Gram Negative Bacteria
1) Some procedures are performed in
vitro and some are performed in
vivo. What does that mean?
2) What characteristics do
Enterobacteriaceae have?
3) What diseases are
Enterobacteriaceae associated with?
4) Who is at high risk for acute
diarrhea?
5) What foods put a person at risk for
getting acute diarrhea?
6) What Gram negative bacteria most
commonly cause acute diarrhea?
7) What are the treatments for GI
diseases such as acute diarrhea?
8) Enteric infection symptoms
In vitro means the procedure is done in a lab, such as
injecting a sperm cell into an egg in a Petri dish to
fertilize the egg.
In vivo means the procedure is in a live organism, such
as implanting a fertilized egg into a woman.
Gram negative rods
Most are motile (peritrichous flagella)
Encapsulated
Virulence factors include LPS, O, H, and K antigens
Many have “serum resistance” (Ab’s can’t attack)
Enteric (GI) infections
Bacteremia
UTI’s
Travelers
Consumers of certain foods
Immunocompromised
Daycare participants
Institutionalized persons (nosocomial infections)
- Chicken, mayonnaise, creams, eggs
(Salmonella, Campylobacter, Shigella)
- Hamburger undercooked (EHEC –
enterohemorrhagic E. coli
- Fried rice (B. cereus)
- Seafood (Salmonella, Vibrio, Hepatitis A)
- Fermented tofu (C. botulinum)
ETEC – enterotoxigenic E. coli
Shigella
Salmonella
Campylobacter
Giardia
- Fluid/electrolyte replacement
Dehydration is the most common cause of death
from diarrhea
- Antibiotics are not used after onset of symptoms
unless systemic/severe
- Antibiotic prophylaxis when traveling to high-risk
countries
Non-inflammatory
- Nausea
- Vomiting
- Diarrhea
Inflammatory
- Dysentery (severe diarrhea containing mucus
and/or blood)
Invasive
- Typhoid Fever (enteric fever)
1
Gram Negative Bacteria
“Common” organisms associated with enteric infections
I
II
III
Mechanism:
Non-inflammatory
(enterotoxin)
Inflammatory (invasive,
cytotoxin)
Penetrating
(invasive, spread)
Location:
proximal small
bowel
colon
distal small bowel
Illness:
Diarrhea
Dysentery
Enteric fever
Stool exam:
no fecal leukocytes
blood, fecal PMNs
(polymorphonuclear
leukocytes = neutrophils)
fecal mononuclear
leukocytes
(monocytes,
lymphocytes)
Example
organisms:
E. coli
Salmonella
V. cholerae
Campylobacter
Giardia
Cryptosporidium
Rotavirus
Shigella
Invasive E. coli
S. enteritidis
C. difficile
E. histolytica
B. coli
Salmonella typhi
Yersinia
enterocolitica
9) What is the mode of transmission
(MOT) of most enteric bacteria?
fecal-oral contamination
10) What are 3 factors the host might
have that increase risk of infection
by enteric bacteria?
11) Pathogenicity of enteric bacterial
toxins:
12) Example of a Gram positive
organism that makes toxins
13) Example of neurotoxin
Low gastric acidity
low numbers of normal enteric microflora
immunocompromised
usually ingested as preformed toxins
14) Enteric Toxins
having a direct effect on intestinal mucosa (elicit fluid
secretions)
15) What are 2 examples of
Enterotoxins?
16) What are attributes of Cytotoxins
Cholera toxin (Vibrio. cholerae)
E. coli toxins
mucosal destruction (often see dysentery)
Shigella dysenteriae
Staphylococcal toxins (Staph. aureus)
Botulinum toxin (Clostridium. botulinum)
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Gram Negative Bacteria
17) What are examples of Cytotoxins?
18) What are attributes of
Enterobacteriaceae?
19) Enterobacteriaceae are members of
family commonly associated with
human disease:
20) Enterobacteriaceae pathogens are
associated with what opportunistic
infections?
Clostridium perfringens
S. aureus
Clostridium difficile
Ubiquious (they are everywhere) - soil, water,
vegetation, normal intestinal flora
Gram negative, facultative anaerobic rods
oxidase negative - no cytochrome oxidase
Escherichia
Salmonella
Shigella
Yersinia
Klebsiella
Serratia
Proteus
septicemia
pneumonia
meningitis
urinary tract infections (UTI)
can also be primary pathogens (unrelated to immune
status)
21) Are E. coli and the serotypes Lactose Lactose positive
positive or Lactose negative?
note: many intestinal pathogens are lactose negative
ex. Salmonella, Shigella, Yersinia
22) How are E. coli and the serotypes
grouped based on surface antigens (serotypes)
grouped?
