what is the only genus of G- cocci that frequently causes disease?
neisseria sp.
- usually diplococci
- n. gonorrhoeae (gonorrhea)
- n. meningitidis (bacterial meningitis and septicemia)
is the neisseria sp. motile?
non-motile (twitching motility from pili)
do neisseria sp. require oxygen?
- aerobes (but can grown anaerobically)
- grow best on media supplemented with blood in presence of CO2
what type of host does neisseria spp. require to live?
-obligate human pathogens: fragile, do not survive long outside host, humans are ONLY reservoirs
how prevalent is gonorrhea among other STDs and the youth?
4th on list of amount of youth who get it
how is gonorrhea diagnosed?
- culture on chocolate agar in presence of CO2
- boiled blood, iron, vitamins
- colonies = nonpigmented, mucoid, non-hemolytic
- modified Thayer-Martin agar (MTM)
- indicative of antibiotic resistance
- catalase and oxidase reactions
- both rxns positive->aerobic
- sugar fermentations
- meningococci:ferment glucose and maltose, but not sucrose or lactose
- gonococci: ferment glucose, but not maltose or sucrose
what are the two major neisseria sp.?
- n. meningitidis (meningococcus)
2. n. gonorrhoeae (gonococcus)
in what habitat does n. meningitidis live?
-throat, human nasopharynx is the only known reservoir
how do we encounter n. meningitidis and how does it enter?
- spread by airborne droplets, viral resp. infections (eg influenza) may enhance the spread
- attach to nasopharyngeal epithelial cells and invade mucous membranes
- asymptomatic carriage induces humoral antibody response
- most individuals acquire immunity by age 20
- invasion of the blood stream only occurs in individuals deficient in complement component (C5-C8)
- type 4 pili: attach organism to meninges in CNS
- lipooligosaccharide (LOS) damages host tissue: elicits host inflamm response, resulting in hemorrhaging of blood into skin and mucous membranes (purpuric rash)
what are the virulence factors for n. meningitidis?
LARGE CAPSULE, outer membrane blebs (LPS endotoxin), hemolysin
what is the habitat for n. gonorrheae?
- mucosal epithelia of male urethra or female cervix
- asymptomatic carriers greater among women
how do we encounter n. gonorrhoeae and how does it enter?
- contact with genital secretions
- upon introduction, attach to columnar epithelia of cervix or urethra (gonococci)
- pili and surface proteins
- adhesins controlled by:
- phase variation-presence/absence
- antigenic variation-composition
what are n. gonorrheae’s virulence factors?
- no capsule
- pili and strong adhesins
- LPS endotoxin
- IgA 1 protease
- phase/antigenic variation
describe the cell surface of n. gonorrhoeae.
classic diplococcus morphology
describe the cell surface of n. meningitidis.
membrane blebs are profuse
describe the phase variation of e. coli.
- expression of gene product is turned on or off at high frequency
- promoter inversion
- promoter on -> fimbriae
- promoter off - no fimbriae
describe the phase variation of n. gonorrhoeae.
- slipped strand mispairing: colony opacity-associated (Opa) genes (10+)-> constantly changing its color
- encode outer membrane proteins
- Opa’s presence results in neutrophil uptake
- ***some gonococci lack Opa and avoid phagocytosis
- *also controls other surf proteins, as well as LPS in gonococci and meningococci
what is the antigenic variation of n. gonorrhoeae?
- changes in composition or structure of surface molecules (eg. pili- host cell attachment)
- reassortment and recombination of pilS loci
**generally, how is gonococci spread and how does it multiply?
- multply rapidly
- shed in genital secretions
- do not have flagella and are not motile
- can enter epithelial cells
- extracellular protease cleaves IgA1
- removes Fc receptor end of antibody
- enables escape from phagocytosis: haemophilus and streptococcis also posses
what type of cells do gonococci attach to and where are they located?
- non-ciliated cells
- human fallopian tubes and columnar epithelial cells have ciliated and non-ciliated cells
- non-ciliated cells have microvilli
what happens once gonococci attached to the non-ciliated cells?
- ciliary statsis: ciliary cell motility slows and ceases
- death of ciliary cells: slough from epithelial surf, can be elicited by LPS and peptidoglycan (G+/G-)
what do the non-ciliated cells do once microvilli contact gonococci?
- engulf bacteria: internalized by “parasite directed endocytosis”
- intracellular replication (protection): gonococci may multiply within vacuoles
- intracellular traffic: vacuoles fuse with basement membrane
- exocytosis: vacuoles discharge bacteria into subepithelial connective tissue
what damage do gonococci cause/do they secrete endotoxin?
- do not secrete endotoxin
- LPS (LOS- lipooliogsaccharide) and other cell wall components cause cell damage by inducing TNF-alpha
- sloughing off of ciliated cells
- non-ciliated cell lysis: release of factors that cause inflamm
how do we fight gonococci?
-serum antibodies recognition that target LPS (LOS), Protein I of the outer membrane and other surf proteins
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G- pathogens of mucosal surfaces pt.155
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G-pathogens of mucosal surfaces pt.269
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Neisseria (G-)33
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Haemophilus (G-)10
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Pseudomonas (G-)31
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Listeria monocytogenes (G+)9
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Small G- Pathogens (chlamydiae, rickettsiae, ehrlichia)72
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Clostridia (G+)66
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Virus Classification, Structure & Replication84
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Childhood Viral Diseases71
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Hepatitis Viruses40
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Neurological Viruses38
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Retroviruses, AIDS, & Tumor Viruses52
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Respiratory Viruses42
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Herpesvirus & Papillomavirus32
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Antivirals & Vaccines24
