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MicroImmuno Exam 3 > Bailey Lecture 3 - Stoeckel Neisseria > Flashcards

Bailey Lecture 3 - Stoeckel Neisseria Flashcards

1
Q

What is the only genus of GRAM NEGATIVE COCCI that frequently cause disease?

A

Neisseria

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2
Q

______ are usually diplococcic

A

Neisseria

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3
Q

What genus is responsible for gonorrhea and bacterial meningitis?

A

Neisseria (note that Neisseria are non-motile, aerobes, and are obligate human pathogens that do not survive long outside the host)

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4
Q

What age group has the highest prevalence of gonorrhea?

A

20-24 followed by 15-19 and 25-29

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5
Q

How many new gonorrhea infections occur each year?

A

820,000 out of 20 million total (most are HPV and chlamydia)

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6
Q

What type of agar is used to identify Neisseria?

A

chocolate agar (boiled blood, iron, vitamins). Colonies are mucoid, non-hemolytic, and nonpigmented. Note that gonorrhea is both catalase and oxidase positive. Meningococci can ferment glucose and maltose while gonococci can only ferment glucose

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7
Q

What is the only known reservoir for N meningitidis?

A

the human nasopharynx

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8
Q

what is the habitat for N. gonorrhoeae?

A

mucosal epithelia of male urethra or female cervix

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9
Q

how is N. meningitidis spread?

A

spread by airborne droplets. Viral respiratory infections such as the flu may enhance the spread

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10
Q

Is N. meningitidis or N. gonorrhoeae encapsulated?

A

meningitidis has a large capsule while gonorrhoeae has no capsule. Note that the gonococcus has pili and strong adhesins and that both species have LPS endotoxin

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11
Q

How can you tell meningitidis and gonorrhoeae apart under microscope?

A

gonorrhoeae look smooth under microscope while meningitidis look “bubbly”

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12
Q

Asymptomatic carriage of meningococci induces ______ antibody response and most individuals acquire immunity by age ____

A

humoral, 20

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13
Q

Invasion of the blood stream by meningitidis is an indication that the individual is deficient in complement components ___ - ___

A

C5 - C8

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14
Q

_____ allows meningitidis to attach to meninges in CNS

A

Type IV pili

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15
Q

Lipooligosaccharide (LOS) of _____ ilicits host inflammatory response, resulting in what?

A

meningococci, skin rash (purpuric rash)

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16
Q

Are asymptomatic carriers of gonococci mostly men or women?

A

women (attach to columnar epithelium of cervix or urethra via pili and surface proteins [adhesins])

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17
Q

What is phase variation as utilized by gonococci?

A

phase variation is the ability of a bacterium to adapt to its environment without requiring mutation. In gonococci, the presence of powerful adhesins on the tips of the pili is dependent on the correct external environment. Our neutrophils are able to recognize some of these phase variation genes such as Opa on gonorrhoeae which results in phagocytosis. Some gonorrhoeae however lack Opa and therefore avoid phagocytosis

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18
Q

Do gonococci spread slowly or rapidly?

A

rapidly. They are shed in genital secretions, do NOT have flagella and therefore are NOT motile. They are able to enter epithelial cells and have an extracellula protease which is able to cleave IgA1, possibly enabling it to escape phagocytosis

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19
Q

Do gonorrhea cells attach to the ciliated or non-ciliated cells of the fallopian tubes?

A

They attach to the non-ciliated cells which results in stasis (non-movement) of the fallopian ciliated cells. As a result, the ciliated cells die and slough from the epithelial surface.

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20
Q

How does internalization of gonorrhea occur?

A

The non-ciliated microvilli engulf the bacteria (AKA they are internalized by “parasite-directed endocytosis”)

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21
Q

Once ingested by non-ciliated epithelial fallopian cells, where do gonorrhea cells multiply?

A

They multiply within vacuoles underneath the epithelial cells. These vacuoles then fuse with the basement membrane and the multiplied bacteria are discharged into subepithelial connective tissue

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22
Q

What exotoxins does gonorrhea have and what is the role of LPS?