O antigen (lipopolysaccharide)
H antigen (flagellar)
K antigen (capsular)
O157:H7 (EHEC – enterohemorrhagic E. coli)
O148:H28 (ETEC – enterotoxigenic E. coli)
23) Describe E. coli serotype
immunologic assay
differentiation
growth on MacConkey agar with sorbitol (called SMac media)
most E. coli can ferment sorbitol (form pink colonies)
E. coli O157:H7 does not ferment sorbitol (colonies
are clear/colorless)
24) Describe 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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Gram Negative Bacteria
25) Pathogenic strains produce virulence
factors found on:
26) Virulence factors include:
27) Pathogenic strains of E. coli include:
28) What happens when there is
destruction of the surface microvilli
(small intestines)
29) Since EPEC pathology - diarrhea is
primarily a disease of the young
(less the 6 months old), what must
be replaced?
30) What are symptoms of EPEC
pathology- diarrhea?
31) Enterotoxigenic E. coli (ETEC) is
also known as?
Plasmids (a DNA molecule that is separate from, and
can replicate independently of, the chromosomal
DNA)
Bacteriophages (viruses that infect bacteria
Fimbriae (allow bacteria to stack up on each other to
shelter themselves from immune system
secretion systems (the process of toxin release) and
toxins
EPEC (enteropathic)
ETEC (enterotoxic)
EHEC (enterohemorrhagic)
EIEC (enteroinvasive)
EAEC (enteroaggregative)
UPEC (uropathogenic)
fever
diarrhea (infantile)
malabsorption of fluids
vomiting/nausea hard to replace fluids
non-bloody stools
common in developing countries (rare in U.S.)
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
“Traveler’s diarrhea”
32) What are the types of ETEC toxins?
heat labile toxins (LT)
similar to cholera toxin (although not as severe)
lack of absorption of fluids = watery diarrhea
heat stabile toxins (ST)
no inflammation, self-limiting
33) ETEC strains are
disease is self-limiting, watery diarrhea common
symptom
exposure provides immunity
adults living in endemic areas,
often immune
children, through exposure to
the many strains, eventually
develop immunity
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Gram Negative Bacteria
34) Therapy for ETEC includes:
35) Enterohemorrhagic E. coli (EHEC)
is usually classified as:
~fluid replacement
~bismuth subsalicylate tablets (Pepto-Bismol, etc.)
~provide antibiotics to travelers in the event they get
sick while abroad
usually O157:H7
strain must have virulence/toxin genes.
36) What are VTECs?
Vero toxin (VTEC) = “shiga-like” toxin (cytotoxin)
aka Shiga toxin-producing E. coli (STEC)
37) What does an AB toxin cause?
“A” inactivates 28S rRNA = stop protein synthesis.
Death of epithelial cells
• Gram-positive cocci, arranged in pairs or
chains, that are facultative anaerobes
• Often categorized based on the Lancefield
classification
Divides the streptococci into serotype groups based
on the bacteria’s antigens
Lancefield groups A and B include the significant
streptococcal pathogens of humans
Group A (GAS) Strep pyogenes
Group B Strep agalactiae
Group D Enterococcus faecalis
Viridans Strep mutans
Hemolysis - beta
Bacitracin - sensitive
Hemolysis – beta
Bacitracin - resistant
Homlysis – Alpha
Bacitracin - resistant
Hemolysis – Alpha or gamma
Bacitracin - resistant
• S. pyogenes forms white colonies surrounded
by zone of beta-hemolysis on blood agar plates
• Only GAS species
• Pathogenic strains often form a capsule
• Normal microbiota are depleted
• Large inoculum enable the streptococci
to establish themselves before
antibodies are formed against them
• Specific immunity is impaired
• Direct contact with mucous
38) Characteristics of Streptococcus
39) Strep classification
40) Identification of S. pyogenes
41) Identification of S. agalactiae
42) Identification of S. pnumoniae
43) Identification of E. faecalis
44) Characteristics of Stre[tococcus
Pyogenes
45) Group A streptococci generally only
cause disease in the following
situations
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Gram Negative Bacteria
46) Group A streptococci Pathogenicity
47) Group A Streptococcal Dieseases
48) What is the major species of
Salmonella?
