Includes the following: Pathogenic Bacteria Lecture
Questions: Host-Parasite Interactions Questions may
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Pathogenic Bacteria Lecture Questions
Host-Parasite Interactions
1. What stages occur during the pathogenesis of a
microbial infection? Why is it important to
understand the mechanisms involved at each stage of
infection by any specific microbe?
In order for a pathogen to establish an infection,
it must first gain access to the host through
contact and entry. It then establishes itself
(colonization). Once a colony is developing, the
infection spreads to other parts of the body. If the
organism is able to survive, it may begin to cause
damage (pathology) to the host.
To fight pathogenic organisms effectively, we must
understand each step of the development of pathology
if we want to block the orderly progression of an
infection.
2. What are the normal flora in each region of the
body? What factors modify the numbers and kinds of
microbes in the normal flora?
Site Normal Flora
Blood none
Tissue none
Skin staphylococci, propionibacterium
Mouth streptococci, neisseria, moraxella
Nasopharynx Staph aureus and those of mouth
Esophagus transient mouth flora
Stomach few (if any)
Small intestine scanty, variable
Large intestine Bifidobacterium, lactobacillus,
strep
Vagina skin / colon flora
Several factors can modify the "normal"flora of any
organ system. The amount and type of nutrients
available, pH, redox potentials, local acting anti
microbials (bile, lysozyme, etc), and competition
for nutrients among bacteria all contribute to the
selection of the "normal" flora. As the host’s
condition changes with illness, pregnancy, age, or
geographic location, the "normal" flora will change.
Some bacteria that are "normal" in one site can
cause disease in another. (ex: E. coli in urinary
tract-->infection)
3. For each model of microbial pathogenesis
discussed in lecture, what kind of virulence factors
are important?
Virulence factors inherent to bacteria (whether
found on the chromosome, plasmid or in a
bacteriophage) allow the bacteria to survive in
conditions that kill other bacteria. The expression
of these virulence factors is tightly regulated in
response to environmental stimuli. Bacteria can
mimic external signals that stimulate host cells,
secrete toxins that damage host cells, block the
release of neuromuscular signals, or inhibit host
protein synthesis.
4. For each model of microbial pathogenesis
discussed in lecture, what kind of microbial
defenses are important for the host?
The host defense against bacteria is a broad system.
Nonspecific and mechanical barriers such as the
external epithelial layer, flushing action of
secretions, and a hostile surface environment (lo
pH, enzymes, etc) are the first line of defense
against pathogens. The immune response mounted
against pathogens that penetrate the host is the
second line of defense. People who cannot mount a
well rounded immune response are at much higher risk
of developing life threatening infections.
Bacterial Toxins
1. How would you investigate whether a newly
discovered pathogenic bacterium that causes
pneumonia produces a toxin that is essential for
pathogenesis?
By using the molecular version of Koch’s postulates,
one could investigate the pathogenesis of a specific
toxin by the following sequence:
1. Clone the gene for the suspected toxin
2. Inactivate the cloned gene in vitro by genetic
engineering
3. Replace the wild type allele in the pathogenic
microbe with the inactivated allele
4. See if the loss of the suspected toxin results in
loss of pathogenesis
2. What are A-B type toxins? What are the functions
of the two domains or subunits of such toxins?
Toxins that must cross the plasma membrane of host
cells to reach an intracellular target are
identified as A-B type toxins. They are bifunctional
proteins with separate domains. The A domain is the
"active" domain and the B domain is the "binding"
domain. The toxins use normal membrane receptors as
points of entry into the cell and susceptibility is
determined by the presence or absence of the
particular receptor on a specific cell. Most toxis
bind their receptor and are then transported, by
endocytosis, into the cytoplasm where they become
active and attack their target.
3. What features are shared by ADP-ribosylating
toxins? What features are unique for each toxin?
What are some possible reasons that many toxins have
ADP-ribosylating activity?
All of the ADP-ribosylating toxins catalyze the
transfer of ADP-ribose from NAD to acceptor
proteins. the NAD binding domain is highly
cconserved among these toxins. But, they recognize
different acceptor proteins and interact with target
cells via defferent cell durface receptors. One
could postulate that the reason many toxins use this
mechanism is its effectiveness in rendering the host
defenseless and lead to the death of the host cell.
One could also postulate that the genetic
information for this toxin has been passed from
species to species over a long period of time and
that each bacteria has modified the toxin to fit its
particular needs.
4. How would you test for immunity to diptheria? To
tetanus?
One could inject a previously immunized person
(either one who has had an infection or one who has
been immunized) with a small amount of the toxoid
from the two diseases and see if an immune response
develops. By measuring the antibody titer to the
disease, one could quantitatively assess host
immunity.
Enteric Bacteria
1. What is the purpose of culturing diarrheic stools
onto media containing lactose?
This would allow one to discern the types of
bacteria growing in a patients GI tract. Salmonella,
Shigella, and Yersinia are all nonfermenters of
lactose. MacConkey agar contains bile salts,
lactose, dyes, nutrients and a pH sensitive
indicator. Bacteria that can ferment lactose will
produce acid, and cause the pH indicator to become
hot pink. Bacteria that are unable to ferment
lactose (Salmonella, Shigella, and Yersinia) will
appear as clear or colorless on the plate.
2. What is meant by endotoxin? Describe the effects
of such a molecule.
Endotoxin is the lipid A portion of LPS that causes
endotoxic shock upon release in the host
circulation. This presents as fever, intravascular
coagulation, hypotension, complement activation, and
B cell stimulation.
3. How are the enterobacteriacea serotyped? For what
purpose is this done?
The enterobacteriacea are serotyped by agglutination
with antisera to three different surface antigens
(O, H and K/Vi). The differences seen on serotyping
allow one to identify the bacterial species.
4. Compare the pathogenesis of Shigella sp. versus
Salmonella typhi. How does each pathogen interact
with macrophages? How does S. typhi disseminate thru
the body? What is the basis for the colonic ulcers
that occur during Shigella infection?
Shigella species passes thru the stomach and small
intestine, when it reaches the colon it interacts
with the M cell, an antigen presenting cell of
Peyer’s patches. It causes death of macrophages in
the lamina propria by inducing apoptosis. It is
rarely disseminated into the bloodstream. The
bacterial invasion of the colon results in acute
inflammation and necrosis. This leads to the
formation of abcesses and ulcers.
S. typhi enters M cells by endocytosis and
eventually macrophages in the submucosal layer.
