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ID Week 5 > ICL 2.25: Francisella, Brucella & Acinetobacter > Flashcards

ICL 2.25: Francisella, Brucella & Acinetobacter Flashcards

1
Q

what is the microbiology of actinobacter?

A

gram (-) coccus

aerobic

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2
Q

what is the microbiology of francisella?

A

gram (-) pleomorphic = coccobacilli

not motile

has a capsule

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3
Q

what is the micropbiology of brucella?

A

gram (-) pleomorphic = coccobacilli

not motile

strict aerobe

no capsule

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4
Q

what are the similarities between francisella and brucella?

A
  1. grow poorly in the lab = need 2+ days to see colonies
  2. non motile
  3. intracellular pathogens
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5
Q

what is the microbiology of francisells tularensis?

A

gram (-) coccobacillus

strict aerobic

non-motile

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6
Q

is francisella tularensis spore-forming?

A

no

but because of its capsule it can survive for months at low temperatures in water, moist soil, hay, straw, and decaying animal carcasses

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7
Q

how do you grow francisella tularensis?

A

chocolate agar

requires cysteine and blood for growth

takes 2+ days for colonies to grow

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8
Q

what are the virulence factors of francisella tularensis?

A
  1. capsule
  2. francisella pathogenicity island (FPI)
  3. LPS
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9
Q

how does the francisella tularensis capsule act as a virulence factor?

A

anti-phagocytic

binds complement = bacteria isn’t lysed

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10
Q

how does the francisella pathogenicity island act as a virulence factor?

A

it’s required for phagosome escape and possible secretion

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11
Q

how does francisella tularensis LPS act as a virulence factor?

A

its LPS has super long acyl chains and only has 4 acyl chains instead of 6

this modified LPS doesn’t stimulate TLR4 = immune evasion

so it’s not endotoxic = no cytokine-mediated inflammation and no TNFα

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12
Q

what kind of pathogen is francisella tularensis?

A

intracellular pathogen

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13
Q

which cells does francisella tularenis infect? what does it do?

A

it infects macrophages, dendritic cells, neutrophils, epithelial cells, etc. (basically everything)

it inhibits phagosome-lysosome fusion!!

then it somehow escapes the phagosome into the cytosol to replicate

it’ll eventually cause apoptosis of the cell so it can be released

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14
Q

what is francisella related to?

A

nothing…

Francisella are not related to any other genus

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15
Q

what are the francisella tularenis subspecies?

A
  1. F. tularensis subsp. tularensis = type A

**type A is the most virulent subspecies; LD50 = 10 bacteria!!

  1. F. tularensis subsp. holarctica = type B
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16
Q

where are F. tularensis type A and B found in the world?

A

type A = strictly north america

type B = North America, Europe, Russia, and Asia

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17
Q

where do most tularemia cases occur in the US?

A
  1. OK
  2. MO
  3. AR
  4. KS
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18
Q

how is F. tularensis transmitted?

A

ticks are the most common

but it can also be biting flies and mosquitoes

also aerosolizing an infected bunny/reservoir and breathing in the bacteria could cause it too or ingesting an infected bunny

no person-person spread

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19
Q

what time of the year is tularemia most common?

A

may, june, july = summer

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20
Q

what is the reservoir for F. tularensis?

A
  1. rabbits
  2. house cats

can also be ground squirrels, hares, muskrats, voles, mice, water rats, and other rodents are reservoir

F. tularensis has also been found in water, soil and vegetation

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21
Q

what are the possible disease states of F. tularensis?

A
  1. typhoidal
  2. pneumonic
  3. ulceroglandular
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22
Q

what is ulceroglandular F. tularensis?

A

you’ll get a cutaneous ulcer at the site of inoculation

you’ll also have proximal lymphadenopathy = super swollen lymph nodes

you can it from ticks or handling infected animals

mortality = 3%

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23
Q

what is pneumonic F. tularensis?

A

you’ll get atypical pneumonia or hilar lymphadenopathy

this is the most likely presentation of F. tularensis if exposed to aerosol

so you can get it from lawn mowing, haymaking, lab exposure or bioterrorism

mortality is 60%

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24
Q

what is typhoidal F. tularensis?

A

you can get septicemia and have systemic involvement

there will be no evidence of skin, mucosal or lymphatic involvement

this is what happens if the other F. tularensis presentations aren’t treated they can progress to typhoidal tularemia

mortality is 60%

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25
Q

what are the clinical symptoms of acute tularemia?

A

lasts 3-5 days

  1. Fever (up to 104∘F), chills
  2. Malaise
  3. Headache
  4. Sore throat
  5. Myalgia
  6. Anorexia
  7. Prostration
  8. Erythema nodosum
26
Q

what are the clinical symptoms of prolonged tularemia?

A

lasts from day 6 to death

has all the symptoms seen in acute tularemia plus:

  1. cough (productive or non-productive)
  2. chest pain
  3. liver dysfunction
27
Q

what is the pathology of an F. tularensis infection?

A

pathology mainly in lymph nodes, lungs, spleen, liver, and kidneys

there’s an influx of neutrophils, macrophages, and lymphocytes that may form granulomas

granulomas develop necrotic centers, sometimes caseating, typical of other granulomatous conditions

the infected macrophages can’t kill the bacteria so they undergo apoptosis –> francisella is released –> it infects new macrophages and travels through the lymphatics and infects other tissues and organs

28
Q

how do you diagnose an F. tularensis infection?

A
  1. risk factors = rabbit hunting, ticks, sick cat
  2. microscopic examination of secretions, exudates, biopsy

but not very sensitive, francisella gram stains poorly and it’s hard to find sufficient organisms in specimens

  1. culture of ulcer scrapings, lymph node biopsy, or sputum = sensitive and specific but just use chocolate agar
  2. serology confirms diagnosis = compare titer with second titer 2 weeks later (4x)
29
Q

how do you treat F. tularensis?

A
  1. doxycycline
  2. ciprofloxacin

F. tularensis produces B-lactamases, so B-lactams are ineffective

30
Q

how do you prevent F. tularensis infections?

A

no vaccine

31
Q

how do you grow brucella?

A

special Brucella medium

requires a week or more for visible growth on media

strict aerobe

32
Q

which tissues does Brucella infect?

A
  1. epididymis
  2. placenta
  3. breast
  4. uterus

prefers to infect organs that are rich in erythritol because it metabolizes easier than glucose

infection causes sterility, abortions, or asymptomatic lifelong carriage

33
Q

what kind of pathogen is brucella?

A

intracellular pathogen

replicates and persists within macrophages

prevents phagolysosome fusion –> persist/multiply within endosomal compartment

34
Q

what are the virulence factors of brucella?

A
  1. urease

2. LPS

35
Q

how does urease act a virulence factor for brucella?

A

buffers bacteria from low pH of stomach

urea –> CO2

36
Q

what are the 2 types of LPS in brucella?

A

alterations in LPS O-antigen result in smooth or rough colony phenotypes –>- smooth isolates much more virulent than rough

rough colonies lack O-antigen (B. canis)

smooth = has O-antigen

rough = lacks O-antigen

either LPS form is much less stimulatory than LPS from other gram negatives

37
Q

how does LPS act as a virulence factor for brucella?

A

has hella long acyl chains that are not recognized by TLR4

this LPS also inhibits apoptosis of infected macrophages

smooth LPS O-antigen groups block complement C3 binding

also the O-antigen amido groups are difficult to degrade so they block MHCII presentation of infected macrophages

38
Q

what are the 4 brucella species that cause human disease?

A
  1. B. melitensis**
  2. B. abortus
  3. B. suis
  4. B. canis
39
Q

where is brucellosis endemic?

A

Mediterranean Basin**

Middle East

Latin America

S.E. Europe

Asia

Africa

40
Q

where is brucellosis common in the US?

A

Most U.S. cases in Texas and California

CA, TX, IL, FL = half of U.S. cases

41
Q

how do you get brucellosis?

A
  1. abraded skin
  2. inhalation
  3. conjunctiva
  4. ingestion

no person-person spread

it’s shed in high numbers in milk, urine, birth products

**human disease is most often associated with consumption of contaminated unpasteurized dairy products (mainly milk and cheese)

42
Q

what disease state does brucellosis cause?

A

causes sterility and abortions (pregnancy tolerance –> bacterial replication)

43
Q

which groups are at risk for brucellosis?

A
  1. ingestion of unpasteurized milk, cheese, other dairy products
  2. slaughterhouse workers (reduced with brucellosis control measures in cattle)
  3. veterinarians (RB51 vaccine is B. abortus rough strain; rifampicin resistant)
  4. lab workers (highly infectious; BSL-3 required)
  5. hunters (feral swine, bison, elk)
44
Q

what are the 3 forms of brucellosis?

A
  1. acute form
  2. undulant form
  3. chronic form
45
Q

what is the acute form of brucellosis?

A

<8 weeks from illness onset

nonspecific “flu-like” symptoms include undulating fever, malodorous sweats, malaise, anorexia, headache, myalgia, and back pain

46
Q

what is the undulant form of brucellosis?

A

<1 year from illness onset

  1. intermittent fevers, arthralgia, myalgia
  2. epididymo-orchitis in males
  3. spontaneous abortions in females
  4. neurologic symptoms may occur ≥ 5% of cases
47
Q

what is the chronic form of brucellosis?

A

> 1 year from onset

symptoms may include chronic fatigue syndrome, depression, and arthritis

hepatomegaly, splenomegaly, lymphadenopathy

endocarditis in only 2% of cases but these can progress to death (80% of brucellosis endocarditis lethal)

48
Q

what are the key symptoms of brucellosis in general?

A
  1. undulating fever
  2. malodorous perspiration
  3. arthralgia
49
Q

how do you diagnose brucellosis?

A
  1. history!!!!
  2. culture from blood i gold standard

must use enriched blood agars to culture; takes 2 weeks to grow

  1. speciic antibodies are present in almost all brucellosis patients

IgM early 1st week then IgG

must see 4x increase in titer for diagnosis

50
Q

what is the Ruiz-Castaneda test?

A

used to diagnose brucellosis

blood sample inoculated into vial containing both agar slant and broth media; must rotate vial daily to allow bacteria from broth to form colonies on agar

but takes 7-21 days to grow….

51
Q

what is the lysis centrifugation test?

A

used to diagnose brucellosis

collect blood –> lyse RBCs in water and sodium citrate –> pellet bacteria –> plate

takes 2-4 days to grow; faster than Ruiz castaneda

52
Q

how do you treat brucellosis?

A

because of slow growth, latency, and granuloma formation, need to treat with at least 2 antibiotics for 6 weeks

doxycycline and rifampicin

***except vets because the RB51 vaccine they give to animals is rifampicin resistant so you treat them with doxy and streptomycin

53
Q

is there a brucellosis vaccine?

A

no

there’s a live attenuated vaccines for B. abortus and B. melitensis are used in animals but not in humans because they cause disease

54
Q

where is actinobacter found in nature?

A

tolerate many environments; soil, skin, water, moist and dry surfaces

also part of normal flora of skin and oropharynx

common in hospitals (burn units, intensive care); easy to culture

55
Q

which acinetobacter species is responsible for most human disease?

A

A. baumannii

it’s not a risk for immunocompotent people!

56
Q

what diseases can A. baumannii cause?

A
  1. pneumonia
  2. septicemia
  3. wound infections
57
Q

what are the risk factors to acinetobacter infections?

A
  1. combat injuries: present in 1/3 of cases from Iraq and Afghanistan**
  2. ventilator-associated pneumonia: 5 - 10% of long-term ICU patients
  3. Burn units and skin/soft tissue wounds: 2%
  4. UTIs: 1.6% catheter-associated
  5. diabetes
  6. chronic lung disease
58
Q

how do you treat acinetobacter infections?

A

alot of acinetobacter is resistant to multiple antibiotics so first perform antimicrobial susceptibility testing

  1. broad-spectrum cephalosporin = ceftazidime or cefepime
  2. β-lactamase inhibitor (sulbactam) with β-lactam (ampicillin)**
  3. carbapenem = imipenem, meropenem, doripenem
  4. colistin**
59
Q

is acinetobacter resistance a problem?

A

often resistant to multiple antibiotics

antibiotic resistance is rapidly spread via integrons, transposons, insertion elements

they’re resistant to B-lactams, aminoglycosides, quinolones, tetracyclines

60
Q

FLASHCARD: micro, virulence factors, epidemiology, clinical, diagnosis, treatment of francisella tularensis

A

MICROBIOLOGY: Gram– coccobacilli but capsule may interfere; non-motile; requires cysteine and blood to culture; slow growing

VIRULENCE FACTORS: LPS is tetra-acylated, acyl chains 16-18 carbons long, monophosphorylated

EPIDEMIOLOGY: Type A (subsp. tularensis) > Type B (subsp. holarctica); ticks > rabbits > other animals; ~120 cases/yr; MO, AR, OK

CLINICAL: flu-like; ulceroglandular lesion may be present

DIAGNOSIS: Culture of ulcer, lymph node or sputum –> Agglut Ab; serology

TREATMENT: Doxycycline or cipro

61
Q

FLASHCARD: micro, pathology, epidemiology, clinical, diagnosis, treatment of brucella

A

MICROBIOLOGY: very small Gram– coccobacilli; no capsule; flagella does not stimulate TLR5

PATHOLOGY: LPS acyl chains 28 carbons long, monophosphorylated , O-Ag blocks complement and MHC-II presentation

EPIDEMIOLOGY: B. melitensis&raquo_space;> B. abortus > B. suis > B. canis; Mediterranean or unpasteurized cheese from C. America; Veterinarians

CLINICAL: Undulating fever, chills, malodorous sweats, arthralgia, malaise, anorexia, headache, myalgia, and back pain

DIAGNOSIS: Blood culture (two weeks) –> Agglut Ab; serology

TREATMENT: Doxycycline and rifampicin 6 weeks

62
Q

FLASHCARD: microbiology, pathology, epidemiology, clinical, diagnosis, treatment of acinetobacter

A

MICROBIOLOGY: Gram– coccobacilli; form biofilms on medical instruments

PATHOLOGY/VIROLOGY: LPS potent inducer of inflammation

EPIDEMIOLOGY: Combat injuries Iraq and Afghanistan; ventilator-associated pneumonia; burn units

CLINICAL: pneumonia, septicemia, wound infections

DIAGNOSIS: Agar culture

TREATMENT: Sulbactam (small mol. B-lactamase inhibitor) with ampicillin; or colistin (polymixin E)

ID Week 5 (13 decks)

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