Transcript Gram Neg Bacteria PPT

Gram Negative Bacteria and
Spirochetes
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REVIEW
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5 Types of bacteria
 Gram positive
 Gram negative
 Spirochetes
Today’s lecture
Today’s lecture
 Acid-fast (Mycobacteria)
 Mycoplasma
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For the Lecture 3 Exam
 The whole test is matching. Be able to match the
following with their description:
 Virulence factors/enzymes
 The three hemolysis patterns
 Disease terms
 Toxins
 Match the disease to the organism
 Know which diseases have which vectors
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Outer membrane
Peptidoglycan
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GRAM NEGATIVE
GRAM POSITIVE
ENDOTOXINS
(GRAM NEGATIVE ONLY)
O Antigen
Inner plasma membrane
LPS
Cell Wall
Lipid A
(endotoxin)
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LPS
(LOS is LPS with shorter O antigen)
Outer plasma
membrane
Gram Negative Bacterial Cell Walls
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Figure 3.13b7
Virulence Factors
 Adhesins (to adhere)
• Enzymes
 Invasins (to get into cells)
 Endotoxin (LPS, LOS, and Lipid A)
 Exotoxins
 Cytotoxins (kills cells)
 Enterotoxin (GI upset)
 Neurotoxins (disrupts nerves)
 H Ag (flagella allows motility)
 K Ag (capsule)
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β lactamase (deactivates penicillins)
Ribosylase (causes diarrhea)
Catalase
Coagulase (causes blood clots)
Staphylokinase (dissolves blood clots)
Streptokinase (dissolves blood clots)
IgA or IgG protease (deactivates Ab’s)
Hyaluronidase (can move thru tissues)
SOD (superoxide dismutase;
deactivates WBC lysosomes)
 Angiotrophic ability (pulls blood vessels close)
 Facultative intracellular pathogens (can survive with and without O2)
 MDR plasmids (genetic drug resistance)
 PG (prostaglandins; promotes inflammation)
END OF REVIEW
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Gram Negative Bacteria
Not Enterobacteriaceae
Enterobacteriaceae
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E. coli
Enterobacter aerogenes
Klebsiella pneumoniae
Proteus vulgaris
Serratia marcescens
Campylobacter jejuni
Salmonella typhi
Shigella dysenteriae
Yersinia enterocolitica and pestis
NOTE: All of the organisms on
this slide are rods except
Neisseria, which are cocci
(diplococci).
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Neisseria gonorrhea and meningitis
Vibrio cholerae
Helicobacteri pylori
Haemophilus influenzae
Bordetella pertussis
Francisella tularensis
Brucella
Pseudomonas aeruginosa
Rickettsia spp
Chlamydia spp
Legionella
Bartonella spp
Pasturella multocida
Spirochetes
 Treponema pallidum
 Borelia burgdorferi
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Enterobacteriaceae
 The Enterobacteriaceae is a large family of Gram-negative bacteria that
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includes, along with many harmless symbionts, many of the more
familiar pathogens, such as Salmonella, Escherichia coli,Yersinia pestis,
Klebsiella and Shigella.
Other disease-causing bacteria in this family include Proteus, Enterobacter,
Serratia, and Citrobacter.
They are Gram negative rods, most of which are normal flora of the
large intestines of humans and animals.
Some are found in water or soil, or are parasites on a variety of
different animals.
When they get into the small intestines (fecal-oral route) or blood, or
elsewhere, they cause serious disease.
Enterobacteriaceae
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Infections associated
with
Enterobacteriaceae
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Enterobacteriaceae
 Gram negative rods, oxidase negative
 Most are motile (peritrichous flagella)
 Most are encapsulated
 LPS is a virulence factor, since they are Gram neg
 Many have “serum resistance”
 inhibitions of complement proteins (Ab’s can’t attack)
 Ubiquious (they are everywhere) - soil, water,
vegetation, normal intestinal flora
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~40 genera, 150 species
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Cytochrome oxidase
 Cytochrome c oxidase is the last enzyme in the
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respiratory electron transport chain.
It transfers the last two H+ electrons to one oxygen molecule,
converting molecular oxygen to water.
The oxidase test is used to determine if a bacterium produces
cytochrome c oxidase.
Those that have the enzyme (oxidase positive) can use oxygen to
break glucose down into ATP (aerobic).
Those that are oxidase negative must use another pathway, such as
fermentation.
All Enterobacteriaceae are oxidase negative.
CH2OH
GLYCOLYSIS
O
OH
OH
Kinase
CH2O(P)
OH
OH
Homolactic
CH3-C-COOO
GLUCOSE-6-P
OH
O
OH
Kinase
CH2O(P)
OH
ATP
ADP
O
OH
Pyruvate
CH3-C-COO-
O
FRUCTOSE-1,6 DiPhosphate
CH2O(P)
2NADH
DiOH Acetone Phosphate (3C)
P-Glyceraldehyde (3C)
OH OH
CH3-C-C-CH3
GLYCOLYSIS
1, 3, P-Glyceric acid
NAD+ NADH2
ADP + Pi
ATP
2 P-Glyceric acid
Acetoin
2NAD+
2, 3, Butanediol
H H
1 GLU + 2ATP + 2NAD = 2PYR +
4ATP + 2NADH2
Kinase
2, 3 Butanediolic Fermentation
2PYR + 2NADH 
Acetoin + NAD + 2 CO2  +2NADH

