ch12 Flashcards
(122 cards)
1
Q
rickettsias
A
tiny, Gram-negative, obligate intracellular
parasites that synthesize only a small amount of
peptidoglycan and thus appear almost wall-less.
2
Q
rickettsias named after
A
The group
as a whole is named after the most common genus of them,
Rickettsia, named for person who discovered
3
Q
rickettsias are viruses?
A
they are not much bigger than a large
virus. Because of their small size, rickettsias were originally considered
viruses, but closer examination has revealed that they
contain both DNA and RNA, functional ribosomes, and Krebs
cycle enzymes and that they reproduce via binary fission—all
characteristics of cells, not viruses.
4
Q
Researchers have proposed several hypotheses to explain
why rickettsias are obligate parasites, even though they have
functional genes for protein synthesis, ATP production, and reproduction.
A
Primary among these hypotheses is that rickettsias
have very “leaky” cytoplasmic membranes and lose small cofactors
(such as NAD+
) unless they are in an environment that
contains an equivalent amount of these cofactors—such as the
cytosol of a host cell.
5
Q
Rickettsia genus
A
Rickettsia is a genus of nonmotile, aerobic, intracellular parasites
that live in the cytosol of their host cells.
6
Q
Rickettsia genus structure
A
They possess minimal
or no cell walls of peptidoglycan and an outer membrane of lipopolysaccharide
with endotoxin activity. A loosely organized slime layer surrounds each cell.
7
Q
Rickettsia genus vector
A
Arthropod vectors transmit all three species of Rickettsia
8
Q
how do Rickettsia genus enter host cells
A
by stimulating endocytosis. Once inside a
host cell, the microbes secrete an enzyme that digests the membrane
of the endocytic vesicle, releasing the bacteria into the cytosol.
As a result, rickettsias avoid the lysis that would ensue if
a lysosome had merged with the endosome
9
Q
Rickettsia rikcettsii causes
A
- spotted fever rickettsiosis (principally
Rocky Mountain spotted fever, RMSF), the most severe and
most reported rickettsial illness.
10
Q
RMSF symptoms
A
About a week after infection, patients experience fever,
headache, chills, muscle pain, nausea, and vomiting. In most
cases (90%), a spotted, nonitchy rash develops on the trunk and
appendages–including palms and soles. In about 50% of patients, the rash develops into subcutaneous
hemorrhages called petechiae
11
Q
R. rickettsii secretes __, and disease is not the product
of the host’s immune response
A
no toxins. Apparently, damage to the
blood vessels leads to leakage of plasma into the tissues, which
may result in low blood pressure and insufficient nutrient and
oxygen delivery to the body’s organs.
12
Q
R rickettsii dormancy
A
R. rickettsii is typically dormant in the salivary glands of
the ticks, and only when the arachnids feed for several hours
are the bacteria activated. Active bacteria are released from the
tick’s salivary glands into the mammalian host’s circulatory
system.
13
Q
epidemic typhus organism
A
R prowazekii
14
Q
In contrast to other rickettsias,
R. prowazekii
A
has humans as its primary hosts.
15
Q
RMSF treatment
A
Physicians treat Rocky Mountain spotted fever by carefully
removing the tick and prescribing doxycycline for most adults
or chloramphenicol for children and pregnant women.
16
Q
RMSF prevention
A
Prevention of infection involves
wearing tight-fitting clothing, using tick repellents, promptly
removing attached ticks, and avoiding tick-infested areas
17
Q
RMSF vectors
A
Hard ticks
in the genus Dermacentor
18
Q
epidemic typhus vector
A
vectored by the human body louse,
Pediculis humanus
19
Q
RMSF tests
A
Serological tests such as latex agglutination and fluorescent
antibody stains are used to confirm an initial diagnosis based
on sudden fever and headache following exposure to hard ticks,
plus a rash on the soles or palms. Nucleic acid probes of specimens
from rash lesions provide specific and accurate diagnosis,
but such tests are expensive and typically are performed only
by trained technicians in special laboratories.
