Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ID Week 4 > ICL 2.14: Neisseria & Moraxella > Flashcards

ICL 2.14: Neisseria & Moraxella Flashcards

1
Q

what’s the microbiology of neisseria?

A

gram (-) coccus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what’s the microbiology of moraxella?

A

gram (-) coccus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

rate these bacteria from leads to most invasive:

N. meningitis (commensal)

N. gonorrhoeae/M. catarrhalis

N. meningitis (N. meningitis)

A

the most nontoxic, highly invasive and causes damage from immune system: N. meningitis (pathogenic)

then N. gonorrhoeae/M. catarrhalis

then lease invasive is n. meningitis (commensal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are the 3 genera in the Neisseriaceae family?

A
  1. Neisseria
  2. Eikenella
  3. Kingella
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

where in the body is Eikenella usually found?

A

E. corrodens is normal inhabitant of upper respiratory tract – fastidious and rarely pathogenic

it’s an opportunistic pathogen that most often causes disease after wounding during fistfights or by human bite

they’re also are sometimes associated with neck cancer and endocarditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

where in the body is Kingella usually found?

A

K. kingae is normal inhabitant of upper respiratory tract

although normally fastidious and non-pathogenic, can disseminate to cause arthritis or endocarditis – much less common in respiratory tract infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

which species of the Neisseria genus are in humans?

A
  1. N. gonorrhoeae

2. N. meningitidis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what kind of pathogens are N. gonorrhoeae and N. meningitidis?

A

opportunistic pathogens

human host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the disease syndromes associated with N. gonorrhoeae?

A
  1. gonorrhea
  2. disseminated disease = purulent arthritis, pustular rashes, fever and rigor
  3. conjunctivitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are the disease syndromes associated with N. meningitidis?

A
  1. meningitis
  2. meningococcemia – Waterhouse-Friderichsen syndrome
  3. pneumonia
  4. arthritis
  5. urethritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is Waterhouse-Friderichsen syndrome?

A

massive, usually bilateral, hemorrhage into the adrenal glands caused by fulminant miningococcemia

WFS is characterised by overwhelming bacterial infection, rapidly progressive hypotension leading to shock, disseminated intravascular coagulation (DIC) with widespread purpura, particularly of the skin, and rapidly developing adrenocortical insufficiency associated with massive bilateral adrenal hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the microbiology of Neisseria?

A

aerobic, non-motile gram (-) cocci

oxidase and catalse positive

usually in pairs = diplococci; adjacent sides are flattened together like coffee beans (really does look like coffee beans)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how are N. gonorrhoeae and N. meningitidis related?

A

they’re closely related

> 80% amino acid similarity

12% of the genes showed no significant homology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

in what media do N. gonorrhoeae grow in?

A

requires complex media and controlled conditions for growth (chocolate or Thayer-Martin agar)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is difference in the pathogenesis of N. gonorrhoeae and N. meningitidis?

A

mechanisms for pathogenesis by N. gonorrhoeae and N. meningitidis are virtually the same and share many virulence factors

the major difference is that N. meningitidis has a capsule, but not N. gonorrhoeae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what role do pili play in N. gonorrhoeae and N. meningitidis?

A

both posses multiple types of pili that mediate different functions

type IV pilus allows initial binding to CD46 on surface of non-ciliated epithelial cells – it has multiple subunits that confer extension, adhesion and contraction

pilus then contracts to bring bacteria close to host cell

Neisseria does not initially bind to ciliated epithelial cells

pili exhibit phase variation and antigenic variation which allows for re-infection because the can evade previous antibody response!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the function of Opa proteins in N. gonorrhoeae and N. meningitidis?

A

Opa proteins mediate tight adherence to epithelial cell

although both species possess Opa proteins, only N. gonorrhoeae become opaque

the bacteria possess multiple alleles that promote binding to different host molecules = Vitronectin, fibronectin, heparan sulfate proteoglycan, CEACAM1, 3, 5 and 6

binding also sends signals that promote invasion of host cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is the function of pili and opa proteins?