A

actually, gonorrhea do not have an exotoxins. LPS is important however because it causes cell damage. LPS (LOS) induces TNF-alpha resulting in the sloughing of ciliated cells and lysis of ciliated cells (causing inflammation)

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23
Q

How can gonorhea survive the host immune response?

A

its LPS can be altered to look like the surface components of red blood cells which may allow for ‘self’ recognition

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24
Q

What are the three main diseases associated with meningococci?

A

1) uncomplicated bacteremic process
2) metastatic infection of the meninges
3) overwhelming systemic infection involving circulatory collapse and disseminated intravascular coagulation (DIC). This can happen when individuals lack the IgG antibodies that are specific to the bacteria’s capsule

*note that these meningococci systemic infections will give the highest known bacterial titers in blood

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25
Q

Do meningococci produce hemolysin?

A

yes

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26
Q

What is pelvic inflammatory disease?

A

it is the gonococcal infection of the female upper reproductive tract which involves inflammation of the uterus and fallopian tubes, scarring of upper tract and adjacent organs (infertility, ectopic pregnancy, chronic pelvic pain)

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27
Q

How does pelvic inflammatory disease (gonococcal) affect men?

A

it manifests as epididymitis where gonococcal infection spreads into the upper reproductive tract of men

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28
Q

Disseminated gonococcal infections can result from the endotoxin of ____

A

endotoxin of pelvic inflammatory disease (PID). It involves pustular lesions of skin, imflammation of tendons and joints, and suppurative arthritis (more common in women)

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29
Q

Can meninococcus survive in the bloodstream? If so, what are the effects?

A

Yes it can, and the effects include skin manifestations, meningitis, shock, and death. These symptoms are due to the immune response mediated by TNF-A and IL-1 to the toxin produced by meningitis. The greater the response, the greater the chance of death

30
Q

What antibiotic are Neisseria mainly resistant to?

A

penicillin (B-lacam drugs). Resistance to other drugs is increasing

31
Q

What is prophylaxis?

A

treatment with antibiotics during a procedue in which secondary infection is likely. Prophylaxis is key during surgical procedures in order to prevent costly extended hospital stays

32
Q

Which of the two Neisseria have vaccines available?

A

meningococci (not gonococci). Does not work for children under the age of 2

33
Q

Haemophilus are (large/small) gram (positive/negative) (anaerobic/aerobic) coccobacilli

A

small gram negative aerobic (some anaerobic)

34
Q

Haemophilus colonizes ______ of almost everyone

A

upper respiratory tract (H. influenzae [note that this is not what causes flu. flu is a virus])

35
Q

What two factors does H. influenzae require for growth?

A

X factor and V factor (NAD+)

36
Q

Other haemophilus species besides H. influenzae only require what factor for growth (on blood agar)?

A

NAD+

37
Q

There are seven antigenically typable H. influenzae strains and several non-typable strains. Describe them

A

the antigenically typable are described by their polysaccharide capsule (a, b, c, d, e, e’, f). The non-typable do not have capsules

38
Q

What are the two meningitis diseases?

A

N. meningitis and H. meningitis

39
Q

What is the most virulent form of H. influenzae?

A

H. influenzae type b (Hib). Causes bacteremia and meningitis in children younger than 2 years

40
Q

What type of Haemophilus bacteria frequently cuse respiratory tract disease in infants, children, and adults?

A

the non-typable strains (not encapsulated)

41
Q

What type of capsule do the Haemophilus genus have?

A

PRP capsule (polyrobosyl ribitol phosphate) that allows resistance to phagocytosis (as long as antibody is not present). The PRP capsule is the basis for he Hib vaccine. PRP capsule is an endotoxin, causing pathogen-directed endocytosis

42
Q

Many H. influenzae and non-typeable isolaes produce B-lactamase. What does this mean?