49) Which organisms cause enteric
fever?
50) How is S. enterica ssp. enterica
serotype typhimurium shorted?
51) With Salmonella subtyping, how are
serotypes determined?
52) How do most clinical labs divide
Salmonella into serogroups?
53) What causes Salmonella diseases?
54) What happens when bacteria from
Salmonella diseases get to the in the
intestinal tract?
55) How does Salmonella alter host
cells?
56) With Salmonella pathology, the
bacteria is disseminated by
macrophages to which areas?
• Structural components
Protein M, which interferes with opsonization and
lysis of the bacteria and a hyaluronic acid capsule,
which acts to camouflage the bacteria
• Enzymes
Streptokinases, deoxynucleases, and C5a peptidase
all facilitate the spread of streptococci through tissues
• Pyrogenic toxins that stimulate macrophages
and helper T cells to release cytokines
• Streptolysins lyse red blood cells, white blood
cells, and platelets
• Pharyngitis (“strep throat”)-inflammation of
the pharynx
• Scarlet fever-rash that begins on the chest and
spreads across the body
• Pyoderma-confined, pus-producing lesion that
usually occurs on the face, arms, or legs
(Impetigo)
• Streptococcal toxic shock syndromebacteremia and severe multisystem infections
S. choleraesuis
S. choleraesuis ssp. Choleraesuis, serovar typhi (often
just called S. typhi, or a better designation is
Salmonella Typhi)
It is shortened to S. typhimurium (Salomonella
Typhimurium)
1. O antigen (LPS outer sugars)
2. Surface Vi antigen (only in sub-types)
Capsule antigens (vi=virulence antigens)
3. H antigens (flagella)
Serogroups (A, B, C1, C2, D, and E) based on Oantigen antisera
Ingestion of bacteria from contaminated food/water
and affects the human intestinal tract.
Organisms get to the small intestines, where the
macrophages often ingest bacteria, however the
bacteria are protected from host responses (e.g.
complement, antibodies, etc)
changes host cell to allow for “bacteria-mediated
endocytosis (absorbing a substance from outside the
cell)”prevents lysosomal enzymes of macrophage from
degrading bacteria
The liver, spleen, lymph nodes and bone marrow.
6
Gram Negative Bacteria
57) What causes systemic symptoms?
These are due to host responses against pathogens
58) What are inflammatory cytokines?
Inflammatory cytokines are secreted by activated
macrophages. (Cytokines are chemicals that call other
WBCs to come to the area)
59) How rare is typhoid Salmonella
It is very rare in the U.S., however 21 millions
infections?
infections worldwide (~200,000 deaths)
60) Compared to typhoid Salmonella,
Non-typhoid is much more common. Humans acquire
how common is non-typhoid
infections from poultry/eggs, dairy, and contaminated
Salmonella?
work surfaces (cutting boards). In the U.S. ~40,000
reported cases (estimated 2 million)
61) What is Enteric (typhoid) fever?
It is a systemic disease caused by S. Typhi or S.
Paratyphi. It is endemic (only occurs in developing
countries. ~70% of U.S. cases are acquired from
international travel)
62) How are Typhoid Fever and Enteric Similar: Fever, nausea, rash and other systemic
Fever similar and different?
symptoms. Was originally called typhoid fever
because of the similar symptoms to typhus.
Differ: Different bacteria, different mechanism of
spreading
63) How is Enteric fever acquired and
The disease is from ingesting contaminated food, and
who are its host?
the only known host is humans.
64) Is the infectious dose low or high?
Dose is low. (~103 versus 106-108 for infections with
other species of Salmonella)
65) What are the 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
66) What is one reason why it is difficult The variable numbers of bacteria throughout the
to diagnose Typhoid Fever?
infection
67) What are 3 potential cultures
1) Stool
(specimens) that can be used to test a
2) Urine
positive diagnosis for Typhoid
3) Bone marrow
Fever?
68) What does MDR mean?
Multi-drug resistant
69) Are some strains of S. Typhi MDR?
YES
70) What causes gastroenteritis?
Salmonella
71) What are 4 symptoms of acute
gastritis?
