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Lecture PowerPoint to accompany
Foundations in
Microbiology
Seventh Edition
Talaro
Chapter 20
The Gram-Negative
Bacilli of Medical
Importance
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
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
3
Aerobic Gram-Negative
Nonenteric Bacilli
• Pseudomonas and Burkholderia – an
opportunistic pathogen
• Brucella and Francisella – zoonotic
pathogens
• Bordetella and Legionella – mainly human
pathogens
4
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
5
Figure 20.1
Pseudomonas aeruginosa
6
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
7
Figure 20.2 Skin rash from
Pseudomonas
8
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
9
Figure 20.3 Pseudomonas (left) and
Staphylococcus (right)
10
20.2 Related Gram-Negative Aerobic Rods
• Genera Burkholderia, Acinetobacter,
Stenotrophomonas
• Similar to pseudomonads
• Wide variety of habitats in soil, water, and related
environments
• Obligate aerobes; do not ferment sugars
• Motile, oxidase positive
• Opportunistic
11
Burkholderia
• Burkholderia cepacia – active in biodegradation
of a variety of substances; opportunistic agent in
respiratory tract, urinary tract, and occasionally
skin infections; drug resistant
• B. pseudomallei – generally acquired through
penetrating injury or inhalation from
environmental reservoir; wound infections,
bronchitis and pneumonia, septicemia
12
Acinetobacter and Stenotrophomonas
• Acinetobacter baumanii – nosocomial and
community acquired infections; wounds, lungs,
urinary tract, burns, blood; extremely resistant –
treatment with combination antimicrobials
• Stenotrophomonas maltophilia – forms biofilms;
contaminant of disinfectants dialysis equipment,
respiratory equipment, water dispensers, and
catheters; clinical isolate in respiratory soft tissue,
blood, CSF; high resistance to multidrugs
13
Brucella and Brucellosis
• Tiny gram-negative coccobacilli
• 2 species:
– Brucella abortus (cattle)
– Brucella suis (pigs)
• Brucellosis, malta fever, undulant fever, and Bang
disease – a zoonosis transmitted to humans from infected
animals
• Fluctuating pattern of fever – weeks to a year
• Combination of tetracycline and rifampin or
streptomycin
• Animal vaccine available
• Potential bioweapon
14
Figure 20.5 Agglutination titer test
for brucellosis
15
Francisella Tularensis and
Tularemia
• Causes tularemia, a zoonotic disease of mammals
endemic to the northern hemisphere, particularly
rabbits
• Transmitted by contact with infected animals, water
and dust or bites by vectors
• Headache, backache, fever, chills, malaise, and
weakness
• 10% death rate in systemic and pulmonic forms
• Intracellular persistence can lead to relapse
• Gentamicin or tetracycline
• Attenuated vaccine
• Potential bioterrorism agent
16
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
17
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
18
Figure 20.7 Prevalence of pertussis
in the United States
19
Alcaligenes
• Live primarily in soil and water
• May become normal flora
• A. faecalis – most common clinical species
– Isolated from feces, sputum, and urine
– Occasionally associated with opportunistic
infections – pneumonia, septicemia, and
meningitis
20
Legionella Pneumophila and
Legionellosis
• Widely distributed in water
• Live in close association with amoebas
• 1976 epidemic of pneumonia afflicted 200 American
Legion members attending a convention in
Philadelphia and killed 29
• Legionnaires disease and Pontiac fever
• Prevalent in males over 50
• Nosocomial disease in elderly patients
• Fever, cough, diarrhea, abdominal pain, pneumonia
fatality rate of 3-30%
• Azithromycin
21
Figure 20.8
Appearance of
Legionella
pneumophila
22
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
23
Figure 20.9
Bacteria that
account for
the majority
of hospital
infections
24
• Facultative anaerobes, grow best in air
• All ferment glucose, reduce nitrates to nitrites,
oxidase negative, and catalase positive
• Divided into coliforms (lactose fermenters) and
non-coliforms (non-lactose fermenters)
• Enrichment, selective and differential media
