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micro quiz 2 > MICRO_042213_Chlamydia and Rickettsia > Flashcards

MICRO_042213_Chlamydia and Rickettsia Flashcards

1
Q

What type of organism is chlamydia?

A

Obligate intracellular bacteria

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2
Q

What does chlamydia rely on the host for?

A

ATP

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3
Q

What are the 2 developmental stages of chlamydia?

A

Elementary bodies (EB) and Initital bodies (IB aka reticulate bodies (RB))

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4
Q

What is the difference between elementary bodies and the initial bodies of chlamydia?

A

ELEMENTARY BODIES (EB) - Small, non-multiplying form with a rigid bacteria-like cell wall. Infectious form - transmits from one cell/person to another. INITIAL BODIES: Larger, multiplying form that Lacks rigid wall; non-infectious form

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5
Q

What is the intracellular growth cycle of chlamydia?

A

1) EB induces host cell to phagocytose them, 2) Once inside the cell, the EB lose their cell wall, grow larger, and synthesize RNA to make Ibs, 3) IBs divide by binary fission; some of it is converted back to EB.

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6
Q

What are the 3 different types of chlamydia that is known to infect humans?

A

1) C. psittaci “parrot fever”, 2) C. pneumonia, 3) C. trachomatis

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7
Q

Of the 3 different types of chlamydia, which one has multiple serotypes?

A

C. trachomatis

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8
Q

How is C. Psittaci “parrot fever” transmitted?

A

it’s a natural parasite of birds; transmitted to humans via fecal matter

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9
Q

What does C. psittaci cause?

A

1) interstitial pneumonia - progressive scarring of lungs, 2) fever, 3) headache

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10
Q

How is C. pneumonia transmitted?

A

aerosol droplets

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11
Q

What does C. pneumonia cause?

A

causes atypical pneumonia or bronchitis, mostly in adults

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12
Q

What is unique about C. pneumonia’s pathology?

A

detected in atherosclerotic lesions; may play a role in coronary atherosclerosis

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13
Q

What are the 4 different serotypes of C. Trachomatis?

A

1) Serotype D-K 2) A, B, C, 3) L1, L2, L3

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14
Q

Which C. Trachomatis serotypes are more invasive?

A

Serotypes A, B, C, and L1, L2, L3

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15
Q

What does C. Trachomatis serotype D-K cause in ADULTS? How is it normally transmitted?

A

Nongonococcal urethritis, a common venereal disease transmitted via sexual contact

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16
Q

What are the symptoms that C. Trachomatis serotype D-K cause in adults?

A

Males/Females are normally ASYMPTOMATIC but both sexes can have more severe diseases involving the epididymis or fallopian tubes that can ultimately lead to sterility

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17
Q

What does C. Trachomatis serotype D-K cause in infants? How is it normally transmitted?

A

Inclusion Conjunctivitis and/or Infant Chlamydial Pneumonia. Transmitted via perinatal transmission (since the bacteria grows in the mother’s cervical cells).

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18
Q

What is infant chlamydial pneumonia?

A

caused by C. Trachomatis serotype D-K; is an extension of the ocular disease (inclusion conjunctivitis)

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19
Q

What does C. Trachomatis serotype A, B, C cause?

A

blindness - it is the leading cause of PREVENTABLE blindness

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20
Q

How is C. Trachomatis serotype A, B, C transmitted?

A

1) Mechanical (finger to the eye), 2) flies/poor hygiene (prevalent in tropical Africa and Asia)

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21
Q

What symptoms do C. Trachomatis serotype A, B, C cause?

A

chronic infection of conjunctiva, which can cause the eyelashes to grow inward, which can cause corneal scarring and blindness

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22
Q

What does C. Trachomatis serotype L1, L2, and L3 cause?

A

painless papule that progresses to a genital ulcerating vesicle and sometimes progress to a painful suppurating disease of regional lymph nodes

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23
Q

How is C. Trachomatis serotype A, B, C transmitted?

A

veneral disease - transmitted via sexual contact

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24
Q

How would you treat chlamydia?

A

Tetracycline and Azithromycin (antibiotics that can enter the cells)

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25
Q

How would you diagnose chlamydia?

A

Intraurethral or endocervical smears: test for specific serotypes (direct immunofluorescence to detect cytoplasmic inclusion bodies, PCR, seroassays)

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26
Q

In the serological tests, what’s the difference between the acute vs convalescent serum samples?

A

ACUTE: on-going symptoms, little or no antibody. CONVALESCENT: >5 d post symptoms, a lot of antibody produced

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27
Q

What is Rickettsia?

A

an intracellular pathogen that’s is normally parasites of arthropods (vector)

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28
Q

What does Rickettsia rely on the host for?