Vomiting, abdominal pain, fever, and diarrhea
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Gram Negative Bacteria
72) What causes shigella?
Acute infectious inflammatory colitis
73) Is mortality from shigella more
common in children or adults?
74) Is shigella a pathogen of animals or
humans?
75) Is it easy to spread shigella to
others?
76) What are the clinical manifestations
of Shigella?
77) What do Shigella virulence proteins
cause?
Children
78) S. dysenteriae produces what toxin?
Humans
Yes, it is highly communicable
abdominal cramps, diarrhea, fever, bloody stools and
large numbers of WBC in stool
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)
79) What are the enteric pathogens of
Yersinia?
Y. enterocolitica, Y. pseudotuberculosis
80) Y. pestis is also known as what?
The bubonic and pneumonic plague
81) The zoonotic disease Yersinia is
primarily found in what animals?
82) The formation of bubos is found in
what disease?
83) What is the mortality rate of
untreated patients suffering from the
pneumonic plague?
84) Is Y. entrocolitica or Yersinia sp.
more common?
85) Does Y. entrocolitica cause severe
or acute enterocolitis?
86) How many different serotypes of Y.
enterocolitica are there?
87) Y. entrocolitica is associated with
what risk factors?
88) Yersinia can be diagnosed from
what type of samples?
89) What is cold enrichment?
Fleas, rodents, swine, cattle, etc
90) What are the therapies for Yersinia?
91) What are two major pathogenic
species of Neisseria?
Y. pestis
High mortality rate - 90%
Y. entrocolitica
acute enterocolitis and mysenteric lymphadenitis (can
mimic appendicitis)
Over 60 (serotypes 3,8, &9 account for most human
infections
Ingestion of contaminated food/ milk (can grow at
lower temperatures 4C), blood transfusion septicemia
Blood or stool
Growth culture at 4-7C for 28 days w/ weekly
subculture on SS agar
Plague- antibiotics and rodent control Enteric- often
self limiting
N. gonorrheae- associated with STDS
N. meningitidis- associated with respiratory and CNS
infections
8
Gram Negative Bacteria
92) In vitro growth is found in:
93) What does LPS stand for?
Obligate aerobes
Sensitive to drying ( delicate) and some products in
blood(that is why one uses Chocolate agar for culture
fastidious-picky
Out-competed by normal flora so grow in presence of
select antibiotics(Thayer-Martin agar)
Need 5% CO2
Lipopolysaccharide
94) What does LOS stand for?
Lipoligosaccharide
95) In Endotoxins, what is the LPS like?
Lipid A, core sugars, outer sugars
96) In Endotoxins, what is the LOS like? Lipid A, core sugars, present in Neisseria
97) In Neisseria gonorrhoeae, what are
the incidences of the disease?
98) How is it transmitted?
99) What are the virulence factors of
Gonococcus?
100) What are the characteristics of the
genital infection Urethritis, found in
men?
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
Efficiently transmitted by:
Male to female via semen
Female to male urethra
Rectal intercourse
Fellatio(jpharyngeal infection)
Perinatal transmission( mother to infant)
Gonorrhea associated with increased transmission of
and susceptibility to HIV infection
Pilus
Phase variation and Antigenic variation(of pilus and
opacity protein)
phase variation-differences in colony appearance
antigenic variation-varying pili antigenic type
development of a vaccine will be difficult
Endotoxin (LOS)
IgA protease-cleaves at hinge region
Serum resistance
inflammation of urethra,
typically purulent or mucopurulent urethral discharge
asymptomatic in 10% of cases
101) What are the characteristics of the inflammation of the epididymis
genital infection Epididymitis, found unilateral testicular pain and swelling
in men?
infrequent
102) Most genital infection in women
are?
 Asymptomatic
9
Gram Negative Bacteria
103) What is Cervicitis?
 Inflammation of the cervix
104) What is Urethritis?
 Inflammation of the urethra
105) What are complications in women
due to gonorrhea?
106) What are the gonorrhea
syndromes in men and women?
107) Gonorrhea infection in perinatal
children causes?
108) What are diagnostic methods for
gonorrhea?
109) Laws and regulations in all states
require that persons diagnosed with
are reported to public health
authorities by clinicians, labs, or
both.
110) What are the diseases caused by
N. meningitides?
111) What are the virulence factors of
Meningococcus?