2, 3 Butanediol + 2NAD
NET GAIN = 4 NAD
O
2NAD+
OH
CH3-C-C-CH3
H
O
2NADH
OH
CO2
C-CH3
CH3-C
Adolase
NET GAIN = 2 ATP
x2
Isomerase
x2
O
Enol Pyruvate
ADP + Pi
Kinase
ATP
Coenzyme A
NAD+ NADH2
Pyruvate
CH3-C-COOH
CO2
Dehydrogenase
O
Isocitric Acid (6C)
NAD+
NADH2
CO2
ά Ketoglutarate Acid (5C)
COO- -CH2-CH2-C-COOO NAD+
NADH2
Tricarboxylic Acid Cycle
(TCA/ Krebs Cycle)
Succinyl CoA
Citric Acid
Acetyl CoA
CH3-C-S-CoA
Oxaloacitic Acid (4C)
O
COO- -CH2-C-COO-
PYRUVATE
ACTIVATION
ETOH
CH3-CH2-OH
Ethanolic Fermentation
PYR + NADH 
Acetaldehyde + NAD + CO2 
+NADH 
ETOH + NAD
NET GAIN = 2 NAD
Pyruvate
CH3-C-COO-
+
O
CO2
NAD+
NADH
O
2, 3 Butanediolic
FRUCTOSE-6-P
CH2OH
CO2
OH
Acetaldehyde
H
CH3-C
NAD+
O
OH
CH2O(P)
NADH
Pyruvate
CH3-C-COO-
Ethanolic
Homolactic Fermentation
PYR + NADH 
Lactic Acid + NAD
NET GAIN = 1 NAD
Lactic Acid
H
CH3-C-COO-
NAD+
NADH
Pyruvate
GLUCOSE
OH
ATP
ADP
O
OH
Isomerase
FERMENTATION
O
TCA
Acetyl CoA + 3NAD +
1 FAD + 1GTP =
3 NADH + 1FADH2 + GTP +
CO2
MULTIPLY THE ABOVE BY
CO2
TOTAL GAIN:
TWO
8 H+
2 GTP
GDP+ GTP
*First energy-producing step
Malate Acid
PYRUVATE ACTIVATION
Succinate
NAD+
NADH2
2 PYR + 2NAD + 2CoA =
Acetyl CoA + 2NADH2 + 2CO2
FAD+
Fumorate Acid
FADH2
ELECRON TRANSPORT SYSTEM (RESPIRATION / OXIDATIVE PHOSPHORYLATION
ETS
16 NADH from
glycolysis need to
be reduced.
H
Ox
Red
+3
H
Red
Ox
Ox
Red
Ox
+2
FMN
Fes
CoQ
Red
Ox
Red
+2
+3
ADP ATP
ATPase
H2
Cyt b
Cyt c
Cyt a1
Ox
Red
Ox
ADP ATP
ATPase
H2O
Cyt a3
Red
Anaerobic phosphorylation endproducts (instead of H2O)
H
ADP ATP
ATPase
O2
H2S
SO4
NH3
NO2
Electron Transport Chain
Cytochrome
oxidase
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Oxidase Test
 Put bacteria on paper and add a drop of reagent. Purple means
oxidase positive. Enterobacteriaceae are oxidase negative, so they
all ferment at least one type of sugar. The sugar is broken down
into lactic acid, which will change fermentation media from red
to yellow.
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Lab identification of the enterics
http://class.fst.ohio-state.edu
www.mc.maricopa.edu
Green sheen; black nucleated centers
MacConkey agar
selective and differential
EMB agar
selective and differential
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Yellow = sugar fermentation
Black = H2S positive
Air bubble = gas production
TSI
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Triple Sugar Iron Agar (TSI)
Lactose in the slant
Sucrose in the slant
Glucose in the butt
Phenol red (pH indicator dye)
Iron (turns black in the presence of sulfur, which indicates the
organism uses sulfur as its electron acceptor instead of oxygen).
All Enterobacteriacea ferment glucose, so butt will turn yellow.
If it also ferments lactose or sucrose, slant and butt will turn yellow.
If it does not ferment lactose or sucrose: slant stays red and butt turns
yellow.
If the whole tube stays red (e.g. Pseudomonas) it does not ferment glucose,
so it is a strict aerobe, not Enterobacteriaceae.
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Salmonella-Shigella differentiation
 Salmonella-Shigella agar (SS agar) or Hecktoen
agar inhibits most Gram +
 (sugar fermenters – red/orange; non-fermenters – green)
 H2S production (black)
K. pneumoniae (L); M. luteus (R)
S. typhimurium (L); P. vulgaris (R)
H2S production (black ppt)
www.austincc.edu/microbugz/
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Note: Shigella is a
non-fermenter,
and does not
produce H2S,
unlike Salmonella
Enterobacteriaceae
 May be primary pathogens (cause disease in healthy
people)
 But they are usually associated with opportunistic
infections:
 Enteric (GI) infections
 Bacteremia (bacteria in the blood)
 Septicemia (bacterial toxins in the blood)
 Pneumonia
 Meningitis
 UTIs (urinary tract infections)
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Enterobacteriaceae and disease
http://www.ratsteachmicro.com
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Hospital-acquired infection
 A hospital-acquired infection, also known as a HAI or in
medical literature as a nosocomial infection, is an infection
whose development is favoured by a hospital environment,
such as one acquired by a patient during a hospital visit or
one developing among hospital staff.
 Such infections include fungal and bacterial infections and are
aggravated by the reduced resistance of individual patients.
 About 100,000 people die each year in the USA from
nosocomial infections.
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Contaminated surfaces increase
cross-transmission
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Nosocomial Infections
 ESKAPE pathogens are a group of the six bacteria with a high rate
of antibiotic resistance that are responsible for the a majority of
nosocomial infections.
 Enterococcus faecium
 Staphylococcus aureus
 Klebsiella pneumoniae
 Acinetobacter baumannii
 Pseudomonas aeruginosa
 Enterobacter species
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Bacteria forces closure of Puerto
Rico hospital intensive care unit
 At least 10 patients at the University of Puerto Rico
Hospital who have since died were carrying the bacteria
Acinetobacter baumannii.
 The health department's epidemiology director blames
the presence of the bacteria on poor hygiene at the
hospital's intensive care unit.
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Diarrhea
 ~1 billion people worldwide suffer from acute diarrhea
at least once/year
 5-8 million deaths/year
 primarily in developing nations
 ~100 million infections in U.S.
 250,000 require hospitalization
 3000 die
 90% of acute diarrhea caused by infectious agents
 fecal-oral contamination
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High risk groups in U.S.
 Travelers – 40% of tourists to Latin America, Africa, Asia
develop “traveler’s diarrhea”
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ETEC – enterotoxigenic E. coli
Shigella
Salmonella
Campylobacter
Giardia (camper’s, swimmers)
 Consumers of certain foods
 Chicken, mayonnaise, creams, eggs: picnic, banquet,
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restaurant (Salmonella, Shigella. Campylobacter)
Hamburger: undercooked (EHEC – enterohemorrhagic E. coli)
Fried rice (B. cereus)
Seafood (Salmonella, Vibrio cholerae, hepatitis A)
Fermented tofu (C. botulinum)
 Immunocompromised
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High risk groups in U.S. (cont.)
 Daycare participants and their family
 Shigella
 Giardia
 Cryptosporidium (protozoan)
 Rotavirus (virus)
 Institutionalized persons
 Nosocomial (acquired in a hospital) infections of hospital
patients
 Clostridium difficile (Gram positive)
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Treatment - gastrointestinal disease
 Fluid/electrolyte replacement
 fluid alone for mild cases
 dehydration most common cause of death due to diarrheal
disease
 Antibiotics
 not used unless systemic/severe
 e.g.
enteric fever
 immunosuppressed
 Antibiotic prophylaxis for those traveling to
high-risk countries (esp. immunocompromised)
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Enteric infections
 Overview of symptoms
 non-inflammatory
 nausea
 vomiting
 diarrhea
 inflammatory
 Dysentery (severe diarrhea containing mucus
and/or blood)
 Invasive (systemic)
 Typhoid Fever (enteric fever)
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“Common” organisms associated with enteric
infections
I
Mechanism: Non-inflammatory
II
(enterotoxin)
(invasive, cytotoxin)
Penetrating
(invasive, spread)
Location:
proximal small bowel
colon
distal small bowel
Illness:
Diarrhea
Dysentery
Enteric fever
blood, fecal PMNs
(polymorphonuclear
leukocytes =
neutrophils)
fecal mononuclear
leukocytes
(monocytes,
lymphocytes)
Shigella
Invasive E. coli
Clostridium difficile
Entamoeba histolytica
Balentidium coli
Salmonella typhi
Yersinia enterocolitica
Stool exam: no fecal leukocytes
Example
organisms:
Vibrio cholerae
E. coli
Salmonella
Campylobacter
Giardia
Inflammatory
III
Cryptosporidium
Rotavirus
Norwalk-like agents
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Diarrhea pathobiology, #1
Agent
Incubation
period
Vomiting
Abdominal
pain
Fever
Diarrhea
Toxin producers
B. cereus
S. aureus
C. perfringens
1-8h
8-24h
3-4+
1-2+
0-1+
3-4+, watery
8-72h
2-4+
1-2+
0-1+
3-4+, watery
1-8d
0-1+
1-3+
0-1+
3-4+, watery
Enterotoxin
V. cholera
ETEC
K. pneumoniae
Enteroadherent
EPEC
EAEC
Giardia
Cryptosporidium
Helminthes
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Harrison’s principles of internal medicine, 2005
Diarrhea pathobiology, #2
Agent
Incubation Vomiting Abdominal
period
pain
Fever
Cytotoxin
producers
C. difficile
1-3+, usually
watery,
occasional
bloody
1-3d
0-1+
EHEC
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12-72h
Diarrhea
3-4+
1-2+
1-3+, initially
watery, quickly
bloody
Diarrhea pathobiology, #3
Agent
Incubation
period
Vomiting
Abdominal
pain
Fever
Diarrhea
1-3d
1-2+
2-3+
3-4+
1-3+,
watery
moderate
inflammation
Salmonella
Camylobacter
V. parahaemolyticus
Yersinia
12h-11d
0-3+
2-4+
3-4+
1-4+,
watery or
bloody
severe inflammation
Shigella
EIEC
E. histolytica
12h-8d
0-1+
3-4+
3-4+
1-2+,
bloody
Invasive
minimal
inflammation
Rotavirus
Norwalk agent
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Pathogenicity of enteric bacteria
 Host factors
 personal hygiene
 fecal-oral contamination
 gastric acidity
 enteric flora (your own colon microbes)
 specific immunity status (how healthy you
are)
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Pathogenicity of enteric bacteria (cont.)
 Microbial factors
 Exotoxins: three categories
 Neurotoxins
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usually ingested as preformed toxins
Staphylococcal toxins (Staph. aureus)
Botulinum toxin (Clostridium botulinum)
 Enterotoxins
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having a direct effect on intestinal mucosa (elicit fluid secretions)
Cholera toxin (Vibrio cholerae)
E. coli toxins
 Cytotoxins
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mucosal destruction (often see dysentery)
Shigella dysenteriae
Clostridium perfringens
Clostridium difficile
S. aureus
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Gram Negative Bacteria
Not Enterobacteriaceae
Enterobacteriaceae
 E. coli
 Enterobacter aerogenes
 Klebsiella pneumoniae
 Proteus vulgaris
 Serratia marcescens
 Campylobacter jejuni
 Salmonella typhi
 Shigella dysenteriae
 Yersinia enterocolitica and pestis
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Neisseria gonorrhea and meningitis
Vibrio cholerae
Helicobacteri pylori
Haemophilus influenzae
Bordetella pertussis
Francisella tularensis
Brucella
Pseudomonas aeruginosa
Rickettsia spp
Chlamydia spp
Legionella
Bartonella spp
Pasturella multocida
E. coli and the serotypes
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Lactase positive
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note: many intestinal pathogens are lactase negative
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ex. Salmonella, Shigella, Yersinia
grouped based on surface antigens
(serotypes)
 O antigen (lipopolysaccharide)
 H antigen (flagellar)
 K antigen (capsular)
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O157:H7 (EHEC – enterohemorrhagic E. coli)
O148:H28 (ETEC – enterotoxigenic E. coli)
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E. coli serotype differentiation
1. immunologic assay
2. Growth on a variant of MacConkey agar called
Sorbital-MacConkey agar (sorbitol is an artificial
sweetener made from corn sugar)
Most E. coli can ferment sorbitol (forms pink colonies)
 E. coli O157:H7 does not ferment sorbitol (colonies
are clear/colorless).
www.komed.com
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E. coli pathology
 most strains of the pathogenic E. coli are capable of
pathology only within the intestinal tract (some
exceptions)
 most pathogenic strains associated with disease in
developing countries (except EHEC is common in
the USA)
 dependent upon strain, different disease
severity/symptoms (e.g. pathotype)
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E. coli pathology (cont.)
 pathogenic strains produce virulence factors
 found on:
 Plasmids (a DNA molecule that is separate from, and can
replicate independently of, the chromosomal DNA)
 Bacteriophages (viruses that infect bacteria)
 virulence factors include:
 Fimbriae (allow bacteria to stack up on each other to shelter
themselves from immune system
 secretion systems (the process of toxin release)
 toxins
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Bacteriophage
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E. coli strains/serotypes
 most normal flora E. coli are non-pathogenic in
intestinal tract
 pathogenic strains:
 EPEC (enteropathic)
 ETEC (enterotoxic)
 EHEC (enterohemorrhagic)
 EIEC (enteroinvasive)
 EAEC (enteroaggregative)
 UPEC (uropathogenic)
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Enteropathogenic E. coli (EPEC)
destruction of surface microvilli (small intestines)
•fever
•diarrhea (infantile)
•malabsorption of fluids
•vomiting/nausea
•hard to replace fluids
•non-bloody stools
common in developing countries (rare in U.S.)
http://www.annauniv.edu/biotech/epec.jpg
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EPEC pathology - diarrhea
 since this is primarily a disease of the young (less
the 6 months old), fluid replacement is important
 intense vomiting - i.v. fluids are usually required
 disease self-limiting (antibiotics usually not required)
 breast feeding seems to have a strong protective
effect
 IgA and other factors decrease bacterial attachment
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Enterotoxigenic E. coli (ETEC)
“Traveler’s diarrhea”
primarily in developing nations
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~650 million cases/year
~80,000 in travelers from the U.S.
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Two types of toxins
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heat labile toxins (LT)
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similar to cholera toxin (although not as severe)
 lack of absorption of fluids = watery diarrhea
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heat stabile toxins (ST)
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no inflammation, self-limiting
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Enterotoxigenic E. coli (ETEC)
many different ETEC strains
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disease is self-limiting
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watery diarrhea common symptom
exposure provides immunity
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adults living in endemic areas, often immune
children, through exposure to the many strains, eventually
develop immunity
therapy
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fluid replacement
bismuth subsalicylate tablets (Pepto-Bismol, etc.)
provide antibiotics to travelers in the event they get sick
while abroad
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Enterohemorrhagic E. coli (EHEC)
usually O157:H7
many different types of E. coli
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identifying O157:H7…finding a slightly different hay in a
large haystack.
strain must have virulence/toxin genes.
Vero toxin (VTEC) = “shiga-like” toxin (cytotoxin)
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aka Shiga toxin-producing E. coli (STEC)
AB toxin
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“A” inactivates 28S rRNA = stop protein synthesis
 death of epithelial cells
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EHEC
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~75,000 cases in U.S./year
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estimated that only ~100 bacterial cells are
enough to cause infection
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~60 deaths
many EHEC serotypes (~50)
in U.S., most diseases due to O157:H7
disease can be mild to severe (hemorrhagic
colitis = bloody diarrhea)
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depends on strain
patient status (age, physiological status)
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EHEC symptoms
 Hemorrhagic (hemorrhagic coilitis)
 bloody, copious diarrhea
 few leukocytes
 afebrile (no fever)
 usually self limiting (in ~1 week)
 Hemolytic Uremic Syndrome (HUS)
 hemolytic anemia
 thrombocytopenia (destroys platelets)
 kidney failure
 5-10% of kids infected with
EHEC
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Found in raw or
undercooked
ground meat, raw
milk and fecal
contamination of
vegetables
EHEC
cattle seem to be the major reservoir
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humans become infected by ingesting undercooked
meat (beef), unpasteurized milk, fruits and fruit juices
(fecal-contaminated fruit), uncooked vegetables
detection: O157 strains do not ferment sorbitol (or do
so slowly)
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follow up with serological/biochemical testing to confirm
therapy
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supportive therapy
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Enteroinvasive E. coli (EIEC )
Dysentery (bloody diarrhea)
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resembles shigellosis (Shigella dysenteriae)
relatively rare in U.S.
common strains: O124, O143, O164
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need relatively large inoculum: 108-1010
invade and destroy colonic epithelium
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usually causing watery diarrhea
some patients will progress to dysentery
organism replicates within cytoplasm of cell
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Enteroaggregative E. coli (EAEC )
associated with persistent watery diarrhea
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> 14 days (especially infants)
traveler’s diarrhea – maybe as important as ETEC
fimbriae allow for bacteria to stack up on each
other
bacteria stimulate
mucous production called
biofilm formation
(bacterial community)
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Uropathogenic E. coli (UPEC)
 most common cause of UTIs
 females more than males
 some serotypes have pili that preferentially binds
to uroepithelial cells
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Gram Negative Bacteria
Not Enterobacteriaceae
Enterobacteriaceae
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E. coli
Enterobacter aerogenes
Klebsiella pneumoniae
Proteus vulgaris
Serratia marcescens
Campylobacter jejuni
Salmonella typhi
Shigella dysenteriae
Yersinia enterocolitica and pestis













Neisseria gonorrhea and meningitis
Vibrio cholerae
Helicobacteri pylori
Haemophilus influenzae
Bordetella pertussis
Francisella tularensis
Brucella
Pseudomonas aeruginosa
Rickettsia spp
Chlamydia spp
Legionella
Bartonella spp
Pasturella multocida
Enterobacter aerogenes
 Normal GI flora that cause opportunistic
infection
 Transmitted by fecal-oral route or aspiration
 Causes diarrhea, pneumonia, or septicemia
60
Klebsiella pneumoniae
 Although found in the normal flora of the mouth,
skin, and intestines, it can cause destructive
changes to human lungs if aspirated.
 It is an important pathogen in nosocomial
infections. This is an ESKAPE organism.
 Its virulence factors include the O antigen, which
is a component of the lipopolysaccharide (LPS),
and the K antigen (a capsule).
61
Klebsiella pneumoniae
 It causes destructive changes to human lungs via
inflammation and hemorrhage with cell death (necrosis) that
sometimes produces a thick, bloody, mucoid sputum (called
currant jelly sputum).
 These bacteria gain access typically after a person aspirates
colonizing oropharyngeal microbes into the lower respiratory
tract.
 Klebsiella infections are seen mostly in people with a
weakened immune system.
 Many of these infections are obtained when a person is in the
hospital for some other reason (a nosocomial infection).
62
Klebsiella pneumoniae
 Klebsiella can also cause infections in the urinary tract,
lower biliary tract, and surgical wound sites.
 For patients with an invasive device in their body,
contamination of the device becomes a risk; for example,
respiratory support equipment and urinary catheters.
 Sepsis and septic shock can follow entry of the bacteria
into the blood.
 Klebsiella organisms are often resistant to multiple
antibiotics.
63
Proteus vulgaris
 The term Proteus means “changeability of form”.
 Proteus vulgaris inhabits the intestinal tracts of humans and
animals. It can be found in soil, water and fecal matter.
 It is grouped with the Enterobacteriaceae and is an
opportunistic pathogen of humans.
 It is known to cause urinary tract infections and wound
infections.
 It is a common agent of nosocomial infections.
64
Proteus vulgaris Virulence Factors
 Flagella for motility
 Fimbrae for attachment
 Interleukon secretion to cause epithelial cells of
the urinary tract to desquamate (fall off).
 Production of urease, an enzyme that breaks urea
down into ammonia to make the urine more
alkaline so it can survive better.
65
Proteus vulgaris Symptoms
 Urinary tract infections
 Bacteremia and sepsis
 Proteus and Pseudomonas are the most common
causes of Gram negative bacteremia.
 Both exhibit “swarming motility”, in which they
rapidly spread across the surface of the agar
medium. This allows them to spread quickly in
the host.
66
Proteus vulgaris Treatment
 Antibiotics should be introduced in much higher
doses than "normal" when P. vulgaris has infected
the sinus or respiratory tissues.
 For example, Ciprofloxacin should be introduced
at a level of at least 2000 mg per day orally in
such a situation, rather than the "standard" 1000
mg per day.
67
Serratia marcescens
 This is a common cause of nosocomial
infections, particularly catheter-associated
bacteremia, urinary tract infections and
wound infections.
 It is commonly found in the respiratory and
urinary tracts of hospitalized adults and in
the gastrointestinal system of children.
68
Serratia marcescens
 Due to its abundant presence in the environment, and its
preference for damp conditions, S. marcescens is commonly
found growing in bathrooms (especially on tile grout, shower
corners, toilet water line, and basin), where it manifests as a
pink discoloration and slimy film feeding off phosphoruscontaining materials or fatty substances such as soap and
shampoo residue.
 Once established, complete eradication of the organism is
often difficult, but can be accomplished by application of a
bleach-based disinfectant.
69
Serratia marcescens
 S. marcescens may also be found in environments such as dirt,
supposedly "sterile" places, and the subgingival biofilm of
teeth. Due to this, and the fact that it produces a reddishorange pigment, it may cause staining of the teeth.
70
What Diseases Do These Cause?
Enterobacteriaceae








E. coli Diarrhea, septicemia, UTI
Enterobacter aerogenes Diarrhea, pneumonia, septicemia
Klebsiella pneumoniae Pneumonia, septicemia
Proteus vulgaris UTI, diarrhea, nosocomial wound infections
Serratia marcescens UTI, wound infections (catheters), pink grout
Campylobacter jejuni
Salmonella typhi
Shigella dysenteriae
 Yersinia enterocolitica
 Yersinia pestis
71
Gram Negative Bacteria
Not Enterobacteriaceae
Enterobacteriaceae