A

adapted to take up ATP, NAD, and other metabolites, but can make their own ATP

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29
Q

What is the typical life-cycle of Rickettsia?

A

1) induces host cell to phagocytose them, 2) multiplies via binary fission, 3) pathogens released via host cell lysis

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30
Q

How do you diagnose Rickettsia?

A

1) PCR, 2) Serological tests for specific antigens or antibody response, 3) immunohistologic detections

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31
Q

How do you treat Rickettsia?

A

Tetracycline and DTT (for lice control)

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32
Q

What are the different types of Rickettsia?

A

1) R. typhi, 2) R. rickettsii, 3) R. akari, 4) prowazekii (think TRAP)

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33
Q

What does rickettsia prowazekii cause?

A

primary epidemic typhus

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34
Q

How is rickettsia prowazekii transmitted?

A

human lice

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35
Q

What is the pathogenesis of rickettsia prowazekii?

A

replicates first in capillary endothelial cells and after ~10d there is an onset of fever and severe headache, followed by a rash 4-7d later

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36
Q

What is a complication of rickettsia prowazekii?

A

recovery does note eliminate rickettsia prowazekii; can resurface as BRILL-ZINSSER disease, especially if the immune response is compromised. Symptoms are the same as primary epidemic typhus

37
Q

What is one additional test that you can do to test for rickettsia prowazekii?

A

liver function tests - usually elevated

38
Q

What is unique about rickettsia typhi?

A

it is antigenically related to R. prowazekii

39
Q

What does rickettsia typhi normally cause?

A

endemic murine typhus, a milder form of primary epidemic typhus

40
Q

How is rickettsia typhi transmitted?

A

humans fleas from ground squirrels or rats

41
Q

What does Rickettsia Rickettsii normally cause?

A

Rocky Mountain Spotted Fever

42
Q

What are the symptoms of Rickettsia Rickettsii?

A

1) rash begins on the palms/soles and spreads rapidly to the trunk, 2) fever, headache, arthritic pains, abdominal pain with nausea and vomiting

43
Q

How is Rickettsia Rickettsii normally transmitted?

A

humans forest ticks that infest many animals

44
Q

What does Rickettsia akari normally cause?

A

Rickettsial pox (a rash that resembles that of chicken pox)

45
Q

What are the symptoms of Rickettsia akari?

A

skin lesion at the site of the bite, followed by systemic symptoms (fevers, chills, headache, rash that resembles that of chicken-pox)

46
Q

How is Rickettsia akari transmitted?

A

humans mouse mites (outbreaks are often confined to a single building/apartment complex)

47
Q

What does coxiella burnetti cause?

A

Q fever

48
Q

How is coxiella burnetti transmitted?

A

humans are infected via inhalation of spore-like c. burnetii that’s present on the placental tissue/carcasses of sheep, goat, cow cat (animal-animal transmission occurs via ticks); usually an occupational exposure

49
Q

What are the symptoms of coxiella burnetti?

A

interstitial pneumonia, fever, headache, sometimes rash

50
Q

How is coxiella burnetti normally diagnosed?

A

1) liver function tests – should be elevated, 2) serologic testing for specific antigens, 3) indirect immunofluorescence assay, 4) immunohistological staining , 5) PCR

51
Q

How would you treat coxiella burnetti?

A

1) Doxycycline, 2) Quinolone antibiotics

52
Q

What is erlichioses?

A

a tick-borne disease

53
Q

What is erlichioses caused by? How are they different?

A

caused by two different obligate intracellular bacteria: 1) MONOCYTIC ehrlichiosis – infects monocytes 2) GRANULOCYTIC ehrlichiosis - infects granulocytes

54
Q

What are some symptoms that ehrlichiosis cause?

A

1) fever, 2) lymphocytopenia (WBCs are being destroyed through infection), 3) elevated liver function tests due to liver damage

55
Q

How would you treat ehrlichiosis?

A

tetracycline

56
Q

What are the two strains of neisseria?

A

1) N. meningitidis 2) N. gonorrhoeae

57
Q

What are the animal reservoir for neisseria?

A

none, humans are the only hosts.

58
Q

What are some charcteristics of neisseria?

A

gram (-), diplococci

59
Q

What conditions do neisseria grow best in?

A

rich medium, with 5-10% CO2

60
Q

How would you test for the different strains of neisseria?

A

sugar fermentation tests

61
Q

How do different strains of Neisseria ferment sugars differently?

A

1) N. gonorrhoeae – ferments glucose only, 2) N. meningitidis – ferments glucose and maltose, 3) N. lactamica (nonpathogenic) – ferments glucose, maltose, and lactose. NOTE that neisseria does NOT ferment sucrose!

