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PHARM/MHD EXAM - 3 > L8 MHD: Spirochetes > Flashcards

L8 MHD: Spirochetes Flashcards

1
Q

Treponema Pallidum:

  1. Light microscopy or Darkfield
  2. Vector/reservoir
  3. Transmission
  4. Disease
A
  1. use Darkfield
  2. NO vector/reservoir
  3. Intimate sexual contact
  4. Disease = SYPHILLIS
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2
Q

Leptospira Interrogans

  1. Light microscopy or Darkfield
  2. Vector/reservoir
  3. Transmission
  4. Disease
A
  1. Use dark field
  2. Rats, mice, wild rodents, dogs, swine, cattle
  3. Contact or ingest urine-contaminated water (surfer’s disease)
  4. Leptospirosis!
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3
Q

Borrelia Recurrentis

  1. Light microscopy or Darkfield
  2. Vector/reservoir
  3. Transmission
  4. Disease
A
  1. Light microscopy
  2. V= louse + tick
    Reservoir = rodents
  3. Transmitted by ticks or lice
  4. RELAPSING fever
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4
Q

Borrelia Burgdorferi

  1. Light microscopy or Darkfield
  2. Vector/reservoir
  3. Transmission
  4. Disease
A
  1. Yes - Light microscopy
  2. Vector = tick

Reservoir = Mouse, deer

  1. Transmission via (ixodes deer) TICKS
  2. Lyme borreliosis
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5
Q

Treponema Pallidum:

  1. Seen on ____ or ____
  2. Outer membrane: Does NOT contain ____
  3. What is the internal flagellum called?
A
  1. Immunofluorescence or darkfield
  2. No LPS
  3. Internal flagellum is called AXIAL FIBRIL
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6
Q

The following are characteristics of _____:

  1. Helical morphology
  2. Flexible peptidoglycan cell wall
  3. Axial fibrils that wind around cell wall
    - covered by outer membrane
A

SPIROCHETES

Treponema & leptospira are THIN and seen only by dark field microscopy

BLT

  • burrelia (can be seen with light microscopy)
  • leptospira
  • treponema
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7
Q

Culture of T. Pallidum:

  1. Cultured on _____
  2. Differentiated by clinical association only, why?
  3. What type of respiration?
A
  1. rabbit epithelial cells
    - Generation time – 30 hours
  2. Because structural & metabolic differences between treponemes have to been found.
    - differentiated by clinical association only
  3. MICROAEROPHILLIC!
    - Outer membrane protein antigens cloned but pathogenicity not well characterized
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8
Q

Syphillis Transmission:

  1. Major contact? With what?
  2. How does congenital infection arise?
  3. Lesions of tertiary syphillis are contagious (T/F)
  4. No sexual spread if greater than ___ years after acquiring infection
A
  1. Intimate sexual contact with infective PRIMARY or SECONDARY lesion
    - genitals, anus, lip
  2. Dissemination through PLACENTA
  3. FALSE: lesions of primary and secondary syphilis are contagious
  4. 4 years!
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9
Q

How have US rates of syphillis changed?

Linked to what 3 things?

Marked increase among what population?

Decreased in ____

A

INCREASED since 2005

  1. Drug use
  2. Truck Routes
  3. core groups

Increase in GAY MEN

Decreased rates among FEMALES

(most common in white non hispanic males)

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10
Q

PATHOGENESIS:

  1. Syphillis passes through ____ or ____
  2. Multiplies locally and disseminates to____ and other organs
  3. Symptoms or signs when number of organisms reaches critical mass
    Primary _____ days after inoculation
  4. What is the pathologic lesion of syphillis?
  5. What stages are self-limiting?
A
  1. Intact mucosa or Abraded skin
  2. lymph nodes
  3. 10-90
  4. OBLITERATIVE ENDARTERITIS
    - Hypersensitivity and autoimmunity may play late role
  5. Primary and secondary stages are self-limiting

(each followed by periods of latency)

  • immunity to reinfection after treatment of early syphillis is NOT enough to prevent reinfection
  • immunity after later stages is more substantial
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11
Q

Primary Syphillis:

  1. What appears at the site of inoculation? This also results in regional _____
  2. Painless papule is called a ____
  3. Describe the ulcer
  4. T/F: systemic manifestations appear in primary stage.
  5. Heals ____
A
  1. ULCERATIVE LESION
    - regional adenopathy
  2. CHANCRE
    - PAINLESS papule that ulcerates
    (10-90 days after initial infection)
  3. Ulcer has smooth , heaped up margins and dry crusted base
    (liquid from base is dark field positive)

+ FIRM LOCAL ADENOPATHY

  1. FALSE: no fever/chills
  2. Heals spontaneously
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12
Q

Secondary Syphillis:

  1. What type of illness?
  2. What type of rash? Is the whole body covered?
  3. In Moist areas, papillose coalesce to form _____
  4. What other sites are affected?
  5. Fever & generalized ______
A
  1. SYSTEMIC flu-like illness
    - may develop 2-10 weeks after primary lesion heals
  2. PAPULOSQUAMOUS rash
    - entire body including pass and soles

ALSO mucocutaneous rash with generalized lymphadenopathy & organ (liver, kidney, CNS involvement)

  1. CONDYLOMA LATA
  2. Hepatitis, aseptic meningitis, periostitis, nephritis (IMMUNE COMPLEX type)
  3. LYMPHADENOPATHY
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13
Q

What is a papulosquamous rash? Which stage of syphillis is this characteristic of?

A
  1. Red, elevated lesion that is easily felt, rough on the surface with a sandpaper texture
    - HYPERKERATOTIC
  2. SECONDARY SYPHILLIS
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14
Q

What is the difference between adenopathy between primary and secondary syphillis?

A
  1. Primary = REGIONAL lymphadenopathy
    - genital area (inguinal etc.)
  2. Secondary = GENERALIZED (neck/axillary)
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15
Q

One third of untreated syphillis cases resolve spontaneously.

The reminder progress to what?

What is positive in this stage?

Clinically what is seen?

A
  1. LATENT SYPHILLIS
  2. presence of POSITIVE treponema serologic test in
  3. the absence of clinical manifestations
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16
Q

(1/3 of untreated cases become LATE syphillis)

Late Syphillis presents in what 3 major organ systems?

A
  1. Neurosyphillis
    - TABES Dorsalis
    - (demyelination of nerves)
  2. Cardiovascular
    - proximal aorta & branches –> causing aneurisms due to AORTITIS
    - can lead to ascending aortic aneurism
    “tree barking of aorta”
    (syphillis destroys the vast vasorum –> smaller vessels that supply the aorta)
  3. Late Benign GUMMATOUS
    - granulomatous lesions in skin, mucocutaneous areas, bones
  • soft growth with firm necrotic center
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17
Q

Describe the 4 kinds of neurosyphilis.

  1. Asymptomatic
  2. Meningovascular
  3. Paresis
  4. Tabes dorsalis (what sensory deficits present?)
A
  1. Asymptomatic
    - CSF infected w/o symptoms or signs (only seen as infection in CSF)
  2. Meningovascular
    - chronic meningitis which can affect major arteries to brain & cranial nerves
    (stroke is possible/ without HTN)
  3. Paresis
    - CORTICAL DEGENERATION w/ mental changes
  4. Tabes dorsalis
    - demyelination of posterior colums & dorsal roots

**LOSS OF PAIN, temp, proprioception
+ ATAXIA

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18
Q

Congenital Syphillis:

  1. Infection occurs ____
  2. T/F: symptoms present at birth
  3. Prevent with what?
  4. What is recommended during pregnancy?
A
  1. IN UTERO infection (typically 1st trimester)
  2. FALSE no symptoms at birth
    - multi system disease later
    a) rhinitis
    b) rash
    c) bone & cartilage involvement
    d) liver, spleen, lymph nodes , CNS
  3. Penicillin during pregnancy (de-sensitize person if allergic, since tetracyclines are contraindicated in pregnancy)
  4. ROUTINE SCREENING recommended
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19
Q

What are the pupils that arise due to tertiary Syphillis?

What congenital defects are associated with syphillis?

