Transcript Document 7170025

Septicemia, bacteremia, “bacteria in the
blood”
500M cases in United States/annum
25% mortality rate
10% of patients with sepsis die of
underlying disease or comorbidity
13th leading cause of death in the United
States
Cost 5-10 billion in annual healthcare
expenditures
50% of all cases of sepsis are caused by gram
negative rods
other etiologies include:
CNS
Staphylococcus aureus
Enterococcus sp
Fungi (yeast)
The numbers of sepsis are predicted to
increase:
larger numbers of immunocompromised
patients
more frequent use of invasive procedures or
devices
greater availability of life-sustaining
technology
higher infection rates of antibiotic resistant
bacteria
increase proportion of patients at the
extremes of age
Among hospitalized in non-coronary intensive
care units, sepsis has been reported to be the
most common cause of death.
The term systemic inflammatory response
syndrome (SIRS)was developed to imply a
clinical response from a non-specific etiology.
SIRS is defined as two or more of the
following:
temperature above 38 C or below 36 C
heart rate above 90 beats/minute
respiratory rate above 20/minute P CO2 less than
32 mm Hg
white blood count above 12M or below 4M
cells/mm3
presence of more than 10% immature neutrophils
A severe form of gangrene (tissue
death) usually caused by Clostridium
perfringens (see also necrotizing
subcutaneous infection). It can also be
from Group A Streptococcus.
Staphlyococcus aureus and Vibrio
vulnificus can also cause similar
infections.
Gas gangrene occurs as a result of
infection by Clostridium bacteria.
Under anaerobic (low oxygen)
conditions, produce toxins that cause
the tissue death and associated
symptoms.
Gas gangrene generally occurs
at the site of trauma or a recent
surgical wound.
Symptoms
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moderate to severe pain around a skin
injury
progressive swelling around a skin
injury
moderate to high fever
skin color initially pale, later dusky
progressing to dark red or purple
Vesicle (blister) formation, coalescent
(combine into large blisters)
blisters filled with brown-red fluid
drainage from the tissues, foulsmelling brown-red or bloody fluid
(serosanguineous discharge)
increased heart rate (tachycardia)
sweating
subcutaneous emphysema (air under
the skin)
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Treatment
◦ Prompt surgical removal of dead,
damaged, and infected tissue
(debridement) is necessary. Amputation
of an arm or leg may be indicated to
control the spread of infection.
◦ Antibiotics, preferably penicillin-type,
should be given. Initially, this is given
intravenously (through a vein).
Analgesics may be required to control
pain. Hyperbaric oxygen has been tried
with varying degrees of success.
◦ Hyperbaric treatment
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Prognosis
◦ Gas gangrene is progressive and
often lethal. Immediate medical
attention is required.
Yersina pestis is the causative
agent.
Three clinical manifestations:
Pneumonic
Septicemic
Bubonic
In early stages of bubonic there is
fever, delirium, and swelling of
lymph nodes. Septicemia develops
and cause hemorragic blackened
lesion therefore black death
Plague is transmitted among
rodents and to humans by flea bite
or ingestion of the feces of fleas.
It can also be transmitted human
to human when a plague victim
develops pneumonia and spreads
infected droplets by coughing.
An epidemic may be started this
way.
Symptoms
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Sudden onset of high fever
Chills
General discomfort, uneasiness, or
ill feeling (malaise)
Muscular pains
Severe headache
Smooth, oval, reddened, painful
swellings of swollen lymph glands
called buboes in the groin, armpits,
neck, or elsewhere in the body. Pain
may occur in the area before the
swelling; the most common area is
in the groin
Seizures
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Treatment
◦ Immediate treatment with
antibiotics such as streptomycin,
chloramphenicol, or tetracycline
is indicated. Oxygen, intravenous
fluids, and respiratory support are
additional treatments.
◦ Patients with pneumonic plague
are strictly isolated from other
patients.
◦ People who have had contact
with anyone infected by
pneumonic plague are observed
closely and are given antibiotics
as a preventive measure.
Prognosis
◦ Half of bubonic plague
victims die if not treated, and
almost all victims of
pneumonic plague die if not
treated. Treatment reduces
the death rate to 5%
Borrelia burgdorferi is a species of Gram negative
bacteria of the spirochete class of the genus
Borrelia. B. burgdorferi is predominant in North
America, but also exists in Europe, and
is the agent of Lyme disease.