utilized for screening samples for pathogens
25
Figure 20.10 Biochemical traits for separating
enteric genera
26
Figure 20.11 Isolation media for enterics
27
Figure 20.12 BBL Enterotube II,
rapid biochemical testing of enterics
28
Antigenic Structures
and Virulence Factors
Complex surface antigens contribute to
pathogenicity and trigger immune response:
• H – flagellar Ag
• K – capsule and/or fimbrial Ag
• O – somatic or cell wall Ag – all have
• Endotoxin
• Exotoxins
29
Figure 20.13 Antigenic structures in
gram-negative enteric rods
30
20.4 Coliform Organisms and
Diseases
31
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
32
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
33
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
34
Figure 20.14 Rapid identification of
E. coli O157:H7
35
Other Coliforms
Clinically important mainly as opportunists
• Klebsiella pneumoniae – normal inhabitant of
respiratory tract, has large capsule, cause of
nosocomial pneumonia, meningitis, bacteremia,
wound infections, and UTIs
• Enterobacter sp. – UTIs, surgical wounds
• Citrobacter sp. – opportunistic UTIs and
bacteremia
• Serratia marcescens – produces a red pigment;
causes pneumonia, burn and wound infections,
septicemia and meningitis
36
Figure 20.15 A capsule stain of
Klebsiella pneumoniae
37
Figure 20.16 Serratia marcescens
38
20.5 Noncoliform Lactose-Negative
Enterics
• Proteus, Morganella, Providencia
• Salmonella and Shigella
39
Opportunists: Proteus and Its
Relatives
Proteus, Morganella, Providencia – ordinarily harmless
saprobes in soil, manure, sewage, polluted water,
commensals of humans and animals
– Proteus sp. – swarm on surface of moist agar in a concentric
pattern
– Involved in UTI, wound infections, pneumonia, septicemia,
and infant diarrhea
– Morganella morganii and Providencia sp. involved in similar
infections
• All demonstrate resistance to several antimicrobials
40
Figure 20.17 Wavelike, swarming
pattern of Proteus vulgaris
41
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
42
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
43
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
44
Figure 20.18 Prevalence of
salmonelloses
45
Figure 20.19
The phases of
typhoid fever
46
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
47
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
48
Figure 20.20 The appearance of the large
intestinal mucosa in Shigella
49
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
50
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
51
Figure 20.21 Gram-stain of Yersinia pestis
52
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
53
Figure 20.22 Infection cycle of
Yersinia pestis
54
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
55
Figure 20.23 The bubo, classic
sign of bubonic plague
56
• 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
57
Oxidase-Positive Nonenteric Pathogens
•
•
•
•
•
•
Pasteurella multocida
Haemophilus influenzae
H. aegyptius
H. ducreyi
H. parainfluenzae
H. aphrophilus
58
Pasteurella Multocida
• Zoonotic genus; normal flora in animals
• Opportunistic infections
• Animal bites or scratches cause local
abscess that can spread to joints, bones, and
lymph nodes
• Immunocompromised are at risk for
septicemia and complications
• Treatment: penicillin and tetracycline
59
Haemophilus
• Tiny gram-negative pleomorphic rods
• Fastidious, sensitive to drying, temperature
extremes, and disinfectants
• None can grow on blood agar without special
techniques – chocolate agar
• Require hemin, NAD, or NADP
• Some species are normal colonists of upper
respiratory tract or vagina (H. parainfluenzae, H.
ducreyi)
• Others are virulent species responsible for childhood
meningitis, and chancroid
60
Haemophilus
• H. influenzae – acute bacterial meningitis,
epiglottitis, otitis media, sinusitis, pneumonia,
and bronchitis
– Subunit vaccine Hib
• H. aegyptius – conjunctivitis, pink eye
• H. ducreyi – chancroid STD
• H. parainfluenzae and H. aphrophilus – normal
oral and nasopharyngeal flora; infective
endocarditis
61
Figure 20.25 Meningitis
in the United States
62
Figure 20.26 Acute conjunctivitis
63