Intracellular bacteria - Chlamydia; Rickettsia & Orientia; Ehrlichia, Anaplasma & Neorickettsia; Coxiella burnetti Flashcards

1
Q

Features & examples of Chlamydia

A
  • Little peptidoglycan
  • infectious form = elementary body
  • EB enters host cell & reproduces in a membrane bound vesicle = reticulate body (replicative form)
  • new EBs produced & release from infected cell
  1. Chlamydia trachomatis
  2. Chalmydophilia psittaci
  3. Chlamydophilia pneumoniae
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2
Q

Features of Chlamydia trachomatis

A
  • acquired primarily from human sources
  • many strains, distinguished by different surface antigens
    1. Oculogenital biovar = A-K
    2. Lymphogranuloma venereum (LGV) biovar = L1-L3
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3
Q

Transmission of serovars A, B, Ba, C (C. trachomatis)

A
  1. Fingers
  2. Flies
  3. Fomites
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4
Q

Clinical presentations of serovars A, B, Ba, C (C. trachomatis)

A

Trachoma (eye inf common in LDCs)

  • repeated infections occur, protective immunity doesn’t develop
    1. Pannus formation (cornea becomes clouded)
    2. Chronic inflamm & scarring of eyelids & cornea
    3. Eventual blindness
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5
Q

Diagnosis of serovars A, B, Ba, C (C. trachomatis)

A

Serology

  1. Complement fixation test (genus specific)
  2. Micro-immunofluorescence species & serovar specific
    - generally only useful for more invasive forms of infections
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6
Q

Treatment & prevention of serovars A, B, Ba, C (C. trachomatis)

A
  • Antibiotics

- Education in better hygiene

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7
Q

Transmission of serovars L1, L2, L3 (C. trachomatis)

A

Sexually transmitted disease

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8
Q

Clinical presentations of serovars L1, L2, L3 (C. trachomatis)

A

Lymphogranulomavenereum (LGV)

  • commonly in tropics/subtropics
    1. Primary lesion: small papule/vesicle on genitalia
    2. Infection spreads to regional lymph nodes which enlarge, suppurate & discharge through sinuses - M: inguinal glands affected, F & homosexual M: perirectal glands suppurate - proctitis & bloody anal discharge
    3. Chronic inflammation - lymphatic blockate - rectal stricture, elephantiasis of genitals
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9
Q

Diagnosis, treatment & prevention of serovars L1, L2, L3 (C. trachomatis)

A
  • Serology - complement fixation test, MIF
  • Antibiotics
  • Contact tracing, screening of high risk groups, use of condoms, education
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10
Q

Transmission of serovars D-K (C. trachomatis)

A
  1. Sexually transmitted disease
  2. Autoinfection (fingers)
  3. Vertical
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11
Q

Clinical presentations of serovars D-K (C. trachomatis) (3)

A
  1. Males: non/post-gonococcal urethritis - asymptomatic carriage is common, inf may spread to epididymis, prostate, proctitis in homosexuals
  2. Females: mucopurulent cervicitis, urethritis, ascending infection causing acute salpingitis/acute PID, spread into peritoneal cavity causing peri-appendicitis/peri-hepatitis (Fitz- Hugh- Curtis syndrome), vaginal discharge, proctitis
  3. Adult inclusion conjunctivitis (due to autoinfection).paratrachoma, ophthalmia neonatorum (due to endocervical inf in mother)
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12
Q

Diagnosis of serovars D-K (C. trachomatis)

A
  1. Molecular (PCR)
  2. Antigen detection (IF/ELISA)
  3. Serology
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13
Q

Treatment & prevention of serovars D-K (C. trachomatis)

A
  • Antibiotics, contact tracing, screening of high risk groups, use of condoms, education
  • Erythromycin as systemic treatment in ophthalmia neonatorum (prevent development of pneumonitis, recurrent conjunctivitis)
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14
Q

Transmission of Chlamydophilia psittaci

A

Zoonosis, from birds

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15
Q

Clinical presentations of Chlamydophilia psittaci

A

Psittacosis, Ornithosis

  • flu-like initial illness leading to pneumonia
  • dissemination - infection of brain, meninges, heart, joints etc
  • rare cause of bacterial endocarditis
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16
Q

