Spiral Bacteria Flashcards

1
Q

Classification of spiral bacteria

A

Spirochaetes

  1. Treponema pallidum
  2. Borrelia
    - Relapsing Fever Group - B. recurrentis, B. duttoni
    - Lyme Disease Group - B. burgdorferi
  3. Leptospira interrogans
  4. Spirillum minus & Streptobacillus monilformis - causes of rat bite fever

Spiral

  1. Campylobacter - jejuni, coli, fetus
  2. Helicobacter - pylori, cinaedi, fennelliae
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2
Q

Features of campylobacter & helicobacter

A
  1. Oxidase positive
  2. Gram negative short spirals
  3. Grow under microaerophilic conditions (less O2)
    - will not grow at normal atmospheric conc of O2/in its absence
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3
Q

Transmission of T. pallidum

A
  • natural syphilis infections only occur in man

1. Sexually transmitted disease - organism is sensitive to drying, only by intimate contact

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4
Q

Clinical presentations of T. pallidum (6)

A
  1. Primary syphilis
    - Chancre (painless ulcer) + enlargement of local lymph nodes
    - often on genitals, also extragenital sites (mouth, lips, anal canal, fingers of HCW)
    - may have multiple, not always painless, increasesd risk of concomitant HIV inf
  2. Secondary syphilis
    - Treponemes spread throughout body - rash (macular, papular, pustular), very infectious, usually involves palms & soles
    - Mucous patches (lesions on mucous membranes), snail track ulcers, oral/genital
    - Condylomata lata (warty lesions) around anus, genitals, warm moist areas
    - generalised enlargement of lymph nodes (lymphadenopathy)
    - fever, acute meningeal involvement
  3. Latent syphilis
    - signs disappear but secondary lesions may relapse
    - 70% never develop further disease, the rest develop chronic symptomatic inf
  4. Meningeal syphilis
    - present within a few months to a year of infection
    - chronic meningitis - headache, nausea, neck stiffness, other neuro signs
  5. Late complications (tertiary, quaternary syphilis)
    - Neurosyphilis - Meningovascular syphilis, General paresis/general paralysis of the insane (GPI), Tabes dorsalis (demyelination of posterior columns of spinal cord & dorsal roots/ganglia - loss of pain & proprioception - ataxic gait, lightning/sudden pains, Charcot’s joint, foot ulcers, Argyll Robertson pupils)
    - Gummatous syphilis/tertiary - granulomatous lesions which become necrotic - gumma on skin, mucous membranes, bone
    - Cardiovascular syphilis - aortitis of thoracic aorta - narrowed origin of coronary arteries, angina, MI, stretching of aortic valve ring, aortic incompetence, aortic aneurysm, weakened/stretched aortic wall
  6. Congenital syphilis (T. pallidum can cross the placenta)
    - may kill the baby, induce abortion
    - bullous rash at delivery (may be absent) - early lesions (resemble sec syphilis) - later lesions (gummatous, neurosyphilis)
    - Hutchinson’s triad: 8th nerve deafness + interstitial keratitis (corneal clouding - blindness) + Hutchinson’s teeth (notched incisors)
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5
Q

Diagnosis of T. pallidum (3)

A
  1. Dark Ground Illumination (DGI)
    - thin, cannot be seen using routine dye staining methods
    - not for oral lesions - other bacteria in flora - not specific
  2. Neurosyphilis: CSF sample - abnormalities in cell count, chemistry, syphilis antibody tests
  3. Serology
    (A) Non-treponemal antibody tests (non specific)
    - VDRL (venereal disease reference laboratory), RPR (rapid plasma reagin)
    - +: titre fluctuates with intensity of disease, falls w successful treatment, -: false positive reactions, VDRL/RPR titres decay naturally without treatment
    (B) Treponemal antibody tests (specific)
    - TPHA (T. pallidum hemagglutinin test), TPPA (TP particle/agglutination test), FTA-Abs (fluorescent treponemal antibody test - absorbed)
    - +: less false positives & fluctuations, -: stay raised for a long time even after successful treatment
  • VDRL + TPHA - if either is positive do FTA-Abs
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6
Q

Treatment of T. pallidum

A
  1. Penicillin/azithromycin

- supervised by experienced STD physicians to manage Jarisch-Herxheimer reactions & careful follow up

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7
Q

Prevention of T. pallidum

A
  • Antenatal screening
  • Serology for all STD patients
  • Contact tracing
  • Screening of donors
  • Education
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8
Q

Transmission & virulence factors of relapsing fever (borrelia)

A
  • louse (B. recurrentis), tick (B. duttoni)

- antigenic variation - relapsing nature of infections

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9
Q

Clinical presentations of relapsing fever (borrelia)

A
  • periods of fever alternate with afebrile intervals

- fevers cease when bacterium has run out of new antigens & immune system catches up

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10
Q

Diagnosis & treatment of relapsing fever (borrelia)

A
  • Peripheral Blood Films

- Doxycycline (watch out for Jarisch-Herxheimer reaction)

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11
Q

Transmission of lyme disease (borrelia)

A

Bite of hard ticks, extensive animal reservoir

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12
Q

Clinical presentations of lyme disease (borrelia) (3)