It is a zoonotic, vector-borne disease transmitted
by ticks and is named after the researcher Willy
Burgdorfer who first isolated the bacterium in
1982.
B. burgdorferi is one of the few pathogenic
bacteria that can survive without iron, having
replaced all of its iron-sulfur cluster enzymes with
enzymes that use manganese, thus avoiding the
problem many pathogenic bacteria face in
acquiring iron.
Borrelia burgdorferi infections have been
linked to non-Hodgkin lymphomas.
Lyme disease is diagnosed based on
symptoms, objective physical findings
(such as erythema migrans, facial palsy,
or arthritis), and a history of possible
exposure to ticks. Validated laboratory
tests can be very helpful but are not
generally recommended when a patient
has erythema migrans.
The Lyme disease bacterium, Borrelia
burgdorferi, normally lives in mice,
squirrels and other small animals.
It is transmitted among these animals
and to humans through the bites of
certain species of ticks. In the
northeastern and north-central
United States, the black-legged tick
(or deer tick, Ixodes scapularis)
transmits Lyme disease.
Antibiotics commonly used for oral treatment
include doxycycline, amoxicillin, or cefuroxime
axetil. Patients with certain neurological or
cardiac forms of illness may require intravenous
treatment with drugs such as ceftriaxone or
penicillin.
Patients treated with antibiotics in the early stages
of the infection usually recover rapidly and
completely.
A few patients, particularly those diagnosed with
later stages of disease, may have persistent or
recurrent symptoms.
Scientists have concluded that longer courses of
antibiotic treatment are not beneficial.
Longer courses of antibiotics have been linked to
serious complications, including death.
Brucellosis is an infectious disease caused
by the bacteria of the genus Brucella.
These bacteria are primarily passed among
animals, and they cause disease in many
different vertebrates.
Various Brucella species affect sheep, goats,
cattle, deer, elk, pigs, dogs, and several other
animals.
Humans become infected by coming in contact
with animals or animal products that are
contaminated with these bacteria.
In humans brucellosis can cause a range of
symptoms that are similar to the flu and may
include fever, sweats, headaches, back pains, and
physical weakness.
Also known as undulating fever (higher at night),
muscle aches, enlarged spleen and lymph nodes
Severe infections of the central nervous systems
or lining of the heart may occur. Brucellosis can
also cause long-lasting or chronic symptoms that
include recurrent fevers, joint pain, and fatigue.
Mainly an infection of livestock.
Human cases are reported as:
60% butchers, meat packers
30% ranchers and hunters
10% people who consume
unpasteurized dairy products
Brucellosis is diagnosed in a
laboratory by finding Brucella
organisms in samples of
blood or bone marrow.
Also, blood tests can be done to
detect antibodies against the
bacteria.
If this method is used, two blood
samples should be collected 2 weeks
apart.
Treatment can be difficult. Doctors can
prescribe effective antibiotics.
Usually, doxycycline and rifampin are used
in combination for 6 weeks to prevent
reoccuring infection.
Depending on the timing of treatment and
severity of illness, recovery may take a few
weeks to several months.
Mortality is low (<2%), and is usually associated
with endocarditis.
Francisella tularensis, the organism
that causes tularemia, is one of the
most infectious pathogenic
bacteria known, requiring
inoculation or inhalation of as few
as 10 organisms to cause disease.
It is considered to be a dangerous
potential biological weapon because of
its extreme infectivity, ease of
dissemination, and substantial capacity
to cause illness and death.
Francisella tularensis is a hardy non-
spore forming organism that is capable
of surviving for weeks at low
temperatures in water, moist soil, hay,
straw or decaying animal carcasses.
Tularemia is a zoonosis. Natural reservoirs
include small mammals such as voles,
mice, water rats, squirrels, rabbits and
hares.
Naturally acquired human infection occurs
through a variety of mechanisms such as:
bites of infected arthropods; handling
infectious animal tissues or fluids; direct
contact or ingestion of contaminated
water, food, or soil; and inhalation of
infective aerosols.
F. tularensis is so infective that
examining an open culture
plate can cause infection.
