Welcome to Pathogen Group 9
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- Betty Barton
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1 Welcome to Pathogen Group 9 Yersinia pestis Francisella tularensis Borrelia burgdorferi Rickettsia rickettsii Rickettsia prowazekii Acinetobacter baumannii
2 Yersinia pestis: Plague gram negative oval bacillus, bipolar staining Enterobacteriaceae Aerobic or facultatively anaerobic No capsule Nonmotile
3 Plague reservoir: rodents vector: fleas sylvatic plague bubonic plague: bubos, fever, chills, headache, malaise, prostration, petechial rash plague pneumonia pneumonic plague
4 blocked spiny valve in flea causes regurgitation during bite
5 plague areas: U. S.
6 Plague in world
7 History of Plague Pandemics 6th Century: killed 100 million Europeans 14th Century: killed 44 million Europeans 20th Century: killed?? Million in China
8 Plague cases per year, U.S.
9 plague transmission
10 plague transmission
11 Francisella tularensis: Tularemia reservoirs: rabbits, other animals, ticks (transovarian transmission in ticks) oval gram - bacilli bipolar staining Strictly aerobic (Tortora is wrong) Capsule Requires enriched media (cysteine added) Highly virulent: ID as low as 10 cells many modes of transmission
12 Transmission of tularemia Bite of tick or deer fly Through inhalation (occupational hazard for gardeners: dust from rodent feces) Through ingestion Through skin contact Splash into eye
13 forms of tularemia ulceroglandular = skin ulcer and lymphadenopathy glandular with no ulcer ocular intestinal - pain, vomiting, diarrhea pneumonic typhoidal (systemic)
14 tularemia primary lesion (ulcer)
15 Tularemia in U.S.
16 Tularemia as bioterrorist weapon Considered ideal: many methods of transmission, especially airborne
17 Borrelia burgdorferi : Lyme disease spirochete reservoir: mice and deer Also affects dogs, cows, horses vector: ticks affects skin, joints, nervous system, and cardiovascular system
18 Increase in Lyme disease
19 Counties with Lyme disease
20 symptoms of Lyme disease Estimated 5-40% of human infections symptomatic initial rash (most reliable symptom) rash usually accompanied by fatigue, fever, headache, stiff neck, arthralgia or myalgia (all are often intermittent) Late symptoms: arthritis meningitis, cranial neuritis, facial palsy disorders of heartbeat
21 Lyme disease bullseye rash around site of tick bite
22 Lyme reservoir and vector
23 Lyme disease reservoir and vector
24 Lyme transmission to human
25 Lyme prevention LYMErix vaccine: no longer manufactured avoid tick bites, remove ticks promptly
26 Rickettsia rickettsii: Rocky Mountain Spotted Fever vector: ticks
27 symptoms of RMSF fever myalgia, headache, petechial rash (usually on palms of hands and soles of feet), vomiting, fever, lethargy Potentially fatal without prompt treatment with antibiotic (doxycycline) 90% of cases April-Sept
28 RMSF rash on hands and abdomen
29 transovarian transmission in ticks
30 RMS fever damage to a person are needed to see this picture.
31 RMS fever: fatal case with gangrene
32 Rickettsia prowazekii: Epidemic Typhus Fever vector: lice (s. louse) fever, chills, headache, prostration, general pains, red rash on 5th day spreads over whole body can be fatal may reoccur years later
33 Acinetobacter baumannii Aerobic, opportunistic, gram-negative coccobacillary rod There have been many reports of A. baumannii infections among American soldiers wounded in Iraq, earning it the nickname "Iraqibacter". [3] Multi-drug resistant Acinetobacter baumannii is abbreviated as MDRAB. Multidrug-resistant Acinetobacter is not a new phenomenon; it has always been inherently resistant to multiple antibiotics. In soil and water Normally inhabits skin, mucous membranes and soil
34 Acinetobacter baumannii Genus Acinetobacter is important opportunistic pathogens in hospital-acquired infections. They cause various types of human infections, including pneumonia, wound infections, urinary tract infections, bacteremia, and meningitis. Of the currently known 31 Acinetobacter species, Acinetobacter baumannii is the most prevalent in clinical specimens. Adherence of bacteria to epithelial cells is an essential step towards colonization and infection. Bacterial adherence to host cells is mediated by fimbria or membrane components. Furthermore, many pathogenic bacteria are capable of invading non-phagocytic cells and evolve to survive within the host cells. The cellular invasion of bacteria contributes to evasion of humoral immunity, persistence in the host, and penetration into deep tissues.
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