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2 PID Unit > 25 Unculturable Bacteria: Spirochetes and Rickettsia > Flashcards

25 Unculturable Bacteria: Spirochetes and Rickettsia Flashcards

1
Q

What are the 3 genera of spirochetes that cause human illnesses?

A

Treponema (syphilis)
Leptospira (leptospirosis)
Borrelia (relapsing fever and lyme disease)

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2
Q

T/F- Spirochetes are long slender rods that are related to gram negatives (LPS-like); they have endoflagella under a sheath (axial fibril-like flagella)

A

True

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3
Q

Treponemes species are defined by disease. Name 4 examples along with the diseases they cause.

A

T. pallidum-syphilis
T. pertenue-yaws
T. carateum-pinta
T. endemicum-bejel

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4
Q

T/F- normal flora do not contain treponemes

A

False. Normal flora may contain non-pathogenic treponemes

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5
Q

T/F- Treponemes have been kept alive in conditions with reduced oxygen, however, genomics predicts they are aerobes, but they have never been cultured on lab media

A

True

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6
Q

What facilitates dissemination of treponemes in the body?

A

readily attach to endothelial cells and pass through blood vessel walls

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7
Q

Treponema pallidum is responsible for disease?

A

Syphilis
-60% probability of transmission if sex with infected parter
-46x more common in gay men than straight men
-more common in men than women
-rates increasing in past several years
-Primary/Secondary disease are most infectious stages
Non-sexual transmission: congenital syphilis (400 cases/yr in U.S.) and Bejel/Siti are disease of children

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8
Q

T/F- syphilis does not change risk of transmitting or acquiring HIV

A

False, it increases risk:

  • Indirect: a portal for HIV entry through lesions and attracting HIV target cells to lesions
  • Direct: possibly upregulates HIV replication
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9
Q

Describe the natural course of a hard chancre in primary syphilis

A
  1. organism penetrates skin/mucous membrane and develops lesion and initial inoculation site
  2. organism replicates at this lesion and then spreads through blood stream (regional lymphadenopathy common). CD4 t cells and macrophages predominate.
  3. Chancre resolves without treatment while bacteria seeds other parts of body
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10
Q

When does secondary syphilis develop and what are the common manifestations?

A
  • develops 6-8 weeks after resolution of primary lesion (CD8 response)
  • maculopapular rash on flank, shoulder, arm, chest, back, hands, soles of feet, malaise, headache, generalized lyphadenopathy (lymphadenopathy resolves in 2 months)
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11
Q

What are some less common manifestations of secondary syphilis?

A

fever, anorexia, mucous patches, condylomata lata (infectious), alopecia, meningitis, myalgia, ocular complaints, hepatic, pulmonary or neuro involvement

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12
Q

What’s latent syphilis?

A

period of disappearance of secondary manifestations until therapeutic cure occurs OR until tertiary symptoms develop. Divided into early and late phases.

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13
Q

Important details of early latent phase (first year of latency)?

A

Many patients experience recurrence of secondary symptoms and remain INFECTIOUS to sexual partners

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14
Q

Important details of Late latent phase (>1 year of latency)?

A

Patients are not considered infectious and even without treatment 72% of T. palladium infected pts with remain symptom free forever. 28% progress to tertiary syphilis.

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15
Q

What is tertiary syphilis?

A
  • few viable bacteria remain
  • hypersensitivity to bacterial antigens causes GUMMA lesions
  • cardio: aortic aneurysm, valvular insufficiency, coronary artery ostial stenosis
  • Neuro: CN palsy, personality changes, delusions
  • Outcome is death for tertiary syphilis
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16
Q

What are GUMMA lesions?

A
  • small rubber granuloma infiltrates of monocytes
  • any organ
  • non-infectious
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17
Q

What is the underlying systemic pathophysiology of syphilis?

A
  • lesions at all stages show vasculopathic changes (enderarteritis and periarteritis)
  • dense local infiltrates (macrophages, lymphocytes, plasma cells, PMNs, histiocytes
  • granulomata often present and assume necrotizing nature
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18
Q

Outcomes of congenital syphilis?

A

-Hutchinson’s teeth, Saddle nose, Saber shins, fulminant disseminated infections, lesions of skin and bone, deafness

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19
Q

T/F- syphilis bacteria can cross the placenta to infect the fetus

A

True

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20
Q

T/F- untreated syphilis in pregnancy can result in spontaneous abortion, still birth, premature delivery, or perinatal death

A

True

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21
Q

T/F- T. pallidum can be grown in culture

A

False. Cannot be grown in culture (makes no amino acids)

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22
Q

T/F- T. pallidum outer membrane does not contain LPS and contains very few proteins

A

True, this allows it to evade the immune system

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23
Q

T/F- binding between T. pallidum outer membrane proteins and host cell glycoproteins (fibronectin, laminin) occurs

A

True

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24
Q

T/F- Treponema is an intracellular pathogen that elicits weak stimulation of the innate, humoral, and cell-mediated defenses that eradicates the bacteria

A

False

  • extracellular pathogen
  • elicits STRONG immune response but it does NOT eradicate the bacteria. Lipoproteins play a crucial role in stimulating the innate mechanism during all stages.
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25
Q

Does microscopy help diagnose syphilis?