A
  • Stage 1: Rash, erythema chronicum migrans - begins at site of bite (macule/papule) - spreads out in a ring (sometimes with central clearing), may be assoc w systemic disease
  • Stage 2: neurological, cardiac, MSK disease, arthritis (weeks to months later)
  • Stage 3: chronic skin, joint, neurological disease (months to years later)
  • congenital infection may occur
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13
Q

Diagnosis & treatment of lyme disease (borrelia)

A
  • Serology
  • culture is difficult
  • Treatment depends on stage of disease
  • ECM: Doxycycline
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14
Q

Features & transmission of Leptospira interrogans

A
  • many serovars depending on surface Ag
  • chronically excreted in urine of rats & other animals
  1. Entry through skin, mucous membranes of URT, eyes
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15
Q

Clinical presentations of Leptospira interrogans (3)

A

Leptospirosis

  1. Septicaemic phase, bacteraemic leptospirosis - flu-like, high fever, muscle pain, possible conjunctival congestion
  2. Immune phase - bacteria cleared from blood as antibodies appear, signs of meningeal irritation (headache, vomiting)
  3. Weil’s disease: Icteric leptospirosis - jaundice, hemorrhage, renal failure, conjunctival congestion, may be fatal
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16
Q

Diagnosis & treatment of Leptospira interrogans

A
  • Microscopy: DGI of blood, urine
  • Serology
  • culture difficult
  • Benzylpenicillin
17
Q

Features of rat bite fever

A
  • rare, local lesion (skin ulcer, abscess), local lymphadenopathy, fever, skin rash
  • may be acquired by oral route (Haverhill fever) via contaminated milk/water (S. moniliformis)
  • caused by Spirillum minus (gram neg spiral, mostly in far east esp Japan, Africa); Streptobacillus moniliformis (pleomorphic gram neg non-spiral)
18
Q

Transmission of campylobacter jejuni & coli

A

Faecal-oral, contaminated food & milk (from animals, poultry meat)

19
Q

Clinical presentations of campylobacter jejuni & coli (5)

A
  • C. jejuni is an impt cause of GI inf, C. coli is less common
    1. incubation 1-7 days, initial flu-like prodromal illness
    2. Sever abdominal pain (sometimes suspected as appendicitis)
    3. Diarrhea (sometimes frank blood w faeces)
    4. usually self limiting
    5. complications: sever local hemorrhage, reactive arthritis, Guillain Barre syndrome)
20
Q

Diagnosis of campylobacter jejuni & coli (2)

A
  1. Stool culture on selective medium w antibiotics to suppress faecal flora
    - microaerophilic conditions, 42C
    - grey spreading oxidase positive colonies
    - gram stain - typical spiral morphology
  2. Serology
21
Q

Treatment of campylobacter jejuni & coli (2)

A
  1. Supportive therapy: rehydration

2. Erythromycin/Ciprofloxacin - for severe symptoms

22
Q

Prevention of campylobacter jejuni & coli (3)

A
  1. eliminate from poultry farms
  2. safe food handling & cooking practices
  3. safe water supplies, pasteurise milk
23
Q

Clinical presentations of campylobacter fetus (3)

A
  • causes abortion in sheeps, cows
    1. Occasional cause of diarrhea
    2. Septicaemia in immunocompromised
    3. Rare cause of septic abortion
24
Q

Features of H. pylori

A
  1. Urease positive

2. Only infects gastric-type mucosa

25
Q

Transmission of H. pylori

A
  1. Faecal-oral

2. Oral-oral

26
Q

Clinical presentations of H. pylori (3)

A
  1. Symptoms ~2 weeks: abdominal pain, flatulence, nausea, bad breath
  2. Chronic active gastritis - provoked by bacterial antigens, may be asymptomatic, stomach pain (non-ulcer dyspepsia) & eventual atrophic gastritis
  3. H. pylori gastritis is linked to 1. peptic ulceration 2. gastric cancer 3. gastric MALT lymphoma
27
Q

Diagnosis of H. pylori (6)

A

Non-invasive - in younger patients with dyspepsia (no alarm symptoms) - if not scope (risk of cancer)

  1. Urea Breath Test - drink solution of urea with 14C, H. pylori breaks down urea into CO2 & NH3, CO2 absorbed into bloodstream & excreted rapidly through lungs
  2. Faecal Antigen Test
    - false negs due to antibiotics, PPIs, acute bleeding
  3. Serology (serum, blood urine, saliva) - false pos in recently treated patients

Invasive

  1. Culture from gastric biopsies taken through fibre-optic endoscope
    - grows micro-aerophilically at 37C
    - colonies are rapidly urease positive
  2. Histology/Microscopy
  3. Rapid Urease Test
    - biopsy added to urease broth
    - positive result seen in a few min because bacterium makes a lot of enzymes
28
Q

Treatment of H. pylori

A
  • several agents to eliminate colonisation

- more complex regimes - higher clearance rates, but expect relapse

29
Q

Prevention of H. pylori (3)

A
  1. Improved living conditions - lower infection rates
  2. Careful disinfection of endoscopes to prevent nosocomial transmission
  3. No vaccine
30
Q

Features of H. cinaedi & fennelliae

A
  • associate with proctitis in homosexual men

- can also cause bacteremia