Pelvic Inflammatory Disease (PID)
Fitz-Hugh-Curtis Syndrome
Conjunctivitis
Disseminated gonococcal infection (DGI)
Infections of the conjunctiva, pharynx, respiratory
tract
 Culture tests
 Gonorrhea
 Meningococcal meningitis
 Meningococcemia, sepsis
 Polysaccharide capsule
 Endotoxin (LOS)
 IgA protease
 Serum resistance
Does NOT display same types of phase/antigenic
variation as seen in NG
Somewhat susceptible to penicillins (although some
degree of resistance reported)
Enteric bacteria such as Escherichia and Salmonella
112) To control Meningococcus how
does the vaccine work?
113) To control Meningococcus how
do microbials work?
114) Members of the Vibrio genus
share many characteristics with what
type of bacteria?
115) Where are Vibrio found?
Water environments
116) What is the most common species
to infect humans?
117) Vibrio causes what?
Vibrio cholerae
118) How do humans become infected
with V. cholerae?
119) What type of communities does
this occur in?
120) What type of inoculum is required
to cause the disease and why?
121) What is the most important
virulence factor of V. Cholerae?
By ingesting contaminated food and water
Cholera
With poor sewage and water treatment
A large inoculum because the bacteria are susceptible
to the acidic stomach environment
Cholera toxin
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Gram Negative Bacteria
122) What are the symptoms of
Cholera?
-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
Usually based on the characteristic diarrhea
123) How does one diagnose for
Cholera?
124) What is the treatment for Cholera? - Fluid and electrolyte replacement
- Antimicrobial drugs are not as important because
they are lost in the watery stool
125) How do you prevent Cholera?
Adequate sewage and water treatment can limit the
spread of V. cholerae
126) What is the most common cause
Campylobacter jejuni
of gastroenteritis in the United States
5-7% of cases?
127) What serves as reservoirs for the
Many animals
bacteria?
128) How do humans become infected Consuming contaminated food, milk, or water
with Campylobacter jejuni?
129) What is the most common source Poultry
of infection?
130) What does the infection cause?
Produce dysenteri and frequent diarrhea that is selflimiting
131) How does the bacteria spread?
- Fecal-oral
- Person-to-person sexual contact
- Unpasteurized raw milk and poultry ingestion
- Waterborne exposure to sick pets, especially puppies
132) What would be considered an
1,000-10,000 bacteria
infectious dose of Campylobacter
jejuni?
133) What is the incubation period?
1-7 days (up to a week)
*Probably related to the dose of organisms ingested
134) A person infected with
- A brief prodrome of fever as high as 40°C
Campylobacter jejuni have what
- Headache, and myalgias lasting up to 24 hours
type of symptoms?
- 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
135) Patients with C. jejuni infection
A longer illness and require hospital admission
who report vomiting, blood diarrhea,
or both tend to have what type of
illness?
11
Gram Negative Bacteria
136) What organism causes most peptic
ulcers?
137) Does Haemophilus influenza have
a capsule?
138) What was the most common form
of meningitis in infants prior to the
use of an effective vaccine?
139) What disease is caused by
Haemophilus aegypticus?
140) What disease is caused by
Haemophilus ducreyi
141) What is Bordetella
142) What is B. Pertussis
143) What are the stages of Bordetella?
144) What is the clinical significance
of B. pertussis-causes whooping
cough?
145) Purtussis toxin in catarrahl
contains how many A subunits and
how many B subunits?
146) The increase of what in Catarrhal
from the combined effects of
pertussis toxin and bacterial
adenylate cyclase inhibits host cell
phagocytic cell responses and the
inhibition of natural killer cell
activity?
147) When is Dermonecrotic toxin in
Catarrhal released?
148) What is Trachael cytotoxin related
to?
149) What is Lipooligosaccharide?
Helicobacter pylori
Yes
Haemophilus influenzae
conjunctivitis with pus
STD with chancre, only painful in men
Small, aerobic, nonmotile coccobacillus
B. Pertussis (the most important)
Causes pertussis, also called whopping cough
Most cases of disease are in children
Produce various adhesions and toxins, including
pertussis toxin, that mediate the disease
Bacteria are first inhaled in aerosols and multiply in
epithelial cells
Then progress through three stages of disease
Catarrhal
Paroxymal
Convalescence
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.
