Exotic Pathogens

Question 1

Bacillus anthracis important properties

Answer 1

large, non-motile gram-positive rod with square ends, often in chains; expresses an anti-phagocytic capsule composed of d-glutamate; capsule is encoded on a plasmid; expresses toxins encoded on a different plasmid; is a spore former

Question 2

Bacillus anthracis transmission

Answer 2

transmission is typically cutaneous contact with animal products; transmission can be via aerosolized droplets containing spores (pneumonic disease), can be person to person ; vector transmission is very rare

Question 3

Bacillus anthracis virulence factors

Answer 3

antiphagocytic capsule; lethal toxin is a protease known as lethal factor (LF) that cleaves host MAP kinases; “edematous toxin” is a deny late cyclase known as edema factor (EF) that interferes with immune responsiveness; “protective antigen” (PA) is a protein that facilitates entry of LF and EF into host cells

Question 4

Bacillus anthracis pathogenesis

Answer 4

multiplies at the infection site and dissemates via lymph nodes; pneumonic type requires high infectious dose and is very fatal

Question 5

Bacillus anthracis clinical course

Answer 5

pneumonic disease has an onset 4-6 days after exposure; after s hort prodromal period with flu like symptoms, a sudden high fever, chills, profuse sweating, dysnpea, hypoxia, and tachycardia develop - usually fatal; CXR shows widened mediastinum with infiltrates and pleural effusions

Question 6

Brucella spp. important properties

Answer 6

small gram-negative coccabacillus without a capsule; intracellular bacterium;3 human pathogens; reservoirs are goats/sheep, cattle, pigs

Question 7

Brucella epidemiology

Answer 7

endemic in Asia, Africa, Europe, and South America; typically contracted from contaminated dairy products or secretions from an infected animal; pasteurization of milk kills the disease; person-to-person transmission is rare

Question 8

Brucella Pathogenesis

Answer 8

the bacteria localize in the reticuloendothelial system; many organisms are killed by macrophages, but some live within the macrophage avoiding antibody; when infection is via inhalation, lung infection occurs resulting in granuloma formation

Question 9

Host respond to Brucella

Answer 9

granulomatous with lymphocytes and epitheliod giant cells, which can progress to form focal abscesses. Endotoxin is involved; no exotoxins are produced

Question 10

Brucella clinical findings

Answer 10

incubation of 1-3 weeks; fever, chills, fatigue, malaise, anorexia, weight loss; enlarged lymph nodes, spleen, liver; pancytopenia; osteomyelitis is most common complication; nodules on CXR

Question 11

Lab Diagonsis for Brucella

Answer 11

require enriched culture media with incubation in 10% CO2; slide agglutination with Brucella antiserum; rise in atinbody titers

Question 12

Treatment of Brucella

Answer 12

Tetracycline or Doxycycline plus Rifampin

Question 13

Burkholderia pseudomallei important properties

Answer 13

small, motile gram-negative rod that is a facultative intracellular bacterium

Question 14

Transmission of Burkholderia

Answer 14

Infection typically results from inhalation of aerosolized bacteria; outbreaks often occur after rain storm that aerosolize it from the soil in endemic areas; person to person is possible via body fluid transfer

Question 15

Burkholderia pathogenesis

Answer 15

thin polysaccharide capsule that is anti-phagocytic; well adapted for living and replicating within macrophages; can mediate lysis of host cell that it replicates in so it can get out and infect others; utilizes the actin network of infected cells to propel itself into adjacent cells; latency that allows it to be dormant for years

Question 16

Burkholderia virulence factors

Answer 16

capsule, LPS, type 3 secretion systems, flagella, pili, type 6 secretion systems, a number of secreted factors and several regulatory genes

Question 17

Burkholderia clinical findings

Answer 17

usually pneumonic infection with typical symptoms; CXR shows small nodule and consolidations of upper lobe, progressive disease can produce cavities (mimic TB), infection can become septic

Question 18

Lab diagnosis of Burkholderia

Answer 18

isolation of it from blood, urine, sputum, or skin lesions; measuring Bp specific antibodies in either acute phase or convalescent phase serum

Question 19

Treament of Burkholderia

Answer 19

Ceftazidime for 8wks unless immunosuppressed in which case 6months; it is intrinsically resistant to antibiotics such as gentamicin and colistin - can help in diagnosis

Question 20

Coxiella burnetii (Q-fever) important properties

Answer 20

gram-negative bacillus that is an obligate intracellular parasite; infects cattle sheep and goats mainly;

Question 21

Transmission of Coxiella

Answer 21

usually to humans via handling of contaminated viscera or drink raw contaminated milk; can be via tick bite; spore like form that can become aerosolized resulting in inhalational transmission

