Small G- Pathogens (chlamydiae, rickettsiae, ehrlichia) Flashcards

1
Q

how small is chlamydiae?

A

.25 micrometers- .8 micrometers

just at limit of light microscopy
similar in size to some viruses

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2
Q

is chlamydia G+ or G-?

A

G-

LPS outer membrane and cytoplasmic membrane

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3
Q

does chlamydiae contain peptidoglycan?

A

no peptidoglycan (murein) in cell walls

  • genes are present
  • structure analogous to murein can be seen by EM
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4
Q

what type of pathogen is chlamydiae?

A
  • obligate intracellular pathogen (cannot grow outside of host): grow only inside cells or on live tissues
  • humans, animals, insects, protozoa
  • small genomes (1-1.2 megabases)

*“energy parasites”: depend on host for ATP, auxotrophic for some amino acids

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5
Q

does chlamydiae have a simple development cycle?

A

NO,

  1. for infection
  2. for replication (metabolically active)
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6
Q

what are the 4 species formally recognized in chlamydia classification?

A
  1. c. trachomatis (3 biovars: multiple strains in each)
  2. c. pneumoniae
  3. c. psittaci
  4. c. pecorum
  • 1 & 2 primarily found in human pathogens
  • 3 &4 primarily animal pathogens, but some capable of causing disease in humans
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7
Q

flip for some general facts on chlamydial infections

A
  • leading cause of preventable blindness in THE WORLD
  • the MOST common agents of sexually transmitted bacterial infections
  • speculation that every living adult has had pneumonia (“walking”) caused by c. pneumoniae
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8
Q

how is chlamydia spread?

A
  • droplet or direct contact infection
  • 4 F’s:
    • fingers
    • flies
    • fomites
    • fornication
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9
Q

where does chlamydia infect?

A

mucosal epithelial cells

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10
Q

is chlamydia infection localized or systemic?

A

localized

-eyes, lungs, genitalia

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11
Q

c. trachomatis infections are infections of the genital tract, what do they cause specifically in men and women?

A

men: prostitis, epididymitis
women: cervicitis, PID, premature births, pelvic pain, newborn eye/lung infections
both: urethritis, infertility, procitis, arthritis

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12
Q

is c. trachomatis usually asymptomatic in men or women?

A

WOMEN

chronic and repeat infections can cause sterility and or ectopic pregnancy

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13
Q

are c. trachomatis infections acute or chronic?

A

either!

there is a silent period- orgs location unknown

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14
Q

T/F: asymptomatic carriage results in most damage and scarring

A

TRUEIE

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15
Q

what two things can happen to infants during birth if the mother has chlamydia?

A

infection leading to:

  • conjunctivitis
  • pneumonia
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16
Q

how is chlamydiae internalized into a cell?

A
  • extracellular
    • elementary body (EB) transit form: not metabolically active
  • entry of EBs into epithelial cells: masquerade as nutrients, growth factors, hormones to bind to specific receptors
  • internalized by receptor-mediated endocytosis (endosomal vesicle that bacteria modifies for growth)
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17
Q

how do the EBs modify the endocytic vesicle?

A
  1. maintain pH above 6.2
  2. prevents vesicle from fusion with lysosomes

*vesicle is also modified with host components (glycolipids) for camouflage

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18
Q

what is a RB (reticulate body)?

A

metabolically active, in inclusion bodies get released from epithelial cells by exocytosis when reach a certain threshold

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19
Q

infectious EB change into larger intracellular active organisms (RB) which do what?

A
  • synthesize molecules using host metabolites and energy

- divide by binary fission

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20
Q

how to RB uptake nutrients?

A
  • tube-like structures (“drinking straws”) that allow them to feed on the eukaryotic host cell without leaving the inclusion vacuole
  • 18-23 hollow tubes that protrude from bacterial cell cytoplasm into host cell cytoplasm
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21
Q

what is trachoma?

A

c. trachomatis strains that cause:
- inflamm of conjunctiva, can cause blindness, scarring cornea

-spread by direct contact with eye, nose,and throat secretions from affected individuals, or contact with objects such as towels and/or washcloths

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22
Q

what is lymphogranuloma venerum?