20
Q
epidemic typhus test
A
Diagnosis must be confirmed by the demonstration of
the bacterium in tissue samples using fluorescent antibody tests.
21
Q
epidemic typhus symptoms
A
Diagnosis is based on the observation of signs and
symptoms—high fever, mental and physical depression, and a
rash that lasts for about two weeks—following exposure to infected
lice.
22
Q
epidemic typhus occurs in
A
Epidemic typhus occurs in crowded, unsanitary living
conditions that favor the spread of body lice; it is endemic in
Central and South America and in Africa.
23
Q
epidemic typhus recurrence
A
It can recur many
years (even decades) following an initial episode. The recurrent
disease (called Brill-Zinsser disease) is mild and brief and
resembles murine typhus.
24
Q
epidemic typhus treatment
A
Epidemic typhus is treated with doxycycline or chloramphenicol.
25
epidemic typhus prevention
Prevention involves controlling lice populations
and maintaining good personal hygiene. An attenuated vaccine
against epidemic typhus is available for use in high-risk
populations.
26
murine typhus organism
R typhi
| ***aka endemic (not epidemic) typhus
27
murine typhus vector
fleas (rat: X cheopis, cat: C felis)
28
murine typhus symptoms
About 10 days following the
bite of an infected flea, an abrupt fever, severe headache, chills,
muscle pain, and nausea occur. A rash typically restricted to the
chest and abdomen occurs in less than 50% of cases.
29
murine typhus test
Diagnosis is initially based on signs and symptoms following
exposure to fleas. An immunofluorescent antibody stain of
a blood smear provides specific confirmation
30
murine typhus treatment
doxycycline or chloramphenicol.
31
scrub typhus oganism
Orentia tsutsugamushi
32
Orentia t vs Rickettsia
It differs
from Rickettsia by having significantly different rRNA nucleotide
sequences, a thicker cell wall, and a minimal slime layer
33
orentia vectors
Mites of
the genus Leptotrombidium, also known
as red mites or chiggers
34
scrub typhus symptoms
Scrub typhus is characterized by
fever, headache, and muscle pain, all of which develop about
11 days after a mite bite. Less than half of patients with scrub
typhus also develop a spreading rash on their trunks and appendages.
35
scrub typhus treatment
Physicians treat scrub typhus in nonpregnant adults with
doxycycline or macrolides. They treat children and pregnant
women with azithromycin.
36
HME organism
Ehrlichia chaffeensis
37
anaplasmosis organism
Anaplasma
| phagocytophilum
38
HME stands for
human monocytic ehrlichiosis
39
HME, anaplasmosis treatment
Doxycycline and tetracycline are effective against both
| Ehrlichia and Anaplasma, but chloramphenicol is not.
40
HME, anaplasmosis test
Immunofluorescent antibodies
against Ehrlichia or against Anaplasma can demonstrate the bacterium
within blood cells, confirming the diagnosis.
41
HME, anaplasmosis symptoms
HME and anaplasmosis resemble Rocky Mountain spotted
fever but without the rash, which only rarely occurs in ehrlichiosis
or anaplasmosis. Leukopenia,which is an
abnormally low leukocyte count, is typically seen.
42
HME, anaplasmosis vector
lone star tick (amblyomma), deer tick (ixodes), dog tick
43
HME, anaplasmosis in cells
Once in the blood, each bacterium triggers its own phagocytosis
by a white blood cell (either a monocyte in HME or a neutrophil
in anaplasmosis). Inside a leukocyte the bacteria grow and reproduce
through three developmental stages: an elementary body,
an initial body, and a morula.
44
Unlike Rickettsia, Ehrlichia and Anaplasma
grow and reproduce within the host cell’s phagosomes. Because
the bacteria are killed if a phagosome fuses with a lysosome,
the bacteria must somehow prevent fusion, but the mechanism
is unknown.
45
chlamydias
vie with rickettsias for
the title “smallest bacterium.” Like rickettsias, chlamydias are nonmotile and grow and multiply only within vesicles in host
cells.
