly killed by
drying, sunlight, moist heat and many disinfectants.
Poor survival at cooler temperature.
N. gonorrhoeae (Gonococcus)
Form opaque and transparent variants; the opaque colonies are
associated with the presence of Opa.
Antigenic structure
1. Pili: enhancing attachment
to host cells and resistance to
phagocytosis; antigenically
different among strains, and a
single strain can make many
antigenically distinct forms of
pilin.
2. Por (protein I): forms porins
and mediates resistance to
serum killing.
3. Opa (protein II): an outer
membrane protein functioning
in attachment to host cells.
4. Rmp protein (protein III):
stimulates Abs that block
serum bactericidal activity.
5. Lipooligosaccharide (LOS):
lacking long-antigenic side
chains; endotoxic.
6. Other proteins.
N. gonorrhoeae is capable of changing its surface antigens
(pilin, Opa, and LOS) rapidly to avoid host defenses.
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.
Symptoms
Male: urethritis with yellow,
creamy pus and painful
urination. The process may
extend to the epididymis. As
suppuration subsides in
untreated infection, fibrosis
occurs, sometimes leading to
urethral strictures.
Female: infection starts from
the endocervix, then, urethra
and vagina, giving rise to
mucopurulent discharge.
Uterine tubes may be involved,
causing salpingitis, fibrosis,
and obliteration of the tubes
(20% may become infertile).
95% infected men and 50% infected women have acute symptoms.
Asymptomatic carriage is more common in women than in men.
Gonococcal bacteremia (1-3% of infected women and much lower
percent of infected men) can lead to skin lesions, tenosynovitis
and suppurative arthritis.
Gonococcal ophthalmia neonatorum (purulent conjunctivitis in
newborns); prevention: tetracycline, erythromycin or silver nitrate.
Immunity
Treatments
Repeated gonococcal
infections are common,
because protective
immunity to reinfection
does not develop due to
the antigenic variation of
gonococci. This makes
development of effective
vaccines difficult.
Resistance to penicillin G
(PPNG: penicillinaseproducing N. gonorrhoeae)
and tetracycline is common.
Ceftriaxon can be used for
gonococci.
In gonococcal infections other
than urethritis in men, cure
should be established by
follow-up, including cultures
from the involved sites.
Laboratory Diagnosis
Gram stain (gram-negative
diplococci in PMNs):
Sensitive (>90%) and specific
(98%) for men with purulent
urethritis.
Less sensitive for
asymptomatic men (<60%).
Relatively insensitive for both
symptomatic and
asymptomatic women.
* Negative results must be
confirmed by culture.
Culture and identification:
Avoid drying of specimen
(genital or rectal) and low
temperature.
Inoculate both the selective
media (containing
antibiotics) and nonselective media (chocolate
blood agar is used for
strains that are sensitive to
antibiotics).
【聯合新聞網】2004.10.29
自91年到93年，台北市接獲通報的梅毒及淋病患者都有顯著增加
的趨勢，以淋病來說，91年的通報人數為257人、92年為469人，
而今年9月為止就有375人，又以梅毒來說，91年通報數為667人，
92年為637人，但今年不到10月就有690人感染，情況嚴重。
儘管通報人數有上升，但台北市性防所護理組主任莊苹卻表示，
實際感染人數應該更多，因為許多人罹患性病都到小診所看病，
而淋病與梅毒的通報必須檢驗確認才行，由於通報沒有獎金加上
必須做檢驗，許多醫生為了省麻煩，只看了病人的性器官，就憑
著症狀開藥，不做檢查也不通報。
不通報造成的後果就是，衛生單位無法追蹤性伴侶或配偶，也無
法確認病患是否治療完成，這不但增加復發率，也增加交叉感染
的危險性。
Epidemiology, Prevention, and Control
Gonorrhea occurs only in
humans.
Infection rate can be
reduced by:
Gonorrhea is transmitted by
sexual contact, often by
women and men with
asymptomatic infections.
1. avoiding multiple
sexual partners;
Chemoprophylaxis is of
limited value.