62
Q

How would you isolate NM and NG from other bacteria?

A

Thayer-martin selective medium

63
Q

How would a Thayer-martin selective medium help isolate NM and NG from other bacteria?

A

it contains: 1) Vancomycin inhibits gram (+), 2) Colistin inhibit gram (-) enterics, 3) Nystatin is antifungal

64
Q

How are pathogenic and non-pathogenic neisseria different in terms of growth conditions?

A

Non-pathogenic Neisseria do not require blood products in the medium, while pathogenic Neisseria do

65
Q

T/F pathogenic and non-pathogenic neisseria are both oxidase positive

A

True. Both are oxidase positive

66
Q

What are some virulence factors that neisseria produces and how does it contribute to their pathogenicity? (3)

A

1) PROTEASE - splits secretory IgA1, 2) PILI and outer membrane protiens (OMPs) contributes to colonization, 3) LOS (like LPS, but without the side-chains) - endotoxin; mediates resistance to serum bactericidal activity

67
Q

Where does NM live?

A

nasopharynx

68
Q

What are some virulence factors specific to NM?

A

1) CAPSULE has anti-phagocytic properties, 2) ENDOTOXIN - damages wall of small vessels

69
Q

When does NM replicate?

A

only when it’s outside of cells. Once it is phagocytosed, it does not multiply

70
Q

How is NM transmitted?

A

respiratory droplets (remember that it resides in the nasopharynx)

71
Q

What is a complication of NM?

A

Waterhouse-Friderichsen Syndrome – meningococcemia causes adrenal failure circulatory collapse, shock, and rapid death

72
Q

What is the Sub-saharan Meningitis Belt?

A

Largest burden of meningococcal meningitis in the world; caused by NM - Type A; due to overcrowded housing and large population displacements (pilgrimages and traditional markets)

73
Q

How do you diagnose NM?

A

CLINICAL PICTURE: 1) URI, 2) high fever, 3) signs of meningitis, 4) Petechiae, followed by large areas of ecchymosis. CULTURE: blood, spinal fluid, nasopharyngeal specimens are cultured, examined for gram (-) diplococcic, followed by sugar fermentation testing

74
Q

How do you treat NM?

A

I.V. penicillin or 3rd generation cephalosporins (ceftriaxone). Rifampin or Ciprofloxacin for those who have come into contact

75
Q

Is there a vaccine for NM?

A

quadravalent vaccine for groups A, C, Y, and W135

76
Q

Why isn’t there a vaccine for NM, type B?

A

the type B capsule is composed of sialic acid, which is not recognized by the C3b component of complement and does not stimulate recruitment of phagocytes

77
Q

Both NM and NG produce an endotoxin. Which one is a major factor in the disease state?

A

NM

78
Q

Where is NG normally found?

A

genitourinary tract

79
Q

T/F NG has a capsule.

A

False. Only NM has a capsule

80
Q

What are some virulence factors specific to NG?

A

PILI - promote sticking to epithelial cells and impairs phagocytosis by PMNs. NOTE: non-piliated strains are NOT virulent

81
Q

How is NG transmitted? (2)

A

1) sex, 2) perinatal transmission

82
Q

Perinatal transmission of NG can cause disease. How do you treat it?

A

ophthalamia neonatorium - can result in blindness in children. Treat with tetracycline or erythromycin ointment or dilute silver nitrate (1%)

83
Q

What is the mechanism of pathogenesis of NG?

A

1) bacteria anchors to cells via their pili and penetrate through the cells to reach subendothelial connective tissue, 2) infection established within an hour of exposure, 3) Inflammation ensues, 4) Infection may spread to the epididymis or prostate in males and fallopian tubes in females

84
Q

What are some of the symptoms of NG?

A

1) Yellow purulent urethral discharge (with burning sensations during urination) occurs
2) Asymptomatic carrier states are common and carriers can still transmit infection

85
Q

What are some complications of NG?

A

1) Arthritis-dermatitis – infection spreads to ≥1 joints; skin lesions are present, 2) Chronic pelvic inflammatory disease – in females

86
Q

How do you diagnose NG?

A

1) Clinical picture of discharge + history of exposure, 2) Stained smears of exudate show gram (-) diplococci within PMNs

87
Q

How would you treat NG?

A

Intramuscular ceftriaxone; but must add 10d oral tetracycline, doxycycline, or azithromycin for chlamydia (assumption: chlamydial infection is present in gonnorhea cases)

88
Q

What antibiotics is NG resistant to?

A

1) Pencillin, 2) Tetracycline, 3) some cephalosporins

89
Q

What vaccines are available to treat NG?

A

none.

micro quiz 2 (8 decks)

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