foundations in microbiology - bellarmine.edu readings/lecture notes 202/chapt20...the enteric...
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Foundations in
MicrobiologySeventh Edition
Chapter 20
The Gram-Negative Bacilli of Medical
Importance
Talaro
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20.1 Aerobic Gram-Negative
Nonenteric Bacilli
• Large, diverse group of non-spore-forming bacteria
• Wide range of habitats – large intestines (enteric), zoonotic, respiratory, soil, water
• Most are not medically important; some are true pathogens, some are opportunists
• All have a lipopolysaccharide outer membrane of cell wall – endotoxin 2
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Aerobic Gram-Negative
Nonenteric Bacilli
• Pseudomonas and Burkholderia – an
opportunistic pathogen
• Brucella and Francisella – zoonotic
pathogens
• Bordetella and Legionella – mainly
human pathogens
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Pseudomonas: The Pseudomonads
• Small gram-negative rods with a single polar flagellum
• Free living– Primarily in soil, sea water, and fresh water; also
colonize plants and animals
• Important decomposers and bioremediators
• Frequent contaminants in homes and clinical settings
• Use aerobic respiration; do not ferment carbohydrates
• Produce oxidase and catalase
• Many produce water soluble pigments
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Figure 20.1
Pseudomonas aeruginosa
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Pseudomonas Aeruginosa
• Common inhabitant of soil and water
• Intestinal resident in 10% normal people
• Resistant to soaps, dyes, quaternary
ammonium disinfectants, drugs, drying
• Frequent contaminant of ventilators, IV
solutions, anesthesia equipment
• Opportunistic pathogen
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Figure 20.2 Skin rash from
Pseudomonas
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Pseudomonas Aeruginosa
• Common cause of nosocomial infections in hosts
with burns, neoplastic disease, cystic fibrosis
• Complications include pneumonia, UTI, abscesses,
otitis, and corneal disease
• Endocarditis, meningitis, bronchopneumonia
• Grapelike odor
• Greenish-blue pigment (pyocyanin)
• Multidrug resistant
• Cephalosporins, aminoglycosides, carbenicillin,
polymixin, quinolones, and monobactams
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Figure 20.3 Pseudomonas (left) and
Staphylococcus (right)
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Bordetella Pertussis
• Minute, encapsulated coccobacillus
• Causes pertussis or whooping cough, a communicable childhood affliction
• Acute respiratory syndrome
• Often severe, life-threatening complications in babies
• Reservoir – apparently healthy carriers
• Transmission by direct contact or inhalation of aerosols
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Bordetella Pertussis
• Virulence factors
– Receptors that recognize and bind to ciliated
respiratory epithelial cells
– Toxins that destroy and dislodge ciliated cells
• Loss of ciliary mechanism leads to buildup of
mucus and blockage of the airways
• Vaccine – DTaP – acellular vaccine contains
toxoid and other Ags
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Figure 20.7 Prevalence of pertussis
in the United States
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20.3 Enterobacteriaceae Family
• Enterics
• Large family of small, non-spore-forming gram-negative rods
• Many members inhabit soil, water, decaying matter, and are common occupants of large bowel of animals including humans
• Most frequent cause of diarrhea through enterotoxins
• Enterics, along with Pseudomonas sp., account for almost 50% of nosocomial infections
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Figure 20.9
Bacteria that
account for
the majority
of hospital
infections
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20.4 Coliform Organisms and
Diseases
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Escherichia Coli: The Most
Prevalent Enteric Bacillus
• Most common aerobic and non-fastidious
bacterium in gut
• 150 strains
• Some have developed virulence through
plasmid transfer, others are opportunists
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Pathogenic Strains of E. Coli
• Enterotoxigenic E. coli causes severe diarrhea due to
heat-labile toxin and heat-stable toxin – stimulate
secretion and fluid loss; also has fimbriae
• Enteroinvasive E. coli causes inflammatory disease of
the large intestine
• Enteropathogenic E. coli linked to wasting form
infantile diarrhea
• Enterohemorrhagic E. coli, O157:H7 strain, causes
hemorrhagic syndrome and kidney damage
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Escherichia coli
• Pathogenic strains frequent agents of infantile
diarrhea – greatest cause of mortality among
babies
• Causes ~70% of traveler’s diarrhea
• Causes 50-80% UTI