Question 22

Coxiella pathogenesis

Answer 22

well adapted for survival and replication within macrophages; considered an obligate intracellular parasite; extremely low infectious dose required; similar to Legionella in how it causes disease

Question 23

Coxiella clinical findings

Answer 23

many are asymptomatic; can cause acute febrile illness or atypical pneumonia; occasional liver and heart involvement; chronic infection can lead to endocarditis or granulomatous hepatitis

Question 24

Coxiella lab diagnosis

Answer 24

serological, looking for high or rising antibody titers to Q fever antigen

Question 25

Coxiella treatment

Answer 25

Most infection resolve spontaneously, but doxycycline will shorten duration and reduce risk of chronic infection

Question 26

Francisella tularensis important properties

Answer 26

small, pleomorphic gram-negative rod, obligate intracellular bacterium; Type A is most virulent and found in US; type B is less virulent and in Europe; expresses atypical LPS that is not recognized by TLR4; may produce a capsule

Question 27

Francisella transmission

Answer 27

typically by tick or blood to blood contact with infected animal; can be aerosol, ingestion in food or water; unknown reservoir; survives in water for long time living inside amoebas

Question 28

Francisella pathogenesis

Answer 28

Pneumonic occurs when Ft is inhaled - has high mortality rate; in the oculoglandular (infection via conjunctiva), glandular, or oculoglandular disease, it can disseminate to the lungs and cause pneumonic form

Question 29

Francisela clinical findings

Answer 29

often sudden onset of flu like symptoms, adenopathy, regional lymph nodes swollen and tender; CXR shows infiltrates in lungs, lobar pneumonia, and pleural exudation

Question 30

Lab diagnosis of Francisella

Answer 30

rarely cultured due to how dangerous the bug is; agglutination tests with serum are most common; fluorescent antibody staining of infected tissue is also available

Question 31

Francisella prevention and treatment

Answer 31

unlicensed vaccine used by military is live attenuated; treatment is with streptomycin

Question 32

Hantavirus Pulmonary Syndrome etiology

Answer 32

caused by Sin Nombre Virus which is transmitted by inhalation of aerosolized rodent piss; usually affects healthy young adults

Question 33

Symptoms of HPS

Answer 33

fever, muscle aches, rapid development of pulmonary edema and respiratory failure, death within 2-5 days of onset

Question 34

Risk factors for Hantavirus

Answer 34

relatively low, contact with rodent excrement, sleeping in confined areas with rodents (hikers/campers); being in a hantavirus area does not put you at risk

Question 35

Clinical signs of HPS

Answer 35

incubation of 14-17 days; early stage of flu like symptoms for 3-5 days, some experience dizziness, n/v/d, ab pain; late stage 4-10 days after symptom onset coughing and SOB, rapidly progressive, non cardiogenic pulmonary edema, severe hypotension

Question 36

HPS findings on CXR

Answer 36

bilateral interstitial infiltrates, bilateral alveolar infiltrates, pleural effusion, normal heart size

Question 37

HPS treatment

Answer 37

early aggressive intensive care, avoidance of hypoxia via ventilation, electrolyte balance, maintain normal BP, Ribavirin with questionable efficacy, careful monitoring

Question 38

Yersinia pestis (plague) important properties

Answer 38

small gram negative rod that is encapsulated (lost in vitro); well adapted for survival within macrophages; extremely virulent exhibits bipolar staining (looks like a safety pin)

Question 39

Yersinia transmission

Answer 39

transmitted among rodents via fleas; humans are affected by fleas; person-to-person transmission via aerosol inhalation

Question 40

Yersinia CXR

Answer 40

lower lung zone airspace disease with bilateral pleural effusions

Question 41

Yersinia pathogenesis

Answer 41

spreads to regional lymph nodes which swell and are tender; can cause bacteremia and abscesses in many organs; endotoxin can cause DIC and cutaneous hemorrhages

Question 42

Yersinia virulence factors

Answer 42

envelope capsular antigen called F1 which protects against phagocytosis, endotoxin (LPS), V/W antigens that allow intra-macrophage survival and growth, Yops that are injected into host cells via type III secretion systems and inhibit phagocytosis and cytokine production by macrophages and neutrophils; exotoxin

Question 43

Yersinia clinical findings

Answer 43

pain and tenderness of lymph nodes, high fever, myalgias, prostration, septic shock, pneumonia(can be caused by inhalation of aerosol or septic emboli)

Question 44

Yersinia lab diagnosis

Answer 44

smear and culture of blood or pus from bubo is best diagnostic procedure; Giemsa or Wayson stain show safety pin appearance; fluorescent antibody staining can be used in tissues; rise in antibody titer can be used retrospectively

Question 45

Yersinia treatment

Answer 45

streptomycin and tetracycline together; treat before lab results come back; incision and drainage of buboes is unnecessary; vaccine exists for bubonic disease but not pneumonic