One A subunit and Five B subunits
cAMP
is released upon cell lysis causing strong
vasoconstrictive effects
to the B. pertussis peptidogycan
-might contribute to the killing and sloughing off of
ciliated cells in the respiratory tract.
Has potent endotoxin activity
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Gram Negative Bacteria
150) Stage of Proxymal
151) Stage of Convalescence
152) What is B. parapertussis?
153) What is B. bronchoseptica?
154) What are the current treatments
for Bordetella?
155) What is the diagnosis for
Bordetella?
156) What are the treatments for
Bordetella?
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:
Increased peripheral lymphocytes
Metabolic alteration such as increased insulin release
and the resulting hypoglycemia
Increased capillary permeability and increased
susceptibility to histamine, serotonin, and endotoxin
shock
-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.
B. parapertussis – causes a mild form of whooping
cough
Widespread in animals where it causes kennel cough.
Occasionally causes respiratory or wound infections
in humans
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).
Diagnosis:
Symptoms of pertussis are usually diagnostic
Treatment:


157) What is the prevention for
Bordetella?
Prevention:


158) What is the classification of
Francisella?
Primarily supportive
Antibacterial drugs have little effect on the
course of the disease
Immunization with the DPT vaccine
Cases in the United States have increased due
to a refusal by some parents to have their
children immunized
Classification – only 1 pathogenic species – F. tularensis
13
Gram Negative Bacteria
159) What are the morphology and
characteristics of Francisella?
Morphology and cultural characteristics:





160) Where is Francisella found?
Found living in water as an intracellular parasite of animals.

161) What are the causes of
Francisella?


162) How is Francisella acquired?
163) If not contained, what can
Francisella progress to?
164) What is the antimicrobial
susceptibility of Francisella?
Spread to humans occurs mainly through the
bite of an infected Dermacentor 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
1. Entry through skin abrasions (ulceroglandular form
of the disease) - after ~ 48 hours a lesion occurs at
the inoculated site.
2. Ingestion (typhoidal form of the disease)
 the focus of infection is the mouth, throat, and GI
tract.
3. 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.
Septicemia, pneumonia, and abscesses throughout the
body.



165)

166) What type of organism is
Brucella?
167) What 4 species of Brucella can
infect humans?
Minute, pleomorphic g- rod that stains poorly
Staining may be bipolar
Nonmotile
Nonencapsulated
Won’t grow on ordinary media – requires
cysteine or cystine for growth
Streptomycin or tetracycline
An attenuated, live vaccine that protects
against the inhalation form of the disease is
available for those exposed to the organism.
A vaccine is available to at risk individuals
Preventing infection is done by avoiding the
major reservoirs of the bacteria
Intracellular




B. abortus
B. suis
B. melitensis
B. canis
14
Gram Negative Bacteria
168) What is the morphology and
characteristics of Brucella?
169) What are the 2 antigens that are
part of the LPS are recognized?
170) Which species of Brucella has the
highest concentration of M antigen,
which causes an infection?
171) What is the virulence factor of
Brucella?
172) Brucella has a tropism for what
type of sugar alcohol?
a. What does Brucella cause?
b. How do you treat Brucella?
c. Are Pseudomonads
problematic in hospitals?
d. What does Pseudomonas
aeruginosa often infect
e. Where does Treponema
pallidum pallidum live?
173) Name the four stages of Syphilis
Small g-cb that stain poorly
A and M
B. melitensis
Endotoxin
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.
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).
Tetracycline for 21 days, sometimes combined with
streptomycin.
Yes, because they can be found in numerous locations
Often infects the lungs of cystic fibrosis patients
Lives naturally only in humans as an obligate parasite
Primary
Secondary
Latent
Tertiary syphilis
Primary
174) Symptoms associated with the
initial infection
175) Related to spread of the organisms Secondary
away from the site of the original
infection
176) The symptoms in primary syphilis Chancre that should heal by itself in 3-6 weeks
are:
painless
genitals
Mouth
Skin
rectum
Enlarged lymph nodes near the chancre the chancre
15
Gram Negative Bacteria
177) The symptoms in Secondary
Syphilis
178) The symptoms of Tertiary
Syphilis
179) How is syphilis is diagnosed
180) What is the drug of choice for
treatment of syphilis?
181) Will penicillin work on tertiary
syphilis?
182) Why not?
183) How can you prevent syphilis?
184) What is Borrelia?