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Humans can contract
tularemia in the following
ways:
direct contact with an
infected animal or carcass via
broken skin
the bite of an infected flea,
deer fly, or tick
ingesting infected meat (rare)
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red spot on the skin,
enlarging to an ulcer
enlarged lymph nodes of
groin or armpits
headache
muscle pains
possible conjunctivitis
shortness of breath
fever
chills
sweating
weight loss
joint stiffness
◦ The goal of treatment is to
eliminate the infection with
antibiotic therapy.
Streptomycin and
tetracycline are commonly
used in this infection.
◦ Tularemia is fatal in about
5% of untreated cases and
in less than 1% with
treatment.
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Complications
◦ meningitis
◦ pneumonia
◦ pericarditis
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Cat scratch disease is an
infectious illness caused
by the bacteria
Bartonella, believed to be
transmitted by cat
scratches, bites, or
exposure to cat saliva.
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More than 40,000 cases
occur annually in the US
Symptoms
◦ A history of contact with a cat
◦ Papule or pustule at site of
injury (inoculation), usually
the first sign
◦ Swelling of the lymph nodes
(adenopathy) occurs in the
area near where the skin was
infected (bitten, scratched,
etc.)
◦ Fever in approximately one
third of patients
◦ Fatigue
◦ Malaise
◦ Headache
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Treatment
◦ Generally, cat scratch
disease is not serious.
Treatment, other than
reassurance, is not usually
recommended. However, in
severe cases treatment with
antibiotics can be helpful.
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Typhus is a rickettsial disease caused
by one of two organisms, Rickettsia
prowazekii (epidemic typhus and Brill
disease) and Rickettsia typhi (murine
or endemic typhus). Epidemic typhus
and Brill disease are uncommon in
the United States.
Murine typhus occurs in the
southeastern and southern states.
There are less than 100 cases per
year. Murine typhus is a milder form
and is seldom fatal (less than 2%).
It is frequently seen in the summer
and fall and typically lasts two to
three weeks. Risk factors for murine
typhus include exposure to rat fleas
or rat feces, or exposure to other
animals (such as cats, opossums,
raccoons, skunks, and rats).
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Epidemic typhus occurs in
poor hygienic conditions
(which is why it is sometimes
called "jail fever"), usually
when the temperature is cold.
It is spread by lice. Although
very rare in the United States,
it has sometimes been spread
by the lice and fleas of flying
squirrels.
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severe headache
fever, high (104 degrees Fahrenheit)
cough in 70% of patients
arthralgia and myalgia, (muscle pain)
severe
chills
falling blood pressure
stupor
delirium
rash that begins on chest and spreads
to rest of trunk and extremities, but not
to palms and soles
early rash is faint and rose colored and
fades with pressure (Later the lesions
become dull, red, and do not fade.
People with severe typhus may also
develop petechiae.)
lights appear very bright, and exposure
to light may hurt the eyes
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Treatment
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Prognosis
◦ The goal of treatment is to
eliminate the infection and to treat
the symptoms with antibiotics
(such as tetracycline, doxycycline,
or chloramphenicol). For epidemic
typhus, intravenous fluids and
oxygen may be necessary to help
stabilize the patient.
◦ Without treatment death may
occur in 10 to 60% of patients with
epidemic typhus. Patients over the
age of 60 have the highest risk of
death. With timely antibiotic
therapy, the affected person is
expected to recover completely.
◦ Less than 2% of untreated patients
with murine typhus may die, and
appropriate antibiotic therapy will
cure virtually all patients.
An infectious disease caused
by Rickettsia rickettsii
transmitted to humans by the
bite of ticks.
Symptoms
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fever
chills
incubation period of 2 to 14 days
severe headache
muscle pain
mental confusion
rash, first appearing on wrists and
ankles, then spreading to most of
the body, usually starts a few days
after fever starts; up to 20% of
people do not get a rash
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Chagas disease is caused by
Trypanosoma cruzi, a
parasite related to the African
trypanosome that causes
sleeping sickness.
It is spread by reduvid bugs
and is one of the major
health problems in South
America, where 20 million
people are infected.
Due to immigration,
approximately 500,000
people in the United States
are believed to be infected.
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Chagas disease has two phases – acute and
chronic. The acute phase may have no
symptoms or have very mild symptoms.