These infected macrophages escape the colonic
structure and eventually seed the bloodstream.
Infections usually spread systemically and come to a
focus in the liver and spleen.
5. Compare the reservoirs, infectious dose, and risk
groups for Shigella, Salmonella typhi, Salmonella
enteriditis, and Y. enterocolotica. Where in the
world are S. flexnerii, S. sonnei, and S. typhi
isolated?
Bacteria Reservoir Infectious dose Hi risk group
Location
Shigella humans 200 institutions or crowding
worlwide
S. sonnei humans 200 children US / 1st world
S. flexnerii humans 200 institutions or crowding
American Indians / 3rd world
Sal. typhi humans 106 children / elderly 3rd world
Sal. enteriditis animals 104 picnics worldwide
Y. enterocolitica animals >109 people who eat
undercooked meat Europe / Scandinavia
6. How might one prevent transmission of S. typhi,
Shigella and S. enterocolitica? For which of these
pathogens is there a vaccine?
All of these diseases can be prevented by practicing
improved sanitation and hygiene. Basic preventive
medicine measures can prevent these illnesses (hand
washing, latrines away from food prep sites, pest
control, etc). There is a vaccine against S. typhi.
7. Which of the enterobacteriaceae can cause
mesenteric lymphadenitis?
Yersinia sp. causes mesenteric lymphadenitis.
Enterics II
1. What are the different ways that E. Coli can
cause diarrhea and enteritis? Which bacteria use
which mechanism?
E. coli can cause diarrhea via several mechanisms.
ETEC produces heat labile and heat stable toxins
that affect the small bowel, producing a watery
diarrhea without blood. EIEC causes diarrhea
identical to a Shigella infection, bloody and loaded
with neutrophils. EPEC causes the "attaching and
effacement" lesions that lead to a watery diarrhea.
EHEC causes bloody diarrhea without WBCs in the
stool.
2. What is the mechanism of heat labile toxin (LT),
stable toxin (ST), and Shiga toxin?
LT activates adenylate cyclase and cAMP in the
intestinal cell (this is identical to the action of
cholera toxin).
ST activates guanylate cyclase and cGMP in the
intestinal cell.
Shiga toxin is cytotoxic and enterotoxic. It
inhibits eukaryotic protein synthesis and has
neurotoxic effects as well.
3. Why are US travelers generally susceptible to
ETEC infection but not to EPEC infection?
EPEC infects susceptible people of all ages who are
exposed to the pathogen. EPEC only infects small
children, possibly due to selection of specific host
characteristics by the pathogen that are present in
infants, but not present in adults.
4. What is the natural habitat of Vibrio and
Campylobacter species? What are some common sources
of infection with these pathogens?
Vibrio is abundant in marine and surface waters.
Drinking water that is infested with the pathogen or
eating aquatic life from infested waters causes
disease in humans.
Campylobacter is a normal GI commensal of many
animals. Consumption of water that is infested with
the pathogen or eating animals contaminated with the
pathogen causes disease in humans.
5. Describe the spectrum of disease caused by Vibrio
Cholerae. Name two virulence factors utilized by
this pathogen and describe the physiological basis
behind the intestinal secretion caused by this
organism.
Cholera can range from an asymptomatic "carrier"
state to full blown "cholera gravis" that is life
threatening due to the massive loss of fluid. The
bacteria use a specific pillus (Tcp) to attach to
the brush border of epithelial cells. The bacteria
then produce the cholera toxin that activates
adenylate cyclase and increases the intracellular
cAMP level. This leads to increased secretion of Cl-,
K+ and HCO3- from cells and decreased NaCl coupled
absorption. The outward flow of ions from the
intestinal cells leads to an osmotic loss of water.
6. Where is cholera endemic? Who is at risk? What
vaccines are available?
Cholera is endemic to Indian, southern Asia, Africa,
Indonesia, South / Central America and the southern
U.S. coastline. Children in endemic areas are at
greatest risk of developing the disease. There is a
parenteral whole cell killed vaccine available that
has some drawbacks.
7. What is the first and formost important form of
treatment for a cholera patient?
Oral or IV fluid and electrolyte replacement is the
most important treatment of cholera.
8. Describe the type of stools that can result from
infection with Campylobacter jejuni. What are the
special conditions needed to culture this organism?
Stools from an infected person resemble those of a
person with Shigella. They can be bloody and contain
neutrophils. This organism must be cultured in CO2
and ¯ O2.
Enteric Bacteria III
1. Describe the pathogenesis of H. Pylori, including
the host response to infection. What are some of the
major virulence factors used by this pathogen?
H. pylori is ingested and passes into the stomach.
It penetrates the gastric mucosa and colonizes the
stomach’s epithelium. Damage to the epithelium leads
to superficial inflammation and is followed by deep
inflammation. The bacteria excrete urease that
allows the bacteria to survive in the low pH of the
stomach. The bacterial flagella may assist in the
penetration of the mucosa and a vacuolating
cytotoxin may assist in damaging cells.
2. Compare the epidemiology of H. Pylori infection
among people of the 1st and 3rd worlds. How is the
infection transmitted?
H. Pylori is found in the feces, oral cavity and
dental plaques of infected individuals. The disease
is transmitted by ingestion of the pathogen.
3. What clinical tests can one use to diagnose H.
Pylori infection?
Detection of urease in gastric biopsies can aid in
the diagnosis. Patients can be given radiolabeled
urea and the detection of radiolabeled CO2 on
exhalation can also assist in diagnosis.
4. Who is most susceptible to uncomplicated UTI? To
complicated UTI?
Uncomplicated UTIs occur in otherwise healthy
people. They are usually (80%) caused by E. coli.
Complicated UTIs are found in people who have
urinary catheters, are immunosuppressed, or have an
anatomical or functional defect that interferes with
the normal voiding of urine.
5. What role does the urease produced by P.
Mirabilis play in urinary tract disease? How might
lateral flagella enable P. mirabilis to establish
pyelonephritis?
The urease produced by P. Mirabilis can lead to the
formation of kidney stones and subsequent blockage
of the urinary tract. The lateral flagella allow the
organism to swim upstream in the urinary tract and
hold on oncce they reach their site of colonization.
6. How are UTI diagnosed in the lab? What is the
importance of a "clean catch" specimen?
Urine specimens are collected after the stream of
urine has begun, and are then cultured. If bacteria
are isolated, a UTI is suspected. Presence of
multiple organisms may imply contamination.
