29-Neisseriae

Question 1

Neisseria- morphology and gram stain

Answer 1

Gram (-) cocci

Question 2

Neisseria- reservoir

Answer 2

Humans

Question 3

N. meningitis- transmission

Answer 3

person-person by aerolization of respiratory tract secretions

Question 4

N. gonnorrhoeae- transmission

Answer 4

STD, carriage can be in asymptomatic people

Question 5

N. gonnorrhoeae- susceptible people

Answer 5

Blacks, ppl ages 15-24, residents of SE USA, ppl with multiple sexual partners (giggity)

Question 6

N. meningitides- susceptible people

Answer 6

children <5, institutionalized ppl

Question 7

Gonorrhea- clinical presentation

Answer 7

purulent discharge of involved site (urethra, cervix, epididymis, prostate, anus after 2-5 incubation days

Question 8

Meningitis- clinical presentation

Answer 8

purulent inflammation of meninges- headache, meningeal signs, fever (high mortality if not treated appropriately and quickly)

Question 9

Disseminated infections (from N. gonnorrhoeae)- clinical presentation

Answer 9

spread of infection from genitourinary tract through blood to skin or joints- pustular rash with erythromatus base and suppurative arthritis in joints

Question 10

Opthalmia neunatorum (from N. gonnorrhoeae)- clinical presentation

Answer 10

purulent ocular infection acquired by neonate at birth (from vagina of infected mother)

Question 11

Meningococcemia (from N. meningitides)- clinical presentation

Answer 11

disseminated infection- thrombosis of small blood vessels and multiorgan involvement- small petechial skin lesions which coalesce into larger hemorrhagic lesions

Question 12

Pneumonia (from N. meningitides)- clinical presentation

Answer 12

milder form of meningococcal disease- bronchopneumonia in patients with underlying pulmonary disease

Question 13

What is the main VF in Neisseria?

Answer 13

Pili

Question 14

What is the function of Pili in Neisseria?

Answer 14

• mediate functions: attachment to host cells, transfer of genetic material, and motility
• composed of repeating protein subunits (pilins)- expression is controlled by the pil gene complex
• pili expression is associated with virulence because of involvement in host attachment to and provide resistance to killing by neutrophils
• lack of immunity to re-infection with N. gonorrhoeae results partially from antigenic variation among pilin proteins and from phase variation in pilin expression.

Question 15

Neisseria- media

Answer 15

modified Thayer-Martin Agar chocolate agar

Question 16

What is opa?

Answer 16

• opacity proteins
• membrane proteins that mediate intimate binding to epithelial and phagocytic cells and are important for cell to cell signaling
• N. gonorrhoeae- Opa proteins are opaque (not transparent)
• Opa associated with clinical disease
• Opaque colonies are in localized disease
• Transparent colonies associated with pelvic inflammatory disease and disseminated diseases

Question 17

Why can’t you use penicillin for gonorrhea infections?

Answer 17

• historically, was the antibiotic of choice for gonorrhea
• not used today because the concentration needed to kill susceptible strains has increased and is now resistant.
• Resistance is caused by the ability of the membrane proteins and antigens to produce β-lactamase or by chromosomally mediated changes in penicillin-binding proteins and in cell wall permeability
• Resistance is also associated with resistance to tetracyclines, erythromycin and aminoglycosides.

Question 18

Why is antigenic variation in Neisseria infections bad?

Answer 18

• the lack of immunity to re-infection by N. gonorrhoeae results partially from the antigenic variation among the pilin proteins and partially from the phase variation among the pilin gene expression. These factors complicate attempts to develop effective vaccines for gonorrhea.

Question 19

What is the fxn of the capsule in Neisseria?

Answer 19

• The polysaccharide capsule also has antiphagocytic properties that protect N. meningitidis against phagocytic destruction. This allows the meningococci bacterium to penetrate through cells, avoid intracellular death while in a phagocytic vesicle, replicate, and then migrate into subepithelial spaces where the infection is established.

Question 20

What is disseminated intravascular coagulation?

Answer 20

• associated with meningococcemia
• begins with thrombosis of small blood vessels and multiorgan involvement
• presents with small petechial skin lesions on trunk and lower extremities – may coalesce to form larger hemorrhagic lesions
• leads to overwhelming disseminated intravascular coagulation with shock along with bilateral destruction of adrenal glands (Waterhouse-Friderichsen syndrome)