A

Argyle - Robinson pupils
- can accommodate but not react to light!
= stay dilated when light is shined

(prostitute pupils)

FIRST AID:

  1. Saber shins
  2. Saddle shaped nose
  3. Hutchinson’s teeth (notched)
  4. Mulberry molars
  5. CN VIII deafness!!
  6. RHAGADES (linear scars at angle of mouth)
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20
Q

Microscopy for syphillis includes what 3 tests:

  1. ___ for primary & secondary lesions
  2. Immunofluorescence with monoclonal antibodies ______
  3. ___ which is not used clinically
A
  1. DARKFIELD
  2. Direct Fluorescent Antibody Test
  3. PCR
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21
Q

Reaginic Antibodies for Syphillis serology are IgG & IgM directed against _____

(not T. Pallidum!)

A
  1. CARDIOLIPIN
    - a lecithin cholesterol mixture present on mitochondrial membrane
  • extracted from beef heart
  • reason for forming these antibodies is unknown
  • antibodies not directed against T. Pallidum
22
Q
  1. What is VDRL?
    - What bodily fluid is used?
    - is it specific?

RPR?

What is common with these tests?

A
  1. VDRL: Veneral Disease Research Lab
    a) - done on CSF to screen for T. Pallidum
    - detects non-specific antibody that reacts with Cardiolipin

b) QUANTITATIVE, SENSITIVE, but NOT specific

  1. Rapid Plasma Reagin
    - directed against SERUM
  2. FALSE POSITIVE is common

V - viral infection
D - drugs
R - rheumatic fever
L - leprosy/lupus

23
Q

The following are examples of what?

  1. FTA - Abs
  2. TPPA
  3. EIA & CIA

Which has high false positive rate when sued to screen low prevalence pop? (but is used widely)

Which includes adsorbed antigens onto gelatin particle or RBC?

Which test is NOT quantitative?

Which is used to confirm a positive RPR?

A

SPECIFIC antibody tests for Treponema

  1. FTA - Abs
    -Absorbed with non-T. pallidum treponeme (dead T. palidum)
    Antigen is killed Reiter strain T. pallidum

Either reactive or NON reactive (not quantitative)

  1. TPPA
    - Treponemal antigens adsorbed onto gelatin particle or RBC
    MHA-TP–Microhemagglutination Treponema pallidum
  2. EIA & CIA
    - Chemiluminescence immunoassay
    Cheap, automated, now in wide use for screening
    - USED to confirm a POSITIVE RPR!!!!

High false positive rate when used to screen low prevalence population

If RPR is positive, but FTA is negative - strong indication that patient DOESN’T HAVE SYPHILLIS

24
Q

What are some conditions that cause false positives in Serologic Treponema tests:

  1. Troponemal (2)
  2. Non treponemal (2)
A
  1. Troponemal:
    - febrile illness
    - pregnancy
  2. Treponemal
    - chronic infections
    - autoimmune disease** (TEST)

V
D
R
L

V - viral infection
D - drugs
R - rheumatic fever
L - Lupus & leprosy

(AUTOIMMUNE DISORDERS CAUSE FALSE POSITIVE = TEST!!!)

25
Q

Treatment of Syphillis:

  1. What type of drug & what route?
  2. Treatment schedules differ according to ____. Must use IV treatment for ___ syphillis (which stage)
  3. What is an alternate to the drug in #1?
  4. Contraindicated in what? (2)
A
  1. Benzathine Penicillin G
    - IV (long duration time)
  2. STAGE
    - IV for LATE stage
  3. DOxycycline (tetracycline)
    BUT contraindicated in NEURSYPHILLIS & pregnancy
    -patient needs to be de-sensitized to PCN if allergic
  • ESPECIALLY PREGNANT & NEURAL patients with syphillis
26
Q

What treponema disease is associated with:

  1. Contaminated utensils; T. pallidum ss. Endemicum
  2. Direct lesion contact; T. pallidum ss. pertenue
  3. Direct lesion contact; T. Carateum
A
  1. Bejel
  2. Yaws
  3. Pinta
27
Q

What is the Jarisch - Herxheimer Reaction?