A
  • Gram stain will not work

- can use phase contrast, dark field, or fluorescent microscopy

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26
Q

Are there screening assays for syphilis?

A
  • -screening assays for non-treponemal antibodies detect IgG and IgM against cardiolipin (most sensitive in secondary and latent infection-100% vs 80% in primary and tertiary)
  • rapid plasmid reagin test (RPR)
  • venereal disease research laboratory test (VDRL) best for neurosyphilis
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27
Q

What confirmatory tests can be used for syphilis?

A
  1. Indirect Fluorescent Antibody (fluorescent treponemal antibody ‘FTA’)
  2. Treponema pallidum particle agglutination test (TP-PA)
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28
Q

How do you treat syphilis?

A
  • treat at all stages of disease with parenteral penicillin injections
  • no resistance to penicillin
  • later stage=longer therapy needed
  • if allergic to penicillin use ceftriaxone or doxycycline
  • can be reinfected after treatment
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29
Q

T/F condoms always prevent syphilis infection

A

False. condom use is not necessarily helpful to prevent transmission of T. pallidum unless the infected area is completely covered and potential exposure site is protected

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30
Q

T/F- there is a vaccine for syphilis

A

False

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31
Q

What organism causes “relapsing fever” and lyme disease?

A

Borrelia

32
Q

Compare epidemic relapsing fever and endemic relapsing fever

A
  • epidemic: caused by B. recurrentis, body louse borne, humans are reservoirs
  • endemic: caused by many Borrelia sp., small mammal reservoirs, transmitted by soft-shelled tick vector
33
Q

What species of Borrelia causes lyme disease in the U.S.? What is it’s vector and reservoir?

A

B. burgdorferi

reservoir: farm animals, rodents, pets
vector: Ixodes scapularis (deer tick)

34
Q

Important details of relapsing fevers

A
  • associated with ospC gene
  • organisms with one ospC gene are cleared but organisms expressing another take over
  • diagnosed by presence of organisms in peripheral blood smear
35
Q

T/F- lyme disease is the most common vector borne disease in the U.S. with peak transmission in late spring (juvenile ticks) and summer (adult ticks) and 10% of B. burgdorferi infections are asymptomatic

A

true

36
Q

Describe time course of Lyme disease

A
  1. early localized phase: bull’s eye rash (erythema migrans) 1-2 weeks after bite with flu like symptoms (20% have no EM and only show fever, headache, malaise)
  2. Late disseminated: if untreated, 60% will progress to this phase, joint swelling/arthritis (high risk in HLA-DR4 pts), neuroborreliosis=>chronic polyneuropathy, encephalopathy, insomnia, malaise, mental changes. Debilitating but rarely fatal.
37
Q

Describe virulence of lyme diseas

A
  • unusual small, linear 950 kb chromosome with 12+ plasmids
  • genome encodes 150 lipoproteins (stimulate innate defense via TLR-2 and CD14 on macrophages
  • OspA, B, C, etc. plasma encoded lipoproteins in an LPS-free outer membrane help adapt and survive in host + stimulate autoimmune response in some, =>T cell response to Osp causes them to recognize synovial and neuronal proteins
38
Q

How is Lyme disease diagnosed?

A
  • clinical features
  • serologic tests (ELISA, IFA are sensitive, western blot is specific) can be used if enough time has passed, but cannot differentiate active from past infection
39
Q

How is lyme disease treated?

A
  • doxycycline for non-pregnat patients >9 yrs old
  • duration depends on stage of disease (localized skin infection:14 days), early disseminated disease (21 days), lyme associated arthritis (30-60 days), late or severe disease with cardiac/neuro involvement use IV antibiotics for 4 weeks
40
Q

T/F- treatment of lyme disease is not required if the tick is unengorged or attached less than two days

A

True

41
Q

T/F- there is no vaccine for lyme disease and getting it once does not confer immunity against future infections

A

True

42
Q

T/F- leptospira causes zoonoses

A

true

43
Q

What are common hosts of leptospira?

A

dogs, rats, livestock, sea lions, opossums etc. Commonly infect renal tubules in reservoirs leading to prolonged shedding in urine=>gets into lakes, contracted while swimming or during floods. humans are incidental hosts.

44
Q

T/F- Leptospira spreads human to human

A

No documented person to person spread

45
Q

What is the mechanism of infection of leptospira?

A

Thin, highly motile leptospires penetrate intact mucous membranes or conjunctiva or enter skin through small cuts or abrasions then spreads through blood to all tissues (and CSF) especially the liver

46
Q

How does leptospirosis present in patients?

A
  • most show no or mild symptoms and do not seek medical care
  • some experience flu like symptoms, myalgia, abdominal pain, conjunctival suffusion, skin rash, aseptic meningitis (up to 25% of cases)
  • 5-10% will have icteric leptospirosis (Weil’s disease) which is the most severe form
47
Q

What is Weil’s disease?

