Exotic Pathogens Flashcards
Bacillus anthracis important properties
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
Bacillus anthracis transmission
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
Bacillus anthracis virulence factors
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
Bacillus anthracis pathogenesis
multiplies at the infection site and dissemates via lymph nodes; pneumonic type requires high infectious dose and is very fatal
Bacillus anthracis clinical course
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
Brucella spp. important properties
small gram-negative coccabacillus without a capsule; intracellular bacterium;3 human pathogens; reservoirs are goats/sheep, cattle, pigs
Brucella epidemiology
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
Brucella Pathogenesis
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
Host respond to Brucella
granulomatous with lymphocytes and epitheliod giant cells, which can progress to form focal abscesses. Endotoxin is involved; no exotoxins are produced
Brucella clinical findings
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
Lab Diagonsis for Brucella
require enriched culture media with incubation in 10% CO2; slide agglutination with Brucella antiserum; rise in atinbody titers
Treatment of Brucella
Tetracycline or Doxycycline plus Rifampin
Burkholderia pseudomallei important properties
small, motile gram-negative rod that is a facultative intracellular bacterium
Transmission of Burkholderia
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
Burkholderia pathogenesis
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
Burkholderia virulence factors
capsule, LPS, type 3 secretion systems, flagella, pili, type 6 secretion systems, a number of secreted factors and several regulatory genes
Burkholderia clinical findings
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
Lab diagnosis of Burkholderia
isolation of it from blood, urine, sputum, or skin lesions; measuring Bp specific antibodies in either acute phase or convalescent phase serum
Treament of Burkholderia
Ceftazidime for 8wks unless immunosuppressed in which case 6months; it is intrinsically resistant to antibiotics such as gentamicin and colistin - can help in diagnosis
Coxiella burnetii (Q-fever) important properties
gram-negative bacillus that is an obligate intracellular parasite; infects cattle sheep and goats mainly;
Transmission of Coxiella
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
Coxiella pathogenesis
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
Coxiella clinical findings
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
Coxiella lab diagnosis
serological, looking for high or rising antibody titers to Q fever antigen
Coxiella treatment
Most infection resolve spontaneously, but doxycycline will shorten duration and reduce risk of chronic infection
Francisella tularensis important properties
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
Francisella transmission
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
Francisella pathogenesis
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
Francisela clinical findings
often sudden onset of flu like symptoms, adenopathy, regional lymph nodes swollen and tender; CXR shows infiltrates in lungs, lobar pneumonia, and pleural exudation
Lab diagnosis of Francisella
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
Francisella prevention and treatment
unlicensed vaccine used by military is live attenuated; treatment is with streptomycin
Hantavirus Pulmonary Syndrome etiology
caused by Sin Nombre Virus which is transmitted by inhalation of aerosolized rodent piss; usually affects healthy young adults
Symptoms of HPS
fever, muscle aches, rapid development of pulmonary edema and respiratory failure, death within 2-5 days of onset
Risk factors for Hantavirus
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
Clinical signs of HPS
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
HPS findings on CXR
bilateral interstitial infiltrates, bilateral alveolar infiltrates, pleural effusion, normal heart size
HPS treatment
early aggressive intensive care, avoidance of hypoxia via ventilation, electrolyte balance, maintain normal BP, Ribavirin with questionable efficacy, careful monitoring
Yersinia pestis (plague) important properties
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)
Yersinia transmission
transmitted among rodents via fleas; humans are affected by fleas; person-to-person transmission via aerosol inhalation
Yersinia CXR
lower lung zone airspace disease with bilateral pleural effusions
Yersinia pathogenesis
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
Yersinia virulence factors
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
Yersinia clinical findings
pain and tenderness of lymph nodes, high fever, myalgias, prostration, septic shock, pneumonia(can be caused by inhalation of aerosol or septic emboli)
Yersinia lab diagnosis
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
Yersinia treatment
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