7. Which members of the Enterobacteriaceae are
common contaminants of parenteral fluid?
Shigella, ETEC, EIEC, EHEC, Vibrio cholerae, and
Campylobacter jejuni are all potential contaminants
of parenteral fluids.
8. What is bacteremia? Sepsis? endotoxic shock?
Bacteremia is defined as the presence of viable
bacteria in the bloodstream. Sepsis is defined as
the presence of bacteria or toxic bacterial
metabolites in the bloodstream or tissues. Endotoxic
shock is the systemic reaction to an overwhelming
presence of bacterial toxins in the bloodstream.
9. What are the lab characteristics of Psuedomonas
aeruginosa? Where is it found in nature? How is it
transmitted?
Psuedomonas aeruginosa are aerobic, gram (-) rods
that are oxidase (+). They oxidize but do not
ferment glucose and posssess polar flagellum. The ar
found ubiquitous in nature and are transmitted in
fluid media. They cause opportunisitic infections in
patients with compromised inate immunity (surgical
wounds, trauma, eye injury, IV catheters, patients
with sepsis).
10. How might the polysaccharide capsule of K.
pneumoniae assist in establishing infection? What is
responsible for the mucoid appearance of Psuedomonas
aeruginosa isolates in CF patients?
The polysaccharide capsule of K. pneumoniae assists
the organism in establishing infections by
inhibiting the actions of host immune responses and
antimicrobial agents. The mucoid appearance in CF
patient is due to the production of and alginate
capsule that is very "sticky."
11. What is the mechanism of action of Psuedomonas
aeruginosa exotoxin A?
Psuedomonas aeruginosa exotoxin A is a potent
inhibitor of mammalian protein synthesis. Its
mechanism is identical to diptheria toxin, in that
it ADP-ribosylates EF-2 and prevent protein
synthesis.
Anaerobes
1. Compare and contrast the mode of action of
botulinus toxin and tetanospasmin.
Botulinum toxin interferes with the release of
acetylcholine at the neuromuscular junction by
cleaving components of the neurosecretory apparatus
® flaccid paralysis.
Tetanus toxin (tetanospasmin) cleaves vAMP and
prevents the release of glycine from inhibitory
interneurons in the spinal cord ® spastic paralysis.
2. What is infant botulism? What are the proposed
mechanisms of pathogenesis?
Infant botulism occurs when the infant’s gut is
colonized by C. botulinum that produces toxin in
vivo. This leads to generalized hypotonia ® "floppy
baby" syndrome.
3. Which of the organisms discussed are gram
positive, spore forming anaerobes? Gram negative
anaerobes? Gram positive anaerobes?
The clostridia species are gram-pos spore forming
rods. Bacteroides species are gram-neg obligate
anaerobic bacillus. Bacillus anthracis is an
aerobic, gram positive rod.
4. What are the primary virulence determinants of B.
Anthracis?
Virulent strains of Bacillus anthracis produce an
anti-phagocytic poly D-glutamic acid capsule that
increases its ability to survive in the host. They
also produce three separate proteins (EF, LF, and
PA) that combine to form a toxin. Edema factor (EF)
is a calmodulin dependent bacterial adenylate
cyclase. Lethal factor (LF) has no known enzymatic
activity. Protective antigen (PA) is a tissue
binding component required for significant disease
in the infected host.
5. How is tetanus prevented? How is botulism
prevented?
Vaccination with tetanus toxoid causes the host to
produce protective antibodies for the disease.
Botulism is prevented by using a trivalent antitixon
vaccine and by proper food handling and preparation
techniques.
6. How does C. perfringens alpha toxin work?
C. perfringens alpha toxin is a lecithinase that
causes hemolysis of the RBC in circulation, destroys
platelets and causes widespread damage.
7. Discuss the pathogenesis of botulism,
pseudomembranous colitis and C. perfringens food
poisoning.
Botulism, pseudomembranous colitis and C.
perfringens food poisoning are all similar in that
they involve ingestion of vegatative cells or
spores. The cells or spores undre anaerobic
conditions in the gut mature to produce an
enterotoxin that has either systemic or local
effects.
8. What is the most common bacterial species in the
human gut?
Bacteroides spp.
9. What is the "preeminent" anaerobic pathogen in
humans?
Bacteroides fragilis is the preeminent anaerobic
pathogen in humans. This is based on virulence,
ubiquity in various sites, and resistance to
antimicrobials. It causes abcesses and tissue
destruction on a regular basis.
Staphylococci
1. Which species of Staphylococci are medically
relevant to human disease?
S. Aureus, S. epidermidis and S. saprophyticus are
medically relavant to humans.
2. How are S. Aureus infections acquired? What are
some of the risk groups for S. aureus invasive
disease?
Most infections of staphylococci occur from
autoinfection of strains that reside on the skin and
mucous membranes (nose, perineum and urinary tract).
Patients whose innate immunity has been compromised
are at increased risk for developing invasive S.
aureus infection. Patients who are diabetic,
elderly, alcoholic, abuse IV drugs, have cystic
fibrosis and those with indwelling catheters are at
increased risk. Surgical patients and others who
have open wounds are also at increased risk.
3. Describe the toxins produced by S. aureus. What
other virulence factors are important in S. aureus
disease?
I. Toxins
-Heat stable enterotoxin------------------->food
poisoning
-Exfoliatin---------------------------------->scalded
skin syndrome
-TSST-1----------------------------------->Toxic
shock syndrome
-Alpha hemolysin (a -toxin)------------->RBC lysis
II. Extracellular products
-Coagulase--------------->causes clot that walls off
bacteria from bloodstream
-Leukocidin------------->permeabilizes and kills
PMNs and macrophages
-Hyaluronidase--------->hydrolizes host
extracellular matrix and allows organism to move
III. Surface components
-Peptidoglycan layer---------------->septic shock
-Ribitol-techoic acid---------------->antigenic and
binds fibronectin
-Protein A--------------------------->binds Fc
portion of IgG --->antiphagocytic activity
-Clumping factor------------------->fibrinogen
binding receptor
-Cell surface bound coagulase---->causes bacteria to
be coated with fibrin and ¯ phagocytosis
4. How does one distinguish Staph species from Strep
species in the lab?
The catalase test distinguishes Staph species from
Strep species in the lab by testing the ability
(inherent enzymatic machinery) of the bacteria to
catalyze the reaction H2O2®H2O + O2. The enzyme
required is "catalase." Staph species are catalse
(+) and strep species are catalase (-).
