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MSI Unit I > 1-20 Spirochetes and Vibrios > Flashcards

1-20 Spirochetes and Vibrios Flashcards

1
Q

Recurring themes of spirochetes

A

cross easily into bloodstream/cross blood brain barrier - spread through entire body quickly (unlike anaerobes that wall themselves off from bloodstream)

primary virulence factor involves immune evasion

diagnosis challenging

once correctly diagnosed, treatment simple

jarish herx reaction to treatment

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2
Q

The primary virulence factor of spirochetes

A

for immune evasion

  • little inflammation
  • few exotoxins
  • low immunogenic surface (no LOS or LPS)
  • no vaccines
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3
Q

describe the issues of spirochete diagnosisis

A

wide variety of symptoms. illness comes in phases. history taking critical

syphillis too small for standard microscopy

lyme has no reliable lab diagnostic

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4
Q

Argyll-robertson?

A

hallmark of neurosyphillis. loss of light pupil constriction.can still constrict when focusing

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5
Q

conjuctivitis?

A

redness with exudate, found in leptospirosis

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6
Q

caught early vs caught late

A

early-curable by standard abx

late- infection still cured easily, but recovery of nerves/immune system takes months/years if ever

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7
Q

Herx?

A

24 hours after abx, body “wakes up” to infection. spirochete evasion tactics fail. flulike, 24-48 hours

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8
Q

treponema pallidum (syphillis) bacteriology

A

spirochetes are motile (corkscrew), not culturable, very slow growing, too slender to gram stain

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9
Q

tranmission of treponoma pallidum

A

intimate contact - sex, mother-baby, rarely through blood transfusion

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10
Q

what does syphilis infect? incidence?

A

endothelium of small blood vessels

increasing in US

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11
Q

treponema pallidum is a _______ infection

A

triphasic

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12
Q

primary syphilis

A

primary (weeks) - initial replication at site of infection, ulcer/chancre. initiates bacterioemia

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13
Q

secondary syphilis

A

months. macropapular rash on palms, soles. papules on mucuous membranes. patchy alopecia. low fever, malaise, anorexia, headache, myalgia,

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14
Q

____ syphilis will resolve, _____ will enter

A

1/3, 1/3 latency

early latency - symptoms come and go, patient remains infectious

late latency - symptoms absent, not infectios

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15
Q

remaining ____ will enter tertiary syphilis

A

1/3

granulomas “gummas”, CNA involvement

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16
Q

congenital syphilis

A

crosses placenta, stillbirth or fetal abnormality

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17
Q

immunity is _____

A

incomplete - reinfection can occur. doesnt cause strong enough immune response

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18
Q

pathogenesis of syphilis does not seem to involve

A

toxins.

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19
Q

diagnosis of syphilis

A

chancre, rash, granulomas, cns symptoms

lab - darkfield microscopy or IF

serology -

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20
Q

efficacy of antibiotics against spirochetes

A

spirochetes are still sensitive against older antibiotics

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21
Q

describe the syphillis bacteria

A

delicate, small, .25mM in size

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22
Q

Describe how to culture T.pallidum

A

cannot culture, syphillis will not grow in culture

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23
Q

highest risk groups for contracting syphillis

A

gay/poor

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24
Q

describe the path of infection by syphillis

A

penetrates mucous membrane, hits bloodstream, enters lymphastics, hits CNS early in infection

25
Q

what factor most complicates treatment of syphillis at the primary/secondary stages?

A

the fact that the lesions go away. Patients will not present primary or secondary lesions.

Also patients who are economically disadvantaged or don’t know a doctor will wait until it goes away, which it does

26
Q

neurological syphillis

A

neurosyphillis - CNS breached
meningitis - within 6 months

meningovascular syphillis - damage to blood vessels of brain, spinal cord

parenchyma neurosyphillis - grows in brain

27
Q

prevent syphillis?

A

penicillin & condoms. if allergic, treat with other abx then check up later

28
Q

Describe the borrelia burgdorferi bacteria

A

motile spirochete, flat wave shape

29
Q

can you get lyme without ever knowing?

A

asymptomatic clearance is possible - but how common this is unknown for obvious reasons

30
Q

weeks after being bitten by tick

A

early localized infection (75%) with erythema migrans (bullseye, getting larger)

31
Q

months after tick bite

A

early disseminated infection. bloodborn bacteria colonize CNS

meningitis, facial palsy, AV block, other rashes

takes time for body to recover after lyme cleared

32
Q

final stage of lyme disease progression

A

late disseminated

bacteria colonize large joins and brain (encephalitis). damage will persist or be permanent

33
Q

describe the proper examination for lyme.

A
  • testing is not clear

- no known exposure or substantial risk of exposure? do not test. “history of outdoor activity?”

34
Q

how will a patient likely present with lyme?

A

EM, high fever, coinfections, flu-like

35
Q

Serology of lyme?