A

Fever, chills, headache, hypotension AFTER TREATMENT

  • Release of toxic products from killed spirochetes

Flu like symptoms (fever, chills, HA, myalgia) after antibiotics started due to killed bacteria releasing endotoxins!

28
Q

Borrelia:

  1. Large or small?
  2. Visible on what?
  3. Reservoir?
  4. Spread to humans via (2)
  5. Result?
A
  1. Large
  2. Visible on stained prep Light Microscopy!!!
  3. Reservoir: mammals (mouse)
  4. Vector: tick or louse
  5. Relapsing Fever or LYME BORRELIOSIS
29
Q

Borrelia Recurrentis:

  1. Seen on ____ stain
  2. ____ code for outer membrane protein antigens
A
  1. Wright- Giemsa’s Stained blood smear

2. Linear plasmids

30
Q
  1. B. recurrentis and related organisms escape immune recognition by doing what?
  2. What is this similar to?
  3. Relapses caused by what?
A
  1. altering their antigenic structure during infection
  2. Gene switch from silent to expression locus (like N. gonorrhoeae) on plasmid
  3. emergence and multiplication of antigenic variants
31
Q

What is exchanged in Borrelia Recurrentis antigenic shift?

A

Vmp21 exchanged for Cmp7

louse transmitts due to variable surface antigens

32
Q

Relapsing fever:

  1. EPIDEMICS of louse borne relapsing fever in times of ____
  2. ENDemic Tick - borne relapsing fever occurs in ____
A
  1. CATASTROPHE - war or famine

2. Endemic = mountain regions of western US

33
Q

What is the reservoir for TICK-BORNE relapsing fever of B. Recurrentis?

A

MICE

34
Q

The following describes B. Recurrentis or Borrelia species:

  1. Tick borne
  2. Organisms in saliva and feces
  3. Ticks infected by feeding on rodent (human – accidental host)
  4. Multiple and incade tissues of tick including salivary glands

TICK BITE TRANSMITS INFECTION

  1. Transovarial passage in ticks perpetuates spirochetes

(if infected, stay in the blood stream!)

A

BORRELIA SPECIS

35
Q

The following describes B. Recurrentis or Borrelia species:

  • **Louse borne
  • Organisms in gut of louse only
  • Lice suck blood & become infected (carried to another individual)
  • Crushing infected louse transmits infection
A

B. Recurrentis

** infection NOT maintained through generations of lice

36
Q

What are the clinical manifestations of of Relapsing Fever?

A

Fever
Chills
Muscle pain
Headache

Relapses – antigenic variation

Resolves 3-5 days, remits after 7-9 days
Each relapse is less severe

37
Q

Diagnosis? (3)

Treatment? (2 major; what reactions are more common than in syphillis)

A
  1. Blood smear
    - culture
    - serology
  2. Tetracycline
    Erythromycin

Jarisch-Herxheimer reactions MORE common (than in syphillis)

38
Q

Lyme borreliosis is a systemic spirochetal disease resembling syphilis in its stages and prominent involvement of skin and CNS

  1. What are the 2 primary reservoirs
  2. Vectors?
  3. Which tick stage is responsible for transmission?
A
  1. Deer
    White footed mouse
  2. Spread by IXODES deer tick (deer = adult host)
    (larva feed on poo of white mouse)
  3. All tick stages feed on humans, but NYMPH responsible for transmission
  • larva & nymph = white footed mouse
  • adult form = deer
39
Q

Where is the ixodes tick found?

What is the pathogenesis of Lyme Borreliosis?

A
  1. Northeastern & Midwestern US

focus in midwest –> wisconsin & minnesota (but diagnostic testing isn’t perfect, many people do not actually have lyme disease)

A LOT IN THE NORTHEAST!!!

  1. Tick bite –> multiply locally & enter lymph or blood

Antibody is associated with near disappearance of spirochetes
Suggests immune pathogenesis in late stage disease

40
Q

Early stage of Lyme disease is characterized by what?