5. What are some epidemiological tools used to study
Staph epidemics?
Bacteriophage typing is based on the fact that staph
species are lysogenic and carry phages to which they
are immune but that are lytic for other species.
Plasmid profiles allow one to characterize genetic
info carried on plasmids (antibiotic resistance,
etc). DNA fingerprinting can also be used to
characterize the genetic info in a given strain and
compare it to other strains.
6. How do Staph acquire antibiotic resistance? What
is signified by MRSA? What are the public health
implication of vancomycin resistant S. aureus
isolates?
Penicillin resistance (and sometimes erythromycin)
is due to a b -lactamase that is coded on a staph
plasmid. Other low molecular weight plasmids encode
resistance to tetracycline, chloramphenicol and
kanamycin. Methycillin resistant staph aureus (MRSA)
resistance to antibiotics is coded for in the
bacterial chromosome. Emerging vancomycin resistance
is probably due to genetic transfer from
Enterococcus species.
7. What type of infection do S. epidermis and S.
saprophyticus cause? How does one distinguish these
species from S. aureus in the lab?
S. epidermis causes nosocomial infections in
patients with indwelling catheters and prosthetic
devices. S. saprophyticus is responsible for 10-20%
of primary UTI in females. S. epidermis and S.
saprophyticus are coagulase (-) and can therefore be
distinguished from coagulase (+) S. Aureus in the
lab.
Streptococci
1. What are the major virulence determinants for
Strep pneumoniae? Strep pyogenes? What immune
mechanisms protect the host against these organisms?
The most important virulence factors for Strep
pneumoniae are the capsular polysaccharides. They
are antigenic, anti-phagocytic, and a loss of the
capsule leads to a loss of virulence. Strep
pneumoniae also produce pneumolysin that injures
pulmonary endothelial cells.
The most important virulence factor for Strep
pyogenes is the production of M protein. It binds to
the host epidermis and is anti-phagocytic. The
capsule of this organism also contains hyaluronic
acid that prevents the host from attacking it (would
lead to autoimmune response to host tissue).
Humoral immunity (opsonization, phagocytosis, and
development of an antibody titer) are the most
important factors in protection for the host.
2. What are the primary disease caused by Strep
pyogenes? Strep pneumoniae? Strep agalactiae? Group
D streptococci? Viridans (a -hemolytic) strep?
Strep pyogenes (group
A)----------------------->impetigo, wound
infections, pharynigitis, cellulitis, necrotizing
fascitis, myositis, rhuematic fever
Strep pneumoniae-------------------------------->pneumonia
Strep agalactiae (group
B)--------------------->neonatal meningitis
Group D streptococci--------------------------->UTI,
bacteremia (post urologic surg), endocarditis,
wound infection
Viridans (a -hemolytic) strep------------------->endocarditis,
dental caries
3. What are the morphologic and physiological
characteristics of all streptococci? In the clinical
lab, how would you distinguish Strep pneumoniae from
viridans (a -hemolytic) strep?
All streptococci species are gram (+) spheres that
grow in pairs or chains. They are non-motile and are
catalase (-).
In the clinical lab one could distinguish Strep
pneumoniae from viridans (a -hemolytic) strep based
on the fact that Strep pneumoniae is optochin
sensitive and viridans strep is not. Furthermore,
viridans will not grow in 6.5% NaCl/bile esculin.
4. Why is it clinically important to distinguish the
enterococci from other group D streptococci?
Enterococci share many characteristics with other
group D streptococci and are normal flora on the
skin and in the GI tract. Enterococci that move to
other sites in the body often cause disease (UTI,
bacteremia, endocarditis, wound infection) and may
exhibit strong antibiotic resistance. The other
group D streptococci are normally non-virulent and
display very little antimicrobial resistance.
5. Describe the extracellular and cell-associated
products of Streptococcus pyogenes. How are these
products used in the diagnosis of group A strep
infections?
One can purchase commercially antibodies to group A
strep that are linked to a staph species via protein
A. When this combination is added to a group A strep
sample, agglutination occurs. This confirms the
presence of the group A strep.
Group A strep also render a (+) PYR (pyrrolidonyl
arylamidase) test.
Neisseria I
1. What are the major virulence determinants of
meningococci? What are the primary host defense
mechanisms against these organisms?
The meningococci are obligate extracellular
parasites. They cannot survive inside PMNs. The
meningococcal capsule is antiphagocytic and is the
major virulence determinant.
The host defense mechanism against meningococci is
primarily a humoral response.
2. How would you isolate and identify N.
meningitidis in the clinical lab? How would you
distinguish it from normal flora neisseria?
Neisseria in general are gram (-) cocci that occur
in pairs. They are non-motile and are non-spore
forming. Pathogenic species will not grow at 220 C
or on a growth agar without blood. They do require
5-10% CO2 for optimal growth. Non-pathogenic species
grow well at 220 C or on a growth agar without
blood. They do not require 5-10% CO2 for optimal
growth.
3. What are the most common causes of bacterial
meningitis by age in the US?
Age #1 #2 #3 #4 #5
<1 month group B strep listeria monocyt strep pneum
1-23 months strep pneum neisseria menin group B
strep haemophilus flu
2-18 yrs neisseria menin strep pneum haemophilus flu
group B strep listeria monocyt
19-59 yrs strep pneum neisseria menin haemophilus
flu listeria monocyt group B strep
>60 yrs strep pneum listeria monocyt neisseria menin
haemophilus flu group B strep
4. Compare and contrast the meningococcal vaccines
with the pnuemococcal vaccines (Who gets them? How
effective are they? etc).
The meningococcal vaccine is available with A, C, Y
and W-135 capsular polysaccharides. It is not a good
immunogen for children >2 yrs of age. There is no
group B vaccine as yet because the capsular
polysaccharide is a poor immunogen even for adults.
The pneumococcal vaccine contains polysaccharide
from each of the 23 serotypes. It is also better for
patients that are >2 yrs of age. It is highly
recommended for people at hi risk® elderly , immune
deficiency, chronic disease patients, sickle cell
anemia, splenectomized, alcoholics.
Neisseria II
1. How does uncomplicated gonorrhea usually manifest
in a male? In a female of reproductive age? In a
pre-adolescent female?