72
E. coli
Enterobacter aerogenes
Klebsiella pneumoniae
Proteus vulgaris
Serratia marcescens
Campylobacter jejuni
Salmonella typhi
Shigella dysenteriae
Yersinia enterocolitica and
pestis













Neisseria gonorrhea and meningitis
Vibrio cholerae
Helicobacteri pylori
Haemophilus influenzae
Bordetella pertussis
Francisella tularensis
Brucella
Pseudomonas aeruginosa
Rickettsia spp
Chlamydia spp
Legionella
Bartonella spp
Pasturella multocida
Campylobacter jejuni
 Likely the most common cause of gastroenteritis in the United
States 5-7% of cases
 Many animals serve as reservoirs for the bacteria
 Humans become infected by consuming contaminated food, milk,
or water
 Poultry is the most common source of infection
 Infections produce dysentery and frequent diarrhea that is self-
limiting
 Spread of the bacteria can be reduced by proper food handling and
preparation
73
Pathophysiology
 Transmission
 fecal-oral, person-to-person sexual contact,
unpasteurized raw milk and poultry ingestion,
and waterborne.
 Exposure to sick pets, especially puppies
 infectious dose is 1000-10,000 bacteria
 incubation period of up to a week
74
Disease
– Patients may have a history of ingesting inadequately cooked
poultry, unpasteurized milk, or untreated water.
• The incubation period is 1-7 days and is probably related to the
dose of organisms ingested.
– A brief prodrome of fever as high as 40°C (104°F)
– headache, and myalgias (muscle pain) lasting up to 24 hours
– crampy abdominal pain (abdominal pain and tenderness may be
localized)
• Pain in the right lower quadrant may mimic acute appendicitis
(pseudoappendicitis).
– Up to 10 watery, frequently bloody, bowel movements per day
– Patients with C jejuni infection who report vomiting, bloody
diarrhea, or both tend to have a longer illness and require hospital
admission.
75
Salmonella

The “L” is silent
Gram negative bacilli, lactase negative
motile, H2S gas production (some exceptions)

~2500 serotypes!


often, the serotypes are considered to be
individual species
 nomenclature is a “mess”

76
Salmonella

S. choleraesuis is the “major” species

organism that causes typhoid (enteric)
fever:

Often just called Salmonella Typhimurium
 Shortened to Salmonella Typhi
77
Salmonella subtyping

Serotypes based on:
 O antigen (LPS outer sugars)
 Flagella H antigens
 Various surface antigens

most clinical labs divide Salmonella into serogroups
(A, B, C1, C2, D, and E) based on O-antigen
78
Salmonella infection

Human intestinal disease due to ingestion of
bacteria (contaminated food/water)
organism gets to small intestines
 macrophages often ingest bacteria
 bacteria are then protected from host responses
(e.g. complement, antibodies, etc)


Salmonella alters host cells:


changes host cell to allow for “bacteria-mediated
endocytosis (absorbing a substance from outside
the cell)”
prevents lysosomal enzymes of macrophage from
degrading bacteria
79
Salmonella pathology

Bacteria is disseminated by macrophages to:


liver, spleen, lymph nodes, bone marrow
Systemic symptoms likely due to host
response against pathogen

inflammatory cytokines secreted by activated
macrophages. Cytokines are chemicals that call
other WBCs to come to the area.
80
Salmonella pathology (cont.)
Non-typhoid and typhoid Salmonella
infections



Typhoid relatively rare in U.S., although 21 million
infections worldwide (~200,000 deaths)
Non-typhoid Salmonella much more common
 Human acquire infections from poultry/eggs,
dairy, and contaminated work surfaces
(cutting boards)
 In U.S., ~40,000 reported cases (estimated 2
million)
81
Enteric (typhoid) fever


systemic disease caused by S. Typhi or S.
Paratyphi
originally called typhoid fever because of some
similarities to typhus (fever, nausea, rash, and
other systemic symptoms)



different bacteria, different mechanism of spread
“better name” is enteric fever
disease from ingesting contaminated food



humans only known hosts of these strains
endemic (commonly occuring) in developing nations
not common in U.S. (food/water/sewage care)
82
Enteric (typhoid) fever (cont.)
~70% of U.S. cases obtained from international
travel
infectious dose is low (~103 versus 106-108 for
infections with other species of Salmonella)
Clinical manifestations







febrile illness
disease more severe by S. typhi as compared to S.
paratyphi
after 10-14 days of initial infection, patients have
gradually increasing fever, headache, myalgia (muscle
pain), malaise (fatigue).
at around 21 days after infection, GI symptoms present
(not seen in all patients) – diarrhea
83
Typhoid fever
 Typhoid fever — also known simply as typhoid — is a
common worldwide bacterial disease transmitted by the
ingestion of food or water contaminated with the feces of an
infected person, which contain the bacterium Salmonella.
84
Went back to work as
a cook in 1914 at a
NYC hospital. Another
25 got sick and 2 died.
85
Mary Mallon in 1931.
Food worker, first diagnosed
as carrier in 1907. She
infected 50 people, 3 of
whom died. Quarantined and
then released in 1910.
Quarantined
permanently to North
Brother island in 1915.
Typhoid Mary
 Mary Mallon (September 23, 1869 – November 11, 1938),
better known as Typhoid Mary, was the first person in the
United States identified as an asymptomatic carrier of the
pathogen associated with typhoid fever.
 She was presumed to have infected some 75 people, 5 of
whom died, over the course of her career as a cook.
 She was forcibly isolated twice by public health authorities
and died after a total of nearly three decades in isolation.
86
 From 1900 to 1907 she worked as a cook in the New York City




87
area. In 1900, within two weeks of her employment, residents
developed typhoid fever.
In 1901 she moved to Manhattan, where members of the family
for whom she worked developed fevers and diarrhea, and the
laundress died.
Mallon then went to work for a lawyer, until seven of the eight
household members developed typhoid.
In 1906, she took a position in Long Island, and within two weeks,
ten of eleven family members were hospitalized with typhoid.
She changed jobs again, and similar occurrences happened in three
more households.
 In late 1906, one family hired a typhoid researcher named George




88
Soper to investigate.
Soper discovered the common element in the outbreaks was an
unmarried, heavyset Irish cook, about forty years old. No one knew her
whereabouts. After each case she left and gave no forwarding address.
Soper traced her to an active outbreak in a Park Avenue penthouse —
two servants were hospitalized and the daughter of the family died.
When Soper approached Mallon about her possible role in spreading
typhoid, she adamantly rejected his request for urine and stool samples.
Since Mary refused to give urine and stool samples, he decided to
compile a five-year history of Mary's employment. Soper found that of
the eight families that hired Mallon as a cook, seven claimed to have
gotten typhoid fever.
On his next visit, he told her he would write a book and give her all the
royalties. She angrily rejected his proposal and locked herself in the
bathroom until he left.
 A few days later, several police officers arrived at Mary's




89
workplace and took her into custody.
Mary attracted so much media attention that in a 1908 issue of the
Journal of the American Medical Association she was called
“Typhoid Mary“.
Under questioning, Mallon said she rarely washed her hands when
cooking and felt there was no need to do so.
Cultures of Mary's urine and stools, taken forcibly with the help of
prison matrons, revealed that her gallbladder was teeming with
typhoid Salmonella.
She refused to have her gallbladder extracted or to give up her
occupation as a cook, maintaining stubbornly that she did not
carry any disease.
 Mallon was held in isolation for three years at a clinic located on
North Brother Island.
 Eventually, the New York State Commissioner of Health decided
that disease carriers should no longer be kept in isolation.
Mallon could be freed if she agreed to stop working as a cook
and take reasonable steps to prevent transmitting typhoid to
others.
 On February 19, 1910, Mary agreed that she prepared to change
her occupation (that of a cook), and would take such hygienic
precautions as would protect those with whom she came in
contact from infection.
 She was released from quarantine and returned to the mainland.
90
 Upon her release, Mallon was given a job as a laundress, which paid
less than cooking. She soon changed her name to Mary Brown, and
returned to her old occupation. For the next five years, she worked in
a number of kitchens; wherever she worked, there were outbreaks of
typhoid. However, she changed jobs frequently, and Dr. Soper was
unable to find her.
 In 1915, a serious epidemic of typhoid erupted among the staff of
New York's Sloane Hospital for Women, with twenty-five cases and
two fatalities. Public health authorities located and arrested Typhoid
Mary, returning her to quarantine on North Brother Island on March
27, 1915. She was confined there for the remainder of her life.
 Mallon became a minor celebrity, and was interviewed by journalists,
who were forbidden to accept even a glass of water from her. Later,
she was allowed to work as a technician in the island's laboratory,
washing bottles.
91
 Other healthy typhoid carriers identified in the first quarter of the
20th century include Tony Labella, an Italian immigrant, presumed
to have caused over 100 cases (with five deaths); an Adirondack
guide dubbed Typhoid John, presumed to have infected 36 people
(with two deaths); and Alphonse Cotils, a restaurateur and bakery
owner.
 Today, Typhoid Mary is a colloquial term for anyone who, knowingly
or not, spreads something undesirable.
 Individuals can develop typhoid fever after ingesting food or water
contaminated during handling by a human carrier. The human
carrier may be a healthy person who has survived a previous episode
of typhoid fever yet who continues to shed the associated bacteria,
Salmonella typhi, in feces and urine.
 Washing hands with soap before touching or preparing food,
washing dishes and utensils with soap and water, and only eating
cooked food are all ways to reduce the risk of typhoid infection.
92
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93
Diagnosis and treatment of typhoid fever
positive diagnosis can be accomplished from stool,
urine, or bone marrow culture



stool culture is often negative in 60-70% early in infection
some strains of S. Typhi have been shown to
be MDR (multidrug resistant)


check for antibiotic susceptibility
carrier state requires ~6 week therapy

if patient has kidney/gall stones, need surgery as well as
antibiotic therapy
94
Gastroenteritis

acute gastritis is characterized by vomiting,
abdominal pain, fever, and diarrhea (many causes)
Gastroenteritis caused by Salmonella:
 S. Typhimurium (~200 serovariants)
 many animal reservoirs (hard to control)
 symptoms often within 8-24hr after ingestion
 often self limiting
 diarrhea can be mild to very severe (watery,
green, offensive)
 symptoms usually last 2-3 days (can be up
to 1 week)

95
Salmonellosis

outbreaks in U.S.

attributed to raw chicken, eggs, processed
foods, and vegetables and fruits (fruit juices)


fecal contaminants
exposure to pets (especially reptiles)
~90% of reptiles carry the bacteria
 1970s – 14% of human cases of salmonellosis
attributed to exposure to turtles
 birds, rodents, dogs, and cats are also potential
reservoirs

96
Salmonella
 Professional food facilities are not allowed to store eggs or
chicken on shelves above other exposed foods in the
refrigerator.
97
Salmonellosis diagnosis and treatment
 stool culture

sent to public health departments for phage
typing


mechanism to identify serotype/serovar
disease generally self-limiting
replace fluids/electrolytes if needed
 antibiotics for infants, elderly,
immunocompromised, and those with bacteremia
 many antibiotic resistant strains

vaccine for those traveling to endemic areas
(especially those going camping)