46
chlamydias viruses?
Scientists once considered chlamydias to be viruses because
of their small size, obligate intracellular lifestyle, and ability to pass
through 0.45-μm pores in filters, which were thought to trap all
cells. However, chlamydias are cellular and possess DNA, RNA,
and functional 70S ribosomes
47
chlamydia structure
Each chlamydial cell is surrounded
by two membranes, similar to a typical Gram-negative bacterium
but without peptidoglycan between the membranes—chlamydias lack cell walls.
48
chlamydias lack
the metabolic
enzymes needed to synthesize ATP, so they must depend on
their host cells for the high-energy phosphate compounds they require;
thus, chlamydias have been called energy parasites.
49
chlamydia life cycle
once an EB attaches
to a host cell 1 , it enters by triggering its own endocytosis
2 . Once inside the endosome, the EB converts into an
RB 3 , which then divides rapidly into multiple RBs 4 . Once
an infected vesicle becomes filled with RBs, it is called an inclusion
body. About 21 hours after infection, RBs within an inclusion
body begin converting back to EBs 5 , and about 19 hours
after that, the EBs are released from the host cell via exocytosis.
50
Three chlamydias cause disease in humans. In order of the
| prevalence with which they infect humans, they are
Chlamydia
| trachomatis, Chlamydophila pneumoniae, and Chlamydophila psittaci
51
EBs vs RBs
Elementary bodies are relatively dormant,
are resistant to environmental extremes, can survive outside
cells, and are the infective forms. Reticulate bodies are noninfective,
obligate intracellular forms that replicate via binary fission
within phagosomes, where they survive by inhibiting the fusion
of a lysosome with the phagosome
52
The clinical manifestations of chlamydial infection
| result from
the destruction of infected cells at the site of infection
and from the inflammatory response this destruction
stimulates
53
LGV
lymphogranuloma venereum. caused by the so-called LGV strain
of C. trachomatis.
54
LGV stage 1
The initial lesion of lymphogranuloma venereum
occurs at the site of infection on the penis, urethra, scrotum, vulva,
vagina, cervix, or rectum. This lesion is often overlooked because
it is small and painless and heals rapidly. Headache, muscle pain,
and fever may also occur at this stage of the disease
55
LGV stage 2
The second stage of the disease involves the development
of buboes (swollen lymph nodes) associated with lymphatic
vessels draining the site of infection. The buboes, which are
accompanied by fever, chills, anorexia, and muscle pain, may
enlarge to the point that they rupture, producing draining
sores.
56
LGV stage 3
In a few cases, lymphogranuloma venereum proceeds to
a third stage characterized by genital sores, constriction of the
urethra, and genital elephantiasis. Arthritis may also occur during
this third stage, particularly in young white males.
57
proctitis
C trachomatis: Proctitis
may occur in men and women as a result of lymphatic
spread of the bacterium from the vagina, vulva, cervix,
or urethra to the rectum.
58
PID
An immune response against reinfections of C. trachomatis in
women can have serious consequences, causing pelvic inflammatory
disease (PID). PID involves chronic pelvic pain; irreversible
damage to the uterine tubes, uterus, and ovaries; and sterility
59
trachoma
The so-called trachoma strains of C. trachomatis cause
| a disease of the eye called trachoma, which is the leading cause of nontraumatic blindness in humans
60
how does C trachomatis cause trachoma
The pathogen multiplies in cells of the conjunctiva and
kills them, triggering a copious, purulent
(pus-filled) discharge
that causes the conjunctiva to become scarred. Such scarring in
turn causes the patient’s eyelids to turn inward such that the
eyelashes abrade, irritate, and scar the cornea, triggering an invasion
of blood vessels into this normally clear surface of the
eye. A scarred cornea filled with blood vessels is no longer
transparent, and the eventual result is blindness.