A

they’re important for attachment of bacteria to host cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what do porin proteins of virulent Neisseria III do?

A

they are integral outer membrane pores that are essential to acquire nutrients

they also interfere with neutrophil function which facilitates invasion of epithelial cells

this promotes resistance to complement-mediated killing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what are the general characteristics of virulent Neisseria III?

A
  1. release peptidoglycan fragments (NAG-NAM) which slows down or kills ciliated epithelial cells and decreases mucociliary clearance
  2. porin proteins that interfere with neutrophil function and facilitates invasion of epithelial cells
  3. iron acquisition proteins that produce a number of receptors for human iron-binding molecules like transferrin, lactoferrin, hemoglobin – the bacteria can then sequester iron from these complex because iron is essential for neisseria species

do not produce siderophores! = a molecule which binds and transports iron in microorganisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are the general characteristics of virulent Neisseria IV?

A
  1. lipooligosaccharide (LOS)
  2. IgA protease
  3. possess several mechanisms for serum resistance (evade complement)
  4. virulent Neisserial strains are phagocytosed and compartmentalized by neutrophils, but often escape intracellular killing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is the function of lipooligosaccharide in neisseria IV?

A

LOS is similar to LPS but lacks the O-antigen polysaccharide

it possesses endotoxin activity that elicits inflammatory response

it’s also Is responsible for the tissue damage associated with Neisserial diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is the function of IgA protease in neisseria IV?

A

it cleaves IgA at the hinge point to produce inactive Fab and Fc fragments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

which mechanisms does Neisseria IV possess for serum resistance?

A

neisseria IV can evade complement by:

  1. Sialylated LOS binds host Factor H
  2. Different porins bind host Factor H and/or C4bp
  3. Capsule (N. meningitidis) is resistant to complement deposition
  4. Patients with deficiencies in C5-C9 are very susceptible to Neisserial infections (especially N. meningitidis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what do Neisseria do in the body?

A

Neisseria invade epithelial cells, kill them, are taken up and persist within PMNs, and eventually establish infection in subepithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Neisseria gonorrhoeae vingette

A

18 year old male has 48 hour history of painful urination with a yellowish penile discharge

he returned 2 days ago from Daytona Beach, where he had been sexually active with several female partners during Spring Break – he denied previous such episodes and said he was in good health

PE found purulent urethral discharge with no sign of genital ulcers, rash, or skin ulcers. Inguinal lymph nodes were not enlarged or tender

gram stain and culture showed gram (-) diplococci with PMN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is the 2nd most commonly reported infectious disease in the US?

A

Neisseria gonorrhoeae

number of cases are probably underreported because cases are often asymptomatic especially in women and they can remain asymptomatic for months to years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what does untreated gonorrhea infection lead to?

A

severe reproductive complications like:

  1. pelvic inflammatory disease (PID)
  2. can lead to tubal-factor infertility and cases of ectopic pregnancy

can also have adverse outcomes for children born to infected mothers:
1. blindness

  1. joint infection
  2. septicemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what’s the national gonorrhea control program?

A

increased use of barrier contraception after the onset of the HIV epidemic probably helped in gonorrhea control

numbers of cases has leveled over past years, but may be seeing increases due to antibiotic resistance

30
Q

which populations commonly have gonorrhea?

A

the actual prevalence of gonorrhea depends on the characteristics of the population studied

  1. young age is the factor that is most strongly associated with infection
  2. Southeastern U.S currently has highest rate
  3. African-American heritage
  4. Inconsistent use of barrier contraceptive methods

also historically, reported cases for gonorrhea infections is higher in men – men are also more likely to exhibit symptoms

but actual incidence is currently similar between sexes

31
Q

how is N. gonorrhoeae transmitted?

A

transmitted mainly during vaginal or anal sex

but also possible through oral sex

32
Q

which cells does gonorrhea infect? what happens?