Uncomplicated gonorrhea in a male is characterized
by urethritis. The patient will present with
frequent, urgent and painful urination. A yellow,
mucopurulent discharge containing neutrophils and
gram (-) diplococci is seen. The incubation period
is 2-7 days after contact with an infected partner.
Uncomplicated gonorrhea in a female of reproductive
age is characterized by cervicitis. This is an
inflammation of the endocervical canal epithelium. A
mucopurulent discharge is often seen. Bartholin’s
glands can also become infected and develop into an
abcess.
Uncomplicated gonorrhea in a pre-adolescent female
is characterized by vulvovaginitis.
2. What are the clinical manifestations of ascended
reproductive tract infection in males and in
females? What post-infection complications might
result?
Ascended reproductive tract infection in males can
lead to epididymitis and prostitis. Endometritis,
salpingitis and pelvic inflammatory disease are
common in females with an ascended infection. These
infections all can lead to sterility if severe
and/or untreated. They can also lead to ectopic
pregnancy in women.
3. What other organisms cause acute urethritis in
men and urethritis / cervicitis in women? How would
you differentially diagnose these agents?
Chlamydia trachomatis, ureaplasma urealyticum,
trichomonas vaginalis and Herpes Simplex Virus all
cause urethritis in men and women. The diagnosis of
the causative agent in a given case is based on a
gram-stain of a sample taken from the patient. One
should attempt to grow pathogens on culture, conduct
antibody titer count and examine genomic information
in order to form a definitive diagnosis.
4. How would you isolate and identify N. gonorrhea
in the clinical laboratory? How would you
distinguish it from N.meningitidis?
First, one obtains a specimen from the patient. This
can be done by swabbing the infected site (urethra,
cervix, anus, etc.). Organisms are then cultured and
classified. N. gonorrhea are gram (-) diplococci,
oxidase (+) and nonmotile.
N. meningitidis is also gram (-) and grows on
maltose. N. gonorrhea grows on glucose but not
maltose.
5. Discuss the evolution and mechanisms of
gonococcal resistance to penicillin. What other
antimicrobial agents are used to treat gonorrhea?
Has resistance developed to these agents? What are
the mechanisms of gonococcal resistance to these
agents?
Gonococcal resistance to penicillin is carried on a
small plasmid. This genetic information for
production of a penicillinase was probably acquired
from H. ducreyi. Resistance can also occur in the
form of altered penicillin binding proteins that are
chromosomally encoded.
Tetracycline is also used to treat gonococcal
infection, but genetic information can transfer such
that the penicillin resistance also affects
sensitivity to tetracycline. This leads to a double
resistant organism.
Fluoroquinolone treatment is effective, but
resistance is developing due to an altered DNA
gyrase.
6. Which surface components of the gonococcus
undergo phase and antigenic variation?
The pili, opacity proteins, and the
lipooligosaccharides undergo phase and antigenic
variation.
7. What are the epidemiological implications of
phase and antigenic variation of the gonococcal
pili?
Because the outer pili of the gonococcal species are
highly variable, it is very difficult to design a
vaccine that can target a conserved structure. N.
gonorrhea do not possess a capsule and this also
increases the difficulty in developing a vaccine.
Mycobacterial infections
1. How is the cell mediated immune (CMI) response
involved in mycobacterial infection?
A host infected with mycobacteria fights the
organism through activated macrophages that kills
the infectious agent. CD4+ T-cells secrete
lymphokines that activate the macrophages. CD8+
T-cells release bacilli from unactivated phagocytes
and allow the organisms to be ingested by activated
macrophages. Patients who have AIDS are at increased
risk of developing mycobacterium tuberculosis
infection because they are CD4+ deficient and cannot
fight off the pathogen.
2. What characteristics of tuberculosis and leprosy
are important when considering the epidemiology of
these diseases?
Tuberculosis is a significant disease in the grand
scheme. Worldwide, there are 5-8 million new cases
per year and 2-3 million deaths. The concentration
of TB is increased in areas of poverty, overcrowding
and generally poor living conditions. TB is
developing significant resistance to antibiotic
therapy. Less than 10 viable bacilli in the airway
of a susceptable host can cause disease. Because TB
declined continuously for several years, public
awareness of the disease waned. As TB reemerges as a
resistant infectious agent, large scale epidemics
could occur.
There are 12 million cases of leprosy worldwide.
Unlike TB, a large dose of bacilli is required to
cause infection in a susceptable host. Leprosy is
sensitive to dapsone, but resistant strains are
present.
3. Compare and contrast the two polar forms of
leprosy.
Tuberculoid leprosy elicits a highly specific CMI
response. Bacilli in this form of the disease growin
the skin, but they also invade Schwann cell and
macrophages that can lead to peripheral
neuropathy.The host is able to kill (CD4+ T-cells)
the bacilli and granulomas form around sites of
dermal infection.
Patients who develop lepromatous leprosy are
deficient in cell mediated immunity. Growth of the
pathogen proceeds relatively unimpeded (unless the
patient is treated with medication) and is spread
via the host’s lymphatic system. Skin lesions are
extensive, symmetrical, and diffuse. The face, lips,
forehead, ears and nose are the most common sites of
infectious lesions. Damage from this form of the
disease is often disfiguring and irreversible.
Corynebacteria and listeria
1. How would you process a clinical specimen to
identify C. diptheria? What properties distinguish
it from Staph Aureus and from Strep pneumoniae?
C. diptheria produces grey to black colonies on
selective medium that contains tellurite. It is an
aerobic, gram (+) rod that is not spore forming and
is catalase (+). Staph aureus and Strep pneumoniae
are gram (+) cocci. Staph aureus is catalase (+) and
Strep pneumoniae is catalase (-).
2. How do the properties of the A and B domains of
diptheria toxin contribute to its mode of action in
intoxicating susceptible human cells?
Diptheria toxin is secreted as a single polypeptide
that is proccessed by proteolysis into two subunits.
Fragment B binds to receptors on the plasma membrane
of susceptible cells and initiates uptake of the
toxin by receptor mediated endocytosis. Fragment A
is transported to the cytosol where it
ADP-ribosylates EF2 and inhibits protein synthesis
by the infected cell. This reaction is virtually
identical to the pathogenic toxin of psuedomonas
aeruginosa but the two toxins recognize different
receptors.
3. What are the roles of antitoxic antibodies in
treatment and prevention of diptheria?
Antitoxic antibodies neutralize the toxicity of
diptheria toxin. Usually, a person who is suspected
or confirmed to have a case of diptheria is given
horse antitoxin. One can also be vaccinated against
diptheria and prevent infection by the use of the
diphteria toxoid immunization that is available.