98
Shigella
 causes acute infectious inflammatory colitis
(colon infection)
 aka – bacillary dysentery
 not all infected develop dysentery
 Gram negative rod (bacillus), non-motile
 lactase negative (S. sonnei is a weak fermenter)
 H2S negative
 genetically similar to Esherichia
 Shigella are thought to be serotypes of E. coli
 historically names have not been changed
99
Shigella
 4 main species, different serotypes within each
species (47 serotypes)
 S. dysenteriae (Group A) – most pathogenic
 S. flexneri (Group B)
 most common cause of shigellosis in developing nations
 S. boydii (Group C) - India
 S. sonnei (Group D) – U.S.
 most common cause of shigellosis in industrial world
 mildest
100
Shigella
 ~200 million cases worldwide
 ~1 million deaths (especially among children)
 ~15,000 cases reported/year in U.S. (real number is
higher - ~500,000/year?)
 pathogen of humans and higher primates
 infection from fecal-oral transmission from infected
humans
 highly communicable (need only ~200 cells to
produce disease)
 high rate of secondary household transmission
101
Shigella pathology
 Clinical manifestation
 abdominal cramps, diarrhea, fever, bloody stools
 large numbers of WBC in stool
 inflammatory damage to intestinal epithelium
 Diagnosis
 standard microbiological testing (selective/differential
media: MacConkey followed by SS or Hektoen-enteric,
etc)
 Therapy
 most cases self-limiting
 antibiotic therapy for those with severe symptoms
 because of high rate of spread, all patients should be treated
102
Shigella pathology
 virulence proteins cause “ruffling” of epithelial
cells
 allows for endocytosis of the bacteria
 actin rearrangement allows for cell-to-cell spread
 S. dysenteriae produces shiga toxin (similar to
EHEC)
103
Yersinia
 Enteric pathogens: Y. enterocolitica, Y.
pseudotuberculosis
 Y. pestis – Black Plague (carried by fleas on rats)
 Gram negative, pleomorphic rods
 primarily found in animals (rodents, swine, cattle,
etc) – all are zoonotic diseases
Y. enterocolitica
104
www.emedicine.com
Y. pestis
 Bubonic and Pneumonic plague
 formation of bubos: live pathogens in lymph nodes
 bacteria resists phagocytosis
 painful inflammatory lesions
 Pneumonic plague – high mortality (90%
of untreated)
 highly infectious
105
Bubonic plague still kills thousands
 Bubonic plague, the deadly
scourge that wiped out half of
Europe during the Middle Ages,
still lurks in pockets of the globe.
 Although plague is now rare in
Europe, it recently sickened
more than 10,000 people in
Congo over a decade, and cases
still occasionally emerge in the
Western United States.
106
Yersinia pestis
 The plague bacteria, Yersinia pestis, had lain dormant in China's
Gobi Desert for centuries. But in the 1300s, it emerged with a
vengeance, fanning out via trade routes from Asia to Europe and
killing millions of people along the way. The plague was
transmitted by fleas harbored by rats, which flourished in the
overcrowded, filthy cities of the Middle Ages. By the end of the
1500s, between a third and half of Europe's population had died
from the Black Death.
 Even during the 1900s, the plague still killed millions of people,
but since then, the advent of better hygiene in cities and swift
treatment with antibiotics has reduced this erstwhile killer into a
rare disease.
107
Yersinia pestis
 In the United States during that time period, 56 people
contracted the plague and seven died. The cases occurred
mainly because plague has become endemic in squirrels and
wild rodents in the American West.
108
Man who contracted bubonic
plague from cat bite
 An Oregon man who escaped death after
contracting the bubonic plague from his
cat has opened up about the terrifying
experience and how lucky he is to be
alive.
 Paul Gaylord was in a coma for 27 days in
2012, on life support as his internal
organs began to fail, his extremities
rotting.
 “I had collapsed lungs, my heart stopped
and my hands and feet turned black.
Technically, I shouldn’t be here.”
 Gaylord’s condition was so bad that the
day before he woke up, doctors
considered pulling the plug.
109
Man who contracted bubonic
plague from cat bite
 “My recovery shocked everybody,. I’d
been told I’d be on dialysis for the rest
of my life, but I had one treatment and
I recovered. Everything in my body
did, except my hands and feet.”
 The retired welder lost all of his
fingers except for parts of both
thumbs, all of his toes and a part of his
right foot.
 Gaylord recalled that his cat Charlie
showed up on the porch, swollen and
choking on a mouse. He tried to pull it
out, but the cat bit his finger and ran
away. The next day Charlie returned,
“clearly suffering.”
110
“It was as if the mouse had died in his mouth and was
rotting, and I was worried about bacteria,” Gaylord
wrote. “I called a friend over to put him down, then
we buried him.”
Gaylord’s own symptoms kicked in at work the next
day. He had a fever and felt sick before his skin turned
grey and his wife rushed him to the hospital.
Man who contracted bubonic
plague from cat bite
 After being given antibiotics for cat
scratch fever, a doctor told Gaylord he
thought bubonic plague was the
correct diagnosis.
 “I had glands under my arms the size
of lemons and that’s one of the
symptoms,” he said.
 Gaylord spent a month in the hospital
— most of it unconscious — before
returning home.
 Health officials dug up Charlie’s body
and determined he was infected with
the plague.

Author: RHEANA MURRAY

http://m.nydailynews.com/1.1600598
111
Gaylord has since retired, and spends his time making
hunting knives in his workshop.
“It’s hard to believe it happened to me, but rather
than feel depressed, I’ve always felt positive and
happy to be alive,” he wrote, calling his experience “a
fluke.”
Y. enterocolitica (and Y. pseudotuberculosis)
 Y. enterocolitica more common than other enteric
Yersinia sp.
 acute enterocolitis
 mesenteric lymphadenitis (can mimic appendicitis)
 over 60 different serotypes
 serotypes 3, 8 and 9 account for most human infections
 ingestion of contaminated food/milk (can grow at
lower temperatures, 4°C or 39°F.
 associated with a blood transfusion septicemia
112
Y. enterocolitica transmission
bold lines = common
spread
113
Yersinia
 Diagnosis for Yersinia
 isolation of organism from stool or blood sample
 may need to do “cold enrichment”
 growth at 4-7°C for 28 days with weekly subculture on SS agar
 Therapy
 Plague
 antibiotics (control rodent population)
 Enteric infections: often self-limiting (except if
progress to septicemia)
114
What Diseases Do These Cause?
Enterobacteriaceae







E. coli Diarrhea, septicemia, UTI
Enterobacter aerogenes Diarrhea, pneumonia, septicemia
Klebsiella pneumoniae Pneumonia, septicemia
Proteus vulgaris UTI, diarrhea, nosocomial wound infections
Serratia marcescens UTI, wound infections (catheters), pink grout
Campylobacter jejuni Diarrhea from poultry, sick puppies; septicemia
Salmonella typhi Diarrhea and typhoid fever; feces on food, raw
chicken, reptiles
 Shigella dysenteriae Bloody diarrhea from human feces
 Yersinia enterocolitica Diarrhea; lymph node inflammation
 Yersinia pestis Bubonic (black) plaque
115
Exotoxins and their classification
 Cytotoxins








Toxic Shock Syndrome toxin (Staph aureus)
Exfolatin (Scalded Skin Syndrome; Staph aureus)
Necrotizing Fasciitis Toxin (group A Strep)
Anthrax
Diphtheria
Verotoxin (Shigella-like toxin; E. coli EHEC)
AB toxin (Kills colon epithelium; E. coli EHEC)
Pertussis and tracheal cytotoxin
 Enterotoxins
 Neurotoxins
 Botulism
 Tetanus
116
These all have endotoxins, but what EXOTOXINS do they produce?






E. coli (EHEC) Verotoxin, AB toxin
E. coli (ETEC) Enterotoxin, heat labile and heat stable toxins
Klebsiella pneumoniae Enterotoxin
Campylobacter jejuni Enterotoxin
Salmonella typhi Enterotoxin
Shigella dysenteriae Shigatoxin
 Vibrio cholerae Cholera toxin
 Bordatella pertussis Pertussis toxin
117
Gram positive exotoxins (no endotoxins)








Staphylococcus aureus Cytotoxins (TSS, NF, exfolatin), Neurotoxin, Enterotoxin
Clostridium difficile Cytotoxin, Enterotoxin
Clostridium perfringens Cytotoxin, Enterotoxin
Clostridium botulinum Neurotoxin (botulism toxin)
Clostridium tetani Neurotoxin (Tetanus toxin)
Bacillus cereus Enterotoxin
Bacillus anthracis Cytotoxin (Anthrax toxin)
Corynebacterium diphtheriae Cytotoxin (Diphtheria toxin)
118
Gram Negative Bacteria
Not Enterobacteriaceae
Enterobacteriaceae








E. coli
Enterobacter aerogenes
Klebsiella pneumoniae
Proteus vulgaris
Serratia marcescens
Campylobacter jejuni
Salmonella typhi
Shigella dysenteriae
 Yersinia enterocolitica and pestis
119
 Neisseria gonorrhea and












meningitis The only Gram neg cocci
Vibrio cholerae
Helicobacter pylori
Haemophilus influenzae
Bordetella pertussis
Francisella tularensis
Brucella
Pseudomonas aeruginosa
Rickettsia spp
Chlamydia spp
Legionella
Bartonella spp
Pasturella multocida
Neisseria gonorrhoeae with pili
120
Neisseria
 two major pathogenic species
 N. gonorrheae
 associated with STDs
 N. meningitidis
 associated with respiratory and CNS
infections
121
Microbiology/Pathology
 Gram-negative intracellular diplococcus
 Contains LOS in outer membrane.
 infects mucus-secreting epithelial cells
 evades host response through alteration of
surface structures
 Oxidase positive
122
In vitro growth
 Obligate aerobes
 Sensitive to drying (“delicate”) and some products in
blood (that is why one uses “Chocolate agar” for
culture)
 called fastidious
 Chocolate agar is blood agar that has been slowly
heated so the red blood cells lyse, to release the
hemoglobin.
 Also needs 5% CO2
123
Endotoxin
 LPS - lipopolysaccharide
 Lipid A, core sugars, outer sugars
 LOS - lipooligosaccharide
 present in Neisseria as well as several other Gram
negative bacteria
124
NG: Incidence and Prevalence
 Significant public health problem in U.S.
 Number of reported cases underestimates incidence
 incidence remains high in some groups defined by
geography, age, race/ethnicity, or sexual risk behavior
 Increasing proportion of gonococcal infections caused
by resistant organisms
125
Gonorrhea — Rates by state: United States and
outlying areas, 2006
67.3
20.7
VT 11.6
NH 13.7
MA 38.0
RI 47.2
CT 74.4
NJ 63.0
DE 176.0
MD 130.8
DC 342.8
10.4
24.0
40.1
64.4
14.4
125.1
47.3
23.6
81.5
115.6
66.3
79.2
92.2
158.2 139.2
36.0
93.4
80.5
89.9
139.5
167.4
52.5 85.6
175.9
78.5
Guam 58.1
100.2
90.7
154.9
199.4
162.6
154.9
242.5
Rate per 100,000
population
216.8
257.1 234.0
133.2
240.6
94.9
69.4
134.8
<=19.0
(n= 5)
19.1-100.0
(n= 27)
>100
(n= 22)
Puerto Rico 7.7
Virgin Is. 31.3
Note: The total rate of gonorrhea for the United States and outlying areas
(Guam, Puerto Rico and Virgin Islands) was 119.4 per 100,000 population.
The Healthy People 2010 target is 19.0 cases per 100,000 population.
126
Men
750
Rate (per 100,000 population)
600
450
300
150
0
6.3
279.1
Age
10-14
0
Women
150
300
605.7
25-29
185.7
294.9
30-34
130.8
40-44
53.0
117.1
125.5
35-39
93.5
45-54
65.7
33.9
12.9
18.4
55-64
2.9
4.2
65+
0.7
Total
750
647.9
20-24
320.9
600
35.1
15-19
454.1
450
124.6
127
Transmission
 Efficiently transmitted by:





Male to female via semen
Female to male urethra
Rectal intercourse
Fellatio (pharyngeal infection)
Perinatal transmission (mother to infant)
 Gonorrhea associated with increased transmission of
and susceptibility to HIV infection
128
Virulence Factors of Gonococcus
 Pilus
 Phase variation and Antigenic variation (of pilus)
 phase variation – differences in colony appearance
 antigenic variation – varying pili antigenic type
 development of a vaccine will be difficult
 Endotoxin (LOS)
 Serum resistance
 IgA protease – cleaves at hinge region
129
Gonorrhea: Gram Stain of
Urethral Discharge
130
Source: CDC/NCHSTP/Division of STD Prevention, STD Clinical Slides
Neutrophils Containing Neisseria
131
biology.clc.uc.edu/Fankhauser/Labs/Microbiolo...
Genital Infection in Men
 Urethritis – inflammation of urethra
 typically purulent or mucopurulent urethral discharge
 asymptomatic in 10% of cases
 Epididymitis – inflammation of the epididymis
 unilateral testicular pain and swelling
 Infrequent
 NOTE:
 Gonorrhea: men have symptoms, women do not
 Chlamydia: women have symptoms, men do not
132
Genital Infection in Women
 most infections are asymptomatic
 Cervicitis – inflammation of the cervix
 non-specific symptoms: abnormal vaginal discharge,
intermenstrual bleeding, dysuria, lower abdominal pain,
or dyspareunia (difficult or painful sexual intercourse)
 clinical findings: mucopurulent or purulent cervical
discharge, easily induced cervical bleeding
 50% of women with clinical cervicitis have no symptoms
 Urethritis – inflammation of the urethra
133
Complications in Women
 Pelvic Inflammatory Disease (PID)
 Pelvic inflammatory disease (PID) is a term for inflammation of the
uterus, fallopian tubes, and/or ovaries as it progresses to scar formation
with adhesions to nearby tissues and organs.
 This can lead to infertility.
 may be asymptomatic
 may present with lower abdominal pain, discharge,
dyspareunia, irregular menstrual bleeding and fever.
134
Pelvic inflammatory disease (PID)
 PID is a vague term and can refer to viral, fungal, parasitic, though
most often bacterial infections.
 In the United States, more than 750,000 women are affected by PID
each year, and the rate is highest with teenagers and young women.
 PID causes over 100,000 women to become infertile in the US each
year.
 N. gonorrhea causes 40–60% of cases of PID.
 There is NO CURE for PID. Women will have severe
pain for the rest of their lives.
 Although the PID infection itself may be cured, effects of
the infection may be permanent, due to the scar tissue
that develops.
135
Syndromes in Men and Women
 Conjunctivitis
 usually autoinoculation in adults
 symptoms/signs: eye irritation with purulent conjunctival
exudate
 Disseminated gonococcal infection (DGI)
 systemic gonococcal infection
 occurs infrequently. More common in women than in men
 associated with gonococcal strain that produce bacteremia
without associated urogenital symptoms
 clinical manifestations: skin lesions, arthralgias, arthritis,
hepatitis, myocarditis, endocarditis, meningitis
136
Gonococcal Ophthalmia
137
Source: CDC/NCHSTP/Division of STD Prevention, STD Clinical Slides
Disseminated
Gonorrhea—
Skin Lesion
138
Source: CDC/NCHSTP/Division of STD Prevention, STD Clinical Slides
Septic
Arthritis
139
www.learningradiology.com/images/boneimages1/...
Gonorrhea Infection in Children
 Perinatal: infections of the
conjunctiva, pharynx, respiratory
tract
 ophthalmia neonatorum
 silver nitrate, antibiotics
 Older children (>1 year):
considered possible evidence of
sexual abuse
140
Diagnostic Methods
• Culture tests
– Thayer-Martin agar
– This is 5% chocolate sheep blood plus antibiotics.
– It is used for culturing and primarily isolating pathogenic Neisseria
bacteria, including Neisseria gonorrhea and Neisseria
meningitides, because this medium inhibits the growth of most
other microorganisms.
– Neisseria is fastidious, so it needs chocolate agar, and it also
needs the below three antibiotics mixed into the medium because
other organisms will out-compete it and it will not grow. The
antibiotics that are used will not kill Neisseria.
1) Vancomycin to kill Gram positives
2) Colistin to kill all other Gram negatives
3) Nystatin to kill most fungi
141
Reporting
 Laws and regulations in all states require that
persons diagnosed with gonorrhea are reported
to public health authorities by clinicians, labs, or
both.
142
Meningococcus
Capsule
143
meningitisuk.org
Diseases caused by N. meningitidis
 Meningococcal meningitis
 Meningococcemia, sepsis
144
Virulence Factors of Meningococcus
 Endotoxin (LOS)
 Polysaccharide capsule
 Serum resistance
 IgA protease
145
Control of Meningococcus
 Vaccine
 does not display same types of phase/antigenic
variation as seen in other Neisseria, so it may not work
against the strains that have mutated.
 Antimicrobials
 somewhat susceptible to penicillins (although some
degree of resistance reported)
146
Gram Negative Bacteria
Not Enterobacteriaceae
Enterobacteriaceae