A
  • severe form of infection by leptospira
  • jaundice, acute renal failure, pulmonary and cardiac symptoms, and ocular manifestations all may occur
  • rapid progression, fatality of 5-15%
48
Q

What are Leptospira’s virulence factors?

A
  • “LPS like” molecule in outer membrane (lower endotoxin activity than LPS)
  • can attach to epithelial cells
  • lipoproteins in outer membrane play a role (similar to other Spirochetes)
49
Q

How is Leptospira treated?

A

penicillin G

Doxycycline

50
Q

Are animal vaccinations available against leptospira?

A

yes, this is used for prevention

51
Q

How is leptospirosis diagnosed?

A
  • Serologic test called microscopic agglutination test (MAT)
  • won’t gram stain, darkfield unreliable
  • Culture is very slow
52
Q

T/F- Rickettsia is an obligate intracellular parasite

A

True

53
Q

What are the 5 “more or less” unrelated bacterial genera that cause somewhat similar “Rickettsial” diseases. What type of pathogens are they?

A

Rickettsia, Ehrlichia, Coxiella, Orientia, Anaplasma.

  • All obligate intracellular pathogens
  • All small gram negative coccobacilli/short rods
54
Q

Why are the Rickettsial diseases obligate intracellular pathogens?

A

Need host to metabolize sugars and synthesize all their nucleotides, lipids, and amino acids

55
Q

How do Rickettsial diseases manifest clinically?

A

acute phase: fever, headache, myalgias, nausea, vomiting, cough, thrombocytopenia, elevated liver enzymes, normal to low WBC counts
later phase: manifestations vary greatly

56
Q

How are Rickettsial infections transmitted?

A

most via arthropod vectors (ticks, mites, fleas, lice) exception is Q fever (due to C. burnetii) which is transmitted via ingestion of milk or aerosols of partition (birth) material from sheep, dogs, other animals.
-Some via inhalation

57
Q

T/F- some rickettsial diseases cause rashes which may be macular, maculopapular, or vesicular in MOST of those infected

A

True, although Q fever rash is rare

58
Q

T/F- some rickettsial diseases cause pneumonitis (pneumonia without pus) because they don’t elicit a massive PMN response

A

True

59
Q

T/F- because rickettsial diseases are intracellular, they cannot cause meningoencephalitis or toxic shock syndrome

A

False, they can cause both of these

60
Q

What is rickettsial pox caused by and how is it spread?

A
  • R. akari
  • spread by mites
  • in cities
  • papule where bitten->wchar->systemic spread (fever, rash)
61
Q

T/F- epidemic (louse-borne) typhus is caused by R. prowazecki which is a human body louse

A

True

62
Q

T/F- endemic (murine) typhus is caused by R. typhi which is a rat flea and spread from rodents

A

True

63
Q

Scrub typhus is caused by Orienta tsutsugamushi and which is associated with chiggers and mites. What symptoms does this cause in humans?

A

Headache, fever, rash

64
Q

What organism causes Q fever? How is it spread and what are the symptoms?

A
  • caused by Coxiella burnetii
  • spread through unpasteurized milk or aerosol of dried placenta of farm animals
  • can be asymptomatic or flu-like with pneumonia, hepatitis, endocarditis
65
Q

How does Coxiella burnetii, which causes Q fever, replicate?

A

in phagolysosomes (needs acidic environment)

66
Q

What are the 2 phases of Q fever?

A

This organism undergoes genetic variation of the cell wall LPS resulting in two phases:
Phase I: infectious, no antibody response
Phase II: acute disease, antibody response

67
Q

What organism is human monocytotropic ehrlichiosis (HME) caused by and what is it’s vector?

A
  • caused by E. chaffeensis

- Lone Star Tick (generally infects leukocytes, particularly monocytes)

68
Q

How does E. chaffeensis (the cause of HME) reproduce?

A

within membrane-bound vacuoles in the cytoplasm

69
Q

What is the micro colony of replicating E. chaffeensis called? If you see this can it be used to diagnose HME?

A

morulae, yes (but only seen in a minority of cases)

70
Q

Are rashes in HME patients more common in kids or adults?

A

30% of adults, 60% of kids

71
Q

What organism causes Rocky Mountain spotted fever? What is the vector?

A

R. rickettsia

-vector: wood tick and american dog tick

72
Q

How do female ticks infected with Rocky mountain spotted fever pass on bacteria?

A

trans-ovariallly (an infected blood meal is not necessarily required)

73
Q

What is the cause of spots in rocky mountain spotted fever?

A

rickettsial infections:

  • increase vascular permeability (disrupt adherents junctions)
  • cause oxidative stress (but no toxins)
  • release of procoagulant factors, activates coagulation cascade
  • spots start peripherally, move centrally
74
Q

How is rocky mountain spotted fever diagnosed?

A
  • diagnosis is diffult in acute stage since 97% of people won’t have characteristic spots yet
  • 7-10 days after onset, diagnosis can be confirmed with serologic test
75
Q

How is rocky mountain spotted fever treated?

A
  • MUST provide empiric treatment before disease is confirmed

- doxycycline is antibiotic of choice for both children and non-pregnant adults

2 PID Unit (13 decks)

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