61
C trachomatis test
Giemsa-stained specimens
may reveal bacteria or inclusion bodies within cells, but
the most specific method of diagnosis involves amplifying the
number of chlamydia by inoculating the specimen into a culture
of susceptible cells. Laboratory technicians then demonstrate
the presence of Chlamydia in the cell culture by means of specific
fluorescent antibodies (Figure 21.9) or nucleic acid probes
62
C pneumoniae
chlamydophila pneumoniae
- pneumonia, bronchiti,s sinusitis
- also been implicated as a cause
of some cases of atherosclerosis—lipid deposits on the walls of
arteries and the first stage of arteriosclerosis, or hardening of
the arteries.
63
C pneumoniae symptoms
Most infections with Chlamydophila pneumoniae are
mild, producing only malaise and a chronic cough, and do not
require hospitalization. Some cases, however, are characterized
by the development of a severe pneumonia that cannot be distinguished
from primary atypical pneumonia, which is caused
by Mycoplasma pneumoniae
64
C pneumoniaae test
Fluorescent antibodies demonstrate the intercellular presence
of C. pneumoniae, which is diagnostic.
65
whats ornithosis
disease of birds that can be transmitted to humans, in whom it typically causes flulike
symptoms.
66
ornithosis transmission
Elementary bodies of Chlamydophila psittaci may be inhaled in
aerosolized bird feces or respiratory secretions or ingested from
fingers or fomites that have contacted infected birds. Pet birds
may transmit the disease to humans via beak-to-mouth contact
67
spirochetes
thin, tightly coiled, helically shaped,
Gram-negative bacteria that share certain unique features—most
notably axial filaments.
68
axial filaments
Axial filaments are composed of endoflagella
located in the periplasmic space between the cytoplasmic
membrane and the outer (wall) membrane (see Figure 3.8). As
its axial filament rotates, a spirochete corkscrews through its
environment—a type of locomotion thought to enable pathogenic
spirochetes to burrow through their hosts’ tissues.
69
spirochete mutants
Mutants lacking
endoflagella are rod shaped rather than helical, indicating
that the axial filaments play a role in maintaining cell shape.
70
ornithosis organism
chlamydophila psittaci
71
syphilis organism
Treponema pallidum pallidum
72
3 genera of spirochetes that cause disease in humans
Treponema, Borrelia, and Leptospira
73
primary syphilis
a small, painless,
reddened lesion called a chancre forms at the site of
infection. The center
of a chancre fills with serum that is extremely infectious because
of the presence of millions of spirochetes.
- 1/3 of cases, ends here
74
2ndary syphilis
, in most infections Treponema has invaded
the bloodstream and spreads throughout the body to cause
the symptoms and signs of secondary syphilis: sore throat, headache, mild fever, malaise, myalgia (muscle pain), lymphadenopathy (diseased
lymph nodes), and a widespread rash. Although this rash
does not itch or hurt, it can persist for months, and like the primary
chancre, rash lesions are filled with spirochetes and are extremely
contagious.
75
latent syphilis
After several weeks or months the rash gradually disappears,
and the patient enters a latent (clinically inactive) phase of
the disease. The majority of cases do not advance beyond this
point, especially in developed countries where antimicrobial
drugs are in use
76
latent syphilis
After several weeks or months the rash gradually disappears,
and the patient enters a latent (clinically inactive) phase of
the disease. The majority of cases do not advance beyond this
point, especially in developed countries where antimicrobial
drugs are in use
77
tertiary syphilis
Latency may last 30 or more years, after which perhaps
a third of the originally infected patients proceed to tertiary
syphilis. This phase is associated not with the direct effects of
Treponema but rather with severe complications resulting from
inflammation and a hyperimmune response against the pathogen.
