1. NEISSERIA
N.meningitidis
N.Gonorrhea
Deepa Babin

2. Family Neisseriaceae
• Genera include Neisseria, Branhamella,
Moraxella
• Gram-negative diplococci
• Residents of mucous membranes of warm
blooded animals
• 2 primary human pathogens:
– Neisseria gonorrhoeae
– Neisseria meningitidis
2

3. Neisseria Gonorrhoeae:
• Gram-negative, bean-shaped, diplococci
• Nonmotile and Non sporing
• Capsulated,Pili
• Strict parasites, do not survive long outside
of the host
• Aerobic or microaerophilic
• Oxidative metabolism
• Produce catalase and cytochrome oxidase
• Pathogenic species require enriched
complex media and CO2
3

4. Neisseria Gonorrhoeae:
Gonococcus
• Causes gonorrhea
(flow of seeds) an
STD
Morphology- Gram
negative diplococci
with adjacent side
concave or pear
shaped,seen
intracellularly
4

5. Epidemiology and Pathology
• Strictly a human infection
• In top 5 STDs
• Infectious dose 100-1,000
• Does not survive more than 1-2
hours on fomites
• Virulence factors:
– Fimbriae, Pili,other surface molecules
for attachment; slows phagocytosis
– IgA protease – cleaves secretory IgA
5

6. Pathogenicity
• Acquire thru sexual contact
• Adhesion on urethra or mucosal
surface(Pili)
• Cocci penetrate thru intercellular
spaces and reach the subepithelial
connective tissue
• IP- 2-8 DAYS

7. Gonorrhea
Infection is asymptomatic in 10% of males and
50% of females
• Males –Extends along urethra-prostate-
seminal vesicle-epididymis causes urethritis,
yellowish discharge, scarring, and infertility
• WATERCAN PERINEUM(Multiple discharging
sinus)
7

8. Gonorrheal damage to the male reproductive
tract
8

9. • Females – vaginitis,
urethritis, salpingitis (PID)
mixed anaerobic abdominal
infection, common cause of
sterility and ectopic tubal
pregnancies

10. Ascending gonorrhea in women
10

11. Extragenital infections –
Gonorrhea in Newborns
• Infected as they pass through birth
canal
• Ophthalmia neonatorum
• Eye inflammation, blindness
• Prevented by prophylaxis immediately
after birth
• Extragenital infections – anal,
pharygeal, conjunctivitis, septicemia,
arthritis
11

12. Lab Diagnosis and Control
• Gram stain – Gram-negative intracellular
(neutrophils) diplococci from urethral,
vaginal, cervical, or eye exudate – presumptive
identification
• Culture-Chocolate agar,Muller Hinton
agar,Thayer Martin Medium
• Treatment-Ceftriazone
+Doxycyline(Erythromycin)
• Combined therapies indicated
• Recurrent infections can occur
• Reportable infectious disease
12

13. Gram stain of urethral pus
13

14. Non specific urethritis
• Gonococci cannot be demonstrated in this
condition
• Some time associated with Reiters
syndrome(urethritis, conjunctvitis ,arthritis)
• L forms of Gonococci not detectable
• Others-Chlamydia trchomatis, Ureaplasma
urealyticum, Mycoplasma hominis, Herpes
virus, Cytomegalovirus,Gardinella vaginalis,
Acinetobacter,Candida,Trichomonas vaginalis

15. Neisseria Meningitidis:
Meningococcus
Morphlogy-Gram
negative diplococci
with adjacent side
flattened
,intracellular
Virulence factors:
– Capsule
– Adhesive fimbriae
– IgA protease
– Endotoxin
• 12 strains; serotypes
A, B, C cause most
cases 15

16. Epidemiology
• Prevalent cause of cerebrospinal meningitis
and meningococcal septicemia and sporadic
or epidemic
• Human reservoir – nasopharynx, 3-30% of
adult population; higher in institutional
settings
• High risk individuals are those living in close
quarters, children 6 months-3 years, children
and young adults 10-20 years
16

17. Pathogenesis
• Infection is acquired through droplet spread via
the carriers
• Incubation period is 3 days
• It spread along the perineural sheath of
olfactory nerve thru cribriform plate to
subarachnoid space
• When bacteria enter bloodstream, cross the
blood-brain barrier, permeate the meninges,
and grow in the cerebrospinal fluid
• Very rapid onset; neurological symptoms;
endotoxin causes hemorrhage and shock; can be
fatal

18. Dissemination of the meningococcus
from a nasopharyngeal infection
18

19. CLINICAL FEATURES
• Acute fever with petechial rash
• Few develop meningococcemia(Waterhouse-
Friderichsen syndrome) characterised by
shock, disseminated intravascular coagulation
and multisystem failure

20. One clinical sign of meningococcemia
20

21. Lab diagnosis
• Specimens-CSF, blood, or nasopharyngeal
sample
• CSF COLLECTION-Lumbar puncture
• THREE PORTIONS OF CSF
• Microscopy-Gram staining- Gram negative
diplococci, intracellular and extracellular
• Culture- Chocolate agar, Blood agar,
Newyork city medium
• Oxidase test-positive
• Rapid tests for capsular polysaccharide
21

24. Treatment and Prevention
• IV penicillin G, Cefotaxime ,Ceftriaxone
• Prophylactic treatment of family
members, medical personnel, or children
in close contact with patient
• Primary vaccine contains specific purified
capsular antigens
24

25. Other causes of meningitis
Bacterial causes:
Three primary pathogens:
N. meningitidis, H influenzae,
S.pneumoniae
N.menningitidis all ages
HI 2m-5y
S.pneumoniae all ages but more
common in adult with underlying illnesses.

26. Other causative bacteria (Continue)
E.coli & other coliforms
Listeria
Strept.group B
Salmonella spp.
Favobacteria..
All common in neonates

27. Other causative bacteria (Continue
After surgery or trauma
S.aureus
S.pneumoniae
AFB chronic meningitis
Spirochaetes

28. Other Causes
Viral :enterovirus, Paramyxovirus,
Herpes viruses, adenoviruses,
arboviruses.
Fungi: yeasts
(Candida,cryptococcus spp.)
Aspergillus spp ,Mucor

29. Normal CSF: BACTERIAL MENINGITIS CSF
Clear , colorless
0-5 lymphocytes Turbid
Sterile 500-20,000 cells mainly polys,few
150-450 mg /l protein lymphocytes
2.8-3.9mmol/l glucose Bacteria in Gram stain
Markedly raised protein
Reduced or absent glucose
CSF in TB meningitis
Clear or slightly turbid
10-500 cells,mainly CSF in VIRAL meningitis
lymphocytes polys early) Clear or slightly turbid
AFB in Z-N stain 10-500 cells mainly lymphocytes
Grow in LJ medium Stool culture, or serology +ve
Moderately raised protein Normal or slightly raised protein
Sugar reduced Normal glucose