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ID Week 3 > ICL 2.3: Mycoplasma & Ureaplasma > Flashcards

ICL 2.3: Mycoplasma & Ureaplasma Flashcards

1
Q

what bacteria classification are mycoplasma and ureaplasma?

A

they don’t have a cell wall!

so they can’t be classified as gram +/- or have a shape

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2
Q

what are the major species of mycoplasma?

A
  1. genitalium
  2. hominis
  3. pneumoniae
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3
Q

what are the major species of ureaplasma?

A
  1. urealyticum
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4
Q

how big are mycoplasma?

A

smallest known free-living organisms

one of the smallest genomes of self-replicating organisms

2 – 3× the size of a medium-sized virus like adenovirus but half the size of e. coli

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5
Q

do mycoplasma have a cell wall?

A

NO

they are bacteria with no peptidoglycan cell wall

**this means they won’t gram stain!!!

instead they have a triple cell membrane

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6
Q

what is the cell membrane of mycoplasma made of?

A

mycoplasma doesn’t have PG cell wall

instead they have triple cell membrane and no cell wall

the cell membrane contains sterols, including cholesterol

***it’s the only bacterial membrane that contains cholesterol!!!

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7
Q

do gram positive bacteria have a cell wall?

A

yes

they have 1 cell membrane plus a thick cell wall made of peptidoglycan

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8
Q

do gram negative bacteria have a cell wall?

A

yes

they have 2 cell membrane layers plus a thin cell wall made of peptidoglycan

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9
Q

where are mycoplasma most commonly found?

A
  1. plants
  2. animals
  3. insects
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10
Q

what are the two important genuses in the mycoplasmataceae family?

A
  1. mycoplasma

2. ureaplasma

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11
Q

which mycoplasmataceae species cause human disease?

A
  1. mycoplasma pneumoniae
  2. mycoplasma genitalium
  3. mycoplasma hominis
  4. ureaplasma urealyticum
  5. mycoplasma fermentans, mycoplasma penetrans
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12
Q

what is the disease and site associated with mycoplasma pneumoniae?

A

site = respiratory tract

disease:
1. primary atypical pneumonia

  1. tracheobronchitis
  2. pharyngitis
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13
Q

what is the disease and site associated with mycoplasma genitalium?

A

site = genitourinary tract

disease:
1. urethritis

  1. cervicitis
  2. endometritis
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14
Q

what is the disease and site associated with mycoplasma hominis?

A

site: 1. genitourinary tract
2. oropharynx

disease:
1. pelvic inflammatory disease

  1. neonatal infections
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15
Q

what is the disease and site associated with ureaplasma urealyticum?

A

site = genitourinary tract

disease:
1. urethritis

  1. neonatal infections
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16
Q

what is the disease and site associated with mycoplasma fermentans, mycoplasma penetrans?

A

site = genitourinary tract

disease = possible HIV cofactor

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17
Q

are mycoplasmidae aerobic or anaerobic?

A

fastidious aerobic bacteria

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18
Q

what do mycoplasmidae need for growth?

A
  1. exogenous lipids
  2. sterols
  3. vitamins
  4. AA

**special media (SP4) with serum is needed to grow them in a lab; isolation isn’t commonly performed

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19
Q

how can you grow mycoplasmidae in a lab?

A

identification/diagnosis often fails because they’re very difficult to grow

it takes 2 − 6 weeks before colonies are visible

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20
Q

how can you see mycoplasmidae?

A

they’re really hard to grow in the lab

instead they’re viewed by dissecting microscope

collonies have “freid egg” appearance

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21
Q

how long does it take to start seeing symptoms of mycoplasma infections?

A

prolonged (1-3 wk) asymptomatic colonization is typical

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22
Q

how does m. pneumoniae cause infections? what’s the pathology?

A
  1. M. pneumoniae attaches to the ciliated respiratory epithelial cells

there are unique attachment structures at one end of the mycoplasma called P1 adhesin

P1 adhesin binds to TLR2 on respiratory epithelial cells at the base of the cilia

  1. after attachment, ciliary movement is stopped
  2. mycoplasma secrete H2O2 and O2-
  3. CARDS toxin is released
  4. cilia desquamate and RBCs lyse

lack of cilia leads to impaired airway clearance

this leads to a vigourous host immune response with lymphocytes, antibody production and cutokines –> *immune response correlates with disease severity

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23
Q

what is P1 adhesin?

A

it’s a unique attachment structure at one end of the mycoplasma that binds to TLR2 on respiratory epithelial cells

P1 adhesin can undergo antigenic variation!

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24
Q

what is CARDS toxin?