A

available but not useful. cant tell if current or past infection or if received vaccine while still on market

36
Q

treatment of lyme?

A

14 days doxy if early, 30 if late. refer for symptoms (psychiatry, rehumatology)

37
Q

how to treat pregnant woman with lyme?

A

avoid doxy. give approved antibiotic for time being, prescribe doxy after delivery

38
Q

Describe vibrios appearance and resovoir

A

curved, gram neg. rods

mostly ocean dwelling. infected humans are resovoir

39
Q

tranmission of vibrios

A

fecal-oral

infection of wounds exposed to ocean water

40
Q

what can vibrios cause?

A

gastroenteritis and peptic ulcers.

41
Q

vibrio example?

A

cholera

42
Q

two types of cholera?

A

non-pathogenic, and pathogenic that received virulence factors from horizontal gene transfer

43
Q

how does cholera spread?

A

-fecal oral
-shed by asymptomatic carriers
-untreated water/under cooked shellfish
ussually killed by stomach acid
-surviving bacteria reach small intestines and colonize

44
Q

growing cholera excrete _____

A

cholera toxin (enterotoxin) called choleragen

-AB subunit, overactivates adenylate cyclase

45
Q

presentation of cholera if little penetration of gut wall

A

watery, not bloody diarrhea

46
Q

what causes morbidity to cholera?

A

dehydration from the toxin

47
Q

When examining a cholera patient, what to look for? treatment?

A

look for dehydration, treat with antibiotics and rehydration with electrolytes (most important)

48
Q

what kind of virulence factor is choleragen?

A

an enterotoxin

49
Q

what is an enterotoxin?

A

gastroenterology

a toxin produced in or affecting the intestines, such as those causing food poisoning or cholera.
50
Q

Transmission of spirochetes

A

Transmission – Sexual contact (Treponema pallidum – syphilis), vector-borne transmission (deer ticks carrying Borrelia burgdorferi – Lyme disease), and environmental transmission.

51
Q

pathogenesis of spirochetes

A

Pathogenesis – They cross easily into the blood stream, and their primarily virulence factors are for immune evasion. They can further immunomodulate the host to suppress any immune response. As a result, no effective vaccines exist. Both syphilis and Lyme disease occur in three stages that can happen over the course of years.

52
Q

diagnosis of spirochetes

A

Spirochetes are particularly challenging to diagnose. Symptoms appear in stages, so a patient history is essential. What’s more, Treponema pallidum are too small to see with a standard light microscope, and there is no quick and clear lab test for Borrelia burgdorferi exposure. In patients with neurosypilis, Argyll-Robertson pupil (one or both pupils fail to constrict due to light) is a good diagnostic tool.

53
Q

treatment of spirochetes

A

Treatment – Treat syphilis with penicillin, prevent by practicing safe sex. Treat patients with early Lyme disease with a ten-to-twenty-day long doxycycline regiment unless pregnant. Antibiotics will cause Jarisch-Herxheimer reaction (about twenty-four hours of flu-like symptoms) twenty-four hours after the beginning of the regiment.

54
Q

tranmission of vibrios

A

Primarily by fecal-oral route, but can also infect wounds contaminated by seawater or ocean debris. V. cholerae in particular is more likely to be transmitted by fecal-oral route in individuals with higher stomach pH (on antacids) or gastrectomies.

55
Q

pathogenesis of vibrios

A

Vibrios have specialized virulence factors for survival in the GI tract. In the case of V. cholerae, when it reaches the small intestine, it secretes mucinase to clear out mucus and reach the brush border where it attaches and colonizes. There, it releases the enterotoxin choleragen. It follows the typical exotoxin AB structure. B binds the ganglioside receptor GM1 on intestinal lining, and A causes massive water and ion loss by the cells while simultaneously blocking microvilli absorption. Massive watery diarrhea results, and patients can die within hours in severe cases.

56
Q

diagnosis of vibrios

A

When testing for V. cholerae, a pinch test is effective to determine if the patient is moderately dehydrated. For severe dehydration, signs to look for include sunken eyes, weak pulse, and coma.

57
Q

treatment of vibrios

A

Rehydration and rebalancing electrolyte levels are critical steps. Then treat with a short course of tetracycline, doxycycline, or furazolidone after IV rehydration to shorten course and reduce shedding.

58
Q

treat c.jejuni with abx but not c.butulinum with abx. Why?

A

c. botulinum dies during ingestion, it is the toxin we are worried baout. even if some bacteria survived, they don’t have any virulence factors we would worry about.
c. jejuni is an enteric bacteria with virulence factors for survival of stomach acid. Needs antibiotics.

59
Q

why do we vaccnate against chickenpox?

A

the virus is very immungenic. raises a strong, long-lived response that prevents reinfection to a host that has been previously exposed.

MSI Unit I (52 decks)

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