Tertiary syphilis may affect virtually any tissue or organ
and can cause dementia, blindness, paralysis, heart failure, and gummas
78
gummas
in tertiary syphilis: syphilitic lesions; rubbery,
painfully swollen lesions that can occur in bones, in nervous tissue,
or on the skin
79
congenital syphilis
Congenital syphilis results when Treponema crosses the placenta
from an infected mother to her fetus. Transmission to the
fetus from a mother experiencing primary or secondary syphilis
often results in the death of the fetus. If transmission occurs
while the mother is in the latent phase of the disease, the result
can be a latent infection in the fetus that causes mental retardation
and malformation of many fetal organs. After birth, newborns
with latent infections usually exhibit a widespread rash at
some time during their first two years of life.
80
syphilis treatment
Penicillin is the drug of choice for treating primary, secondary,
latent, and congenital syphilis, but it is not efficacious for tertiary
syphilis because this phase is caused by a hyperimmune response,
not an active infection.
81
syphilis diagnosis
- primary, 2ndary, congenital: easy and rapid using specific antibody tests
- tertiary: extremely difficult to diagnose
because it mimics many other diseases, because few (if
any) spirochetes are present, and because the signs and symptoms
may occur years apart and seem unrelated to one another
82
other members of treponema
cause three nonsexually transmitted
diseases in humans: bejel, yaws, and pinta. These diseases
are seen primarily in impoverished children in Africa, Asia, and
South America who live in unsanitary conditions. The spirochetes
that cause these diseases look like Treponema pallidum pallidum.
- diagnose by appearance
- penicillin
- preventing: prevent contact w/ lesions
83
bejel
treponema palidum endemicum --
a disease seen in children in Africa, Asia, and Australia. In bejel, the
spirochetes are spread by contaminated eating utensils, so it is not
surprising that the initial lesion is an oral lesion, which typically is
so small that it is rarely observed. As the disease progresses, larger
and more numerous secondary lesions form around the lips and
inside the mouth. In the later stages of the disease, gummas form
on the skin, bones, or nasopharyngeal mucous membranes.
84
yaws
treponema pallidum pertenue --
characterized initially by granular skin lesions that, although
unsightly, are painless. Over time the lesions develop into large,
destructive, draining lesions of the skin, bones, and lymph
nodes (Figure 21.13). The disease is spread via contact with spirochetes
in fluid draining from the lesions
85
pinta
spirochetes are spread among the children by skin-to-skin contact. After one to
three weeks of incubation, hard, pus-filled lesions called papules
form at the site of infection; the papules enlarge and persist for
months or years, resulting in scarring and disfigurement.
86
borrelia
lightly staining,
Gram-negative. These spirochetes cause two diseases in humans: Lyme
disease and relapsing fever.
87
Lyme disease organism
hard ticks of genus Ixodes transmitted the spirochete Borrelia burgdorferi to human hosts
88
Borrelia burgdorferi
B. burgdorferi is an unusual bacterium in that it lacks ironcontaining
enzymes and iron-containing proteins in its electron
transport chains. By utilizing manganese rather than iron,
the spirochete circumvents one of the body’s natural defense
mechanisms: the lack of free iron in human tissues and fluids.
89
lyme disease characterized by
dermatological, cardiac, and neurological abnormalities
in addition to the observed arthritis. Infected children
may have paralysis of one side of their face (Bell’s palsy).
- Lyme disease mimics many other diseases, and its range
of signs and symptoms is vast.
90
ixodes
An Ixodes tick lives for two years, during which it passes
through three stages of development: a six-legged larva, an
eight-legged nymph, and an eight-legged adult. During each
stage it attaches to an animal host for a single blood meal. After
each of its three feedings, the tick drops off its host and lives in
leaf litter or on brush.
91
lyme disease phases
1. expanding red bulls eye rash (75p patients)
2. neurological symptoms, cardiac dysfunction (10p patients)
3. severe arthritis that can last for years
The pathological conditions of the latter phases of Lyme
disease are due in large part to the body’s immunological response;
rarely is Borrelia seen in the involved tissue or isolated
in cultures of specimens from these sites
92
lyme disease phases
1. expanding red bulls eye rash (75p patients)
2. neurological symptoms, cardiac dysfunction (10p patients)
3. severe arthritis that can last for years
The pathological conditions of the latter phases of Lyme
disease are due in large part to the body’s immunological response;
rarely is Borrelia seen in the involved tissue or isolated
in cultures of specimens from these sites
93
lyme disease dianosis
rarely confirmed
by detecting Borrelia in blood smears; instead, the diagnosis
is confirmed through the use of serological tests.