A
  • STD
  • systemic, invasive infection apparent in the lymph nodes that drain the genital tract
  • predominately in developing countries:
  • rare in US (200-400 cases)
  • more common in africa, asia, india, s. america
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23
Q

T/F: chlamydophila pneumoniae perhaps is the least prevalent chamydial pathogen in the human population

A

FALSE its the most

50% of people up to the age of 20 have been infected, 80% of older adults

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24
Q

what kind of body response is elicited in chlamydophila pneumoniae infections?

A
  • usually asymptomatic or acute respiratory response

- chronic resp. infections have been associated with asthma, CF, lung cancer

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25
Q

what type of condition is closely associated with chlamydophila pneumoniae infections?

A

ATHEROSCLEROTIC HEART LESIONS

40-100% of people with the previous have this infection
-usually not problematic unless you have some other disease with it

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26
Q

how are chlamydial infections treated?

A
  • metabolic active RB forms are targets of antimicrobials
  • four membrane layer to penetrate
    1. host cell plasma mem
    2. inclusion membrane
    3. chlamydial outer membrane
    4. chlamydial cytoplasmic mem
  • orgs grow slow so antibiotics must be maintained for long time
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27
Q

are EBs susceptible to antibiotic treatement

A

no because they are not metabolically active

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28
Q

rickettsiae is in what shape?

A

small G- rods that don’t stain well

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29
Q

what type of pathogen are rickettsiae?

A

obligate intracellular bacteria

30
Q

how are rickettsiae transmitted?

A

zoonoses: infections transmitted from animals to humans

31
Q

are rickettsiae energy parasites like chlamydiae?

A

NO they can synthesize some of their own ATP and are capable of INDEPENDENT METABOLISM but they prefer to use host’s

32
Q

do rickettsiae have flagella or endospores?

A

nopers

33
Q

how are rickettsiae cultured?

A
  • in animals
  • in embryonated eggs
  • in cell cultures in the lab
34
Q

describe rickettsiae transmission? what is the common vector?

A
  • rocky mountain wood tick and american dog tick
  • once infected, a tick can carry the pathogen for life
  • adult ticks feed on large mammals, including humans, larval and nymph forms feast on small rodents
  • most tick species require blood meal before developing into next life stage
  • during feeding as larva or nymph, ticks may become infected with the R. rickettsii bacteria
  • bacteria pass on the infection to humans as adult ticks, during blood meal
  • bacteria spread via bloodstream
35
Q

how do rickettsiae attach for spread and multiplication?

A
  • attach to VASCULAR ENDOTHELIAL CELLS (small blood vessels): induce endocytosis
  • once inside, presumably lyse the phagosome (PHOSPHOLIPASE) and enter the cytosol
  • engulfed through receptor mediated endocytosis
  • mode of exit from cell VARIES
36
Q

where does rickettsiae replicate?

A

cytosol

37
Q

how does R. prowazekii exit the cell?

A

lysis

38
Q

how does R. rickettsii exit the cell?

A
  • gets extruded from the cell through local projections (filopodia)
  • actin in the host cell associates with R. rickettsii and the actin helps to “push” the bacteria thru the filopodia
39
Q

how does R. tsutsugamushi exit the cell?

A
  • exits by budding thru the cell membrane
  • remains enveloped in the host cell membrane as it infects other cells
  • binds to neighboring cells=merging of membranes
40
Q

T/F: the degree of injury to the host is proportional to the number of intracellular bacteria

A

TRUE

41
Q

how are hemorrhagic spots created in infections with rickettsiae?

A

from lysis of cells resulting in the leakage of blood (rash)

42
Q

can rickettsiae travel to the heart and brain?

A

for sure

43
Q

T/F: 10% of patients will clear the infection even before antimicrobial treatment

A

75%%%%%

44
Q

what are the 3 typhus group fevers caused by?

A
  1. R. prowazekii
  2. R. typhi
  3. Orientia (formeraly rickettsia) tsutsugamushi
45
Q

describe the fever from R. prowazekii

A

typhus fever purplish rash, RECRUDESCENT typhus (reactivation of the dormant agent seen in US), transmitted by human lice

46
Q

describe the fever from R. typhi

A

more prevalent and wide spread, MURINE TYPHUS, transmitted by rats and rat fleas

47
Q

describe the fever from orientia tsutsugamushi

A

SCRUB TYPHUS, variety of antigenic types, NO RASH

48
Q

what type of pathogen is Ehrlichia?