E. coli
Enterobacter aerogenes
Klebsiella pneumoniae
Proteus vulgaris
Serratia marcescens
Campylobacter jejuni
Salmonella typhi
Shigella dysenteriae
 Yersinia enterocolitica and pestis
147













Neisseria gonorrhea and meningitis
Vibrio cholerae
Helicobacteri pylori
Haemophilus influenzae
Bordetella pertussis
Francisella tularensis
Brucella
Pseudomonas aeruginosa
Rickettsia spp
Chlamydia spp
Legionella
Bartonella spp
Pasturella multocida
Vibrio
 Vibrio are small Gram negative rods, shaped like a comma.
 Members of this genus share many characteristics with enteric
bacteria such as Escherichia and Salmonella
 Found in water environments worldwide
 Vibrio cholerae is the most common species to infect humans
 Causes cholera
 Humans become infected with V. cholerae by ingesting contaminated
food and water
 Found most often in communities with poor sewage and water
treatment
148
Haiti cholera outbreak after
earthquake, 2010
 The ongoing Haiti cholera outbreak is the worst epidemic of
cholera in recent history, according to the U.S. Centers for
Disease Control and Prevention. After the 2010 earthquake,
in little over two years, as of August 2013, it has killed at
least 8,231 Haitians. Since the outbreak began in October
2010, more than 6% of Haitians have had the disease.
 Then, hurricane Sandy struck in 2012, and the subsequent
cases of cholera caused more deaths than the cyclone took in
all countries combined.
149
Cholera Outbreaks After Storms
 Hurricane Sandy (Oct 2012)
 Cholera outbreak
150
Cholera Outbreaks
 Outbreaks occur seasonally and are associated with poverty and poor
sanitation.
Serious disasters, such as hurricanes, typhoons, or earthquakes, cause
a disruption in water systems resulting in the mixing of drinking and
waste waters.
 Compared to diseases like smallpox and tuberculosis, which have
been around for thousands of years, cholera is a relatively new disease.
Its origins can be traced to India in 1826, but by 1830, 40,000 people
a year were dying from cholera. In 1831, nearly 200,000 Russians
died. The same year, cholera spread to Poland, Hungary, and
Germany, killing hundreds of thousands. As it spread throughout
Europe, the death toll rose dramatically. In 1848, Russia alone
suffered 3 million deaths!
151
Cholera Outbreaks
 Cholera spread throughout the world in seven large pandemics. The
seventh pandemic began in 1961 in Indonesia and subsequently
affected approximately 100 more countries. In some areas, more than
20 percent of the people got sick and often half of them died because
medical treatment was not available. The pandemic reached Africa in
1970 and moved rapidly throughout the region. By the end of 1971,
25 African countries were reporting cholera outbreaks. Between
3,000 and 43,000 cholera cases were reported in Africa every year
until 1990. The following year, a large epidemic affected 14 countries
and resulted in more than 100,000 cases and 10,000 deaths.
152
Cholera Vaccine
 There are two oral vaccines with few side
effects that are given outside the United
States.
 These vaccines provide 60 to 100 percent
protection against major outbreak strains,
but the vaccine only lasts for six months.
153
Vibrio
 A large inoculum is required to cause disease
because the bacteria are susceptible to the
acidic stomach environment.
 Cholera toxin is the most important virulence
factor of V. cholerae.
154
Cholera Pathology
 Some infections are asymptomatic or cause mild
diarrhea
 Can cause severe disease resulting in abrupt watery
diarrhea and vomiting
 “Rice-water stool” is characteristic
 Results in severe fluid and electrolyte loss
 Can progress to coma and death
155
Rice water stools
156
Cholera Beds
157
Diagnosis, Treatment, and Prevention
 Diagnosis
 Usually based on the characteristic diarrhea
 Treatment
 Fluid and electrolyte replacement
 Antimicrobial drugs are not as important because they are
lost in the watery stool
 Prevention
 Adequate sewage and water treatment can limit the spread
of V. cholerae
158
Florida officials warn of deadly
seawater bacteria after man's death
 Sept, 2013, authorities in Florida are advising residents
to avoid eating raw shellfish and exposing open wounds
in seawater.
 59-year-old Henry "Butch" Konietzky died after he was
exposed to bacteria called Vibrio vulnificus. He had been
fishing for crabs in the Halifax River.
 Statewide, 29 cases and nine deaths have been linked to
the bacteria this year.
159
Florida officials warn of deadly seawater
bacteria after man's death
 Vibrio vulnificus is a bacterium that normally lives in warm
seawater and is in the same family as cholera. Symptoms include
diarrhea, vomiting and abdominal pain. Health officials say people
should wear gloves and wash their hands after handling raw
shellfish.
 He noticed lesions on his legs several hours after fishing and went
to the emergency room with his wife. But the bacteria had already
spread through his body, causing his kidneys to shut down.
160
Gram Negative Bacteria
Not Enterobacteriaceae
Enterobacteriaceae









161
E. coli
Enterobacter aerogenes
Klebsiella pneumoniae
Proteus vulgaris
Serratia marcescens
Campylobacter jejuni
Salmonella typhi
Shigella dysenteriae
Yersinia enterocolitica and pestis













Neisseria gonorrhea and meningitis
Vibrio cholerae
Helicobacteri pylori
Haemophilus influenzae
Bordetella pertussis
Francisella tularensis
Brucella
Pseudomonas aeruginosa
Rickettsia spp
Chlamydia spp
Legionella
Bartonella spp
Pasturella multocida
Helicobacter pylori
 Slightly helical, highly motile bacterium that colonizes the
stomach of its hosts
 Causes most (if not all) peptic ulcers
 H.pylori produces numerous virulence factors that enable it to
colonize the stomach
 Many people have this organism in their stomach, but don't get
an ulcer or gastritis.
 Coffee drinking, smoking, and drinking alcohol increase your risk for
an ulcer
162
Symptoms
 If you are a carrier of H. pylori, you may have no
symptoms.
 Symptoms of an ulcer or gastritis include:
 Abdominal pain
 Bloating and fullness
 Dyspepsia or indigestion
 Feeling very hungry 1 to 3 hours after eating
 Mild nausea (may be relieved by vomiting)
163
Diagnosis
 Simple blood, breath, and stool tests can determine if you are
infected with H. pylori.
 The most accurate way to diagnose is through upper endoscopy of
the esophagus, stomach, and duodenum.
 Because this procedure is invasive, it is generally only done on
people suspected to have an ulcer, or who are at high risk for
ulcers or other complications from H. pylori, such as stomach
cancer.
 Risk factors include being over 45 or having symptoms such as:
 Anemia
 Difficulty swallowing
 Gastrointestinal bleeding
 Unexplained weight loss
164
Treatment
 Patients who have H. pylori and also have an ulcer are
most likely to benefit from being treated.
 Patients who only have heartburn or acid reflux and H.
pylori are less likely to benefit from treatment.
 The treatment does not work in all patients.
 Treatment must be taken for 10 to 14 days. Medications
may include:
 Two different antibiotics
 Proton-pump inhibitor (inhibits acid secretion)
 Bismuth subsalicylate (Pepto-Bismol)
165
Haemophilus
 Small, pleomorphic (various shaped) bacilli
 Obligate parasites due to their requirement of heme
and NAD+ for growth
 Colonize the mucous membranes of humans and
some animals
 Contains LOS in outer membrane.
166
Lipooligosaccharides (LOS)
 LOS is like LPS, except it lacks the O-antigen and possesses
only the lipid A.
 LOS are glycolipids found in the outer membrane of some
types of Gram negative bacteria, such as Neisseria,
Haemophilus, and Bordetella.
 LOS allows for bacteria to display antigenic diversity, aiding
in the evasion of host immune defenses and thus contributing
to the virulence of these bacterial strains.
167
Haemophilus influenzae
 Most strains have a polysaccharide capsule that resists
phagocytosis and is used in classification of the bacteria
 H.influenzae type b is the most significant
 Was the most common form of meningitis in infants prior to the use of
an effective vaccine
 Can cause a number of other diseases in young children
 Use of the Hib vaccine has eliminated much of the disease caused by
H.influenzae b
 Other strains still cause a variety of diseases
168
169
Other Species of Haemophilus
 H. aegypticus
 Causes conjunctivitis with pus
 H.ducreyi
 Causes a sexually transmitted disease
 Results in the formation of a genital ulcer called a chancroid
 Often asymptomatic in women but in men the chancroid is often
painful
 H.aphrophilus causes a rare type of endocarditis
 Other species primarily cause opportunistic infections
170
Gram Negative Bacteria
Not Enterobacteriaceae
Enterobacteriaceae








E. coli
Enterobacter aerogenes
Klebsiella pneumoniae
Proteus vulgaris
Serratia marcescens
Campylobacter jejuni
Salmonella typhi
Shigella dysenteriae
 Yersinia enterocolitica and pestis
171
NOTE: All of the organisms on
this slide are rods except
Neisseria, which are cocci
(diplococci).













Neisseria gonorrhea and meningitis
Vibrio cholerae
Helicobacteri pylori
Haemophilus influenzae
Bordetella pertussis
Francisella tularensis
Brucella
Pseudomonas aeruginosa
Rickettsia spp
Chlamydia spp
Legionella
Bartonella spp
Pasturella multocida
Bordetella
 Small, aerobic, nonmotile coccobacillus (partly round and
partly rod-shaped)
 B. pertussis is the most important
 Causes pertussis, also called whopping cough
 Most cases of disease are in children
 Produce various adhesins and toxins, including pertussis
toxin, that mediate (causes) the disease
 Bacteria are first inhaled in aerosols and multiply in epithelial
cells
 Then progress through three stages of disease
172
Stages
 Catarrhal (coughing)
 Paroxymal (comes and goes)
 Convalescence
173
Bordetella
 Clinical significance
 B. pertussis – causes whooping cough
 Acquired by inhalation of droplets containing
the organism
 The organism attaches to the ciliated cells of
the respiratory tract.
 During an incubation period of 1-2 weeks,
the organism multiplies and starts to
liberate its toxins.
174
Catarrhal Stage (Coughing)
 Pertussis toxin
 Has one A subunit
(toxic part), plus five
different kinds of B
subunits (involved in
binding).
175
Catarrhal
 The pertussis toxin (cytotoxic) inhibits host cell
phagocytic cell responses and the inhibition of
natural killer cell activity.
 The toxin also causes strong vasoconstriction
effects.
176
Catarrhal
 Tracheal cytotoxin – is related to the B.
pertussis peptidoglycan.
 might contribute to the killing and
sloughing off of ciliated cells in the
respiratory tract.
 Lipooligosaccharide (LOS) has potent
endotoxin activity.
177
Paroxymal Stage (comes and goes)
Lasts 4-6 weeks.
The patient has rapid, consecutive coughs with a rapid intake of
air between the coughs (has a whooping sound).
mucous has accumulated, and the patient is trying to cough up the
mucous accumulations.
The coughs are strong enough to break ribs!
Other symptoms due to the activity of the released toxins
include:
oIncreased peripheral lymphocytes
oMetabolic alteration such as increased insulin release and the
resulting hypoglycemia
oIncreased capillary permeability and increased susceptibility to
histamine, serotonin, and endotoxin shock
178
Convalescence Stage
 Symptoms gradually subside.
 This can last for months.
 B. pertussis rarely spreads to other sites, but a lot of
damage may occur, such as CNS dysfunction which
occurs in ~10 % of the cases and is due to an
unknown cause.
 Secondary infections such as pneumonia and otitis
media are common.
179
Bordetella
 B. parapertussis – causes a mild form of whooping cough
 B. bronchoseptica
 Widespread in animals where it causes kennel cough.
 Occasionally causes respiratory or wound infections in
humans.
 Current treatment
 Erythromyin – only effective in early stages of the disease
before the toxin(s) have been released
 Vaccination P part of DPT (killed, encapsulated organism);
a subunit vaccine has also been developed (purified
pertussis toxin).
180
Diagnosis, Treatment, and Prevention
 Diagnosis
 Symptoms of pertussis are usually diagnostic
 Treatment
 Primarily supportive
 Antibacterial drugs have little effect on the course of the
disease
 Prevention
 Immunization with the DPT vaccine
 Cases in the United States have increased due to a refusal
by some parents to have their children immunized
181
DPT Vaccine
 The vaccine components include diphtheria and tetanus
toxoids, and killed whole cells of the organism that causes
pertussis.
 The usual course of childhood immunization is five doses
between 2 months and 15 years.
 While vaccinations helped eradicate pertussis from the
United States in the latter half of the 20th century, in recent
years the disease resurfaced and resulted in fatalities.
 Many parents decline to vaccinate their children against the
disease for fear of side effects.
182
Vaccine refusal contributes to
whooping cough outbreaks
 The 2010 whooping cough outbreak in California may have
been fueled by clusters of parents who refused to vaccinate
their children, a new study suggests.
 Researchers found increased rates of whooping cough in
children entering kindergarten with "non-medical" vaccine
exemptions, meaning parents or guardians applied for an
exemption from school policies requiring vaccines due to
personal beliefs, rather than for medical reasons.
 In 2010, the year the state experienced a whooping cough
outbreak that caused 9,120 cases and 10 deaths from the
disease.
183
whooping cough
 San Diego County had a particularly high degree of pertussis
cases. There were 980 pertussis cases in the county, and the
area in and around Escondido, a city in San Diego County,
had more than 5,100 exemptions.
 Although the overall rate of vaccination in California
remained high (90 percent of kindergartners in 2010 were
fully vaccinated), some regions had lower immunization
rates.
 In 2010, some schools reported non-medical exemption rates
as high as 84 percent.
184
NEXT TUESDAY
 We will start in the lab room and finish this lecture after
dinner.
 Run a PCR and gel electrophoresis on your soil sample.
 Use your unknown organism to inoculate the following
tubes and place them in the incubator to examine on the
following Thursday. Just flame your loop once and do all of
the inoculations with your unknown organism. There are 3
tubes total for each lab group.
Glucose fermentation tube
Lactose fermentation tube
Sucrose fermentation tube
Gram Negative Bacteria
Not Enterobacteriaceae
Enterobacteriaceae