Areas with high incidence of
PPNG: Asia, parts of Africa
and some places in USA.
2. early diagnosis and
treatment;
3. finding cases and
contacts through
education and
screening of
population at high risk.
N. meningitidis (Meningococcus)
【大紀元1月30日訊】安徽近期發生C群流腦疫情，自2004年12月20日～
2005年1月28日，除了3名在南京死亡的安徽病人外，安徽還有5人死
亡、7人隔離、49人治癒，61個「新型C群流行性腦膜炎」病例已涉及全
省17個城市中的11個城市的22個縣（區）。
據安徽省衛生廳副廳長杜昌智說，自2004年12月下旬以來，在安徽蕪
湖、滁州、安慶、巢湖、合肥等地的個別學校先後暴發流腦疫情，其他
部分地區陸續出現散發病例。發病者以中小學生為主，占病例總數的77
％，年齡多在13歲～18歲之間--已報告的在安徽死亡的5名死者，都是
合肥、蕪湖、滁州等地的在校學生。
此次流腦疫情具有以下特點：一是流腦發病數比去年同期有所上升，由
14例上升為61例；二是病例呈散發狀態，疫點涉及11個市的22個縣
（區）；三是引起流腦局部傳播流行的主要是C群腦膜炎雙球菌，這一
群種是近年來新發現報告的菌群，冬春季節是此病的高發期。
C群流腦具有易傳播、隱性感染比例高、起病急、病程進展快、死亡率
高等特點，臨床上常表現為暴發型、可在發病後24小時內死亡。C群流
腦感染者以高熱為首發症狀、伴有頭痛、全身酸痛、咽痛、咳嗽等，部
分病人出現皮膚瘀斑、瘀點，頸部強直、噴射性嘔吐等。
Antigenic structure
1. Capsular polysaccharide: more than 13 serogroups have
been identified (serogroups A, B, C, X, Y, and W135 are
most commonly isolated).
2. Pili
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.
Pathogenesis, Pathology, and Clinical Finding
Meningococci are pathogenic only for humans under
natural conditions.
Both gonococci and meningococci are able to invade the
epithelial cells. The capsule of meningococci protects the
bacteria from phagocytic destruction.
Nasopharynx is the portal of entry
attach to epithelial
cells with the aid of pili (may colonize without producing
symptoms)
reach the blood stream, producing
bacteremia.
Upper respiratory tract infection.
Fulminant meningococcemia.
Fulminant meningococcemia
High fever and hemmorrhagic rash.
There may be disseminated intravascular coagulation
and circulatory collapse.
Meningitis is the most common complication of
meningococcemia.
Symptoms: begins
suddenly, with intense
headache, vomiting, and
stiff neck, and progress to
coma within a few hours.
Meningococcemia can be
prevented by specific
bactericidal antibodies in
serum.
Immunity
Laboratory Diagnosis
Protective immunity is the
group- or type-specific,
complement dependent,
bactericidal antibodies.
Specimen: blood and
cerebrospinal fluid (CSF). >107
bacteria/ml of CSF are normally
found in untreated patients.
Treatments
Gram stain: gram-negative
diplococci in PMNs.
Penicillin G is the drug of
choice.
Culture and identification.
Epidemiology, Prevention, and Control
Meningococcal meningitis occurs in epidemic (in developing
countries) and sporadic cases (in developed countries).
Transmitted by respiratory droplets among people in close
contact (family members; soldiers in military barracks;
direct contact with the respiratory secretions of an infected
person.) Reduction of personal contacts in a population
with a high carrier rate is important for prevention.
Riphampicin or minocycline can often eradicate the carrier
state and serve as chemoprophylaxis.
Vaccination of specific capsular polysaccharides of groups
A, C, Y, and W-135 is used for protecting susceptible
persons against infection.
Lipopolysaccharide (LPS)
is also called endotoxin.
LPS is composed of lipid A,
core polysaccharide, and Ospecific polysaccharide.
Lipid A anchors LPS in the lipid
bilayer. It causes symptoms
associated with endotoxin.
O-specific polysaccharide can
be used to identify certain
species and strains.
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