Rickettsia and Spiral Organisms Flashcards

1
Q

Intracellular gram negative organisms

A

Rickettsia and Orientia
(Erlichia and Anaplasma)
Coxiella Burnetii (Q fever)

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2
Q

Spiral organisms

A

Treponema pallidum
Leptospira
Borrelia burgdoferi (Lyme disease)

Only seen under dark field micropscopy

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3
Q

Rickettsia - growth characteristics, transmission

A

Obligate intracellular parasite
Small (0.3x1-2 mcm)

Can’t grow on agar plates - requires tissue cultures
Readily inactivated by heat/disinfectants

Transmission:

  • Spotted fever group - ticks and fleas
    • tick restricted, flea worldwide
  • Typhus group
  • -> murine typhus - rodent flea
  • -> epidemic typhus - human body louse
  • Scrub typhus - larval stage of mites
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4
Q

Rickettsia - general pathogenesis, clinical manifestations, labs

A

Pathogenesis
- infect endothelial cells, especially vasculitis –> microinfarcts with necrosis and thrombosis in small vessels

Clinical manifestation depends on organ e.g. petechiae, interstitial pneumonitis, myocarditis
Site of bite may necrose and form black eschar (common in scrub typhus)

Usually 1-2 wks after arthropod bite (often at hidden skin creases/groin area)
– FEVER, RASH, HEADACHE

Lab: neutrophil + Plt low; ALT moderately high

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5
Q

Spotted Fever Group - species, vector, clinical presentations

A

Rocky mountain spotted fever

  • R. rickettsii (tick borne)
  • fever, headache, rash, myalgia, anorexia
  • can be complicated with pneumonitis, myocarditis, renal failure, DIC, CNS involvement

Other spotted fevers
- R. japonica, R. conorii, R. felis

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6
Q

Typhus Group - species, vector, clinical presentations

A

Murine typhus

  • R. typhi (flea borne)
  • acute febrile illness, rash, headache
  • rare fatality

Epidemic typhus

  • R. prowazekii (human body louse)
  • typical outbreaks where pediculosis is common
  • Brill-Zinsser disease (milder form of disease)
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7
Q

Scrub Typhus - species, vector, clinical presentations

A

Orientia tsutsugamushi
Mite borne (low lying scrubs/ transitional vegetation)
SE Asia

Eschar in 20% patients
Fatality <10% if left untreated

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8
Q

Rickettsia - diagnosis and management

A

Diagnosis:

  • clinical suspicion (need specific tests ordered)
  • PCR
  • SEROLOGY (Weil-Felix)
  • -> detect anti-rickettsial Ab in patient’s serum by inducing cross reaction with Proteus OX antigens
  • -> Ab detection e.g. IF stain

Spotted fever: OX2, OX19 for R. rickettsii
Murine: OX19
Epidemic: OX19
Scrub Typhus: OXK

Serology: 4x rise in Ab or single titre >512; or OXK >320 for scrub typhus

Management:

  • Doxycycline 7-14 days
  • Prevention by personal protection/long sleeves in rural areas, insect repellents, rodents control
  • NOTIFIABLE DISEASES
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9
Q

Q fever - organism, geographical distribution, source, transmission, pathogenesis

A

Coxiella burnetii
Intracellular pleomorphic GN bacilli

Worldwide zoonotic agent - cattle, sheep, goats
(can be maintained in ticks - minor)

Transmission:

  • inhalation of aerosol particles from parturient or slaughter ruminants or tick faeces
  • ingestion of unpasteurised milk or milk products
  • high concentration in placenta
  • LOW INFECTIVE DOSE (1-10 cells only)

Pathogenesis:
- infect alveolar macrophages and cause acute or chronic infection

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10
Q

Q fever - clinical presentations acute and chronic

A

Incubation 2-5 wks

Acute Q fever:

  • self limiting febrile illness (fever, headache, myalgia, night sweats, LFT derangement) ==> usually resolve in 10-14 days
  • atypical pneumonia
  • anicteric hepatitis (normal bilirubin, no jaundice)
  • -> may develop sterilising or non-sterilising immunity –> chronic Q fever

Chronic Q fever:

  • CULTURE NEGATIVE ENDOCARDITIS
  • intravascular infections (not common)
  • chronic granulomatous hepatitis (Doughnut granulomata)
  • osteoarticular infections
  • abortion, still birth
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11
Q

Q fever - diagnosis

A

Diagnosis:

  • clinical suspicion (PUO + sepsis workup negative + empirical antibiotics ineffective or clear exposure history or culture negative endocarditis)
  • SEROLOGY
  • -> acute: 4x change in phase II IgG
  • -> chronic: >800 phase I IgG
  • blood or tissue PCR
  • CAN’T CULTURE!
  • HISTOLOGY - doughnut ring granuloma, IHC of heart valve
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12
Q

Q fever - management

A

Acute
- Doxycycline 2 wks

Chronic
- Doxycycline AND Hydroxychloroquine >18 months
(HCQ increases pH of phagolysosome which makes doxycycline bactericidal)

Pregnancy
- Septrin for duration or pregnancy

NOTIFIABLE DISEASE

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13
Q

Treponema pallidum - size, transmission, clinical presentations, treatment

A

Difficult to stain and non-cultivable
Visualised in fresh exudate by dark ground microscopy
Killed rapidly by exposure to air/desiccation
10-20 mcm long, 100-200nm width
Transmission: sexual, congenital

Clinical disease: Syphillis

Congenital syphilis

Acquired syphilis:

  • incubation 9-90 days
  • primary – PAINLESS genital ulcers (Chancre)
  • secondary – skin rash (papulosquamous at palms and soles)
  • latent – asymptomatic, slowly develop CVS and CNS complications
  • neurosyphilis

Treatment: Benzathine penicillin G IM (longer/higher dose if late latent); Penicillin G high dose if neurosyphilis

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14
Q

Treponema pallidum - diagnosis

A

Microscopy
- dark ground, requiring fresh exudate from chancres (rarely done now)

SEROLOGY

  • non-treponemal test (VDRL, RPR)
  • -> non-specific
  • -> titres can be used as markers for treatment efficacy (decreases after treatment)
  • -> biological false positive if AI disease, pregnancy
  • treponemal test (TPHA, TPPA)
  • -> Ab remain elevated even after treatment (but not sterilising immunity)
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15
Q

Leptospirosis - organism, source, at risk population

A

Leptospira interrogans serovar icterohaemorrhagiae

Zoonosis
- direct/ indirect contact of urine of infected rodents via abrasions or cuts in the skin or conjunctiva

At risk population = sewage workers, soldiers, farmers, kayaking

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16
Q

Leptospirosis - clinical presentations

A

Majority subclinical infections
Minority have febrile illness with non-specific signs and symptoms

BIPHASIC

  • incubation 2-26 days
  • ACUTE SEPTICAEMIC phase followed by IMMUNE LEPTOSPIURIC phase with Ab production and excretion of leptospires in urine

Anicteric leptospirosis (mild)

  • 1 wk, biphasic fever, aseptic meningitis
  • mortality almost 0

Icteric leptospirosis (WEIL’S DISEASE)

  • 5-10% cases
  • jaundice, multi-system involvement with renal failure, pulmonary haemorrhage, ARDS, thrombocytopenia
  • severe and rapidly progressive
  • 5-15% mortality
17
Q

Leptospirosis - diagnosis, treatment

A

Serology as mainstay

  • Leptospiral microscopic agglutination test (LMAT)
  • titre >1600 = confirmed
  • titre 400-1600 = probable
  • but tedious and difficult to interpret

Treatment:
- Pencillin G/ Doxycycline

NOTIFIABLE DISEASE

18
Q

Lyme disease - organism, vector, prevalence

A

Borrelia burgdorferi
Most common tick-borne disease in USA
No local case in HK yet

Vector: hard bodies, blacklegged Ixodid ticks

19
Q

Lyme disease - clinical manifestations

A

Multisystem inflammatory disorder
3-32 days incubation

Early localised disease (few days - 1mnth)

  • ERYTHEMA MIGRANS (central clearing and necrotic centre at site of bite)
  • fatigue, malaise, lethargy, arthralgia, regional LN

Early disseminated disease (wks-mnths)
- carditis, lymphocytic meningitis, migratory arthralgia, multiple erythema migrans lesions, hepatitis, conjunctivitis etc.

Late or chronic disease (mnths-yrs)

  • intermittent arthritis
  • peripheral neuropathy/encephalomyelitis
  • localised scleroderma-like lesions
20
Q

Lyme disease - diagnosis, treatment

A

Diagnosis
- Serology (2 tiered testing)

Treatment

  • Doxycycline (early phase)
  • Rocephin (late phase)