186
E. coli
Enterobacter aerogenes
Klebsiella pneumoniae
Proteus vulgaris
Serratia marcescens
Campylobacter jejuni
Salmonella typhi
Shigella dysenteriae
Yersinia enterocolitica and pestis










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

Neisseria gonorrhea and meningitis
Vibrio cholerae
Helicobacteri pylori
Haemophilus influenzae
Bordetella pertussis
Francisella tularensis
Brucella
Pseudomonas aeruginosa
Rickettsia spp
Chlamydia spp
Legionella
Bartonella spp
Pasturella multocida
Francisella tularensis
 Morphology and cultural characteristics
 Small, pleomorphic (various shapes) rods
 Non-motile
 Non-encapsulated
 Won’t grow on ordinary media – requires
cysteine (an amino acid) for growth
187
Tularemia (“Rabbit Fever”)
 Found in rabbits and is transmitted to humans by
hard ticks and deer flies.
 The disease is named after
Tulare County, California,
where it was first
identified.
From May to October 2000, an
outbreak of tularemia in Martha's
Vineyard resulted in one fatality.
This is the only place in the world
of a documented case of tularemia
resulting from lawn mowing.
188
Francisella tulerensis
 Found living in water as an intracellular parasite of animals
 Causes the zoonotic disease tuleremia
 Spread to humans occurs mainly through the bite of an
infected Dermacentor tick or by contact with an infected
animal
 The bacteria can spread through unbroken skin and mucous
membranes, making it highly infectious
 Tuleremia produces symptoms common to other bacterial
and viral diseases and may be misdiagnosed
189
Francisella tularensis: Disease = Tularemia
 Tularemia has three possible forms:
 Cutaneous (ulceroglandular form)
 Ingestion (typhoidal form)
 Inhalation (pneumonic form)
190
Francisella
 Cutaneous: entry through skin abrasions (ulceroglandular
form of the disease) - after ~ 48 hours a lesion occurs at
the inoculated site.
 Symptoms
 Ulcer
 Headaches
 Pain, Fever
 Adjacent lymph nodes become enlarged.
 If not contained, this can progress to septicemia,
pneumonia, and abscesses throughout the body.
 The organism survives for long periods of time inside
phagocytic cells.
191
Francisella
 Ingestion (typhoidal form of the disease)
 the focus of infection is the mouth, throat, and GI
tract.
 Inhalation (pneumonic form of the disease)
 This is the most severe form of the disease and it
manifests as a pneumonia with a high mortality rate
of 30% in untreated cases.
 Antimicrobial susceptibility
 Streptomycin or tetracycline
 An attenuated, live vaccine that protects against the
inhalation form of the disease is available for those
exposed to the organism.
192
Prevention
 A vaccine is available to at risk individuals
 Preventing infection is done by avoiding the
major reservoirs of the bacteria.
193
Gram positive exotoxins (no endotoxins)
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194
Staphylococcus aureus Cytotoxins (TSS, NF, exfolatin), Neurotoxin, Enterotoxin
Clostridium difficile Cytotoxin, Enterotoxin
Clostridium perfringens Cytotoxin, Enterotoxin
Clostridium botulinum Neurotoxin (botulism toxin)
Clostridium tetani Neurotoxin (Tetanus toxin)
Bacillus cereus Enterotoxin
Bacillus anthracis Cytotoxin (Anthrax toxin)
Corynebacterium diphtheriae Cytotoxin (Diphtheria toxin)
These all have endotoxins, but what
EXOTOXINS do they produce?

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
E. coli (EHEC) Verotoxin, AB toxin
E. coli (ETEC) Enterotoxin, heat labile and heat stable toxins
Klebsiella pneumoniae Enterotoxin
Campylobacter jejuni Enterotoxin
Salmonella typhi Enterotoxin
Shigella dysenteriae Shigatoxin
 Vibrio cholerae Cholera toxin
 Bordatella pertussis Pertussis toxin
195
What Diseases Do These Cause?
Enterobacteriaceae
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E. coli Diarrhea, septicemia, UTI
Enterobacter aerogenes Diarrhea, pneumonia, septicemia
Klebsiella pneumoniae Pneumonia, septicemia
Proteus vulgaris UTI, diarrhea, nosocomial wound infections
Serratia marcescens UTI, wound infections (catheters), pink grout
Campylobacter jejuni Diarrhea from poultry, sick puppies; septicemia
Salmonella typhi Diarrhea and typhoid fever; feces on food, raw
chicken, reptiles
 Shigella dysenteriae Bloody diarrhea from human feces
 Yersinia enterocolitica Diarrhea; lymph node inflammation
 Yersinia pestis Bubonic (black) plaque
196
What Diseases Do These Cause?

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197
Neisseria gonorrhea Gonorrhea
Neisseria meningitis Meningitis
Vibrio cholerae Cholera
Helicobacteri pylori Stomach and duodenal ulcers
Haemophilus influenzae Meningitis (infants), conjunctivitis, STD, endocarditis
Bordetella pertussis Whooping cough, kennel cough in dogs
Francisella tularensis Rabbit Fever
Gram Negative Bacteria
Not Enterobacteriaceae
Enterobacteriaceae


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


E. coli
Enterobacter aerogenes
Klebsiella pneumoniae
Proteus vulgaris
Serratia marcescens
Campylobacter jejuni
Salmonella typhi
Shigella dysenteriae
 Yersinia enterocolitica and pestis
198
NOTE: All of the organisms on
this slide are rods except
Neisseria, which are cocci
(diplococci).

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

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

Neisseria gonorrhea and meningitis
Vibrio cholerae
Helicobacteri pylori
Haemophilus influenzae
Bordetella pertussis
Francisella tularensis
Brucella
Pseudomonas aeruginosa
Rickettsia spp
Chlamydia spp
Legionella
Bartonella spp
Pasturella multocida
Brucella
 Classification
 Are all intracellular organisms
 Small, pleomorphic (various shapes) coccobacilli
 4 species can infect humans
 B. abortus
 B. suis
 B. canis
 B. melitensis causes the most serious infections
199
Brucella
 Virulence factors
 Endotoxin (LPS)
 Clinical significance
 Has a tropism (preference) for erythritol
 Animal fetal tissues and placenta, other than those in
humans, are rich in erythritol and, therefore, the
organisms often cause abortions in these animals.
200
Brucella
 Causes Brucellosis or undulent fever in man following
ingestion of contaminated milk or cheese from goats (B.
melitensis), cows (B. abortus), pigs (B. suis), or canines (B. canis).
 Man can also acquire the organism via contact with infected
animals.
 Clinical manifestations range from subclinical, to chronic
with low grade symptoms of low fever and muscular stiffness,
to acute with fever and chills.
 The fever typically spikes each evening and this
coincides with the release of organisms from phagocytes
(hence the name undulent fever).
 The patient may also experience malaise, weakness, enlarged
lymph nodes, weight loss, and arthritis.
201
Brucella
 Antibiotic susceptibility
 Chemotherapy is difficult because of the
intracellular survival of the organism.
 Tetracycline for 21 days, sometimes combined
with streptomycin.
202
Gram Negative Bacteria
Not Enterobacteriaceae
Enterobacteriaceae

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203
E. coli
Enterobacter aerogenes
Klebsiella pneumoniae
Proteus vulgaris
Serratia marcescens
Campylobacter jejuni
Salmonella typhi
Shigella dysenteriae
Yersinia enterocolitica and pestis













Neisseria gonorrhea and meningitis
Vibrio cholerae
Helicobacteri pylori
Haemophilus influenzae
Bordetella pertussis
Francisella tularensis
Brucella
Pseudomonas aeruginosa
Rickettsia spp
Chlamydia spp
Legionella
Bartonella spp
Pasturella multocida
Pseudomonas
 Gram-negative, aerobic bacilli
 Ubiquitous in soil, decaying organic matter, and almost every moist
environment
 Problematic in hospitals because they can be found in numerous
locations
 Opportunistic pathogens
204
Pseudomonas aeruginosa
 Rarely part of the normal microbiota
 Opportunistic pathogen of immunocompromised patients
 Common in ulcers and burn wounds…turns it green
 Can colonize almost every organ and system and result in various
diseases
 Often infects the lungs of cystic fibrosis patients
 The bacteria form a biofilm that protects them from phagocytosis
 Increases the likelihood of death in these patients
205
Pseudomonas aeruginosa
 Diagnosis can be difficult as the presence of bacteria may
represent contamination of the sample
 Treatment is difficult because P. aeruginosa is resistant to many
antibacterial drugs.
 Silvadene cream on ulcers or burns is used.
206
Gram Negative Bacteria
Not Enterobacteriaceae
Enterobacteriaceae
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207
E. coli
Enterobacter aerogenes
Klebsiella pneumoniae
Proteus vulgaris
Serratia marcescens
Campylobacter jejuni
Salmonella typhi
Shigella dysenteriae
Yersinia enterocolitica and pestis













Neisseria gonorrhea and meningitis
Vibrio cholerae
Helicobacteri pylori
Haemophilus influenzae
Bordetella pertussis
Francisella tularensis
Brucella
Pseudomonas aeruginosa
Rickettsia spp
Chlamydia spp
Legionella
Bartonella spp
Pasturella multocida
Rickettsias
 Extremely small (not much bigger than a smallpox virus)
 Appear almost wall-less due to the small amount of peptidoglycan
present
 Obligate intracellular parasites
 Unusual because they have functional genes for protein synthesis,
ATP production, and reproduction
 Five genera cause disease in humans
 Rickettsii, Prowasekii, Typhi, Orienta, Ehrlichia
208
Characteristics of Rickettsias
209
Table 21.1
Rocky Mountain Spotted Fever
 Symptoms usually develop about 2 to 14 days after the tick

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210
bite. They may include:
Chills & Fever
Severe headache
Muscle pain
Mental confusion & Hallucinations
Rash
Abnormal sensitivity to light
Diarrhea
Excessive thirst
Loss of appetite
Nausea &Vomiting
Spread by ticks
Typhus vs. Typhoid Fever
 Typhus is any of several similar diseases caused by Rickettsia
bacteria. The name comes from the Greek “typhos” meaning
smoky or hazy, describing the state of mind of those affected
with typhus. The causative organism, Rickettsia is an obligate
parasite bacterium that cannot survive for long outside living
cells. Typhus should not be confused with typhoid fever.
While "typhoid" means "typhus-like", the diseases are
distinct and are caused by different species of bacteria.
Condition
211
Bacteria
Vetor
Epidemic typhus
Rickettsia prowazekii
Lice on humans
Endemic typhus (murine
typhus)
Rickettsia typhi
Fleas on rats
Endemic Typhus
 Chills
 Cough
 Delirium
 High fever (104 degrees Fahrenheit)
 Joint pain (arthralgia)
 Light may hurt the eyes
 Low blood pressure
 Rash that begins on the chest and spreads to the rest of the body
(except the palms of the hands and soles of the feet)
 Severe headache
 Severe muscle pain Stupor
 Spread by fleas
212
Epidemic Typhus
 Abdominal pain
Spread by lice
 Backache
 Dull red rash that begins on the middle of the body and spreads
 Extremely high fever (105 - 106 degrees Fahrenheit), which may

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213
last up to 2 weeks
Hacking, dry cough
Headache
Joint pain (arthralgia)
Nausea
Vomiting
Gram Negative Bacteria
Enterobacteriaceae
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214
E. coli
Enterobacter aerogenes
Klebsiella pneumoniae
Proteus vulgaris
Serratia marcescens
Campylobacter jejuni
Salmonella typhi
Shigella dysenteriae
Yersinia enterocolitica and pestis
Not Enterobacteriaceae

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
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