185) Borrelia causes two diseases in
humans
186) What are the 3 phases of lyme
disease
187) In untreated patients?
188) What is the pathology of Lyme
Disease?
189) What can treat the first stage of
Lyme Disease?
190) Why is treatment difficult of the
later stages of Lyme Disease?
191) What are the two types of
Relapsing Fever?
192) What are the Mortality Rate of
Epidemic Relapsing Fever?
Spotted rash all over
Fever
general ill feeling
loss of appetite
muscle aches
joint pain
enlarged lymph nodes
hair loss may occur.
Cardiovascular syphilis causes aneurysms or valve
disease
Central nervous system disorders (neurosyphilis)
Infiltrative tumors of skin, bones, or liver (gumma)
Primary, secondary, and congenital can be readily
diagnosed with antibody tests against bacterial
antigens
Tertiary syphilis is difficult to diagnose
penicillin
No
It is hyperimmune response and not an active infection
Abstinence and safe sex are the primary ways to avoid
contracting syphilis
Lightly staining, Gram-negative spirochetes
Lyme disease
Relapsing fever
*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
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
2 types of relapsing fever
 Epidemic relapsing fever
 Endemic relapsing fever
Mortality rate is 1% with treatment; 30-70% without
treatment
16
Gram Negative Bacteria
193) What transmits Epidemic
Relapsing Fever?
194) What can cause Endemic
Relapsing Fever?
195) How is it transmitted?
196) How are the two types of
Relapsing fever characterized?
197) What is the primary method of
diagnosis?
198) What can treat Relapsing fever?
Transmitted by lice
Several Borrelia species can cause this disease
Transmitted to humans by soft ticks of the genus
Ornithodoros
Both types of relapsing fever are characterized by
recurring episodes of fever and septicemia separated
by symptom free intervals
Observation of the spirochetes
Successful treatment is with antimicrobial drugs
199) How to prevent Relapsing fever?
Prevention involves avoidance of ticks and lice, good
personal hygiene, and use of repellent chemicals
200) Characteristics of Mycoplasma:
1. Smallest free-living microbes
2. Lack cytochromes, enzymes of the Krebs
cycle, and cell walls
3. Often have sterols in their cytoplasmic
membranes which other prokaryotes lack
4. Require various growth factors that must be
acquired from a host or supplied in laboratory
media
5. Can colonize the mucous membranes of the
respiratory and urinary tracts
201) What does Mycoplasma
Attaches specifically to receptors located at the bases
pneumonia attaches to?
of cilia on epithelial cells lining the respiratory tracts
of humans
202) What can Mycoplasma pneumonia Causes primary atypical pneumonia, or walking
cause?
pneumonia
203) Symptoms of primary atypical
Symptoms such as fever, headache, and sore throat are
pneumonia or walking pneumonia
not typical of other types of pneumonia
204) How is primary atypical
Spread by nasal secretions among people in close
pneumonia or walking pneumonia
contact
spread?
205) Why is diagnosing Mycoplasma
Mycoplasmas are small and grow slowly
pneumoniae difficult?
a. Why is prevention of
Patient can be infective for long periods of time
Mycoplasma pneumoniae
without signs or symptoms
difficult?
206) Characteristics of Rickettsias
Extremely small
Appear almost wall-less due to small amount of
peptidoglycan present
Obligate intracellular parasites-unusual as they have
function genes for protein synthesis, ATP production
and reproduction
17
Gram Negative Bacteria
Three main genera cause disease in humans-Rickettsia,
Prowasekii, and typhi. There are two more that we will
not cover: Orienta (scrub typhus) and Ehrlichia
(Erlichiosis)
207) Signs and Symptoms of Rocky
Chills & Fever
Mountain Spotted Fever usually
Severe Headache
develop 2 to 14 days after a tick bite Muscle Pain
Mental Confusion & Hallucinations
Rash
Abnormal sensitivity to light
Diarrhea
Excessive thirst
Loss of appetite
Nausea & Vomiting
208) Signs and Symptoms of Endemic Chills
Typhus spread by fleas
Cough
Delirium
High Fever (104 degrees F)
Joint Pain (arthralgia)
Light may hurt eyes
Hypotension
Rash that begins on the chest & spreads to the rest of
the body (except palms of hands and soles of feet)
Severe headache
Severe muscle pain stupor
209) Signs and Symptoms of Epidemic Abdominal Pain
Typhus spread by lice
Backache
Dull red rash that spreads from the middle of the body
Extremely high fever (105-106 degrees F), may last up
to 2 weeks
Hacking, dry cough
Headache
Joint Pain (arthralgia)
Nausea
Vomiting
210) Characteristics of Chlamydia
Do NOT have cell walls- have two membranes but
without any peptidoglycan between them
Grow & 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
211) Characteristics of Chlamydia
Has limited host range-one strain infects mice, all
trachomatis
others infect humans
Infect the conjunctiva, lungs, urinary tract, or genital
tract. Enters the body through abrasions and
lacerations. Clinical manifestations result from the
18
Gram Negative Bacteria
212) What two main types of diseases
does Chlamydia trachomatis cause?