A

it initially infects the single-cell columnar epithelial layers of:

  1. endocervix of women = vaginal epithelium is too acidic
  2. urethra for men = burning sensation when urinating

then it invades, transcytoses and establishes infection killing the epithelial cells

when this happens, there’s a large influx of PMNs, shedding of epithelial cells and purulent discharge

if left untreated, symptoms will cease and asymptomatic infection can establish

33
Q

are gonorrhea infections symptomatic or asymptomatic?

A

95% of men have acute symptoms

50-80% of women are asymptomatic

subclinical infection with women is DANGEROUS because gonorrhea can be passed along to child during birth

34
Q

what causes PID?

A

PID = pelvic inflammatory disease

˜45% of women with gonococcal cervicitis will develop an ascending infection into fallopian tubes and this is the pre-requisite to PID

35
Q

what does PID cause?

A

PID can cause infertility or more commonly, ectopic pregnancy – PID is a major cause of sterility and ectopic pregnancy and is the major cause of maternal death during pregnancy

also infection of the fallopian tubes produces severe salpingitis, adhesions, scarring and tubal occlusions

36
Q

what causes dissseminated gonoccoccemia infections? what are they?

A

although N. gonorrhoeae infection are usually localized, 1-3% of infected women develop disseminated infections usually from untreated asymptomatic infections (this is less likely to happen in men)

this is when the bacteria travel through blood to seed different tissues = bacteremia, fever, shaking chills

37
Q

what is a common symptom of gonorrhea bacteremia?

A

skin lesions are seen in 75% of patients with bacteremia

usually painless but number between 5-40

usually on extremities and trunk

wide variety of lesions! = vesicles, bullae, urticaria, etc.

bacteria usually can not be cultured from lesions

38
Q

is there a gonorrhea vaccine?

A

there is currently no vaccine for gonorrhea

also lasting immunity rarely develops after gonorrhea infection becaues most surface antigens have multiple alleles…

so that means people can be re-infected by different strains…

39
Q

how do you detect gonorrhea?

A
  1. gram stain of urethral or cervical discharge –> look for gram (-) diplococci inside of or around neutrophils (cervical samples are less reliable)
  2. growth on chocolate agar then test colonies for oxidase positive gram (-) diplococci
  3. urine tests (less reliable)
  4. PCR from endocervical or urethral swabs
40
Q

how do you treat gonorrhea?

A

historically, β lactams were the treatment of choice, but more recently the 3rd generation cephalosporins have been DOC

currently, only certain 3rd generation cephalosporins are favored together with something that also treats Chlamydia = ceftriaxone together with either oral doxycycline or azithromycin (for chlamydia co-infection)

*azithromycin may be favorable over doxycycline because only a single does and less bacterial resistance

after a week, test to see if the patient has been cured!

41
Q

what drug is no longer recommended as DOC for gonorrhea?

A

Cefixime orally (single dose) has just been “de-recommended” as first choice

this is because of increased resistance in clinical isolates that indicate that may not achieve MIC via oral route

it can still be an alternative treatment though

42
Q

who is recommended to get annual screenings for N. gonorrhoeae infections?

A
  1. all sexually active women aged <25 years
  2. older women at increased risk for infection
  3. those who have a new sex partner
  4. more than one sex partner
  5. a sex partner with concurrent partners
  6. sex partner who has an STI

additional risk factors include:

  1. inconsistent condom use among persons who are not in mutually monogamous relationships
  2. previous or coexisting sexually transmitted infections
  3. exchanging sex for money or drugs
43
Q

what is the pathology of N. gonorrhoeae?

A

N. gonorrhoeae is acquired via sexual contact and establishes infection in the urogenital tract

initial interaction with non-ciliated epithelial cells results in cellular invasion –> infection often leads to inflammation and PMN influx

N. gonorrhoeae is engulfed by PMN are secreted in PMN-rich exudate

toxic damage to ciliated epithelial cells of mucosal surfaces can be caused by: TNF from phagocytes or gonococcal products like PG and LOS

different molecular mechanisms are involved during the establishment of gonococci on the mucosal surfaces of males and females

infection of the lower female genital tract is typically asymptomatic

44
Q

FLASHCARD: microbiology, pathology, epidemiology, clinical symptoms, diagnosis and treatment of neisseria gonorrhea

A

MICROBIOLOGY: Gram – cocci, facultative anaerobe, non-motile, NO capsule, often seen in neutrophils.