Neisseria gonorrhea and meningitis
Vibrio cholerae
Helicobacteri pylori
Haemophilus influenzae
Bordetella pertussis
Francisella tularensis
Brucella
Pseudomonas aeruginosa
Rickettsia spp
Chlamydia spp
Legionella
Bartonella spp
Pasturella multocida
Chlamydias
 Do not have cell walls
 Have two membranes but without any peptidoglycan between them
 Grow and multiply only within the vesicles of host cells
 Have a unique developmental cycle involving two forms
 Both forms can occur within the phagosome of a host cell
215
Chlamydia trachomatis
 Has a limited host range
 One strain infects mice, all others infect humans
 Infect the conjunctiva, lungs, urinary tract, or genital tract
 Enters the body through abrasions and lacerations
 Clinical manifestations result from the destruction of infected cells
at the infection site, and from the resulting inflammatory response
216
Chlamydia trachomatis
 Causes two main types of disease
 Sexually transmitted diseases
 Causes the most common sexually transmitted disease in the United States
 Symptomatic in women but not men
 Women can develop pelvic inflammatory disease if reinfected with C. trachomatis
 Ocular disease called trachoma
 Occur particularly in children
 Endemic in crowded, poor communities with poor hygiene, inadequate sanitation,
and inferior medical care
 In the USA, All newborns receive silver nitrate drops in the eyes at birth to prevent
this disease, which causes blindness.
217
Chlamydia—Rates by Sex, United States, 1990–2009
Rate (per 100,000 population)
600
Men
Women
Total
500
400
300
200
100
0
1990
1992
1994
1996
1998
2000
2002
2004
Year
NOTE: As of January 2000, all 50 states and the District of Columbia had regulations that required chlamydia cases to be
reported.
2006
2008
Trachoma
 Disease of the eye
 Leading cause of nontraumatic blindness in humans
 Bacteria multiply in the conjunctival cells resulting in scarring
 The scarring causes the eyelashes to turn inwards and abrade the
eye that can eventually result in blindness
 Typically a disease of children who have been infected during birth
 Infection of the eye with bacteria from the genitalia can also result
in disease
219
Diagnosis, Treatment, and Prevention
 Diagnosis
 Demonstration of the bacteria inside cells from the
site of infection
 Treatment
 Antibiotics can be administered for genital and ocular
infections
 Surgical correction of eyelid deformities from
Trachoma may prevent blindness
220
Diagnosis, Treatment, and Prevention
 Prevention
 Abstinence and safe sex can prevent sexually
transmitted chlamydial infection
 Blindness can only be prevented by prompt
treatment with antibacterial agents and preventing
reinfections
221
Gram Negative Bacteria
Not Enterobacteriaceae
Enterobacteriaceae

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222
E. coli
Enterobacter aerogenes
Klebsiella pneumoniae
Proteus vulgaris
Serratia marcescens
Campylobacter jejuni
Salmonella typhi
Shigella dysenteriae
Yersinia enterocolitica and pestis













Neisseria gonorrhea and meningitis
Vibrio cholerae
Helicobacteri pylori
Haemophilus influenzae
Bordetella pertussis
Francisella tularensis
Brucella
Pseudomonas aeruginosa
Rickettsia spp
Chlamydia spp
Legionella
Bartonella spp
Pasturella multocida
Legionella pneumophila
 Aerobic, slender, pleomorphic bacteria
 Universal inhabitants of water
 Humans acquire the disease by inhaling the bacteria
in aerosols from various water sources
 Intracellular parasites
223
Legionella pneumophila
 Causes Legionnaires’ disease
 Results in pneumonia
 Immunocompromised individuals are more
susceptible
 Elimination of the bacteria is not feasible but reducing
their number is a successful control measure
 What you should know about this disease:
 http://fxn.ws/Ou9EGv
224
Bartonella
 Gram-negative aerobic bacilli
 Found in animals but only cause disease in humans
 3 species are pathogenic
 Bartonella bacilliformis
 Bartonella quintana
 Bartonella henselae
225
Bartonella bacilliformis
Bartonellosis -Carrión’s Disease
Transmitted by blooding-sucking sand flies
Acute phase: (Carrion's disease)
fever
pallor, malaise,
nonpainful hepatomegaly,
jaundice,
lymphadenopathy,
splenomegaly.
This phase is characterized by severe
hemolytic anemia and transient
immunosuppression.
• The case fatality ratios of untreated patients
exceeded 40% but reach around 90% when
opportunistic infection with Salmonella
occurs.
•
•
•
•
•
•
•
•
226
Sand Fly
 This looks like a
mosquito, except its
body is hairy and the
wings are feathery.
 Remember, Leishmaniasis (a
protozoan) is another disease
transmitted by this insect.
227
Bartonella quintana
 Trench fever
 Spread person to person by human body lice
 Also causes disease in immunocompromised patients
 The disease is classically a five-day fever of the relapsing
type
228
Bartonella henselae
 Cat scratch fever
 Introduced into humans through cat scratches or bites
229
Pasteurella multocida
 Normal flora in cats that can infect others if
bitten.
 Causes avian cholera (deadly) in birds
 In humans, causes septicemia, endocarditis,
menigitis
230
Family Sues Petco After Son's
Death from Rat-Bite Fever
 A San Diego family is suing Petco following the death of their
10-year-old son from a bacterial infection that they say he
contracted from his pet rat. Aidan became sick two weeks
after the family bought the rat, and died the next day, hours
after being rushed to the hospital with severe stomach pains.
The San Diego County Medical Examiner's Office ruled the
cause of death was streptobacillus moniliformis infection,
commonly known as rat-bite fever, after exposure to an
infected rat. A breeder would have to test eight rats to be 95
percent certain a colony of 100 rats or more did not have the
disease. The test costs $40 per rat, and a rat costs between
$6 and $11 at Petco.
231
What Diseases Do These Cause?
Enterobacteriaceae







E. coli Diarrhea, septicemia, UTI
Enterobacter aerogenes Diarrhea, pneumonia, septicemia
Klebsiella pneumoniae Pneumonia, septicemia
Proteus vulgaris UTI, diarrhea, nosocomial wound infections
Serratia marcescens UTI, wound infections (catheters), pink grout
Campylobacter jejuni Diarrhea from poultry, sick puppies; septicemia
Salmonella typhi Diarrhea and typhoid fever; feces on food, raw
chicken, reptiles
 Shigella dysenteriae Bloody diarrhea from human feces
 Yersinia enterocolitica Diarrhea; lymph node inflammation
 Yersinia pestis Bubonic (black) plaque
232
What Diseases Do These Cause?


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
233
Neisseria gonorrhea Gonorrhea
Neisseria meningitis Meningitis
Vibrio cholerae Cholera
Helicobacteri pylori Stomach and duodenal ulcers
Haemophilus influenzae Meningitis (infants), conjunctivitis, STD, endocarditis
Bordetella pertussis Whooping cough, kennel cough in dogs
Francisella tularensis Rabbit Fever
What Diseases Do These Cause?







234
Brucella Undulant fever, abortions
Pseudomonas aeruginosa Infects ulcers and burns, cellulitis, otitis
Rickettsia spp Rocky Mt spotted fever, endemic and epidemic typhus
Chlamydia spp STD and trachoma
Legionella Legionnaires’ disease (pneumonia)
Bartonella spp Carrion's disease, Trench Fever, Cat Scratch Fever
Pasturella multocida Bird Cholera
Spirochetes
Treponema pallidum
Borelia burgdorferi and other spp.
235
Spirochetes
 Spirochetes are Gram negative, but they are too small to be
seen with a light microscope after a Gram stain.
 They are best seen with a dark field microscope, in which
Gram stain does not show up.
 Unlike other Gram negative bacteria, they do not have
endotoxin in their cell walls.
Spirochetes seen
with dark field
microscopy
236
Spirochetes
 Thin, tightly coiled, helically shaped bacteria
 Moves in a corkscrew fashion through its environment
 This movement is thought to enable pathogenic spirochetes to burrow
through their hosts’ tissues
 3 genera cause human disease
 Treponema, Borrelia, and Leptospira
237
Treponema pallidum
Cannot survive in the environment
Lives naturally only in humans as an obligate parasite
Causative agent of syphilis
Syphilis occurs worldwide
Transmission is almost solely via sexual contact
Endemic among sex workers, men who have sex with men,
and users of illegal drugs
 Can also be spread from an infected mother to her fetus
 Often results in the death of the fetus or in mental
retardation and malformation


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
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
238
Treponema pallidum
• Syphilis can proceed through three stages
– Primary-symptoms associated with the
initial infection: painless chancer (ulcer)
– Secondary-related to spread of the
organisms away from the site of the original
infection (spotted rash)
– Tertiary syphilis - invades brain and also
causes gummas (large invasive ulcers)
239
Primary Syphilis
• Symptoms include:
– Chancre that should
•
240
heal by itself in 3-6
weeks
• painless
– genitals
– Mouth
– Skin
– rectum
Enlarged lymph nodes
near the chancre
Secondary Syphilis
 Spotted rash all over
 Fever
 general ill feeling
 loss of appetite
 muscle aches
 joint pain
 enlarged lymph nodes
 hair loss may occur.
241
Tertiary Syphilis
 Cardiovascular syphilis
causes aneurysms or valve
disease
 Central nervous system
disorders (neurosyphilis)
 Infiltrative tumors of skin,
bones, or liver (gumma)
242
Diagnosis, Treatment, and Prevention
 Diagnosis
 Primary, secondary, and congenital can be readily
diagnosed with antibody tests against bacterial antigens
 Tertiary syphilis is difficult to diagnose
 Treatment
 Penicillin is the drug of choice except with tertiary
syphilis which is a hyperimmune response and not an
active infection
 Prevention
 Abstinence and safe sex are the primary ways to avoid
contracting syphilis
243
Borrelia
• Lightly staining, Gram-negative spirochetes
• Cause two diseases in humans
– Lyme disease
– Relapsing fever
244
3D Image of Lyme Disease
Spirochete
Lyme Disease
 Borrelia burgdorferi is the causative agent
 Bacteria are transmitted to humans via a tick bite
 Hard ticks of the genus Ixodes are the vectors of Lyme disease
246
247
Transmission
 Transmitted by the Ixodes




