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micro_db > chlamydia, mycoplasma, rickettsia and coxiella > Flashcards

chlamydia, mycoplasma, rickettsia and coxiella Flashcards

1
Q

what antibiotics are generally used to treat chlamydia species?

A

tetracyclines and macrolides

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2
Q

what type of cells commonly affect chlamydia species

A

columnar epithelial cells of the membranes

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3
Q

C. psittaci mainly affects the genitourinary tract.

True/False

A

False

C. pneumonia and psittaci affect the respiratory tract

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4
Q

what systems are affected by chlamydia trachomatis?

A

eyes, respiratory tract and genitourinary tract

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5
Q

list the diseases that can be caused by C. trachomatis

A
  • Trachoma and inclusion conjunctivitis
  • Urethritis
  • Lymphogranuloma venereum
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6
Q

what are the risk factors of C. trachomatis infection?

A
  • Poor access to water

* Overcrowding (facilitating transfer of infected secretions)

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7
Q

what are the factors associated with decreased risk of trachoma?

A

– facial cleanliness

– reducing fly contact (via insecticide spraying, building toilet facilities, etc)

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8
Q

what scaring complication of Cl trachomatis is more in females than males?

A

Thought to reflect frequent contact with children (the primary reservoir of infection).

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9
Q

what is trichiasis

A

abnormally positioned eyelashes that grow back toward the eye, touching the cornea or conjunctiva. This can be caused by infection, inflammation, autoimmune conditions, congenital defects, eyelid agenesis and trauma such as burns or eyelid injury. It is the leading cause of infectious blindness in the world.

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10
Q

compare active vs cicatricial phases of trachoma

A

1) Active phase: conjunctival follicles (with eventual involution forming Herbert pits), inflamed upper tarsal conjunctiva
2) cicatricial phase: chronic/recurring inflammation in both eyes → conjunctival scarring → progressive conjunctival shrinkage → corneal ulcers and opacities, superficial neovascularization with cellular infiltration (corneal pannus), entropion, trichiasis

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11
Q

follicle formation occurs in cicatricial phase of trachoma.

True/False

A

False
During active phase: conjunctival follicles (with eventual involution forming Herbert pits), inflamed upper tarsal conjunctiva

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12
Q

what is the inclusion conjunctivitis (paratrachoma)?

A

conjunctivitis in newborns due to transmission during labor

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13
Q

what serotypes of C. trachomatis cause inclusion conjunctivitis?

A

Chlamydia trachomatis types D–K

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14
Q

what are the clinical features of inclusion conjunctivitis?

A
  • Conjunctival follicles
  • Papillary hypertrophy
  • Corneal pannus (superficial vascularization of the cornea with cellular infiltration)
  • Preauricular lymphadenopathy
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15
Q

what is the prevention of inclusion conjunctivitis?

A

oral azithromycin, erythromycin

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16
Q

inclusion conjunctivitis arises immediately after birth.

True/False

A

False

5-14 days postpartum (vs chemical-during first few days, gonorrheal-during first week)

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17
Q

what is the lymphogranuloma venerum?

A

sexually transmitted disease caused by L1–3 serovars of Chlamydia trachomatis. Patients initially develop a small, painless papule in the genital region that may ulcerate but will heal and disappear within one week. 2–4 weeks after the initial lesion, patients present with painful, suppurative, bilateral inguinal lymphadenopathy, and systemic symptoms such as fever, malaise, chills, and/or myalgia.

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18
Q

which serovars of chlamydia cause lymphogranuloma venerum?

A

L1-L3

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19
Q

Lymphogranuloma venerum is widespread in developed countries.
True/False

A

False

it is common in tropics

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20
Q

what other systemic manifestation can be seen in neonatal infection with Cl. trachomatis

A

pneumonia

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21
Q

Chlamydia pneumoniae cause lobar pneumonia

True/False

A

False

with Mycoplasma pneumoniae they are a common cause of atypical pneumonia

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22
Q

How Chlamydia pneumoniae is transmitted

A

via respiratory droplets

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23
Q

what are the risk factors of pneumonia with Chlamydia pneumoniae

A
  • Outbreaks: living in close-quarters (e.g., nursing homes)
  • More common in older adults (seroprevalence increases with age)
    although atypical pneumonia is common in young adults
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24
Q

how much is the incubation period of pneumonia caused by Chlamydia pneumoniae

A

3-4 weeks

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25
Q

what are the phases of pneumonia caused by Chlamydia pneumoniae

A

symptoms commonly occur in two phases: symptoms of upper respiratory tract infection appear first, followed by symptoms of pneumonia after the first week.

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26
Q

what symptoms of URT infection are typical to Chlamydia pneumoniae

A

pharyngitis, hoarseness

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27
Q

what are the extra-pulmonary manifestations of Chlamydia pneumoniae

A
  • Meningoencephalitis
  • Guillain-Barre syndrome
  • Reactive arthritis
  • Myocarditis
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28
Q

what is reactive arthritis

A

an immune-mediated condition that typically occurs 1-4 weeks after bacterial infection of the gastrointestinal or genitourinary tract. Particularly common after infection with Shigella, Yersinia, Salmonella, Campylobacter, or Chlamydia.

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29
Q

where outbreaks of Cl psittaci occurs

A

pet shops, aviaries, veterinary hospital, poultry flocks, turkey and duck processing

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30
Q

what age group is at higher risk of Cl psittaci

A

Young and middle-aged adults, although it has been described in all age groups

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31
Q

Cl psittaci is antroponosis. True/False

A

False
It is zoonosis
A group of infections that are transmitted from animals to humans. Typically endemic to specific geographical regions. Examples include Q fever, babesiosis, and epidemic typhus.

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32
Q

how Cl psittaci is transmitted?

A

Airborne: Inhalation of dried infected droppings and/or secretions of infected birds (alive or dead!)

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33
Q

how much is the incubation period of pneumonia caused by Cl psittaci

A

1-3 weeks

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34
Q

what are the manifestations of pneumonia caused by Cl psittaci

A

• Infection often asymptomatic (or mild symptoms)
• Acute flu-like symptoms esp. fever
• Pneumonia
Complications rare but severe:
• Respiratory failure, hepatitis, endocarditis, and encephalitis.
• Infection in pregnancy may be life-threatening

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35
Q

what are the ways to diagnose Cl pneumonia and psittaci

A
  • Nucleic acid amplification testing (PCR)
  • Serology to detect specific IgG

–A 4-fold rise in titer

• [cell culture] Obligate intracellular pathogens, i.e. need living cells to survive

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36
Q

why penicillin is ineffective for the treatment of chlamydia

A

penicillin disrupts cell wall peptidoglycan, chlamydia and mycoplasma does not have peptidoglycan

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37
Q

what is the leading infectious caused of blindness worldwide?

A

C. trachomatis

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38
Q

what is the cicatricial phase caused by C. trachomatis

A
  • -Active phase: conjunctival follicles (with eventual involution forming Herbert pits), inflamed upper tarsal conjunctiva
  • -Cicatricial phase: chronic/recurring inflammation in both eyes → conjunctival scarring → progressive conjunctival shrinkage → corneal ulcers and opacities, superficial neovascularization with cellular infiltration (corneal pannus), entropion, trichiasis
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39
Q

how C. trachomatis is transmitted?

A

– Direct (human to human - eye, nose, throat secretions).

– Indirect (fomites contaminated with secretions - handkerchiefs, towels, flies)

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40
Q

how trachoma is diagnosed?

A

clinically

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41
Q

what is the treatment of trachoma

A

– Surgical correction of trichiasis (ingrown eyelashes) prevents the development of corneal opacification,
– Antibiotics (azithromycin / tetracycline)
– Facial cleanliness
– Environmental improvements may disrupt the cycle of reinfection.

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42
Q

how inclusion conjunctivitis is diagnosed?

A

Conjunctival scraping – antigen detection / nucleic acid amplification testing (NAAT)

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43
Q

how STD caused by C. trachomatis is diagnosed?

A
  • -Nucleic acid amplification testing (NAAT) vulvo-vaginal swabs / endo-cervical swabs/ first-catch urine/ urethral swabs/ rectal swabs
  • -Antigen etection
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44
Q

how lymphogranuloma venerum is diagnosed?

A
  • NAAT of aspirated fluid

* Serology

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45
Q

what is the treatment of lymphogranuloma venerum

A
  • Aspirate buboes
  • Doxycycline
  • Treat the partners too
  • Check for other causes of STI
46
Q

do partners of patients with chlamydial STD need to be treated?

A

Yes

no in Bacterial Vaginosis, the rest yes

47
Q

what is the difference of sexual infection with C. trachomatis in male vs female

A

1) cause urethritis, 50% are symptomatic: dysuria, frequency, discharge
2) cervicitis: the majority are asymptomatic, non-specific symptoms include discharge, ost-coital bleeding

48
Q

what is the complication in females of sexually transmitted C. trachomatis infection?

A

Pelvic inflammatory diseases and resulting complications of pregnancy: PPROM, preterm delivery

49
Q

what are the other manifestations of sexually transmitted C. trachomatis infection in males?

A

acute epididymitis and proctitis

50
Q

what are the clinical features of acute epididymitis

A

U/L testicular pain, tenderness and palpable swelling

51
Q

Clmaydia are G+ obligate extracellular pathogens

True/False

A

False

Gram negative obligate intracellular pathogen

52
Q

why Chlamydia cannot replicate outside the cell?

A

cannot produce its own ATP and rely on host cell ATP for protein synthesis

53
Q

describe the cell wall of clamydia

A

The unique cell wall of Chlamydia is thought to be one of its virulence factors, as it inhibits phagolysosome fusion in phagocytes. The cell wall contains an outer lipopolysaccharide membrane but lacks peptidoglycan. It instead contains cysteine-rich proteins that are likely the functional equivalent of peptidoglycan. This unique cell wall structure allows for intracellular division and extracellular survival.

54
Q

chlamydia cannot survive outside the cell.

True/False

A

False

They can survive and are stable but cannot replicate

55
Q

what are the 2 phases of the life cycle of chlamydia?

A

First phase: elementary bodies

second phase: reticulate bodies

56
Q

describe the elementary bodies of chlamydia

A

characterize the infectious stage of Chlamydiaceae; metabolically almost inactive and environmentally stable

  • -Attachment of extracellular elementary bodies to target cells (mostly on the respiratory or urogenital epithelium)
  • -Endocytosis
  • -Transformation into reticulate bodies in the endosome
  • -Fusion of the endosome with lysosomes does not occur in the infected cell, allowing the pathogen to survive unharmed and persist within the cell.
57
Q

describe the reticulate bodies of chlamydia

A

represent the obligate intracellular, replicative, and metabolically active form of chlamydia

  • -Multiplication and aggregation of various reticulate bodies in the endosome, which take over most of the infected cells, at which point they are called inclusion bodies. Inclusion bodies are visible under light microscopy.
  • -Transformation of reticulate bodies to elementary bodies
  • -Lysis of endosomes
  • -Release of newly formed elementary bodies and exit from the cell
  • -New start of the cycle
58
Q

the reticulate body is the infectious form of the chlamydia

True/False

A

False

It is the active form, an infectious form is an elementary body which exit the cell and affect others

59
Q

inclusion bodies seen with chlamydia infections represent reticulate or elementary bodies?

A

reticulate as it is the intracellular form

60
Q

what serotypes cause trachoma vs inclusion trachomatis

A

A-C vs D-K

61
Q

the respiratory tract is affected by L serotypes of chlamydia
True/False

A

False
D-K
L serotypes cause Lymphogranuloma venerum

62
Q

what is the Coxiella burnetii?

A

A gram-negative intracellular organism that causes Q fever. Transmitted by inhalation of aerosols from the secretions of livestock or ingestion of raw milk produced by infected animals. The primary reservoir includes cattle, sheep, and goats. It can survive in harsh environments in an endospore form.

63
Q

what is the reservoir of Coxiella burnetii

A

– Reservoir: cattle / sheep / goats

– May also be present in smaller animals, such as cats, dogs or rabbits

64
Q

how Coxiella burnetii is transmitted?

A

– Inhalation of contaminated aerosols arising from the placenta or parturient fluids of infected livestock
– Ingestion of raw milk produced by infected animals (rare)

65
Q

does Coxiella burnetii produce spores?

A

Yes

Can form spores which can survive for prolonged periods outside of the host

66
Q

what are the risk groups for acquiring Coxiella burnetii

A

Farmers, abattoir workers, vets i.e., occupational exposure

67
Q

what are the clinical features of acute Q fever

A 
•	Asymptomatic (50%) 
•	Flu-like illness 
•	Atypical pneumonia
•	Hepatitis
•	Pregnancy: 
--usually asymptomatic but: ↑ risk of  IU death/growth retardation / premature delivery
68
Q

what are the clinical features of chronic Q fever

A

• 1-5% infected people
• Commonest manifestation – culture-negative endocarditis
• osteomyelitis, vascular graft infection
• More likely if
–pregnant, immunocompromised, underlying valvular or vascular disease

69
Q

what is the most common manifestation of chronic Q-fever?

A

culture-negative endocarditis

70
Q

Q fever causes lobar pneumonia.

True/False

A

Mainly atypical pneumonia (lobar is possible)

71
Q

what are the pregnancy risks of acute Q fever?

A

• usually asymptomatic but: ↑ risk of IU death/growth retardation / premature delivery

72
Q

what are the diagnostic tests of Q fever?

A

– Serology
– Nucleic acid amplification testing (NAAT) (not commonly available)
– Culture: biosafety level 3 containment due to extreme infectivity

73
Q

what is the phase 1 vs 2 antigens of Coxiella burnetii?

A

–phase I antigens: seen when C. burnetii is highly infectious
–Phase II antigens: seen when C. burnetii is less infectious
Antigenic shift essential to differentiating acute Q fever from the chronic variant

74
Q

antibodies against phase 1 or 2 Coxiella antigens develop first?

A

Although phase I antigens indicate a high level of infectiousness, the antibodies to phase II antigens develop first and are characteristic markers of acute Q fever.

75
Q

how acute vs chronic Q fever is diagnosed?

A

1) anti-phase II antibody IgG titers ≥ 200 and IgM titers ≥ 50
- -In cases of negative IFA but high clinical suspicion, perform PCR on serum or tissue samples before administering antibiotics.
2) Anti-phase I antibody IgG titers > 800 or persistently high levels of anti-phase I antibody 6 months after completing therapy

76
Q

what is the treatment of Q fever?

A
  • Acute: Doxycycline

* Chronic: Combination therapy (e.g. doxycycline + rifampicin) for a prolonged period (years)

77
Q

what is the treatment of chronic Q-fever?

A
  • -First-line: doxycycline and hydroxychloroquine for ≥ 18 months
  • -Second-line: rifampin and doxycycline/ciprofloxacin
  • -Valve repair may be required in the case of endocarditis.
  • -The patient is treated until phase I antigen titers decrease. Hydroxychloroquine alkalinizes the acidic phagolysosome and allows doxycycline to act against C. burnetii.
78
Q

how Q fever is prevented?

A
  • Appropriate disposal of the placenta, birth products, etc from facilities housing sheep and goats
  • Consuming only pasteurized milk and milk products
  • Quarantining imported animals
  • Locating holding facilities for sheep away from populated areas
79
Q

in what cell Coxiella inhabitants?

A

Intracellular pathogen

Usual host cell = macrophage (unable to kill it - lives and multiplies in a vacuole)

80
Q

which antigen is the infectious form?

A

Phase I antigen = highly infectious and a single bacterium is sufficient to infect a human!!

81
Q

what is the Rickettsia rickettsii

A

small, gram-negative, obligate, intracellular coccobacillus responsible for Rocky Mountain Spotted Fever. It infects Dermacentor ticks, which then pass on the pathogen to humans.

82
Q

Rickettsia are an extracellular organism.

True/False

A
  • Gram-negative

* Depends on the host cell for nutrition and metabolism = can’t replicate outside the host cell (obligate intracellular)

83
Q

what cells predominantly are affected by Rickettsia?

A

A predilection for vascular endothelial cells (causes vasculitis)

84
Q

with ticks transmits Rickettsia rickettsii

A

Dermacentor andersoni

85
Q

how rickettsia species are transmitted to humans?

A

Transmitted from a vertebrate host by an insect, e.g., body louse, rat flea, tick, mite

86
Q

what are etiologic agents of RMSF vs Epidemic typhus vs Murine Typhus

A
  • -Rickettsia rickettsii
  • -Rickettsia prowazekii
  • -Rickettsia typhi
87
Q

how RSMF vs Epidemic typhus vs Murine typhus transmitted?

A

ticks vs body lice vs fleas

88
Q

what are the reservoirs of RMSF vs EPIDEMIC and Murine Typhus

A

1) dogs, rodents, ticks
2) humans
3) rats, mice cats

89
Q

what is the geographical distribution of MSF vs EPIDEMIC and Murine Typhus

A

1) North, Central, and South America
2) Africa, South America, Mexico, Asia
3) worldwide

90
Q

what is the pathophysiology of Rickettsia

A

Multiply at the site of inoculation from which they disseminate throughout the body –with localization in the endothelial cells of small blood vessels

91
Q

what are the common clinical manifestations of Rickettsia

A
  • Fever, headache, and intense myalgias, often in association with rash and organ involvement
  • Relative bradycardia despite fever (typhus)
  • GI symptoms common
92
Q

what is the mortality of RMSF or Epidemic typhus?

A
  • RMSF – overall mortality 4% (even with treatment)

* Epidemic typhus – 20% - 50% mortality (untreated)

93
Q

what is the Weil-Felix test?

A

A diagnostic test for rickettsial infections, whereby suspensions of proteus antigens (OX 19, OX 2, or OX K) are mixed with a patient’s serum. Agglutination occurs in the serum of patients infected with Rickettsia (antibodies cross-react with Proteus mirabilis antigens)

94
Q

how rickettsial diseases are commonly diagnosed?

A

Serology

– 4 fold rise in titers

95
Q

what antibiotic is the treatment of choice of Rickettsial diseases?

A

doxycycline

96
Q

how rickettsial diseases need to be prevented?

A
  • Wear long sleeved protective clothing and broad brimmed hat to reduce the risk when undertaking activities where human contact with ticks, lice, mites or fleas may occur, such as bushwalking and camping in infected areas.
  • DEET containing insect repellent
  • Examine skin for possible bites (especially behind the ears, on the back of the head, in the groin, armpits and behind the knees) following the above activities.
97
Q

describe Mycoplasma species

A

A type of bacteria characterized by the lack of a cell wall, making them resistant to antibiotics that target cell-wall synthesis. Common subspecies that cause infections in humans are Mycoplasma pneumoniae (atypical pneumonia) and Mycoplasma hominis (e.g., pelvic inflammatory disease).

98
Q

describe the cell wall of mycoplasma species

A

The murine layer is absent (so they are pleomorphic), cholesterol is present in the cell membrane, which is obtained from the host organism

99
Q

how mycoplasma pneumoniae spread?

A

Respiratory droplets. Person to person spread

100
Q

what age group is at risk for contracting Mycoplasma pneumonia?

A
  • -Outbreaks: living in close quarters

- -More common in young children than in adolescents and adults

101
Q

what are the clinical features of Mycoplasma pneumoniae infection?

A
  • Cough, pharyngitis, rhinorrhea, ear pain

* Pneumonia (10%)

102
Q

what are the extra-pulmonary manifestations of Mycoplasma pneumoniae

A

– Hemolysis (rarely clinically significant),
– Skin rash including Erythema Multiforme and Stevens-Johnson syndrome,
– Carditis
– Encephalitis (more common in children)

103
Q

how mycoplasma pneumoniae is diagnosed?

A

– Serology

– Nucleic acid amplification testing (NAAT)

104
Q

what antibiotics are used to treat mycoplasmal infections?

A

macrolides / doxycycline

105
Q

what mycoplasma species affect the genito-urinary tract?

A

Mycoplasma hominis

Ureaplasma urealyticum

106
Q

what agar is used to grow Mycoplasma species?

A

Eaton agar,

Colonies classically have a “fried egg” appearance.

107
Q

does Mycoplasma species can be part of normal genital flora?

A

Yes
–Many healthy asymptomatic adults have genitourinary colonization with Mycoplasma and Ureaplasmaspp – increases with sexual activity

108
Q

what are the manifestations of M hominis infection?

A

Chorioamnionitis. Possible association with PID less well established. Non-genitourinary tract infections also reported

109
Q

what are the manifestations of Ureaplasma urealyticum infection?

A

Chorioamnionitis, postpartum and postabortal fever, and pneumonia, bacteremia, and abscesses in neonates

110
Q

how genital mycoplasma infections are treated?

A

with doxycycline

111
Q

what are the virulence factors of My. Pneumoniae

A

Adhesins attach to epithelial cells/affinity for respiratory tract

112
Q

how hemolysis is caused in Mycoplasma infection

A

Some pathogenic features of infection, outside of the respiratory tract = immune-mediated rather than caused by direct bacterial invasion

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