Uncommon Bacterial Pathogens Flashcards

1
Q

Bacillus Antracis –
Bacteriology

  • what is the distinctive morphology?
  • Where does it live? How is it transmitted ?
A

Gram positive rods – large “boxcars”

forms spores in the laboratory and in the field

Non motile; facultative anaerobic

Lives in the soil and in herbivores

Transmitted by coming into contact with spores or contaminated meat
-NOT TRANSMITTED PERSON TO PERSON

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2
Q

Describe the pathogenesis and virulence factors of Anthrax:

A

Two Plasmids:
1) Encodes Poly D Glutamic Acid Capsule– (unique bc its not an amino acid capsule, not a polysaccharide)

2) Tripartite Toxin Plasmid:
- Protective Antigen
- Edema Factor
- Lethal Factor

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3
Q

Describe the mechanism of Edema Factor and Lethal Factor?

what organism produces these?

A

Bacillus Antrhacis

  • Edema factor (A subunit) – Adenylate Cyclase; raises cAMP; intereferes with phagocytosis and signaling of phagocytes

Lethal Factor (A subunit): metalloproteases; MAP kinase Kinase which paralyzes lymphocytes leading to death

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4
Q

What are the three disease types than can manifest from anthracis?

Briefly Describe the presentation of each

A

Cutaneous

Gastrointestinal –

Inhalation

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5
Q

Describe the cutaneous form of anthrax –

  • presentation
  • what is the mortality rate?
A

Cutaneous – Most common (95%)

Spores enter through breaks in the skin.

Presents as painless pruiritic pustule that quickly enlarges leave BLACK ESCHAR + EDEMA
No Fever or LAD

20% mortality rate

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6
Q

Describe GI anthrax:

How do you get it?
Presentation?
mortality rate

A

Gastro-intestinal:

spores ingested (eg from contaminated beef).

Can survive high temperatures, so cooking it doesn’t kill it.

Symp - fever, gastroenteritis, vomiting, hematemesis, bloody diarrhea… Toxemia –> Death

Symptoms are non specific
higher mortality rate (50+%) bc its hard to recognize

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7
Q

Describe Inhalation anthrax

  • How do you get it?
  • Initial presentation?
  • terminal presentation?
  • what is distinct about the CXR?
A
  • Spores are inhaled
  • gereminate in the lung macrophages

Symptoms (2-5 days) fever, malaise, cough, myalgia

CXR: Widened mediastinum (hemorrhagic adenitis of the hilum)

Late symptoms (1-2 days): hemorrhagic pleural effusions, hypoxia, cyanosis, dyspnea, shock and death

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8
Q

Treatment of Anthrax:

Prevention of Anthrax

A

Traditional : PCN + Doxycyclin

Animal studies: Cipro

2001 Survivors: FQ + clinda OR Rifampin

Vaccine: noncapsulated strain that has protective antigen but not the other toxins

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9
Q

Yersinia Pestis

  • Bacteriology
  • how are humans infected ?
  • what is the reservoir in the environement
A

GN coccobaccilus

Humans infected from flea bite

Reservoirs: rats, squierrels, rabbits

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10
Q

Virlence factors of Yersina Pestis

A
  • 2 plasmids which encode:

type 3 secertions

Fibrinolysis

(if no fibrinolysis, cannot become invasive; stays as local infection)

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11
Q

Disease forms of Yersinia Pestis?

  • how does each present ?
A

Bubonic Plague:
Bubo = large infected LN
Sx: Bubo, HA, malaise, myalgia
Pap/Purpuric lesion at the site of the flea bite

Pneumonic Plague: Highly contagious;
HA, mailse, fever, cough, dyspnea, cyanosis, hemoptysis, respiratory failure

Septicemia: No Obvious Bubo or PNA; patient’s present with sepsis. Die from shock and DIC

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12
Q

Medical management of Yersinia

A

FQs (cipro)
Tetracycline
TMP/SMX

Genitmicin/streptomycin

Prophylaxis:
- bubonic contacts: TMP/SMX, tetracyclines,

Pneumonic contacts: cipro, tetracyclines

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13
Q
• Francisella tularensis
- Epidemiology: 
what part of the world is it found? what animals harbor it? 
What is the ID? 
how is it transmitted?
A
  • Found in the norther hemisphere
  • Rabbits (Skinning)
    and ticks

Very low ID: 1-10 CFU

no person to person trasmission

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14
Q

What are the important clinical forms of • Francisella tularensis

A

Ulceroglandular: ulcer with regional adenopathy at site of tick bite

Pneumonic: similar to pneumonic plague presentation
Abrupt onset fever, chills, HA, myalgia, non productive cough,

CXR: segmental, lobar infiltrates, hilar adenopathy

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15
Q

Treatment of • Francisella tularensis

is there a vaccine?

A

Tetracyclines or FQ

(Strepto and gentimicin in the past)

No Vaccine

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16
Q

• Listeria monocytogenes

bacteriology:

A

GPR, facultative anaerobe, motile

Beta Hemolytic

17
Q

Listeria Monocytogenes
Epi:
how is it transmitted
what foods are implicated

where can it grow?

A

Foodborne pathogen — milk, cheese, meats, coleslaw, cantaloupe
undercooked chicken, microwaved hotdogs

Can grow at wide range of temperatures (1C - 45C); including your fridge

18
Q

Pathogenesis of lysteria monocytogenes

what proteins are used to help it infect and spread

A

Internalin: bind to the tip of exposed E cadherins

Invades macrophages

Lysteriolysisn – escapes the phagsome within the macrophage

Act A – activates polymerization of actin; pushing towards neighboring cells to infect (act A is unevenly distributed on dividing lysteria, therefore will move uni-directionally)

Phospholipases

19
Q

Risk Factors for Lysteria infection

-

A

Certain foods (unpastuerized diary, etc)

98% of cases have underlying disease/condition

Extremes of Age
Pregnancy
Immunocompromised (steroids, AIDS, cancer, transplant)

20
Q

Describe the pregnancy associated form of listerosis

A

Pregnancy Associated:
Mothers won’t develop the disease outright

3rd Trimester - may present with fever, chills, myalgias, bacteremia

Septic Amnionitis: crosses the placenta and passed to the child leading to septic abortion/premature labor

The neonate: 
- acquires the disease in utero: 
overwhelemd with microabscesses: 
granulomatous infantiseptica
dies in utero 
  • may present healthy for first month of life and develop meningitis later
21
Q

what is the divide between the clinical presentations of listerosis?

A

Pregnancy associated

non pregnancy associated

22
Q

Describe the non pregnancy associated form of listerosis ?

A

Leading cause of meningitis in immunocompromised patients

meningoenchephalitis, gasteroenteritis; some cases of enteric abscess

Presentation: fever, HA, altered sensorium; some have focal neurological signs (seizures, cranial nerves, hemiparesis)

23
Q

Treatment of Listeria monocytogenes

What is it resistant to?

A

Treatment: penicillin or ampicillin
Amp + clavulonate
TMP-SMX

Resistant to ALL CEPHALOSPORINS and vancomycin

24
Q

How do you treat a 70 yo male presenting with meningitis?

A

What causes meningitis?
Strep pnuemo – use ceftriaxone (has good csf coverage)

But ALSO listeria — use Ampicillin

25
Q

Bartonella henselae
Bacteriology
what is this also known as ?
how is it transmitted

A

cat Scratch Fever

Transmitted by cats bit, scratch or fleas

GNR, Slow growing

26
Q

Presentation of Bartonella Henselae in kids

Treatment:

A

unilateral adenopathy, but patient is mostly fine

happens mostly in kids

Treatment: abx would shorten the duration but not 100% indicated

27
Q

Presentation of Bartonella Henselae in HIV patients

Treatment

A

Bacillary Angiomatosis -

Cutaneous or visceral disease that has proliferation of RBCs

Erythematous papules on the skin

Treat: macrolides and tetracyclines

28
Q

• Brucella spp.
bacteriology:

how is it transmitted:

Presentation:

A

tiny, fastidious, gram negative cocco bacilli

direct contact or contaminated milk/milk products, esp unpasteurized milk/milk products

Presentation; Fever, malaise, without localizing symptoms

Can cause osteomyelitis, or infectious arthritis

29
Q

Treatment of Brucella:

A

long course of tetracyclines, initially combined with aminogylcosides