A

obligate intracellular bacteria

49
Q

how is Ehrlichia transmitted?

A

by lone star tick

50
Q

what immune cells does Ehrlichia infect?

A
  • monocytes and macrophages

- human granulocytic ehrlichiosis (HGE) and human monocytic ehrlichiosis (HME)

51
Q

what symptoms arise from infection with Ehrlichia?

A

fever, malaise, headache and myalgia

52
Q

how does Ehrlichia develop first?

A

develops first as reticulate cells (RC) and then as dense-core cells (DC)

53
Q

how are rickettsioses diagnosed?

A
  • problematic:
  • during 1st visit, pts don’t typically have fever or rash, and may not be aware of tick bite
  • require eukaryotic cell cultures or innoculation of animals
  • handling is notoriously hazardous
  • clinical diagnostic tests
  • antibody titers
  • fluorescent antibody assay
  • complement fixation
  • latex agglutination
54
Q

what is mycoplasma?

A

-smallest organisms capable of growth on cell-free media

55
Q

what does mycoplasma require?

A

sterol (cholesterol) because bacteria don’t have a cell wall

56
Q

what characteristic appearance does mycoplasma have?

A

fried egg appearance

57
Q

does mycoplasma grow in small or large colonies and at a fast or slow rate?

A

small and slow

58
Q

what does mycoplasma lack?

A

cell wall (no murein) so not sensitive to penicilin

59
Q

where is mycoplasma found?

A

humans, other mammals, and birds

60
Q

what are the 4 mycoplasma species that cause disease?

A
  1. m. pneumoniae: prototype mycoplasma, primary atypical pneumonia
  2. m. genitalium
  3. m. hominis
  4. ureaplasma urealyticum
    * *2-4 are genitourinary tract infections
61
Q

T/F: some mycoplasmas are part of the normal human oral flora

A

TRUEEE

62
Q

what is the only reservoir of m. pneuominae?

A

humans

-unlike pneumococci, prolonged asymptomatic colonization is uncommon

63
Q

are m. pneumoniae infections contagious?

A

mild and moderately contagious

spread through close-contact group

passed by respiratory droplets

64
Q

describe “walking pneumonia.”

A

primary atypical pneumonia not cleared by penicillin, presents differently because just affecting respiratory epithelium

65
Q

what epithelium does m. pneumoniae adhere to?

A

respiratory epithelium: terminal adhesion structures, tip-mediated attachment organelle

66
Q

what are the main cells of the inflammatory response to mycoplasmas?

A

lymphocytes

67
Q

what is unusual about the spread of mycoplasmas?

A
  • largely limited to the respiratory mucosa that lines the airways
  • doesn’t get into the lung alveoli
  • bronchopneumonia
68
Q

do mycoplasmas cause a lot of tissue destruction?

A
  • no highly destructive of tissues, but ciliary function of bronchioles is impaired
    • tissue toxic substances may include H2O2
    • inflamm mediators
69
Q

what other damage can mycoplasmas cause?

A
  • hemolytic anemia
    • IgM=cold hemagglutinins
    • at lower temps, these antibodies cause RBCs to stick together & partial lysis, @ mucosal surfaces
    • detectable in 50% of cases
    • clinically significant hemolysis is rare
  • encephalitis: spread to brain
  • erythma multiforme (rash): systemic
70
Q

which of the genital mycoplasmas is the newest emerging human pathogen, what can it cause, and where is it isolated from?

A

m. genitalium:
- urethritis, cervicitis, endometritis, PID
- isolated from synovial and resp fluids
- a lot like m. pneumoniae

71
Q

which two genital mycoplasmas are frequently associated with disease in newborns?

A
  • m. hominis and u. urealyticum
  • commonly found in resp and genitourinary tracts
  • present in most of the sexually active population
72
Q

how are m. hominis and u. urealyticum isolated in newborns and do they always cause disease?

A

spinal fluid and they only cause disease in susceptible individuals