Symptoms of the acute phase include
swelling and reddening at the site of
infection (where the blood-sucking insect
caused the initial infection).
This may be followed by swelling of one
eye. Lymph nodes that drain the area of
the insect bite may become swollen. As the
parasite spreads from the bite site, the
patient develops fever, malaise, and
generalized swelling of the lymph nodes.
The liver and spleen may become enlarged.
The disease goes into remission after the
acute phase and may become chronic with
no further symptoms for many years. When
symptoms finally develop, they appear as
cardiac disease (cardiomyopathy) and
digestive abnormalities.
Patients may develop
congestive heart failure.
Swallowing difficulties may
be the first symptom of
digestive disturbances and
may lead to malnutrition.
Patients who have parasitic
infection of the colon may
experience abdominal pain and
constipation. Death is usually
caused by heart disease.
◦ history of exposure in an area
where Chagas disease is
known to occur
◦ swollen red area at site of
previous insect bite
◦ enlarged lymph nodes
◦ swelling of one eye
◦ fever
◦ irregular heartbeat
(arrhythmia)
◦ rapid heartbeat (tachycardia)
◦ swallowing difficulties
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Treatment
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Prognosis
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The acute phase should be treated.
Benznidazole has been shown to be
effective. Experimental treatment may
include nifurtimox. Treating the chronic
phase with antibiotics is not helpful.
Instead, the symptoms of heart and
intestinal disease should be treated.
Approximately 30% of infected and
untreated people will develop chronic
or symptomatic Chagas disease. It may
take more than twenty years from the
time of the original infection to develop
heart or digestive problems.
Abnormal heart rhythms (arrythmias,
ventricular tachycardia) may cause
sudden death. Once congestive heart
failure develops, death usually occurs
within several years.
Leishmania are tiny protozoa. Their
parasitic life cycle includes the
sandfly and an appropriate host.
Humans are one of those hosts.
Leishmania infection can cause
skin disease (called cutaneous
leishmaniasis).
It can affect the mucous membranes
with a wide range of appearance, most
frequently ulcers. It may cause skin
lesions that resemble those of other
diseases including cutaneous
tuberculosis, syphilis, leprosy, skin
cancer (basal cell carcinoma), and
fungus infections.
Symptoms
◦ history of exposure to the bite of
sandflies
◦ history in being in an area known for
leishmaniasis
◦ Systemic illness (visceral
leishmaniasis)
◦ fever, persistent, long duration
(weeks), may cycle irregularly
◦ night sweats
◦ fatigue
◦ weakness
◦ appetite loss (anorexia)
◦ weight loss
◦ abdominal discomfort, vague
◦ vomiting (children)
◦ diarrhea (children)
◦ cough (children)
◦ skin, scaly
◦ skin, gray, dark, ashen
◦ hair, thinning
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Skin disease (cutaneous
leishmaniasis)
Symptoms on the skin
include:
◦ macule or papule,
erythematous
◦ skin ulcer, forms at site of
original lesion
◦ ulcer heals very slowly over
a matter of months
◦ smaller lesions may form
around the ulcer (satellite
lesions)
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Treatment
◦ Antimony-containing compounds are
the principal medications used to treat
leishmaniasis. These include:
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meglumine antimonate
sodium stibogluconate
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pentamidine
amphotericin B
Miltefosine
◦ Other drugs that may be used include:
◦ Plastic surgery may be required to
correct disfigurement by destructive
facial lesions (mucocutaneous
leishmaniasis). Removal of the spleen
(splenectomy) may be required in
drug-resistant cases (visceral
leishmaniasis).
Causes and risks
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Schistosoma infections are contracted
through contact with contaminated
water. The parasite in its infective
stages is called a cercaria. It swims
freely in open bodies of water.
On contact with humans, the parasite
burrows into the skin, matures into
another larval stage (schistosomula),
then migrates to the lungs and liver
(where it matures into the adult form).
The adult worm then migrates to the
anatomic area of its preference,
depending on which species is involved.
Likely areas include the bladder,
rectum, intestines, liver, portal venous
system, spleen, and lungs.
Schistosomiasis is not usually found in
the United States. However, it is
prevalent in many tropical or
subtropical areas, and it is a common
illness thought to affect more than 200
million people.