A
  1. Erythema Migrans
    - expanding erythematous lesion at site of tick bite

-Organisms cultured from biopsy
- Accompanied by flu-like illness** (fever + chills)
may have central clearing with BULL’S EYE CLEARING!!! (sketchy)

41
Q

What is the Early Disseminated Lyme disease characterized by?

A
  • Days to weeks after primary infection

***Fatigue, headache, fever, malaise = SYSTEMIC SIGNS

Multiple skin lesions

  1. Neurologic: Meningitis, radiculitis
    - FACIAL NERVE PALSY
  2. HEART BLOCK, myocarditis
  3. Arthritis
42
Q

Which stage of Lyme disease is characterized by facial nerve paralysis, heart block, meningitis, and arthritis?

A

EARLY DISSEMINATED stage

  • days to weeks after infection

A key LYME to the FACE

F - facial nerve palsy
A - arthritis
C - cardiac block
E - Erythema chronicum migrans (early stage)

43
Q

What are 3 conditions that are associated with LATE STAGE Lyme Disease?

A
  1. Arthritis
  2. Encephalopathy (neuroplogic)
  3. Acrodermatitis Chronica Atrophicans
    - skin rash indicative of the third or late stage of LYME BORRELIOSIS
    - widespread atrophy
44
Q

Because a culture is usually not available for Lyme Borreliosis, what is used instead to diagnosis this condition in the lab? (2)

A
  1. ELISA or IFA
    - both IgM and IgG responses measured
  2. Western Blot to confirm
45
Q

What is the treatment of Lyme borreliosis?

1) early
2) late

T/F there is a vaccine for Lyme Borreliosis

A
  1. Doxycyline,
    amoxicillin,
    cefuroxime ORALLY
  2. Oral as above
    or PENICILLIN G or CEFRIAXONE parenterally (give for 4 weeks for arthritis)
  • all used in early and late disease
    3. TRUE: Recombinant OspA vaccine removed from market

Prevention – remove tick!!
( needs 24 hours to transfer disease, unlike Relapsing fever which only needs a few minutes)

46
Q

Leptospirosis:

Humans acquire the organism by contact with ______ usually through contaminated water

A
  1. infected animal urine
    - SPECIFIC SYNDROMES ASSOCIATED WITH EACH SEROTYPE ARE NOT DISTINCTIVE
  • 2 periplasmic flagella
  • cultivated in liquid media
47
Q

What are the hosts for Leptospirosis?

Transmitted via?

A
  1. ZOONOSIS with many animal hosts
    - Rats, mice, wild rodents, dogs, swine, cattle

2.Transmission
Ingestion of or direct contact with food or water contaminated with infected animal URINE

Leptospirosis- common infection when a FLOOD occurs
(or those who participate in triathlons)

48
Q

Pathogenesis of Leptospirosis:

  1. After infection, spirochetes invade bloodstream and affect endothelial cell integrity causing _____ in many organs
  2. _____found in kidney*
  3. Organisms excreted in ____
A
  1. vasculitis
  2. Immune complexes
  3. urine
49
Q

What clinical manifestations are associated with the first stage of Leptospirosis?

Second Stage?

Severe stage?

A
  1. First stage (Bacteremia)

Fever, headache, myalgias, CONJUCTIVAL SUFFUSION, abdominal pain
- leptospires present in blood/other areas

  1. Second stage (Immune)
    Aseptic meningitis or generalized illness with myalgias, headache, uveitis and rash
    liver enzymes are elevated + renal changes with elevated Creatinine
    organisms only found in urine (no longer in blood)
  2. STAGES BLEND
    - hepatitis w/ jaundice
    - kidney –> renal failure
    - hemmorhage
50
Q

How is Leptospirosis diagnosed?

a) early
b) late

After first week?

A

1.

a) early = blood & CSF culture
b) late = Urine

  1. Serology:
    Microscopic agglutination test (MAT) after first week
  • ELISA and IHA tests less standardized

( not as accurate as MAT!)
- difficult to get this test done since involves agglutinating leptospires on a slide

PCR is VERY SENSITIVE

3.

51
Q

What is the treatment for leptospirosis?

A

Penicillin or Doxycyline

PHARM/MHD EXAM - 3 (21 decks)

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