94
relapsing fever organism
A disease called louse-borne relapsing
fever results when Borrelia recurrentis is transmitted
between humans by the human body louse Pediculus humanus.
A disease known as tick-borne relapsing fever occurs when
any of several species of Borrelia are transmitted between humans
by soft ticks in the genus Ornithodoros
95
relapsing fever symptoms
septicemia (aka bacteremia, bloodstream bacterial infection) and fever separated by symptom-free
intervals—a pattern that results from the body’s repeated efforts to remove the spirochetes, which continually change their antigenic
surface components
96
leptospira
l interrogans: alludes to the fact that one end of the spirochete
is hooked in a manner reminiscent of a question mark. This thin, pathogenic spirochete is an obligate
aerobe that is highly motile by means of two axial filaments,
each of which is anchored at one end.
97
leptospirosis
Humans contract the zoonotic disease leptospirosis through direct contact with the
urine of infected animals or indirectly via contact with the
spirochetes in contaminated streams, lakes, or moist soil,
environments in which the organisms can remain viable for
six weeks or more. Person-to-person spread has not been
observed.
98
leptospira in the body
After Leptospira gains initial access to the body through
invisible cuts and abrasions in the skin or mucous membranes,
it corkscrews its way through these tissues. It then
travels via the bloodstream throughout the body, including
the central nervous system, damaging cells lining the
small blood vessels and triggering fever and intense pain.
Infection may lead to hemorrhaging and to liver and kidney
dysfunction. Eventually, the bacteremia resolves, and the
spirochetes are found only in the kidneys. As the disease
progresses, spirochetes are excreted in urine
99
vibrios
- slightly curved bcteria
- The more important pathogenic vibrios of
humans are in the genera Vibrio, Campylobacter, and Helicobacter.
100
vibrio genus structure
- Gram-negative, slightly curved
bacilli
- Vibrio shares many characteristics with enteric
bacteria, such as Escherichia and Salmonella, including O polysaccharide
antigens
- polar flagellum
- The bacterium appears to vibrate
when moving—giving rise to the genus name.
101
vibrio vs enteric bacteria
- O polysaccharide antigens
- Vibrio is oxidase positive and has a polar flagellum,
unlike enteric bacteria, which are oxidase negative and have peritrichous flagella
102
vibrio env
Vibrio lives naturally in estuarine and marine environments
| worldwide. It prefers warm, salty, and alkaline water
103
cholera transmission
Humans become infected with Vibrio cholerae by ingesting
contaminated food and water. Cholera is most frequent in communities
with poor sewage and water treatment.
104
vibrio cholerae in the body
After entering
the digestive system, Vibrio is confronted with the inhospitable
acidic environment of the stomach. Most cells die, which is why
a high inoculum—at least 10^8
cells—is typically required for the
disease to develop.
- Recent research indicates that only the environment within
a human body activates Vibrio virulence genes. Thus, Vibrio shed
in feces is more virulent than its counterparts in the environment.
105
cholera symptoms
Although cholera infections may be asymptomatic or cause
mild diarrhea, some result in rapid, severe, and fatal fluid and
electrolyte loss. Symptoms usually begin two to three days following
infection, with explosive watery diarrhea and vomiting.
As the disease progresses, the colon is emptied, and the stool
becomes increasingly watery, colorless, and odorless. The stool,
which is typically flecked with mucus, is called rice-water stoo.
106
v cholerae virulence factor
The most important virulence factor of V. cholerae is a potent
exotoxin called cholera toxin, which is composed of five identical
B subunits and a single A subunit.
107
action of cholera toxin
1 One of the B subunits binds to a glycolipid receptor in the
cytoplasmic membrane of an intestinal epithelial cell.