A

This means that they will be resistant to penicillin or ampicillin. Therefore, chloramphenicol is the drug of choice as well as third-generation cephalosporins

43
Q

Pseudomonas aeruginosa are gram (positive/negative) (cocci/bacilli/spirochetes) that are found pretty much everywhere. They are (motile/nonmotile), (do/do not) have pili & flagella, and are (aerobic/anaerobic)

A

gram negative rods, have flagella and pili, are aerobic (some strains anaerobic)

44
Q

Pseudomonas aeruginosa produce water-soluble pigments that function as _____

A

antibacterials that produce a fruity odor

45
Q

Pseudomonas aeruginose grow (fast/slow) and (are/aren’t) fragile

A

grow fast and aren’t fragile

46
Q

pseudomonas (do/don’t) ferment sugars

A

don’t. All they need is aceate and ammonia as carbon and nitrogen sources. Most organic compounds can provide this including petroleum and toxic wastes. They can survive in hand cremes, soaps, and dilute antiseptics

47
Q

What shields Pseudomonas aeruginosa from the immune system?

A

mucoid polysaccharide capsule with elastase, exotoxin A, and phospholipase C

48
Q

What are the three spreading factors for pseudomonas?

A

collagenase, elastase, and exoenzymes (cause tissue damage)

49
Q

What bodily element do pseudomonas desire and how do they get it?

A

They want iron and compete with transferrin for it. When there is a low amount of iron available, the bacteria will increase production o elastase and endotoxin A in order to create conditions that increase accessibility of iron

50
Q

What role does phospholipase C play for pseudomonas?

A

phospholipase C hydrolyzes phospholipids in the eukaryotic membrane, releasing usable phosphate

51
Q

What common place can pseudomonas prosper?

A

hot tubs (folliculitis, dermatitis)

52
Q

Is pseudomonas an opportunistic pathogen or not?

A

yes, its opportunistic and mainly goes after immunocompromised patiens

53
Q

True or false: pseudomonas adheres poorly to healthy epithelium

A

true. it prefers to enter through abrasions, cuts, etc.

54
Q

After pseudomonas entry, the ability to spread and multiply depends on two things. What are they?

A

1) avoiding phagocytosis
2) successful adherence to a surface

55
Q

Does pseudomonas have an endotoxin?

A

yes. Lipid A is its LPS endotoxin and in interacts with host TLR4 (toll-like-receptor) to initiate inflammatory response (fever, hypotension, gram-negative sepsis)

56
Q

What in the pseudomonas is responsible for resistance to human serum, antibiotics, and detergents?

A

The long O-antigen side chains

57
Q

What exotoxins do pseudomonas produce and what is the result?

A

pseudomonas produce exotoxin A which can kill host cells… exotoxin A is highly regulated

58
Q

What two things does elastase do?

A

it cleaves elastin and collagen causing direct tissue damage (it also cleaves proteinase inhibitors and immune system components)

59
Q

What does LasA do in the context of pseudomonas?

A

it is a serine protease that works with elastase to degrade elastin

60
Q

Why are pseudomonas exotoxins highly regulated?

A

it costs the cell energy to make them

61
Q

What are two important strains of P. aeruginosa morphologically speaking?

A

one has pili and the other does not. The one with pili adheres beter to epithelium than the non piliated strain

62
Q

People with cystic fibrosis lose what which causes what?

A

they lose the cystic fibrosis transmembrane conductance regulator (CTFR) and the result is that they lose the ability to transport Cl-. This is hereditary

63
Q

CTFR causes decreased what?

A

decreased sialyation of surface glycolipids (P. aeruginosa bind to these asialo-glycolipids)

64
Q

What causes sepsis from Pseudomonas?

A

The LPS (endotoxin) triggers a severe immune response from TNF and IL-1

65
Q

What type of pseudomonas predominate in some hospitals?

A

antibiotic-resistant pseudomonas (resistance is due to limited permeability of outer membrane, efflux pumps, and antibiotic resistance genes). This frequently requires antibiotic synergism to treat

66
Q

Is Listeria gram positive or negative?

A

Gram positive (found in the intestinal tract of vertebrates, sewage, soil, and water). It is a common food-bourne pathogen that is especialy heat and cold resistant (lunch meat).

67
Q

Is listeria motile?

A

yes, it has peritrichous flagella

68
Q

Are there asymptomatic carriers of Listeria?

A

yes, 5-10% (transmitted via fecal-oral)

69
Q

Where does Listeria multiply?

A

Within the cellular cytoplasm

70
Q
A

MicroImmuno Exam 3 (5 decks)

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