4. What environmental and host factors predispose to
infection by Listeria monocytogenes? How would you
distinguish Listeria monocytogenes in a cultured
clinical specimen from Streptococcus penumoniae or
from Corynebacterium diptheria?
Persons who are HIV (+) and/or are immunosuppresed
are at increased risk of infection from Listeria.
Most infections in humans are food borne, but
infection of a pregnant woman can lead to abortion,
stillbirth, and transplacental infection of the
infant.
Listeria monocytogenes is a short, gram (+) rod that
is non-sporulating, aerobic to microaerophilic and
is catalase (+). Strep pneumoniae is a gram (+)
cocci that is catalase (-). Corynebacterium
diptheria produces grey to black colonies on
selective medium that contains tellurite. It is an
aerobic, gram (+) rod that is not spore forming and
is catalase (+).
Haemophilus, Moraxella and Bordetella
1. What are the primary virulence determinants of
Haemophilus influenzae? Bordetella pertussis? What
immune mechanisms are important in defense against
these organisms?
The primary virulence determinant of Haemophilus
influenzae is a capsular polysaccharide that is
antiphagocytic. Non-encapsulated forms are normal
flora of the URT that can cause some diseases
(otitis media, sinusitis, conjunctivitis, etc).
The primary virulence determinants of Bordetella
pertussis are toxins. The primary toxin activates
the mebrane adenylate cyclaase of eukaryotic cells
via ADP-ribosylation of regulatory protein G1. This
leads to an increase in cAMP and increased fluid
secretion in the URT. Bordetella pertussis also
produces adhesive factors and a tracheal cytotoxin.
Anti-capsular antibodies (humoral immunity) against
Haemophilus influenzae are protective. They coat the
pathogen and mediate complemtn dependent
phagocytosis / lysis.
Protection against Bordetella pertussis is somewhat
elusive. Antibodies are produced during active
infection with the disease and from immunization.
Naturally acquired immunity is not lifelong, second
attacks are common. Newborns and infants that are
not immunized are highly susceptible, reflecting a
low level of antibody being passed from the adult
mother to the newborn child.
2. What are the in vitro growth requirements for H.
influenzae? How do these compare with H. ducreyi? B.
pertussis?
Haemophilus influenze requires X (hemin, heat
stable) or V (can be replaced by NAD / NADP, heat
labile). These factors are provided by chocolate
agar. The organism grows best in 5-10% CO2.
Heamophilus ducreyi also grows best on enriched
chocolate agar in 10% CO2 and at 350 C.
Bordatella pertussis requires enriched media that
binds fatty acids. Bordet-Gengou agar (contains
potato extract, 30% blood and glycerol) is ideal.
3. What is the chemical composition of the type b
capsule? How does this compare with the capsule of
S. pneumoniae? B. anthracis? E. coli K-1?
The Haemophilus influenzae type b capsule is
composed of polyribose-ribitol phosphate (PRP).
The capsule of S. pneumoniae is composed of a very
diverse group of polysaccharides, choline, acetyl,
and phosphate groups. Over 80 different combinations
have been classified.
The capsule of Bacillus anthracis is D-glutamic acid
polypeptide.
E. coli K-1 species produce a capsular
polysaccharide that contains sialic acid and is
structurally identical to the group B polysaccharide
of Neisseria meningitidis.
4. What are the similarities and differences in mode
of action of cholera toxin, diptheria toxin, and
pertussis toxin?
Cholera toxin, diptheria toxin and pertussis toxin
are all ADP-ribosylases. Their most significant
difference is their target. Cholera toxin affects
the stimulatory G protein (GS)of the adenylate
cyclase complex. Pertussis toxin attacks the
inhibitory protein (GI) of the same complex.
Diptheria toxin affects elongation factor 2 (EF2)
that leads to a blockage of host cell protein
synthesis.
5. Compare the vaccines against pertussis and H.
influenzae type b with regard to composition and
efficacy.
The current pertussis vaccine is composed of a
mixture of purified, inactivated B. pertussis
products. It is very effective in producing immunity
to the disease and has only local side effects.
The H. influenzae type b (Hib) vaccine is a
conjugation of Hib with diptheria toxoid. It is
highly effective and serves as a model for the
development of future vaccines.
6. How does B. pertussis colonize the respiratory
tract? Is it an invasive organism? How does the
pathogenesis of pertussis compare with that of
diptheria? Cholera?
B. pertussis colonizes the ciliated bronchial
epithelium without invading the tissue. It does this
via filamentous attachment. The bacteria first
attach to and immobilize the cilia. The ciliated
epithelial cells are then slowly destroyed by
bacterial toxins.
The diseases caused by infection with Vibrio cholera
and corynebacteria diptheriae are due to the
production of ADP-robosylating toxins by the
organism that lead to altered host cell function.
Mycoplasma and legionella infections
1. How do mycoplasms differ from other bacteria?
What characteristics do they have in common? How do
these organisms appear under a microscope?
Mycoplasm do not have a cell wall. They are much
smaller than other bacteria, and contain DNA
genomes. Under a microscope, mycoplasm stain poorly
or not at all and because of their small size, they
are difficult to see.
2. What are the major disease syndromes caused by
mycoplasma? What pathogenic mechanisms are involved?
Mycoplasma pneumonia causes primary atypical
pneumonia (walking pneumonia). Mycoplasma hominis
causes genital infections. Many other clinical
syndromes (wheezing, pharyngitis, rhinitis, erythema
multiforme, myringitis, otitis media, et al) are
associated with mycoplasma infection.
Mycoplasma enter the respiratory tract via
inhalation and attach to cells in the lower part of
the tract. The pathogens remain extracellular and
intefere with ciliary action. The immune response to
infection may lead to an autoimmune attack on the
host in some cases.
3. What are the most common clinical signs of
infection with M. pnuemoniae?
One sees non-specific pulmonary infiltrates, fever,
malaise, myalgia, sore throat, and cough
(nonproductive, productive, or paroxysmal).
4. Why do you think that Legionella pneumoniae was
not discovered until the mid 1970’s? What are its
characteristic properties?
Legionella pneumoniae is a motile, gram (-) rod that
is difficult to stain. It is very difficult to
culture due to restrictive growth criteria (requires
cysteine and iron). Because it is very small
(.5-.7mm wide and 2-20mm long) and difficult to
stain, isolation and identification is very
difficult.