Tick
Tick saliva carries the
spirochete during blood
feedings
Usually goes unnoticed
because tick is in nymphal
stage and is very small
Roughly only 1% of tick bites
results in Lyme Disease
(CDC 2012)
Spirochete is
problematic
Lyme Disease Pathology
 Shows a broad range of signs and symptoms
 3 phases of disease in untreated patients
 In most cases an expanding red “bull’s eye” rash occurs at the site
of infection
 Neurological symptoms and cardiac dysfunction
 Severe arthritis that can last for years
 Pathology of this stage is largely a result of the body’s immune response
249
3 Stages of Lyme Disease
 There are 3 stages of Lyme disease
 Stage 1 is called early localized Lyme disease. The
infection is not yet widespread throughout the
body
 Stage 2 is called early disseminated Lyme disease.
The bacteria have begun to spread throughout the
body
 Stage 3 is called late disseminated Lyme disease.
The bacteria have spread throughout the body
Risk Factors
 Doing outside activities that increase tick
exposure (for example, gardening, hunting,
or hiking) in an area where Lyme disease is
known to occur
 Having a pet that may carry ticks home
 Walking in high grasses
Important Facts
 In most cases, a tick must be attached to your body for
24 - 36 hours to spread the bacteria to your blood.
 Blacklegged ticks can be so small that they are almost
impossible to see. Many people with Lyme disease
never even saw a tick on their body.
 Most people who are bitten by a tick do not get Lyme
disease.
 To remove a tick, cover its body and legs with Vaseline
so it cannot breathe. Wait for it to back out on its own.
Bull’s Eye Rash
Erythema Chronicum Migrans
Symptoms
 Stage 1
 Body-wide itching
 Bull’s-eye rash (erythema chronicum migrans)
 Thought to occur in 80% of infections
 Fever
 General ill-feeling
 Headache
 Light-headedness
 Myalgia
 Stiff neck
Symptoms
 Stage 2 (early disseminated Lyme Disease)
 Paralysis or weakness in the muscles of the face
 Muscle pain and pain or swelling in the knees
and other large joints
 Heart problems, such as palpitations and
arrhythmias
Symptoms
 Stage 3 (Late disseminated Lyme Disease)
 Abnormal muscle movement
 Muscle and joint pain
 Muscle weakness
 Numbness and tingling
 Speech problems
Detection
 Blood test can be performed to detect antibodies to the
bacteria that cause Lyme Disease
 Called the ELISA for Lyme Disease Test
 ELISA stands for “Enzyme-linked immunosorbant assay”
 Other tests include:
 Electrocardiogram
 Echocardiogram to look at the heart
 Spinal tap (lumbar puncture to examine spinal fluid
 MRI of the brain
Treatments
 Most common treatment is 2-4 week course of antibiotics
 Controversy surrounds treatment for Post-treatment Lyme
disease syndrome or “PTLDS”
 Persistent symptoms after 2-4 weeks treatment of antibiotics
 Long-term IV antibiotics are used despite the Infectious Disease
Society of America’s guideline strictly prohibiting such
treatment
 Many physicians view PTLDS as an accumulation of diseases
rather than long-term Lyme disease
Lyme Disease Pathology
 The increase of cases is a result of humans coming in closer
association with ticks infected with Borrelia
 Antimicrobial drugs can effectively treat the first stage of Lyme
disease
 Treatment of later stages is difficult because symptoms result from
the immune response rather than the presence of bacteria
 Prevention is best achieved by taking precautions to avoid ticks
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Prevention
 Avoid wooded or bushy
areas, or areas with
high grasses and leaf
litter.
 Walk in the center of
trails.
 Check yourself and
your pets frequently
during and after your
walk or hike.
Erythema Migrans
Erythema Migrans
Erythema Migrans
The first stage of
Lyme disease is
a target shaped
rash like this,
which appears
3-30 days after
the bite.
Erythema Migrans
When to get treatment for tick bite
 Just because you get a tick bite does not mean the tick was
carrying a disease. The only tick that carries Lyme disease is a
deer tick. They are tiny and have a red abdomen (the tick on
the penny). The engorged tick is on the far right picture. If it
was not engorged when you removed it, it will not have
transmitted the disease.
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 Only ticks that are attached and have finished feeding or are
near the end of their meal can transmit Lyme disease. After
arriving on the skin, the tick that spreads Lyme disease
usually takes 24 hours before feeding begins. Even if a tick is
attached, it must have taken a blood meal to transmit Lyme
disease. At least 36 to 48 hours of feeding is required for a
tick to have fed and then transmit the bacterium that causes
Lyme disease. After this amount of time, the tick will be
engorged (full of blood). An engorged tick has a globular
shape and is larger than an unengorged one.The risk of
acquiring Lyme disease from an observed tick bite, for
example, is only 1.2 to 1.4 percent, even in an area where
the disease is common.
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 The Infectious Diseases Society of America (IDSA) recommends preventive treatment
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with antibiotics only in people who meet ALL of the following criteria:
Attached tick identified as an adult or nymphal I. scapularis (deer) tick
Tick is estimated to have been attached for =36 hours (based upon how
engorged the tick appears or the amount of time since outdoor exposure)If
the person meets ALL of the above criteria, the recommended dose of doxycycline is a
single dose of 200 mg for adults and 4 mg/kg, up to a maximum dose of 200 mg, in
children = 8 years. If the person cannot take doxycycline, the IDSA does not
recommend preventive treatment with an alternate antibiotic for several reasons: there
are no data to support a short course of another antibiotic, a longer course of antibiotics
may have side effects, antibiotic treatment is highly effective if Lyme disease were to
develop, and the risk of developing a serious complication of Lyme disease after a
recognized bite is extremely low.
Antibiotic treatment can begin within 72 hours of tick removal
The local rate of tick infection with B. burgdorferi is =20 percent (known to occur in parts
of New England, parts of the mid-Atlantic states, and parts of Minnesota and Wisconsin)
The person can take doxycycline (eg, the person is not pregnant or breastfeeding or a
child <8 years of age)
Relapsing Fever
 Relapsing fever is a vector-borne disease caused by infection with certain
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bacteria in the genus Rickettsia and Borrelia, which are transmitted through the
bites of lice or soft-bodied ticks.
People get sick 1-2 weeks after they are bitten. Symptoms include fever,
headaches, and muscle or joint aches.
The symptoms continue for 10 days, then disappear.
This cycle may continue for several weeks if the person is not treated. It is easily
cured with antibiotics.
Relapsing fever caused a series of plagues in late-medieval and early-renaissance
England. At the time, they were called sweating sicknesses.
Relapsing Fever
 The diagnosis of relapsing fever can be made on blood smear
as evidenced by the presence of spirochetes.
 Other spirochete illnesses (Lyme disease, syphilis,
leptospirosis) do not show spirochetes on blood smear.
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Louse-borne Epidemic Relapsing Fever
 Along with Rickettsia prowazekii and Bartonella quintana,
Borrelia recurrentis is one of three pathogens of which the body
louse is a vector.
 Louse-borne epidemic relapsing fever is more severe than
tick-borne endemic relapsing fever.
 Louse-borne epidemic relapsing fever occurs in epidemics
amid poor living conditions, famine and war in the
developing world. It is currently prevalent in Ethiopia and
Sudan.
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Tick-borne Endemic Relapsing Fever
 Tick-borne endemic relapsing fever is found
primarily in Africa, Spain, Saudi Arabia, Asia in and
certain areas of Canada and the western United
States.
 Borrelia hermsii is the most common cause of
Endemic relapsing fever in the United States.
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Relapsing Fever
 2 types of relapsing fever
 Epidemic relapsing fever (lice)
 Endemic relapsing fever (ticks)
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Don’t confuse this with epidemic
and endemic typhus!
Epidemic Relapsing Fever
 Mortality rate is 1%
with treatment; 3070% without
treatment
 Transmitted by
lice
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Endemic Relapsing Fever
 Several Borrelia species can cause this
disease
 Transmitted to humans by soft ticks of the
genus Ornithodoros
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Relapsing Fever
 Both types of relapsing fever are
characterized by recurring episodes of fever
and septicemia separated by symptom free
intervals
 Pattern results from the body’s repeated efforts
to remove the spirochetes, which continually
change their antigenic surface components
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Relapsing Fever
 Observation of the spirochetes is the primary
method of diagnosis
 Successful treatment is with antimicrobial drugs
 Prevention involves avoidance of ticks and lice,
good personal hygiene, and use of repellent
chemicals
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What Diseases Do These Cause?
Enterobacteriaceae
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E. coli Diarrhea, septicemia, UTI
Enterobacter aerogenes Diarrhea, pneumonia, septicemia
Klebsiella pneumoniae Pneumonia, septicemia
Proteus vulgaris UTI, diarrhea, nosocomial wound infections
Serratia marcescens UTI, wound infections (catheters), pink grout
Campylobacter jejuni Diarrhea from poultry, sick puppies; septicemia
Salmonella typhi Diarrhea and typhoid fever; feces on food, raw
chicken, reptiles
 Shigella dysenteriae Bloody diarrhea from human feces
 Yersinia enterocolitica Diarrhea; lymph node inflammation
 Yersinia pestis Bubonic (black) plaque
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What Diseases Do These Cause?
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Neisseria gonorrhea Gonorrhea
Neisseria meningitis Meningitis
Vibrio cholerae Cholera
Helicobacteri pylori Stomach and duodenal ulcers
Haemophilus influenzae Meningitis (infants), conjunctivitis, STD, endocarditis
Bordetella pertussis Whooping cough, kennel cough in dogs
Francisella tularensis Rabbit Fever
What Diseases Do These Cause?
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Brucella Undulant fever, abortions
Pseudomonas aeruginosa Infects ulcers and burns, cellulitis, otitis
Rickettsia spp Rocky Mt spotted fever, endemic and epidemic typhus
Chlamydia spp STD and trachoma
Legionella Legionnaires’ disease (pneumonia)
Bartonella spp Carrion's disease, Trench Fever, Cat Scratch Fever
Pasturella multocida Bird Cholera
Review
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For the Lecture 3 Exam
 The whole test is matching. Be able to match the
following with their description:
 Virulence factors/enzymes
 The three hemolysis patterns
 Disease terms
 Toxins
 Match the disease (or characteristic symptom) to the organism
 Know which diseases have which vectors
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Virulence Factors
 Adhesins (to adhere)
• Enzymes
 Invasins (to get into cells)
 Endotoxin (LPS, LOS, and Lipid A)
 Exotoxins
 Cytotoxins (kills cells)
 Enterotoxin (GI upset)
 Neurotoxins (disrupts nerves)
 H Ag (flagella allows motility)
 K Ag (capsule)
•
•
•
•
•
•
•
•
•
β lactamase (deactivates penicillins)
Ribosylase (causes diarrhea)
Catalase (deactivates H2O2)
Coagulase (causes blood clots)
Staphylokinase (dissolves blood clots)
Streptokinase (dissolves blood clots)
IgA or IgG protease (deactivates Ab’s)
Hyaluronidase (can move thru tissues)
SOD (superoxide dismutase;
deactivates WBC lysosomes)
 Angiotrophic ability (pulls blood vessels close)
 Facultative intracellular pathogens (can survive with and without O2)
 MDR plasmids (genetic drug resistance)
 PG (prostaglandins; promotes inflammation)
Hemolysis
 Hemolysin Patterns:
  (alpha hemolysis; partially breaks down RBC
membranes. Turn blood agar green)
  (beta hemolysis; completely ruptures RBCs.
Turns blood agar clear)
  (gamma hemolysis is no RBC lysis; no color
change on blood agar)
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Disease Terms
 Furuncle (boil; infected hair follicles)
 Carbuncles (mass of boils)
 Cellulitis/ soft tissue infections.
 Scalded Skin Syndrome  exfolatin toxin from Staph aureus
 Necrotizing Faciitis: destroys muscle and fat tissue
 Toxic Shock: Bacteremia (bacteria in blood) and multisystem failure
 Enterointoxication (enterotoxin-mediated diarrhea). This is Dz, not
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infection.
Pneumonia (fluid in the lungs)
Osteomyelitis (bone infection). Requires 6-8 weeks of iv antibiotics
Renal Abscess  infarcts (seeds from renal artery, forms abscess, clots
blood beyond that site)
Endocarditis (heart valve infection) --> destruction of valve --> blood clot
forms, breaks off, travels as a septic embolism
ENDOTOXINS
(GRAM NEGATIVE ONLY)
O Antigen
Inner plasma membrane
LPS
Cell Wall
Lipid A
(endotoxin)
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LPS
(LOS is LPS with smaller or missing O antigen)
Outer plasma
membrane
Exotoxins and their classification
 Cytotoxins
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Verotoxin (Shigella-like toxin; E. coli EHEC)
AB toxin (Kills colon epithelium; E. coli EHEC)
Toxic Shock Syndrome toxin (Staph aureus)
Exfolatin (Scalded Skin Syndrome; Staph aureus)
Necrotizing Fasciitis Toxin (group A Strep)
Anthrax
Diphtheria
Pertussis and tracheal cytotoxin
 Enterotoxins
 Neurotoxins
 Botulism
 Tetanus
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Gram positive exotoxins (no endotoxins)
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Staphylococcus aureus Cytotoxins (TSS, NF, exfolatin), Neurotoxin, Enterotoxin
Clostridium difficile Cytotoxin, Enterotoxin
Clostridium perfringens Cytotoxin, Enterotoxin
Clostridium botulinum Neurotoxin (botulism toxin)
Clostridium tetani Neurotoxin (Tetanus toxin)
Bacillus cereus Enterotoxin
Bacillus anthracis Cytotoxin (Anthrax toxin)
Corynebacterium diphtheriae Cytotoxin (Diphtheria toxin)
These all have endotoxins, but what
EXOTOXINS do they produce?
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E. coli (EHEC) Verotoxin, AB toxin
E. coli (ETEC) Enterotoxin, heat labile and heat stable toxins
Klebsiella pneumoniae Enterotoxin
Campylobacter jejuni Enterotoxin
Salmonella typhi Enterotoxin
Shigella dysenteriae Shigatoxin
 Vibrio cholerae Cholera toxin
 Bordatella pertussis Pertussis toxin
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What Diseases Do These Cause?
Enterobacteriaceae
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E. coli Diarrhea, septicemia, UTI
Enterobacter aerogenes Diarrhea, pneumonia, septicemia
Klebsiella pneumoniae Pneumonia, septicemia
Proteus vulgaris UTI, diarrhea, nosocomial wound infections
Serratia marcescens UTI, wound infections (catheters), pink grout
Campylobacter jejuni Diarrhea from poultry, sick puppies; septicemia
Salmonella typhi Diarrhea and typhoid fever; feces on food, raw
chicken, reptiles
 Shigella dysenteriae Bloody diarrhea from human feces
 Yersinia enterocolitica Diarrhea; lymph node inflammation
 Yersinia pestis Bubonic (black) plaque
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What Diseases Do These Cause?
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Neisseria gonorrhea Gonorrhea
Neisseria meningitis Meningitis
Vibrio cholerae Cholera
Helicobacteri pylori Stomach and duodenal ulcers
Haemophilus influenzae Meningitis (infants), conjunctivitis, STD, endocarditis
Bordetella pertussis Whooping cough, kennel cough in dogs
Francisella tularensis Rabbit Fever
What Diseases Do These Cause?
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Brucella Undulant fever, abortions
Pseudomonas aeruginosa Infects ulcers and burns, cellulitis, otitis
Rickettsia spp Rocky Mt spotted fever, endemic and epidemic typhus
Chlamydia spp STD and trachoma
Legionella Legionnaires’ disease (pneumonia)
Bartonella spp Carrion's disease, Trench Fever, Cat Scratch Fever
Pasturella multocida Bird Cholera
What Diseases do these cause?
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Gram Positive bacteria
 Gram Positive Cocci
 Staphylococcus
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poisoning, scalded skin syndrome, impetigo, folliculitis, furuncles,
S. aureus Food
toxic shock, bacteremia, endocarditis, pneumonia, osteomyelitis, MRSA
S. haemolyticus Skin infections
S. epidermidis Wound and internal fixation devices infections
S. saprophyticus UTI
 Streptococcus
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Strep throat, Scarlet fever, Impetigo, Toxic Shock
Group A (Strep. Pyogenes) Syndrome, Necrotizing fasciitis, Rheumatic fever
Group B (Streptococcus agalactiae) neonatal sepsis and meningitis in infants
Group D (Enterococcus faecalis) Nosocomial infections
Viridins (Steptococcus pneumoniae) Pneumonia, meningitis, endocarditis,
cavities, sinus and ear infections
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What Diseases do these cause?
• Gram Positive Rods
• Bacillis cereus Food poisoning
anthrax
• Bacillis anthracis
• Clostridium perfringins Food poisoning, gas gangrene
• Clostridium difficile Diarrhea from antibiotics, pseudomembranous colitis
• Clostridium botulinum Botulism
• Clostridium tetani Tetanus
• Listeria Food poisoning
• Proprionibacterium acnes acne
• Corynebacterium diptheriae
Diphtheria
• Nocordia asteroides Pneumonia, wounds, CNS infections
• Actinomyces israelii Maxillary osteomyelitis, human bite wounds
• Acid-fast bacteria
Tuberculosis
• Mycobacterium tuburclulosis
• Mycobacterium leprae Hansen’s disease
• Non-acid-fast, non-gram staining
Walking pneumonia
• Mycoplasma pneuomoniae
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Vectors and their Diseases
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Organism
Francisella tularensis
Disease
Tularemia (“Rabbit Fever”)
Rickettsia rickettsii
Rocky Mountain Spotted Fever
Vector
Dermacentor ticks (hard tick) and deer
flies
Ticks
Rickettsia typhi
Endemic typhus
Fleas
Rickettsia prowazekii
Epidemic typhus
Lice
Bartonella bacilliformis
Carrión’s Disease
Sand flies
Borrelia burgdorferi
Lyme Disease
Ixodes ticks (hard tick)
Borrelia recurrentis
Epidemic Relapsing Fever
Lice
Borrelia hermsii
Endemic Relapsing Fever
Ornithodoros (Soft tick)
Yersinia pestis
Bubonic plague
Fleas
How do you eat an elephant?
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