PATHOLOGY: Causes venereal disease. Bacteria introduced via sexual contact. Preferentially infect columnar epithelial layers (cervix in women, urethra in men) to cause persistent infection. Large sloughing of epithelium and immigrating neutrophils produce purulent discharge. Women are often asymptomatic whereas men usually symptomatic, particularly when urinating. If untreated, women will often develop an ascending infection into fallopian tubes, eventually causing asymptomatic (usually) inflammation that damages the fallopian tubes and associated tissues/organs.

EPIDEMIOLOGY: Vast majority of the cases in the US are acquired via sexual contact (include oral & anal). Most common in ages 15-25 for both men & women. Also predisposed to lack of barrier contraception, new or multiple sexual partners, African heritage, & living in the South/Midwest US.

CLINICAL: Women are often subclinical; discharge only apparent during exam. Men develop urethritis that causes painful urination and strangury, along with discharge. Untreated women often develop chronic infection in fallopian tubes & associated tissue, leading to pelvic inflammatory disease. Can lead to blockage of fallopian tubes, with infertility and/or develop ectopic pregnancy.

DIAGNOSIS: Gram stain of urethral/cervical discharge shows Gram-negative cocci, sometimes within neutrophils. Can culture on chocolate agar to see oxidase positive colonies. Most commonly, detect in discharge or scrapings via PCR to detect bacterial DNA.

TREATMENT: Clinical strains have become very antibiotic resistant. Currently, only certain 3rd generation cephalosporins (ceftriaxone) are favored, together with something that also treats potential Chlamydia co-infections. Follow-up patients to determine if antibiotic-resistant.

45
Q

neisseria meningitidis vingette

A

-year-old white male college student with 12-hour history of high fever, chills, stiff neck, and severe headache

after arriving at ED, he vomitted twice, loked confued and highly agitated

was admitted and within 2 hours developed purpuric skin lesions

had received all immunizations and otherwise healthy

begin high dose cefotaxime & vancomycin

lab tests showed CSF contained high WBC with 91% PMN, gram (-) diplococci

also blood and CSF cultures grew Gram (-) diplococci

46
Q

how old are most people with neisseria meningitidis?

A

most endemic cases are between 0.5 and 2 years of age

this is after maternal antibody is lost and before their own immunity has developed

but in the US, 75% of epidemic cases are over the age of 2

47
Q

what time of the year are neisseria meningitidis most common?

A

december/january

48
Q

what is the meningitis belt?

A

Sub-Saharan African countries (Guana, Niger, Chad, etc..)

occurs during the dry season = march-may maybe because there’s better transmission or patients are more stressed in dry conditions

49
Q

what is the meningitis vaccine project?

A

Started in response to the 1996-1997 outbreak

develop, test, license, and introduce an affordable conjugate vaccine for Africa

In Dec. 2010, start 1st immunization with MenAfriVac against serotype A

50
Q

how is neisseria meningitidis differentiated from other neisseria infections?

A

differentiated from other Neisseria species by its production of acid from oxidation of glucose and maltose

however it does share the most virulence factors with N. gonorrhoeae

51
Q

what is the most important unique virulence factor of neisseria meningitidis?

A

the capsule!

it produces resistance to phagocytosis, complement deposition, and intracellular killing by phagocytes

it includes different sialic acid polymers which promote association with factor H

there’s 13 capsular serotypes

52
Q

how does the meningococcal capsule act as a virulence factor?