5. What are some ecological niches for L.
pneumoniae? How is it transmitted?
Legionella pneumoniae hides in air conditioning
equipment that uses water internally (cooling towers
and condensers). Shower heads, faucet taps, and
vegetable misters can also harbor the organism.
The pathogen is transmitted by inhalation of the
aerosolized bacteria. It is not easily (if at all)
spread from person to person.
6. How is legionellosis diagnosed in the lab?
Demonstration in culture of the bacteria taken from
tissue or secretions is useful for diagnosis.
Bacteria can be demonstrated in tissue by using a
silver impregnation technique that highlights the
intracellular pathogen. Direct immunofluorescence
can detect the organism in pleural fluid or lung
tissue. A 4-fold rise in the antibody titer of a
suspected patient is strong evidence for infection.
Chlamydial infections
1. Why are chlamydial infections often misdiagnosed?
Chlamydial infection can range from a chronic /
persistent infection to acute infection, or totally
inapparent to the host. The symptoms of chlamydial
infection are common to many other STDs. Microscopic
examination of specimens in an attempt to identify
the organism is very difficult because of the size
of the pathogen. Growing these organisms in culture
is very difficult. The diagnosis of chlamydia is
usually made when a patient presents with symptoms
of STD and no gonococci can be demonstrated in a
specimen. Many times, an infection with gonococci
masks an infection with chlamydia.
2. Why are chlamydial infections often
inappropriately treated?
Because chlamydia is difficult to diagnose,
treatment for the patient’s symptoms can be
ineffective against the pathogen. If one treats for
a gonococci infection without including
antimicrobials against chlamydia, the infection may
not be cleared by the host.
3. How would you interrupt the cycle of transmission
of trachoma? Nongonococcal urethritis? Psittacosis?
Lymphogranuloma venereum?
4. How do reticulate bodies (Rbs) differ from
elementary bodies (Ebs)?
EB RB
Morphology small and dense large, homogenous
Size .25 mm .6-1.0 mm
Stage extracellular/infectious
intracellular/replicative
Osmotic fragility --- +++
Metabolic activity --- +++
Outer membrane cross-linked not cross-linked
5. What antibiotics are most effective in treating
chlamydial infections? Why?
Doxycycline (tetracycline) is the anitbiotic of
choice. Chlamydia do not possess a peptidoglycan
layer in their cell membrane. Therefore, antibiotics
directed toward cell wall synthesis are ineffective.
Chlamydia is an intracellular pathogen and
tetracycline is effective against it because the
drug is very hydrophobic. This decreases its ability
to enter and attack host cells. However, once inside
the host cell the drug is actively taken up by the
pathogen whose ribosomes are very sensitive to its
action.
Spirochetes
1. What features do all spirochetes have in common?
What features distinguish the genera Treponema,
Borrelia and Leptospira?
Spirochetes are spiral shaped organisms that don’t
gram stain. They are also very difficult to culture
in vitro. The periodicity of the coil and the
overall size of the organism varies among the genera
and species in the spirochete family. Spirochetes
are prokaryotes with inner and outer membranes. They
also display corkscrew motility.
Treponema are 5 to 15 mm in length with regular
spirals 1mm in length and an amplitude of .3 mm.
Borellia is a large spirochete 10 to 30m m long and
.3 m m wide. It contains 15 to 20 axial flagella.
The spirals are irregular with a 2 to 4 m m
wavelength.
Leptospira is a slim (.15m m) spirochete 5-15 m m
long. It displays a single axial filament, fine
closely wound sprials, and hooked ends.
2. What are the clinical stages of syphillis? Where
are the organisms located during each stage? What
are the host responses to infection at each stage?
How is the diagnosis of syphillis established by lab
tests?
10 syphillis presents with a hard, painless genital
chancre that is teeming with infective organisms.
Patients in this phase are at increased risk of
spreading HIV. Lymphocytes, monocytes and plasma
cells surround the lesion. The chancre heals
spontaneously but systemic infection remains.
20 syphillis presents with papulosquamous rashes on
the soles, palms, and mucous mebranes. Painless,
mucosal warty lesions in the perineal and genital
area, known as condyloma lata, is seen in this
stage. Regional adenopathy and tenderness may be
present. Latent syphillis is an asymptomatic
infection (carrier).
30 syphillis appears as early as 5 years, and as
late as 20 years, after the initial infection.
Patients present with syphilitic aortitis, CNS
effects, and gummas (granulomatous lesions in any
organ of the body). These effects are most likely
due to a DTH response to the spirochete or
autoimmunity to host tissues infected with
spirochetes.
Syphillis is diagnosed with non-treponemal and
treponemal assays, direct demonstration of
spirochetes from lesions, and detection of
treponemal specific IgM antibody.
3. What are the risk factors for acquiring
syphillis? Relapsing fever? Lyme disease?
Leptospirosis? What is the significance of these
diseases for civilian and military populations? What
are the major clinical features of these diseases?
Persons who practice "unsafe" sex with multiple
partners, use IV drugs, and are HIV (+) are at
increased risk of contracting syphillis.
Persons who are exposed to wild animals (deer,
ticks, fleas, etc) are at risk for developing lyme
disease and relapsing fever.
Persons who wade in water that has bovine urine in
it are at increased risk of developing
leptospirosis.
These diseases do not have high mortality rates, but
they do have high morbidity rates. Therefore, the
prevention of these diseases through prophylaxis and
behavior modification is of particular interest to
the military, in order to conserve fighting
strength.
Bacterial Vaginosis and Trichamonas Infections
1. Why is transmission of T. vaginalis infection
difficult to control?
T. vaginalis is a very hardy organism. It can live
outside of the human body for some time in a warm,
moist environment. Many people who are infected with
T. vaginalis are asymptomatic and spread the disease
via sexual contact to their partners. If people have
multiple partners, epidemics can develop before
anyone is aware of the infection.
2. How do hydrogenosomes differ from mitochondria?
What drugs are uniquely targeted to hydrogenosome
enzymes?
Hydrogenosomes house the enzymatic machinery that
can carry out anaerobic oxidation of pyruvate to
acetate. This is coupled to ferredoxin mediated
electron transport. Metronidazole targets the
pyruvate::ferredoxin reductase enzyme used in this
pathway.
3. What are the major virulence factors of T.
vaginalis? What are the major host defenses against
this parasite?