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Symptoms
◦ Symptoms vary with the species of
worm and the phase of infection.
◦ Initial invasion of the skin may cause
itching and a rash (swimmer's itch).
◦ Heavy infestation may cause fever,
chills, lymph node enlargement, and
liver and spleen enlargement.
◦ Urinary symptoms may include
frequency, painful urination (dysuria),
and blood in urine (hematuria).
◦ Intestinal symptoms include
abdominal pain and diarrhea (which
may be bloody).
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Treatment
◦ Praziquantel
◦ With acute infection,
corticosteroids may be given
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Prognosis
◦ Treatment before significant
damage or severe
complications usually
produces good results.
Toxoplasmosis is caused by the
protozoan parasite Toxoplasma
gondii. In the United States it is
estimated that 22.5% of the
population 12 years and older
have been infected with
Toxoplasma.
In various places throughout the
world, it has been shown that up
to 95% of some populations have
been infected with Toxoplasma.
Infection is often highest in
areas of the world that have hot,
humid climates and lower
altitudes.
Toxoplasmosis is not passed
from person-to-person,
except in instances of
mother-to-child
(congenital) transmission
and blood transfusion or
organ transplantation.
People typically become
infected by three principal
routes of transmission.
Foodborne transmission
The tissue form of the parasite (a
microscopic cyst consisting of
bradyzoites) can be transmitted to
humans by food. People become
infected by:
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Eating undercooked, contaminated
meat (especially pork, lamb, and
venison)
Accidental ingestion of undercooked,
contaminated meat after handling it and
not washing hands thoroughly
(Toxoplasma cannot be absorbed
through intact skin)
Eating food that was contaminated by
knives, utensils, cutting boards, or
other foods that had contact with raw,
contaminated meat
Cats play an important role in the spread of toxoplasmosis.
They become infected by eating infected rodents, birds,
or other small animals. The parasite is then passed in
the cat's feces in an oocyst form, which is microscopic.
Kittens and cats can shed millions of oocysts in their feces
for as long as 3 weeks after infection. Mature cats are
less likely to shed Toxoplasma if they have been
previously infected. A Toxoplasma-infected cat that is
shedding the parasite in its feces contaminates the litter
box. If the cat is allowed outside, it can contaminate the
soil or water in the environment as well.
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People can accidentally swallow the oocyst form of
the parasite. People can be infected by:
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Accidental ingestion of oocysts after cleaning a cat's
litter box when the cat has shed Toxoplasma in its
feces
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Accidental ingestion of oocysts after touching or
ingesting anything that has come into contact with a
cat's feces that contain Toxoplasma
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Accidental ingestion of oocysts in contaminated soil
(e.g., not washing hands after gardening or eating
unwashed fruits or vegetables from a garden)
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Drinking water contaminated with the Toxoplasma
parasite
People can accidentally swallow the
oocyst form of the parasite. People
can be infected by:
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Accidental ingestion of oocysts after
cleaning a cat's litter box when the
cat has shed Toxoplasma in its
feces
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Accidental ingestion of oocysts after
touching or ingesting anything that
has come into contact with a cat's
feces that contain Toxoplasma
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Accidental ingestion of oocysts in
contaminated soil (e.g., not washing
hands after gardening or eating
unwashed fruits or vegetables from
a garden)
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Drinking water contaminated with
the Toxoplasma parasite
Most healthy people recover from
toxoplasmosis without treatment.
Persons who are ill can be treated
with a combination of drugs such as
pyrimethamine and sulfadiazine, plus
folinic acid.
Pregnant women, newborns, and infants
can be treated, although the parasite
is not eliminated completely. The
parasites can remain within tissue
cells in a less active phase; their
location makes it difficult for the
medication to completely eliminate
them.
Persons with ocular toxoplasmosis are
sometimes prescribed medicine to treat
active disease by their ophthalmologist.
Whether or not medication is
recommended depends on the size of
the eye lesion, the location, and the
characteristics of the lesion (acute
active, versus chronic not progressing).
Persons with compromised immune
systems need to be treated until they
have improvement in their condition.
For AIDS patients, continuation of
medication for the rest of their lives
may be necessary, or for as long as they
are immunosuppressed.