NeisseriaN. gonorrhoeae (gonococcus): gonorrheaN. meningitidis: meningitis

Gram-negative cocci (ki

dney-shaped), usually

in pairs.

Human pathogens (i.e.

N. gonorrhoeae and

N. meningitidis) are ty

pically found associat

ed with or inside PMN

cells.

Morphology and Identification

Morphology and Identification

Both meningococci and gonococci are encapsulated:

menigococci have a polysaccharide capsule; gonococc

i have a loose capsule-like structure.

Grow best under aerobic conditions

Produce oxidase (oxidase-positive).

Meningococci and gonococci grow best in medium con

taining complex organic substances (e.g. blood, hemin,

and animal proteins), and in an atmosphere containing

5% CO2.

Meningococci and gonococci are rapidly killed by dryin

g, 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.

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 III): stimulates Abs that block serum bactericidal activity.

5. Lipooligosaccharide (LOS): lacking long-antigenic side chains; endotoxic.

6. Other proteins.

Antigenic structure

N. gonorrhoeae is capable of changing its surface antigens (pilin, Opa, and LOS) rapidly to avoid host defenses.

Pathogenesis and PathologyGonococci 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.

SymptomsMale: urethritis with yellow, cr

eamy 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.

Resistance to penicillin G (PPNG: penicillinase-producing 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.

Immunity

Treatments

Repeated gonococcal infect

ions are common, because

protective immunity to reinf

ection does not develop du

e to the antigenic variation

of gonococci. This makes d

evelopment of effective vac

cines difficult.

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:

Avoid drying of specimen (genital or rectal) and low temperature.

Inoculate both the selective media (e.g., modified Thayer-Martin) and non-selective media (e.g., chocolate blood agar; for strains that are sensitive to vancomycin).

Identification:

N. gonorrhoeae is distinguished from other species by acid production from glucose but not from other sugars.

Commercial genetic probes for direct detection of bacteria in clinical specimens.

【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.

Gonorrhea is transmitted by

sexual contact, often by

women and men with

asymptomatic infections.

Chemoprophylaxis is of

limited value.

Areas with high incidence of

PPNG: Asia, parts of Africa

and some places in USA.

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.

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 2

0 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。

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 vascul

ar damage in meningococcal infections.

*Twenty serotypes have been identified based on the dif

ferences in outer membrane proteins and LOS.

Antigenic structure

Pathogenesis, Pathology, and Clinical FindingMeningococci are pathogenic only for humans under natu

ral 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 c

ells with the aid of pili (may colonize without producing sy

mptoms) reach the blood stream, producing bacteremi

a.

Upper respiratory tract infection.

Fulminant 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.

Fulminant meningococcemiaHigh fever and hemmorrhagic rash.

There may be disseminated intravascular coagulation and circulatory collapse.

Meningitis is the most common complication of meningococcemia.

Immunity

Protective immunity is the group- or type-specific, complement dependent, bactericidal antibodies.

Treatments

Penicillin G is the drug of choice.

Laboratory Diagnosis

Specimen: blood and cerebrospinal fluid (CSF). >107 bacteria/ml of CSF are normally found in untreated patients.

Gram stain: gram-negative diplococci in PMNs.

Culture: alternative blood culture methods are required because additives in the blood culture broths can be toxic for this organism.

Identification: acid formation with gl

ucose and maltose, but not others.

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.

Back

Lipopolysaccharide (LPS)

is also called endotoxin.

LPS is composed of lipid A, cor

e polysaccharide, and O-specif

ic polysaccharide.

Lipid A anchors LPS in the lipid

bilayer. It causes symptoms a

ssociated with endotoxin.

O-specific polysaccharide can

be used to identify certain spec

ies and strains.