T. vaginalis produces adhesive proteins that help
the organism adhere to the vaginal epithelium. The
organism possesses a surface cysteine proteinase
that is involved in both cytoadherance and
cytotoxicity. The immunodominant surface
glycoprotein undergoes phenotypic variation by
harboring an RNA virus in its cytoplasm.
4. Why do bacterial vaginosis and trichamoniasis
frequently occur together?
Bacterial vaginosis is an overgrowth of the normal
vaginal flora that leads to a more alkaline pH and
loss of H2O2. Several anaerobic species that are
normal flora in the vagina proliferate and increase
the production of succinate. This inhibits the
chemotaxis of white blood cells. All of these
conditions, when combined, favor establishment and
proliferation of T. vaginalis.
5. Metronidazole is used to treat Giardia, Entamoeba
histolytica, and Helicobacter pylori. What can you
infer about the energy metabolism of these GI tract
pathogens?
If metronidazole is effective against these
organisms, they must share the enzymatic machinery
described above for T. vaginalis. According to
Lange’s Pharmacology (p. 828), Entameoba and Giardia
do not possess a hydrogenosome, but they do use the
same enzyme that metronidazole targets in T.
vaginalis infections.
6. Why do bacterial vaginosis and vaginal
yeast infections frequently recur?
Because these diseases are overgrowths of the normal
flora, the immune response to these infections is
limited. Once an infection is cleared with
medication, the only thing necessary for overgrowth
(recurrence) to return is an imblance in the
environmental conditions of the vagina.
Yersinia, Brucella and Francisella
1. How do Y. pestis, Brucella sp. and Francisella
tularensis evade host defense mechanisms?
Y. pestis possesses a capsule that is
antiphagocytic. All three organisms are facultative
intracellular organisms that by living in
macrophages, resist being killed by macrophages.
Cell mediated immunity against the infected cells is
required in order to end the infection without
medical intervention.
2. What kind of vaccine would be optimal to protect
an individual against infection with Y. pestis?
A vaccine that would increase cell mediated immunity
against the capsular antigen of Y. pestis or the
YOMPs would be effective.
3. What zoonotic infections have we discussed to
date?
Disease Etiologic agent Reservoir
Anthrax Bacillus anthracis cattle, sheep, goats
Campylobacter infection C. jejuni wild mammals,
cattle, sheep, pets
Leptospirosis Leptospira sp. cattle, rodents
Lyme disease Borellia burgdorferi deer, rodents
Plague Y. pestis rodents
Relapsing fever Borellia sp. rodents, ticks
Salmonellosis Salmonella sp. poultry, livestock
RMSF R. rickettsii rodents, ticks, mites
Murine typhus Rickettsia typhi rodents
Q fever Coxiella burnettii cattle, sheep, goats
4. Compare and contrast the in vitro growth
requirements and characterisitics of Y. pestis, B.
abortus, and F. tularensis.
Y. pestis is not considered fastidious and grow
optimally at 280 C. Most virulence traits are
expressed at 370 C (temperature inside human body).
Brucella abortus is a slow growing organism that is
very fastidious and requires CO2 for growth.
F. tularensis can be grown in vitro if the culture
medium contains cysteine.
5. Who is most likely to get bubonic plague?
Pneumonic plague? Brucellosis? Infected with F.
tularensis?
Bubonic plague results from being bitten by an
infected flea that feeds on infected rodents or
other small animals. Anyone who is exposed to
infected fleas or rodents could contract the
disease.
Pneumonic plague can be contracted by inhaling
aerosolized secretions or droplets expelled from the
respiratory tract of someone infected with Y.
pestis.
Brucellosis is contracted by contact with infected
animals. Veterinarians, slaughter house workers, and
farmers are at risk for infection. Anyone who drinks
raw milk from an infected animal could also contract
the disease.
People who lead an active, outdoor lifestyle and
come into contact with wild rabbits, muskrats, ticks
or deerflies are at highest risk for developing
tularemia.
Rickettsia
1. Compare and contrast chlamydia, E. coli,
rickettsia, and mycoplasma.
Chlamydia are obligate intracellular parasites. They
multiply by binary fision and have DNA, RNA and 70s
ribosomes. They carry plasmids, and their cell
envelope is similar to a gram (-) species, but they
do not possess a peptido-glycan layer.
E. coli are gram (-) rods that live in the lower GI
tract. They are able to ferment lactose.
Ricketssia are pleomorphic coccobacilli that can be
visualized with Wright-Giemsa stain. They multiply
by binary fission and require a supply of co-factors
(NAD, ATP, CoA) from the host for survival.
Mycoplasma are the smallest free living organism.
They do not have a cell wall, and are distinguished
based on serotype. Some species are normal flora,
while others are frank pathogens.
2. How are the rickettsia classified?
The rickettsia are classified based on clinical
features, epidemiologic aspects, and immunologic
characteristics.
3. What are the characteristic pathological features
of most rickettsial diseases?
Vasculitis caused by the proliferation of the
organism in the endothelial lining of small blood
vessels. This leads to the clinical manifestations
of infection that are commonly seen: rash, fever,
headache, malaise, prostration, hepatosplenomegaly.
4. Which rickettsia are:
able to grow on cell-free media®Bartonella sp. very
resistant to drying®Coxiella burnetii transmitted by
mites®Orientia tsutsugamushi and Rickettsia akari
transmitted by ticks®Rickettsia rickettsii, Ehrlicia
chaffeenis, Coxiella burnettii,
not transmitted by an arthropod vector®Rickettsia
prowazekii, Rickettsia typhi, Rickettsia akari,
Bartonella sp.
5. Compare and contrast the clinical manifestations
of epidemic typhus and RMSF.
Epidemic typhus presents with a severe systemic
infection and prostration. The fever may last for 2
weeks. A rash is noted that spreads from the axilla
and trunk, outward to the extremities. The face,
palms, and soles are spared from the rash.
RMSF presents with an acute, febrile illness with
mylagia, malaise, and a rash. The rash of RMSF
begins on the palms and soles and moves inward. The
rash may involve the entire body.
6. How would you treat RMSF?
Tetracycline and / or chloramphenicol is the
treatment of choice for RMSF.
7. What lab tests are used to confirm the diagnosis
of rickettsial disease?
Skin biopsies may reveal the pathogenic organism by
immunofluoresence. Serologic response to specific
antigens can also be used to confirm the diagnosis.
8. What is the most common tick-borne infection in
the US?
Rocky Mountain Spotted Fever
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