Neisseria

o Gram negativediplococci
o Kidney shaped N.gonorrhoeae
o Occcur in pairs N.meningitidis
o Intracellular within polynorphnuclear leukocyte or extracellular They are homologically related.
o Commensals of upper respiratory tract




N.gonorrhoeae N.meningitidis
STD(sexually transmitted disease) Respiratory tract
Carrier (-) (+) nasopharynx
Polysaccharide capsule (-) (+)
Vaccine (-) (+)
Plasmid (+) (-)
Antibiotic resistance (+) (-)

Sugar fermentation test Capsule !"ိရင် vaccine ထ)တလ
် ရ
ိ) ့
Glucose (+) for N.gonorrhoea G for G
Plasmid !"ိရင် antigen variation
Maltose (+) for both N.gonorrhoea and Maltose က both
(resistance) ြဖစ်ဖိ)လွ
့ ယ်
N.meningitidis


Questions for Neisseria
1. Etiology
2. Pathogenesis of N.gonorrhoea
3. Pathogenesis of N.meningitidis



















Etiology of gonorrhoea
Causal organism – Neisseria gonorrhoea

Morphology
o Gram negativediplococci
o Kidney shaped
o Occcur in pairs
o Intracellular within polynorphnuclear leukocyte or extracellular

1. Growth characteristics
Ø Facultative anaerobe
Ø Fastidious – grow only on chocolate agar (heme)
Ø Selective media -Thayer-Martin media with VCN
(vancomycin, neomycin, amphotericin B)
- Martin-Lewis media, New York City media

Ø Grow best in 5% carbon dioxide containing atmosphere
Ø Oxidase positive
2. Reaction to physical and chemical agents
Ø Rapidly killed by drying, sunlight, moist heat and many disinfectants
Ø Produce autolytic enzyme – result in rapid swelling and lysis in vitro at 25C

3. Antigenic structures (******)
i. Pili
Ø Made up of pili protein, antigenically different
Ø Enhance the attachment to host cell
Ø Resist phagocytosis
ii. Por
Ø Form pores through which nutrients enter into the cell
iii. Ope protein
Ø For adhesion of gonococci,
Ø Produce opaque colonies
Ø For attachment of gonococci to host cells
iv. Rmp (reduction modifiable protein)
Ø Association with Pro in formation of pores
v. Lipooligosaccharides (LOS)
Ø Gonococcal LPS does not have long O antigen side chain
Ø Toxicity of gonococcal infection is due to endotoxic effects of LOS
Ø Structurally resemble human cell membrane glycosphingolipid (molecular
mimicry) escape from immune recognition.
vi. Other proteins
Ø Fbp(iron binding protein) – expressed when available iron is limited
vii. Lip(lipoprotein)
Ø surface expose protein
viii. Ig A1 protease
Ø Split and inactivate Ig A1


***** antigenic variation
-gonococci rapidly switch from one antigenic form to another
-helps the gonococci elude the host immune system Bacteria which produce Ig A1 protease (CQ)
-gonococci contain several plasmid which contain gene for B-lactamase i. Neisseria gonorrhoeae
production ii. Neisseria meningitidis
iii. Streptococcus pneumoniae
4. Antibiotic resistance iv. Haemophilus influenzae
-penicillin resistance (penicillin producing N.gonorrhoeae——-
PPNG)
-high level resistance to tetracycline
-resistance tospectinomycin and other (eg. Fluroquinolone resistance)














Pathogenesis of gonorrhoea How to answer pathogenesis
1. causal organism – Neisseria gonorrhoeae 1. Causal organism
2. Source of infection – infected person 2. Source of infection
3. Mode of transmission 3. Mode of transmission
I. Acute and chronic gonorrhoea in adults 4. Diseases explanation
(MOT-sexual contact)
II. Gonococcal vulvovaginitis in prepubertal girls (young female children)(MOT-
contact due to poor hygiene, sexual abuse)
III. Gonococcal ophthalmia neonatorum in neonates (MOT-direct contact during
delivery)

I. Acute and chronic gonorrhoea

-gonococci attack mucous membrane of genito-urinary tract
-pili,por,opa protein mediate attachment and penetration into cells
- bacteria multiply inside cells and pass to sub-epithelial space
-gonococcal LOS stimulates release of tumor necrosis factor alpha (TNF- )
-acute suppuration lead to tissue invasion followed by chronic inflammation, fibrosis

Clinical features
Male
§ Usually symptomatic
§ Primary site of infection is urethra
§ Urethritis – present with yellow creamy discharge, painful urination (dysuria)
§ Urethral strictures – fibrosis after suppuration subsides in untreated infections leading to
urethral strictures
§ Anorectal gonorrhoea in homosexual men
Female
§ Asymptomatic
§ Primary site of infection is endocervix
§ Spread to vagina and urethra, present with mucopurulent discharge of urethra
§ Spread to uterine tube- salphingitis – fibrosis – obliteration of tubes – infertility (sterility) in 20%
of women with gonococcal salphingitis
Both sex
 § Proctitis

Gonococcal bacteremia
§ Found in patient with complement deficiency (C5b,6,7,8,9) and leads to:
§ Skin lesions (hemorrhagic pa pulse and pustules) on hands, forearms, arms, legs
§ Tenisynovitis and suppurative arthritis, usually of the knees, ankles, and wrists, endocarditis ,
meningitis, pharyngitis, and eye infection in adults.

II. Gonococcal vulvovaginitis

§ Loss of oestrogen – no glycogen deposition in vaginal epithelium – no fermentation by
lactobacilli – no acidity (acid pH)
§ Clinical features are vaginal discharge, vaginitis – pain, inflammation present

III. Gonococcal ophthalmia neonatorum

§ Infection of eye of newborn, acquired during passage through infected birth canal purulent
conjunctivitis if untreated lead to blindness
§ Prevented by tetracycline or erythromycin into conjunctiva of the newborn

 Pathogenesis of N.meningitidis
Causal agent -Neisseria meningitidis
Source – patients and carriers
Mode of transmission – air borne droplet
Carrier site – nasopharynx (5-30% in normal population)
• Portal of entry is nasopharynx
• The organisms attach to specific receptors for meningococcal pili present on
nasophyrangeal epithelial cell and multiply, form part of transient flora without
producing symptoms.
• Bacteria are internalized by phagocytes.The polysaccharide capsule protects the
bacteria against phagocytic destruction.
• Bacateria aggregates in nasopharynx and bacteria are released into airways , person to
person spread – nasophyrangitis
• From nasopharynx, meningococci reach the blood stream (bacteraemia)
• Bacteraemia spreads meningococci to specific sites such as the meninges or joints
• Fulminant meningococcemia is more severe, with high fever and with hemorrhagic
rash, disseminated intravascular coagulation and circulatory collapse (Waterhouse
Friedrichsen syndrome) – due to LPS
• Meningitis, sudden onset of intense headache, vomiting, stiff neck, then progress t
coma within a few hours
• Interstitial myocarditis, arthritis, and skin lesion

Mechanism diseases

ဝင် 1. Local – nasopharyngitis
ပွါး 2. Blood – bacteraemia,
meningococcemia (W-F $)
ထွက် 3. Specific site – meningitis ,
arthritis , myocarditis
ထွက် တာ ၃ ေန ရာ
Local , blood (transportation), favorite
site(သ45ကိ7က်တေ ဲ့ နရာ)