213) Sexually Transmitted Diseases
214) Lymphogranuloma veneruem
215) What does the trachoma disease
affect?
216) What can it cause?
217) How does bacteria affect the eye?
218) What does the scarring cause?
219) Who does trachoma typically
affect?
220) What else may result in the
disease?
221) How is trachoma diagnosed?
222) How is trachoma treated?
223) How can Trachoma be prevented?
destruction of infected cells at the infection site, and
from the resulting inflammatory response.
Sexually transmitted diseases- causes the most
common sexually transmitted disease in the US
Trachoma-Ocular Disease-Occurs particularly in
children-Endemic in crowded, poor communities with
poor hygiene, inadequate sanitation and inferior
medical care.
Lymphogranuloma veneruem-Characterized by a
transient genital lesion and swollen, painfully
inflamed, inguinal lymph nodes
Occurs in three stages Initial Stage- produces a lesion at the infection
site that is a small painless, and heals rapidly
 Second Stage-buboes develop at the infection
site
 Third Stage-only some cases progress to this
stage-characterized by genital sores,
constriction of the urethra and genital
elephantiasis.
Most infections in women are symptomatic but men
may or may not have symptoms
Women can develop pelvic inflammatory disease if
reinfected with C. trachomatis
The eye
Nontraumatic blindness in humans
Bacteria multiply in the conjunctival cell resulting in
scarring
Causes the eyelashes to turn inwards and abrade the
eye eventually resulting in blindness
Children who have been infected during birth
Infection of the eye with bacteria from the genitalia.
There must be bacterial inside cells from the site of
infection
-Antibiotics can be administered for genital and ocular
infections
-Surgical correction of eyelid deformities from
Trachoma may prevent blindness
Abstinence and safe sex can prevent a chlamydial
infection
19
Gram Negative Bacteria
224) How can blindness be prevented?
225) What type of bacteria is
Legionella pneumophila?
226) Where does L. pneumophila
inhabit?
227) How do humans acquire the
disease?
228) Are L. pneumophila intracellular
parasites?
229) What does Legionnaires’ disease
result in?
230) Are immunocompromised
individuals more susceptible to the
disease?
231) Is elimination of the bacteria
feasible?
232) What type of bacteria is
Bartonella?
233) Where is it typically found?
234) Which species are pathogenic?
235) What is B. bacilliformis also
known as?
236) How is it transmitted?
237) What are the signs and symptoms
of the acute phase?
238) What else is this phase
characterized by?
239) What is the case fatality rate?
By prompt treatment with antibacterial agents and
preventing reinfections
Aerobic, slender, pleomorphic bacteria
Water
-By inhaling the bacteria in aerosols from various
water sources.
Yes
Pneumonia
Yes
No, but reducing their number is a successful control
measure
Gram negative aerobic bacilli
It is found in animals but only cause disease in humans
B. bacilliformis
B. quintana
B. henselae
Bartonellosis-Carrion’s disease
By blood sucking sand flies
240) What disease is B. quintana?
241) How is B. quintana spread?
Fever, pallor, malaise, nonpainful hepatomegaly,
jaundice, lymphadenopathy, splenomegaly
Severe hemolytic anemia and transient
immunosuppression
Of untreated patients, greater than 40%, but reach 90%
when opportunistic infection with Salmonella occurs
Trench fever
From person to person by human body lice
242) What may this disease result in?
Disease in immunocompromised patients
243) How does the disease classically
present?
244) What is caused by B. henselae?
245) How is it introduced to humans?
As a five day fever of the relapsing type
Cat scratch fever
Through cat scratches or bites
20