A

it’s released by mycoplasma pneumoniae

it causes epithelial cell death in the respiratory tract

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25
Q

how is mycoplasma pneumoniae transmitted?

A

transmitted person-to-person via respiratory droplets

*1-3 week interval between diseases in individuals; 20% are asymptomatic

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26
Q

which populations are at risk for m. pneumoniae infections?

A

it’s transmitted person-to-person via respiratory droplets so infection spreads among families and closed populations

  1. military
  2. colleges*
  3. hospitals
  4. religious communities
27
Q

what time of the year are m. pneumoniae infections common?

A

year round disease, but peak incidence in fall and winter

there are epidemics every 4-8 years; we don’t know why but maybe it’s because of P1 variation?

28
Q

what is walking pneumonia?

A

caused by m. pneumoniae

aka atypical pneumonia

it’s pneumonia that fails to respond to penicillin/β-lactams and not easily isolated

29
Q

what’s the most common cause of pneumonia in young adults?

A

m. pneumoniae

recent studies suggest that the highest rates of mycoplasma-induced pneumonia is in 15-20 yr olds and elderly (>60 yr old)

30
Q

what is the incubation period of m. pneumoniae?

A

1-3 weeks

31
Q

what are the symptoms m. pneumoniae infection?

A

after 1- 3 week incubation period, there is gradual onset of low-grade fever, malaise, headache, dry cough, little sputum

cough is severe, often painful, but non-productive

chills present but rigors are rare

sometimes patients are anemic

32
Q

what would the PE of a an m. pneumoniae infection show?

A

PE often unremarkable

but chest X-ray reveals interstitial infiltrates, typically in lower lobe

microphage and neutrophil infiltrates with hemolysis!

33
Q

do mycoplasma infections stimulate antibody production?

A

yes

Ab develop early in disease (7 - 10 days after infection) and persist for months

34
Q

what are the types of antibodies generated during a m. pneumoniae infection?

A
  1. anti-mycoplasma antibodies

protective immunity generally develops after infection but immunity is not long lasting

  1. autoantibodies

during an m. pneumoniae infection there are IgM antibodies which binds to RBC surface antigen I causing agglutination and lysis at cold temperaturs = hemolytic anemia

there is also cold agglutinin antibody in 60% of patients

35
Q

what is the Cold agglutinin test?

A

done to test for m. pneumoniae infections

  1. take 1 cc of blood in a glass tube with an anticoagulant (citrate) and place on ice for 3 minutes
  2. RBCs agglutinate on the sides of the tube due to IgM antibodies at 4 °C

it looks grainy

  1. rewarm the tube to 37°C and the agglutination disappears

the issue is that this test is positive in only 50% of mycoplasma infections

plus this result could also occur during influenza and adenovirus infections

36
Q

what are the extrapulmonary complications involved with m. pneumoniae infections?

A

mycoplasma induces autoantibodies against important things in your body like RBCs etc.

  1. rash
  2. nonspecific myalgia and arthralgia
  3. CNS complications
  4. Raynaud’s phenomenon
  5. cardiac abnormalities
  6. Guillain-Barre syndrome
  7. asthma association
  8. COPD association
37
Q

mycoplasma induces autoantibodies against what?

A
  1. RBCs
  2. Myosin
  3. Keratin
  4. Fibrinogen
  5. CNS components
  6. Kidney
  7. Smooth muscle
  8. Lung
38
Q

how do m. pneumoniae cause rash?

A

damage to microvasculature and dermal layers

*Erythema multiforme (mild)

Stevens-Johnson syndrome (severe)

sometimes referred to as target lesions

rash happens in 25% of patients

39
Q

what types of CNS complications does m. pneumoniae cause?

A

encephalitis most common in older adults and children

antibodies against myelin detected in 100% of M. pneumoniae patients with CNS complications

other CNS complications including cerebellar syndrome (ataxia), meningitis, confusion, cranial nerve palsies, etc.

0.1% of all patients; 6-7% of hospitalized patients

40
Q

what is Raynaud’s phenomenon?

A

transient, reversible vasospasm of digit blood vessels upon exposure to cold

41
Q

which cardiac abnormalities can be caused by m. pneumoniae?

A

1-8% of patients

  1. pericarditis
  2. myocarditis
  3. conduction defects
  4. heart failure
42
Q

how is m. pneumonia associated with asthma?

A

bacteria is blieved to over-stimulate immune system

43
Q

in what patient population are m. pneumoniae infections more severe?

A

disease is more severe in patients with hemoglobinopathies

ex. digital necrosis in sickle cell patients

44
Q

how do diagnose m. pneumoniae infections?