A

capsules of several ‘disease’ serogroups contain sialic acid

the sialic acid in type B is identical to those produced in humans

sialic acid is present on human endothelial cells and erythrocytes and it inhibits the complement cascade in the vascular compartment

so this means that sialic acid containing capsules on the surface of the meningococcus and other pathogens down-regulate the activity of the alternative pathway

this reduces amplification of C3b production

the mechanism for this is unknown, but believed due to ability to bind host Factor H & fHLP

53
Q

what is the reservoir of N. meningitidis?

A

nasopharynx of healthy adults

1-40% carry Nm without developing disease

54
Q

when does epidemic spread of N. meningitidis occur?

A

epidemic spread occurs when new serogroup is introduced into immunologically naïve population

55
Q

how is N. meningitidis transmitted?

A

respiratory droplets

bacteria establishes intimate contact with non-ciliated mucosal epithelial cells of the upper respiratory tract

it may enter the cells briefly before migrating back to the apical surfaces of the cells for transmission to a new host

56
Q

which groups are at risk for N. meningitidis?

A

Infants, household contacts of patients with meningococcal disease, military personnel and college students living in dormitories

Close contact with patients with meningococcal disease increases the risk of infection by 500-2000 fold

risk factors = age, crowded living conditions, complement deficiency, smoking recent URT infection, smoking

57
Q

how can smoking cause N. meningitidis?

A

it cause damage to respiratory epithelium which in turn facilitate Nm crossing the respiratory mucosa and reach the blood stream

58
Q

what’s the incubation period of N. meningitidis?

A

onset of symptoms is ABRUPT

incubation period is ~3-4 days

59
Q

what are the clinical symptoms of meningitis?

A

fever, headache, vomiting, neck stiffness, altered mental status

if left untreated: mortality rate of 100%

still poorly understood how N. meningitidis crosses the blood brain barrier to reach meninges – capsule is involved

60
Q

what are the clinical symptoms of meningococcal fulminant sepsis

A

septicemia, septic shock

characterized by appearance of small skin petechial lesions/purpuric rash

Waterhouse-Friderichsen syndrome = a massive, usually bilateral, hemorrhage into the adrenal glands caused by fulminant meningococcemia

fatality rate of 18-53%

61
Q

how does N. meningitidis cause infection?

A

bacteria establishes intimate contact with non-ciliated mucosal epithelial cells of the upper respiratory tract

may enter the cells briefly before migrating back to the apical surfaces of the cells for transmission to a new host

besides transcytosis, N. meningitidis can cross the epithelium either directly following damage to the monolayer integrity or through phagocytes in a ‘Trojan horse’ manner

asymptomatic carriage is common in healthy adults because bacteria that enter the body by crossing the epithelial barrier are eliminated

but in susceptible individuals, once inside the blood, N. meningitidis may survive, multiply rapidly and disseminate throughout the body and the brain – causes vascular damage and skin rash

meningococcal passage across the brain vascular endothelium (or the epithelium of the choroid plexus) may then occur resulting in infection of the meninges and the cerebrospinal fluid

62
Q

how do you diagnose meningococcal disease?

A

requires isolation of N. meningitidis from sterile site (CSF, blood) – then you should find gram (-) diplococcus associated with PMNs

63
Q

how do you determine the capsular serotype of meningitis?

A
  1. agglutination test (latex beads coated with antibodies)
  2. PCR

amplify/sequence ctrA gene which is present in serotype B, C, Y, W135 but not A

amplify serotype A-specific gene sac

64
Q

how do you treat meningococcal?

A
  1. before specific diagnosis:
    3rd gen cephalosporin & vancomycin

Doxycycline during tick season

  1. after diagnosis:

IV ceftriaxone or penicillin (7 days)

65
Q

is there a meningitis vaccine?

A

yes = Aventis Pasteur Merieux

it’s a mixture of 4 capsular polysaccharides

it elicits Abs that opsonize Nm

but it’s poorly effective in children under 3

also it’s NOT a conjugated vaccine that does not elicit long lasting immunity or lead to herd immunity

does not contain serotype B!!!

66
Q

which groups are recommended to get menomune (MPSV4) vaccine?