2 The A subunit is cleaved, and a portion (called A1) enters
the cell’s cytosol.
3 A1 acts as an enzyme that activates adenylate cyclase (AC).
4 Activated AC enzymatically converts ATP into cyclic AMP
(cAMP).
5 cAMP stimulates the active secretion of excess amounts of
electrolytes (sodium, chlorine, potassium, and bicarbonate
ions) from the cell.
6 Water follows the movement of electrolytes from the cell
and into the intestinal lumen via osmosis.
108
Severe fluid and electrolyte losses result in
dehydration,
metabolic acidosis (decreased pH of body fluids) due
to loss of bicarbonate ions, hypokalemia, and hypovolemic
shock caused by reduced blood volume in the body. These conditions can produce muscle cramping, irregularities in
heartbeat, kidney failure, and coma. Death may occur within
hours of onset
109
cholera diagnosis
diagnosis is usually
based on the characteristic diarrhea. Vibrio can be cultured
on many laboratory media designed for stool cultures, but clinical
specimens must be collected early in the disease (before the
volume of stool dilutes the number of cells) and inoculated
promptly because Vibrio is extremely sensitive to drying
110
cholera treatment
Health care providers must promptly treat cholera patients
with fluid and electrolyte replacement before hypovolemic
shock ensues. Antimicrobial drugs are not as important
as with many other bacterial diseases because they are lost in
the watery stool; nevertheless, they may reduce the production
of exotoxin and ameliorate the symptoms.
111
cholera prevention
adequate sewage and
| water treatment
112
other diseases of vibrio
Vibrio parahaemolyticus causes choleralike
gastroenteritis following ingestion of shellfish harvested
from contaminated estuaries; fortunately, only rarely is it severe
enough to be fatal. Typically the disease is characterized by a
self-limiting, explosive diarrhea accompanied by headache,
nausea, vomiting, and cramping for 72 hours.
V. vulnificus is responsible for septicemia
(blood poisoning) following consumption of contaminated
shellfish and for infections resulting from the washing of
wounds with contaminated seawater. Wound infections are
characterized by swelling and reddening at the site of infection
and are accompanied by fever and chills.
113
campylobacter jejuni
most common cause of bacterial gastroenteritis in the United
| States; zoonotic
114
campylobacter jejuni
Like Vibrio, it is Gram negative, slightly curved, oxidase
| positive, and motile by means of polar flagella. comma shaped.
115
campylobacter transmission
Humans acquire the
bacterium by consuming food, milk, or water contaminated w/ infected animal feces. The most common source of infection
is contaminated poultry
116
c jejuni symptoms
C. jejuni infections commonly produce
malaise, fever, abdominal pain, and bloody and frequent
diarrhea—10 or more bowel movements per day are not uncommon.
The disease is self-limiting; as bacteria are expelled
from the intestinal tract, the symptoms abate.
117
helicobacter pylori
a slightly helical,
highly motile bacterium that colonizes the stomachs of its
hosts.
- causes gastritis and most peptic ulcers
- The portal of entry for H. pylori is the mouth. Studies have
shown that H. pylori in feces on the hands, in well water, or
on fomites may infect humans.
118
peptic ulcers
erosions of the mucous membrane of
the stomach or of the initial portion of the small intestine—
is accepted as fact
119
h pylori virulence factor
has urease, an enzyme that degrades urea, which
is present in gastric juice, to produce highly alkaline ammonia,
which neutralizes stomach acid.
120
ulcer treatment
2 antimicrobial drugs + drugs that inhibit diarrhea and acid production, allowing the stomach lining to regenerate
121
h pylori prevntion
Prevention of infection involves
good personal hygiene, adequate sewage treatment, water purification,
and proper food handling.
122
h pylori ulcer process
1. Bacteria invade mucus and attach to
gastric epithelial cells.
2. Helicobacter, its toxins, and inflammation
cause the layer of mucus to become thin, allowing
3. Gastric acid destroys epithelial cells and
underlying tissue.