Diagnosis & treatment/prevention of Chlamydophilia psittaci

A
  • Serology

- Quarantine & treatment of infected birds

17
Q

Clinical presentations of Chlamydophilia pneumoniae

A
  • from human sources
  1. Mild pneumonia in young adults
    - both upp & lower resp tract symptoms
    - reinfection/chronic infection in older patients, roles in asthma, COPD, bronchitis etc
  2. May contribute to atherosclerosis & CHD
  • diagnosis: serology
18
Q

Features of rickettsia & orientia

A
  1. Small gram neg bacilli
  2. Obligate intracellular pathogens
  3. Reproduce in endothelial cells lining blood vessels
19
Q

Transmission of rickettsia & orientia

A

Zoonosis, by arthropod vectors

  1. Typhus Group - louse or flea
  2. Spotted Fever Group - mostly by ticks (R. akari by mouse mite, R. felis by cat flea)
  3. Scrub Typhus Group - chiggers (parasitic larval stage of mite)
20
Q

Clinical presentations of rickettsia & orientia (3)

A

Triad of fever + rash + tick bite

  1. PUO with headache & muscle pain
  2. Skin Rash (macular/papular/petechial/vesicular in rickettsial pox), if severe - damage of blood vessels - hypotension & hypoperfusion of organs - multiple organ failure - SIRS, death
  3. Bite mark, eschar (ulcer w dark/black crust, in spotted fever/scrub typhus)
21
Q

Classification of rickettsia & orientia

A

Typhus Group

  • Epidemic typhus: R. prowazekii - spread person to person by body louse, infection kills louse vector, inf may reactivate after many years: Brill-Zinsser Disease
  • Murine typhus: R. typhi (assoc w rats, fleas are the vector)

Spotted Fever Group

  • R. rickettsi (rocky mountain, spotted fever, ecchymotic rash)
  • R. conorii (boutonneuse fever)
  • R. africae (African tick bite fever)
  • R. akari (rickettsial pox)
  • R. felis (flea-borne SF)

Scrub Typhus Group
- Orientia tsutsugamushi

22
Q

Diagnosis of rickettsia & orientia

A

Serology - no longer use Weil-Felix test due to low sensitivity & specificity

23
Q

Treatment of rickettsia & orientia

A

Doxycycline

- antibiotic resistant O. tsutsugamushi detected in N Thailand

24
Q

Prevention of rickettsia & orientia (2)

A
  1. Delouse at risk populations

2. Physician awareness & stringent rodent control measures

25
Q

Features of ehrlichia, anaplasma & neorickettsia

A
  1. Obligate intracellular pathogens of WBCs - replicate in leukocytes
26
Q

Features of E. chaffeensis, A. phagocytophilum, E. ewingii

A
  • E. chaffeensis infects human monocytes/macrophages
  • A. phagocytophilum & E. ewingii infect granulocytes
  • transmitted via tick bite, animal reservoirs
  • fever, sometimes rash & severe multi-system disease, may develop secondary opportunistic infections
27
Q

Features of Neorickettsia sennetsu

A
  • infections found in Japan & Malaysia, infects human macrophages
  • transmitted via eating raw fish containing infected trematodes (flukes)
  • glandular fever like illness (infectious mononucleosis) with chills, fever & enlarged cervical lymph nodes
  • rash is rare, usually a mild infection
28
Q

Diagnosis of ehrlichia, anaplasma & neorickettsia

A
  1. Serology

2. Morula seen in cytoplasm of leukocytes - intracellular inclusion w replicating bacteria

29
Q

Treatment of ehrlichia, anaplasma & neorickettsia

A

Doxycycline

30
Q

Features of Coxiella burnetti

A
  1. Obligate intracellular pathogen
  2. Replicates in acidified vesicle (phagolysosome) within macrophages
  3. Spore-forming (resistant spore-like structures), survive drying & other environmental stresses
31
Q

Transmission of Coxiella burnetti

A
  • naturally infects many animal species - sheep, cattle, goats, shed in large numbers in urine, faeces, milk, birth products

Zoonosis (airborne or drinking infected milk)

32
Q

Clinical presentations of Coxiella burnetti (2)

A
  1. Acute Q fever
    - many infected asymptomatically/minor symptoms, some with pneumonia, hepatitis, PUO
  2. Chronic Q fever
    - endocarditis (“culture negative endocarditis” as organism does not grow in conventional blood culture systems), rarely cholecystitis
33
Q

Diagnosis of Coxiella burnetti

A

Serology, PCR, culture

34
Q

Treatment of Coxiella burnetti (2)

A
  1. Acute infection: Doxycycline + Rifampicin

2. Endocarditis: difficult, combinations of drugs for long periods or valve replacement