A

not recommended for routine use in general population

it’s appropriate for risk groups like:

  1. military
  2. people who might have been infected during outbreaks
  3. travelers to regions of the world where meningococcal disease is common
  4. Anyone with removed or damaged spleen
  5. anyone with complement deficiency
  6. lab workers routinely exposed to Nm
67
Q

what is MCV4?

A

Menactra meningococcal conjugate vaccine!

contains the same 4 meningococcal PSs along with diphtheria toxoid with high effectivity and no side effects

but the difference is that it elicits an Ab response that appears to be more durable and rude carriage

based on these findings, the CDC considered recommending the conjugate vaccine beyond the high risk groups

this is now the preferred vaccine for people 2-55

68
Q

what is the current vaccine recommendation?

A

MCV4 is now the preferred vaccine for people ages 2 through 55

adolescents should be routinely immunized at ages 11 to 12 years and receive a booster at age 16 years

69
Q

what type of vaccination series should people at risk for meningococcal disease get?

A

persons at increased risk for meningococcal disease should receive a 2-dose primary series 2-months apart. Then boosters every 5 years

ex. persons with terminal complement component deficiencies
ex. persons with anatomic or functional asplenia

other “older” unimmunized people that should get 2-dose primary include:

  1. microbiologists that are routinely exposed to isolates of N. meningitidis
  2. travelers to or residents of countries in which N. meningitidis meningitis is hyperendemic or epidemic
  3. persons entering the military
70
Q

FLASHCARD: microbiology, pathology, epidemiology, clinical, diagnosis, treatment of neisseria meningitidis

A

MICROBIOLOGY: Gram – cocci, facultative anaerobe, non-motile, capsule, often seen within neutrophils

PATHOLOGY: Can be normal flora in throat, where kept in check by antibodies. However, new strains often become invasive to enter bloodstream or cross the blood-brain barrier. Carbohydrate capsule is important virulence mechanism, as helps evade immunity and cross blood-brain barrier. Inability to clear leads to outgrowth in blood and/or meninges and leakage from vessels, leading to sepsis and/or meningitis mediated via bacterial LOS.

EPIDEMIOLOGY: Common flora of throat. Disease usually occurs when contract a new strain (most common in military or college age; new host have no antibodies to capsule of new strain), those who have respiratory tract infect or smoking compromise mucosa, or have complement deficiency.

CLINICAL: Become sick very quick and untreated can die within 24-48h of symptoms. Initially develop high fever, chills, stiff neck, and severe headache. Become disorientated and agitated. Develop diffuse rash that rapidly progress to larger pupuric skin rash. Eventually leads to sepsis and/or meningitis; untreated is fatal.

DIAGNOSIS: Must diagnose quickly to start treatment. Initial diagnosis is on clinical symptoms and epidemiology. Gram stain of blood or CSF can visualize Gram-negative cocci alone or within neutrophils. Eventually determine serotype for reporting purposes.

TREATMENT: Treatment before diagnosis is 3rd gen cephalosporin & vancomycin. After diagnosis, use iv ceftriaxone or penicillin. Are 2 types of vaccines approved: MCV4 possesses 4 serotypes of capsule conjugated to protein carrier (preferred). Alternative (MPSV4) have the 4 serotypes of capsule, but no protein carrier (alternative). Infection with B serotype are not covered by the vaccine.

71
Q

what is the microbiology of moraxella catarrhalis?

A

Gram-negative diplococcus bacterium

human-specific

oxidase positive

non-encapsulated

can be observed within PMNs during Gram-stain of samples

72
Q

what is moraxella catarrhalis?

A

commensal organism but an opportunistic pathogen

it’s responsible for approximately 15-20% of otitis media (OM) cases in U. S.

80% of U.S. children will have at least one episode of OM by 3 years of age

repeated bouts of OM can lead to the retardation of a child’s social and educational development

it also causes up to 30% of bacterial exacerbations in patients with chronic obstructive pulmonary disease (COPD)

there is no vaccine and antibiotic resistant strains are beginning to emerge

ID Week 4 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions