Exotic and Biohazard Pneumonias Flashcards

1
Q

Describe Bacillus anthracis

A

gram positive rod with square ends, usually found in chains and expresses an anti-phagocytic capsule that is composed of d-glutamate

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2
Q

Does Bacillus anthracis produce toxins?

A

anthrax toxins (encoded on a different plasmid than the capsule)

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3
Q

T or F. Bacillus anthracis can form spores

A

T. Facultative intracellular pathogen

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4
Q

How is Bacillus anthracis spread?

A
  • cutaneous contact with infected animal products (e.g. wool, so its aka Woolsorter’s disease)
  • person to person via aerosolized droplets
  • vector transmission
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5
Q

What is the significance of Bacillus anthracis having a capsule?

A

it prevents PAMP binding

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6
Q

What other virulence factors does Bacillus anthracis use?

A

1) Lethal toxin, a protease known as lethal factor that cleaves host MAP kinases
2) Edematous toxin known as edema factor that attenuates immune response
3) protective antigen that facilitates entry of LF and EF into host cells

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7
Q

What are the forms of Bacillus anthracis?

A
  • cutaneous (most common)
  • GI anthrax
  • pneumonic form
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8
Q

How deadly is the cutaneous form?

A

fatal in 5-20% of untreated cases, but less than 1% in treated cases

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9
Q

How deadly is the GI form?

A

25-75%

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10
Q

How deadly is the pneumonic form?

A

results in death in 90-100% of untreated cases, with treatment reducing that rate significantly if initiated before the disease becomes fulminant.

It is estimated that inhalation of between 8,000 and 40,000 spores is required to transmit anthrax via the aerosol route.

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11
Q

When does disease onset occur after inhalation of anthrax species?

A

4-6 days but it can take up 6 weeks because spores can persist within macrophages for long periods (up to 100 days)

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12
Q

How does anthrax present?

A

The initial symptoms include a non-productive cough, sore throat, mild fever, muscle aches, and a
headache.

Soon afterward, more pronounced symptoms suddenly appear. These symptoms include sudden high fever, chills, profuse sweating, dyspnea, hypoxia, and tachycardia.

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13
Q

What does X-ray show in anthrax infection?

A

widened mediastinum with infiltrates and pleural effusions

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14
Q

How does anthrax cause death?

A

1) Blockage of pneumonic lymphatic vessels can result in progressive
pulmonary edema, eventually causing death.

2) Macrophages responding to the infection make cytokines that can result in septic shock and death.

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15
Q

How is anthrax diagnosed?

A

suspected anthrax is done by performing chest X-rays and/or CT scans to determine if the patient has developed mediastinal widening or pleural effusion

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16
Q

How is anthrax diagnosed confirmed?

A

anthrax-specific antibody titers in the serum can be measured or samples from the patient (blood or respiratory secretions) can be tested directly for the presence of either Ba or anthrax toxins.

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17
Q

How is anthrax treated?

A

60 day course of ciprofloxacin
OR

IV chipper with another drug (ampicillin, penicillin g, meropenem, vanco) if severe

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18
Q

Describe Brucella Spp. (Brucellosis or Malta fever)

A

small gram negative cocbacillius WITHOUT a capsule. Intracellular

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19
Q

What are the three species of Brucella and their host?

A

melintensis (goat and sheep)- most severe

abortus (cattle)- self-limited

suis (pigs)

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20
Q

How are humans typically infected by Brucella?

A

from contaminated dairy products (milk or cheese) or direct secretions of infected animals. Uncommon in the U.S. because of pasteurization techniques used here

human to human transmission is rare

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21
Q

Where does Brucella reside in humans?

A

macrophages (where they are protected from antibody) and following infection, they tend to localize in the reticuloendothelial tissue (nodes, liver, spleen)

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22
Q

How does Brucella evade host immune responses?

A
  • granuloma formation (which can progress to form focal abscesses)
  • LPS endotoxin
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23
Q

Mortality rate of Brucella?

A

low, 2%

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24
Q

How does Brucella infection present?

A

fever, chills, fatigue, malaise, anorexia, and weight loss. Enlarged liver, spleen, and lymph nodes are usually evident, and
pancytopenia is also a typical finding.

Some patients develop osteomyelitis, and a few patients experience an undulating fever pattern.

25
Q

How long does it take Brucella to present after infection?

A

incubation for 1-3 weeks and onset can be either acute or gradual

26
Q

What is an undulating fever?

A

fever that rises and falls

27
Q

In pneumonic cases of Brucella, what are typically noted upon CXR?

A

granuloma nodules

28
Q

How is Brucella cultured?

A

not usually done because it requires enriched medium and incubation at 10% CO2

29
Q

How is Brucella identifed normally?

A

-slide agglutination test with Brucella antiserum

30
Q

What is the best diagnostic for Brucella?

A

detecting a rise in Brucella-specific antibodies. Convalescent titer of at least 1:60 is needed diagnostically

31
Q

How is Brucella treated?

A

tetracycline or doxycycline plus rifampin (resistance not seen)

32
Q

T or F. Brucella can be aerosolized easily

A

T. So can Ft, Yersinia pestis, Coxiella burnetii, Burkholderia pseudomallei, and anthrax

33
Q

Burkholderia mallei is the causal agent of what disease?

A

Glander’s disease

34
Q

Major difference between Burkholderia mallei and Burkholderia pseudomallei?

A

B. mallei does not live in the soil, is not motile, and is a strict enzootic pathogen.

35
Q

Burkholderia pseudomallei is the causal agent of what disease?

A

Whittier’s disease or meliodosis

36
Q

Describe Bp

A

small motile gram-negative bacterium and a facultative intracellular pathogen that can survive for long periods of time in water and soil (rice paddies)

37
Q

Where is Bp endemic?

A

southeast Asia and Australia

38
Q

How does human infection occur?

A
  • inhalation of aerosolized bacteria
  • cutaneous infection
  • fluid transfer person-to-person
  • contaminated water
39
Q

What hosts can Bp habitat?

A

sheep, goats, cattle, and horses

40
Q

What virulence factors does Bp have?

A
  • capsule
  • can inhabit amoebas, allowing it to survive in water
  • LPS
  • Type III secretion systems
41
Q

How is Bp spread?

A

(1) host cell lysis: Bp can mediate lysis of the
host cell that it is infecting, allowing rapid escape of progeny from the host cell, allowing them to invade new uninfected cells within the host; and

(2) Bp expresses proteins that allow it to utilize the actin network of its host cell to propel itself into adjacent cells without ever being exposed to the extracellular milieu.

42
Q

Why is BP called the Vietnamese time-bomb.

A

Bp uses a mechanism that remains undefined that allows it to remain dormant for many years within its host. In fact, some U.S. servicemen that served in the Vietnam War
returned home asymptomatically but began showing symptoms of melioidosis up to
decades after their probable exposure to Bp.

43
Q

Bp can be sub-acute, acute or chronic. What is the most common infection route?

A

inhalation, so the acute pneumonic form of disease is the most prevalent.

44
Q

What is the incubation period of Bp?

A

The typical incubation period is 2-3 days, but in some cases can be many years. There is no current explanation for the apparent latency that is
observed in some cases.

45
Q

How does Bp present?

A

high fever, headache, anorexia, general muscle soreness, chest pain, and either a productive (with normal sputum) or non-productive cough.

Chest X-ray typically reveals consolidations of the upper lobe of the lung with small nodules (granulomas), and progressive disease can produce cavities. The clinical picture closely resembles tuberculosis.

46
Q

Seriousness of Bp?

A

Bp infection can become septic. Melioidosis is a very serious disease that results in death in 20-50% of cases, even with appropriate treatment. In cutaneous cases, dissemination to the lungs CAN OCCUR.

47
Q

How is Bp diagnosed?

A

1) Isolation of Bp from blood, urine, sputum, or skin lesions (in the case of a cutaneous infection). This must be done very carefully to prevent exposure of lab personnel to aerosolized bacteria because the LD50 of Bp via the pneumonic route is very low (less than 100 CFU).
2) Measurement of Bp-specific antibodies in either acute- or convalescent phase serum

48
Q

How is Bp treated?

A

ceftazidime for at least 8 weeks. In the case of an immunosuppressed patient, treatment is recommended for 6 months.

49
Q

Which antibiotics is Bp resistant to?

A

intrinsically resistant to many antibiotics including gentamicin and colistin; this fact comes in handy sometimes when attempting to diagnose the disease.

50
Q

T or F. Bp can be easily aerosolized

A

T. So can Coxiella brunetii (Q fever)

51
Q

Describe Coxiella burnetii (aka Q-fever)

A

obligate intracellular gram negative bacillus

52
Q

What are the main reservoirs for Coxiella (aka Q fever)?

A

cattle, sheep, and goats

53
Q

How is Coxiella transmitted to humans?

A

1) ingestion or contact with contaminated milk or dairy products, or via contact with contaminated animal viscera, most prominently during birthing of one of these animals.
2) insect vector (ticks)
3) Inhalation via aerosolized spores like form (most severe)

54
Q

T or F. Humoral immune systems do not play a main role in Cb clearance

A

T. It is intracellular

55
Q

Where does Cb live in humans?

A

macrophages (similar to Legionella in many ways)

56
Q

How severe is Q-fever?

A

Q-fever is typically not a very severe disease syndrome, and in fact, 30-50% of cases are asymptomatic, and the infection often resolves naturally without any type of treatment. The typical course of disease is an acute febrile illness with an atypical pneumonia that lasts for 2-4 weeks. The mortality rate is below 2%.

57
Q

What are possible complications of Q fever?

A

Sometimes the disease has liver and heart involvement and becomes chronic. When a chronic infection results in endocarditis or granulomatous hepatitis, the mortality rate approaches 100% if left
untreated.

58
Q

How is Q fever diagnosed?

A

typically dependent on serological screening for increasing titers of Cb-specific antibodies in patient serum.

59
Q

How is Q fever treated?

A

doxycycline is the antibiotic of choice, and it results in shortened duration of the illness and mitigation of the risk of chronic infection.