• Coliform count – indicator of fecal
contamination in water
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Figure 20.14 Rapid identification
of E. coli O157:H7
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20.5 Noncoliform Lactose-
Negative Enterics
• Proteus, Morganella, Providencia
• Salmonella and Shigella
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Salmonella and Shigella
• Well-developed virulence factors,
primary pathogens, not normal human
flora
• Salmonelloses and Shigelloses
– Some gastrointestinal involvement and
diarrhea but often affect other systems
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Typhoid Fever and Other
Salmonelloses• Salmonella typhi – most serious pathogen of
the genus; cause of typhoid fever; human host
• S. cholerae-suis – zoonosis of swine
• S. enteritidis – includes 1,700 different serotypes based on variation on O, H, and Vi
• Flagellated; survive outside the host
• Resistant to chemicals – bile and dyes
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Typhoid Fever
• Bacillus enters with ingestion of fecally
contaminated food or water; occasionally spread by
close personal contact; ID 1,000-10,000 cells
• Asymptomatic carriers; some chronic carriers shed
bacilli from gallbladder
• Bacilli adhere to small intestine, cause invasive
diarrhea that leads to septicemia
• Treat chronic infections with chloramphenicol or
sulfatrimethoprim
• 2 vaccines for temporary protection
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Figure 20.18 Prevalence of
salmonelloses
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Figure 20.19
The phases of
typhoid fever
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Animal Salmonelloses
• Salmonelloses other than typhoid fever are called enteric fevers, Salmonella food poisoning, and gastroenteritis
• Usually less severe than typhoid fever but more prevalent
• Caused by one of many serotypes of Salmonella enteritidis; all zoonotic in origin but humans can become carriers– Cattle, poultry, rodents, reptiles, animal, and dairy
products
– Fomites contaminated with animal intestinal flora
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Shigella and Bacillary
Dysentery• Shigellosis – incapacitating dysentery
• S. dysenteriae, S. sonnei, S. flexneri, and S. boydii
• Human parasites
• Invades villus of large intestine, does not
perforate intestine or invade blood
• Enters Peyer’s patches instigate inflammatory
response; endotoxin and exotoxins
• Treatment – fluid replacement and ciprofloxacin
and sulfatrimethoprim
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Figure 20.20 The appearance of the
large intestinal mucosa in Shigella
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The Enteric Yersinia Pathogens
• Yersinia enterocolitica – domestic and wild
animals, fish, fruits, vegetables, and water
– Bacteria enter small intestinal mucosa, some
enter lymphatic and survive in phagocytes;
inflammation of ileum can mimic appendicitis
• Y. pseudotuberculosis – infection similar to
Y. enterocolitica, more lymph node
inflammation
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Nonenteric Yersinia Pestis and
Plague
• Nonenteric
• Tiny, gram-negative rod, unusual bipolar
staining and capsules
• Virulence factors – capsular and envelope
proteins protect against phagocytosis and
foster intracellular growth
– Coagulase, endotoxin, murine toxin
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Figure 20.21 Gram-stain of Yersinia pestis
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Yersinia Pestis
• Humans develop plague through contact with
wild animals (sylvatic plague) or domestic or
semidomestic animals (urban plague) or
infected humans
• Found in 200 species of mammals – rodents,
without causing disease
• Flea vectors – bacteria replicates in gut,
coagulase causes blood clotting that blocks the
esophagus; flea becomes ravenous
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Figure 20.22 Infection cycle of
Yersinia pestis
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Pathology of Plague
• ID 3-50 bacilli
• Bubonic – bacillus multiplies in flea bite, enters lymph, causes necrosis and swelling called a bubo in groin or axilla
• Septicemic – progression to massive bacterial growth; virulence factors cause intravascular coagulation subcutaneous hemorrhage and purpura – black plague
• Pneumonic – infection localized to lungs, highly contagious; fatal without treatment
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Figure 20.23 The bubo, classic
sign of bubonic plague
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• Diagnosis depends on history, symptoms,
and lab findings from aspiration of
buboes
• Treatment: streptomycin, tetracycline, or
chloramphenicol
• Killed or attenuated vaccine available
• Prevention by quarantine and control of
rodent population in human habitats