A
  1. clinical findings
  2. serology
  3. cold agglutinin test (not very specific)
  4. culture of sputum (hard to obtain)
  5. antigen detection (P1 adhesin)
  6. PCR/DNA probes (not widely available)
45
Q

what are the clinical findings of m. pneumoniae infections?

A

Fever, malaise, headache, dry cough, little sputum, chest pain

X-ray: lower lobe, diffuse infiltrates, one lobe, hilar adenopathy

46
Q

what is the serology test you can do to diagnose m. pneumoniae?

A

you’re looking to see if there are antibodies against bacterial antigens

titer increase

47
Q

what are the three classes of antibiotics used to treat m. pneumoniae?

A
  1. macrolides*
  2. tetracyclines
  3. quinolones

you can’t use any antibiotics that target the cell wall

48
Q

which macrolide drugs are used to treat m. pneumoniae?

A

erythromycin

azithromycin

49
Q

which tetracycline drugs are used to treat m. pneumoniae?

A

doxycycline

50
Q

which quinolone drugs are used to treat m. pneumoniae?

A

levofloxacin

51
Q

how do you treat m. pneumoniae?

A

with either macrolides, tetracyclines or quinolines

penicillins and cephalosporins inactive

treat for 7-10 days

antibiotic resistance is uncommon but there is some macrolide resistance recently

treating with antibiotics shortens course of illness and reduces transmission to others

52
Q

how are m. homins/genitalium and ureaplasma transmitted?

A

vertical transmission: colonization in humans begins with passage through infected vaginal canal at birth

colonization decreases beyond age 2 and increases again after puberty

colonization rate increases with the number of sex partners

they all cause diseases in the genitourinary tract

53
Q

what are the symptoms of m. homins/genitalium and ureaplasma infections?

A

in neonates, affects lower respiratory tract and CNS

in adults, diseases include non-gonococcal urethritis, post-abortion/postpartum fever, cervicitis, endometritis, pelvic inflammatory disease (PID), pyelonephritis (rare)

54
Q

what is PID?

A

PID = pelvic inflammatory disease

*M. hominis accounts for approx. 10% of PID cases

usually more than one organism involved (polymicrobic infection)

55
Q

which bacteria is most often the cause of PID?

A

m. hominis

PID = pelvic inflammatory disease

56
Q

what is postabortal/postpartum fever?

A

self-limiting episode of fever without sepsis 24 hours after delivery or abortion (spontaneous or therapeutic)

m. hominis is recovered from blood cultures in 10% of cases

57
Q

which bacteria causes non-gonoccal and non-chlamydial urethritis?

A

ureaplasma accounts for approx. 20% of cases

M. genitalium accounts for rare urethritis cases

58
Q

how do you diagnose m. homins/genitalium and ureaplasma infections?

A
  1. clinical presentation

2. culture from blood/urine

59
Q

how do you treat m. homins/genitalium and ureaplasma infections?

A

Ureaplasma: Use erythromycin; resistant to tetracyclines

M. hominis: Use clindamycin; resistant to erythromycin and tetracyclines

60
Q

which bacteria is responsible for this?

A 21-year-old female developed fever, headache, and a gradually progressive dry cough. Over the next 2 days, her cough worsened, producing small amounts of clear sputum.

History: Previously healthy. Her 19-year-old brother had similar symptoms 2 weeks earlier.

Physical exam: Slightly pale appearance, mild pharyngeal erythema, chest exam was normal (no rales)

Lab results: WBCs 8,600/µL

CXR: bilateral patchy infiltrates

A

m. pneumoniae!

61
Q

FLASHCARD: micro, epidemiology, clinical features, diagnosis and treatment for m. pneumoniae

A

MICRO: gram-indeterminant; no PG; 3 membranes; smallest bacterium; difficult to grow in lab; media needs lipids/sterols; fried-egg appearance; P1 adhesin with antigen variation

EPIDEMIOLOGY: Respiratory pathogen; < 20 yrs old; atypical or walking pneumonia; 2-3 week incubation after close contact with 1°

Clinical: Gradual onset of low-grade fever, malaise, headache, dry cough, patchy infiltrates on CXR

Diagnosis: clinical findings and serology; cold agglutinin

Treatment: Erythromycin or doxycycline

62
Q

FLASHCARD: clinical features and treatment for m. hominis/genitalium

A

M. hominis

Clinical: PID, neonatal infections (respiratory or CNS), postpartum or postabortal fever

Treatment: clindamycin (erythromycin resistant)

63
Q

FLASHCARD: clinical features and treatment of ureaplasma

A

Clinical: non-gonococcal urethritis, intrapartum infections

Treatment: erythromycin

ID Week 3 (25 decks)

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